CHOPCHOP accepts a wide range of inputs (gene identifiers, genomic regions or pasted sequences) and provides an array of advanced options for target selection. ... The ease-of-use and speed of CHOPCHOP make it a valuable tool for genome engineering.
Nucleic acid and its related compounds, such as pyrimidines and purines, are well known to absorb UV light at a wavelength of 260 nm
Ohtsuka K1, Osakabe MM.Author informationAbstractThe herbivorous spider mite Tetranychus urticae usually remains on the lower leaf surfaces of its host plants. Although terrestrial animals are generally thought to be well protected from damage because of UV radiation, insect herbivory frequently increases when solar UV-B (280-315 nm) radiation is attenuated. As UV transmission through leaves is generally low because of the accumulation of compounds that act as selective sunscreens (e.g., phenolics), we hypothesized that T. urticae avoids solar UV-B radiation by staying on lower leaf surfaces. We examined whether artificial UV irradiation and solar UV affected the survival and reproduction of T. urticae and whether staying on lower leaf surfaces was beneficial to their performance under ambient UV radiation. We found that T. urticae was not well protected from UV-B radiation, because artificial UV-B irradiation strongly decreased survivorship and egg production. More importantly; compulsory solar UV irradiation treatments also had lethal effects on T. urticae, whereas the mites could avoid them if they remained on the lower leaf surfaces of their host plants. These results showed that access to habitats protected from sunlight, such as lower leaf surfaces, is likely essential for T. urticae survival under ambient UV-B radiation. The lethal effects of solar UV radiation may also affect the population dynamics of spider mites, and habitat (resource) limitation may increase the probability of interspecific interactions, such as competition and predation. In turn, the occurrence of these interactions in sheltered areas may be associated with observed increases in herbivory under conditions of solar UV-B-attenuation. Screening, in medicine, is a strategy used in a population to identify the possible presence of an as-yet-undiagnoseddisease in individuals without signs or symptoms. This can include individuals with pre-symptomatic or unrecognized symptomatic disease. As such, screening tests are somewhat unique in that they are performed on persons apparently in good health.
Screening interventions are designed to identify disease in a community early, thus enabling earlier intervention and management in the hope to reduce mortality and suffering from a disease. Although screening may lead to an earlier diagnosis, not all screening tests have been shown to benefit the person being screened; overdiagnosis, misdiagnosis, and creating a false sense of security are some potential adverse effects of screening. For these reasons, a test used in a screening program, especially for a disease with low incidence, must have good sensitivity in addition to acceptablespecificity.[1] Several types of screening exist: universal screening involves screening of all individuals in a certain category (for example, all children of a certain age). Case finding involves screening a smaller group of people based on the presence of risk factors (for example, because a family member has been diagnosed with a hereditary disease). Screening interventions are not designed to be diagnostic, and often have significant rates of both false positive and false negative results. Contents [hide]
Principles of screening[edit]In 1968 the World Health Organization published guidelines on the Principles and practice of screening for disease, which often referred to as Wilson's criteria.[2]The principles are still broadly applicable today:
Synthesis of emerging screening criteria proposed over the past 40 years • The screening programme should respond to a recognized need. • The objectives of screening should be defined at the outset. • There should be a defined target population. • There should be scientific evidence of screening programme effectiveness. • The programme should integrate education, testing, clinical services and programme management. • There should be quality assurance, with mechanisms to minimize potential risks of screening. • The programme should ensure informed choice, confidentiality and respect for autonomy. • The programme should promote equity and access to screening for the entire target population. • Programme evaluation should be planned from the outset. • The overall benefits of screening should outweigh the harm. [3] Types of screening[edit] A mobile clinic used to screen coal miners at risk of black lung disease
Medical equipment used in screening[edit]Medical equipment used in screening tests is usually different from equipment used in diagnostic tests as screening tests are used to indicate the likely presence or absence of a disease or condition in people not presenting symptoms; while diagnostic medical equipment is used to make quantitative physiological measurements to confirm and determine the progress of a suspected disease or condition. Medical screening equipment must be capable of fast processing of many cases, but may not need to be as precise as diagnostic equipment. Limitations of screening[edit]Screening can detect medical conditions at an early stage before symptoms present while treatment is more effective than for later detection. In the best of cases lives are saved. Like any medical test, the tests used in screening are not perfect. The test result may incorrectly show positive for those without disease (false positive), or negative for people who have the condition (false negative). Limitations of screening programmes can include:
Analysis of screening[edit]To many people, screening instinctively seems like an appropriate thing to do, because catching something earlier seems better. However, no screening test is perfect. There will always be the problems with incorrect results and other issues listed above. Before a screening program is implemented, it should ideally be looked at to ensure that putting it in place would do more good than harm. The best studies for assessing whether a screening test will increase a population's health are rigorous randomized controlled trials. When studying a screening program using case-control or, more usually, cohort studies, various factors can cause the screening test to appear more successful than it really is. A number of different biases, inherent in the study method, will skew results. Screening can certainly improve outcomes, but this must be confirmed with proper statistical analysis, not simplistic comparison of numbers. Lead time bias[edit]For more details on this topic, see Lead time bias. Lead time bias leads to longer perceived survival with screening, even if the course of the disease is not alteredThe intention of screening is to diagnose a disease earlier than it would be without screening. Without screening the disease may be discovered later, when symptoms appear. Even if in both cases a person will die at the same time, because we diagnosed the disease earlier with screening thesurvival time since diagnosis is longer with screening; but life span has not been prolonged, and there will be added anxiety as the patient must live with knowledge of the disease for longer. Looking at statistics of survival time since diagnosis, screening will show an increase (this gain is called lead time). If we do not think about what survival time actually means in this context, we might attribute success to a screening test that does nothing but advance diagnosis; comparing statistics of mortality due to a disease in a screened and unscreened population gives more meaningful information. Length time bias[edit]For more details on this topic, see Length time bias. Length time bias leads to better perceived survival with screening, even if the course of the disease is not altered.Many screening tests involve the detection of cancers. It is often hypothesized that slower-growing tumors have better prognoses than tumors with high growth rates. Screening is more likely to detect slower-growing tumors (due to longer pre-clinical sojourn time), which may be less deadly. Thus screening may tend to detect cancers that would not have killed the patient or even been detected prior to death from other causes. Selection bias[edit]For more details on this topic, see Selection bias.Not everyone will partake in a screening program. There are factors that differ between those willing to get tested and those who are not. If people with a higher risk of a disease are more likely to be screened, for instance women with a family history of breast cancer are more likely than other women to join a mammography program, then a screening test will look worse than it really is: negative outcomes among the screened population will be higher than for a random sample. Selection bias may also make a test look better than it really is. If a test is more available to young and healthy people (for instance if people have to travel a long distance to get checked) then fewer people in the screening population will have negative outcomes than for a random sample, and the test will seem to make a positive difference. Overdiagnosis[edit]For more details on this topic, see Overdiagnosis.Screening may identify abnormalities that would never cause a problem in a person's lifetime. An example of this is prostate cancer screening; it has been said that "more men die with prostate cancer than of it".[6] Autopsy studies have shown that a high proportion of elderly men who have died of other causes are found to have had prostate cancer. Aside from issues with unnecessary treatment (prostate cancer treatment is by no means without risk), overdiagnosis makes a study look good at picking up abnormalities, even though they are sometimes harmless. Overdiagnosis occurs when all of these people with harmless abnormalities are counted as "lives saved" by the screening, rather than as "healthy people needlessly harmed by overdiagnosis". Avoidance of bias[edit]The best way to minimise these biases is to use a randomized controlled trial. These need to be very large[clarification needed], and very strict in terms of research procedure. Such studies take a long time and are expensive, but provide the best information for evidence-based medicine. AbstractThe two-spotted spider mite, Tetranychus urticae was exposed to UV-C (250 nm), UV-B (300 nm), and UV-A (350 nm). In non-diapausing females, the median effective doses for 50% mortality plus escape incidence (ED50) were 21 (UV-C) and 104 kJ m−2 (UV-B); those for 50% oviposition rate in continuous darkness-treated mites were 6.2 (UV-C) and 41 kJ m−2 (UV-B). No significant effects of UV-A on mortality and oviposition rate were observed. The ED50 values for UV-B were similar to the natural UV-B observed for 2–5 days in summer when T. urticae inhabits the undersides of leaves. Therefore, T. urticaepossibly uses leaves as a filter to avoid the deleterious effects of UV-B. In diapausing females, low mortality was observed even at high doses of UV radiation, but more than half escaped even at low doses. The orange body color of diapausing females results from accumulation of carotenoids, a scavenger for UV-induced reactive oxygen species; this may explain the low mortality of diapausing females. Diapausing females may overcome the deleterious effects of UV-B during winter in the absence of leaves by emigrating to UV-free environments and by accumulating carotenoids.
Keywords
From Wikipedia, the free encyclopedia Look up diapause in Wiktionary, the free dictionary. Part of a series on Animal dormancy
Diapause, when referencing animal dormancy, is the delay in development in response to regularly and recurring periods of adverse environmental conditions.[1][2] It is considered to be a physiological state of dormancy with very specific initiating and inhibiting conditions. Diapause is a mechanism used as a means to survive predictable, unfavorable environmental conditions, such as temperature extremes, drought, or reduced food availability. Diapause is most often observed in arthropods, especially insects, and in the embryos of many of the oviparousspecies of fish in the order Cyprinodontiformes.[3] (Diapause does not occur in embryos of the viviparous andovoviviparous species of Cyprinodontiformes.) Diapause is not only induced in an organism by specific stimuli or conditions, but once it is initiated, only certain other stimuli are capable of bringing the organism out of diapause. The latter feature is essential in distinguishing diapause as a different phenomenon from other forms of dormancy, such as stratification and hibernation. Activity levels of diapausing stages can vary considerably among species. Diapause may occur in a completely immobile stage, such as the pupae and eggs, or it may occur in very active stages that undergo extensive migrations, such as the adult Monarch butterfly, Danaus plexippus. In cases where the insect remains active, feeding is reduced and reproductive development is slowed or halted. CarotenoidFrom Wikipedia, the free encyclopedia
The orange ring surroundingGrand Prismatic Spring is due to carotenoid molecules, produced by mats of algae and bacteria.Carotenoids, also called tetraterpenoids, are organic pigments that are found in the chloroplasts and chromoplasts of plants and some other photosynthetic organisms, including some bacteria and some fungi. Carotenoids can be produced from fats and other basic organic metabolic building blocks by all these organisms. The only animals known to produce carotenoids are aphids and spider mites, which acquired the ability and genes from fungi.[1] Carotenoids from the diet are stored in the fatty tissues of animals, and exclusively carnivorous animals obtain the compounds from animal fat. There are over 600 known carotenoids; they are split into two classes, xanthophylls (which contain oxygen) andcarotenes (which are purely hydrocarbons, and contain no oxygen). All derivatives of tetraterpenes, meaning that they are produced from 8 isoprene molecules and contain 40 carbon atoms. In general, carotenoids absorb wavelengths ranging from 400-550 nanometers (violet to green light). This causes the compounds to be deeply colored yellow, orange, or red. Carotenoids are the dominant pigment in autumn leaf coloration of about 15-30% of tree species, but many plant colors, especially reds and purples, are due to other classes of chemicals. Carotenoids serve two key roles in plants and algae: they absorb light energy for use in photosynthesis, and they protect chlorophyll from photodamage.[2]Carotenoids that contain unsubstituted beta-ionone rings (including beta-carotene, alpha-carotene, beta-cryptoxanthin and gamma-carotene) have vitamin Aactivity (meaning that they can be converted to retinol), and these and other carotenoids can also act as antioxidants. In the eye, certain other carotenoids (lutein, astaxanthin,[3] and zeaxanthin) apparently act directly to absorb damaging blue and near-ultraviolet light, in order to protect the macula of the retina, the part of the eye with the sharpest vision. Contents [hide]
Biosynthesis[edit]CRT is the gene cluster responsible for the biosynthesis of carotenoids. Properties[edit]Main articles: carotenes and xanthophyllsCarotenoids belong to the category of tetraterpenoids (i.e., they contain 40 carbon atoms, being built from four terpene units each containing 10 carbon atoms). Structurally, carotenoids take the form of a polyene hydrocarbon chain which is sometimes terminated by rings, and may or may not have additional oxygen atoms attached.
Their color, ranging from pale yellow through bright orange to deep red, is directly linked to their structure. Xanthophylls are often yellow, hence their class name. The double carbon-carbon bonds interact with each other in a process called conjugation, which allows electrons in the molecule to move freely across these areas of the molecule. As the number of conjugated double bonds increases, electrons associated with conjugated systems have more room to move, and require less energy to change states. This causes the range of energies of light absorbed by the molecule to decrease. As more frequencies of light are absorbed from the short end of the visible spectrum, the compounds acquire an increasingly red appearance. Carotenoids are usually lipophilic due to the presence of long unsaturated aliphatic chains as in some fatty acids. The physiological absorption of these fat-soluble vitamins in humans and other organisms depends directly on the presence of fats and bile salts.[5] Physiological effects[edit]Supplements[edit]A 2014 review found that antioxidant supplements (including carotenoids) do not confer any health benefit and appear to increase the risk of getting certain cancers.[6] In foods[edit]Reviews of epidemiological studies seeking correlations between carotenoid consumption in food and clinical outcomes have come to various conclusions:
Simplified carotenoid synthesispathway.Plant colors[edit]The most common carotenoids include lycopene and the vitamin A precursor β-carotene. In plants, the xanthophylllutein is the most abundant carotenoid and its role in preventing age-related eye disease is currently under investigation. Lutein and the other carotenoid pigments found in mature leaves are often not obvious because of the masking presence of chlorophyll. When chlorophyll is not present, as in autumn foliage, the yellows and oranges of the carotenoids are predominant. For the same reason, carotenoid colors often predominate in ripe fruit after being unmasked by the disappearance of chlorophyll. Carotenoids give the characteristic color to carrots, corn, canaries, and daffodils, as well as egg yolks, rutabagas,buttercups, and bananas. Carotenoids are responsible for the brilliant yellows and oranges that tint deciduous foliage (such as dying autumn leaves) of certain hardwood species as hickories, ash, maple, yellow poplar, aspen, birch, black cherry, sycamore,cottonwood, sassafras, and alder. Carotenoids are the dominant pigment in autumn leaf coloration of about 15-30% of tree species.[14] However, the reds, the purples, and their blended combinations that decorate autumn foliage usually come from another group of pigments in the cells called anthocyanins. Unlike the carotenoids, these pigments are not present in the leaf throughout the growing season, but are actively produced towards the end of summer.[15] Aroma chemicals[edit]Products of carotenoid degradation such as ionones, damascones and damascenones are also important fragrance chemicals that are used extensively in theperfumes and fragrance industry. Both β-damascenone and β-ionone although low in concentration in rose distillates are the key odor-contributing compounds in flowers. In fact, the sweet floral smells present in black tea, aged tobacco, grape, and many fruits are due to the aromatic compounds resulting from carotenoid breakdown. Disease[edit]Some carotenoids are produced by bacteria to protect themselves from oxidative immune attack. The golden pigment that gives some strains ofStaphylococcus aureus their name (aureusis = golden) is a carotenoid called staphyloxanthin. This carotenoid is a virulence factor with an antioxidant action that helps the microbe evade death by reactive oxygen species used by the host immune system.[16] Question of synthesis in the corpus luteum[edit]Following a 1968 report that beta-carotene was synthesized in laboratory conditions in slices of corpus luteum from cows, an organ known to concentrate beta-carotene (hence its color and name), attempts have been made to replicate these findings, but have not succeeded. The idea is not presently accepted by the scientific community.[17] Rather, the mammalian corpus luteum, like the macula lutea in the retina of the mammalian eye, merely concentrates carotenoids from the diet. Artificial synthesis[edit]Microorganisms can be genetically modified[18] to produce certain C40 carotenoids, including lycopene and beta carotene.[19] Naturally occurring carotenoids[edit]
Choice experiment 1. Male Tetranychus urticae behaviour when presented with one female (♀) cadaver in stage 1 and one healthy ♀ quiescent deutonymph on leaf discs in a Petri dish. Stage 1=Dry non-sporulating cadaver killed by Neozygites floridana. (A) Leaf disc choice index (mean+SE) tested at three male (♂) densities. Index>0.5 indicates a preference for the leaf disc with cadaver. (B) Proportion of Petri dishes in which touching and guarding the two females were observed at least once tested at three ♂ densities.
Fatal attraction: Male spider mites prefer females killed by the mite-pathogenic fungus Neozygites floridana - Scientific Figure on ResearchGate. Available from: https://www.researchgate.net/275058361_fig2_Choice-experiment-1-Male-Tetranychus-urticae-behaviour-when-presented-with-one-female [accessed 5 Apr, 2016]
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