HERBARIUM

In botany, a herbarium (plural: herbaria ) – sometimes known by the Anglicized term herbar – is a collection of preserved plant specimens. These specimens may be whole plants or plant parts: these will usually be in a dried form, mounted on a sheet, but depending upon the material may also be kept in alcohol or other preservative. The same term is often used in mycology to describe an equivalent collection of preserved fungi, otherwise known as a fungarium . The term can also refer to the building where the specimens are stored, or the scientific institute that not only stores but researches these specimens. The specimens in a herbarium are often used as reference material in describing plant taxa ; some specimens may be types . A xylarium is a herbarium specialising in specimens of wood. A hortorium (as in the Liberty Hyde Bailey Hortorium) is one specialising in preserved specimens of cultivated plant. Specimen preservation Preparing a plant for mounting To preserve their form and color, plants collected in the field are spread flat on sheets of newsprint and dried, usually in a plant press, between blotters or absorbent paper. The specimens, which are then mounted on sheets of stiff white paper, are labeled with all essential data, such as date and place found, description of the plant, altitude, and special habitat conditions. The sheet is then placed in a protective case. As a precaution against insect attack, the pressed plant is frozen or poisoned and the case disinfected. Certain groups of plants are soft, bulky, or otherwise not amenable to drying and mounting on sheets. For these plants, other methods of preparation and storage may be used. For example, conifer cones and palm fronds may be stored in labeled boxes. Representative flowers or fruits may be pickled in formaldehyde to preserve their three-dimensional structure. Small specimens, such as mosses and lichens, are often air-dried and packaged in small paper envelopes. No matter the method of preservation, detailed information on where and when the plant was collected, habitat, color (since it may fade over time), and the name of collector is usually included. Collections management A large herbarium may have hundreds of cases filled with specimens. Most herbaria utilize a standard system of organizing their specimens into herbarium cases. Specimen sheets are stacked in groups by the species to which they belong and placed into a large lightweight folder that is labelled on the bottom edge. Groups of species folders are then placed together into larger, heavier folders by genus. The genus folders are then sorted by taxonomic family according to the standard system selected for use by the herbarium and placed into pigeonholes in herbarium cabinets. Locating a specimen filed in the herbarium requires knowing the nomenclature and classification used by the herbarium. It also requires familiarity with possible name changes that have occurred since the specimen was collected, since the specimen may be filed under an older name. Modern herbaria often maintain electronic databases of their collections. Many herbaria have initiatives to digitize specimens to produce a virtual herbarium . These records and images are made publicly accessible via the Internet when possible. Uses Herbaria are essential for the study of plant taxonomy , the study of geographic distributions, and the stabilizing of nomenclature. Thus it is desirable to include in a specimen as much of the plant as possible (e.g., flowers, stems, leaves, seed, and fruit). Linnaeus' herbarium now belongs to the Linnean Society in England. Specimens housed in herbaria may be used to catalogue or identify the flora of an area. A large collection from a single area is used in writing a field guide or manual to aid in the identification of plants that grow there. With more specimens available, the author of the guide will better understand the variability of form in the plants and the natural distribution over which the plants grow. Herbaria also preserve a historical record of change in vegetation over time. In some cases, plants become extinct in one area, or may become extinct altogether. In such cases, specimens preserved in an herbarium can represent the only record of the plant's original distribution. Environmental scientists make use of such data to track changes in climate and human impact. Many kinds of scientists use herbaria to preserve voucher specimens; representative samples of plants used in a particular study to demonstrate precisely the source of their data. They may also be a repository of viable seeds for rare species.[1] Largest herbaria The Swedish Museum of Natural History (S) . Main article: List of herbaria Many universities, museums, and botanical gardens maintain herbaria. Herbaria have also proven very useful as sources of plant DNA for use in taxonomy and molecular systematics . The largest herbaria in the world, in approximate order of decreasing size, are: Muséum National d'Histoire Naturelle (P) (Paris, France) New York Botanical Garden (NY) (Bronx, New York, USA) Komarov Botanical Institute (LE) (St. Petersburg, Russia) Royal Botanic Gardens (K) (Kew, England, UK) Conservatoire et Jardin botaniques de la Ville de Genève (G) (Geneva, Switzerland) Missouri Botanical Garden (MO) (St. Louis, Missouri, USA) British Museum of Natural History (BM) (London, England, UK) Harvard University (HUH) (Cambridge, Massachusetts, USA) Swedish Museum of Natural History (S) (Stockholm, Sweden) United States National Herbarium (Smithsonian Institution ) (US) (Washington, DC, USA) Nationaal Herbarium Nederland (L) (Leiden, the Netherlands) Université Montpellier (MPU) (Montpellier, France) Université Claude Bernard (LY) (Villeurbane Cedex, France) Herbarium Universitatis Florentinae (FI) (Florence, Italy) National Botanic Garden of Belgium (BR) (Meise, Belgium) University of Helsinki (H) (Helsinki, Finland) Botanischer Garten und Botanisches Museum Berlin- Dahlem, Zentraleinrichtung der Freien Universität Berlin (B) (Berlin, Germany) The Field Museum (F) (Chicago, Illinois, USA) University of Copenhagen (C) (Copenhagen, Denmark) Chinese National Herbarium, (Chinese Academy of Sciences) (PE) (Beijing, People's Republic of China) University and Jepson Herbaria (UC/JEPS) (Berkeley, California, USA) Herbarium Bogoriense (BO) (Bogor, West Java, Indonesia) Royal Botanic Garden, Edinburgh (E) (Edinburgh, Scotland, UK) See also Herbal List of herbaria Plant collecting Plant taxonomy Systematics Virtual herbarium External links Wikimedia Commons has media related to: Herbarium For links to a specific herbarium or institution, see the List of herbaria Index Herbariorum Linnean Herbarium Lamarck's Herbarium (online database with 20.000 sheets in HD) French Herbaria Network

NOMENCULATURE

Nomenclature is a term that applies to either a list of names or terms, or to the system of principles, procedures and terms related to naming - which is the assigning of a word or phrase to a particular object or property. [1][clarification needed] The principles of naming vary from the relatively informal conventions of everyday speech to the internationally- agreed principles, rules and recommendations that govern the formation and use of the specialist terms used in scientific and other disciplines. Naming "things" is a part of our general communication using words and language: it is an aspect of everyday taxonomy as we distinguish the objects of our experience, together with their similarities and differences, which we identify , name and classify. The use of names, as the many different kinds of nouns embedded in different languages, connects nomenclature to theoretical linguistics, while the way we mentally structure the world in relation to word meanings and experience relates to the philosophy of language . Onomastics, the study of proper names and their origins, includes: anthroponymy , concerned with human names, including personal names, surnames and nicknames; toponymy the study of place names; and etymology , the derivation, history and use of names as revealed through comparative and descriptive linguistics . The scientific need for simple, stable and internationally- accepted systems for naming objects of the natural world has generated many formal nomenclatural systems. Probably the best known of these nomenclatural systems are the five codes of biological nomenclature that govern the Latinized scientific names of organisms. Definition & criteria Nomenclature is a system of words used in particular discipline. It is used in respect of giving names systematically following the rules to all known living.It is applied to many chemical components, mainly used in carbon and hydrogen components. Etymology The word nomenclature is derived from the Latin nomen - name, calare - to call; the Ancient Greek ονοματοκλήτωρ from όνομα or onoma meaning name and equivalent to the Old English nama and Old High German namo which is derived from Sanskrit nama. The Latin term nomenclatura refers to a list of names as does the word nomenclator which can also indicate a provider or announcer of names. Onomastics and nomenclature Main article: Onomastics The study of proper names is known as onomastics,[2] which has a wide-ranging scope encompassing all names, all languages, all geographical and cultural regions. The distinction between onomastics and nomenclature is not readily clear: onomastics is an unfamiliar discipline to most people and the use of nomenclature in an academic sense is also not commonly known. Although the two fields integrate, nomenclature concerns itself more with the rules and conventions that are used for the formation of names.[citation needed] Naming as a cultural activity Main article: Philosophy of language Names provide us with a way of structuring and mapping the world in our minds so, in some way, they mirror or represent the objects of our experience. Names, words, language and meaning Main articles: Proper name (philosophy) and Semantics Elucidating the connections between language (especially names and nouns), meaning and the way we perceive the world has provided a rich field of study for philosophers and linguists. Relevant areas of study include: the distinction between proper names and proper nouns;[3] and the relationship between names, [4] their referents, [5] meanings (semantics), and the structure of language. Folk taxonomy Main articles: Folk taxonomy and Binomial nomenclature Modern scientific taxonomy has been described as "basically a Renaissance codification of folk taxonomic principles."[6] Formal scientific nomenclatural and classification systems are exemplified by biological classification. All classification systems are established for a purpose. The scientific classification system anchors each organism within the nested hierarchy of internationally-accepted classification categories. Maintenance of this system involves formal rules of nomenclature and periodic international meetings of review. This modern system evolved from the folk taxonomy of pre-history. [7] Folk taxonomy can be illustrated through the Western tradition of horticulture and gardening. Unlike scientific taxonomy, folk taxonomies serve many purposes. Examples in horticulture would be the grouping of plants, and naming of these groups, according to their properties and uses: annuals, biennials and perennials (nature of life cycle); vegetables , fruits, culinary herbs and spices (culinary use); herbs, trees and shrubs (growth habit); wild and cultivated plants (whether they are managed or not), and weeds (whether they are considered to be a nuisance or not) and so on. Folk taxonomy is generally associated with the way rural or indigenous peoples use language to make sense of and organise the objects around them. Ethnobiology frames this interpretation through either "utilitarianists" like Bronislaw Malinowski who maintain that names and classifications reflect mainly material concerns, and "intellectualists" like Claude Lévi-Strauss who hold that they spring from innate mental processes.[8] The literature of ethnobiological classifications was reviewed in 2006.[9] Folk classification is defined by the way in which members of a language community name and categorize plants and animals whereas ethnotaxonomy refers to the hierarchical structure, organic content, and cultural function of biological classification that ethnobiologists find in every society around the world. [10] Ethnographic studies of the naming and classification of animals and plants in non- Western societies have revealed some general principles that indicate pre- scientific man’s conceptual and linguistic method of organising the biological world in a hierarchical way. [11][12][13][14] Such studies indicate that the urge to classify is a basic human instinct.[15][16] in all languages natural groups of organisms are distinguished (present- day taxa) these groups are arranged into more inclusive groups or ethnobiological categories in all languages there are about five or six ethnobiological categories of graded inclusiveness these groups (ethnobiological categories) are arranged hierarchically, generally into mutually exclusive ranks the ranks at which particular organisms are named and classified is often similar in different cultures The levels are — moving from the most to least inclusive: level 1 - "unique beginner" --e.g. plant or animal. A single all- inclusive name rarely used in folk taxonomies but loosely equivalent to an original living thing, a "common ancestor" level 2 - “life form” --------------e.g. tree, bird, grass and fish These are usually primary lexemes (basic linguistic units) loosely equivalent to a phylum or major biological division. level 3 - "generic name" ------e.g. oak, pine, robin, catfish This is the most numerous and basic building block of all folk taxonomies, the most frequently referred to, the most important psychologically, and among the first learned by children. These names can usually be associated directly with a second level group. Like life-form names these are primary lexemes. level 4 - "specific name" ------e.g. white fir, post oak More or less equivalent to species. A secondary lexeme and generally less frequent than generic names. level 5 - "varietal name"--------e.g. baby lima bean, butter lima bean. In almost all cultures objects are named using one or two words equivalent to "kind" (genus) and "particular kind" (species). [6] When made up of two words (a binomial) the name usually consists of a noun (like salt, dog or star) and an adjectival second word that helps describe the first, and therefore makes the name, as a whole, more "specific", for example, lap dog, sea salt, or film star. The meaning of the noun used for a common name may have been lost or forgotten (whelk, elm, lion, shark, pig) but when the common name is extended to two or more words much more is conveyed about the organism's use, appearance or other special properties (sting ray, poison apple, giant stinking hogweed, hammerhead shark). These noun-adjective binomials are just like our own names with a family or surname like Simpson and another adjectival Christian- or forename name that specifies which Simpson, say Homer Simpson. It seems reasonable to assume that the form of scientific names we call binomial nomenclature is derived from this simple and practical way of constructing common names - but with the use of Latin as a universal language. In keeping with the "utilitarianist" view other authors maintain that ethnotaxonomies resemble more a "complex web of resemblances" than a neat hierarchy.

METABOLISM

Metabolism (from Greek: μεταβολή "metabolē", "change" or Greek: μεταβολισμός metabolismos, "outthrow") is the set of chemical reactions that happen in the cells of living organisms to sustain life. These processes allow organisms to grow and reproduce, maintain their structures, and respond to their environments. Metabolism is usually divided into two categories. Catabolism breaks down organic matter, for example to harvest energy in cellular respiration. Anabolism uses energy to construct components of cells such as proteins and nucleic acids. The chemical reactions of metabolism are organized into metabolic pathways , in which one chemical is transformed through a series of steps into another chemical, by a sequence of enzymes . Enzymes are crucial to metabolism because they allow organisms to drive desirable reactions that require energy and will not occur by themselves, by coupling them to spontaneous reactions that release energy. As enzymes act as catalysts they allow these reactions to proceed quickly and efficiently. Enzymes also allow the regulation of metabolic pathways in response to changes in the cell's environment or signals from other cells. The metabolism of an organism determines which substances it will find nutritious and which it will find poisonous. For example, some prokaryotes use hydrogen sulfide as a nutrient, yet this gas is poisonous to animals.[1] The speed of metabolism, the metabolic rate, influences how much food an organism will require, and also affects how it is able to obtain that food. A striking feature of metabolism is the similarity of the basic metabolic pathways and components between even vastly different species. [2] For example, the set of carboxylic acids that are best known as the intermediates in the citric acid cycle are present in all known organisms, being found in species as diverse as the unicellular bacteria Escherichia coli and huge multicellular organisms like elephants.[3] These striking similarities in metabolic pathways are likely due to their early appearance in evolutionary history , and being retained because of their efficacy. [4][5] Key biochemicals Further information: Biomolecule, cell (biology) and biochemistry Structure of a triacylglycerol lipid Most of the structures that make up animals, plants and microbes are made from three basic classes of molecule: amino acids, carbohydrates and lipids (often called fats). As these molecules are vital for life, metabolic reactions either focus on making these molecules during the construction of cells and tissues, or breaking them down and using them as a source of energy, in the digestion and use of food. Many important biochemicals can be joined together to make polymers such as DNA and proteins. These macromolecules are essential. Type of molecule Name of monomer forms Name of polymer forms Examples of polymer forms Amino acids Amino acids Proteins (also called polypeptides) Fibrous proteins and globular proteins Carbohydrates Monosaccharides Polysaccharides Starch, glycogen and cellulose Nucleic acids Nucleotides Polynucleotides DNA and RNA Amino acids and proteins Proteins are made of amino acids arranged in a linear chain and joined together by peptide bonds. Many proteins are the enzymes that catalyze the chemical reactions in metabolism. Other proteins have structural or mechanical functions, such as the proteins that form the cytoskeleton , a system of scaffolding that maintains the cell shape.[6] Proteins are also important in cell signaling, immune responses, cell adhesion, active transport across membranes, and the cell cycle .[7] Lipids Lipids are the most diverse group of biochemicals. Their main structural uses are as part of biological membranes such as the cell membrane, or as a source of energy. [7] Lipids are usually defined as hydrophobic or amphipathic biological molecules that will dissolve in organic solvents such as benzene or chloroform.[8] The fats are a large group of compounds that contain fatty acids and glycerol ; a glycerol molecule attached to three fatty acid esters is a triacylglyceride .[9] Several variations on this basic structure exist, including alternate backbones such as sphingosine in the sphingolipids, and hydrophilic groups such as phosphate in phospholipids. Steroids such as cholesterol are another major class of lipids that are made in cells.[10] Carbohydrates Glucose can exist in both a straight-chain and ring form. Carbohydrates are aldehydes or ketones with many hydroxyl groups that can exist as straight chains or rings. Carbohydrates are the most abundant biological molecules, and fill numerous roles, such as the storage and transport of energy (starch, glycogen ) and structural components (cellulose in plants, chitin in animals).[7] The basic carbohydrate units are called monosaccharides and include galactose, fructose, and most importantly glucose. Monosaccharides can be linked together to form polysaccharides in almost limitless ways.

VERNALISATION

Vernalization (from Latin: vernus, of the spring) is the acquisition of a plant's ability to flower or germinate in the spring by exposure to the prolonged cold of winter. After vernalization, plants have acquired the ability to flower, but they may require additional seasonal cues or weeks of growth before they will actually flower. Many plants grown in temperate climates require vernalization and must experience a period of low winter temperature to initiate or accelerate the flowering process. This ensures that reproductive development and seed production occurs in spring and summer, rather than in autumn.[1] The needed cold is often expressed in chill hours. Typical vernalization temperatures are between 5 and 10 degrees Celsius (40 and 50 degrees Fahrenheit). For many perennial plants, such as fruit tree species, a period of cold is needed to break dormancy, prior to flowering. Many monocarpic annuals and biennials, including some ecotypes of Arabidopsis thaliana [2] and winter cereals such as wheat, must go through a prolonged period of cold before flowering occurs. History of vernalization research In the history of agriculture , farmers observed a traditional distinction between "winter cereals," whose seeds require chilling, and "spring cereals," whose seeds can be sown in spring and flower soon thereafter. [3] The word "vernalization" is a translation of "Jarovization," a word coined by Trofim Lysenko to describe a chilling process he used to make the seeds of winter cereals behave like spring cereals ("Jarovoe" in Russian).[3] Scientists had also discussed how some plants needed cold temperatures to flower, as early as the 18th century, with the German plant physiologist Gustav Gassner often mentioned for his 1918 paper.[3][4] Lysenko's 1928 paper on vernalization and plant physiology drew wide attention due to its practical consequences for Russian agriculture. Severe cold and lack of winter snow had destroyed many early winter wheat seedlings. By treating wheat seeds with moisture as well as cold, Lysenko induced them to bear a crop when planted in spring.[4] Later however, Lysenko inaccurately asserted that the vernalized state could be inherited - i.e., that the offspring of a vernalized plant would behave as if they themselves had also been vernalized and would not require vernalization in order to flower quickly. [5] Early research on vernalization focused on plant physiology; the increasing availability of molecular biology has made it possible to unravel its underlying mechanisms.[5] For example, longer days as well as cold temperatures are required for winter wheat plants to go from the vegetative to the reproductive state; the three interacting genes are called VRN1, VRN2, and FT (VRN3). [6] Due to plant flowering requiring the successful co- operation of several metabolic pathways , computer models that incorporate vernalization have also been made. [7] Vernalization in Arabidopsis thaliana Arabidopsis thaliana rosette before vernalization, with no floral spike Arabidopsis thaliana, also known as "thale cress," is a much-studied model species. In 2000, the entire genome of its five chromosomes was completely sequenced. [8] Some variants, called "winter annuals", require vernalization to flower; others ("summer annuals") do not.[9] The genes that underlie this difference in plant physiology have been intensively studied. [5] The reproductive phase change of A. thalliana occurs by a sequence of two related events: first, the bolting transition (flower stalk elongates), then the floral transition (first flower appears).[10] Bolting is a robust predictor of flower formation, and hence a good indicator for vernalization research.[10] In arabidopsis winter annuals, the apical meristem is the part of the plant that needs to be chilled. Vernalization of the meristem appears to confer competence to respond to floral inductive signals on the meristem. A vernalized meristem retains competence for as long as 300 days in the absence of an inductive signal. [9] Before vernalization, flowering is repressed by the action of a gene called Flowering Locus Controller (FLC).[1] Vernalization activates a gene called Frigida (FRI), which progressively turns off FLC expression over a period of six weeks. Since vernalization also occurs in flc mutants (lacking FLC), vernalization must also activate a non-FLC pathway. [11] A day-length mechanism is also important.

PHOTOPERIODISM

Photoperiodism is the physiological reaction of organisms to the length of day or night. It occurs in plants and animals. Photoperiodism can also be defined as the developmental responses of plants to the relative lengths of the light and dark periods. Here it should be emphasized that photoperiodic effects relate directly to the timing of both the light and dark periods. In plants Many flowering plants use a photoreceptor protein , such as phytochrome or cryptochrome , to sense seasonal changes in night length, or photoperiod, which they take as signals to flower. In a further subdivision, obligate photoperiodic plants absolutely require a long or short enough night before flowering, whereas facultative photoperiodic plants are more likely to flower under the appropriate light conditions, but will eventually flower regardless of night length. Photoperiodic flowering plants are classified as long- day plants or short-day plants, though the regulatory mechanism is actually governed by hours of darkness, not the length of the day. Modern biologists believe [citation needed] that it is the coincidence of the active forms of phytochrome or cryptochrome, created by light during the daytime, with the rhythms of the circadian clock that allows plants to measure the length of the night. Other than flowering, photoperiodism in plants includes the growth of stems or roots during certain seasons, or the loss of leaves. Long-day plants A long-day plant requires fewer than a certain number of hours of darkness in each 24-hour period to induce flowering. These plants typically flower in the northern hemisphere during late spring or early summer as days are getting longer. In the northern hemisphere, the longest day of the year is on or about 21 June (solstice). After that date, days grow shorter (i.e. nights grow longer) until 21 December (solstice). This situation is reversed in the southern hemisphere (i.e. longest day is 21 December and shortest day is 21 June). In some parts of the world, however, "winter" or "summer" might refer to rainy versus dry seasons, respectively, rather than the coolest or warmest time of year. Some long-day obligate plants are:Carnation (Dianthus) Henbane (Hyoscyamus) Oat (Avena) Ryegrass (Lolium) Clover (Trifolium) Bellflower (Campanula carpatica) Some long-day facultative plants are: Pea (Pisum sativum) Barley (Hordeum vulgare) Lettuce (Lactuca sativa) Wheat (Triticum aestivum, spring wheat cultivars) Turnip (Brassica rapa) Arabidopsis thaliana (model organism) Short-day plants Short-day plants flower when the night is longer than a critical length. They cannot flower under long days or if a pulse of artificial light is shone on the plant for several minutes during the middle of the night; they require a consolidated period of darkness before floral development can begin. Natural nighttime light, such as moonlight or lightning, is not of sufficient brightness or duration to interrupt flowering. In general, short-day (i.e. long-night) plants flower as days grow shorter (and nights grow longer) after 21 June in the northern hemisphere, which is during summer or fall. The length of the dark period required to induce flowering differs among species and varieties of a species. Photoperiod affects flowering when the shoot is induced to produce floral buds instead of leaves and lateral buds. Note that some species must pass through a "juvenile" period during which they cannot be induced to flower—common cocklebur is an example of a plant species with a remarkably short period of juvenility and plants can be induced to flower when quite small. Some short-day obligate plants are: Chrysanthemum Coffee Poinsettia Strawberry Tobacco, var. Maryland Mammouth Common duckweed , (Lemna minor) Cocklebur (Xanthium) Maize – tropical cultivars only[citation needed] Some short-day facultative plants are: Hemp (Cannabis) Cotton (Gossypium) Rice Sugar cane Day-neutral plants Day-neutral plants, such as cucumbers, roses and tomatoes, do not initiate flowering based on photoperiodism at all; they flower regardless of the night length. They may initiate flowering after attaining a certain overall developmental stage or age, or in response to alternative environmental stimuli, such as vernalisation (a period of low temperature), rather than in response to photoperiod.

ETHYLENE

Ethylene (IUPAC name: ethene ) is a gaseous organic compound with the formula C2H4. It is the simplest alkene (older name: olefin from its oil-forming property). Because it contains a carbon-carbon double bond, ethylene is classified as an unsaturated hydrocarbon . Ethylene is widely used in industry and is also a plant hormone.[3] Ethylene is the most produced organic compound in the world; global production of ethylene exceeded 107 million tonnes in 2005.[4] To meet the ever increasing demand for ethylene, sharp increases in production facilities are added globally, particularly in the Persian Gulf countries and in China.[5] Structure and properties Orbital description of bonding between ethylene and a transition metal. This hydrocarbon has four hydrogen atoms bound to a pair of carbon atoms that are connected by a double bond. All six atoms that comprise ethylene are coplanar. The H-C- H angle is 119°, close to the 120° for ideal sp² hybridized carbon. The molecule is also relatively rigid: rotation about the C-C bond is a high energy process that requires breaking the π-bond. The π-bond in the ethylene molecule is responsible for its useful reactivity. The double bond is a region of high electron density , thus it is susceptible to attack by electrophiles. Many reactions of ethylene are catalyzed by transition metals, which bind transiently to the ethylene using both the π and π* orbitals. Being a simple molecule, ethylene is spectroscopically simple. Its UV-vis spectrum is still used as a test of theoretical methods. [6] Uses Major industrial reactions of ethylene include in order of scale: 1) polymerization , 2) oxidation , 3) halogenation and hydrohalogenation , 4) alkylation , 5) hydration , 6) oligomerization, and 7) hydroformylation . In the United States and Europe, approximately 90% of ethylene is used to produce three chemical compounds— ethylene oxide , ethylene dichloride, and ethylbenzene —and a variety of kinds of polyethylene .[7] Main industrial uses of ethylene. Clockwise from the upper right: its conversions to ethylene oxide , precursor to ethylene glycol, to ethylbenzene , precursor to styrene , to various kinds of polyethylene , to ethylene dichloride, precursor to vinyl chloride. Polymerization See also: Ziegler-Natta catalyst and Polyethylene Polyethylenes of various types consume more than half of world ethylene supply. Polyethylene, also called polythene, is the world's most widely-used plastic, being primarily used to make films used in packaging, carrier bags and trash liners. Linear alpha- olefins, produced by oligomerization (formation of short polymers) are used as precursors, detergents, plasticisers, synthetic lubricants, additives, and also as co-monomers in the production of polyethylenes. [7] Oxidation Ethylene is oxidized to produce ethylene oxide , a key raw material in the production of surfactants and detergents by ethoxylation . Ethylene oxide also hydrolyzed to produce ethylene glycol , widely used as an automotive antifreeze as well as higher molecular weight glycols and glycol ethers. Main article: Wacker process Ethylene undergoes oxidation by palladium to give acetaldehyde . This conversion remains a major industrial process (10M kg/y). [8] The process proceeds via the initial complexation of ethylene to a Pd(II) center. Halogenation and hydrohalogenation Major intermediates from the halogenation and hydrohalogenation of ethylene include ethylene dichloride, ethyl chloride and ethylene dibromide . The addition of chlorine entails "oxychlorination," i.e. chlorine itself is not used. Some products derived from this group are polyvinyl chloride , trichloroethylene , perchloroethylene , methyl chloroform, polyvinylidiene chloride and copolymers , and ethyl bromide .[9] Alkylation Major chemical intermediates from the alkylation with ethylene is ethylbenzene , precursor to styrene . Styrene is used principally in polystyrene for packaging and insulation, as well as in styrene-butadiene rubber for tires and footwear. On a smaller scale, ethyl toluene, ethylanilines, 1,4-hexadiene, and aluminium alkyls. Products of these intermediates include polystyrene , unsaturated polyesters and ethylene- propylene terpolymers .[9] Oxo reaction The hydroformylation (oxo reaction) of ethylene results in propionaldehyde , a precursor to propionic acid and n-propyl alcohol.[9] Hydration Ethylene can be hydrated to give ethanol, but this method is rarely used industrially. Niche uses An example of a niche use is as an anesthetic agent (in an 85% ethylene/15% oxygen ratio).[10] It can also be used to hasten fruit ripening, as well as a welding gas. [7][11] Production In 2006, global ethylene production was 109 million tonnes.[12] By 2010 ethylene was produced by at least 117 companies in 55 countries.[5] Ethylene is produced in the petrochemical industry by steam cracking . In this process, gaseous or light liquid hydrocarbons are heated to 750–950 °C, inducing numerous free radical reactions followed by immediate quench to stop these reactions. This process converts large hydrocarbons into smaller ones and introduces unsaturation. Ethylene is separated from the resulting complex mixture by repeated compression and distillation. In a related process used in oil refineries, high molecular weight hydrocarbons are cracked over zeolite catalysts. Heavier feedstocks, such as naphtha and gas oils require at least two "quench towers" downstream of the cracking furnaces to recirculate pyrolysis-derived gasoline and process water. When cracking a mixture of ethane and propane, only one water quench tower is required. [9] The areas of an ethylene plant are: 1. steam cracking furnaces: 2. primary and secondary heat recovery with quench; 3. a dilution steam recycle system between the furnaces and the quench system; 4. primary compression of the cracked gas (3 stages of compression); 5. hydrogen sulfide and carbon dioxide removal (acid gas removal); 6. secondary compression (1 or 2 stages); 7. drying of the cracked gas; 8. cryogenic treatment; 9. all of the cold cracked gas stream goes to the demethanizer tower. The overhead stream from the demethanizer tower consists of all the hydrogen and methane that was in the cracked gas stream. Cryogenically (−250 °F (−157 °C)) treating this overhead stream separates hydrogen from methane. Methane recovery is critical to the economical operation of an ethylene plant. 0. the bottom stream from the demethanizer tower goes to the deethanizer tower. The overhead stream from the deethanizer tower consists of all the C2,'s that were in the cracked gas stream. The C2 stream contains acetylene, which is explosive above 200 kPa (29 psi).[13] If the partial pressure of acetylene is expected to exceed these values, the C 2 stream is partially hydrogenated. The C2's then proceed to a C2 splitter. The product ethylene is taken from the overhead of the tower and the ethane coming from the bottom of the splitter is recycled to the furnaces to be cracked again; 1. the bottom stream from the de-ethanizer tower goes to the depropanizer tower. The overhead stream from the depropanizer tower consists of all the C 3's that were in the cracked gas stream. Before feeding the C3's to the C3 splitter, the stream is hydrogenated to convert the methylacetylene and propadiene (allene) mix. This stream is then sent to the C3 splitter. The overhead stream from the C3 splitter is product propylene and the bottom stream is propane which is sent back to the furnaces for cracking or used as fuel. 2. The bottom stream from the depropanizer tower is fed to the debutanizer tower. The overhead stream from the debutanizer is all of the C 4's that were in the cracked gas stream. The bottom stream from the debutanizer (light pyrolysis gasoline) consists of everything in the cracked gas stream that is C 5 or heavier. [9] Since ethylene production is energy intensive, much effort has been dedicated to recovering heat from the gas leaving the furnaces. Most of the energy recovered from the cracked gas is used to make high pressure (1200 psig) steam. This steam is in turn used to drive the turbines for compressing cracked gas, the propylene refrigeration compressor, and the ethylene refrigeration compressor. An ethylene plant, once running, does not need to import steam to drive its steam turbines. A typical world scale ethylene plant (about 1.5 billion pounds of ethylene per year) uses a 45,000 horsepower (34,000 kW) cracked gas compressor, a 30,000 hp (22,000 kW) propylene compressor, and a 15,000 hp (11,000 kW) ethylene compressor.

CYTOKININ

Cytokinins (CK) are a class of plant growth substances (phytohormones ) that promote cell division , or cytokinesis , in plant roots and shoots. They are involved primarily in cell growth and differentiation , but also affect apical dominance, axillary bud growth, and leaf senescence. Folke Skoog discovered their effects using coconut milk in the 1940s at the University of Wisconsin–Madison. [1] There are two types of cytokinins: adenine-type cytokinins represented by kinetin , zeatin, and 6- benzylaminopurine , and phenylurea-type cytokinins like diphenylurea and thidiazuron (TDZ). Most adenine-type cytokinins are synthesized in roots. [2]Cambium and other actively dividing tissues also synthesize cytokinins. [3] No phenylurea cytokinins have been found in plants.[4] Cytokinins participate in local and long-distance signalling, with the same transport mechanism as purines and nucleosides.[5] Typically, cytokinins are transported in the xylem .[2] Cytokinins act in concert with auxin , another plant growth hormone.[2] Mode of Action The ratio of auxin to cytokinin plays an important role in the effect of cytokinin on plant growth. Cytokinin alone has no effect on parenchyma cells. When cultured with auxin but no cytokinin, they grow large but do not divide. When cytokinin is added, the cells expand and differentiate. When cytokinin and auxin are present in equal levels, the parenchyma cells form an undifferentiated callus. More cytokinin induces growth of shoot buds, while more auxin induces root formation.[2] Cytokinins are involved in many plant processes, including cell division and shoot and root morphogenesis. They are known to regulate axillary bud growth and apical dominance. The "direct inhibition hypothesis" posits that these effects result from the cytokinin to auxin ratio. This theory states that auxin from apical buds travels down shoots to inhibit axillary bud growth. This promotes shoot growth, and restricts lateral branching. Cytokinin moves from the roots into the shoots, eventually signaling lateral bud growth. Simple experiments support this theory. When the apical bud is removed, the axillary buds are uninhibited, lateral growth increases, and plants become bushier. Applying auxin to the cut stem again inhibits lateral dominance.[2] While cytokinin action in vascular plants is described as pleiotropic, this class of plant hormones specifically induces the transition from apical growth to growth via a three-faced apical cell in moss protonema. This bud induction can be pinpointed to differentiation of a specific single cell, and thus is a very specific effect of cytokinin. [6] Cytokinins have been shown to slow aging of plant organs by preventing protein breakdown, activating protein synthesis, and assembling nutrients from nearby tissues. [2] A study that regulated leaf senescence in tobacco leaves found that wild-type leaves yellowed while transgenic leaves remained mostly green. It was hypothesized that cytokinin may affect enzymes that regulate protein synthesis and degradation. [7] Biosynthesis Adenosine phosphate- isopentenyltransferase (IPT) catalyses the first reaction in the biosynthesis of isoprene cytokinins. It may use ATP, ADP, or AMP as substrates and may use dimethylallyl diphosphate (DMAPP) or hydroxymethylbutenyl diphosphate (HMBDP) as prenyl donors .[8] This reaction is the rate-limiting step in cytokinin biosynthesis. DMAPP and HMBDP used in cytokinin biosynthesis are produced by the methylerythritol phosphate pathway (MEP). [8] Cytokinins can also be produced by recycled tRNAs in plants and bacteria.[8][9] tRNAs with anticodons that start with a uridine and carrying an already- prenylated adenosine adjacent to the anticodon release on degradation the adenosine as a cytokinin. [8] The prenylation of these adenines is carried out by tRNA- isopentenyltransferase .[9] Auxin is known to regulate the biosynthesis of cytokinin. [10] Uses Because cytokinin promotes plant cell division and growth, produce farmers use it to increase crops. One study found that applying cytokinin to cotton seedlings led to a 5– 10% yield increase under drought conditions. [11] Cytokinins have recently been found to play a role in plant pathogenesis.

PLASMIC GROWTH

MESISTEM

A meristem is the tissue in most plants consisting of undifferentiated cells (meristematic cells ), found in zones of the plant where growth can take place. The meristematic cells give rise to various organs of the plant, and keep the plant growing. The Shoot Apical Meristem (SAM) gives rise to organs like the leaves and flowers. The cells of the apical meristems - SAM and RAM (Root Apical Meristem) - divide rapidly and are considered to be indeterminate, in that they do not possess any defined end fate. In that sense, the meristematic cells are frequently compared to the stem cells in animals, that have an analogous behavior and function. The term meristem was first used in 1858 by Karl Wilhelm von Nägeli (1817–1891) in his book Beiträge zur Wissenschaftlichen Botanik. [1] It is derived from the Greek word merizein (μερίζειν), meaning to divide, in recognition of its inherent function. In general, differentiated plant cells cannot divide or produce cells of a different type. Therefore, cell division in the meristem is required to provide new cells for expansion and differentiation of tissues and initiation of new organs, providing the basic structure of the plant body. Meristematic cells are incompletely or not at all differentiated , and are capable of continued cellular division (youthful). Furthermore, the cells are small and protoplasm fills the cell completely. The vacuoles are extremely small. The cytoplasm does not contain differentiated plastids (chloroplasts or chromoplasts), although they are present in rudimentary form (proplastids). Meristematic cells are packed closely together without intercellular cavities. The cell wall is a very thin primary cell wall. Maintenance of the cells requires a balance between two antagonistic processes: organ initiation and stem cell population renewal. Meristematic zones Apical meristems are the completely undifferentiated (indeterminate) meristems in a plant. These differentiate into three kinds of primary meristems. The primary meristems in turn produce the two secondary meristem types. These secondary meristems are also known as lateral meristems because they are involved in lateral growth. At the meristem summit, there is a small group of slowly dividing cells, which is commonly called the central zone. Cells of this zone have a stem cell function and are essential for meristem maintenance. The proliferation and growth rates at the meristem summit usually differ considerably from those at the periphery. Meristems also are induced in the roots of legumes such as soybean , Lotus japonicus, pea, and Medicago truncatula after infection with soil bacteria commonly called Rhizobium. Cells of the inner or outer cortex in the so-called "window of nodulation" just behind the developing root tip are induced to divide. The critical signal substance is the lipo-oligosaccharide Nod- factor, decorated with side groups to allow specificity of interaction. The Nod factor receptor proteins NFR1 and NFR5 were cloned from several legumes including Lotus japonicus, Medicago truncatula and soybean (Glycine max). Regulation of nodule meristems utilizes long distance regulation commonly called "Autoregulation of Nodulation" (AON). This process involves a leaf- vascular tissue located LRR receptor kinases (LjHAR1, GmNARK and MtSUNN), CLE peptide signalling , and KAPP interaction, similar to that seen in the CLV1,2,3 system. LjKLAVIER also exhibits a nodule regulation phenotype though it is not yet known how this relates to the other AON receptor kinases Apical meristems Organisation of an apical meristem (growing tip) 1 - Central zone 2 - Peripheral zone 3 - Medullary (i.e. central) meristem 4 - Medullary tissue The apical meristem , or growing tip, is a completely undifferentiated meristematic tissue found in the buds and growing tips of roots in plants. Its main function is to begin growth of new cells in young seedlings at the tips of roots and shoots (forming buds, among other things). Specifically, an active apical meristem lays down a growing root or shoot behind itself, pushing itself forward. Apical meristems are very small, compared to the cylinder-shaped lateral meristems (see 'Secondary Meristems' below). Apical meristems are composed of several layers. The number of layers varies according to plant type. In general the outermost layer is called the tunica while the innermost layers are the corpus . In monocots, the tunica determine the physical characteristics of the leaf edge and margin. In dicots, layer two of the corpus determine the characteristics of the edge of the leaf. The corpus and tunica play a critical part of the plant physical appearance as all plant cells are formed from the meristems. Apical meristems are found in two locations: the root and the stem. Some Arctic plants have an apical meristem in the lower/middle parts of the plant. It is thought that this kind of meristem evolved because it is advantageous in Arctic conditions[citation needed]. Shoot apical meristems The source of all above- ground organs. Cells at the shoot apical meristem summit serve as stem cells to the surrounding peripheral region, where they proliferate rapidly and are incorporated into differentiating leaf or flower primordia. The shoot apical meristem is the site of most of the embryogenesis in flowering plants. Primordia of leaves, sepals, petals, stamens and ovaries are initiated here at the rate of one every time interval, called a plastochron. It is where the first indications that flower development has been evoked are manifested. One of these indications might be the loss of apical dominance and the release of otherwise dormant cells to develop as axillary shoot meristems, in some species in axils of primordia as close as two or three away from the apical dome. The shoot apical meristem consists of 4 distinct cell groups: -. Stem cells The immediate daughter cells of the stem cells A subjacent organising centre Founder cells for organ initiation in surrounding regions The four distinct zones mentioned above are maintained by a complex signalling pathway. In Arabidopsis thaliana , 3 interacting CLAVATA genes are required to regulate the size of the stem cell reservoir in the shoot apical meristem by controlling the rate of cell division .[2] CLV1 and CLV2 are predicted to form a receptor complex (of the LRR receptor like kinase family) to which CLV3 is a ligand.[3][4][5] CLV3 shares some homology with the ESR proteins of maize, with a short 14 amino acid region being conserved between the proteins. [6][7] Proteins that contain these conserved regions have been grouped into the CLE family of proteins.[6][7] CLV1 has been shown to interact with several cytoplasmic proteins that are most likely involved in downstream signalling . For example, the CLV complex has been found to be associated with Rho/Rac small GTPase- related proteins.[2] These proteins may act as an intermediate between the CLV complex and a mitogen- activated protein kinase (MAPK), which is often involved in signalling cascades. [8] KAPP is a kinase-associated protein phosphatase that has been shown to interact with CLV1.[9] KAPP is thought to act as a negative regulator of CLV1 by dephosphorylating it. [9] Another important gene in plant meristem maintenance is WUSCHEL (shortened to WUS), which is a target of CLV signalling.[10]WUS is expressed in the cells below the stem cells of the meristem and its presence prevents the differentiation of the stem cells.[10] CLV1 acts to promote cellular differentiation by repressing WUS activity outside of the central zone containing the stem cells. [10]STM also acts to prevent the differentiation of stem cells by repressing the expression of Myb genes that are involved in cellular differentiation.

STROKE

A stroke , also known as a cerebrovascular accident (CVA ), is the rapid loss of brain function(s) due to disturbance in the blood supply to the brain. This can be due to ischemia (lack of blood flow) caused by blockage (thrombosis, arterial embolism), or a hemorrhage (leakage of blood). [1] As a result, the affected area of the brain cannot function, which might result in an inability to move one or more limbs on one side of the body , inability to understand or formulate speech, or an inability to see one side of the visual field .[2] A stroke is a medical emergency and can cause permanent neurological damage, complications, and death. It is the leading cause of adult disability in the United States and Europe and the second leading cause of death worldwide. [3]Risk factors for stroke include old age, hypertension (high blood pressure), previous stroke or transient ischemic attack (TIA), diabetes, high cholesterol, cigarette smoking and atrial fibrillation .[2] High blood pressure is the most important modifiable risk factor of stroke. [2] A silent stroke is a stroke that does not have any outward symptoms, and the patients are typically unaware they have suffered a stroke. Despite not causing identifiable symptoms, a silent stroke still causes damage to the brain, and places the patient at increased risk for both transient ischemic attack and major stroke in the future. Conversely, those who have suffered a major stroke are at risk of having silent strokes. [4] In a broad study in 1998, more than 11 million people were estimated to have experienced a stroke in the United States. Approximately 770,000 of these strokes were symptomatic and 11 million were first-ever silent MRI infarcts or hemorrhages. Silent strokes typically cause lesions which are detected via the use of neuroimaging such as MRI. Silent strokes are estimated to occur at five times the rate of symptomatic strokes. [5][6] The risk of silent stroke increases with age, but may also affect younger adults and children, especially those with acute anemia.[5][7] An ischemic stroke is occasionally treated in a hospital with thrombolysis (also known as a "clot buster"), and some hemorrhagic strokes benefit from neurosurgery. Treatment to recover any lost function is termed stroke rehabilitation, ideally in a stroke unit and involving health professions such as speech and language therapy, physical therapy and occupational therapy . Prevention of recurrence may involve the administration of antiplatelet drugs such as aspirin and dipyridamole , control and reduction of hypertension , and the use of statins. Selected patients may benefit from carotid endarterectomy and the use of anticoagulants.[2] Classification A slice of brain from the autopsy of a person who suffered an acute middle cerebral artery (MCA) stroke Strokes can be classified into two major categories: ischemic and hemorrhagic.[8] Ischemic strokes are those that are caused by interruption of the blood supply, while hemorrhagic strokes are the ones which result from rupture of a blood vessel or an abnormal vascular structure. About 87% of strokes are caused by ischemia, and the remainder by hemorrhage. Some hemorrhages develop inside areas of ischemia ("hemorrhagic transformation"). It is unknown how many hemorrhages actually start as ischemic stroke. [2] Ischemic Main articles: Cerebral infarction and Brain ischemia In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain tissue in that area. There are four reasons why this might happen: 1. Thrombosis (obstruction of a blood vessel by a blood clot forming locally) 2. Embolism (obstruction due to an embolus from elsewhere in the body, see below), [2] 3. Systemic hypoperfusion (general decrease in blood supply, e.g., in shock)[9] 4. Venous thrombosis.[10] Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin); this constitutes 30-40% of all ischemic strokes. [2][11] There are various classification systems for acute ischemic stroke. The Oxford Community Stroke Project classification (OCSP, also known as the Bamford or Oxford classification) relies primarily on the initial symptoms; based on the extent of the symptoms, the stroke episode is classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four entities predict the extent of the stroke, the area of the brain affected, the underlying cause, and the prognosis.[12][13] The TOAST (Trial of Org 10172 in Acute Stroke Treatment) classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete investigation). [2][14] Hemorrhagic Main articles: Intracranial hemorrhage and intracerebral hemorrhage An intraparenchymal bleed (bottom arrow) with surrounding edema (top arrow) Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the brain). Intra-axial hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). The main types of extra-axial hemorrhage are epidural hematoma (bleeding between the dura mater and the skull, subdural hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of the hemorrhagic stroke syndromes have specific symptoms (e.g., headache, previous head injury). Signs and symptoms Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases do not progress further. The symptoms depend on the area of the brain affected. The more extensive the area of brain affected, the more functions that are likely to be lost. Some forms of stroke can cause additional symptoms. For example, in intracranial hemorrhage, the affected area may compress other structures. Most forms of stroke are not associated with headache, apart from subarachnoid hemorrhage and cerebral venous thrombosis and occasionally intracerebral hemorrhage. Early recognition Various systems have been proposed to increase recognition of stroke by patients, relatives and emergency first responders. A systematic review , updating a previous systematic review from 1994, looked at a number of trials to evaluate how well different physical examination findings are able to predict the presence or absence of stroke. It was found that sudden-onset face weakness, arm drift (i.e., if a person, when asked to raise both arms, involuntarily lets one arm drift downward) and abnormal speech are the findings most likely to lead to the correct identification of a case of stroke (+ likelihood ratio of 5.5 when at least one of these is present). Similarly, when all three of these are absent, the likelihood of stroke is significantly decreased (– likelihood ratio of 0.39).[15] While these findings are not perfect for diagnosing stroke, the fact that they can be evaluated relatively rapidly and easily make them very valuable in the acute setting. Proposed systems include FAST (stroke) (face, arm, speech, and time),[16] as advocated by the Department of Health (United Kingdom) and The Stroke Association , the American Stroke Association (www.strokeassociation.org) , National Stroke Association (US www.stroke.org), the Los Angeles Prehospital Stroke Screen (LAPSS) [17] and the Cincinnati Prehospital Stroke Scale (CPSS).[18] Use of these scales is recommended by professional guidelines.[19] For people referred to the emergency room , early recognition of stroke is deemed important as this can expedite diagnostic tests and treatments. A scoring system called ROSIER (recognition of stroke in the emergency room) is recommended for this purpose; it is based on features from the medical history and physical examination. [19][20] Subtypes If the area of the brain affected contains one of the three prominent central nervous system pathways — the spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include: hemiplegia and muscle weakness of the face numbness reduction in sensory or vibratory sensation initial flaccidity (hypotonicity), replaced by spasticity (hypertonicity), hyperreflexia, and obligatory synergies. [21] In most cases, the symptoms affect only one side of the body ( unilateral). Depending on the part of the brain affected, the defect in the brain is usually on the opposite side of the body. However, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms, the presence of any one of these symptoms does not necessarily indicate a stroke. In addition to the above CNS pathways, the brainstem give rise to most of the twelve cranial nerves . A stroke affecting the brain stem and brain therefore can produce symptoms relating to deficits in these cranial nerves: altered smell, taste, hearing, or vision (total or partial) drooping of eyelid ( ptosis) and weakness of ocular muscles decreased reflexes: gag, swallow, pupil reactivity to light decreased sensation and muscle weakness of the face balance problems and nystagmus altered breathing and heart rate weakness in sternocleidomastoid muscle with inability to turn head to one side weakness in tongue (inability to protrude and/ or move from side to side) If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms: aphasia (difficulty with verbal expression, auditory comprehension, reading and/or writing Broca's or Wernicke's area typically involved) dysarthria (motor speech disorder resulting from neurological injury) apraxia (altered voluntary movements) visual field defect memory deficits (involvement of temporal lobe) hemineglect (involvement of parietal lobe) disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe) anosognosia (persistent denial of the existence of a, usually stroke-related, deficit) If the cerebellum is involved, the patient may have the following: trouble walking altered movement coordination vertigo and or disequilibrium Associated symptoms Loss of consciousness, headache, and vomiting usually occurs more often in hemorrhagic stroke than in thrombosis because of the increased intracranial pressure from the leaking blood compressing the brain. If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.

CERIBRAL HEMMORAGE

A cerebral hemorrhage or haemorrhage (or intracerebral hemorrhage , ICH ) is a subtype of intracranial hemorrhage that occurs within the brain tissue itself. Intracerebral hemorrhage can be caused by brain trauma, or it can occur spontaneously in hemorrhagic stroke . Non-traumatic intracerebral hemorrhage is a spontaneous bleeding into the brain tissue.[1] A cerebral hemorrhage is an intra-axial hemorrhage ; that is, it occurs within the brain tissue rather than outside of it. The other category of intracranial hemorrhage is extra-axial hemorrhage, such as epidural, subdural, and subarachnoid hematomas, which all occur within the skull but outside of the brain tissue. There are two main kinds of intra-axial hemorrhages: intraparenchymal hemorrhage and intraventricular hemorrhages. As with other types of hemorrhages within the skull, intraparenchymal bleeds are a serious medical emergency because they can increase intracranial pressure, which if left untreated can lead to coma and death. The mortality rate for intraparenchymal bleeds is over 40%. [2] Signs and symptoms Patients with intraparenchymal bleeds have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed. [3] Other symptoms include those that indicate a rise in intracranial pressure due to a large mass putting pressure on the brain.[3] Intracerebral hemorrhages are often misdiagnosed as subarachnoid hemorrhages due to the similarity in symptoms and signs. A severe headache followed by vomiting is one of the more common symptoms of intracerebral hemorrhage. Some patients may also go into a coma before the bleed is noticed. Causes CT scan showing hemorrhage in the posterior fossa[1] Intracerebral bleeds are the second most common cause of stroke , accounting for 30–60% of hospital admissions for stroke. [1]High blood pressure raises the risks of spontaneous intracerebral hemorrhage by two to six times. [1] More common in adults than in children, intraparenchymal bleeds due to trauma are usually due to penetrating head trauma, but can also be due to depressed skull fractures. Acceleration- deceleration trauma,[4][5][6] rupture of an aneurysm or arteriovenous malformation (AVM), and bleeding within a tumor are additional causes. Amyloid angiopathy is a not uncommon cause of intracerebral hemorrhage in patients over the age of 55. A very small proportion is due to cerebral venous sinus thrombosis. Infection with the k serotype of Streptococcus mutans may also be a risk factor, due to its prevalence in stroke patients and production of collagen- binding protein.[7] Risk factors for ICH include: [8] Hypertension Diabetes Menopause Current cigarette smoking Alcoholic drinks (≥2/day) Tramautic intracerebral Hematomas are divided into acute and delayed. Acute intracerebral Hematomas occur at the time of the injury while delayed intracerebral Hematomas have been reported from as early as 6 hours post injury to as long as several weeks. It is important to keep in mind that intracerebral Hematomas can be delayed because if symptoms begin to appear several weeks after the injury, concussion is no longer considered and the symptoms may not be connected to the injury. Diagnosis Spontaneous ICH with hydrocephalus on CT scan[1] Intraparenchymal hemorrhage can be recognized on CT scans because blood appears brighter than other tissue and is separated from the inner table of the skull by brain tissue. The tissue surrounding a bleed is often less dense than the rest of the brain due to edema, and therefore shows up darker on the CT scan. Treatment Treatment depends substantially of the type of ICH. Rapid CT scan and other diagnostic measures are used to determine proper treatment, which may include both medication and surgery. Medication Antihypertensive therapy in acute phases. The AHA/ ASA and EUSI guidelines (American Heart Association/American Stroke Association guidelines and the European Stroke Initiative guidelines) have recommended antihypertensive therapy to stabilize the mean arterial pressure at 110 mmHg. One paper showed the efficacy of this antihypertensive therapy without worsening outcome in patients of hypertensive intracerebral hemorrhage within 3 hours onset.[9] Giving Factor VIIa within 4 hours limits the bleeding and formation of a hematoma. However, it also increases the risk of thromboembolism.[10] Mannitol is effective in acutely reducing raised intracranial pressure. Acetaminophen may be needed to avoid hyperthermia , and to relieve headache. [10] Frozen plasma, vitamin K , protamine, or platelet transfusions are given in case of a coagulopathy.[10] Fosphenytoin or other anticonvulsant is given in case of seizures or lobar hemorrhage.[10] H2 antagonists or proton pump inhibitors are commonly given for stress ulcer prophylaxis, a condition somehow linked with ICH. [10] Corticosteroids, in concert with antihypertensives, reduces swelling. [11] Surgery Surgery is required if the hematoma is greater than 3 cm (1 in), if there is a structural vascular lesion or lobar hemorrhage in a young patient.[10] A catheter may be passed into the brain vasculature to close off or dilate blood vessels, avoiding invasive surgical procedures.[12] Aspiration by stereotactic surgery or endoscopic drainage may be used in basal ganglia hemorrhages, although successful reports are limited.[10] Other treatment Tracheal intubation is indicated in patients with decreased level of consciousness or other risk of airway obstruction. [10] IV fluids are given to maintain fluid balance, using normotonic rather than hypotonic fluids. [10] Prognosis The risk of death from an intraparenchymal bleed in traumatic brain injury is especially high when the injury occurs in the brain stem.[2] Intraparenchymal bleeds within the medulla oblongata are almost always fatal, because they cause damage to cranial nerve X, the vagus nerve , which plays an important role in blood circulation and breathing.[4] This kind of hemorrhage can also occur in the cortex or subcortical areas, usually in the frontal or temporal lobes when due to head injury, and sometimes in the cerebellum. [4][13] For spontaneous ICH seen on CT scan, the death rate (mortality ) is 34–50% by 30 days after the insult, [1] and half of the deaths occur in the first 2 days. [14] The inflammatory response triggered by stroke has been viewed as harmful, focusing on the influx and migration of blood-borne leukocytes, neutrophils, and macrophages. New area of interest are the Mast Cells.[15] Epidemiology It accounts for 20% of all cases of cerebrovascular disease in the US, behind cerebral thrombosis (40%) and cerebral embolism (30%).[16] It is two or more times more prevalent in black American patients than it is in white.

AUXIN

Auxins are a class of plant hormones (or plant growth substances) with some morphogen-like characteristics. Auxins have a cardinal role in coordination of many growth and behavioral processes in the plant's life cycle and are essential for plant body development. Auxins and their role in plant growth were first described by the Dutch scientist Frits Went.[1]Kenneth V. Thimann isolated this phytohormone and determined its chemical structure as indole-3-acetic acid. Went and Thiman then co-authored a book on plant hormones, Phytohormones, in 1937. Native auxins indole-3-acetic acid (IAA) is the most abundant and the basic auxin natively occurring and functioning in plants. It generates the majority of auxin effects in intact plants, and is the most potent native auxin. There are three more native — endogenous auxins [2] All auxins are compounds with aromatic ring and a carboxylic acid group [3]: 4-chloroindole-3-acetic acid (4-CI-IAA) 2-phenylacetic acid (PAA) Indole-3-butyric acid (IBA) For representatives of synthetic auxins see chapter Synthetic auxins Overview Auxins derive their name from the Greek word αυξειν (auxein - "to grow/increase"). They were the first of the major plant hormones to be discovered. The (dynamic and to environment responsive) pattern of auxin distribution within the plant is a key factor for plant growth, its reaction to its environment, and specifically for development of plant organs [4][5] (such as leaves or flowers ). It is achieved through very complex and well coordinated active transport of auxin molecules from cell to cell throughout the plant body — by the so- called polar auxin transport .[4] Thus, a plant can (as a whole) react to external conditions and adjust to them, without requiring a nervous system . Auxins typically act in concert with, or in opposition to, other plant hormones. For example, the ratio of auxin to cytokinin in certain plant tissues determines initiation of root versus shoot buds. On the molecular level, all auxins are compounds with an aromatic ring and a carboxylic acid group. [3] The most important member of the auxin family is indole-3- acetic acid (IAA). [2] IAA generates the majority of auxin effects in intact plants, and is the most potent native auxin. And as native auxin, its stability is controlled in many ways in plants, from synthesis, through possible conjugation to degradation of its molecules, always according to the requirements of the situation. However, molecules of IAA are chemically labile in aqueous solution, so it is not used commercially as a plant growth regulator. The four naturally occurring (endogenous) auxins are IAA, 4- chloroindole-3-acetic acid, phenylacetic acid and indole-3-butyric acid ; only these four were found to be synthesized by plants. [2] However, most of the knowledge described so far in auxin biology and as described in the article below, apply basically to IAA; the other three endogenous auxins seems to have rather marginal importance for intact plants in natural environments. Alongside endogenous auxins, scientists and manufacturers have developed many synthetic compounds with auxinic activity. Synthetic auxin analogs include 1-naphthaleneacetic acid, 2,4- dichlorophenoxyacetic acid (2,4-D),[2] and many others. Some synthetic auxins, such as 2,4-D and 2,4,5- trichlorophenoxyacetic acid (2,4,5-T), are used also as herbicides. Broad-leaf plants (dicots), such as dandelions, are much more susceptible to auxins than narrow-leaf plants (monocots) such as grasses and cereal crops, so these synthetic auxins are valuable as synthetic herbicides. Auxins are also often used to promote initiation of adventitious roots, and are the active ingredient of the commercial preparations used in horticulture to root stem cuttings. They can also be used to promote uniform flowering and fruit set, and to prevent premature fruit drop. Hormonal activity Auxins coordinate development at all levels in plants, from the cellular level, through organs, and ultimately to the whole plant. The plant cell wall is made up of cellulose, proteins, and, in many cases, lignin. It is very firm and prevents any sudden expansion of cell volume (and, without the contribution of auxins, any expansion at all). Molecular mechanisms Auxin molecules present in cells may trigger responses directly through stimulation or inhibition of the expression of sets of certain genes.[6] or by means independent of gene expression. One of the pathways leading to the changes of gene expression involves the reception of auxin by TIR1 protein. In 2005, the F-box protein TIR1, which is part of the ubiquitin ligase complex SCFTIR1, was demonstrated to be an auxin receptor. [7] Upon binding of auxin, TIR1 recruits specific transcriptional repressors (the Aux/IAA repressors) for ubiquitination by the SCF complex. This marking process leads to the degradation of the Aux/ IAAs repressors by the proteasome. The degradation of the repressors leads, in turn, to potentiation of auxin response factor-mediated transcription of specific genes in response to auxins. [8]) Another protein, auxin- binding protein 1 (ABP1), is a putative receptor for different signaling pathway, but its role is as yet unclear. Electrophysiological experiments with protoplasts and anti-ABP1 antibodies suggest ABP1 may have a function at the plasma membrane, and cells can possibly use ABP1 proteins to respond to auxin through means faster and independent of gene expression. On a cellular level On the cellular level, auxin is essential for cell growth , affecting both cell division and cellular expansion. Auxin concentration level, together with other local factors, contributes to cell differentiation and specification of the cell fate. Depending on the specific tissue, auxin may promote axial elongation (as in shoots), lateral expansion (as in root swelling), or isodiametric expansion (as in fruit growth). In some cases (coleoptile growth), auxin- promoted cellular expansion occurs in the absence of cell division. In other cases, auxin- promoted cell division and cell expansion may be closely sequenced within the same tissue (root initiation, fruit growth). In a living plant, auxins and other plant hormones nearly always appear to interact to determine patterns of plant development. Organ patterns Growth and division of plant cells together result in growth of tissue, and specific tissue growth contributes to the development of plant organs. Growth of cells contributes to the plant's size, unevenly localized growth produces bending, turning and directionalization of organs- for example, stems turning toward light sources (phototropism), roots growing in response to gravity ( gravitropism ), and other tropisms originated because cells on one side grow faster than the cells on the other side of the organ. So, precise control of auxin distribution between different cells has paramount importance to the resulting form of plant growth and organization. Uneven distribution of auxin To cause growth in the required domains, auxins must of necessity be active preferentially in them. Auxins are not synthesized in all cells (even if cells retain the potential ability to do so, only under specific conditions will auxin synthesis be activated in them). For that purpose, auxins have to be not only translocated toward those sites where they are needed, but also they must have an established mechanism to detect those sites. For that purpose, auxins have to be translocated toward those sites where they are needed. Translocation is driven throughout the plant body, primarily from peaks of shoots to peaks of roots (from up to down). For long distances, relocation occurs via the stream of fluid in phloem vessels, but, for short-distance transport, a unique system of coordinated polar transport directly from cell to cell is exploited. This short-distance, active transport exhibits some morphogenetic properties. This process, the polar auxin transport , is directional, very strictly regulated, and based in uneven distribution of auxin efflux carriers on the plasma membrane, which send auxins in the proper direction. Pin-formed (PIN) proteins are vital in transporting auxin. [5][9] The regulation of PIN protein localisation in a cell determines the direction of auxin transport from cell, and concentrated effort of many cells creates peaks of auxin, or auxin maxima (regions having cells with higher auxin - a maximum). [5] Proper and timely auxin maxima within developing roots and shoots are necessary to organise the development of the organ. [4] [10][11] Surrounding auxin maxima are cells with low auxin troughs, or auxin minima. For example, in the Arabidopsis fruit, auxin minima have been shown to be important for its tissue development.

DANDRUFF

Dandruff [1] (Latin: Pityriasis simplex capillitii [1]) is the shedding of dead skin cells from the scalp (not to be confused with a dry scalp). Dandruff is sometimes caused by frequent exposure to extreme heat and cold. As it is normal for skin cells to die and flake off, a small amount of flaking is normal and common; about 487,000 cells/ cm2 get released normally after detergent treatment. [2] Some people, however, either chronically or as a result of certain triggers, experience an unusually large amount of flaking, up to 800,000 cells/ cm2, which can also be accompanied by redness and irritation. Most cases of dandruff can be easily treated with specialized shampoos. Zoomed version of microscopic picture of human dandruff Dandruff is a common scalp disorder affecting almost half of the population at the pre- pubertal age and of any sex and ethnicity. In some cultures dandruff is considered aesthetically displeasing. It often causes itching. It has been well established that keratinocytes play a key role in the expression and generation of immunological reactions during dandruff formation. The severity of dandruff may fluctuate with season as it often worsens in winter. [2] Those affected by dandruff find that it can cause social or self-esteem problems. Treatment may be important for both physiological and psychological reasons. [3] Causes As the epidermal layer continually replaces itself, cells are pushed outward where they eventually die and flake off. In most people, these flakes of skin are too small to be visible. However, certain conditions cause cell turnover to be unusually rapid, especially in the scalp. For people with dandruff, skin cells may mature and be shed in 2–7 days, as opposed to around a month in people without dandruff. The result is that dead skin cells are shed in large, oily clumps, which appear as white or grayish patches on the scalp, skin and clothes. Malassezia furfur species causes dandruff Dandruff has been shown to be the result of three required factors:[4] 1. Skin oil commonly referred to as sebum or sebaceous secretions[5] 2. The metabolic by-products of skin micro-organisms (most specifically Malassezia yeasts )[6][7][8] [9][10] 3. Individual susceptibility Older literature cites the fungus Malassezia furfur (previously known as Pityrosporum ovale) as the cause of dandruff. While this species does occur naturally on the skin surface of both healthy people and those with dandruff, in 2007 it was discovered that the responsible agent is a scalp specific fungus, Malassezia globosa,[11] that metabolizes triglycerides present in sebum by the expression of lipase, resulting in a lipid byproduct oleic acid (OA). During dandruff, the levels of Malassezia increase by 1.5 to 2 times its normal level. [2] Penetration by OA of the top layer of the epidermis, the stratum corneum, results in an inflammatory response in susceptible persons which disturbs homeostasis and results in erratic cleavage of stratum corneum cells.[8] Rarely, dandruff can be a manifestation of an allergic reaction to chemicals in hair gels, sprays, and shampoos, hair oils, or sometimes even dandruff medications like ketoconazole .[citation needed] There is some evidence that excessive perspiration and climate have significant roles in the pathogenesis of dandruff.[citation needed] Dandruff composition Dandruff scale is a cluster of corneocytes, which have retained a large degree of cohesion with one another and detach as such from the surface of the stratum corneum. The size and abundance of scales are heterogeneous from one site to another and over time. Parakeratotic cells often make up part of dandruff. Their numbers are related to the severity of the clinical manifestations, which may also be influenced by seborrhea.[2] Seborrhoeic dermatitis Main article: Seborrhoeic dermatitis Flaking is a symptom of seborrhoeic dermatitis. Joseph Bark notes that "Redness and itching is actually seborrheic dermatitis, and it frequently occurs around the folds of the nose and the eyebrow areas, not just the scalp." Dry, thick, well-defined lesions consisting of large, silvery scales may be traced to the less common psoriasis of the scalp. The spectrum of dandruff is difficult to define because it blurs with seborrhoeic dermatitis and some other scaly conditions. The inflammation and extension of scaling outside the scalp exclude the diagnosis of dandruff from seborrhoeic dermatitis.[5] However, many reports suggest a clear link between the two clinical entities - the mildest form of the clinical presentation of seborrhoeic dermatitis as dandruff, where the inflammation is minimal and remain subclinical. Histological examination reveals the scattered presence of lymphoid cells and squirting capillaries in the papillary dermis with hints of spongiosis and focal parakeratosis. [12][13] Seasonal changes, stress, and immuno-suppression seem to affect seborrheic dermatitis. [2] Treatment Shampoos use a combination of ingredients to control dandruff. The pathogenesis of dandruff involves hyperproliferation of keratinocytes, resulting in deregulation of keratinization. The corneocytes clump together, manifesting as large flakes of skin. Essentially, keratolytic agents such as salicylic acid and sulphur loosen the attachments between the corneocytes and allow them to get swiped off. Regulators of keratinization Zinc pyrithione (ZPT) heals the scalp by normalizing the epithelial keratinization or sebum production or both. Some studies have shown a significant reduction in the number of yeasts after use of ZPT, which is an antifungal and antibacterial agent. [14] A study by Warner et al. [15] demonstrates a dramatic reduction of structural abnormalities found in dandruff with the use of ZPT; the population abundance of Malassezia decreases, parakeratosis gets eliminated and corneocytes lipid inclusions are diminished.[2] Steroids The parakeratotic properties of topical corticosteroids depend on the structure of the agent, the vehicle and the skin onto which it is used. Corticosteroids work via their anti-inflammatory and antiproliferative effects. [16] Selenium sulfide It is believed that selenium sulfide controls dandruff via its anti Malassezia effect rather than by its antiproliferative effect, although it has an effect in reducing cell turnover. It has anti- seborrheic properties as well as cytostatic effect on cells of the epidermal and follicular epithelium. The excessive oiliness after use of this agent has been reported in many patients as adverse drug effect. Imidazole antifungal agents Imidazole topical antifungals such as ketoconazole act by blocking the biosynthesis of ergosterol, the primary sterol derivative of the fungal cell membrane. Changes in membrane permeability caused by ergosterol depletion are incompatible with fungal growth and survival. [17] Ketoconazole is a broad spectrum, antimycotic agent that is active against both Candida and M. furfur . Of all the imidazoles, ketoconazole has become the leading contender among treatment options because of its effectiveness in treating seborrheic dermatitis as well. [2]

CHIKENPOX

Malaria is a mosquito-borne infectious disease of humans and other animals caused by eukaryotic protists of the genus Plasmodium. The disease results from the multiplication of Plasmodium parasites within red blood cells, causing symptoms that typically include fever and headache, in severe cases progressing to coma or death. It is widespread in tropical and subtropical regions, including much of Sub-Saharan Africa , Asia, and the Americas. Five species of Plasmodium can infect and be transmitted by humans. Severe disease is largely caused by Plasmodium falciparum while the disease caused by Plasmodium vivax , Plasmodium ovale ,[1] and Plasmodium malariae is generally a milder disease that is rarely fatal. Plasmodium knowlesi is a zoonosis that causes malaria in macaques but can also infect humans. [2] [3] Malaria transmission can be reduced by preventing mosquito bites by distribution of mosquito nets and insect repellents, or by mosquito- control measures such as spraying insecticides and draining standing water (where mosquitoes breed). Despite a clear need, no vaccine offering a high level of protection currently exists. Efforts to develop one are ongoing.[4] A number of medications are also available to prevent malaria in travelers to malaria-endemic countries (prophylaxis ). A variety of antimalarial medications are available. Severe malaria is treated with intravenous or intramuscular quinine or, since the mid-2000s, the artemisinin derivative artesunate,[5] which is superior to quinine in both children and adults.[6] Resistance has developed to several antimalarial drugs, most notably chloroquine.[7] There were an estimated 225 million cases of malaria worldwide in 2009. [8] An estimated 655,000 people died from malaria in 2010,[9] a 5% decrease from the 781,000 who died in 2009 according to the World Health Organization's 2011 World Malaria Report, accounting for 2.23% of deaths worldwide. [8] Ninety percent of malaria- related deaths occur in sub- Saharan Africa, with the majority of deaths being young children. Plasmodium falciparum, the most severe form of malaria, is responsible for the vast majority of deaths associated with the disease.[10] Malaria is commonly associated with poverty, and can indeed be a cause of poverty [11] and a major hindrance to economic development . Signs and symptoms Main symptoms of malaria. [12] Typical fever patterns of malaria Symptoms of malaria include fever , shivering , arthralgia (joint pain), vomiting , anemia (caused by hemolysis ), jaundice, hemoglobinuria, retinal damage,[13] and convulsions . The classic symptom of malaria is cyclical occurrence of sudden coldness followed by rigor and then fever and sweating lasting four to six hours, occurring every two days in P. vivax and P. ovale infections, and every three days for P. malariae.[14]P. falciparum can have recurrent fever every 36–48 hours or a less pronounced and almost continuous fever. For reasons that are poorly understood, but that may be related to high intracranial pressure, children with malaria frequently exhibit abnormal posturing, a sign indicating severe brain damage. [15] Malaria has been found to cause cognitive impairments, especially in children. It causes widespread anemia during a period of rapid brain development and also direct brain damage. This neurologic damage results from cerebral malaria to which children are more vulnerable. [16][17] Cerebral malaria is associated with retinal whitening, [18] which may be a useful clinical sign in distinguishing malaria from other causes of fever. [19] Severe malaria is almost exclusively caused by Plasmodium falciparum infection, and usually arises 6– 14 days after infection. [20] Consequences of severe malaria include coma and death if untreated—young children and pregnant women are especially vulnerable. Splenomegaly (enlarged spleen), severe headache, cerebral ischemia, hepatomegaly (enlarged liver), hypoglycemia , and hemoglobinuria with renal failure may occur. Renal failure is a feature of blackwater fever , where hemoglobin from lysed red blood cells leaks into the urine. Severe malaria can progress extremely rapidly and cause death within hours or days. [20] In the most severe cases of the disease, fatality rates can exceed 20%, even with intensive care and treatment. [21] In endemic areas, treatment is often less satisfactory and the overall fatality rate for all cases of malaria can be as high as one in ten.[22] Over the longer term, developmental impairments have been documented in children who have suffered episodes of severe malaria. [23] Cause A Plasmodium sporozoite traverses the cytoplasm of a mosquito midgut epithelial cell in this false-color electron micrograph. Malaria parasites are members of the genus Plasmodium (phylum Apicomplexa ). In humans malaria is caused by P. falciparum, P. malariae, P. ovale , P. vivax and P. knowlesi .[24][25] While P. vivax is responsible for the largest number of malaria infections worldwide, infections by P. falciparum account for about 90% of the deaths from malaria.[26] Parasitic Plasmodium species also infect birds, reptiles, monkeys, chimpanzees and rodents.[27] There have been documented human infections with several simian species of malaria; however, with the exception of P. knowlesi, these are mostly of limited public health importance.[28] Malaria parasites contain apicoplasts, an organelle usually found in plants, complete with their own functioning genomes. These apicoplast are thought to have originated through the endosymbiosis of algae[29] and play a crucial role in various aspects of parasite metabolism e.g. fatty acid bio- synthesis. [30] To date, 466 proteins have been found to be produced by apicoplasts [31] and these are now being looked at as possible targets for novel anti-malarial drugs. Life cycle The parasite's secondary hosts are humans and other vertebrates. Female mosquitoes of the Anopheles genus are the primary, i.e. definitive hosts and act as transmission vectors . Young mosquitoes first ingest the malaria parasite by feeding on an infected human carrier and the infected Anopheles mosquitoes carry Plasmodium sporozoites in their salivary glands. A mosquito becomes infected when it takes a blood meal from an infected human. Once ingested, the parasite gametocytes taken up in the blood will further differentiate into male or female gametes and then fuse in the mosquito's gut. This produces an ookinete that penetrates the gut lining and produces an oocyst in the gut wall. When the oocyst ruptures, it releases sporozoites that migrate through the mosquito's body to the salivary glands, where they are then ready to infect a new human host. This type of transmission is occasionally referred to as anterior station transfer.[32] The sporozoites are injected into the skin, alongside saliva, when the mosquito takes a subsequent blood meal. Only female mosquitoes feed on blood while male mosquitoes feed on plant nectar,[33] thus males do not transmit the disease. The females of the Anopheles genus of mosquito prefer to feed at night. They usually start searching for a meal at dusk, and will continue throughout the night until taking a meal. Malaria parasites can also be transmitted by blood transfusions, although this is rare.[34] Recurrent malaria Malaria recurs after treatment for three reasons. Recrudescence occurs when parasites are not cleared by treatment, whereas reinfection indicates complete clearance with new infection established from a separate infective mosquito bite; both can occur with any malaria parasite species. Relapse is specific to P. vivax and P. ovale and involves re- emergence of blood-stage parasites from latent parasites (hypnozoites) in the liver. Describing a case of malaria as cured by observing the disappearance of parasites from the bloodstream can, therefore, be deceptive. The longest incubation period reported for a P. vivax infection is 30 years. [20] Approximately one in five of P. vivax malaria cases in temperate areas involve overwintering by hypnozoites (i.e., relapses begin the year after the mosquito bite).[35] Pathogenesis Further information: Plasmodium falciparum biology The life cycle of malaria parasites in the human body. A mosquito infects a person by taking a blood meal. First, sporozoites enter the bloodstream, and migrate to the liver. They infect liver cells (hepatocytes), where they multiply into merozoites, rupture the liver cells, and escape back into the bloodstream. Then, the merozoites infect red blood cells, where they develop into ring forms, trophozoites and schizonts which in turn produce further merozoites. Sexual forms (gametocytes) are also produced, which, if taken up by a mosquito, will infect the insect and continue the life cycle. Malaria develops via two phases: an exoerythrocytic and an erythrocytic phase. The exoerythrocytic phase involves infection of the hepatic system, or liver, whereas the erythrocytic phase involves infection of the erythrocytes, or red blood cells. When an infected mosquito pierces a person's skin to take a blood meal, sporozoites in the mosquito's saliva enter the bloodstream and migrate to the liver . Within minutes of being introduced into the human host, the sporozoites infect hepatocytes , multiplying asexually and asymptomatically for a period of 8–30 days. [36] Once in the liver, these organisms differentiate to yield thousands of merozoites, which, following rupture of their host cells, escape into the blood and infect red blood cells, thus beginning the erythrocytic stage of the life cycle. [36] The parasite escapes from the liver undetected by wrapping itself in the cell membrane of the infected host liver cell. [37] Within the red blood cells, the parasites multiply further, again asexually, periodically breaking out of their hosts to invade fresh red blood cells. Several such amplification cycles occur. Thus, classical descriptions of waves of fever arise from simultaneous waves of merozoites escaping and infecting red blood cells. Some P. vivax and P. ovale sporozoites do not immediately develop into exoerythrocytic-phase merozoites, but instead produce hypnozoites that remain dormant for periods ranging from several months (6–12 months is typical) to as long as three years. After a period of dormancy, they reactivate and produce merozoites. Hypnozoites are responsible for long incubation and late relapses in these two species of malaria. [38] The parasite is relatively protected from attack by the body's immune system because for most of its human life cycle it resides within the liver and blood cells and is relatively invisible to immune surveillance. However, circulating infected blood cells are destroyed in the spleen. To avoid this fate, the P. falciparum parasite displays adhesive proteins on the surface of the infected blood cells, causing the blood cells to stick to the walls of small blood vessels, thereby sequestering the parasite from passage through the general circulation and the spleen.[39] This "stickiness" is the main factor giving rise to hemorrhagic complications of malaria. High endothelial venules (the smallest branches of the circulatory system) can be blocked by the attachment of masses of these infected red blood cells. The blockage of these vessels causes symptoms such as in placental and cerebral malaria. In cerebral malaria the sequestrated red blood cells can breach the blood brain barrier possibly leading to coma.[40] Micrograph of a placenta from a stillbirth due to maternal malaria. H&E stain. Red blood cells are anuclear; blue/black staining in bright red structures (red blood cells) indicate foreign nuclei from the parasites Although the red blood cell surface adhesive proteins (called PfEMP1, for Plasmodium falciparum erythrocyte membrane protein 1) are exposed to the immune system, they do not serve as good immune targets, because of their extreme diversity; there are at least 60 variations of the protein within a single parasite and even more variants within whole parasite populations.[39] The parasite switches between a broad repertoire of PfEMP1 surface proteins, thus staying one step ahead of the pursuing immune system. Some merozoites turn into male and female gametocytes . If a mosquito pierces the skin of an infected person, it potentially picks up gametocytes within the blood. Fertilization and sexual recombination of the parasite occurs in the mosquito's gut. (Because sexual reproduction of the parasite defines the definitive host , the mosquito is the definitive host, whereas humans are the intermediate host.) New sporozoites develop and travel to the mosquito's salivary gland, completing the cycle. Pregnant women are especially attractive to the mosquitoes, [41] and malaria in pregnant women is an important cause of stillbirths, infant mortality and low birth weight, [42] particularly in P. falciparum infection, but also in other species infection, such as P. vivax.

MALERIA

Malaria is a mosquito-borne infectious disease of humans and other animals caused by eukaryotic protists of the genus Plasmodium. The disease results from the multiplication of Plasmodium parasites within red blood cells, causing symptoms that typically include fever and headache, in severe cases progressing to coma or death. It is widespread in tropical and subtropical regions, including much of Sub-Saharan Africa , Asia, and the Americas. Five species of Plasmodium can infect and be transmitted by humans. Severe disease is largely caused by Plasmodium falciparum while the disease caused by Plasmodium vivax , Plasmodium ovale ,[1] and Plasmodium malariae is generally a milder disease that is rarely fatal. Plasmodium knowlesi is a zoonosis that causes malaria in macaques but can also infect humans. [2] [3] Malaria transmission can be reduced by preventing mosquito bites by distribution of mosquito nets and insect repellents, or by mosquito- control measures such as spraying insecticides and draining standing water (where mosquitoes breed). Despite a clear need, no vaccine offering a high level of protection currently exists. Efforts to develop one are ongoing.[4] A number of medications are also available to prevent malaria in travelers to malaria-endemic countries (prophylaxis ). A variety of antimalarial medications are available. Severe malaria is treated with intravenous or intramuscular quinine or, since the mid-2000s, the artemisinin derivative artesunate,[5] which is superior to quinine in both children and adults.[6] Resistance has developed to several antimalarial drugs, most notably chloroquine.[7] There were an estimated 225 million cases of malaria worldwide in 2009. [8] An estimated 655,000 people died from malaria in 2010,[9] a 5% decrease from the 781,000 who died in 2009 according to the World Health Organization's 2011 World Malaria Report, accounting for 2.23% of deaths worldwide. [8] Ninety percent of malaria- related deaths occur in sub- Saharan Africa, with the majority of deaths being young children. Plasmodium falciparum, the most severe form of malaria, is responsible for the vast majority of deaths associated with the disease.[10] Malaria is commonly associated with poverty, and can indeed be a cause of poverty [11] and a major hindrance to economic development . Signs and symptoms Main symptoms of malaria. [12] Typical fever patterns of malaria Symptoms of malaria include fever , shivering , arthralgia (joint pain), vomiting , anemia (caused by hemolysis ), jaundice, hemoglobinuria, retinal damage,[13] and convulsions . The classic symptom of malaria is cyclical occurrence of sudden coldness followed by rigor and then fever and sweating lasting four to six hours, occurring every two days in P. vivax and P. ovale infections, and every three days for P. malariae.[14]P. falciparum can have recurrent fever every 36–48 hours or a less pronounced and almost continuous fever. For reasons that are poorly understood, but that may be related to high intracranial pressure, children with malaria frequently exhibit abnormal posturing, a sign indicating severe brain damage. [15] Malaria has been found to cause cognitive impairments, especially in children. It causes widespread anemia during a period of rapid brain development and also direct brain damage. This neurologic damage results from cerebral malaria to which children are more vulnerable. [16][17] Cerebral malaria is associated with retinal whitening, [18] which may be a useful clinical sign in distinguishing malaria from other causes of fever. [19] Severe malaria is almost exclusively caused by Plasmodium falciparum infection, and usually arises 6– 14 days after infection. [20] Consequences of severe malaria include coma and death if untreated—young children and pregnant women are especially vulnerable. Splenomegaly (enlarged spleen), severe headache, cerebral ischemia, hepatomegaly (enlarged liver), hypoglycemia , and hemoglobinuria with renal failure may occur. Renal failure is a feature of blackwater fever , where hemoglobin from lysed red blood cells leaks into the urine. Severe malaria can progress extremely rapidly and cause death within hours or days. [20] In the most severe cases of the disease, fatality rates can exceed 20%, even with intensive care and treatment. [21] In endemic areas, treatment is often less satisfactory and the overall fatality rate for all cases of malaria can be as high as one in ten.[22] Over the longer term, developmental impairments have been documented in children who have suffered episodes of severe malaria. [23] Cause A Plasmodium sporozoite traverses the cytoplasm of a mosquito midgut epithelial cell in this false-color electron micrograph. Malaria parasites are members of the genus Plasmodium (phylum Apicomplexa ). In humans malaria is caused by P. falciparum, P. malariae, P. ovale , P. vivax and P. knowlesi .[24][25] While P. vivax is responsible for the largest number of malaria infections worldwide, infections by P. falciparum account for about 90% of the deaths from malaria.[26] Parasitic Plasmodium species also infect birds, reptiles, monkeys, chimpanzees and rodents.[27] There have been documented human infections with several simian species of malaria; however, with the exception of P. knowlesi, these are mostly of limited public health importance.[28] Malaria parasites contain apicoplasts, an organelle usually found in plants, complete with their own functioning genomes. These apicoplast are thought to have originated through the endosymbiosis of algae[29] and play a crucial role in various aspects of parasite metabolism e.g. fatty acid bio- synthesis. [30] To date, 466 proteins have been found to be produced by apicoplasts [31] and these are now being looked at as possible targets for novel anti-malarial drugs. Life cycle The parasite's secondary hosts are humans and other vertebrates. Female mosquitoes of the Anopheles genus are the primary, i.e. definitive hosts and act as transmission vectors . Young mosquitoes first ingest the malaria parasite by feeding on an infected human carrier and the infected Anopheles mosquitoes carry Plasmodium sporozoites in their salivary glands. A mosquito becomes infected when it takes a blood meal from an infected human. Once ingested, the parasite gametocytes taken up in the blood will further differentiate into male or female gametes and then fuse in the mosquito's gut. This produces an ookinete that penetrates the gut lining and produces an oocyst in the gut wall. When the oocyst ruptures, it releases sporozoites that migrate through the mosquito's body to the salivary glands, where they are then ready to infect a new human host. This type of transmission is occasionally referred to as anterior station transfer.[32] The sporozoites are injected into the skin, alongside saliva, when the mosquito takes a subsequent blood meal. Only female mosquitoes feed on blood while male mosquitoes feed on plant nectar,[33] thus males do not transmit the disease. The females of the Anopheles genus of mosquito prefer to feed at night. They usually start searching for a meal at dusk, and will continue throughout the night until taking a meal. Malaria parasites can also be transmitted by blood transfusions, although this is rare.[34] Recurrent malaria Malaria recurs after treatment for three reasons. Recrudescence occurs when parasites are not cleared by treatment, whereas reinfection indicates complete clearance with new infection established from a separate infective mosquito bite; both can occur with any malaria parasite species. Relapse is specific to P. vivax and P. ovale and involves re- emergence of blood-stage parasites from latent parasites (hypnozoites) in the liver. Describing a case of malaria as cured by observing the disappearance of parasites from the bloodstream can, therefore, be deceptive. The longest incubation period reported for a P. vivax infection is 30 years. [20] Approximately one in five of P. vivax malaria cases in temperate areas involve overwintering by hypnozoites (i.e., relapses begin the year after the mosquito bite).[35] Pathogenesis Further information: Plasmodium falciparum biology The life cycle of malaria parasites in the human body. A mosquito infects a person by taking a blood meal. First, sporozoites enter the bloodstream, and migrate to the liver. They infect liver cells (hepatocytes), where they multiply into merozoites, rupture the liver cells, and escape back into the bloodstream. Then, the merozoites infect red blood cells, where they develop into ring forms, trophozoites and schizonts which in turn produce further merozoites. Sexual forms (gametocytes) are also produced, which, if taken up by a mosquito, will infect the insect and continue the life cycle. Malaria develops via two phases: an exoerythrocytic and an erythrocytic phase. The exoerythrocytic phase involves infection of the hepatic system, or liver, whereas the erythrocytic phase involves infection of the erythrocytes, or red blood cells. When an infected mosquito pierces a person's skin to take a blood meal, sporozoites in the mosquito's saliva enter the bloodstream and migrate to the liver . Within minutes of being introduced into the human host, the sporozoites infect hepatocytes , multiplying asexually and asymptomatically for a period of 8–30 days. [36] Once in the liver, these organisms differentiate to yield thousands of merozoites, which, following rupture of their host cells, escape into the blood and infect red blood cells, thus beginning the erythrocytic stage of the life cycle. [36] The parasite escapes from the liver undetected by wrapping itself in the cell membrane of the infected host liver cell. [37] Within the red blood cells, the parasites multiply further, again asexually, periodically breaking out of their hosts to invade fresh red blood cells. Several such amplification cycles occur. Thus, classical descriptions of waves of fever arise from simultaneous waves of merozoites escaping and infecting red blood cells. Some P. vivax and P. ovale sporozoites do not immediately develop into exoerythrocytic-phase merozoites, but instead produce hypnozoites that remain dormant for periods ranging from several months (6–12 months is typical) to as long as three years. After a period of dormancy, they reactivate and produce merozoites. Hypnozoites are responsible for long incubation and late relapses in these two species of malaria. [38] The parasite is relatively protected from attack by the body's immune system because for most of its human life cycle it resides within the liver and blood cells and is relatively invisible to immune surveillance. However, circulating infected blood cells are destroyed in the spleen. To avoid this fate, the P. falciparum parasite displays adhesive proteins on the surface of the infected blood cells, causing the blood cells to stick to the walls of small blood vessels, thereby sequestering the parasite from passage through the general circulation and the spleen.[39] This "stickiness" is the main factor giving rise to hemorrhagic complications of malaria. High endothelial venules (the smallest branches of the circulatory system) can be blocked by the attachment of masses of these infected red blood cells. The blockage of these vessels causes symptoms such as in placental and cerebral malaria. In cerebral malaria the sequestrated red blood cells can breach the blood brain barrier possibly leading to coma.[40] Micrograph of a placenta from a stillbirth due to maternal malaria. H&E stain. Red blood cells are anuclear; blue/black staining in bright red structures (red blood cells) indicate foreign nuclei from the parasites Although the red blood cell surface adhesive proteins (called PfEMP1, for Plasmodium falciparum erythrocyte membrane protein 1) are exposed to the immune system, they do not serve as good immune targets, because of their extreme diversity; there are at least 60 variations of the protein within a single parasite and even more variants within whole parasite populations.[39] The parasite switches between a broad repertoire of PfEMP1 surface proteins, thus staying one step ahead of the pursuing immune system. Some merozoites turn into male and female gametocytes . If a mosquito pierces the skin of an infected person, it potentially picks up gametocytes within the blood. Fertilization and sexual recombination of the parasite occurs in the mosquito's gut. (Because sexual reproduction of the parasite defines the definitive host , the mosquito is the definitive host, whereas humans are the intermediate host.) New sporozoites develop and travel to the mosquito's salivary gland, completing the cycle. Pregnant women are especially attractive to the mosquitoes, [41] and malaria in pregnant women is an important cause of stillbirths, infant mortality and low birth weight, [42] particularly in P. falciparum infection, but also in other species infection, such as P. vivax.