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Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
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A 2012 review could not find strong evidence for any cause, although many theories have been discredited. Because twins and relatives are more likely to get myopia under similar circumstances, there must be a hereditary factor. Myopic shifts seen during growth spurts of childhood and adolescence, as well as in acromegaly, indicates a relationship between the timing of myopic development and the release of human growth hormone. However, the lack of correlation between height and myopia seems to suggest the relationship between human growth hormone and myopia is complex.
Myopia has been increasing rapidly throughout the developed world, suggesting environmental factors must be important. Quite similarly, the mechanisms of emmetropization are still unclear. Emmetropization is the process by which a child's eye grows and changes to become less hyperopic. It is thought that the same triggers and signals that cause this growth may also play a role in the eye growing beyond the point of emmetropia and into myopia.
In one study, heredity was an important factor associated with juvenile myopia, with smaller contributions from more near work, higher school achievement, and less time in sports activity.
Long hours of exposure to daylight appears to be a protective factor. Lack of outdoor play could be linked to myopia.
Other personal characteristics, such as value systems, school achievements, time spent in reading for pleasure, language abilities, and time spent in sport activities all correlated to the occurrence of myopia in studies.
Patients with keratoconus typically present initially with mild astigmatism and myopia, commonly at the onset of puberty, and are diagnosed by the late teenage years or early 20s. The disease can, however, present or progress at any age; in rare cases, keratoconus can present in children or not until later adulthood. A diagnosis of the disease at an early age may indicate a greater risk of severity in later life. Patients' vision will seem to fluctuate over a period of months, driving them to change lens prescriptions frequently, but as the condition worsens, contact lenses are required in the majority of cases. The course of the disorder can be quite variable, with some patients remaining stable for years or indefinitely, while others progress rapidly or experience occasional exacerbations over a long and otherwise steady course. Most commonly, keratoconus progresses for a period of 10 to 20 years before the course of the disease generally ceases in the third and fourth decades of life.
The National Eye Institute reports keratoconus is the most common corneal dystrophy in the United States, affecting about one in 2,000 Americans, but some reports place the figure as high as one in 500. The inconsistency may be due to variations in diagnostic criteria, with some cases of severe astigmatism interpreted as those of keratoconus, and" vice versa". A long-term study found a mean incidence rate of 2.0 new cases per 100,000 population per year. Some studies have suggested a higher prevalence amongst females, or that people of South Asian ethnicity are 4.4 times as likely to suffer from keratoconus as Caucasians, and are also more likely to be affected with the condition earlier.
Keratoconus is normally bilateral (affecting both eyes) although the distortion is usually asymmetric and is rarely completely identical in both corneas. Unilateral cases tend to be uncommon, and may in fact be very rare if a very mild condition in the better eye is simply below the limit of clinical detection. It is common for keratoconus to be diagnosed first in one eye and not until later in the other. As the condition then progresses in both eyes, the vision in the earlier-diagnosed eye will often remain poorer than that in its fellow.
As the name implies, it is the bulge of weak sclera lined by ciliary body, which occurs about 2–3 mm away from the limbus. Its common causes are thinning of sclera following perforating injury, scleritis & absolute glaucoma.
it is part of anterior staphyloma
It is the name given to the localised bulge in limbal area, lined by the root of the iris. It results due to ectasia of weak scar tissue formed at the limbus, following healing of a perforating injury or a peripheral corneal ulcer. There may be associated secondary angle closure glaucoma, may cause progression of the bulge if not treated. Defective vision occurs due to marked corneal astigmatism. Treatment consists of localised staphylectomy under heavy doses of oral steroids.
A galactosemic cataract is cataract which is associated with the consequences of galactosemia.
Galactosemia is one of the most mysterious of the heavily-researched metabolic diseases. It is a hereditary disease that results in a defect in, or absence of, galactose-metabolizing enzymes. This inborn error leaves the body unable to metabolize galactose, allowing toxic levels of galactose to build up in human body blood, cells, and tissues. Although treatment for galactosemic infants is a strict galactose-free diet, endogenous (internal) production of galactose can cause symptoms such as long-term morbidity, presenile development of cataract, renal failure, cirrhosis, and cognitive, neurologic, and female reproductive complications. Galactosemia used to be confused with diabetes due to the presence of sugar in a patient's urine. However, screening advancements have allowed the exact identity of those sugars to be determined, thereby distinguishing galactosemia from diabetes.
The disease incidence varies widely depending on the geographical location. The most extensive epidemiological survey on this subject has been carried out by Dharmasena et al. who analysed the number of neonates who developed neonatal conjunctivitis in England from 2000 to 2011. In addition to the incidence of this sight threatening infection they also investigated the time trends of the disease. According to them the incidence of Neonatal conjunctivitis (Ophthalmia Neonatorum) in England was 257 (95% confidence interval: 245 to 269) per 100,000 in 2011.
Papillorenal syndrome, also called renal-coloboma syndrome or isolated renal hypoplasia, is an autosomal dominant genetic disorder marked by underdevelopment (hypoplasia) of the kidney and colobomas of the optic nerve.
Approximately half of patients with papillorenal syndrome do not have defects in the "Pax2". This suggests that other genes play a role in the development of the syndrome, though few downstream effectors of "Pax2" have been identified.
Chemical irritants such as silver nitrate can cause chemical conjunctivitis, usually lasting 2–4 days. Thus, prophylaxis with a 1% silver nitrate solution is no longer in common use. In most countries neomycin and chloramphenicol eye drops are used instead. However, it is possible for newborns to suffer from neonatal conjunctivitis due to reactions with chemicals in these common eye drops. Additionally, a blocked tear duct may be another non-infectious cause of neonatal conjunctivitis.
As of 2009, loiasis is endemic to 11 countries, all in western or central Africa, and an estimated 12–13 million people have the disease. The highest incidence is seen in Cameroon, Republic of the Congo, Democratic Republic of Congo, Central African Republic, Nigeria, Gabon, and Equatorial Guinea. The rates of "Loa loa" infection are lower but it is still present in and Angola, Benin, Chad and Uganda. The disease was once endemic to the western African countries of Ghana, Guinea, Guinea Bissau, Ivory Coast and Mali but has since disappeared.
Throughout "Loa loa"-endemic regions, infection rates vary from 9 to 70 percent of the population. Areas at high risk of severe adverse reactions to mass treatment (with Ivermectin) are at present determined by the prevalence in a population of >20% microfilaremia, which has been recently shown in eastern Cameroon (2007 study), for example, among other locales in the region.
Endemicity is closely linked to the habitats of the two known human loiasis vectors, "Chrysops dimidiata" and "C. silicea".
Cases have been reported on occasion in the United States but are restricted to travelers who have returned from endemic regions.
In the 1990s, the only method of determining "Loa loa" intensity was with microscopic examination of standardized blood smears, which is not practical in endemic regions. Because mass diagnostic methods were not available, complications started to surface once mass ivermectin treatment programs started being carried out for onchocerciasis, another filariasis. Ivermectin, a microfilaricidal drug, may be contraindicated in patients who are co-infected with loiasis and have associated high microfilarial loads. The theory is that the killing of massive numbers of microfilaria, some of which may be near the ocular and brain region, can lead to encephalopathy. Indeed, cases of this have been documented so frequently over the last decade that a term has been given for this set of complication: neurologic serious adverse events (SAEs).
Advanced diagnostic methods have been developed since the appearance the SAEs, but more specific diagnostic tests that have been or are currently being development (see: Diagnostics) must to be supported and distributed if adequate loiasis surveillance is to be achieved.
There is much overlap between the endemicity of the two distinct filariases, which complicates mass treatment programs for onchocerciasis and necessitates the development of greater diagnostics for loiasis.
In Central and West Africa, initiatives to control onchocerciasis involve mass treatment with Ivermectin. However, these regions typically have high rates of co-infection with both "L. loa" and "O. volvulus", and mass treatment with Ivermectin can have severe adverse effects (SAE). These include hemorrhage of the conjunctiva and retina, heamaturia, and other encephalopathies that are all attributed to the initial L. loa microfilarial load in the patient prior to treatment. Studies have sought to delineate the sequence of events following Ivermectin treatment that lead to neurologic SAE and sometimes death, while also trying to understand the mechanisms of adverse reactions to develop more appropriate treatments.
In a study looking at mass Ivermectin treatment in Cameroon, one of the greatest endemic regions for both onchocerciasis and loiasis, a sequence of events in the clinical manifestation of adverse effects was outlined.
It was noted that the patients used in this study had a "L. loa" microfilarial load of greater than 3,000 per ml of blood.
Within 12–24 hours post-Ivermectin treatment (D1), individuals complained of fatigue, anorexia, and headache, joint and lumbar pain—a bent forward walk was characteristic during this initial stage accompanied by fever. Stomach pain and diarrhea were also reported in several individuals.
By day 2 (D2), many patients experienced confusion, agitation, dysarthria, mutism and incontinence. Some cases of coma were reported as early as D2. The severity of adverse effects increased with higher microfilarial loads. Hemorrhaging of the eye, particularly the retinal and conjunctiva regions, is another common sign associated with SAE of Ivermectin treatment in patients with "L. loa" infections and is observed between D2 and D5 post-treatment. This can be visible for up to 5 weeks following treatment and has increased severity with higher microfilarial loads.
Haematuria and proteinuria have also been observed following Ivermectin treatment, but this is common when using Ivermectin to treat onchocerciasis. The effect is exacerbated when there are high "L. loa" microfilarial loads however, and microfilariae can be observed in the urine occasionally. Generally, patients recovered from SAE within 6–7 months post-Ivermectin treatment; however, when their complications were unmanaged and patients were left bed-ridden, death resulted due to gastrointestinal bleeding, septic shock, and large abscesses.
Mechanisms for SAE have been proposed. Though microfilarial load is a major risk factor to post-Ivermectin SAE, three main hypotheses have been proposed for the mechanisms.
The first mechanism suggests that Ivermectin causes immobility in microfilariae, which then obstructs microcirculation in cerebral regions. This is supported by the retinal hemorrhaging seen in some patients, and is possibly responsible for the neurologic SAE reported.
The second hypothesis suggests that microfilariae may try to escape drug treatment by migrating to brain capillaries and further into brain tissue; this is supported by pathology reports demonstrating a microfilarial presence in brain tissue post-Ivermectin treatment.
Lastly, the third hypothesis attributes hypersensitivity and inflammation at the cerebral level to post-Ivermectin treatment complications, and perhaps the release of bacteria from L. loa after treatment to SAE. This has been observed with the bacteria "Wolbachia" that live with "O. volvulus".
More research into the mechanisms of post-Ivermectin treatment SAE is needed to develop drugs that are appropriate for individuals suffering from multiple parasitic infections.
One drug that has been proposed for the treatment of onchocerciasis is doxycycline. This drug has been shown to be effective in killing both the adult worm of "O. volvulus" and "Wolbachia", the bacteria believed to play a major role in the onset of onchocerciasis, while having no effect on the microfilariae of "L. loa". In a study done at 5 different co-endemic regions for onchocerciasis and loiasis, doxycycline was shown to be effective in treating over 12,000 individuals infected with both parasites with minimal complications. Drawbacks to using Doxycycline include bacterial resistance and patient compliance because of a longer treatment regimen and emergence of doxycycline-resistant "Wolbachia". However, in the study over 97% of the patients complied with treatment, so it does pose as a promising treatment for onchocerciasis, while avoiding complications associated with L. loa co-infections.
Human loiasis geographical distribution is restricted to the rain forest and swamp forest areas of West Africa, being especially common in Cameroon and on the Ogooué River. Humans are the only known natural reservoir. It is estimated that over 10 million humans are infected with "Loa loa" larvae.
An area of tremendous concern regarding loiasis is its co-endemicity with onchocerciasis in certain areas of west and central Africa, as mass ivermectin treatment of onchocerciasis can lead to serious adverse events (SAEs) in patients who have high "Loa loa" microfilarial densities, or loads. This fact necessitates the development of more specific diagnostics tests for "Loa loa" so that areas and individuals at a higher risk for neurologic consequences can be identified prior to microfilaricidal treatment. Additionally, the treatment of choice for loiasis, diethylcarbamazine, can lead to serious complications in and of itself when administered in standard doses to patients with high "Loa loa" microfilarial loads.
Melanism, meaning a mutation that results in completely dark skin, does not exist in humans. Melanin is the primary determinant of the degree of skin pigmentation and protects the body from harmful ultraviolet radiation. The same ultraviolet radiation is essential for the synthesis of vitamin D in skin, so lighter color of skin - less melanin - is an adaptation for the prehistoric movement of humans away from equatorial regions, as there is less exposure to sunlight at higher latitudes. People from parts of Africa have very dark skin, but this is not melanism.
Diethylcarbamazine has been shown as an effective prophylaxis for "Loa loa" infection.
A study of Peace Corps volunteers in the highly Loa—endemic Gabon, for example, had the following results: 6 of 20 individuals in a placebo group contracted the disease, compared to 0 of 16 in the DEC-treated group. Seropositivity for antifilarial IgG antibody was also much higher in the placebo group. The recommended prophylactic dose is 300 mg DEC given orally once weekly. The only associated symptom in the Peace Corps study was nausea.
Researchers believe that geo-mapping of appropriate habitat and human settlement patterns may, with the use of predictor variables such as forest, land cover, rainfall, temperature, and soil type, allow for estimation of Loa loa transmission in the absence of point-of-care diagnostic tests. In addition to geo-mapping and chemoprophylaxis, the same preventative strategies used for malaria should be undertaken to avoid contraction of loiasis. Specifically, DEET-containing insect repellent, permethrin-soaked clothing, and thick, long-sleeved and long-legged clothing ought to be worn to decrease susceptibility to the bite of the mango or deer fly vector. Because the vector is day-biting, mosquito (bed) nets do not increase protection against loiasis.
Vector elimination strategies are an interesting consideration. It has been shown that the "Chrysops" vector has a limited flying range, but vector elimination efforts are not common, likely because the insects bite outdoors and have a diverse, if not long, range, living in the forest and biting in the open, as mentioned in the vector section.
No vaccine has been developed for loiasis and there is little report on this possibility.
Buruli ulcer commonly affects poor people in remote rural areas with limited access to health care. The disease can affect all age groups, although children under the age of 15 years (range 2–14 years) are predominantly affected. There are no sex differences in the distribution of cases among children. Among adults, some studies have reported higher rates among women than males (Debacker "et al." accepted for publication). No racial or socio-economic group is exempt from the disease. Most ulcers occur on the extremities; lesions on the lower extremities are almost twice as common as those on the upper extremities. Ulcers on the head and trunk accounted for less than 8% of cases in one large series.
Melanism is a development of the dark-colored pigment melanin in the skin or its appendages and is the opposite of albinism. The word "melanism" is derived from the ("black pigment").
Pseudo-melanism, also called abundism, is another variant of pigmentation, characterized by dark spots or enlarged stripes, which cover a large part of the body of the animal, making it appear melanistic.
A deficiency in or total absence of melanin pigments is called amelanism.
The morbid deposition of black matter, often of a malignant character causing pigmented tumors, is called melanosis. For a description of melanin-related disorders, see melanin and ocular melanosis.
Prevention focuses on protecting against mosquito bites in endemic regions. Insect repellents and mosquito nets are useful to protect against mosquito bites. Public education efforts must also be made within the endemic areas of the world to successfully lower the prevalence of "W. bancrofti" infections.
The WHO is coordinating an effort to eradicate filariasis. The mainstay of this programme is the mass use of antifilarial drugs on a regular basis for at least five years.
In April 2011, Sri Lanka was certified by the WHO as having eradicated this disease.
Afro-textured hair is the natural hair texture of certain populations in Africa, the African diaspora, Australia and Asia, which has not been altered by hot combs, flat irons or chemicals (through perming, relaxation or other straightening methods). Each strand of this hair type grows in a tiny, spring-like helix shape. The overall effect is such that, compared to straight, wavy or curly hair, afro-textured hair appears denser.
Buruli ulcer has been reported from at least 32 countries around the world, mostly in tropical areas:
- West Africa: Benin, Burkina Faso, Côte d'Ivoire, Ghana, Liberia, Nigeria, Togo, Guinea, Sierra Leone.
- Other African Countries: Angola, Cameroon, Congo, Democratic Republic of Congo, Equatorial Guinea, Gabon, Sudan, Uganda.
- Western Pacific: Australia, Papua New Guinea, Kiribati.
- Americas: French Guiana, Mexico, Peru, Suriname.
- Asia: China, Malaysia, Japan.
In several of these countries, the disease is not considered to be a public health problem, hence the current distribution and the number of cases are not known. Possible reasons include:
- the distribution of the disease is often localized in certain parts of endemic countries;
- Buruli ulcer is not a notifiable disease
- In most places where the disease occurs, patients receive care from private sources such as voluntary mission hospitals and traditional healers. Hence the existence of the disease may not come to the attention of the ministries of health.
It most commonly occurs in Africa: Congo and Cameroon in Central Africa, Côte d'Ivoire, Ghana and Benin in West Africa. Some Southeast Asian countries (Papua New Guinea) and Australia have major foci, and there have been a few patients reported from South America (French Guyana and Surinam) and Mexico. Focal outbreaks have followed flooding, human migrations, and man-made topographic modifications such as dams and resorts. Deforestation and increased basic agricultural activities may significantly contribute to the recent marked increases in the incidence of "M. ulcerans" infections, especially in West Africa, where the disease is rapidly emerging.
HIV infection rates in central Africa are generally moderate to high.
Tropical spastic paraparesis (TSP), also called HTLV-I-associated myelopathy (HAM) or HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a medical condition that causes weakness, muscle spasms, and sensory disturbance by human T-lymphotropic virus resulting in paraparesis, weakness of the legs. As the name suggests, it is most common in tropical regions, including the Caribbean. Blood transfusion products are screened for HTLV-1 antibodies, as a preventive measure.
In areas where there is little iodine in the diet, typically remote inland areas and semi-arid equatorial climates where no marine foods are eaten, iodine deficiency gives rise to hypothyroidism, symptoms of which are extreme fatigue, goiter, mental slowing, depression, weight gain, and low basal body temperatures.
Iodine deficiency is the leading cause of preventable mental retardation, a result which occurs primarily when babies or small children are rendered hypothyroidic by a lack of the element. The addition of iodine to table salt has largely eliminated this problem in the wealthier nations, but as of March 2006, iodine deficiency remained a serious public health problem in the developing world.
Iodine deficiency is also a problem in certain areas of Europe. In Germany it has been estimated to cause a billion dollars in health care costs per year. A modelling analysis suggests universal iodine supplementation for pregnant women in England may save £199 (2013 UK pounds) to the health service per pregnant woman and save £4476 per pregnant woman in societal costs.
HIV infection rates in eastern Africa are generally moderate to high.