Leukoencephalopathy ( leukodystrophy -like diseases) is all of the brain white matter diseases, whether their molecular cause is known or not. [1] It can refer specifically to any of these diseases: Progressive multifocal leukoencephalopathy Toxic leukoencephalopathy Leukoencephalopathy with vanishing white matter Leukoencephalopathy with neuroaxonal spheroids Reversible posterior leukoencephalopathy syndrome Megalencephalic leukoencephalopathy with subcortical cysts . It can also refer to gene MLC1 or Megalencephalic leukoencephalopathy with subcortical cysts 1 , a human gene related to the former disease. Hypertensive leukoencephalopathy The classification of leukoencephalopathies is a matter of debate. Some authors divide leukoencephalopathies into hereditary disorders and acquired disorders. The hereditary demyelinating disorders are then classified according to the localization of the underlying metabolic defect, and they include the leukodystrophies when myelin growth is the underlying problem.
Avoid and exclude mosquitoes Limit exposure to mosquitoes by: Repairing any tears in the screens on windows, doors and camping gear Using mosquito netting over strollers and cribs Using mosquito netting when sleeping outdoors Selecting self-care products that don't have scents Use insect repellent Use insect repellent when mosquitoes are active. ... Some sporting goods stores sell clothing pretreated with permethrin. Don't wash bed nets or set them in sunlight, as this breaks down permethrin.
Information concerning histiocytosis and clinicians located in European countries may be found in many languages at the web portal of Euro Histio Net (EHN). This is a project funded by the European Union, coordinated by Jean Donadieu, APHP , Paris, France. ... Archived from the original on 2007-09-28 . Retrieved 2007-05-07 . ^ James, William D.; Berger, Timothy G.; et al. (2006).
Occupational heat stress is the net load to which a worker is exposed from the combined contributions of metabolic heat, environmental factors , and clothing worn which results in an increase in heat storage in the body. [1] Heat stress can result in heat-related illnesses , such as heat stroke , hyperthermia , heat exhaustion , heat cramps or heat rashes. [2] Although heat exhaustion is less severe, hyperthermia is a medical emergency and requires emergency treatment , which if not provided can even lead to death . [3] Heat stress causes illness but also may account for an increase in workplace accidents , and a decrease in worker productivity . [4] Worker injuries attributable to heat include those caused by: sweaty palms, fogged-up safety glasses, and dizziness . [2] Burns may also occur as a result of accidental contact with hot surfaces or steam. ... Workers who are not acclimatized or who are wearing impermeable equipment or clothing should be monitored every 15 minutes. [25] NIOSH and OSHA have also created a Heat Index App for mobile devices that provides information on temperature, humidity, risk of heat illness, as well as hourly forecasts of temperature and information on how to prevent and treat heat illnesses. [26] Prevention [ edit ] Working in hot conditions can make the body lose fluids through sweating, so workers must drink extra water in these conditions to replenish those fluids and prevent dehydration . [27] Employers can establish prevention programs, which focus on having protocols to gradually increases workloads and concede on allowing on more breaks for new hired workers. [28] Employers can control heat stress through engineering controls, work practices, providing training, implementing an acclimatization schedule, providing water and encouraging workers to drink often, and ensuring workers take appropriate rest breaks to cool down. [29] Engineering controls [ edit ] Employers can provide air conditioners for indoor work spaces and for indoor break areas. ... Retrieved 2020-11-03 . ^ "OSHA-NIOSH Heat Safety Tool App | NIOSH | CDC" . www.cdc.gov . 2020-02-20 .
The application of insecticides and/or insect repellents ) to strategic surfaces such as clothing, skin, buildings, insect habitats, and bed nets . The use of a mosquito net over a bed (also known as a "bed net") to reduce nighttime transmission, since certain species of tropical mosquitoes feed mainly at night. ... NIH/National Institute of Allergy and Infectious Diseases (2007, December 28). "Neglected Tropical Diseases Burden Those Overseas, But Travelers Also At Risk" . ScienceDaily . Retrieved 2007-12-28 . Colombian Institute of Tropical Medicine ICMT-CES University v t e Public health General Auxology Biological hazard Chief Medical Officer Cultural competence Deviance Environmental health Euthenics Genomics Globalization and disease Health economics Health literacy Health policy Health system Health care reform Public health law Health politics Maternal health Medical anthropology Medical sociology Mental health ( Ministers ) Pharmaceutical policy Public health intervention Public health laboratory Reproductive health Social psychology Sociology of health and illness Preventive healthcare Behavior change Theories Family planning Health promotion Human nutrition Healthy diet Preventive nutrition Hygiene Food safety Hand washing Infection control Oral hygiene Occupational safety and health Human factors and ergonomics Hygiene Injury prevention Medicine Nursing Patient safety Organization Pharmacovigilance Safe sex Sanitation Emergency Fecal–oral transmission Open defecation Sanitary sewer Waterborne diseases School hygiene Smoking cessation Vaccination Vector control Population health Biostatistics Child mortality Community health Epidemiology Global health Health impact assessment Health system Infant mortality Open-source healthcare software Public health informatics Social determinants of health Health equity Race and health Social medicine Biological and epidemiological statistics Case–control study Randomized controlled trial Relative risk Statistical hypothesis testing Analysis of variance (ANOVA) Regression analysis ROC curve Student's t -test Z -test Statistical software Infectious and epidemic disease prevention Asymptomatic carrier Epidemics List Notifiable diseases List Public health surveillance Disease surveillance Quarantine Sexually transmitted infection Social distancing Tropical disease Vaccine trial Food hygiene and safety management Food Additive Chemistry Engineering Microbiology Processing Safety Safety scandals Genetically modified food Good agricultural practice Good manufacturing practice HACCP ISO 22000 Health behavioral sciences Diffusion of innovations Health belief model Health communication Health psychology Positive deviance PRECEDE-PROCEED model Social cognitive theory Social norms approach Theory of planned behavior Transtheoretical model Organizations, education and history Organizations Caribbean Caribbean Public Health Agency China Center for Disease Control and Prevention Europe Centre for Disease Prevention and Control Committee on the Environment, Public Health and Food Safety India Ministry of Health and Family Welfare U.S.
Others, again, might be swept into the widespread net of dementia praecox . This state of affairs cannot be regarded as satisfactory, for they are not truly cases of melancholia, paranoia, dementia praecox or any other described affection.
Also, in terms of health risks, people who have had a cryptogenic stroke are more likely to have a PFO than the general population. [2] A cardiac shunt is the presence of a net flow of blood through a defect, either from left to right or right to left. ... Eisenmenger's syndrome [ edit ] Main article: Eisenmenger's syndrome If a net flow of blood exists from the left atrium to the right atrium, called a left-to-right shunt, then an increase in the blood flow through the lungs happens. ... Because the atria are linked via the atrial septal defect, inspiration produces no net pressure change between them, and has no effect on the splitting of S2. ... If the pulmonary arterial pressure is more than two-thirds of the systemic systolic pressure, a net left-to-right shunt should occur at least 1.5:1 or evidence of reversibility of the shunt when given pulmonary artery vasodilators prior to surgery. ... PMID 31547797 . ^ "Atrial Septal Defect Types – Mayo Clinic" . Archived from the original on 28 September 2007 . Retrieved 2007-10-14 . ^ Fix, James D.; Dudek, Ronald W. (1998).
A number sign (#) is used with this entry because of evidence that atrial septal defect-6 (ASD6) is caused by heterozygous mutation in the TLL1 gene (606742) on chromosome 4q32. For a general phenotypic description and discussion of genetic heterogeneity in atrial septal defect, see ASD1 (108800). Molecular Genetics Based on data from mouse models of incomplete heart septation associated with inactivation of mouse Tll1, Stanczak et al. (2009) analyzed the candidate gene TLL1 in 19 unrelated patients with atrial septal defect and identified heterozygosity for 3 missense mutations in 3 patients (606742.0001-606742.0003, respectively). One of the patients had an isolated ostium primum defect; the other 2 patients, who had ostium secundum defects, displayed additional features including interatrial aneurysm and cardiac arrhythmias. INHERITANCE - Autosomal dominant CARDIOVASCULAR Heart - Atrial septal defect, type I or II - Aneurysm of interatrial septum (in some patients) - Atrial fibrillation (in some patients) - Bradycardia (in some patients) MOLECULAR BASIS - Caused by mutation in the tolloid-like 1 gene (TLL1, 606742.0001 ) ▲ Close
A number sign (#) is used with this entry because of evidence that atrial septal defect-5 (ASD5) is caused by heterozygous mutation in the ACTC1 gene (102540) on chromosome 15q14. For a phenotypic description and discussion of genetic heterogeneity in atrial septal defect, see ASD1 (108800). Mapping Matsson et al. (2008) studied 2 large Swedish families segregating autosomal dominant isolated secundum atrial septal defect (ASD) with variable clinical expression. Genotyping with microsatellite markers in 'family 1' revealed a specific haplotype in all affected individuals spanning a 15.1-cM region of chromosome 15q13-q21; analysis of 'family 2' identified a minimal haplotype with significant linkage to ASD consisting of markers GT44248, GATA12322, and ACTC. All affected individuals genotyped had identical allele sizes for the marker haplotype, suggesting a shared ancestral mutation for the 2 families.
A number sign (#) is used with this entry because atrial septal defect-2 (ASD2) is caused by heterozygous mutation in the GATA4 gene (600576) on chromosome 8p23. For discussion of genetic heterogeneity in atrial septal defect, see ASD1 (108800). Clinical Features Garg et al. (2003) identified a large kindred spanning 5 generations in which 16 individuals had congenital heart defects. Detailed clinical evaluations reviewed for all available family members demonstrated an autosomal dominant pattern of inheritance. All affected family members had atrial septal defects. Eight individuals had additional congenital heart defects, including ventricular septal defects (VSD), atrioventricular septal defects (AVSD), pulmonary valve thickening, or insufficiency of the cardiac valves.
Description Secundum atrial septal defect (ASD) is a common congenital heart malformation that occurs as an isolated anomaly in 10% of individuals with congenital heart disease. Uncorrected ASD can cause pulmonary overcirculation, right heart volume overload, and premature death (summary by Benson et al., 1998). Genetic Heterogeneity of Atrial Septal Defect The ASD1 locus has been mapped to chromosome 5p. Other forms of atrial septal defect that are associated with other congenital heart disease but no conduction defects or noncardiac abnormalities include ASD2 (607941), caused by mutation in the GATA4 gene (600576), and ASD4 (611363), caused by mutation in the TBX20 gene (606061). ASD3 (614089) and ASD5 (612794), in which atrial septal defect is not associated with other cardiac abnormalities, are caused by mutation in the MYH6 (160710) and ACTC1 (102540) genes, respectively.
A congenital cardiac malformation characterized by a communication between the atrial chambers of the heart. Epidemiology Overall, openings between the atrial chambers account for about 6 to 8% of all congenitally malformed hearts. As a group, the prevalence at birth is between 6 to 9/10000; however, this is likely an underestimated due to the asymptomatic nature of the disease. The female-to-male ratio is 2-4:1. Clinical description There are four types of defects, named according to their position relative to the atrial septum. The ostium secundum defect is the most common type, accounting for three-quarters of all cases, located to the region of the oval fossa, most commonly due to a deficiency of the primary atrial septum (septum primum) but deficiency of the septum secundum (superior interatrial fold) may also contribute.
A number sign (#) is used with this entry because of evidence that atrial septal defect-8 (ASD8) can be caused by heterozygous mutation in the CITED2 gene (602937) on chromosome 6q23.3. For discussion of genetic heterogeneity of atrial septal defect, see ASD1 (108800). Molecular Genetics Sperling et al. (2005) screened a cohort of 392 patients with congenital heart defects and 192 controls for mutations in the CITED2 gene and identified a 27-bp insertion (602937.0002) in a patient with a secundum atrial septal defect, and a 6-bp deletion (602937.0003) in a patient with a sinus venosus atrial septal defect and abnormal pulmonary venous return to the right atria. Functional analysis of the mutations, which were not found in controls, revealed that both significantly reduced the capacity of CITED2 to transrepress HIF1A (603348). INHERITANCE - Autosomal dominant CARDIOVASCULAR Heart - Atrial septal defect, secundum type (in some patients) - Atrial septal defect, sinus venosus type (in some patients) Vascular - Abnormal pulmonary venous return to right atria (in some patients) MOLECULAR BASIS - Caused by mutation in the CBP/p300-interacting transactivator, with glu/asp-rich C-terminal domain, 2 gene (CITED2, 602937.0001 ) ▲ Close
Overview An atrial septal defect (ASD) is a hole in the heart between the upper chambers (atria). The hole increases the amount of blood that flows through the lungs. The condition is present at birth (congenital heart defect). Small atrial septal defects might be found by chance and never cause a concern. Others close during infancy or early childhood. A large, long-term atrial septal defect can damage the heart and lungs. Surgery may be needed to repair an atrial septal defect and to prevent complications.
A number sign (#) is used with this entry because of evidence that atrial septal defect-9 (ASD9) is caused by heterozygous mutation in the GATA6 gene (601656) on chromosome 18q11. For discussion of genetic heterogeneity of atrial septal defect (ASD), see ASD1 (108800). Molecular Genetics Lin et al. (2010) analyzed the GATA6 gene in 270 unrelated Chinese patients with congenital heart defects and identified heterozygosity for a missense mutation in the GATA6 gene (S184N; 601656.0005) in 2 Chinese children with atrial septal defect. One of the ASD patients was a 3-year-old girl with an ostium secundum ASD and mild pulmonary arterial hypertension, whereas the other was a 4-year-old boy with an ostium secundum ASD and mild tricuspid valve disease and pulmonary valve replacement. The S184N mutation was detected in the unaffected father of the girl as well as in the clinically unaffected mother of the boy; the latter parent was found to have bicuspid aortic valve on echocardiography.
] and the use of large-bore tubes inserted into the esophagus to forcefully lavage it. [17] [ unreliable medical source? ] Endoscopic [ edit ] The Roth net can be inserted through the endoscope to remove pieces of the obstructed food. ... Traditional endoscopic techniques involved the use of an overtube, a plastic tube inserted into the esophagus prior to the removal of the food bolus, in order to reduce the risk of aspiration into the lungs at the time of endoscopy. [7] However, the "push technique", which involves insufflating air into the esophagus, and gently pushing the bolus toward the stomach instead, has emerged as a common and safe way of removing the obstruction. [7] [18] Other tools may be used to remove food boluses. The Roth Net is a mesh net that can be inserted through the endoscope, and opened and closed from the outside; it can be used to retrieve pieces of obstructed food.
These tests are easily transported and can be performed by people without special training. [28] They are useful for screening large numbers of people and testing people who cannot access healthcare facilities, but their sensitivity is relatively low, [2] and it is recommended that a second method is used to confirm a positive result. [28] [29] T. cruzi can be isolated from samples through blood culture or xenodiagnosis , or by inoculating animals with the person's blood. ... Xenodiagnosis involves feeding the person's blood to triatomine insects, then examining their feces for the parasite 30 to 60 days later. [28] These methods are not routinely used, as they are slow and have low sensitivity. [27] [28] Prevention [ edit ] Bed nets can be used in endemic areas to prevent bites from triatomine bugs. [15] Efforts to prevent Chagas disease have largely focused on vector control to limit exposure to triatomine bugs. ... Eleven triatomine species are native to the United States and some southern states have persistent cycles of disease transmission between insect vectors and animal reservoirs, [2] [23] which include woodrats, possums, raccoons, armadillos and skunks. [49] However, locally acquired infection is very rare: only 28 cases were documented from 1955 to 2015. [2] [48] As of 2013, the cost of treatment in the United States was estimated to be US$900 million annually (global cost $7 billion), which included hospitalization and medical devices such as pacemakers. [40] Chagas disease affects approximately 68,000 to 123,000 people in Europe as of 2019. [50] Spain, which has a high rate of immigration from Latin America, has the highest prevalence of the disease. ... Archived from the original on 4 December 2014 . Retrieved 28 November 2014 . ^ a b c d e f g h i j k Despommier DD, Griffin DO, Gwadz RW, Hotez PJ, Knirsch CA (2019). ... Wikipedia's health care articles can be viewed offline with the Medical Wikipedia app . Chagas disease at Curlie Chagas information at the U.S.
These types of residences are more likely to harbor triatomine bugs. Use insecticide-soaked netting over your bed when sleeping in thatch, mud or adobe houses.
A tropical disease mainly found in latin America and transmitted by triatomine insects (mostly Triatoma infestans and Rhodnius prolixus and Panstrongylus megistus ) harboring the hemoflagellate protozoan parasite Trypanosoma cruzi . The disease is characterized by an acute phase which is either asymptomatic or manifest with fever, inflammation at the inoculation site (inoculation chancre or chagoma), unilateral palpebral edema called the Romaña sign (when the triatomine bite occurs near the eye), enlarged lymph nodes, and splenomegaly. The chronic phase is lifelong and development of chagasic cardiomyopathy (30%; complex arrhythmias, heart failure, and thromboembolic events), digestive (10%; megaoesophagus and megacolon), neurological (10%; stroke, peripheral neuropathy and autonomic dysfunction), or mixed alterations (10%) may be observed. These can all lead to high morbidity and mortality rates.
"Problematic Internet use two decades later: apps to wean us off apps". CNS Spectrums . 24 (4): 371–373. doi : 10.1017/S109285291800127X . ... PMID 30507371 . ^ Brandless Support (28 June 2012). "Nomophobia: The Fear of Being Without a Gnome...er, Phone" . ... Clinical Practice and Epidemiology in Mental Health . 10 : 28–35. doi : 10.2174/1745017901410010028 .
Other possible causes of deprivation and occlusion amblyopia include obstruction in the vitreous and aphakia . [28] Deprivation amblyopia accounts for less than 3% of all individuals affected by amblyopia. [28] Pathophysiology [ edit ] Amblyopia is a developmental problem in the brain, not any intrinsic, organic neurological problem in the eyeball (although organic problems can lead to amblyopia which can continue to exist after the organic problem has resolved by medical intervention). [29] The part of the brain receiving images from the affected eye is not stimulated properly and does not develop to its full visual potential. ... Also, the chance of achieving 20/20 vision is greater if treatment is initiated early. [39] One of the German public health insurance providers, Barmer, has changed its policy to cover, as of 1 April 2014, the costs for an application for amblyopic children whose condition has so far not improved through patching. The app offers dedicated eye exercises that the patient performs while wearing an eyepatch. [40] Evidence for vision therapy is unclear as of 2011. [41] Older age [ edit ] Tentative evidence shows that perceptual training may be beneficial in adults. [42] [43] Epidemiology [ edit ] Amblyopia occurs in between 2 and 5% of the population in Western countries [ which? ... Comparable results may be achieved using different types of brain stimulation, [50] such as anodal transcranial direct current stimulation [51] and theta burst rTMS . [52] A 2013 study concluded that converging evidence indicates decorrelated binocular experience plays a pivotal role in the genesis of amblyopia and the associated residual deficits. [53] Another study of 2013 [54] suggests that playing a version of the popular game Tetris that is modified such that each eye sees separate components of the game may also help to treat this condition in adults. [55] Furthermore, the effects of this kind of therapy may be further enhanced by noninvasive brain stimulation [50] as shown by a recent study using anodal tDCS . [56] A 2014 Cochrane review sought to determine the effectiveness of occlusion treatment on patients with sensory deprivation amblyopia, but no trials were found eligible to be included in the review. [28] However, good outcomes from occlusion treatment for sensory deprivation amblyopia likely rely on compliance with the treatment. ... BMJ . 324 (7353): 1549. doi : 10.1136/bmj.324.7353.1549 . PMC 116606 . PMID 12089090 . ^ "App auf Rezept: Barmer bezahlt internetbasierte Behandlung" [Prescription app: Barmer pays for internet-based treatment]. www.aerztezeitung.de (in German). 28 March 2014.
In Dogger Bank itch, sensitivity is acquired after repeated handling of the sea chervils that become entangled in fishing nets. [ citation needed ] The specific toxin responsible for the rash was determined to be the sulfur -bearing salt (2-hydroxyethyl) dimethylsulfoxonium chloride. [3] This salt is also found in some sea sponges and has potent in vitro activity against leukemia cells. [4] Treatment [ edit ] A study of two cases in 2001 suggests that the rash responds to oral ciclosporin . ... The sea chervil, abundant in the area, frequently came up with the fishing nets and had to be thrown back into the water.
Neuropathologic examination showed severe neuronal loss and ovoid tau-positive argyrophilic intraneuronal inclusions consistent with Pick bodies. Beta-amyloid (see APP; 104760) plaques were not detected. ... Van Leeuwen et al. (2006) detected aberrant frameshifted proteins, APP+1 and UBB+1 (UBB; 191339), within the neuropathologic hallmarks of Alzheimer disease, as well as other MAPT-related dementias, including Pick disease, progressive supranuclear palsy, and less commonly frontotemporal dementia. Van Leeuwen et al. (2006) postulated that accumulation of APP+1 and UBB+1, which represents defective proteasome function, contributes to various forms of dementia.
Van Leeuwen et al. (2006) detected aberrant frameshifted proteins, APP+1 (APP; 104760) and UBB+1 (UBB; 191339), within the neuropathologic hallmarks of Alzheimer disease and other MAPT-related dementias, including Pick disease, progressive supranuclear palsy, and less commonly frontotemporal dementia. Van Leeuwen et al. (2006) postulated that accumulation of APP+1 and UBB+1, which represents defective proteasome function, contributes to various forms of dementia. ... In the 7-generation family studied by Murrell et al. (1997), a limited genomic screen by use of DNA samples from 28 family members localized the gene for this disorder to a 3-cM region on chromosome 17, between markers THRA1 (190120) (which maps to 17q11.2) and D17S791.
Semantic dementia (SD) is a form of frontotemporal dementia (FTD; see this term), characterized by the progressive, amodal and profound loss of semantic knowledge (combination of visual associative agnosia, anomia, surface dyslexia or dysgraphia and disrupted comprehension of word meaning) and behavioral abnormalities, attributable to the degeneration of the anterior temporal lobes.
Main articles: Aphasia and Primary progressive aphasia Semantic dementia Other names semantic variant primary progressive aphasia Specialty Neurology Semantic dementia ( SD ), also known as semantic variant primary progressive aphasia (svPPA), is a progressive neurodegenerative disorder characterized by loss of semantic memory in both the verbal and non-verbal domains. However, the most common presenting symptoms are in the verbal domain (with loss of word meaning). [1] [2] [3] Semantic dementia is a disorder of semantic memory that causes patients to lose the ability to match words or images to their meanings. [4] However, it is fairly rare for patients with semantic dementia to develop category specific impairments, though there have been document cases of it occurring. [5] Typically, a more generalized semantic impairment results form dimmed semantic representations in the brain. [6] SD is one of the three canonical clinical syndromes associated with frontotemporal lobar degeneration (FTLD), with the other two being frontotemporal dementia and progressive nonfluent aphasia . SD is a clinically defined syndrome but is associated with predominantly temporal lobe atrophy (left greater than right) and hence is sometimes called temporal variant FTLD (tvFTLD). [7] SD is one of the three variants of primary progressive aphasia (PPA), which results from neurodegenerative disorders such as FTLD or Alzheimer's disease . It is important to note the distinctions between Alzheimer’s disease and semantic dementia with regard to types of memory affected. In general, Alzheimer’s disease is referred to as disorder affecting mainly episodic memory, defined as the memory related to specific, personal events distinct for each individual.
A form of hereditary cerebral hemorrhage with amyloidosis characterized by an age of onset of 20-30 years, major systemic amyloidosis and recurrent lobar intracerebral hemorrhages. Unlike other forms of hereditary cerebral hemorrhage with amyloidosis, this subtype is due to a mutation in the CST3 gene (20p11.2), encoding the precursor protein cystatin C.
Retiform parapsoriasis Specialty Dermatology Retiform parapsoriasis is a cutaneous condition, considered to be a type of large-plaque parapsoriasis . [1] It is characterized by widespread, ill-defined plaques on the skin, that have a net-like or zebra-striped pattern. [2] Skin atrophy , a wasting away of the cutaneous tissue , usually occurs within the area of these plaques. [1] See also [ edit ] Parapsoriasis Poikiloderma vasculare atrophicans List of cutaneous conditions References [ edit ] ^ a b Lambert WC, Everett MA (Oct 1981).
