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Agnosia Wikipedia

If the actual object representation was damaged, this would not allow the object to be stored in visual memory, and therefore the individual would not be able to recognize the object. [28] During the time of Wernicke, Kussmaul and Lissauer there was little known about the cerebral cortex . ... Archived from the original on 2013-01-28. ^ a b c d "NINDS Agnosia Information Page" . ... Archived from the original on 2013-01-27 . Retrieved 2012-03-28 . ^ a b "Agnosia" . [ dead link ] ^ Zeki, S (1991).

BMPR1A, PMS2, TREM2, MLH3, FAN1, TYROBP, TGFBR2, RPS20, PMS1, GRIN2A, PIK3CA, MSH2, MLH1, EPCAM, KRAS, MSH6, SEMA4A
- Agnosia Gard
  
  Agnosia is characterized by an inability to recognize and identify objects and/or persons. Symptoms may vary, according to the area of the brain that is affected. It can be limited to one sensory modality such as vision or hearing; for example, a person may have difficulty in recognizing an object as a cup or identifying a sound as a cough. Agnosia can result from strokes, traumatic brain injury, dementia, a tumor, developmental disorders, overexposure to environmental toxins (e.g., carbon monoxide poisoning), or other neurological conditions. Visual agnosia may also occur in association with other underlying disorders.
Granulomatosis With Polyangiitis Wikipedia

Some affected individuals are able to lead relatively normal lives and remain in remission for 20+ years after treatment. [26] Epidemiology [ edit ] The incidence is 10–20 cases per million per year. [27] [28] It is exceedingly rare in Japan and in African Americans . [28] History [ edit ] Scottish otolaryngologist Peter McBride (1854–1946) first described the condition in 1897 in a BMJ article entitled "Photographs of a case of rapid destruction of the nose and face". [29] Heinz Karl Ernst Klinger (born 1907) added information on the anatomical pathology . ... Current Opinion in Ophthalmology (Review). 28 (6): 613–16. doi : 10.1097/ICU.0000000000000422 .

PRTN3, HLA-DPB1, HLA-DPA1, CTLA4, PTPN22, FCGR3B, WG, MPO, GYPA, SERPINA1, IL10, HLA-DRB1, KRT20, IL4, ACR, CD28, MS4A1, TNF, CCR5, ANP32B, CD226, TNFSF13, TNFSF11, IL2, IL1B, NT5E, TGFB1, IFNG, SEMA6A, FCGR3A, ETS1, CRP, RBM45, TST, DEFB104A, SERPINA13P, CDR3, VDI, MIR142, VCAM1, TNFRSF4, DEFB104B, IGHV3OR16-7, TP53, TNXB, DEFB4B, TNFRSF1A, TNFAIP3, LINC-ROR, TLR4, TIMP3, LOC102723407, USO1, BANF1, TNFRSF18, GREM1, IGHV3-69-1, FOXP3, GCA, TLR9, SMUG1, THBD, SEC14L2, CYCS, GBA3, KDM6B, NOD2, SLC27A5, PPARGC1A, TNFSF13B, PARP9, NXF1, MAMLD1, TIMP1, PLAT, TGFB2, DHX15, HLA-DQA1, HLA-A, GLA, FLNB, F2RL1, FBL, ELANE, DPP4, DEFB4A, DEFB1, ACE, IGH, CTSK, CTSC, CEL, CDK6, SERPINA6, CALCR, C5AR1, C5, BTK, BPI, HLA-DRB4, IL6, XCL1, NBN, S100A7, RXRB, RING1, PTX3, PNN, PML, AGT, PDCD1, SERPINA5, NME1, MMP9, IL17A, MMP8, MMP2, MIP, MIF, CIITA, MDM2, LEPR, KRT3, KLRB1, IRF5, LOC102724971
- Granulomatosis With Polyangiitis Gard
  
  Granulomatosis with polyangiitis (GPA) is a type of vasculitis or swelling (inflammation) of the blood vessels. The disease can cause swelling of the blood vessels anywhere in the body but mainly impacts the sinuses, nose, trachea (windpipe), lungs, and kidneys. The swelling can limit the flow of blood to these body parts, causing damage. Symptoms of the disease can include sinus pain, recurrent respiratory infections, joint pain , tiredness ( fatigue ), and skin lesions. The exact cause of GPA is unknown, but it is a type of autoimmune disease.
- Granulomatosis With Polyangiitis Medlineplus
  
  Granulomatosis with polyangiitis (GPA) is a condition that causes inflammation that primarily affects the respiratory tract (including the lungs and airways) and the kidneys. This disorder is formerly known as Wegener granulomatosis. A characteristic feature of GPA is inflammation of blood vessels (vasculitis), particularly the small- and medium-sized blood vessels in the lungs, nose, sinuses, windpipe, and kidneys, although vessels in any organ can be involved. Polyangiitis refers to the inflammation of multiple types of vessels, such as small arteries and veins. Vasculitis causes scarring and tissue death in the vessels and impedes blood flow to tissues and organs. Another characteristic feature of GPA is the formation of granulomas, which are small areas of inflammation composed of immune cells that aid in the inflammatory reaction.
- Granulomatosis With Polyangiitis Orphanet
  
  A rare anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis characterized by necrotizing inflammation of small and medium vessels (capillaries, venules and arterioles), resulting in tissue ischemia. Epidemiology The prevalence is estimated between 1/6,400 - 42,000 worldwide with annual incidence between 1/84,000-475,000. There is geographic and/or ethnic variation, with a higher incidence in colder regions and among Caucasians. Childhood-onset disease is characterized by female predominance, and adult-onset by a slight male predominance. Clinical description The average age of onset is 45 years but the disease may manifest at any age including childhood.
- Granulomatosis With Polyangiitis Mayo_clinic
  
  Overview Granulomatosis with polyangiitis is an uncommon disorder that causes inflammation of the blood vessels in your nose, sinuses, throat, lungs and kidneys. Formerly called Wegener's granulomatosis, this condition is one of a group of blood vessel disorders called vasculitis. It slows blood flow to some of your organs. The affected tissues can develop areas of inflammation called granulomas, which can affect how these organs work. Early diagnosis and treatment of granulomatosis with polyangiitis might lead to a full recovery. Without treatment, the condition can be fatal. Symptoms Signs and symptoms of granulomatosis with polyangiitis can develop suddenly or over several months.
- Granulomatosis With Polyangiitis Omim
  
  Description Granulomatosis with polyangiitis, formerly termed Wegener granulomatosis, is a systemic disease with a complex genetic background. It is characterized by necrotizing granulomatous inflammation of the upper and lower respiratory tract, glomerulonephritis, vasculitis, and the presence of antineutrophil cytoplasmatic autoantibodies (ANCAs) in patient sera. These ANCAs are antibodies to a defined target antigen, proteinase-3 (PR3, PRTN3; 177020), which is present within primary azurophil granules of neutrophils (PMNs) and lysozymes of monocytes. On cytokine priming of PMNs, PR3 translocates to the cell surface, where PR3-ANCAs can interact with their antigens and activate PMNs. PMNs from patients with active GPA express PR3 on their surface, produce respiratory burst, and release proteolytic enzymes after activation with PR3-ANCAs.
Abortion In Arizona Wikipedia

This information is then collected by Department of Health Services who provide the state with an annual report on abortions in the state, along with information on the how abortions are paid for in the state. [17] In 2019, women in Arizona were eligible for pregnancy related disability associated medical care that included abortion or miscarriage. [21] [22] As of May 14, 2019, abortion was legally not allowed after the fetus was viable, generally some point between week 24 and 28. This period uses a standard defined by the US Supreme Court in 1973 with the Roe v. ... They alleged that Arizona's laws made it so difficult for women to get abortions that it was almost impossible for them to legally get an abortion. [17] Clinic history [ edit ] Number of abortion clinics in Arizona by year Between 1982 and 1992, the number of abortion clinics in the state decreased by 9, going from 37 in 1982 to 28 in 1992. [25] In 2014, there were 9 abortion clinics in the state. [26] 80% of the counties in the state did not have an abortion clinic. ... In 2019, Northern Arizona was served by only one clinic that performed abortions, and that was a Planned Parenthood clinic which could only provide induced abortions using medication. [17] In March 2016, there were 10 Planned Parenthood clinic in the state. [28] In 2017, there were 10 Planned Parenthood clinics in a state with a population of 1,525,996 women aged 15 – 49 of which 4 offered abortion services. [29] Statistics [ edit ] In the period between 1972 and 1974, there were zero recorded illegal abortion deaths in the state. [30] In 1990, 448,000 women in the state faced the risk of an unintended pregnancy. [25] In 2001, Arizona, Florida, Iowa, Louisiana, Massachusetts, and Wisconsin did not provide any residence related data regarding abortions performed in the state to the Centers for Disease Control . [31] In 2014, 49% of adults said in a poll by the Pew Research Center that abortion should be legal in all or most cases. [32] In 2017, the state had an infant mortality rate of 5.7 deaths per 1,000 live births. [9] Number of reported abortions, abortion rate and percentage change in rate by geographic region and state in 1992, 1995 and 1996 [33] Census division and state Number Rate % change 1992–1996 1992 1995 1996 1992 1995 1996 US Total 1,528,930 1,363,690 1,365,730 25.9 22.9 22.9 –12 Mountain 69,600 63,390 67,020 21 17.9 18.6 –12 Arizona 20,600 18,120 19,310 24.1 19.1 19.8 –18 Colorado 19,880 15,690 18,310 23.6 18 20.9 –12 Idaho 1,710 1,500 1,600 7.2 5.8 6.1 –15 Montana 3,300 3,010 2,900 18.2 16.2 15.6 –14 Nevada 13,300 15,600 15,450 44.2 46.7 44.6 1 New Mexico 6,410 5,450 5,470 17.7 14.4 14.4 –19 Utah 3,940 3,740 3,700 9.3 8.1 7.8 –16 Wyoming 460 280 280 4.3 2.7 2.7 –37 Number, rate, and ratio of reported abortions, by reporting area of residence and occurrence and by percentage of abortions obtained by out-of-state residents, US CDC estimates Location Residence Occurrence % obtained by out-of-state residents Year Ref No.
Alice In Wonderland Syndrome Wikipedia

Nonetheless, it is usually easy to rule out psychosis as those with Alice in Wonderland syndrome are typically aware that their hallucinations and distorted perceptions are not 'real'. [27] Younger patients may struggle to describe their unusual symptoms, and thus, one recommended approach is to encourage children to draw their visual illusions during episodes. [28] Symptoms of AiWS do not appear to change in severity over the course of the syndrome, and though the symptoms may acutely impact the patient's life while they are present, Alice in Wonderland syndrome typically resolves itself within weeks or months. [29] Furthermore, AiWS symptoms tend to for short periods of time during the day, with most patients describing their symptoms as lasting anywhere between 10 seconds to 10 minutes [ citation needed ] . ... "The phenomenology of perceptual hallucinations in alcohol-induced delirium tremens". Psychopathology . 28 (5): 247–55. doi : 10.1159/000284935 . ... Journal of the American Academy of Child and Adolescent Psychiatry . 28 (4): 493–6. doi : 10.1097/00004583-198907000-00004 .

SMUG1
Plague Of Justinian Wikipedia

In 568, the Lombards invaded Northern Italy , defeated the small Byzantine army that had been left behind and established the Kingdom of the Lombards . [16] [23] Gaul suffered severely, so it is unlikely that Britain escaped. [24] Epidemiology [ edit ] Genetics of the Justinian plague strain [ edit ] The Plague of Justinian is generally regarded as the first historically recorded epidemic of Yersinia pestis . [25] [26] This conclusion is based on historical descriptions of the clinical manifestations of the disease [27] and the detection of Y. pestis DNA from human remains at ancient grave sites dated to that period. [28] [29] Genetic studies of modern and ancient Yersinia pestis DNA suggest that the origin of the Justinian plague was in Central Asia . ... May 20, 2013. ^ Maria Cheng (January 28, 2014). "Plague DNA found in ancient teeth shows medieval Black Death, 1,500-year pandemic caused by same disease" . ... PMID 26496604 . Retrieved September 28, 2018 . ^ McGrath, Matt (12 October 2011).
Immature Teratoma Wikipedia

In most cases, the implants are better differentiated than the primary tumors. [8] Gliomatosis peritonei, a rare condition often associated with immature ovarian teratoma, is characterized by the presence of mature glial implants in the peritoneum . [25] Yoon et al. (2012) , reported that immature ovarian teratoma patients with Gliomatosis peritonei have larger tumors, more frequent recurrence and higher CA-125 levels than immature ovarian teratoma patients without gliomatosis peritonei. [26] A high degree of immaturity in the primary tumor, one that corresponds with a grade 3 diagnosis is a sign of poor prognosis. [23] [8] [27] [28] Grade 3 tumors often display chromosomal abnormalities , also an indication of poor prognosis. [24] Tumor grade is the most important factor for relapse in immature teratomas. [27] Vicus et al. (2011) , reported that grade 2 or 3 tumors are associated with a greater chance of relapse that can be fatal, predominantly within 2 years of diagnosis. [29] Among grade 3 patients, the stage was significantly associated with relapse . [29] In the past, survival rates were low for high-grade immature teratomas. ... "Teratome des Ovars". Der Pathologe (in German). 28 (3): 203–208. doi : 10.1007/s00292-007-0909-7 . ... "Gliomatosis peritonei: a clinicopathologic and immunohistochemical study of 21 cases" . Modern Pathology . 28 (12): 1613–1620. doi : 10.1038/modpathol.2015.116 .
Primary Polydipsia Wikipedia

Such persons typically prefer to possess bottled water that is ice-cold, consume water and other fluids at excessive levels. [ medical citation needed ] However, a preference for ice-cold water is also seen in diabetes insipidus. [25] [26] Treatment [ edit ] Estimation of serum sodium levels from weight gain and suggested interventions [27] Weight gained (% body mass) Estimated serum sodium (mmol/L) Suggested intervention 0-3 140 - 134 No direct intervention, monitoring 3-5 133 - 130 Redirection from water sources 5-7 129–126 Oral NaCl and redirection 7–10 125–120 Oral NaCl and redirection, possibly restraint > 10 < 120 Slow IV saline , seizure precautions Treatment for psychogenic polydipsia depends on severity and may involve behavioural and pharmacological modalities. [28] Acute hyponatraemia [ edit ] If the patient presents with acute hyponatraemia (overhydration) caused by psychogenic polydipsia, treatment usually involves administration of intravenous hypertonic (3%) saline until the serum sodium levels stabilise to within a normal range, even if the patient becomes asymptomatic. [29] Fluid restriction [ edit ] If the patient is institutionalised , monitoring of behaviour and serum sodium levels is necessary. ... Behavioural [ edit ] Behavioural treatments may involve the use of a token economy to provide positive reinforcement to desirable behaviour. [28] Furthermore, cognitive therapy techniques can be used to address the thought patterns that lead to compulsive drinking behaviour. ... PMID 23181904 . ^ a b "Polydipsia linked to brain alterations in schizophrenia" . News-Medical.net . 2012-11-28 . Retrieved 2016-12-08 . ^ "Psychogenic polydipsia – Diagnosis – Approach" .

AVP, AQP2
Post-Chemotherapy Cognitive Impairment Wikipedia

Modafinil is a wakefulness-promoting agent that can improve alertness and concentration, and studies have shown it to be effective at least among women treated for breast cancer. [28] [29] While estrogen hormone supplementation may reverse the symptoms of PCCI in women treated for breast cancer, [3] this carries health risks, including possibly promoting the proliferation of estrogen-responsive breast cancer cells. ... "Adverse late effects of childhood cancer and its treatment on health and performance" . Annu Rev Public Health . 28 (1): 278–302. doi : 10.1146/annurev.publhealth.28.021406.144049 . ... The European Journal of Neuroscience . 28 (2): 323–330. doi : 10.1111/j.1460-9568.2008.06325.x .
Mastocytosis Wikipedia

Archived from the original on 2013-12-28 . Retrieved 2017-11-02 . ^ Hermine, Olivier; Lortholary, Olivier; Leventhal, Phillip S.; Catteau, Adeline; Soppelsa, Frédérique; Baude, Cedric; Cohen-Akenine, Annick; Palmérini, Fabienne; Hanssens, Katia; Yang, Ying; Sobol, Hagay; Fraytag, Sylvie; Ghez, David; Suarez, Felipe; Barete, Stéphane; Casassus, Philippe; Sans, Beatrice; Arock, Michel; Kinet, Jean Pierre; Dubreuil, Patrice; Moussy, Alain; Soyer, H. Peter (28 May 2008). "Case-Control Cohort Study of Patients' Perceptions of Disability in Mastocytosis" . ... "Everyday life and mastocytosis from a patient perspective-a qualitative study" . Journal of Clinical Nursing . 28 (7–8): 1114–1124. doi : 10.1111/jocn.14676 .

KIT, FOXF1, TET2, SRSF2, ASXL1, NTRK1, CD34, PDGFRA, IL2RA, TNFRSF8, ISG20, STAT5B, STAT5A, IL6, IL9, CD274, FIP1L1, TPSAB1, IL31, JAK2, TPSD1, NGF, IGHE, TPM3, TLR2, RASGRP4, TLR4, TAC1, TACR1, STAT3, SST, SOAT1, SNCA, SLC16A1, TPT1, TPSB2, UBE2N, SF3B1, SLAMF8, MCPH1, TLR9, ZMYND10, CPA4, MCAT, IL37, IL33, VIP, CCL26, IKZF1, CCL2, TNFRSF10A, TNFSF10, KIDINS220, TRPV1, SPATA2, ABL1, RPL17, RUNX2, HBM, FGFR1, CPA3, CD72, CD44, TNFSF8, RUNX1T1, RUNX1, CASP3, PTPN11, CEACAM1, BDNF, BCR, BCL2L1, BCL2, RERE, AR, ALK, HSPG2, IDH2, IL4, IL4R, SERPINB6, ENPP3, PDGFRB, ABL2, PDCD1, NRAS, NPM1, MPL, MITF, KITLG, KRT14, KRAS, KIR2DL4, ITGAV, ITGA5, IL13, IL6R, RPL17-C18orf32
- Mastocytosis Gard
  
  Mastocytosis occurs when too many mast cells accumulate in the skin and/or internal organs such as the liver, spleen, bone marrow , and small intestines. Mast cells are a type of white blood cell in the immune system. Mast cells are responsible for protecting the body from infection and releasing chemicals to create inflammatory responses . The signs and symptoms of mastocytosis vary based on which parts of the body are affected. There are two main forms of mastocytosis. Cutaneous mastocytosis only affects the skin and is more common in children. Systemic mastocytosis affects more than one part of the body and is more common in adults.
- Mastocytosis, Cutaneous Omim
  
  A number sign (#) is used with this entry because of evidence that some cases of cutaneous mastocytosis (MASTC) are caused by heterozygous germline mutation in the KIT gene (164920) on chromosome 4q12. Systemic mastocytosis and some cases of cutaneous mastocytosis are caused by somatic mutation in the KIT gene. Description Mastocytosis, or mast cell disease, is a heterogeneous group of clinical disorders characterized by the abnormal accumulation of mast cells in various tissues, especially in the skin and hematopoietic organs. Mastocytosis usually appears in infancy or early adulthood. In most pediatric cases, the disease is limited to the skin, but it can be associated with systemic symptoms due to the release of mediators from mast cells, even when there is no systemic infiltration. It usually has a good prognosis, with substantial improvement or spontaneous resolution before puberty.
Fryns Syndrome Wikipedia

Bamforth et al. (1987) and Hanssen et al. (1992) also described patients with this syndrome who survived the neonatal period. [28] [29] In the report of Hanssen et al. (1992), 2 older sibs had died in utero . [29] The reports suggested that survival beyond the neonatal period is possible when the diaphragmatic defect and lung hypoplasia are not present. ... "Diaphragmatic defects, craniofacial dysmorphism, cleft palate and distal limb deformities. — a new lethal syndrome". J Genet Hum . 28 (1): 57–60. PMID 7400786 . ^ Fitch N (February 1988). ... Further evidence for autosomal recessive inheritance". Clin. Genet . 28 (6): 516–20. doi : 10.1111/j.1399-0004.1985.tb00419.x .

PIGN, HTC2, IGHV1-12
- Fryns Syndrome Gene_reviews
  
  Summary Clinical characteristics. Fryns syndrome is characterized by diaphragmatic defects (diaphragmatic hernia, eventration, hypoplasia, or agenesis); characteristic facial appearance (coarse facies, wide-set eyes, a wide and depressed nasal bridge with a broad nasal tip, long philtrum, low-set and anomalous ears, tented vermilion of the upper lip, wide mouth, and a small jaw); short distal phalanges of the fingers and toes (the nails may also be small); pulmonary hypoplasia; and associated anomalies (polyhydramnios, cloudy corneas and/or microphthalmia, orofacial clefting, renal dysplasia / renal cortical cysts, and/or malformations involving the brain, cardiovascular system, gastrointestinal system, and/or genitalia). Survival beyond the neonatal period is rare. Data on postnatal growth and psychomotor development are limited; however, severe developmental delay and intellectual disability are common. Diagnosis/testing. The clinical diagnosis of Fryns syndrome can be established in a proband based on six proposed criteria (diaphragmatic defect, characteristic facial appearance, distal digital hypoplasia, pulmonary hypoplasia, at least one characteristic associated anomaly, and a family history consistent with autosomal recessive inheritance). The molecular diagnosis can be established in a proband with suggestive findings and biallelic pathogenic variants in PIGN identified by molecular genetic testing. Management. Treatment of manifestations: For congenital diaphragmatic hernia, the neonate is immediately intubated to prevent inflation of herniated bowel, surgery, and/or supportive measures as for the general population.
- Fryns Syndrome Medlineplus
  
  Fryns syndrome is a condition that affects the development of many parts of the body. The features of this disorder vary widely among affected individuals and overlap with the signs and symptoms of several other disorders. These factors can make Fryns syndrome difficult to diagnose. Most people with Fryns syndrome have a defect in the muscle that separates the abdomen from the chest cavity (the diaphragm ). The most common defect is a congenital diaphragmatic hernia, which is a hole in the diaphragm that develops before birth. This hole allows the stomach and intestines to move into the chest and crowd the heart and lungs.
- Fryns Syndrome Orphanet
  
  A rare multiple congenital anomaly syndrome characterized by dysmorphic facial features, congenital diaphragmatic hernia, pulmonary hypoplasia, and distal limb hypoplasia, in addition to variable expression of additional malformations. Epidemiology The birth prevalence of Fryns syndrome (FS) has been estimated at 1/14,000 births. Clinical description Polyhydramnios is often noted during pregnancy and neonates present with a spectrum of various malformations at birth. The classical features of FS include CDH (unilateral in 75% of cases), dysmorphic craniofacial features (coarse facies, ocular hypertelorism, microphthalmia, low-set, poorly formed ears, a broad and flat nasal bridge, thick nasal tip with anteverted nares, long philtrum, tented upper lip, macrostomia and microretrognathia), and limb malformations (mainly distal limb hypoplasia that includes short and broad hands, short digits, short terminal phalanges, hypoplastic or absent nails, and clinodactyly). Thorax is small with widely spaced nipples. Brain (ventricular dilation, hydrocephalus) and cardiac malformations (atrial and ventricular septal defects, aortic abnormalities) are reported frequently in affected individuals.
- Fryns Syndrome Omim
  
  Description Fryns syndrome is an autosomal recessive multiple congenital anomaly syndrome that is usually lethal in the neonatal period (Alessandri et al., 2005). Fryns (1987) reviewed the syndrome. Also see Tonne-Kalscheuer syndrome (300978), an X-linked disorder with overlapping features. Clinical Features Fryns et al. (1979) reported 2 stillborn sisters with a multiple congenital anomaly syndrome characterized by coarse facies with cloudy corneae, diaphragmatic defects, absence of lung lobulation, and distal limb deformities. A sporadic case was reported by Goddeeris et al. (1980). Fitch (1988) claimed that she and her colleagues were the first to describe this disorder. In 1978 they reported a single infant, born of second-cousin parents, who had absent left hemidiaphragm, hydrocephalus, arhinencephaly, and cardiovascular anomalies (Fitch et al., 1978).
- Fryns Syndrome Gard
  
  Fryns syndrome is a condition that affects the development of many parts of the body. Signs and symptoms vary widely among affected individuals. Many indiivduals with this condition have defects of the diaphragm such as a congenital diaphragmatic hernia (a hole in the diaphragm present at birth). This may allow the stomach and intestines to move into the chest, which can result in pulmonary hypoplasia (underdevelopment of the lungs). Other signs and symptoms may include abnormalities of the fingers and toes; distinctive facial features; severe developmental delay and intellectual disability; and abnormalities of the brain, cardiovascular system, gastrointestinal system, kidneys, and genitalia. survival beyond the neonatal period is rare. The cause of Fryns syndrome is not known, but it is thought to be genetic and appears to be inherited in an autosomal recessive manner.
Dental Plaque Wikipedia

Conditions and diseases can include: Atheromas [26] Cardiovascular disease [27] Respiratory disease [28] Diabetes mellitus [29] Caries [ edit ] Representation of the progression of dental caries Dental caries is an infectious disease caused primarily by Streptococcus mutans , characterized by acid demineralization of the enamel, which can progress to further breakdown of the more organic, inner dental tissue ( dentin ). [1] The bacterial community would mainly consist of acidogenic and acid-tolerating species (e.g. ... "Bacterial and host interactions of oral streptococci" . DNA and Cell Biology . 28 (8): 397–403. doi : 10.1089/dna.2009.0868 . ... Journal of Clinical Periodontology . 38 Suppl 11 (s11): 28–35. doi : 10.1111/j.1600-051X.2010.01673.x .

ACACB, PTEN, OR10A4, FBRS, RBPJP4, PACC1, ZDHHC2, VSX1, AGO2, FBXO8, AIM2, CCN6, S100A9, TAS2R38, APP, PPP1R1A, HPD, HSD17B10, F12, DEFB1, DCN, CD70, CAT, CAST, BGN, BCL2A1, BOP
Neonatal Jaundice Wikipedia

However, it does not appear to reduce the requirement for phototherapy in the treatment of neonatal jaundice. [28] There is currently no reliable evidence about whether home-based or hospital-based phototherapy is more effective for full term infants with jaundice. [29] Exchange transfusions [ edit ] Much like with phototherapy the level at which exchange transfusion should occur depends on the health status and age of the newborn. ... Retrieved 11 December 2017 . ^ a b c d "Jaundice in newborn babies under 28 days | Guidance and guidelines" . ... Retrieved 11 December 2017 . ^ a b c d e "Jaundice in newborn babies under 28 days" . NICE . October 2016 . Retrieved 11 December 2017 . ^ Olusanya, BO; Teeple, S; Kassebaum, NJ (February 2018).

NR1I2, G6PD, UGT1A1, UGT1A, GSTM1, GSTK1, NR1I3, SLCO1B1, GGTLC1, SLCO6A1, ABO, SMIM10L2B, GGTLC5P, GGTLC3, GGT2, GGTLC4P, SMIM10L2A, SPTA1, SLC35A2, ACP1, PRL, OSM, NPC1, HMOX1, HK1, GSTT1, GPI, GCLC, GGT1, GALT, BTD, ADA, LOC102724197
- Infant Jaundice Mayo_clinic
  
  Overview Infant jaundice is yellow discoloration of a newborn baby's skin and eyes. Infant jaundice occurs because the baby's blood contains an excess of bilirubin (bil-ih-ROO-bin), a yellow pigment of red blood cells. Infant jaundice is a common condition, particularly in babies born before 38 weeks' gestation (preterm babies) and some breast-fed babies. Infant jaundice usually occurs because a baby's liver isn't mature enough to get rid of bilirubin in the bloodstream. In some babies, an underlying disease may cause infant jaundice. Most infants born between 35 weeks' gestation and full term need no treatment for jaundice.
Pulp Necrosis Wikipedia

The risk of pulp necrosis in permanent teeth with extrusion or lateral luxation and concomitant crown fractures without pulp exposure". Dental Traumatology . 28 (5): 379–85. doi : 10.1111/j.1600-9657.2011.01100.x . ... International Journal of Paediatric Dentistry . 28 (5): 432–442. doi : 10.1111/ipd.12372 . ... The risk of pulp necrosis in permanent teeth with extrusion or lateral luxation and concomitant crown fractures without pulp exposure". Dental Traumatology . 28 (5): 379–385. doi : 10.1111/j.1600-9657.2011.01100.x .

MMP2, CCL4, CCL20, SCAP, CTNNBL1
Copper Toxicity Wikipedia

Alzheimer's disease [ edit ] Elevated free copper levels exist in Alzheimer's disease , [27] which has been hypothesized to be linked to inorganic copper consumption. [28] Copper and zinc are known to bind to amyloid beta proteins in Alzheimer's disease. [29] This bound form is thought to mediate the production of reactive oxygen species in the brain. [30] Diagnosis [ edit ] ICD-9-CM [ edit ] ICD-9-CM code 985.8 Toxic effect of other specified metals includes acute & chronic copper poisoning (or other toxic effect) whether intentional, accidental, industrial etc. ... S2CID 205770002 . ^ Federal Register / Vol. 65, No. 8 / Wednesday, January 12, 2000 / Rules and Regulations. pp. 1976. ^ a b US EPA Region 5 (2011-12-28). "Ecological Toxicity Information" . ... "The risk of copper toxicity contributing to cognitive decline in the aging population and to Alzheimer's disease". J. Am. Coll. Nutr . 28 (3): 238–42. doi : 10.1080/07315724.2009.10719777 .
Head Lice Infestation Wikipedia

Items may also be frozen for 24 hours well below the freezing point of water to ensure that ice crystals form within the cells of the lice. [27] Epidemiology [ edit ] Reliable data describing the usual incidence of infestation in the general public, in the average school community, or during specific times of the year are lacking. — Janis Hootman, 2002 [28] The number of cases of human louse infestations (or pediculosis ) has increased worldwide since the mid-1960s, reaching hundreds of millions annually. [29] It is estimated between 1 and 20% of specific groups in Europe are infected. [6] Despite improvements in medical treatment and prevention of human diseases during the 20th century, head louse infestation remains stubbornly prevalent. ... Archived from the original on 7 March 2010 . Retrieved 28 May 2010 . ^ a b Devore CD, Schutze GE (May 2015). ... Cdc.gov. 22 October 2012. Archived from the original on 28 October 2012 . Retrieved 22 November 2012 . ^ Michigan Head Lice Manual .

COX1, CYTB, KDR, TRNS1, WDHD1, TNRC6C-AS1
- Head Lice Mayo_clinic
  
  Overview Head lice are tiny insects that feed on blood from the human scalp. Head lice most often affect children. The insects usually spread through direct transfer from the hair of one person to the hair of another. Head lice Head lice feed on blood from the scalp. The female louse lays eggs (nits) that stick to hair shafts. Having head lice isn't a sign of poor personal hygiene or an unclean living environment. Head lice don't carry bacterial or viral diseases. Nonprescription and prescription medications can help treat head lice.
Vaccine Adverse Event Wikipedia

Awards are based on medical expenses, lost earnings and pain and suffering (capped at $250,000). [28] From 1988 until March 3, 2011, 5,636 claims relating to autism, and 8,119 non-autism claims, were made to the VICP. 2,620 of these claims, one autism-related, were compensated, with 4,463 non-autism and 814 autism claims dismissed; awards (including attorney's fees) totaled over $2 billion. ... "A postmodern Pandora's box: anti-vaccination misinformation on the Internet". Vaccine . 28 (7): 1709–16. doi : 10.1016/j.vaccine.2009.12.022 . ... Ministère de la Santé et des Services sociaux. April 28, 2017. Archived from the original on May 15, 2017.
Pyelonephritis Wikipedia

If no abnormality is identified, some studies suggest long-term preventive treatment with antibiotics, either daily or after sexual activity . [26] In children at risk for recurrent urinary tract infections, not enough studies have been performed to conclude prescription of long-term antibiotics have a net positive benefit. [27] Drinking cranberry juice does not appear to provide much if any benefit in decreasing urinary tract infections. [28] Management [ edit ] In people suspected of having pyelonephritis, a urine culture and antibiotic sensitivity test is performed, so therapy can eventually be tailored on the basis of the infecting organism. [5] As most cases of pyelonephritis are due to bacterial infections, antibiotics are the mainstay of treatment. [5] The choice of antibiotic depends on the species and antibiotic sensitivity profile of the infecting organism, and may include fluoroquinolones , cephalosporins , aminoglycosides , or trimethoprim/sulfamethoxazole , either alone or in combination. [15] Simple [ edit ] In people who do not require hospitalization and live in an area where there is a low prevalence of antibiotic-resistant bacteria, a fluoroquinolone by mouth such as ciprofloxacin or levofloxacin is an appropriate initial choice for therapy. [5] In areas where there is a higher prevalence of fluoroquinolone resistance, it is useful to initiate treatment with a single intravenous dose of a long-acting antibiotic such as ceftriaxone or an aminoglycoside, and then continuing treatment with a fluoroquinolone. ... "Pyelonephritis: Radiologic-Pathologic Review" . RadioGraphics . 28 (1): 255–276. doi : 10.1148/rg.281075171 . ... Archived (PDF) from the original on 2013-12-28. ^ Goodman, TR; McHugh K; Lindsell DR (1998).

PIM1, B2M, IL3, CRP, BMP7, CYB5A, HOXA13, KCTD1, BNC2, XDH, CFI, TLR4, UMOD, CXCL8, PRADC1, TIMP1, SFTPD, PROZ, SELE, SLC5A2, ASAP2, IL18R1, EBI3, TLR1, TLR5, PAPOLA, MRPS30, CCL5, PDAP1, TUSC2, ASAP1, VUR, MTPAP, PAPOLG, WDR26, RNASE7, REG3G, SFTPA1, CXCL12, ACP3, CCL2, CXCL2, AFA, AMBP, APRT, AR, BSG, CAT, COX8A, DPEP1, EMP1, GATA6, CBLIF, GLI2, CXCL1, IL6, SCNN1G, IL15, IRF3, LCN2, MFAP1, CXCL9, MMP9, SERPINE1, SERPINB2, REG3A, SLC25A3, ADM, PTX3, RBMS2, SFTPA2
Rh Disease Wikipedia

If he is heterozygous, there is a 50% chance of offspring to be positive for the antigen. [10] Prevention [ edit ] All RhD negative pregnant women should receive RhoGam at 28 weeks gestation and within 72 hours after childbirth in addition to doses with any sensitizing event (miscarriage, trauma, bleeding). ... Seminars in Fetal and Neonatal Medicine . 21 (1): 28–34. doi : 10.1016/j.siny.2015.10.006 . ... Seminars in Fetal and Neonatal Medicine . 21 (1): 28–34. doi : 10.1016/j.siny.2015.10.006 .
Kidney Failure Wikipedia

Overuse of common drugs such as ibuprofen , and acetaminophen (paracetamol) can also cause chronic kidney failure. [25] Some infectious disease agents, such as hantavirus , can attack the kidneys, causing kidney failure. [26] Genetic predisposition [ edit ] The APOL1 gene has been proposed as a major genetic risk locus for a spectrum of nondiabetic renal failure in individuals of African origin, these include HIV-associated nephropathy (HIVAN), primary nonmonogenic forms of focal segmental glomerulosclerosis , and hypertension affiliated chronic kidney disease not attributed to other etiologies. [27] Two western African variants in APOL1 have been shown to be associated with end stage kidney disease in African Americans and Hispanic Americans. [28] [29] Diagnostic approach [ edit ] Measurement for CKD [ edit ] Stages of kidney failure Chronic kidney failure is measured in five stages, which are calculated using the person's GFR, or glomerular filtration rate . ... Nephrology: Clinical Cases Uncovered . John Wiley & Sons. p. 28. ISBN 9781405189903 . ^ a b Ferri, Fred F. (2017). ... PMID 17898101 . ^ Rughooputh, Mahesh Shumsher; Zeng, Rui; Yao, Ying; Sands, Jeff M (28 December 2015). "Protein Diet Restriction Slows Chronic Kidney Disease Progression in Non-Diabetic and in Type 1 Diabetic Patients, but Not in Type 2 Diabetic Patients: A Meta-Analysis of Randomized Controlled Trials Using Glomerular Filtration Rate as a Surrogate" .

TLR4, EDN1, ACE, AGT, MYH9, EPO, APOE, GLA, TRPC6, IFNG, CYBA, PPARG, MME, INF2, INS, CYP24A1, LEPR, LMX1B, CFHR5, IDH2, NOX4, IFNA2, KL, IL1B, PPARGC1A, TBXA2R, CD80, MT1A, SLCO4C1, TLR2, HIF1A, SLC22A2, RHCG, PHEX, PARP1, NAMPT, ACMSD, MT2A, UMOD, PKD1, PTH, REN, TGFB1, ALB, LCN2, TNF, MPO, MTHFR, RAPGEF5, CD2AP, APRT, APOL1, FGF23, ACTN4, ADIPOQ, SERPINA5, HNF1B, LPA, CLCN5, SCARB2, IGAN1, CCL2, IL18, ADAMTS13, B2M, HAMP, VDR, AGTR1, NPHS2, NOS3, CST3, CFH, CRP, IL6, UTS2, CASR, BSND, SLC17A5, ADM, LEP, MMP2, AGXT, KLK1, LAMB2, COL4A3, ANPEP, COL4A4, COL4A5, AQP2, COPD, LRSAM1, CLDN16, CNDP1, NT5C1A, PAX2, ABCB1, TSC2, IL1A, PKD2, VEGFA, SLC5A2, CABIN1, FGF21, PODXL, SPP1, LCAT, SERPINE1, NPHP1, TP53, STAT4, MUC1, CD46, NR3C2, LAMA5, PON1, IFNA13, RMND1, F5, STX2, ELANE, EGFR, DSPP, DPP4, IFNA1, CYP3A4, CCR5, BTBD8, C3, BCL2, AVP, MIR499A, ANGPT1, CCR2, ADCYAP1, G6PC, CYP11B2, IL1RN, APLN, EPX, ITGA8, DGKE, SLCO1B3, DESI1, DEGS1, RUVBL1, USO1, FRMD3, NRP1, SLC7A7, SLC9C1, CLDN1, RGN, KLF4, ADGRF5, SLC35G1, CBLL2, GDF15, MTRF1, IQCB1, KLB, TAM, MRPS7, IL34, WT1, IL20, RN7SL263P, MIR499B, TIMM23, ZGLP1, GGTLC4P, BEST1, SOST, UGT1A, VWF, XDH, NXPH1, GGT2, GGTLC3, GGTLC5P, PAX8, SMARCAL1, MIR216A, MIR21, NR4A3, CUBN, SLC26A5, CLDN19, DIANPH, MAP1S, SEC14L2, MUL1, WNK4, KIF3A, SLC2A6, RASSF1, NOD2, BNC2, ADGRL4, TRPV4, SQOR, PADI4, FERMT2, WDR19, SMUG1, FJX1, SUCNR1, SLC2A9, ANKH, ACSS2, PLA2G15, PPP6R3, NAT10, DHX40, ATRNL1, KEAP1, NXF1, RBM45, FBXO32, ACCS, ATP6AP2, GLIS2, PDLIM3, GDF11, SEMA3A, MZB1, KIRREL2, ASRGL1, CCDC51, SLC34A2, PDLIM5, COQ8B, HBS1L, IL17B, CCL27, INVS, SOX18, EHMT1, NLGN3, ADIPOR1, ACTB, UCP2, F3, FN1, FLT1, FLNB, FLII, FLI1, FECH, EYA1, DECR1, ETF1, ESRRG, EPOR, EPHB2, EGR1, DNMT3B, GATA3, GCG, GCNT2, GGT1, CBLIF, GLP1R, GOT1, GPT, GSN, GUCA2A, HAGH, HLA-B, HLA-DQB1, HLA-DRB1, HLF, HP, HSPG2, DLG1, DCN, TTR, APOA1, ATHS, SERPINC1, ARSL, APOH, APOC3, APOA4, ANGPT2, CYP2D6, AMBP, ALPP, AKR1B1, JAG1, ADRB1, ADD1, BMP7, VPS51, CASP6, CAT, CAV1, CD5L, CD6, CD59, CISH, CLCNKB, CCR6, COL4A6, CLDN7, CSF2, CCN2, CTNNB1, CX3CR1, IGF1, IL2, IL2RA, PTH1R, SCT, SALL1, RENBP, RELA, KDM5A, RAC1, PTHLH, CXCR1, PTGS2, PTGS1, PRTN3, MASP1, MAPK1, CTSA, CCL5, CCL20, SDC1, SDC2, SELL, SLPI, SREBF1, SREBF2, TERT, TFPI, TGFBR2, THBD, TIMP1, TIMP2, TM7SF2, TRPC5, TSC1, PLG, PLAU, PKHD1, MMP9, IL10, ILK, ISG20, ITGB1, ITGB2, KCNMB1, KIR2DS4, KNG1, KRT18, LDLR, LYZ, MBL2, MECP2, MEN1, MPV17, PIK3C3, MSH2, MSX2, COX1, COX2, MTX1, MYB, NPY, NPHS1, NPR3, OCRL, SIX6, PRKN, ENPP1, PGF, MTCO2P12
Harlequin-Type Ichthyosis Wikipedia

She died on March 3, 2017, at age 23. [28] Mason van Dyk (born 2013), despite being given a life expectancy of one to five days, was five years old as of July 2018. [29] Doctors told his mother Lisa van Dyke that he was the first case of harlequin ichthyosis in South Africa, and that she has a one-in-four chance to have another child with the disease . [30] Hunter Steinitz (born October 17, 1994) is one of only twelve Americans living with the disease and is profiled on the National Geographic "Extraordinary Humans: Skin" special. [31] Mui Thomas (born in 1992 in Hong Kong ) qualified as first rugby referee with harlequin ichthyosis. [32] A female baby born in Nagpur , India in June 2016 died after two days. ... Archived from the original on July 28, 2017 . Retrieved July 18, 2017 . ^ a b c d e f Glick, JB; Craiglow, BG; Choate, KA; Kato, H; Fleming, RE; Siegfried, E; Glick, SA (January 2017). ... Archived from the original on February 2, 2017 . Retrieved January 28, 2017 . ^ THE SNAKE SKIN WOMAN: EXTRAORDINARY PEOPLE , Channel 5, March 22, 2017. ^ Rajpopat, Shefali; Moss, Celia; Mellerio, Jemima; Vahlquist, Anders; Gånemo, Agneta; Hellstrom-Pigg, Maritta; Ilchyshyn, Andrew; Burrows, Nigel; Lestringant, Giles; Taylor, Aileen; Kennedy, Cameron; Paige, David; Harper, John; Glover, Mary; Fleckman, Philip; Everman, David; Fouani, Mohamad; Kayserili, Hulya; Purvis, Diana; Hobson, Emma; Chu, Carol; Mein, Charles; Kelsell, David; O'Toole, Edel (2011).

ABCA12, CST6, PIGA, PRSS8, SNHG31