Made by DATEXIS (Data Science and Text-based Information Systems) at Beuth University of Applied Sciences Berlin
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)
Funded by The Federal Ministry for Economic Affairs and Energy; Grant: 01MD19013D, Smart-MD Project, Digital Technologies
Actinic keratosis is very common, with an estimated 14% of dermatology visits related to AKs. It is seen more often in fair-skinned individuals, and rates vary with geographical location and age. Other factors such as exposure to ultraviolet (UV) radiation, certain phenotypic features, and immunosuppression can also contribute to the development of AKs.
Men are more likely to develop AK than women, and the risk of developing AK lesions increases with age. These findings have been observed in multiple studies, with numbers from one study suggesting that approximately 5% of women ages 20–29 develop AK compared to 68% of women ages 60–69, and 10% of men ages 20–29 develop AK compared to 79% of men ages 60–69.
Geography seems to play a role in the sense that individuals living in locations where they are exposed to more UV radiation throughout their lifetime have a significantly higher risk of developing AK. Much of the literature on AK comes from Australia, where prevalence of AK is estimated at 40–50% in adults over 40, as compared to the United States and Europe, where prevalence is estimated at under 11–38% in adults. One study found that those who immigrated to Australia after age 20 had fewer AKs than native Australians in all age groups.
It is thought that UV radiation induces mutations in the keratinocytes of the epidermis, promoting the survival proliferation of these atypical cells. Eventually, this leads to the formation of AKs. In particular, mutations in the p53 tumor suppressor gene have been found in 30–50% of AK lesion skin samples.
- Extent of sun exposure: Cumulative sun exposure leads to an increased risk for development of AKs. In one U.S. study, AKs were found in 55% of fair-skinned men with high cumulative sun exposure, and in only 19% of fair-skinned men with low cumulative sun exposure in an age-matched cohort (the percents for women in this same study were 37% and 12% respectively). Furthermore, the use of sunscreen (SPF 17 or higher) has been found to significantly reduce the development of AK lesions, and also promotes the regression of existing lesions.
- History of sunburn: Studies show that even a single episode of painful sunburn as a child can increase an individual's risk of developing AK as an adult. Six or more painful sunburns over the course of a lifetime was found to be significantly associated with the likelihood of developing AK.
AC is caused by chronic and excessive exposure to ultraviolet radiation in sunlight.
Risk factors include:
- Outdoor lifestyle: e.g. farmers, sailors, fishermen, windsurfers, mountaineers, golfers, etc. This has given rise to synonyms for this condition such as "sailor's lip" and "farmer's lip". The prevalence in agricultural workers in a semi-arid region of Brazil is reported to be 16.7%.
- Light skin complexion: the condition typically affects individuals with lighter skin tones, particularly Caucasians living in tropical regions. In one report, 96% of persons with AC had phenotype II according to the Fitzpatrick scale.
- Age: AC typically affects older individuals, and rarely those under the age of 45.
- Gender: the condition affects males more commonly than females. Sometimes this ratio is reported as high as 10:1.
Additional factors may also play a role, including tobacco use, lip irritation, poor oral hygiene, and ill-fitting dentures.
To prevent AC from developing, protective measures could be undertaken such as avoiding mid-day sun, or use of a broad-brimmed hat, lip balm with anti UVA and UVB ingredients (e.g. para-aminobenzoic acid), or sun blocking agents (e.g. zinc oxide, titanium oxide) prior to sun exposure.
Fiddler’s neck does not usually form unless the musician is practicing or playing for more than a few hours each day, and only seems to develop after a few years of serious playing. Thus, when not infected or otherwise problematic, fiddler’s neck may be known as a benign practice mark and may be worn proudly as an indication of long hours of practice. Blum & Ritter (1990) found that 62% of 523 professional violinists and violists in West Germany experienced fiddler’s neck, with the percentage among violists being higher (67%) than among violinists (59%). Viola players are believed to be more predisposed to developing fiddler’s neck than violinists because the viola is larger and heavier, but this has not been empirically confirmed.
The development of fiddler’s neck does not depend on preexisting skin problems, and Blum & Ritter find that only 23% of men and 14% of women in their study reported cutaneous disorders in other parts of the face (mainly acne and eczema) that were independent of playing the violin or viola. Fiddler’s neck may exacerbate existing acne, but acne may also be limited solely to the lesion and not appear elsewhere. Nonetheless, musicians with underlying dermatologic diseases like acne and eczema are more endangered by fiddler’s neck than others. Males may develop folliculitis or boils due to involvement of beard hair.
Gardasil 6 is an HPV vaccine aimed at preventing cervical cancers and genital warts. Gardasil is designed to prevent infection with HPV types 16, 18, 6, and 11. HPV types 16 and 18 currently cause about 70% of cervical cancer cases, and also cause some vulvar, vaginal, penile and anal cancers. HPV types 6 and 11 are responsible for 90% of documented cases of genital warts.
Gardasil 9, approved in 2014 protects against HPV types 6, 11, 16, 18, 31, 33, 45, 52, and 58.
HPV vaccines do not currently protect against the virus strains responsible for plantar warts (verrucas).
Tobacco smoking or chewing is the most common causative factor, with more than 80% of persons with leukoplakia having a positive smoking history. Smokers are much more likely to suffer from leukoplakia than non-smokers. The size and number of leukoplakia lesions in an individual is also correlated with the level of smoking and how long the habit has lasted for. Other sources argue that there is no evidence for a direct causative link between smoking and oral leukoplakia. Cigarette smoking may produce a diffuse leukoplakia of the buccal mucosa, lips, tongue and rarely the floor of mouth. Reverse smoking, where the lit end of the cigarette is held in the mouth is also associated with mucosal changes. Tobacco chewing, e.g. betel leaf and areca nut, called paan, tends to produce a distinctive white patch in a buccal sulcus termed "tobacco pouch keratosis". In the majority of persons, cessation triggers shrinkage or disappearance of the lesion, usually within the first year after stopping.
Although the synergistic effect of alcohol with smoking in the development of oral cancer is beyond doubt, there is no clear evidence that alcohol is involved in the development of leukoplakia, but it does appear to have some influence. Excessive use of a high alcohol containing mouth wash (> 25%) may cause a grey plaque to form on the buccal mucosa, but these lesions are not considered true leukoplakia.
The disease can last for a considerably long time. Occasionally, "spontaneous cure" may ensue, particularly in young girls.
Lichen sclerosus is associated with a higher risk of cancer. Skin that has been scarred as a result of lichen sclerosus is more likely to develop skin cancer. Women with lichen sclerosus may develop vulvar carcinoma. Lichen sclerosus is associated with 3–7% of all cases of vulvar squamous cell carcinoma. In women, it has been reported that 33.6 times higher vulvar cancer risk is associated with LS. A study in men reported that "The reported incidence of penile carcinoma in patients with BXO is 2.6–5.8%".
IBS is an autosomal dominant genetic condition caused by a mutation in the gene for keratin 2e on chromosome 12.
This means an affected person has a 50% chance of passing the condition on to their child. Around half of cases of IBS, however, have no parent with the condition and have the genetic fault due to a spontaneous mutation.
The virus is relatively hardy and immune to many common disinfectants. Exposure to 90% ethanol for at least 1 minute, 2% glutaraldehyde, 30% Savlon, and/or 1% sodium hypochlorite can disinfect the pathogen.
The virus is resistant to drying and heat, but killed by and ultraviolet radiation.
Hyperkeratosis is thickening of the stratum corneum (the outermost layer of the epidermis), often associated with the presence of an abnormal quantity of keratin, and also usually accompanied by an increase in the granular layer. As the corneum layer normally varies greatly in thickness in different sites, some experience is needed to assess minor degrees of hyperkeratosis.
It can be caused by vitamin A deficiency or chronic exposure to arsenic.
Hyperkeratosis can also be caused by B-Raf inhibitor drugs such as Vemurafenib and Dabrafenib.
It can be treated with urea-containing creams, which dissolve the intercellular matrix of the cells of the stratum corneum, promoting desquamation of scaly skin, eventually resulting in softening of hyperkeratotic areas.
Lichen sclerosus may have a genetic component. Higher rates of lichen sclerosus have been reported among twins and among family members.
"Follicular hyperkeratosis" dass (also called "phrynoderma") is a skin condition characterized by excessive development of keratin in hair follicles, resulting in rough, cone-shaped, elevated papules. The openings are often closed with a white plug of encrusted sebum.
This condition has been shown in several small-scale studies to respond well to supplementation with vitamins and fats rich in essential fatty acids. Deficiencies of vitamin E, vitamin A, and B complex vitamins have been implicated in causing the condition.
PVA usually has an underlying cause, attributed to existing skin diseases and disorders associated with a cutaneous lymphoma or inflammation. Mycosis fungoides is the common lymphoma believed to cause PVA, although it may be considered a precursor when the lymphoma is (hidden) and undiagnosed. Large plaque parapsoriasis is another common causes of PVA. Less common causes include autoimmune-related connective tissue diseases such as lupus, dermatomyositis and scleroderma. Dermatoses and those that are genetically inspired, called genodermatoses, may also be an underlying cause of PVA. Among them, xeroderma pigmentosum and Rothmund-Thomson syndrome (poikiloderma congenita) are thought to be the most prominent. Ingestion of substances containing arsenic, such as arsphenamine, has also been suggested as a least common cause. PVA can also be idiopathic (of unknown cause), as seen in a small number of cases.
The proximal causes of fiddler’s neck are friction and pressure, but both repetitive shearing stress and occlusion with consequent trapping of sweat give rise to progressive damage. This damage along with poor hygiene predisposes the area to local infection, and such infection can progress to scarring and other long-term effects. Hot weather is reported to exacerbate fiddler’s neck, as are tiredness, playing emotional music, and playing in smaller groups where individual stress is higher. Type I hypersensitivity reactions may also be involved, particularly to rosewood and ebony in the chinrest and tailpiece, as well as to varnish of the instrument body when chinrests are not used and to rosin deposits on the instrument and on chin cloths. Nickel or other metal allergies are common causes if the chin rest has a metal clip that comes into constant contact with the skin. Rosin exposure in particular may lead to abietic acid dermatitis.
Vitamins are one of many of the nutritional factors that change the outward appearance of a dog. The fat soluble vitamins A and E play a critical role in maintaining skin health. Vitamin A, which can also be supplemented as beta-carotene, prevents the deterioration of epithelial tissues associated with chronic skin diseases and aging. A deficiency in vitamin A can lead to scaly of skin and other dermatisis related issues like alopecia Vitamin E is an antioxidant. Vitamin E neutralizes free radicals that accumulate in highly proliferative cells like skin and prevent the deterioration of fibrous tissue caused by these ionized molecules. There are also a couple of water-soluble vitamins that contribute to skin health. Riboflavin (B2) is a cofactor to the metabolism of carbohydrates and when deficient in the diet leads to cracked, brittle skin. Biotin (B7) is another B vitamin that, when deficient, leads to alopecia.
The challenge has always been how to deliver the siRNA using a topical method or retroviral vectors and ex vivo gene transfer. In 2011/12 a team at Northwestern University claim to have solved the topical delivery of siRNA dilemma. Personalized siRNA can be delivered in a commercial moisturizer or phosphate-buffered saline, and do not require barrier disruption or transfection agents, such as liposomes, peptides, or viruses. "Topical application of nucleic acids offers many potential therapeutic advantages for suppressing genes in the skin, and potentially for systemic gene delivery. However, the epidermal barrier typically precludes entry of gene-suppressing therapy unless the barrier is disrupted. We now show that spherical nucleic acid nanoparticle conjugates (SNA-NCs), gold cores surrounded by a dense shell of highly oriented, covalently immobilized siRNA, freely penetrate almost 100% of keratinocytes in vitro, mouse skin, and human epidermis within hours after application."
This new discovery may soon offer hope to all suffering from mono-genetic diseases such as EHK. This may lead to promising personalized, topically delivered gene therapy of cutaneous tumors, skin inflammation, and dominant negative genetic skin disorders.
UPDATE: OCTOBER 2014
As of late, Paller reports "we are using a new nanotechnology-based technique called 'spherical nucleic acids' (SNAs) to suppress the production of the abnormal keratin 10 gene that is the most common change leading to epidermolytic ichthyosis. We continue to screen candidate SNAs to find a few that clearly suppress the abnormal keratin 10 gene much more than the normal keratin 10 gene. In the meantime, we have developed several tools towards this effort, which can also be used by other researchers. Most recently we've developed a special 'lentivirus reporter construct' in which we can see through changes in fluorescence whether or not our SNA works."
Dr. Paller and her team recently received more good news with regard to progressing their research. "We just received a grant from the National Institutes of Health (NIH) to continue this effort based on our preliminary data collected with FIRST's funding support. FIRST has been instrumental in furthering our research efforts related to ichthyosis," she said.
There is no cure for IBS but in the future gene therapy may offer a cure.
Treatments for IBS generally attempt to improve the appearance of the skin and the comfort of the sufferer. This is done by exfoliating and increasing the moisture of the skin. Common treatments include:
- Emollients: moisturisers, petroleum jelly or other emolients are used, often several times a day, to increase the moisture of the skin.
- Baths: long baths (possibly including salt) several times a week are used to soften the skin and allow exfoliation.
- Exfoliating creams: creams containing keratolytics such as urea, salicylic acid and lactic acid may be useful.
- Antiseptic washes: antiseptics may be used to kill bacteria in the skin and prevent odour.
- Retenoids: very severe cases may use oral retinoids to control symptoms but these have many serious side effects including, in the case of IBS, increased blistering.
Poikiloderma vasculare atrophicans (PVA), sometimes referred to as parapsoriasis variegata or parapsoriasis lichenoides is a cutaneous condition (skin disease) characterized by hypo- or hyperpigmentation (diminished or heightened skin pigmentation, respectively), telangiectasia and skin . Other names for the condition include prereticulotic poikiloderma and atrophic parapsoriasis. The condition was first described by pioneer American pediatrician Abraham Jacobi in 1906. PVA causes areas of affected skin to appear speckled red and inflamed, yellowish and/or brown, gray or grayish-black, with scaling and a thinness that may be described as "cigarette paper". On the surface of the skin, these areas may range in size from small patches, to plaques (larger, raised areas), to neoplasms (spreading, tumor-like growths on the skin).
Mycosis fungoides, a type of skin lymphoma, may be a cause of PVA. The condition may also be caused by, associated with or accompany any of the following conditions or disorders: other skin lymphomas, dermatomyositis, lupus erythematosus, Rothmund-Thompson syndrome, Kindler syndrome, dyskeratosis congenita, and chronic radiodermatitis. Rare causes include arsenic ingestion, and the condition can also be idiopathic.
PVA may be considered a rare variant of cutaneous T-cell lymphoma, a non-Hodgkin's form of lymphoma affecting the skin. It may also be included among a number of similar conditions that are considered as precursors to mycosis fungoides. PVA is believed to be a syndrome closely associated with large-plaque parapsoriasis and its cohort retiform parapsoriasis; including PVA, all three conditions fit within an updated view of the once ambiguous classification scheme known as parapsoriasis.
Until gene therapy solutions finally become reality, EHK sufferers must treat their fragile skin carefully. Most have learned that taking regular extended baths allows patients to care for their fragile skin and keep it manageable. Baths that include sea salt seem to improve the process of softening and removing the thickened skin.
Ointments like Petroleum Jelly, Aveeno, and other barrier type ointment help hold the moisture in the skin after a bath.
Overheating: The scaling of the skin prevents normal sweating so hot weather and/or vigorous exercise can cause problems.
Eye problems: The eyelids can be pulled down by the tightness of the skin and this can make eyelids (but usually just the lower one) very red and they are prone to drying and irritation.
Constriction bands: Very rarely children with this condition can have tight bands of skin around their fingers or toes (usually at the tips) that can prevent proper blood circulation to the area.
Hair loss: Severe scaling of the skin on the scalp can lead to patchy loss of hair, but this is rarely permanent.
Minerals have many roles in the body, which include acting as beneficial antioxidants. Selenium is an essential nutrient, that should be present in trace amounts in the diet. Like other antioxidants, selenium acts as a cofactor to neutralize free radicals. Other minerals act as essential cofactors to biological processes relating to skin health. Zinc plays a crucial role in protein synthesis, which aids in maintaining elasticity of skin. By including zinc in the diet it will not only aid in the development of collagen and wound healing, but it will also prevent the skin from becoming dry and flaky. Copper is involved in multiple enzymatic pathways. In dogs, a deficiency in copper results in incomplete keratinization leading to dry skin and hypopigmentation. The complicated combination of trace minerals in the diet are a key component of skin health and a part of a complete and balanced diet.
The cause of prurigo nodularis is unknown, although other conditions may induce PN. PN has been linked to Becker's nevus, linear IgA disease, an autoimmune condition, liver disease and T cells. Systemic pruritus has been linked to cholestasis, thyroid disease, polycythaemia rubra vera, uraemia, Hodgkins disease, HIV and other immunodeficiency diseases. Internal malignancies, liver failure, renal failure, and psychiatric illnesses have been considered to induce PN, although more recent research has refuted a psychiatric cause for PN. Patients report an ongoing battle to distinguish themselves from those with psychiatric disorders such as delusions of parasitosis and other psychiatric conditions.
Many conditions affect the human integumentary system—the organ system covering the entire surface of the body and composed of skin, hair, nails, and related muscle and glands. The major function of this system is as a barrier against the external environment. The skin weighs an average of four kilograms, covers an area of two square meters, and is made of three distinct layers: the epidermis, dermis, and subcutaneous tissue. The two main types of human skin are: glabrous skin, the hairless skin on the palms and soles (also referred to as the "palmoplantar" surfaces), and hair-bearing skin. Within the latter type, the hairs occur in structures called pilosebaceous units, each with hair follicle, sebaceous gland, and associated arrector pili muscle. In the embryo, the epidermis, hair, and glands form from the ectoderm, which is chemically influenced by the underlying mesoderm that forms the dermis and subcutaneous tissues.
The epidermis is the most superficial layer of skin, a squamous epithelium with several strata: the stratum corneum, stratum lucidum, stratum granulosum, stratum spinosum, and stratum basale. Nourishment is provided to these layers by diffusion from the dermis, since the epidermis is without direct blood supply. The epidermis contains four cell types: keratinocytes, melanocytes, Langerhans cells, and Merkel cells. Of these, keratinocytes are the major component, constituting roughly 95 percent of the epidermis. This stratified squamous epithelium is maintained by cell division within the stratum basale, in which differentiating cells slowly displace outwards through the stratum spinosum to the stratum corneum, where cells are continually shed from the surface. In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.
The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.
The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance. Functionally, the subcutaneous fat insulates the body, absorbs trauma, and serves as a reserve energy source.
Conditions of the human integumentary system constitute a broad spectrum of diseases, also known as dermatoses, as well as many nonpathologic states (like, in certain circumstances, melanonychia and racquet nails). While only a small number of skin diseases account for most visits to the physician, thousands of skin conditions have been described. Classification of these conditions often presents many nosological challenges, since underlying etiologies and pathogenetics are often not known. Therefore, most current textbooks present a classification based on location (for example, conditions of the mucous membrane), morphology (chronic blistering conditions), etiology (skin conditions resulting from physical factors), and so on. Clinically, the diagnosis of any particular skin condition is made by gathering pertinent information regarding the presenting skin lesion(s), including the location (such as arms, head, legs), symptoms (pruritus, pain), duration (acute or chronic), arrangement (solitary, generalized, annular, linear), morphology (macules, papules, vesicles), and color (red, blue, brown, black, white, yellow). Diagnosis of many conditions often also requires a skin biopsy which yields histologic information that can be correlated with the clinical presentation and any laboratory data.