A pigment is a material that changes the color of reflected or transmitted light as the result of wavelength-selective absorption. This physical process differs from fluorescence and other forms of luminescence, in which a material emits light. Most materials selectively absorb certain wavelengths of light. Materials that humans have chosen and developed for use as pigments have special properties that make them useful for coloring other materials. A pigment must have a high tinting strength relative to the materials colors, it must be stable in solid form at ambient temperatures. For industrial applications, as well as in the arts and stability are desirable properties. Pigments that are not permanent are called fugitive. Fugitive pigments fade over time, or with exposure to light, while some blacken. Pigments are used for coloring paint, plastic, cosmetics and other materials. Most pigments used in manufacturing and the visual arts are dry colorants ground into a fine powder. For use in paint, this powder is added to a binder, a neutral or colorless material that suspends the pigment and gives the paint its adhesion.
A distinction is made between a pigment, insoluble in its vehicle, a dye, which either is itself a liquid or is soluble in its vehicle. A colorant can act as either a dye depending on the vehicle involved. In some cases, a pigment can be manufactured from a dye by precipitating a soluble dye with a metallic salt; the resulting pigment is called a lake pigment. The term biological pigment is used for all colored substances independent of their solubility. In 2006, around 7.4 million tons of inorganic and special pigments were marketed worldwide. Asia has the highest rate on a quantity basis followed by North America; the global demand on pigments was US$20.5 billion in 2009. Pigments appear colored because they selectively reflect and absorb certain wavelengths of visible light. White light is a equal mixture of the entire spectrum of visible light with a wavelength in a range from about 375 or 400 nanometers to about 760 or 780 nm; when this light encounters a pigment, parts of the spectrum are absorbed by the pigment.
Organic pigments such as diazo or phthalocyanine compounds feature conjugated systems of double bonds. Some inorganic pigments, such as vermilion or cadmium yellow, absorb light by transferring an electron from the negative ion to the positive ion; the other wavelengths or parts of the spectrum are scattered. The new reflected. Pigments, unlike fluorescent or phosphorescent substances, can only subtract wavelengths from the source light, never add new ones; the appearance of pigments is intimately connected to the color of the source light. Sunlight has a high color temperature and a uniform spectrum and is considered a standard for white light, while artificial light sources tend to have strong peaks in parts of their spectra. Viewed under different lights, pigments will appear different colors. Color spaces used to represent colors. Lab color measurements, unless otherwise noted, assume that the measurement was taken under a D65 light source, or "Daylight 6500 K", the color temperature of sunlight.
Other properties of a color, such as its saturation or lightness, may be determined by the other substances that accompany pigments. Binders and fillers added to pure pigment chemicals have their own reflection and absorption patterns, which can affect the final spectrum. For example, in pigment/binder mixtures, individual rays of light may not encounter pigment molecules and may be reflected unchanged; these stray rays of source light make. Pure pigment allows little white light to escape, producing a saturated color, while a small quantity of pigment mixed with a lot of white binder will appear unsaturated and pale due to incident white light escaping unchanged. Occurring pigments such as ochres and iron oxides have been used as colorants since prehistoric times. Archaeologists have uncovered evidence that early humans used paint for aesthetic purposes such as body decoration. Pigments and paint grinding equipment believed to be between 350,000 and 400,000 years old have been reported in a cave at Twin Rivers, near Lusaka, Zambia.
Before the Industrial Revolution, the range of color available for art and decorative uses was technologically limited. Most of the pigments in use were pigments of biological origin. Pigments from unusual sources such as botanical materials, animal waste and mollusks were harvested and traded over long distances; some colors were impossible to obtain, given the range of pigments that were available. Blue and purple came to be associated with royalty because of their rarity. Biological pigments were difficult to acquire, the details of their production were kept secret by the manufacturers. Tyrian Purple is a pigment made from the mucus of one of several species of Murex snail. Production of Tyrian Purple for use as a fabric dye began as early as 1200 BCE by the Phoenicians, was continued by the Greeks and Romans until 1453 CE, with the fall of Constantinople; the pigment was expensive and complex to produce, items colored with it became associated with power and wealth. Greek historian Theopompus, writing in the 4th century BCE, reported that "purple for dyes fetched its weight in silver at Colophon."Mineral pigments were traded over long distances.
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A DNA virus is a virus that has DNA as its genetic material and replicates using a DNA-dependent DNA polymerase. The nucleic acid is double-stranded DNA but may be single-stranded DNA. DNA viruses belong to either Group Group II of the Baltimore classification system for viruses. Single-stranded DNA is expanded to double-stranded in infected cells. Although Group VII viruses such as hepatitis B contain a DNA genome, they are not considered DNA viruses according to the Baltimore classification, but rather reverse transcribing viruses because they replicate through an RNA intermediate. Notable diseases like smallpox and the chickenpox are caused by such DNA viruses. Genome organization within this group varies considerably; some have circular genomes. Some families have circularly permuted linear genomes. Others have linear genomes with covalently closed ends. A virus infecting archaea was first described in 1974. Several others have been described since: most have head-tail morphologies and linear double-stranded DNA genomes.
Other morphologies have been described: spindle shaped, rod shaped, filamentous and spherical. Additional morphological types may exist. Orders within this group are defined on the basis of morphology rather than DNA sequence similarity, it is thought that morphology is more conserved in this group than sequence similarity or gene order, variable. Three orders and 31 families are recognised. A fourth order — Megavirales — for the nucleocytoplasmic large DNA viruses has been proposed; this proposal has yet to be ratified by the ICTV. Four genera are recognised. Fifteen families are enveloped; these include all three families in the order Herpesvirales and the following families: Ascoviridae, Asfarviridae, Fuselloviridae, Guttaviridae, Iridoviridae, Lipothrixviridae and Poxviridae. Bacteriophages belonging to the families Tectiviridae and Corticoviridae have a lipid bilayer membrane inside the icosahedral protein capsid and the membrane surrounds the genome; the crenarchaeal virus Sulfolobus turreted.
The genomes in this group vary from ~10 kilobases to over 2.5 megabases in length. The largest bacteriophage known is Klebsiella Phage vB_KleM-RaK2 which has a genome of 346 kilobases; the virophages are a group of viruses. A virus with a novel method of genome packing infecting species of the genus Sulfolobus has been described; as this virus does not resemble any known virus it has been classified into a new family, the Portogloboviridae. Another Sulfolobus infecting virus - Sulfolobus ellipsoid virus 1 - has been described; this enveloped virus may be classified into a new taxon. Species of the order Caudovirales and of the families Corticoviridae and Tectiviridae infect bacteria. Species of the order Ligamenvirales and the families Ampullaviridae, Clavaviridae, Globuloviridae, Guttaviridae and Turriviridae infect hyperthermophilic archaea species of the Crenarchaeota. Species of the order Herpesvirales and of the families Adenoviridae, Iridoviridae, Papillomaviridae and Poxviridae infect vertebrates.
Species of the families Ascovirus, Hytrosaviridae and Polydnaviruses and of the genus Nudivirus infect insects. Species of the family Mimiviridae and the species Marseillevirus, Mavirus virophage and Sputnik virophage infect protozoa. Species of the family Nimaviridae infect crustaceans. Species of the family Phycodnaviridae and the species Organic Lake virophage infect algae; these are the only known dsDNA viruses. Species of the family Plasmaviridae infect species of the class Mollicutes. Species of the family Pandoraviridae infect amoebae. Species of the genus Dinodnavirus infect dinoflagellates; these are the only known viruses. Species of the genus Rhizidiovirus infect stramenopiles; these are the only known dsDNA viruses. Species of the genus Salterprovirus and Sphaerolipoviridae infect species of the Euryarchaeota. Order Caudovirales Family Myoviridae—includes Enterobacteria phage T4 Family Podoviridae—includes Enterobacteria phage T7 Family Siphoviridae—includes Enterobacteria phage λ Order Herpesvirales Family Alloherpesviridae Family Herpesviridae—includes human herpesviruses, Varicella Zoster virus Family Malacoherpesviridae Order Ligamenvirales Family Lipothrixviridae Family Rudiviridae Unassigned families Family Adenoviridae—includes viruses which cause human adenovirus infection Family Ampullaviridae Family Ascoviridae Family Asfarviridae—includes African swine fever virus Family Baculoviridae Family Bicaudaviridae Family Clavaviridae Family Corticoviridae Family Fuselloviridae Family Globuloviridae Family Guttaviridae Family Hytrosaviridae Family Iridoviridae Family Lavidaviridae Family Marseilleviridae Family Mimiviridae Family Nudiviridae Family Nimaviridae Family Pandoraviridae Family Papillomaviridae Family Phycodnaviridae Family Plasmaviridae Family Polydnaviruses Family Polyomaviridae—includes Simian virus 40, JC virus, BK virus Family Poxviridae—includes Cowpox virus, smallpox Family Sphaerolipoviridae Family Tectiviridae Family Tristromaviridae Family Turriviridae Unassigned genera Dinodnavirus Salterprovirus Rhizidiovirus Unassigned species Abalone shriveling syndrome-associated virus Bandicoot papillomatosis carcinomatosis vi
Vesicle (biology and chemistry)
In cell biology, a vesicle is a large structure within a cell, or extracellular, consisting of liquid enclosed by a lipid bilayer. Vesicles form during the processes of secretion and transport of materials within the plasma membrane. Alternatively, they may be prepared artificially. If there is only one phospholipid bilayer, they are called unilamellar liposome vesicles; the membrane enclosing the vesicle is a lamellar phase, similar to that of the plasma membrane and vesicles can fuse with the plasma membrane to release their contents outside the cell. Vesicles can fuse with other organelles within the cell. Vesicles perform a variety of functions; because it is separated from the cytosol, the inside of the vesicle can be made to be different from the cytosolic environment. For this reason, vesicles are a basic tool used by the cell for organizing cellular substances. Vesicles are involved in metabolism, buoyancy control, temporary storage of food and enzymes, they can act as chemical reaction chambers.
The 2013 Nobel Prize in Physiology or Medicine was shared by James Rothman, Randy Schekman and Thomas Südhof for their roles in elucidating the makeup and function of cell vesicles in yeasts and in humans, including information on each vesicle's parts and how they are assembled. Vesicle dysfunction is thought to contribute to Alzheimer's disease, some hard-to-treat cases of epilepsy, some cancers and immunological disorders and certain neurovascular conditions. Vacuoles are cellular organelles which contain water. Plant cells have a large central vacuole in the center of the cell, used for osmotic control and nutrient storage. Contractile vacuoles are found in certain protists those in Phylum Ciliophora; these vacuoles take water from the cytoplasm and excrete it from the cell to avoid bursting due to osmotic pressure. Lysosomes are involved in cellular digestion. Food can be taken from outside the cell into food vacuoles by a process called endocytosis; these food vacuoles fuse with lysosomes which break down the components so that they can be used in the cell.
This form of cellular eating is called phagocytosis. Lysosomes are used to destroy defective or damaged organelles in a process called autophagy, they fuse with the membrane of the damaged organelle. Transport vesicles can move molecules between locations inside the cell, e.g. proteins from the rough endoplasmic reticulum to the Golgi apparatus. Membrane-bound and secreted proteins are made on ribosomes found in the rough endoplasmic reticulum. Most of these proteins mature in the Golgi apparatus before going to their final destination which may be to lysosomes, peroxisomes, or outside of the cell; these proteins travel within the cell inside of transport vesicles. Secretory vesicles contain materials. Cells have many reasons to excrete materials. One reason is to dispose of wastes. Another reason is tied to the function of the cell. Within a larger organism, some cells are specialized to produce certain chemicals; these chemicals are released when needed. Synaptic vesicles are located at presynaptic terminals in neurons and store neurotransmitters.
When a signal comes down an axon, the synaptic vesicles fuse with the cell membrane releasing the neurotransmitter so that it can be detected by receptor molecules on the next nerve cell. In animals endocrine tissues release hormones into the bloodstream; these hormones are stored within secretory vesicles. A good example is the endocrine tissue found in the islets of Langerhans in the pancreas; this tissue contains many cell types. Secretory vesicles hold the enzymes that are used to make the cell walls of plants, fungi and Archaea cells as well as the extracellular matrix of animal cells. Bacteria, Archaea and parasites release membrane vesicles containing varied but specialized toxic compounds and biochemical signal molecules, which are transported to target cells to initiate processes in favour of the microbe, which include invasion of host cells and killing of competing microbes in the same niche. Extracellular vesicles are produced by all domains of life including complex eukaryotes, both Gram-negative and Gram-positive bacteria and fungi.
Exosomes: membraneous vesicles of endocytic origin enriched in CD63 and CD81. Microvesicle, that are shed directly from the plasma membrane. Membrane particles, or large membranous vesicles CD133+, CD63− Apoptotic blebs or blebbing vesicles: released by dying cells; these are separated by density by differential centrifugation. Ectosomes were named in 2008. In humans, endogenous extracellular vesicles play a role in coagulation, intercellular signaling and waste management, they are implicated in the pathophysiological processes involved in multiple diseases, including cancer. Extracellular vesicles have raised interest as a potential source of biomarker discovery because of their role in intercellular communication, release into accessible body fluids and the resemblance of their molecular content to that of the releasing cells; the extracellular vesicles of stem cells known as the secretome of stem cells, are being researched and applied for therapeutic purposes, predominantly degenerative, auto-immune and/or inflammatory diseases.
Nil Fyodorovich Filatov was a physician, considered the founder of Russian paediatrics. His nephew Vladimir Filatov was a prominent ophthalmologist. Having graduated from the Moscow University, he practised as a country doctor in his native region. In 1872-1874, Filatov took additional training in Vienna, Berlin and Prague. In 1876, he upheld a thesis on bronchitis and pneumonia, obtained a doctor degree. Nil Filatov is most famous for describing infectious mononucleosis in 1887 and Dukes' disease in 1885. In cooperation with Georgy Gabrichevsky he introduced serumal treatment of diphtheria in 1894, he created a number of handbooks on paediatrics, which were not only popular in Russia, but translated into German, Italian and Hungarian. In 1892, Filatov established the Society of Paediatricians in Moscow; the oldest children's hospitals in Moscow, in Russia are named after him. Nil Filatov at Who Named It? Biography by the 1st MSMU
Herpes simplex virus
Herpes simplex virus 1 and 2 known by their taxonomical names Human alphaherpesvirus 1 and Human alphaherpesvirus 2, are two members of the human Herpesviridae family, a set of viruses that produce viral infections in the majority of humans. Both HSV-1 and HSV-2 are common and contagious, they can be spread. About 67% of the world population under the age of 50 has HSV-1. In the United States more than one-in-six people have HSV-2. Although it can be transmitted through any intimate contact, it is one of the most common sexually transmitted infections. Many of those who are infected never develop symptoms. Symptoms, when they occur, may include watery blisters in the skin or mucous membranes of the mouth, nose, or genitals. Lesions heal with a scab characteristic of herpetic disease. Sometimes, the viruses cause mild or atypical symptoms during outbreaks. However, they can cause more troublesome forms of herpes simplex; as neurotropic and neuroinvasive viruses, HSV-1 and -2 persist in the body by hiding from the immune system in the cell bodies of neurons.
After the initial or primary infection, some infected people experience sporadic episodes of viral reactivation or outbreaks. In an outbreak, the virus in a nerve cell becomes active and is transported via the neuron's axon to the skin, where virus replication and shedding occur and cause new sores. HSV-1 and HSV-2 are transmitted by contact with an infected person who has reactivations of the virus. HSV-2 is periodically shed in the human genital tract, most asymptomatically. Most sexual transmissions occur during periods of asymptomatic shedding. Asymptomatic reactivation means that the virus causes atypical, subtle, or hard-to-notice symptoms that are not identified as an active herpes infection, so acquiring the virus is possible if no active HSV blisters or sores are present. In one study, daily genital swab samples found HSV-2 at a median of 12–28% of days among those who have had an outbreak, 10% of days among those suffering from asymptomatic infection, with many of these episodes occurring without visible outbreak.
In another study, 73 subjects were randomized to receive valaciclovir 1 g daily or placebo for 60 days each in a two-way crossover design. A daily swab of the genital area was self-collected for HSV-2 detection by polymerase chain reaction, to compare the effect of valaciclovir versus placebo on asymptomatic viral shedding in immunocompetent, HSV-2 seropositive subjects without a history of symptomatic genital herpes infection; the study found that valaciclovir reduced shedding during subclinical days compared to placebo, showing a 71% reduction. About 88% of patients treated with valaciclovir had no recognized signs or symptoms versus 77% for placebo. For HSV-2, subclinical shedding may account for most of the transmission. Studies on discordant partners show that the transmission rate is 5 per 10,000 sexual contacts. Atypical symptoms are attributed to other causes, such as a yeast infection. HSV-1 is acquired orally during childhood, it may be sexually transmitted, including contact with saliva, such as kissing and mouth-to-genital contact.
HSV-2 is a sexually transmitted infection, but rates of HSV-1 genital infections are increasing. Both viruses may be transmitted vertically during childbirth. However, the risk of infection transmission is minimal if the mother has no symptoms or exposed blisters during delivery; the risk is considerable when the mother is infected with the virus for the first time during late pregnancy. Herpes simplex viruses can affect areas of skin exposed to contact with an infected person. An example of this is herpetic whitlow, a herpes infection on the fingers; this was a common affliction of dental surgeons prior to the routine use of gloves when conducting treatment on patients. Animal herpes viruses all share some common properties; the structure of herpes viruses consists of a large, double-stranded, linear DNA genome encased within an icosahedral protein cage called the capsid, wrapped in a lipid bilayer called the envelope. The envelope is joined to the capsid by means of a tegument; this complete particle is known as the virion.
HSV-1 and HSV-2 each contain at least 74 genes within their genomes, although speculation over gene crowding allows as many as 84 unique protein coding genes by 94 putative ORFs. These genes encode a variety of proteins involved in forming the capsid and envelope of the virus, as well as controlling the replication and infectivity of the virus; these genes and their functions are summarized in the table below. The genomes of HSV-1 and HSV-2 are complex and contain two unique regions called the long unique region and the short unique region. Of the 74 known ORFs, UL contains 56 viral genes, whereas US contains only 12. Transcription of HSV genes is catalyzed by RNA polymerase II of the infected host. Immediate early genes, which encode proteins that regulate the expression of early and late viral genes, are the first to be expressed following infection. Early gene expression follows, to allow the synthesis of enzymes involved in DNA replication and the production of certain envelope glycoproteins.
Expression of late genes occurs last. Five proteins from form the viral capsid - UL6, UL18, UL35, UL38, the major capsid p
Infection of the skin is distinguished from dermatitis, inflammation of the skin, but a skin infection can result in skin inflammation. Skin inflammation due to skin infection is called infective dermatitis. Bacterial skin infections affected about 155 million people and cellulitis occurred in about 600 million people in 2013. Bacterial skin infections include: Folliculitis is an infection of the hair follicle that can resemble pimples. Impetigo is a contagious bacterial skin infection most common among pre-school children, it is caused by Staphylococcus aureus, sometimes by Streptococcus pyogenes. Erysipelas is an acute streptococcus bacterial infection of the deep epidermis with lymphatic spread. Cellulitis is a diffuse inflammation of connective tissue with severe inflammation of dermal and subcutaneous layers of the skin. Cellulitis can be caused by normal skin flora or by exogenous bacteria, occurs where the skin has been broken: cracks in the skin, blisters, insect bites, surgical wounds, intravenous drug injection or sites of intravenous catheter insertion.
Skin on the face or lower legs is most affected by this infection, though cellulitis can occur on any part of the body. Fungal skin infections may present as either a superficial or deep infection of the skin, and/or nails; as of 2010, they affect about one billion people globally. Parasitic infestations and bites in humans are caused by several groups of organisms belonging to the following phyla: Annelida, Bryozoa, Cnidaria, Echinodermata, Nemathelminthes and Protozoa. Virus-related cutaneous conditions are caused by two main groups of viruses–DNA and RNA types–both of which are obligatory intracellular parasites. Dempster-Shafer Theory is used for detecting skin infection and displaying the result of the detection process
Human alphaherpesvirus 3
Human alphaherpesvirus 3 referred to as the varicella-zoster virus, is one of eight herpesviruses known to infect humans. It causes chickenpox, a disease most affecting children and young adults, shingles in adults. VZV is a worldwide pathogen known by many names: chickenpox virus, varicella virus, zoster virus, Human herpesvirus 3. VZV infections are species-specific to humans, but can survive in external environments for a few hours, maybe a day or two. VZV multiplies in the lungs, causes a wide variety of symptoms. After the primary infection, the virus goes dormant in the nerves, including the cranial nerve ganglia, dorsal root ganglia, autonomic ganglia. Many years after the person has recovered from chickenpox, VZV can reactivate to cause neurologic conditions. Primary varicella zoster virus infection results in chickenpox, which may result in complications including encephalitis, pneumonia, or bronchitis; when clinical symptoms of chickenpox have resolved, VZV remains dormant in the nervous system of the infected person, in the trigeminal and dorsal root ganglia.
VZV enters through the respiratory system. Having an incubation period of 10–21 days, averaging at 14 days. Targeting the skin and peripheral nerve, the period of illness is from 3 to 4 days. 1 -- 2 days before the rashes appear, is. Some signs and symptoms are vesicles that fill with pus and scab before healing. Lesions tend to stay towards the face and lower back sometimes on the chest and shoulders. Shingles stay located around the waist. In about 10–20% of cases, VZV reactivates in life, producing a disease known as shingles or herpes zoster. VZV can infect the central nervous system, with a 2013 article reporting an incidence rate of 1.02 cases per 100,000 inhabitants in Switzerland, an annual incidence rate of 1.8 cases per 100,000 inhabitants in Sweden. Other serious complications of varicella zoster infection include postherpetic neuralgia, Mollaret's meningitis, zoster multiplex, inflammation of arteries in the brain leading to stroke, herpes ophthalmicus, or zoster sine herpete. In Ramsay Hunt syndrome, VZV affects the geniculate ganglion giving lesions that follow specific branches of the facial nerve.
Symptoms may include painful blisters on the tongue and ear along with one sided facial weakness and hearing loss. If infected during initial stages of pregnancy severe damage to the fetus can take place. Reye’s syndrome can happen after initial infection, continuous vomiting and shows signs of brain dysfunction: extreme drowsiness or combative behavior. In some cases, death or coma can follow. Reye’s syndrome affects children and teenagers, using aspirin during infection can increase this risk. VZV is related to the herpes simplex viruses, sharing much genome homology; the known envelope glycoproteins correspond with those in HSV. VZV fails to produce the LAT that play an important role in establishing HSV latency. VZV virons are 180 -- 200 nm in diameter, their lipid envelope encloses the 100 nm nucleocapsid of 162 hexameric and pentameric capsomeres arranged in an icosahedral form. Its DNA is a single, double-stranded molecule, 125,000 nt long; the capsid is surrounded by loosely associated proteins known collectively as the tegument.
The tegument is in turn covered by a lipid envelope studded with glycoproteins that are displayed on the exterior of the virion, each 8 nm long. The genome was first sequenced in 1986, it is a linear duplex DNA molecule, a laboratory strain has 124,884 base pairs. The genome has 2 predominant isomers, depending on the orientation of the S segment, P and IS which are present with equal frequency for a total frequency of 90–95%; the L segment can be inverted resulting in a total of four linear isomers. This is distinct from HSV's equiprobable distribution, the discriminatory mechanism is not known. A small percentage of isolated molecules are circular genomes. There are at least 70 open reading frames in the genome. There are at least five clades of this virus. Clades 1 and 3 include European/North American strains. Clade 4 includes some strains from Europe but its geographic origins need further clarification. Commonality with HSV1 and HSV2 indicates a common ancestor. Relation with other human herpes viruses is less strong, but many homologues and conserved gene blocks are still found.
There are four genotypes that do not fit into these clades. The current distribution of these clades is Europe. Allocation of VZV strains to clades required sequence of whole virus genome. All molecular epidemiological data on global VZV strains distribution obtained with targeted sequencing of selected regions. Phylogenetic analysis of VZV genomic sequences resolves wild-type strains into 9 genotypes. Complete sequences for M3 and M4 strains are unavailable, but targeted analyses of representative strains suggest they are stable, cir