Retrieved 9 August 2020 . v t e Psychology History Philosophy Portal Psychologist Basic psychology Abnormal Affective science Affective neuroscience Behavioral genetics Behavioral neuroscience Behaviorism Cognitive / Cognitivism Cognitive neuroscience Social Comparative Cross-cultural Cultural Developmental Differential Ecological Evolutionary Experimental Gestalt Intelligence Mathematical Moral Neuropsychology Perception Personality Positive Psycholinguistics Psychophysiology Quantitative Social Theoretical Applied psychology Anomalistic Applied behavior analysis Assessment Clinical Coaching Community Consumer Counseling Critical Educational Ergonomics Feminist Forensic Health Industrial and organizational Legal Media Medical Military Music Occupational health Pastoral Political Psychometrics Psychotherapy Religion School Sport and exercise Suicidology Systems Traffic Methodologies Animal testing Archival research Behavior epigenetics Case study Content analysis Experiments Human subject research Interviews Neuroimaging Observation Psychophysics Qualitative research Quantitative research Self-report inventory Statistical surveys Psychologists Wilhelm Wundt (1832–1920) William James (1842–1910) Ivan Pavlov (1849–1936) Sigmund Freud (1856–1939) Edward Thorndike (1874–1949) Carl Jung (1875–1961) John B.
This range includes: Alcohol-related neurodevelopmental disorder — intellectual disabilities or behavioral and learning problems caused by drinking alcohol during pregnancy Alcohol-related birth defects — physical birth defects caused by drinking alcohol during pregnancy Fetal alcohol syndrome — the severe end of the fetal alcohol spectrum disorders, which includes both neurodevelopmental disorder and birth defects caused by drinking alcohol during pregnancy Partial fetal alcohol syndrome — presence of some signs and symptoms of fetal alcohol syndrome caused by drinking alcohol during pregnancy, but the criteria for the diagnosis are not met Neurobehavioral disorder associated with prenatal alcohol exposure — problems functioning due to neurocognitive impairments, such as problems with mental health, memory, impulse control, communication and daily living skills, caused by drinking alcohol during pregnancy If one child in a family is diagnosed with fetal alcohol syndrome, it may be important to evaluate his or her siblings to determine whether they also have fetal alcohol syndrome, if the mother drank alcohol during these pregnancies.
Fetal alcohol syndrome (FAS) is a rare malformation syndrome caused by excessive maternal consumption of alcohol during pregnancy. It is characterized by prenatal and/or postnatal growth deficiency (weight and/or height <10th percentile), a unique cluster of minor facial anomalies (short palpebral fissures, flat and smooth philtrum, and thin upper lip) and severe central nervous system (CNS) abnormalities including microcephaly, and cognitive and behavioral impairment (intellectual disability, deficit in general cognition, learning and language, executive function, visual-spatial processing, memory, and attention).
The polycystin-1 and polycystin-2 proteins appear to be involved in both autosomal dominant and recessive polycystic kidney disease due to defects in both proteins. [14] Both proteins have communication with calcium channel proteins, and causes reduction in resting (intracellular) calcium and endoplasmic reticulum storage of calcium. [15] The disease is characterized by a ‘second hit’ phenomenon, in which a mutated dominant allele is inherited from a parent, with cyst formation occurring only after the normal, wild-type gene sustains a subsequent second genetic ‘hit’, resulting in renal tubular cyst formation and disease progression. [16] PKD results from defects in the primary cilium , an immotile, hair-like cellular organelle present on the surface of most cells in the body, anchored in the cell body by the basal body. [16] In the kidney, primary cilia have been found to be present on most cells of the nephron, projecting from the apical surface of the renal epithelium into the tubule lumen.
Find out as much as you can about vitiligo and your treatment options so that you can help decide what steps to take. Communicate your feelings. Let your health care provider know if you're feeling depressed.
These records can include your child's IEP or 504 Plan, report cards, written communications from school noting concerns, and a limited number of your child's work samples.
A number sign (#) is used with this entry because of evidence that mutation in the TRPM7 gene (605692), encoding a member of the transient receptor potential cation channel family, influences susceptibility to the disorder. See also PARK7 (606324) for discussion of a similar phenotype, which has been shown to be caused by a double homozygous mutation in the DJ1 gene (602533.0006) in 1 family. Description Amyotrophic lateral sclerosis-parkinsonism/dementia complex of Guam is a neurodegenerative disorder with unusually high incidence among the Chamorro people of Guam. Both ALS and parkinsonism-dementia are chronic, progressive, and uniformly fatal disorders in this population. Both diseases are known to occur in the same kindred, the same sibship, and even the same individual.
., in the amygdala ) and also implicated in neurotransmitters and neurotransmitter receptors known to be involved in anxiety disorders. [29] More specifically, genes studied for their relationship to development of GAD or demonstrated to have had a relationship to treatment response include: PACAP (A54G polymorphism): remission after 6 month treatment with Venlafaxine suggested to have a significant relationship with the A54G polymorphism (Cooper et al. (2013)) [29] HTR2A gene (rs7997012 SNP G allele): HTR2A allele suggested to be implicated in a significant decrease in anxiety symptoms associated with response to 6 months of Venlafaxine treatment (Lohoff et al. (2013)) [29] SLC6A4 promoter region (5-HTTLPR): Serotonin transporter gene suggested to be implicated in significant reduction in anxiety symptoms in response to 6 months of Venlafaxine treatment (Lohoff et al. (2013)) [29] Pathophysiology [ edit ] Amygdala (in red) brain structures linked to anxiety disorders The pathophysiology of GAD is an active and ongoing area of research often involving the intersection of genetics and neurological structures. [32] Generalized anxiety disorder has been linked to changes in functional connectivity of the amygdala and its processing of fear and anxiety. [13] Sensory information enters the amygdala through the nuclei of the basolateral complex (consisting of lateral, basal and accessory basal nuclei). [13] The basolateral complex processes the sensory-related fear memories and communicates information regarding threat importance to memory and sensory processing elsewhere in the brain, such as the medial prefrontal cortex and sensory cortices. [13] Neurological structures traditionally appreciated for their roles in anxiety include the amygdala, insula and orbitofrontal cortex (OFC). [32] It is broadly postulated that changes in one or more of these neurological structures are believed to allow greater amygdala response to emotional stimuli in individuals who have GAD as compared to individuals who do not have GAD. [32] Individuals who GAD have been suggested to have greater amygdala and medial prefrontal cortex (mPFC) activation in response to stimuli than individuals who do not have GAD. [32] However, the exact relationship between the amygdala and the frontal cortex (e.g., prefrontal cortex or the orbitofrontal cortex (OFC)) is not fully understood because there are studies that suggest increased or decreased activity in the frontal cortex in individuals who have GAD. [32] Consequently, because of the tenuous understanding of the frontal cortex as it relates to the amygdala in individuals who have GAD, it an open question as to whether individuals who have GAD bear an amygdala that is more sensitive than an amygdala in an individual without GAD or whether frontal cortex hyperactivity is responsible for changes in amygdala responsiveness to various stimuli. [32] Recent studies have attempted to identify specific regions of frontal cortex (e.g., dorsomedial prefrontal cortex (dmPFC)) that may be more or less reactive in individuals who have GAD [32] or specific networks that may be differentially implicated in individuals who have GAD. [13] Other lines of study investigate whether activation patterns vary in individuals who have GAD at different ages with respect to individuals who do not have GAD at the same age (e.g., amygdala activation in adolescents with GAD). [32] Treatment [ edit ] Traditional treatment modalities broadly fall into two (2) categories - i.e., psychotherapeutic and pharmacological intervention . [14] In addition to these two conventional therapeutic approaches, areas of active investigation include complementary and alternative medications (CAMs), brain stimulation, exercise, therapeutic massage and other interventions that have been proposed for further study. [33] Treatment modalities can, and often are utilized concurrently so that an individual may pursue psychological therapy (i.e., psychotherapy) and pharmacological therapy. [34] Both cognitive behavioral therapy (CBT) and medications (such as SSRIs ) have been shown to be effective in reducing anxiety.
Wearing a medical identification tag can help inform health care providers in the event the person is unable to communicate. Situs inversus also complicates organ transplantation operations as donor organs will more likely come from situs solitus (normal) donors.
Situs inversus is a condition in which the arrangement of the internal organs is a mirror image of normal anatomy. It can occur alone (isolated, with no other abnormalities or conditions) or it can occur as part of a syndrome with various other defects. Congenital heart defects are present in about 5-10% of affected people. The underlying cause and genetics of situs inversus are complex. Familial cases have been reported.
A rare, genetic, developmental defect during embryogenesis characterized by total mirror-image transposition of both thoracic and abdominal viscera across the left-right axis of the body. Congenital abnormalities, such as primary ciliary dyskinesia, Kartagener type, polysplenia syndrome, biliary atresia, congenital heart disease, and midgut malrotation, as well as vascular anomalies (e.g. absence of retrohepatic inferior vena cava, preduodenal portal vein, aberrant hepatic arterial anatomy) and malignancy, are frequently associated.
Hurler did not mention Hunter's paper. Because of the communications interruptions caused by World War I , it is likely that she was unaware of his study.
Mucopolysaccharidosis type I (MPS I) is a condition that affects many parts of the body. This disorder was once divided into three separate syndromes: Hurler syndrome (MPS I-H), Hurler-Scheie syndrome (MPS I-H/S), and Scheie syndrome (MPS I-S), listed from most to least severe. Because there is so much overlap between each of these three syndromes, MPS I is currently divided into the severe and attenuated types. Children with MPS I often have no signs or symptoms of the condition at birth, although some have a soft out-pouching around the belly-button (umbilical hernia) or lower abdomen (inguinal hernia). People with severe MPS I generally begin to show other signs and symptoms of the disorder within the first year of life, while those with the attenuated form have milder features that develop later in childhood.
They suggested that coronary insufficiency can occur but that Hurler patients are prohibited by their retarded development to communicate this effectively. Renteria et al. (1976) described the cardiac disease in 5 necropsy cases of Hurler syndrome.
Hurler syndrome is the most severe form of mucopolysaccharidosis type 1 (MPS1; see this term), a rare lysosomal storage disease, characterized by skeletal abnormalities, cognitive impairment, heart disease, respiratory problems, enlarged liver and spleen, characteristic facies and reduced life expectancy. Epidemiology The prevalence of the Hurler subtype of MPS1 is estimated at 1/200,000 in Europe. Clinical description Patients present within the first year of life with musculoskeletal alterations including short stature, dysostosis multiplex, thoracic-lumbar kyphosis, progressive coarsening of the facial features (including large head with bulging frontal bones, depressed nasal bridge with broad nasal tip and anteverted nostrils, full cheeks and enlarged lips), cardiomyopathy and valvular abnormalities, neurosensorial hearing loss, enlarged tonsils and adenoids, and nasal secretion. Developmental delay is usually observed between 12 and 24 months of life and is primarily in the realm of speech with progressive cognitive and sensorial deterioration. Hydrocephaly can occur after the age of two. Diffuse corneal compromise leading to corneal opacity becomes detectable from three years of age onwards.
However, this is an area of hot debate within the head and neck pathology community, and some pathologists still regard OKC as a neoplasm despite the reclassification.
A rare odontogenic tumor characterized by an unilocular or multilocular cyst most commonly located in the posterior body and lower ramus of the mandible, often surrounding the crown of the third molar. Histopathologically, the lesion shows a lining of parakeratinized stratified squamous epithelium with palisading hyperchromatic basal cells. Patients may be asymptomatic or present with local infection and/or signs and symptoms of mass effect. Recurrence is rare after complete surgical removal. Some patients have multiple cysts (metachronous or synchronous), especially in the context of nevoid basal cell carcinoma syndrome (Gorlin syndrome).
Family-focused therapy. Family support and communication can help you stick with your treatment plan and help you and your loved ones recognize and manage warning signs of mood swings. ... Psychotherapy can help children and teens manage their routines, develop coping skills, address learning difficulties, resolve social problems, and help strengthen family bonds and communication. And, if needed, it can help treat substance abuse problems common in older children and teens with bipolar disorder.
For a phenotypic description and a discussion of genetic heterogeneity of bipolar disorder, see 125480. Mapping Jamra et al. (2007) performed a genomewide interaction and locus heterogeneity linkage scan in bipolar affective disorder (BPAD), using a large linkage dataset (52 families of European descent; 448 participants and 259 affected individuals). The results provided the strongest evidence of interaction between BPAD genes on chromosome 2q22-q24 (MAFD5) and 6q23-q24 (MAFD6; 611536), which was observed symmetrically in both directions; nonparametric lod (NPL) scores of 7.55 on 2q and 7.63 on 6q; P less than 0.0001 and P = 0.0001, respectively, after a genomewide permutation procedure. The second-best BPAD interaction evidence was observed between 2q22-q24 and 15q26. Here, Jamra et al. (2007) also observed a symmetric interaction. Whereas chromosome 6q23-q24 showed evidence within the 1-dimensional linkage scan, the chromosome 2q22-q24 locus was detectable only in the 2-dimensional linkage scan.
This issue diminished with an increased following of the DSM criteria in the last part of the twentieth century. [107] [108] The diagnosis of childhood bipolar disorder, while formerly controversial, [109] has gained greater acceptance among childhood and adolescent psychiatrists. [110] American children and adolescents diagnosed with bipolar disorder in community hospitals increased 4-fold reaching rates of up to 40% in 10 years around the beginning of the 21st century, while in outpatient clinics it doubled reaching 6%. [109] Studies using DSM criteria show that up to 1% of youth may have bipolar disorder. [107] The DSM-5 has established a diagnosis— disruptive mood dysregulation disorder —that covers children with long-term, persistent irritability that had at times been misdiagnosed as having bipolar disorder, [111] distinct from irritability in bipolar disorder that is restricted to discrete mood episodes. [110] Elderly Bipolar disorder is uncommon in older patients, with measured lifetime prevalence of 1% in over 60s and 12-month prevalence of 0.1 to 0.5% in people over 65. ... Long-term inpatient stays are now less common due to deinstitutionalization , although these can still occur. [115] Following (or in lieu of) a hospital admission, support services available can include drop-in centers , visits from members of a community mental health team or an Assertive Community Treatment team, supported employment , patient-led support groups , and intensive outpatient programs .
Large ones grow, mainly outward, from the bowel wall until the point where they outstrip their blood supply and necrose (die) on the inside, forming a cavity that may eventually come to communicate with the bowel lumen. When GIST is suspected—as opposed to other causes for similar tumors—the pathologist can use immunohistochemistry (specific antibodies that stain the molecule CD117 [also known as c-kit ] —see below). 95% of all GISTs are CD117-positive (other possible markers include CD34 , DOG-1, desmin , and vimentin ). ... If the tumor outstrips its blood supply, it can necrose internally, creating a central fluid-filled cavity with bleeding and cavitations that can eventually ulcerate and communicate into the lumen of the bowel.
WHO did not recommend screening of travelers upon arrival or traveling restrictions. [72] [73] United States [ edit ] On 2 May 2014, the Centers for Disease Control and Prevention (CDC) confirmed the first diagnosis of MERS in the United States at Community Hospital in Munster, Indiana . ... Zaki and co-authors from the Erasmus Medical Center published more details, including a tentative name, Human Coronavirus-Erasmus Medical Center (HCoV-EMC), the virus's genetic makeup, and closest relatives (including SARS). [9] In May 2013, the Coronavirus Study Group of the International Committee on Taxonomy of Viruses adopted the official designation, the Middle East Respiratory Syndrome Coronavirus (MERS-CoV), which was adopted by WHO to "provide uniformity and facilitate communication about the disease". [106] Prior to the designation, WHO had used the non-specific designation 'Novel coronavirus 2012' or simply 'the novel coronavirus'. [107] Research [ edit ] When rhesus macaques were given interferon-α2b and ribavirin and exposed to MERS, they developed less pneumonia than control animals. [108] Five critically ill people with MERS in Saudi Arabia with acute respiratory distress syndrome (ARDS) and on ventilators were given interferon-α2b and ribavirin but all ended up dying of the disease.
Nutrition: Findings from the Canadian Community Health Survey . Ottawa, Ontario: Statistics Canada. ^ Lau DC, Douketis JD, Morrison KM, Hramiak IM, Sharma AM, Ur E (April 2007). "2006 Canadian clinical practice guidelines on the management and prevention of obesity in adults and children summary" . ... Wellington: Ministry of Health. ^ "Obesity in the Pacific Too Big To Ignore" (PDF) . Secretariat of the Pacific Community . WHO. 2002 . Retrieved 2008-09-30 .
Tourism Video games COVID-19 Portal v t e The COVID-19 pandemic was confirmed to have spread to Africa on 14 February 2020, with the first confirmed case announced in Egypt . [2] [3] The first confirmed case in sub-Saharan Africa was announced in Nigeria at the end of February. [4] Within three months, the virus had spread throughout the continent, as Lesotho , the last African sovereign state to have remained free of the virus, reported a case on 13 May. [5] [6] By 26 May, it appeared that most African countries were experiencing community transmission, although testing capacity was limited. [7] Most of the identified imported cases arrived from Europe and the United States rather than from China where the virus originated. [8] It is believed that there is widespread under-reporting in many African countries with less developed healthcare systems . [9] Experts have worried about COVID-19 spreading to Africa, because many of the healthcare systems on the continent are inadequate, having problems such as lack of equipment, lack of funding, insufficient training of healthcare workers, and inefficient data transmission. ... Measures are being taken by the government and the community together strictly to suppress the further spreading of this deadly virus. ... The COVID-19 Africa Open Data Project provides additional data on healthcare workers infected, health services, urgent needs and local laboratories. [204] Innovative uses of technology in health and other sectors such as drone delivery of test kits to isolated areas have been piloted. [200] Local businesses have financially supported response efforts and initiated the manufacture of masks and hand sanitizers. [200] There have been significant efforts to combat COVID-19 disinformation and provide accurate information to support the response to COVID-19. [200] [205] Social influencers and celebrities have joined voices with public health experts urging people to practice social distancing. [200] The “Verified” social media initiative of the United Nations utilised “information volunteers” to help debunk false claims about vaccine trials and fake cures. [205] UNESCO #DontGoViral initiative crowdsourced culturally relevant, open-sourced information in local languages. [205] The Communications agency 35-North partnered with the COVID-19 Africa Open Data Project to combat misinformation through Telegaram and WhatsApp. [206] Africa Centres for Disease Control and Prevention director John Nkengasong warned on December 10 that Africa might not see vaccines until after the second quarter of 2021.