<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Mosquito and can you explain it in depth? [/INST] Mosquitoes (or mosquitos) are members of a group of almost 3,600 species of small flies within the family Culicidae (from the Latin culex meaning "gnat"). The word "mosquito" (formed by mosca and diminutive -ito) is Spanish and Portuguese for "little fly". Mosquitoes have a slender segmented body, one pair of wings, one pair of halteres, three pairs of long hair-like legs, and elongated mouthparts.
The mosquito life cycle consists of egg, larva, pupa, and adult stages. Eggs are laid on the water surface; they hatch into motile larvae that feed on aquatic algae and organic material. These larvae are important food sources for many freshwater animals, such as dragonfly nymphs, many fish, and some birds such as ducks. The adult females of most species have tube-like mouthparts (called a proboscis) that can pierce the skin of a host and feed on blood, which contains protein and iron needed to produce eggs. Thousands of mosquito species feed on the blood of various hosts — vertebrates, including mammals, birds, reptiles, amphibians, and some fish; along with some invertebrates, primarily other arthropods.
The mosquitos saliva is transferred to the host during the bite, and can cause an itchy rash. In addition, many species can ingest pathogens while biting, and transmit them to future hosts. In this way, mosquitoes are important vectors of parasitic diseases such as malaria and filariasis, and arboviral diseases such as yellow fever, Chikungunya, West Nile, dengue fever, and Zika. By transmitting diseases, mosquitoes cause the deaths of more people than any other animal taxon: over 700,000 each year. It has been claimed that almost half of the people who have ever lived have died of mosquito-vectored disease, but this claim is disputed, with more conservative estimates placing the death toll closer to 5% of all humans. Mosquitoes cannot live or function properly when the air temperature is below 10 degrees Celsius (50 degrees Fahrenheit). They are mostly active at 15–25 degrees Celsius (60–80 degrees Fahrenheit).

Fossil record and evolutionary history
The oldest known mosquitoes are known from amber dating to the Late Cretaceous. Three species of Cretaceous mosquito are currently known, Burmaculex antiquus and Priscoculex burmanicus are known from Burmese amber from Myanmar, which dates to the earliest part of the Cenomanian stage of the Late Cretaceous, around 99 million years ago. Paleoculicis minutus, is known from Canadian amber from Alberta, Canada, which dates to the Campanian stage of the Late Cretaceous, around 79 million years ago. Priscoculex burmanicus can be definitively assigned to Anophelinae, one of the two subfamilies of mosquitoes alongside Culicinae, indicating the split between these two subfamilies occurred over 99 million years ago. Molecular estimates suggest that the split between the two subfamilies occurred 197.5 million years ago, during the Early Jurassic, but that major diversification did not take place until the Cretaceous.The mosquito Anopheles gambiae is currently undergoing speciation into the M(opti) and S(avanah) molecular forms. Consequently, some pesticides that work on the M form no longer work on the S form.
Over 3,500 species of the Culicidae have already been described. They are generally divided into two subfamilies which in turn comprise some 43 genera. These figures are subject to continual change, as more species are discovered, and as DNA studies compel rearrangement of the taxonomy of the family. The two main subfamilies are the Anophelinae and Culicinae, with their genera as shown in the subsection below. The distinction is of great practical importance because the two subfamilies tend to differ in their significance as vectors of different classes of diseases. Roughly speaking, arboviral diseases such as yellow fever and dengue fever tend to be transmitted by Culicine species, not necessarily in the genus Culex. Some transmit various species of avian malaria, but it is not clear that they ever transmit any form of human malaria. Some species transmit various forms of filariasis, much as many Simuliidae do.

Taxonomy
Family
Mosquitoes are members of a family of nematoceran flies: the Culicidae (from the Latin culex, genitive culicis, meaning "midge" or "gnat"). Superficially, mosquitoes resemble crane flies (family Tipulidae) and chironomid flies (family Chironomidae).

Subfamilies
Anophelinae
Culicinae

Genera
Mosquitoes have been classified into 112 genera, some of the more common of which appear below.

Species
Over 3,500 species of mosquitoes have thus far been described in the scientific literature.

Genomics
An analysis by Matthews et al 2018 suggests mosquito species all carry a large and diverse number of transposable elements.

Morphology
As true flies, mosquitoes have one pair of wings, with distinct scales on the surface. Their wings are long and narrow, as are their long, thin legs. They have slender and dainty bodies of length typically 3–6 mm, with dark grey to black coloring. Some species harbor specific morphological patterns. When at rest they tend to hold their first pair of legs outward. They are similar in appearance to midges (Chironomidae), another ancient family of flies. Tokunagayusurika akamusi, for example, is a midge fly that looks very much like mosquitoes in that they also have slender and dainty bodies of similar colors, though larger in size. They also have only one pair of wings, but without scales on the surface. Another distinct feature to tell the two families of flies apart is the way they hold their first pair of legs – mosquitoes hold them outward, while midges hold them forward.

Life cycle
Overview
Like all flies, mosquitoes go through four stages in their life cycles: egg, larva, pupa, and adult or imago. The first three stages—egg, larva, and pupa—are largely aquatic. Each of the stages typically lasts 5 to 14 days, depending on the species and the ambient temperature, but there are important exceptions. Mosquitoes living in regions where some seasons are freezing or waterless spend part of the year in diapause; they delay their development, typically for months, and carry on with life only when there is enough water or warmth for their needs. For instance, Wyeomyia larvae typically get frozen into solid lumps of ice during winter and only complete their development in spring. The eggs of some species of Aedes remain unharmed in diapause if they dry out, and hatch later when they are covered by water.
Eggs hatch to become larvae, which grow until they are able to change into pupae. The adult mosquito emerges from the mature pupa as it floats at the water surface. Bloodsucking mosquitoes, depending on species, sex, and weather conditions, have potential adult lifespans ranging from as short as a week to as long as several months. Some species can overwinter as adults in diapause.

Breeding
In most species, adult females lay their eggs in stagnant water: some lay near the waters edge while others attach their eggs to aquatic plants. Each species selects the situation of the water into which it lays its eggs and does so according to its own ecological adaptations. Some breed in lakes, some in temporary puddles. Some breed in marshes, some in salt-marshes. Among those that breed in salt water (such as Opifex fuscus), some are equally at home in fresh and salt water up to about one-third the concentration of seawater, whereas others must acclimatize themselves to the salinity. Such differences are important because certain ecological preferences keep mosquitoes away from most humans, whereas other preferences bring them right into houses at night.
Some species of mosquitoes prefer to breed in phytotelmata (natural reservoirs on plants), such as rainwater accumulated in holes in tree trunks, or in the leaf-axils of bromeliads. Some specialize in the liquid in pitchers of particular species of pitcher plants, their larvae feeding on decaying insects that had drowned there or on the associated bacteria; the genus Wyeomyia provides such examples — the harmless Wyeomyia smithii breeds only in the pitchers of Sarracenia purpurea.Some of the species of mosquitoes that are adapted to breeding in phytotelmata are dangerous disease vectors. In nature, they might occupy anything from a hollow tree trunk to a cupped leaf. Such species typically take readily to breeding in artificial water containers. Such casual puddles are important breeding places for some of the most serious disease vectors, such as species of Aedes that transmit dengue and yellow fever. Some with such breeding habits are disproportionately important vectors because they are well-placed to pick up pathogens from humans and pass them on. In contrast, no matter how voracious, mosquitoes that breed and feed mainly in remote wetlands and salt marshes may well remain uninfected, and if they do happen to become infected with a relevant pathogen, might seldom encounter humans to infect, in turn.

Eggs and oviposition
Mosquito habits of oviposition, the ways in which they lay their eggs, vary considerably between species, and the morphologies of the eggs vary accordingly. The simplest procedure is that followed by many species of Anopheles; like many other gracile species of aquatic insects, females just fly over the water, bobbing up and down to the water surface and dropping eggs more or less singly. The bobbing behavior occurs among some other aquatic insects as well, for example mayflies and dragonflies; it is sometimes called "dapping". The eggs of Anopheles species are roughly cigar-shaped and have floats down their sides. Females of many common species can lay 100–200 eggs during the course of the adult phase of their life cycles. Even with high egg and intergenerational mortality, over a period of several weeks, a single successful breeding pair can create a population of thousands.

Some other species, for example members of the genus Mansonia, lay their eggs in arrays, attached usually to the under-surfaces of waterlily pads. Their close relatives, the genus Coquillettidia, lay their eggs similarly, but not attached to plants. Instead, the eggs form layers called "rafts" that float on the water. This is a common mode of oviposition, and most species of Culex are known for the habit, which also occurs in some other genera, such as Culiseta and Uranotaenia. Anopheles eggs may on occasion cluster together on the water, too, but the clusters do not generally look much like compactly glued rafts of eggs.
In species that lay their eggs in rafts, rafts do not form adventitiously; the female Culex settles carefully on still water with its hind legs crossed, and as it lays the eggs one by one, it twitches to arrange them into a head-down array that sticks together to form the raft.Aedes females generally drop their eggs singly, much as Anopheles do, but not as a rule into water. Instead, they lay their eggs on damp mud or other surfaces near the waters edge. Such an oviposition site commonly is the wall of a cavity such as a hollow stump or a container such as a bucket or a discarded vehicle tire. The eggs generally do not hatch until they are flooded, and they may have to withstand considerable desiccation before that happens. They are not resistant to desiccation straight after oviposition, but must develop to a suitable degree first. After that, they can enter diapause for several months if they dry out. Clutches of eggs of the majority of mosquito species hatch as soon as possible, and all the eggs in the clutch hatch at much the same time. In contrast, a batch of Aedes eggs in diapause tends to hatch irregularly over an extended period of time. This makes it much more difficult to control such species than those mosquitoes whose larvae can be killed all together as they hatch. Some Anopheles species do also behave in such a manner, though not to the same degree of sophistication.

Larva
The mosquito larva has a well-developed head with mouth brushes used for feeding, a large thorax with no legs, and a segmented abdomen.
Larvae breathe through spiracles located on their eighth abdominal segments, or through a siphon, so must come to the surface frequently. The larvae spend most of their time feeding on algae, bacteria, and other microbes in the surface microlayer.
Mosquito larvae have been investigated as prey of other Dipteran flies. Species such as Bezzia nobilis within the family Ceratopogonidae have been observed in experiments to prey upon mosquito larvae.They dive below the surface when disturbed. Larvae swim either through propulsion with their mouth brushes, or by jerky movements of their entire bodies, giving them the common name of "wigglers" or "wrigglers".
Larvae develop through four stages, or instars, after which they metamorphose into pupae. At the end of each instar, the larvae molt, shedding their skins to allow for further growth.

Pupa
As seen in its lateral aspect, the mosquito pupa is comma-shaped. The head and thorax are merged into a cephalothorax, with the abdomen curving around underneath. The pupa can swim actively by flipping its abdomen, and it is commonly called a "tumbler" because of its swimming action. As with the larva, the pupa of most species must come to the surface frequently to breathe, which they do through a pair of respiratory trumpets on their cephalothoraxes. They do not feed during this stage; typically they pass their time hanging from the surface of the water by their respiratory trumpets. If alarmed, say by a passing shadow, they nimbly swim downwards by flipping their abdomens in much the same way as the larvae do. If undisturbed, they soon float up again.
After a few days or longer, depending on the temperature and other circumstances, the dorsal surface of its cephalothorax splits, and the adult mosquito emerges. The pupa is less active than the larva because it does not feed, whereas the larva feeds constantly.

Adult
The period of development from egg to adult varies among species and is strongly influenced by ambient temperature. Some species of mosquitoes can develop from egg to adult in as few as five days, but a more typical period of development in tropical conditions would be some 40 days or more for most species. The variation of the body size in adult mosquitoes depends on the density of the larval population and food supply within the breeding water.
Adult mosquitoes usually mate within a few days after emerging from the pupal stage. In most species, the males form large swarms, usually around dusk, and the females fly into the swarms to mate.
Males typically live for about 5–7 days, feeding on nectar and other sources of sugar. After obtaining a full blood meal, the female will rest for a few days while the blood is digested and eggs are developed. This process depends on the temperature, but usually takes two to three days in tropical conditions. Once the eggs are fully developed, the female lays them and resumes host-seeking.
The cycle repeats itself until the female dies. While females can live longer than a month in captivity, most do not live longer than one to two weeks in nature. Their lifespans depend on temperature, humidity, and their ability to successfully obtain a blood meal while avoiding host defenses and predators.
The length of the adult is typically between 3 mm and 6 mm. The smallest known mosquitoes are around 2 mm (0.1 in), and the largest around 19 mm (0.7 in). Mosquitoes typically weigh around 5 mg. All mosquitoes have slender bodies with three segments: a head, a thorax and an abdomen.
The head is specialized for receiving sensory information and for feeding. It has eyes and a pair of long, many-segmented antennae. The antennae are important for detecting host odors, as well as odors of breeding sites where females lay eggs. In all mosquito species, the antennae of the males in comparison to the females are noticeably bushier and contain auditory receptors to detect the characteristic whine of the females.

The compound eyes are distinctly separated from one another. Their larvae only possess a pit-eye ocellus. The compound eyes of adults develop in a separate region of the head. New ommatidia are added in semicircular rows at the rear of the eye. During the first phase of growth, this leads to individual ommatidia being square, but later in development they become hexagonal. The hexagonal pattern will only become visible when the carapace of the stage with square eyes is molted.The head also has an elongated, forward-projecting, stinger-like proboscis used for feeding, and two sensory palps. The maxillary palps of the males are longer than their proboscises, whereas the females’ maxillary palps are much shorter. In typical bloodsucking species, the female has an elongated proboscis.
The thorax is specialized for locomotion. Three pairs of legs and a pair of wings are attached to the thorax. The insect wing is an outgrowth of the exoskeleton. The Anopheles mosquito can fly for up to four hours continuously at 1 to 2 km/h (0.6–1 mph), traveling up to 12 km (7.5 mi) in a night. Males beat their wings between 450 and 600 times per second.The abdomen is specialized for food digestion and egg development; the abdomen of a mosquito can hold three times its own weight in blood. This segment expands considerably when a female takes a blood meal. The blood is digested over time, serving as a source of protein for the production of eggs, which gradually fill the abdomen.

Feeding by adults
Typically, both male and female mosquitoes feed on nectar, aphid honeydew, and plant juices, but in many species the mouthparts of the females are adapted for piercing the skin of animal hosts and sucking their blood as ectoparasites. In many species, the female needs to obtain nutrients from a blood meal before it can produce eggs, whereas in many other species, obtaining nutrients from a blood meal enables the mosquito to lay more eggs. A mosquito has a variety of ways of finding nectar or its prey, including chemical, visual, and heat sensors. Both plant materials and blood are useful sources of energy in the form of sugars, and blood also supplies more concentrated nutrients, such as lipids, but the most important function of blood meals is to obtain proteins as materials for egg production.When a female reproduces without such parasitic meals, it is said to practice autogenous reproduction, as in Toxorhynchites; otherwise, the reproduction may be termed anautogenous, as occurs in mosquito species that serve as disease vectors, particularly Anopheles and some of the most important disease vectors in the genus Aedes. In contrast, some mosquitoes, for example, many Culex, are partially anautogenous: they do not need a blood meal for their first cycle of egg production, which they produce autogenously; subsequent clutches of eggs are produced anautogenously, at which point their disease vectoring activity becomes operative.Among humans, the feeding preferences of mosquitoes typically include: those with type O blood, heavy breathers, an abundance of skin bacteria, high body heat, and pregnant women. Individuals attractiveness to mosquitoes also has a heritable, genetically-controlled component.Female mosquitoes hunt their blood host by detecting organic substances such as carbon dioxide (CO2) and 1-octen-3-ol (mushroom alcohol, found in exhaled breath) produced from the host, and through visual recognition. Mosquitoes prefer some people over others. The preferred victims sweat smells more attractive than others because of the proportions of the carbon dioxide, octenol, and other compounds that make up body odor. The most powerful semiochemical that triggers the keen sense of smell of Culex quinquefasciatus is nonanal. Another compound identified in human blood that attracts mosquitoes is sulcatone or 6-methyl-5-hepten-2-one, especially for Aedes aegypti mosquitoes with the odor receptor gene Or4. A large part of the mosquitos sense of smell, or olfactory system, is devoted to sniffing out blood sources. Of 72 types of odor receptors on its antennae, at least 27 are tuned to detect chemicals found in perspiration. In Aedes, the search for a host takes place in two phases. First, the mosquito exhibits a nonspecific searching behavior until the perception of a hosts stimulants, then it follows a targeted approach.Most mosquito species are crepuscular (dawn or dusk) feeders. During the heat of the day, most mosquitoes rest in a cool place and wait for the evenings, although they may still bite if disturbed. Some species, such as the Asian tiger mosquito, are known to fly and feed during daytime.Prior to and during blood feeding, blood-sucking mosquitoes inject saliva into the bodies of their source(s) of blood. This saliva serves as an anticoagulant; without it the female mosquitos proboscis might become clogged with blood clots. The saliva also is the main route by which mosquito physiology offers passenger pathogens access to the hosts bloodstream. The salivary glands are a major target to most pathogens, whence they find their way into the host via the saliva.
A mosquito bite often leaves an itchy weal, a raised bump, on the victims skin, which is caused by histamines trying to fight off the protein left by the attacking insect.Mosquitoes of the genus Toxorhynchites never drink blood. This genus includes the largest extant mosquitoes, the larvae of which prey on the larvae of other mosquitoes. These mosquito eaters have been used in the past as mosquito control agents, with varying success.

Host animals
Many, if not all, blood-sucking species of mosquitoes are fairly selective feeders that specialise in particular host species, though they often relax their selectivity when they experience severe competition for food, defensive activity on the part of the hosts, or starvation. Some species feed selectively on monkeys, while others prefer particular kinds of birds, but they become less selective as conditions become more difficult. For example, Culiseta melanura sucks the blood of passerine birds for preference, and such birds are typically the main reservoir of the Eastern equine encephalitis virus in North America. Early in the season while mosquito numbers are low, they concentrate on passerine hosts, but as mosquito numbers rise and the birds are forced to defend themselves more vigorously, the mosquitoes become less selective of hosts. Soon the mosquitoes begin attacking mammals more readily, thereby becoming the major vector of the virus, and causing epidemics of the disease, most conspicuously in humans and horses. Multiple mosquitoes withdrawal of blood from a host can add up to a large volume. In rare cases, heavy mosquito densities have directly killed livestock as large as cattle and horses.Even more dramatically, in most of its range in North America, the main vector for the Western equine encephalitis virus is Culex tarsalis, because it is known to feed variously on mammals, birds, reptiles, and amphibians. Even fish may be attacked by some mosquito species if they expose themselves above water level, as mudskippers do.In 1969 it was reported that some species of anautogenous mosquitoes would feed on the haemolymph of caterpillars although its nutritional value is questionable. Other observations include mosquitoes feeding on cicadas and mantids. In 2014, it was shown that malaria-transmitting mosquitoes actively seek out some species of caterpillars and feed on their haemolymph, and do so to the caterpillars apparent physical detriment.

Mouthparts
Mosquito mouthparts are very specialized, particularly those of the females, which in most species are adapted to piercing skin and then sucking blood. Apart from bloodsucking, the females generally also drink assorted fluids rich in dissolved sugar, such as nectar and honeydew, to obtain the energy they need. For this, their blood-sucking mouthparts are perfectly adequate. In contrast, male mosquitoes are not bloodsuckers; they only drink sugary fluids. Accordingly, their mouthparts do not require the same degree of specialization as those of females.Externally, the most obvious feeding structure of the mosquito is the proboscis. More specifically, the visible part of the proboscis is the labium, which forms the sheath enclosing the rest of the mouthparts. When the mosquito first lands on a potential host, its mouthparts are enclosed entirely in this sheath, and it will touch the tip of the labium to the skin in various places. Sometimes, it will begin to bite almost straight away, while other times, it will prod around, apparently looking for a suitable place. Occasionally, it will wander for a considerable time, and eventually fly away without biting. Presumably, this probing is a search for a place with easily accessible blood vessels, but the exact mechanism is not known. It is known that there are two taste receptors at the tip of the labium which may well play a role.The female mosquito does not insert its labium into the skin; it bends back into a bow when the mosquito begins to bite. The tip of the labium remains in contact with the skin of the host, acting as a guide for the other mouthparts. In total, there are six mouthparts besides the labium: two mandibles, two maxillae, the hypopharynx, and the labrum.
The mandibles and the maxillae are used for piercing the skin. The mandibles are pointed, while the maxillae end in flat, toothed "blades". To force these into the skin, the mosquito moves its head backwards and forwards. On one movement, the maxillae are moved as far forward as possible. On the opposite movement, the mandibles are pushed deeper into the skin by levering against the maxillae. The maxillae do not slip back because the toothed blades grip the skin.
The hypopharynx and the labrum are both hollow. Saliva with anticoagulant is pumped down the hypopharynx to prevent clotting, and blood is drawn up the labrum.
To understand the mosquito mouthparts, it is helpful to draw a comparison with an insect that chews food, such as a dragonfly. A dragonfly has two mandibles, which are used for chewing, and two maxillae, which are used to hold the food in place as it is chewed. The labium forms the floor of the dragonflys mouth, the labrum forms the top, while the hypopharynx is inside the mouth and is used in swallowing. Conceptually, then, the mosquitos proboscis is an adaptation of the mouthparts that occur in other insects. The labium still lies beneath the other mouthparts, but also enfolds them, and it has been extended into a proboscis. The maxillae still "grip" the "food" while the mandibles "bite" it. The top of the mouth, the labrum, has developed into a channeled blade the length of the proboscis, with a cross-section like an inverted "U". Finally, the hypopharynx has extended into a tube that can deliver saliva at the end of the proboscis. Its upper surface is somewhat flattened so, when the lower part of the hypopharynx is pressed against it, the labrum forms a closed tube for conveying blood from the host.

Saliva
For the mosquito to obtain a blood meal, it must circumvent the vertebrates physiological responses. The mosquito, as with all blood-feeding arthropods, has mechanisms to effectively block the hemostasis system with their saliva, which contains a mixture of secreted proteins. Saglin is a protein produced by the salivary glands of mosquitoes. Mosquito saliva acts to reduce vascular constriction, blood clotting, platelet aggregation, angiogenesis and immunity, and creates inflammation. Universally, hematophagous arthropod saliva contains at least one anti-clotting, one anti-platelet, and one vasodilatory substance. Mosquito saliva also contains enzymes that aid in sugar feeding, and antimicrobial agents to control bacterial growth in the sugar meal. The composition of mosquito saliva is relatively simple, as it usually contains fewer than 20 dominant proteins. As of the early 2000s, scientists still were unable to ascribe functions to more than half of the molecules found in arthropod saliva. One promising application of components of mosquito saliva is the development of anti-clotting drugs, such as clotting inhibitors and capillary dilators, that could be useful for managing cardiovascular disease.
It is now well recognized that feeding ticks, sandflies, and, more recently, mosquitoes, have an ability to modulate the immune response of the animals (hosts) on which they feed. The presence of this activity in vector saliva is a reflection of the inherent overlapping and interconnected nature of the host hemostatic and inflammatory/immunological responses and the intrinsic need to prevent these host defenses from disrupting successful feeding. The mechanism for mosquito saliva-induced alteration of the host immune response is unclear, but the data have become increasingly convincing that such an effect occurs. Early work described a factor in saliva that directly suppresses TNF-α release, but not antigen-induced histamine secretion, from activated mast cells. Experiments by Cross et al. (1994) demonstrated that the inclusion of Ae. aegypti mosquito saliva into naïve cultures led to a suppression of interleukin (IL)-2 and IFN-γ production, while the cytokines IL-4 and IL-5 are unaffected. Cellular proliferation in response to IL-2 is clearly reduced by prior treatment of cells with mosquito salivary gland extract. Correspondingly, activated splenocytes isolated from mice fed upon by either Ae. aegypti or Cx. pipiens mosquitoes produce markedly higher levels of IL-4 and IL-10 concurrent with suppressed IFN-γ production. Unexpectedly, this shift in cytokine expression is observed in splenocytes up to 10 days after mosquito exposure, suggesting natural feeding of mosquitoes can have a profound, enduring, and systemic effect on the immune response.T cell populations are decidedly susceptible to the suppressive effect of mosquito saliva, showing increased mortality and decreased division rates. Parallel work by Wasserman et al. (2004) demonstrated that T and B cell proliferation was inhibited in a dose dependent manner with concentrations as low as 1/7 of the saliva in a single mosquito. Depinay et al. (2005) observed a suppression of antibody-specific T cell responses mediated by mosquito saliva and dependent on mast cells and IL-10 expression.A 2006 study suggests mosquito saliva can also decrease expression of interferon−α/β during early mosquito-borne virus infection. The contribution of type I interferons (IFN) in recovery from infection with viruses has been demonstrated in vivo by the therapeutic and prophylactic effects of administration of IFN inducers or IFN itself, and different research suggests mosquito saliva exacerbates West Nile virus infection, as well as other mosquito-transmitted viruses.Studies in humanized mice bearing a reconstituted human immune system have suggested potential impact of mosquito saliva in humans. Work published in 2018 from the Baylor College of Medicine using such humanized mice came to several conclusions, among them being that mosquito saliva led to an increase in natural killer T cells in peripheral blood; to an overall decrease in ex vivo cytokine production by peripheral blood mononuclear cells (PBMCs); changes to proportions of subsets of PBMCs; changes in the prevalence of T cell subtypes across organs; and changes to circulating levels of cytokines.

Egg development and blood digestion
Most species of mosquito require a blood meal to begin the process of egg development. Females with poor larval nutrition may need to ingest sugar or a preliminary blood meal before their ovarian follicles can reach their resting stage. Once the follicles have reached the resting stage, digestion of a sufficiently large blood meal triggers a hormonal cascade that leads to egg development. Upon completion of feeding, the mosquito withdraws her proboscis, and as the gut fills up, the stomach lining secretes a peritrophic membrane that surrounds the blood. This membrane keeps the blood separate from anything else in the stomach. Like many Hemiptera and other insects that survive on dilute liquid diets, many adult mosquitoes must excrete unwanted aqueous fractions even as they feed. (See the photograph of a feeding Anopheles stephensi: Note that the excreted droplet patently is not whole blood, being far more dilute). As long as they are not disturbed, this permits mosquitoes to continue feeding until they have accumulated a full meal of nutrient solids. As a result, a mosquito replete with blood can continue to absorb sugar, even as the blood meal is slowly digested over a period of several days. Once blood is in the stomach, the midgut of the female synthesizes proteolytic enzymes that hydrolyze the blood proteins into free amino acids. These are used as building blocks for the synthesis of vitellogenin, which are the precursors for egg yolk protein.In the mosquito Anopheles stephensi, trypsin activity is restricted entirely to the posterior midgut lumen. No trypsin activity occurs before the blood meal, but activity increases continuously up to 30 hours after feeding, and subsequently returns to baseline levels by 60 hours. Aminopeptidase is active in the anterior and posterior midgut regions before and after feeding. In the whole midgut, activity rises from a baseline of approximately three enzyme units (EU) per midgut to a maximum of 12 EU at 30 hours after the blood meal, subsequently falling to baseline levels by 60 hours. A similar cycle of activity occurs in the posterior midgut and posterior midgut lumen, whereas aminopeptidase in the posterior midgut epithelium decreases in activity during digestion. Aminopeptidase in the anterior midgut is maintained at a constant, low level, showing no significant variation with time after feeding. Alpha-glucosidase is active in anterior and posterior midguts before and at all times after feeding. In whole midgut homogenates, alpha-glucosidase activity increases slowly up to 18 hours after the blood meal, then rises rapidly to a maximum at 30 hours after the blood meal, whereas the subsequent decline in activity is less predictable. All posterior midgut activity is restricted to the posterior midgut lumen. Depending on the time after feeding, greater than 25% of the total midgut activity of alpha-glucosidase is located in the anterior midgut. After blood meal ingestion, proteases are active only in the posterior midgut. Trypsin is the major primary hydrolytic protease and is secreted into the posterior midgut lumen without activation in the posterior midgut epithelium. Aminopeptidase activity is also luminal in the posterior midgut, but cellular aminopeptidases are required for peptide processing in both anterior and posterior midguts. Alpha-glucosidase activity is elevated in the posterior midgut after feeding in response to the blood meal, whereas activity in the anterior midgut is consistent with a nectar-processing role for this midgut region.

Ecology
Distribution
Mosquitoes are cosmopolitan (world-wide): they are in every land region except Antarctica and a few islands with polar or subpolar climates. Iceland is such an island, being essentially free of mosquitoes.The absence of mosquitoes in Iceland and similar regions is probably because of quirks of their climate, which differs in some respects from mainland regions. At the start of the uninterrupted continental winter of Greenland and the northern regions of Eurasia and America, the pupa enters diapause under the ice that covers sufficiently deep water. The imago emerges only after the ice breaks in late spring. In Iceland, the weather is less predictable. In mid-winter it frequently warms up suddenly, causing the ice to break, but then to freeze again after a few days. By that time the mosquitoes will have emerged from their pupae, but the new freeze sets in before they can complete their life cycle. Any anautogenous adult mosquito would need a host to supply a blood meal before it could lay viable eggs; it would need time to mate, mature the eggs and oviposit in suitable wetlands. These requirements would not be realistic in Iceland and in fact the absence of mosquitoes from such subpolar islands is in line with the islands low insect biodiversity; Iceland has fewer than 1,500 described species of insects, many of them probably accidentally introduced by human agency. In Iceland most ectoparasitic insects live in sheltered conditions or actually on mammals; examples include lice, fleas and bedbugs, in whose living conditions freezing is no concern, and most of which were introduced inadvertently by humans.Some other aquatic Diptera, such as Simuliidae, do survive in Iceland, but their habits and adaptations differ from those of mosquitoes; Simuliidae for example, though they, like mosquitoes, are bloodsuckers, generally inhabit stones under running water that does not readily freeze and which is totally unsuited to mosquitoes; mosquitoes are generally not adapted to running water.Eggs of species of mosquitoes from the temperate zones are more tolerant of cold than the eggs of species indigenous to warmer regions. Many even tolerate subzero temperatures. In addition, adults of some species can survive the winter by taking shelter in suitable microhabitats such as buildings or hollow trees.

Pollination
Several flowers are pollinated by mosquitoes, including some members of the Asteraceae, Roseaceae and Orchidaceae.

Activity
In warm and humid tropical regions, some mosquito species are active for the entire year, but in temperate and cold regions they hibernate or enter diapause. Arctic or subarctic mosquitoes, like some other arctic midges in families such as Simuliidae and Ceratopogonidae may be active for only a few weeks annually as melt-water pools form on the permafrost. During that time, though, they emerge in huge numbers in some regions and may take up to 300 ml of blood per day from each animal in a caribou herd.

Means of dispersal
Worldwide introduction of various mosquito species over large distances into regions where they are not indigenous has occurred through human agencies, primarily on sea routes, in which the eggs, larvae, and pupae inhabiting water-filled used tires and cut flowers are transported. They have also been carried by personal vehicles, delivery trucks, trains, and aircraft. Man-made areas such as storm water retention basins, or storm drains also provide sprawling sanctuaries. Sufficient quarantine measures have proven difficult to implement. In addition, outdoor pool areas make a perfect place for them to grow.

Climate and global distribution
Seasonality
In order for a mosquito to transmit a disease to the host there must be favorable conditions, referred to as transmission seasonality. Seasonal factors that impact the prevalence of mosquitoes and mosquito-borne diseases are primarily humidity, temperature, and precipitation. A positive correlation between malaria outbreaks and these climatic variables has been demonstrated in China; and El Niño has been shown to impact the location and number of outbreaks of mosquito-borne diseases observed in East Africa, Latin America, Southeast Asia and India. Climate change impacts each of these seasonal factors and in turn impacts the dispersal of mosquitoes.

Past and future patterns
Climatology and the study of mosquito-borne disease have been developed only over the past 100 years. Historical records of weather patterns and distinct symptoms associated with mosquito-borne diseases can be utilized to trace the prevalence of these diseases in relation to the climate over longer time periods. Further, statistical models are being created to predict the impact of climate change on vector-borne diseases using these past records, and these models can be utilized in the field of public health in order to create interventions to reduce the impact of these predicted outcomes.
Two types of models are used to predict mosquito-borne disease spread in relation to climate: correlative models and mechanistic models. Correlative models focus primarily on vector distribution, and generally function in 3 steps. First, data is collected regarding geographical location of a target mosquito species. Next, a multivariate regression model establishes the conditions under which the target species can survive. Finally, the model determines the likelihood of the mosquito species to become established in a new location based on similar living conditions. The model can further predict future distributions based on environmental emissions data. Mechanistic models tend to be broader and include the pathogens and hosts in the analysis. These models have been used to recreate past outbreaks as well as predict the potential risk of a vector-borne disease based on an areas forecasted climate.Mosquito-borne diseases are currently most prevalent in East Africa, Latin America, Southeast Asia, and India. An emergence in Europe was recently observed. A weighted risk analysis demonstrated associations to climate for 49% of infectious diseases in Europe including all transmission routes. One statistical model predicts by 2030, the climate of southern Great Britain will be climatically suitable for malaria transmission Plasmodium vivax for 2 months of the year. By 2080 it is predicted that the same will be true for southern Scotland.

Vectors of disease
Mosquitoes can act as vectors for many disease-causing viruses and parasites. Infected mosquitoes carry these organisms from person to person without exhibiting symptoms themselves. Mosquito-borne diseases include:

Viral diseases, such as yellow fever, dengue fever, and chikungunya, transmitted mostly by Aedes aegypti. Dengue fever is the most common cause of fever in travelers returning from the Caribbean, Central America, South America, and South Central Asia. This disease is spread through the bites of infected mosquitoes and cannot be spread person to person. Severe dengue can be fatal, but with good treatment, fewer than 1% of patients die from dengue. Work published in 2012 from Baylor College of Medicine suggested that for some diseases, such as dengue fever, which can be transmitted via mosquitoes and by other means, the severity of the mosquito-transmitted disease could be greater.
The parasitic diseases collectively called malaria, caused by various species of Plasmodium, carried by female mosquitoes of the genus Anopheles.
Lymphatic filariasis (the main cause of elephantiasis) which can be spread by a wide variety of mosquito species.
West Nile virus is a significant concern in the United States but there are no reliable statistics on worldwide cases.
Dengue viruses are a significant health risk globally. Severe cases of dengue often require hospitalization and can be life-threatening shortly after infection. Symptoms include a high fever, aches and pains, vomiting, and rashes. Warning signs of severe dengue infection include vomiting blood, bleeding from the gums or nose, and stomach tenderness/pain.
Equine encephalitis viruses, such as Eastern equine encephalitis virus, Western equine encephalitis virus, and Venezuelan equine encephalitis virus, can be spread by mosquito vectors such as Aedes taeniorhynchus.
Tularemia, a bacterial disease caused by Francisella tularensis, is variously transmitted, including by biting flies. Culex and Culiseta are vectors of tularemia, as well as arbovirus infections such as West Nile virus.
Zika, recently notorious, though rarely deadly, causes fever, joint pain, rashes and conjunctivitis. The most serious consequence appears when the infected person is a pregnant woman, since during pregnancy this virus can originate a birth defect called microcephaly.
St. Louis Encephalitis, a mosquito-borne disease that is characterized by fever and headaches upon initial onset of infection, arises from mosquitoes who feed on birds who are infected with the illness, and can result in death. The most common vector of this disease is Culex pipiens, also known as the common house mosquito.
Heartworm disease, a parasitic roundworm infection that affects dogs and other canids. Mosquitoes transmit larvae to the definitive host through bites. Adult heart worms infest the right heart and pulmonary artery, where they can cause serious complications including congestive heart failure.Potential transmission of HIV was originally a public health concern, but practical considerations and detailed studies of epidemiological patterns suggest that any transmission of the HIV virus by mosquitoes is at worst extremely unlikely.Various species of mosquitoes are estimated to transmit various types of disease to more than 700 million people annually in Africa, South America, Central America, Mexico, Russia, and much of Asia, with millions of resultant deaths. At least two million people annually die of these diseases, and the morbidity rates are many times higher still.
Methods used to prevent the spread of disease, or to protect individuals in areas where disease is endemic, include:

Vector control aimed at mosquito control or eradication
Disease prevention, using prophylactic drugs and developing vaccines
Prevention of mosquito bites, with insecticides, nets, and repellentsSince most such diseases are carried by "elderly" female mosquitoes, some scientists have suggested focusing on these to avoid the evolution of resistance.

Control
Many measures have been tried for mosquito control, including the elimination of breeding places, exclusion via window screens and mosquito nets, biological control with parasites such as fungi and nematodes, or predators such as fish, copepods, dragonfly nymphs and adults, and some species of lizard and gecko. Another approach is to introduce large numbers of sterile males. Genetic modification methods including cytoplasmic incompatibility, chromosomal translocations, sex distortion and gene replacement, solutions seen as inexpensive and not subject to vector resistance, have been explored.According to an article in Nature discussing the idea of totally eradicating mosquitoes, "Ultimately, there seem to be few things that mosquitoes do that other organisms can’t do just as well—except perhaps for one. They are lethally efficient at sucking blood from one individual and mainlining it into another, providing an ideal route for the spread of pathogenic microbes." The control of disease-carrying mosquitoes may in the future be possible using gene drives.

Repellents
Insect repellents are applied on skin and give short-term protection against mosquito bites. The chemical DEET repels some mosquitoes and other insects. Some CDC-recommended repellents are picaridin, eucalyptus oil (PMD), and ethyl butylacetylaminopropionate (IR3535). Pyrethrum (from Chrysanthemum species, particularly C. cinerariifolium and C. coccineum) has been reviewed favorably in research published in 2021. Others are indalone, dimethyl phthalate, dimethyl carbate, and ethyl hexanediol.
Electronic insect repellent devices that produce ultrasounds intended to keep away insects (and mosquitoes) are marketed. No EPA or university study has shown that these devices prevent a human from being bitten by a mosquito.

Bites
Mosquito bites lead to a variety of mild, occasionally serious, and, rarely, life-threatening allergic reactions. These include ordinary wheal and flare reactions and mosquito bite allergies (MBA). The MBA, also termed hypersensitivity to mosquito bites (HMB), are excessive reactions to mosquito bites that are not caused by any toxin or pathogen in the saliva injected by a mosquito at the time it takes its blood-meal. Rather, they are allergic hypersensitivity reactions caused by the non-toxic allergenic proteins contained in the mosquitos saliva. Studies have shown or suggest that numerous species of mosquitoes can trigger ordinary reactions as well as MBA. These include Aedes aegypti, Aedes vexans, Aedes albopictus, Anopheles sinensis, Culex pipiens, Aedes communis, Anopheles stephensi, Culex quinquefasciatus, Ochlerotatus triseriatus, and Culex tritaeniorhynchus. Furthermore, there is considerable cross-reactivity between the salivary proteins of mosquitoes in the same family and, to a lesser extent, different families. It is therefore assumed that these allergic responses may be caused by virtually any mosquito species (or other biting insect).

The mosquito bite allergies are informally classified as 1) the Skeeter syndrome, i.e. severe local skin reactions sometimes associated with low-grade fever; 2) systemic reactions that range from high-grade fever, lymphadenopathy, abdominal pain, and/or diarrhea to, very rarely, life-threatening symptoms of anaphylaxis; and 3) severe and often systemic reactions occurring in individuals that have an Epstein-Barr virus-associated lymphoproliferative disease, Epstein-Barr virus-negative lymphoid malignancy, or another predisposing condition such as Eosinophilic cellulitis or chronic lymphocytic leukemia.

Mechanism
Visible, irritating bites are due to an immune response from the binding of IgG and IgE antibodies to antigens in the mosquitos saliva. Some of the sensitizing antigens are common to all mosquito species, whereas others are specific to certain species. There are both immediate hypersensitivity reactions (types I and III) and delayed hypersensitivity reactions (type IV) to mosquito bites. Both reactions result in itching, redness and swelling </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Chromoblastomycosis and can you explain it in depth? [/INST] Chromoblastomycosis  is a long-term fungal infection of the skin and subcutaneous tissue (a chronic subcutaneous mycosis).It can be caused by many different types of fungi which become implanted under the skin, often by thorns or splinters. Chromoblastomycosis spreads very slowly.It is rarely fatal and usually has a good prognosis, but it can be very difficult to cure. The several treatment options include medication and surgery.The infection occurs most commonly in tropical or subtropical climates, often in rural areas.

Symptoms and signs
The initial trauma causing the infection is often forgotten or not noticed. The infection builds at the site over a period of years, and a small red papule (skin elevation) appears. The lesion is usually not painful, with few, if any symptoms. Patients rarely seek medical care at this point.Several complications may occur. Usually, the infection slowly spreads to the surrounding tissue while still remaining localized to the area around the original wound. However, sometimes the fungi may spread through the blood vessels or lymph vessels, producing metastatic lesions at distant sites. Another possibility is secondary infection with bacteria. This may lead to lymph stasis (obstruction of the lymph vessels) and elephantiasis. The nodules may become ulcerated, or multiple nodules may grow and coalesce, affecting a large area of a limb.

Cause
Chromoblastomycosis is believed to originate in minor trauma to the skin, usually from vegetative material such as thorns or splinters; this trauma implants fungi in the subcutaneous tissue. In many cases, the patient will not notice or remember the initial trauma, as symptoms often do not appear for years. The fungi most commonly observed to cause chromoblastomycosis are:

Fonsecaea pedrosoi
Cladophialophora bantiana causes both cutaneous chromoblastomycosis and systemic phaeohyphomycosis
Phialophora verrucosa
Cladophialophora carrionii
Fonsecaea compacta

Mechanism
Over months to years, an erythematous papule appears at the site of inoculation. Although the mycosis slowly spreads, it usually remains localized to the skin and subcutaneous tissue. Hematogenous and/or lymphatic spread may occur. Multiple nodules may appear on the same limb, sometimes coalescing into a large plaque. Secondary bacterial infection may occur, sometimes inducing lymphatic obstruction. The central portion of the lesion may heal, producing a scar, or it may ulcerate.

Diagnosis
The most informative test is to scrape the lesion and add potassium hydroxide (KOH), then examine under a microscope. (KOH scrapings are commonly used to examine fungal infections.) The pathognomonic finding is observing medlar bodies (also called muriform bodies or sclerotic cells). Scrapings from the lesion can also be cultured to identify the organism involved </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Gastric atresia and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Antenatal depression and can you explain it in depth? [/INST] Antenatal depression, also known as prenatal or perinatal depression, is a form of clinical depression that can affect a woman during pregnancy, and can be a precursor to postpartum depression if not properly treated. It is estimated that 7% to 20% of pregnant women are affected by this condition. Any form of prenatal stress felt by the mother can have negative effects on various aspects of fetal development, which can cause harm to the mother and child. Even after birth, a child born from a depressed or stressed mother feels the affects. The child is less active and can also experience emotional distress. Antenatal depression can be caused by the stress and worry that pregnancy can bring, but at a more severe level. Other triggers include unplanned pregnancy, difficulty becoming pregnant, history of abuse, and economic or family situations.Commonly, symptoms involve how the patient views herself, how she feels about going through such a life changing event, the restrictions on the mothers lifestyle that motherhood will place, or how the partner or family feel about the baby. Pregnancy places significant strain on a womans body, so stress, mood swings, sadness, irritability, pain, and memory changes are to be expected. Left untreated, antenatal depression can be extremely dangerous for the health of the mother and the baby. It is highly recommended that mothers who feel they are experiencing antenatal depression have a discussion about it with their health care provider. Mothers with a history of mental health issues should also talk to their doctor about it early in the pregnancy to help with possible depressive symptoms.

Signs and symptoms
Antenatal depression is classified based on a womans symptoms. During pregnancy, a lot of changes to mood, memory, eating habits, and sleep are common. When these common traits become severe, and begin to alter ones day-to-day life, that is when it is considered to be antenatal depression. Symptoms of antenatal depression are:

Inability to concentrate.
Overwhelming anxiety and fear.
Difficulty remembering.
Feeling emotionally numb.
Extreme irritability.
Sleeping too much or not enough, or restless sleep.
Extreme or unending fatigue.
Desire to over eat, or not eat at all.
Weight loss/gain unrelated to pregnancy.
Loss of interest in sex.
A sense of dread about everything, including the pregnancy.
Feelings of failure, or guilt.
Persistent sadness.
Thoughts of suicide, or death.Other symptoms can include the inability to get excited about the pregnancy, and/or baby, a feeling of disconnection with the baby, and an inability to form/feel a bond with the developing baby. This can drastically affect the relationship between the mother and the baby, and can drastically affect the mothers capacity for self-care. Such inadequacies can lead to even greater risk factors for the mother. Antenatal depression can be triggered by various causes, including relationship problems, family or personal history of depression, infertility, previous pregnancy loss, complications in pregnancy, and a history of abuse or trauma.

Onset and duration of symptoms
Antenatal depression can be caused by many factors. Often it is associated with the fear and stress of the pregnancy. Other factors include unintended pregnancy, hyperemesis gravidarum, financial issues, living arrangements and relationships with the father and family. Typically, depression symptoms associated with pregnancy are categorized as postnatal depression, due to the onset of symptoms occurring after childbirth has occurred. The following is a breakdown of when a group of various women began to feel the onset of symptoms associated with depression:

11.8 percent at 18 weeks
13.5 percent at 32 weeks
9.1 percent 8 weeks after the birth
8.1 percent 8 months after the birthIn a recent article posted by The BabyCenter, the authors stated that "For years, experts mistakenly believed that pregnancy hormones protected against depression, leaving women more vulnerable to the illness only after the baby was born and their hormone levels plunged." This is a possible explanation as to why antenatal depression has just recently been identified.

Prevalence and causes
The prevalence of antenatal depression differs slightly by region of world. In the United States, antenatal depression is experienced in as many as 16% of pregnant women, while in South Asia it is experienced in as many as 24% of pregnant women. Its becoming more prevalent as more medical studies are being done. Antenatal depression was once thought to simply be the normal stress associated with any pregnancy, and was waved off as a common ailment. It can be caused by many factors, usually though involving aspects of the mothers personal life, such as family, economic standing, relationship status, etc. It can also be caused by hormonal and physical changes that are associated with pregnancy. Additional risk factors include lack of social support, marital dissatisfaction, discriminatory work environments, history of domestic abuse, and unplanned or unwanted pregnancy. Studies have determined that there may be a connection between antenatal and postpartum depression in women with lower vitamin D levels. There is a higher risk of antenatal depression in woman living in low-income countries who deal with less access to quality healthcare, have economic issues, and dont have a good support system.

Screening
Perinatal mental health screenings are important in detecting and diagnosing antenatal and postpartum depression early. The American College of Obstetricians and Gynecologists is one of the many maternal health organizations that strongly encourage universal screening for expectant and postpartum women for depression as part of routine obstetric care. In fact, many states, including California have already legislated laws that require providers to screen patients during visits because they recognize that early screenings can expedite the process in receiving effective treatment. The Patient Health Questionnaire 9 (PHQ-9) is a screening tool typically used to detect depression. Another tool, the Edinburgh Postnatal Depression Scale, was developed for the postnatal period, but has also been validated for use during pregnancy.PHQ-9 is a reliable depression severity scale that was formulated in accordance with DSM-IV criteria for depression, consisting of 9 items correlating to the 9 criteria listed in DSM-IV. It is a shortened version of the PHQ and has been assessed for comparable sensitivity and specificity. The screening test is self-administered to patients and are usually performed at the primary care clinic.However, it is not enough to just provide mental health screenings to at risk patients. Interventions such as referrals to treatment and mental health monitoring should be implemented in health care systems in order to ensure these women are helped consistently throughout their recovery journey.Studies suggest that obese woman tend to develop mental health issues more frequently and should discuss any symptoms with their doctor at the first prenatal appointment.

Treatment
Treatment for antenatal depression poses many challenges because the baby is also affected by any treatment given to the mother. There are both non-pharmacological and pharmacological treatment options which can be considered by women with antenatal depression.

Non-pharmacological Therapy
Psychotherapy
Psychotherapy is recommended for any woman with antenatal depression, as it is an effective way for the mother to express her feelings in her own words. Specifically, Cognitive Behavioral Therapy effectively helps decrease symptoms of antenatal depression. In addition to psychotherapy, being seen by a psychiatrist is recommended as they can assess if medications will be beneficial and make specific medication recommendations, if warranted. Familial support may also play a role in helping with the emotional aspects of antenatal depression.While mental health specialists are trained in providing counseling interventions, results from a recent systematic review and meta-analysis of the literature found that nonspecialist providers, such as lay counselors, nurses, midwives, and teachers with no formal training in counseling interventions, often fill a gap in providing effective services related to depression and anxiety treatments.

Exercise Therapy
Studies suggest that forms of exercise can help with depressive symptoms both before and after birth, but not prevent it entirely.Exercise options that have been studied to help reduce symptoms:

Yoga
Walking
Stretching
Aerobic exercise

Medications
When discussing medication options for antenatal depression, it is important to ask the prescribing healthcare provider to share more details about all the risks and benefits of the available medications. During pregnancy, there are two main kinds of antidepressants used during pregnancy; tricyclic antidepressants (TCAs) and selective serotonin reuptake inhibitors (SSRIs). Once prescribed, anti-depressant medication has been found to be extremely effective in treating antenatal depression. Patients can expect to feel an improvement in mood in roughly 2 to 3 weeks on average, and can begin to feel themselves truly connect with their baby. Reported benefits of medication include returned appetite, increased mood, increased energy, and better concentration. Side effects are minor, though they are reported in some cases. Currently, no abnormalities of the baby have been associated with the use of antidepressants during pregnancy. It may be true that maternal SSRI use during pregnancy can lead to difficulty for their newborn adjusting to conditions outside of the womb immediately following birth. Some studies indicate that infants with exposure to SSRIs in the second and third trimester were more likely to be admitted to intensive care following their birth for respiratory, cardiac, low weight and other reasons, and that infants with prenatal SSRI exposure exhibited less motor control upon delivery than infants who were not exposed to SSRIs. Newborns who were exposed to SSRIs for five months or more prior to birth were at a greater risk for lower Apgar scores 1 and 5 minutes after delivery, indicating they were of lesser health than newborns who were not exposed to SSRIs before birth. However, prenatal SSRI exposure was not found to have a significant impact the long-term mental and physical health of the children. These results are not independent of any effects of prenatal depression on infants.

Connection to postpartum depression and parenting stress
Studies have found a strong link between antenatal depression and postpartum depression in women. In other words, women who have antenatal depression are very likely to also develop postpartum depression. The cause of this is based on the continuation of the antenatal depression into postpartum. In a logistical light, it makes sense that women who are depressed during their pregnancy will also be depressed following the birth of their child. This being said there are some factors that determine exclusively the presence of postpartum depression that are not necessarily linked with antenatal depression. These examples include variables like socioeconomic class, if a pregnancy was planned or not, and the parents relationship prior to conception and delivery of the child.In reference to a recent study by Coburn et al., the authors found that in addition to prenatal effects, higher maternal depressive symptoms during the postpartum period (12 weeks) were associated with more infant health concerns. This is consistent with other findings among low-SES Mexican-American women and their infants. Women with prenatal depressive symptoms are more likely to develop postpartum depression, which can also have negative consequences on children, such as emotional and behavior problems, attachment difficulties, cognitive deficits, physical growth and development, and feeding habits and attitudes. Related, maternal depression affects parenting behaviors, which in turn could affect child outcomes. Thus, womens mental health throughout the perinatal period should be a priority, not only to support women, but also to promote optimal functioning for their infants.

Antenatal Depression and Infant Health
Depression during pregnancy is associated with an increased risk of spontaneous abortion. In a review by Frazier et al., acute and chronic stress during pregnancy can diminish proper immunological activity crucial during pregnancy, and can possibly induce spontaneous abortion. There is still a debate on whether the miscarriage is due to the depressive disease state or the anti-depressant medication. A large study conducted in Denmark observed that there was a higher incidence of first trimester miscarriage in depressed women not exposed to SSRI compared to non-depressed women exposed to SSRI, indicating that the miscarriage may be associated with the psychological state of the mother rather than the anti-depressant.
Depressive symptoms in pregnant women are linked with poor health outcomes in infants. The rates of hospitalization are found increased for infants who are born to women with high depression levels during pregnancy. Reduced breastfeeding, poor physical growth, lower birth weight, early gestational age and high rates of diarrheal infection are some of the reported outcomes of poor health among infants born to depressed pregnant women. In fact, positive antenatal screenings administered in the first or third trimester are found to be high risk factors for early cessation in breastfeeding. Studies also report that the environmental effects of maternal depression affect the developing fetus to such an extent that the impact can be seen during adulthood of the offspring. The effects are worse for women from low socio-economic backgrounds. In a recent study by Coburn et al., maternal prenatal depressive symptoms predicted significantly higher number of infant health concerns at 12-weeks (3 months) of age. The health concerns included rash, colic, cold, fever, cough, diarrhea, ear infections, and vomiting. Additional concerns for women in low-income backgrounds includes low birth rate and preterm births.An interesting and informative area of research has been done to see the role of confounding variables in relationship of maternal prenatal depression with infant health concerns. Age of mother, romantic partner, education, household income, immigrant status, and number of other children, breastfeeding, gestational age, birth weight are some of the mediating or moderating factors which are found correlated with infant health concerns. The studies of post-partum depressive symptoms are relatively more than those of prenatal depression and the studies should look into the role of various factors during pregnancy that may impact the health of infants, even continuing into adulthood.

Male Perspective for Antenatal Depression
Fathers can also experience depression during their partners pregnancy, commonly displayed as fatigue or changes in sleep and eating patterns. Men whose partners are women struggling with antenatal or postnatal depression often find themselves receiving less affection and intimacy from their partners </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Laryngo-onycho-cutaneous syndrome and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Oral mucocele and can you explain it in depth? [/INST] Oral mucocele (also mucous extravasation cyst, mucous cyst of the oral mucosa, and mucous retention and extravasation phenomena.) is a condition caused by two related phenomena - mucus extravasation phenomenon and mucous retention cyst.
Mucous extravasation phenomenon is a swelling of connective tissue consisting of a collection of fluid called mucus. This occurs because of a ruptured salivary gland duct usually caused by local trauma (damage) in the case of mucous extravasation phenomenon and an obstructed or ruptured salivary duct in the case of a mucus retention cyst. The mucocele has a bluish, translucent color, and is more commonly found in children and young adults.
Although these lesions are often called cysts, mucoceles are not true cysts because they have no epithelial lining. Rather, they are polyps.

Signs and symptoms
The size of oral mucoceles vary from 1 mm to several centimeters and they usually are slightly transparent with a blue tinge. On palpation, mucoceles may appear fluctuant, but can also be firm. Their duration lasts from days to years, and may have recurrent swelling with occasional rupturing of its contents.

Locations
The most common location to find a mucocele is the inner surface of the lower lip. It can also be found on the inner side of the cheek (known as the buccal mucosa), on the anterior ventral tongue, and the floor of the mouth. When found on the floor of the mouth, the mucocele is referred to as a ranula. They are rarely found on the upper lip. As their name suggests, they are basically mucus-lined cysts and they can also occur in the paranasal sinuses, most commonly the frontal sinuses, the frontoethmoidal region, and the maxillary sinus. Sphenoid sinus involvement is extremely rare.  When the lumen of the vermiform appendix of the intestine gets blocked due to any factor, a mucocele can also form there.

Variations
A variant of a mucocele is found on the palate, retromolar pad, and posterior buccal mucosa. Known as a "superficial mucocele", this type presents as single or multiple vesicles and bursts into an ulcer. Despite healing after a few days, superficial mucoceles recur often in the same location. Other causes of bumps inside lips are aphthous ulcer, lipoma, benign tumors of salivary glands, submucous abscesses, and haemangiomas.

Diagnosis
Microscopically, mucoceles appears as granulation tissue surrounding mucin </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Fibrous hamartoma of infancy and can you explain it in depth? [/INST] Fibrous hamartoma of infancy (FHI) is a rare, typically painless, benign tumor that develops in the subcutaneous tissues of the axilla (i.e. armpit), arms, external genitalia, or, less commonly, various other areas. It is diagnosed in children who are usually less than 2 years old or, in up to 20% of cases, develops in utero and is diagnosed in an infant at birth.The cells involved in FHI include bland fibroblasts/myofibroblasts, mature fat cells, and primitive-appearing spindle-shaped and/or star-shaped cells. The tumor was first described by R.D. Reye in 1956 who termed the disorder "subdermal fibromatous tumor of infancy" and regarded it as a reactive lesion. In a 1964 study of 30 patients, F.M. Enzinger renamed the tumor hamartoma of infancy; he regarded it to be a hamartoma (i.e. a local malformation of various normal cell types due to a systemic genetic condition) rather than a reactive lesion. However, subsequent studies have found gene mutations in FHI tumor cells and conclude that it is a true neoplasm, i.e. a growth of cells which is uncoordinated with that of the normal surrounding tissue and persists in growing abnormally even if the original trigger is removed. In 2020, the World Health Organization classified FHI in the category of benign fibroblastic and myofibroblastic tumors.Fibrous hamartoma of infancy is generally a benign tumor but may be locally aggressive, locally infiltration, and in uncommon cases produce symptoms such as tenderness. Surgical excision is the treatment of choice for FHI tumors.

Presentation
The largest study to date examined 197 cases of FHI. In this study, most individuals presented with a slowly growing, symptomless, subcutaneous mass although rarely these masses were rapidly growing, and/or were tender, painful, warm, and/or were accompanied by skin changes, pigmentation, sweat gland enlargement, and/or increased hair overlaying the tumor. Sixty-eight percent of these cases were diagnosed in the first year of life, 23% were diagnoses at birth, and 9% were diagnosed in children 2–5 years old. The male-to female ratio was 2.4. The tumors were most common in the axilla (23% of cases), upper arm (12.5%), lower arm (10.5%), external genitalia area (9.5%),  and inguinal region (7.5%); less common or rare sites for these tumors were the buttocks, back of the head, back of the neck, back of the torso, lower arm, leg, foot, chest, and anal area. Most cases presented as solitary masses but 3 cases presenting with 2 tumors and 1 case presenting with 5 tumors. Overall, the size of these tumors varied between 0.5 and 4.0 cm but in rare cases were as large as 20 cm. Two subsequent studies of 145 and 60 individuals agreed with all of these results but also did diagnose  FHI in individuals as old as 8 and 14 years, respectively.

Pathology
On gross pathological examination, FHI tumors are soft, poorly demarcated, fibro-fatty masses located in subcutaneous tissues. These tumor masses tend to blend with the surrounding fat tissues, may be lobulated, and in rare cases, especially when large, extend into nearby muscles, nerves, and/or fibrous/connective tissue structures. Microscopic histopathological analyses of hematoxylin and eosin stained FHI tumor tissues consistently reveal three very different component zones in virtually all cases: 1) haphazardly arranged, intersecting bundles of bland fibroblast-like/myofibroblast-like cells; 2) mature adipose (i.e. fat) tissue; and 3) highly vascular, myxoid (i.e. connective tissue appearing more blue or purple than normal connective) nodules of primitive-appearing spindled-shaped to star-shaped cells. Chronic inflammatory cell (e.g. lymphocytes, macrophages, and plasma cells) aggregates are commonly present in these lesion. The relative proportion of fibroblast/myofibroblast, adipose tissue, and myxoid zones commonly vary from case to case.Earlier Immunohistochemical analyses of FHI tumor tissues in a small number of cases have given varying results. A more recent and larger study reported that 75% of tested cases showed variable expression of smooth muscle actin proteins by the cells located primarily in fibroblast/myofibroblast zones and occasionally by the cells located in myxoid zones; the S100 protein was expressed by the fat cells of the adipose tissue zone in all cases; CD34 protein was expressed by the cells in myxoid and fibroblast/myofibroblast zones in all cases; and cells expressing the desmin protein were not detected in any case. A smaller, more recent study also found that 8 of 13 FHI cases had tumor cells in the fibroblast/myofibrobalast zone that expressed smooth-muscle actin protein, 6 of 8 cases had tumor cells in the myxoid zone that expressed the CD34 protein, and 7 of 7 cases had tumor cells in the adipose tissue zone express the S100 protein. The expression pattern of one or more of these proteins has not yet been found to be of help in distinguishing FHI from other tumor types.

Chromosome and gene abnormalities
The EGFR gene which codes for the production of the epidermal growth factor receptor protein is located at band 11.2 on the short (or "p") arm of chromosome 7. Studies using next-generation sequencing targeted to the EGFR gene chromosomal area and confirmed by Sanger sequencing have detected insertion and/or deletion mutations in exon 20 of this gene in the tumor cells of 13 of 13 test FHI cases. While the activity of the normal EGFR protein is blocked by tyrosine kinase inhibitor drugs, most proteins coded by EGFR exon 20-mutated genes do not respond to these drugs due the structural configuration of their EGFR kinase domains; however, certain protein variants coded by these mutated EGFR genes may still be sensitive, and offer a potential treatment option, for a subset of FHI cases. In any event, the identification of these EGFR can help distinguish FHI from other pediatric spindle cell neoplasms with morphologies similar to FHI such as giant cell fibroblastoma.Genomic microarray analyses performed on the two FHI cases with tumors that had areas of sarcoma-like morphology found sarcoma-like cells hyperdiploid (i.e. cell with at least 2 more chromosomes than the normal 48), near tetraploid (i.e </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Sciatic nerve and can you explain it in depth? [/INST] The  sciatic nerve, also called the ischiadic nerve, is a large nerve in humans and other vertebrate animals which is the largest branch of the sacral plexus and runs alongside the hip joint and down the lower limb. It is the longest and widest single nerve in the human body, going from the top of the leg to the foot on the posterior aspect. The sciatic nerve has no cutaneous branches for the thigh. This nerve provides the connection to the nervous system for the skin of the lateral leg and the whole foot, the muscles of the back of the thigh, and those of the leg and foot. It is derived from spinal nerves L4 to S3. It contains fibers from both the anterior and posterior divisions of the lumbosacral plexus.

Structure
In humans, the sciatic nerve is formed from the L4 to S3 segments of the sacral plexus, a collection of nerve fibres that emerge from the sacral part of the spinal cord. The lumbosacral trunk from the L4 and L5 roots descends between the sacral promontory and ala and the S1 to S3 roots emerge from the ventral sacral foramina. These nerve roots unite to form a single nerve in front of the piriformis muscle. The nerve passes beneath piriformis and through the greater sciatic foramen, quitting the pelvis.: 422–4  From here, it travels down the posterior thigh to the popliteal fossa. The nerve travels in the posterior compartment of the thigh behind (superficial to) the adductor magnus muscle, and is itself in front of (deep to) the long head of the biceps femoris muscle. At the popliteal fossa, the nerve divides into its two branches:: 532
The tibial nerve, which travels down the posterior compartment of the leg into the foot
The common fibular nerve (also called the common peroneal nerve), which travels down the anterior and lateral compartments of the leg into the footThe sciatic nerve is the largest nerve in the human body.: 422–4

Development
Function
The sciatic nerve supplies sensation to the skin of the foot, as well as the entire lower leg (except for its inner side). Sensation to skin to the sole of the foot is provided by the tibial nerve, and the lower leg and upper surface of the foot via the common fibular nerve.: 422–4 The sciatic nerve also innervates muscles </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Tufted angioma and can you explain it in depth? [/INST]  </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Ablepharon macrostomia syndrome and can you explain it in depth? [/INST] Ablepharon macrostomia syndrome (AMS) is an extremely rare, autosomal dominant genetic disorder characterized by abnormal phenotypic appearances that primarily affect the head and face as well as the skull, skin, fingers and genitals. AMS generally results in abnormal ectoderm-derived structures. The most prominent abnormality is the underdevelopment (microblepharon) or absence of eyelids – signifying the ablepharon aspect of the disease – and a wide, fish-like mouth – macrostomia. Infants presenting with AMS may also have malformations of the abdominal wall and nipples. Children with AMS might also experience issues with learning development, language difficulties and intellectual disabilities.
AMS is caused by mutations in the TWIST2 gene, among others. It is closely related to Barber–Say syndrome in terms of phenotypic abnormalities.

Signs and symptoms
AMS is generally characterized by abnormal appearances of the skin, eyes, fingers, genitals, head and face. Infants with AMS will have thin, redundantly wrinkled skin and excessive facial creases; wide-set eyes with absent or severely underdeveloped eyelids and down-turned lower eyelids; and a wide, fish-like mouth that may be fused together at the corners. Other appearances of the face and head include: broad nasal bridge, wide, flared nostrils and thick and flared alae nasi (edges of the nostrils).Abnormalities can also be seen in the hands and fingers, as infants with AMS will also have webbed fingers with limited ability to flex and extend the fingers. Infants with AMS will also display small, rudimentary ears that are atypically low-set on the skull. Absence of the zygomatic bone is also possible. Skin may be dry and coarse, excessively wrinkled around the face and loose around the hands yet tight around the finger joints, leading to diminished use of the fingers.Genital defects may include: ambiguous genitalia, a displaced and/or atypically small penis (micropenis), an absent scrotum around the testes and undescended testicles. Finally, alopecia and thin, sparse hair are also frequently observed.

Causes
Like Barber–Say syndrome, AMS is caused by mutations in the TWIST2 gene that affect a highly conserved residue of TWIST2 (twist-related protein 2). TWIST2 is a basic helix-loop-helix transcription factor that binds to E-box DNA motifs (5-CANNTG-3) as a heterodimer and inhibits transcriptional activation. Because TWIST2 mediates mesenchymal stem cell differentiation and prevents premature or ectopic osteoblast differentiation, mutations in TWIST2 that disrupt these functions by altering DNA-binding activity could explain many of the phenotypes of AMS. Current research points to the substitution of the wild-type amino acid for Lysine at TWIST2 residue 75 as a significant genetic cause of AMS.AMS is inherited in an autosomal dominant manner, in which an affected individual needs only one copy of the mutant allele in order to express the disease.

Mechanism
The mesenchyme is a mesodermal embryonic tissue that can develop into a multitude of different tissues depending on the needs of the developing embryo. The mesenchyme can develop into blood, cartilage, and membranes. In a normal patient, TWIST2 is highly expressed during embryonic development, specifically in the craniofacial development and chondrogenisis. TWIST2 works to prevent the premature maturation of chondrogenic cells and osteoblasts, the cells that will form cartilage and bone respectively. The dominant mutation in TWIST2 leads to the chondrogenic and osteoblastic cells becoming mature prematurely. This then leads to the primary craniofacial deformities seen in AMS patients.

Diagnosis
Ablepharon macrostomia syndrome can be diagnosed at birth by identification of characteristic physical findings, clinical evaluation, and specialized imaging techniques such as CT scans. CT scans can confirm the absence of the zygomatic arch and abnormalities in the cranial and mandibular bones. An ophthalmologist can diagnose abnormalities in the eyelids and confirm microblepharon or ablepharon. Teams of specialist will typically work together to confirm diagnosis and assess treatment options. Pediatricians, gastroenterologists, dermatologists, urologists, and other care providers can be expected to aid in the diagnosis and treatment.

Treatment
Primary treatment focuses on relief of immediate symptoms such as providing lubrication to the eyes to relieve pain and dryness; antibiotics may also be prescribed to prevent infections and inflammation </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Vitreomacular adhesion and can you explain it in depth? [/INST] Vitreomacular adhesion (VMA) is a human medical condition where the vitreous gel (or simply vitreous, AKA vitreous humour) of the human eye adheres to the retina in an abnormally strong manner. As the eye ages, it is common for the vitreous to separate from the retina. But if this separation is not complete, i.e. there is still an adhesion, this can create pulling forces on the retina that may result in subsequent loss or distortion of vision. The adhesion in of itself is not dangerous, but the resulting pathological vitreomacular traction (VMT) can cause severe ocular damage.
The current standard of care for treating these adhesions is pars plana vitrectomy (PPV), which involves surgically removing the vitreous from the eye. A biological agent for non-invasive treatment of adhesions called ocriplasmin has been approved by the FDA on October 17, 2012.

Symptom and signs
Traction caused by VMA is the underlying pathology of an eye disease called symptomatic VMA. There is evidence that symptomatic VMA can contribute to the development of several well-known eye disorders, such as macular hole and macular pucker, that can cause visual impairment, including blindness. It may also be associated with age-related macular degeneration (AMD), diabetic macular edema (DME), retinal vein occlusion, and diabetic retinopathy (DR).

Pathology
Over time, it is common for the vitreous within the human eye to liquify and collapse in processes known as syneresis and synchisis respectively. This creates fluid-filled areas that can combine to form pockets of vitreous gel that are mostly liquid with very small concentrations of collagen. If these liquid pockets are close enough to the interface between the vitreous gel and the retina, they can cause complete separation of the vitreous from the retina in a normally occurring process in older humans called posterior vitreous detachment (PVD). PVD in of itself is not dangerous and a natural process.If the separation of the vitreous from the retina is not complete, areas of focal attachment or adhesions can occur, i.e. a VMA. The pulling forces or traction from this adhesion on the retinal surface can sometimes cause edema within the retina, damage to retinal blood vessels causing bleeding, or damage to the optic nerve causing disruption in the nerve signals sent to the brain for visual processing. It is important to note that while the VMA itself is not dangerous, the resultant pulling on the retina called vitreomacular traction (VMT) causes the above damage. The size and strength of the VMA determine the variety of resulting pathologies or symptoms.VMA can also lead to the development of VMT/traction-related complications such as macular puckers and macular holes leading to distorted vision or metamorphopsia; epiretinal membrane; tractional macular oedema; myopic macular retinoschisis; visual impairment; blindness. The incidence of VMA is reported as high as 84% for patients with macular hole, 100% for patients with vitreomacular traction syndrome, and 56% in idiopathic epimacular membrane.

Diagnosis
Careful eye examination by an ophthalmologist or optometrist is critical for diagnosing symptomatic VMA. Imaging technologies such as optical coherence tomography (OCT) have significantly improved the accuracy of diagnosing symptomatic VMA.

Treatment
A new FDA approved drug was released on the market late 2013. Jetrea (Brand name) or Ocriplasmin (Generic name) is the first drug of its kind used to treat vitreomacular adhesion.Mechanism of Action: Ocriplasmin is a truncated human plasmin with proteolytic activity against protein components of the vitreous body and vitreoretinal interface. It dissolves the protein matrix responsible for the vitreomacular adhesion.
Adverse drug reactions: Decreased vision, potential for lens subluxation, dyschromatopsia (yellow vision), eye pain, floaters, blurred vision.
New Drug comparison Rating gave Jetea a 5 indicating an important advance.
Previously, no recommended treatment was available for the patient with mild symptomatic VMA. In symptomatic VMA patients with more significant vision loss, the standard of care is pars plana vitrectomy (PPV), which involves surgically removing the vitreous from the eye, thereby surgically releasing the symptomatic VMA. In other words, vitrectomy induces PVD to release the traction/adhesion on the retina </s>