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Hematocolpos
Wikipedia
Journal of Ultrasound in Medicine . 28 (7): 949–53. doi : 10.7863/jum.2009.28.7.949 . ... S2CID 11211408 . ^ a b c d e f g Kotter, Haleigh; Weingrow, Daniel; Canders, Caleb (2017-07-28). "Hematometrocolpos in a Pubescent Girl with Abdominal Pain" .
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Diogenes Syndrome
Wikipedia
Psychiatric Bulletin . 22 (5): 319–320. doi : 10.1192/pb.22.5.319 . ^ (01-28-2006) by Alicia M. Canto , in: "Uso y abuso de Diógenes" ^ Marcos, M; Gomez-Pellin, MC. (2008). ... External links [ edit ] 'Husband let wife starve to death' – BBC News item, Friday, 28 March 2008
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Cerebral Autosomal Recessive Arteriopathy With Subcortical Infarcts And Leukoencephalopathy
Wikipedia
. ^ a b c d e f g h i j k l m n o Carasil. (2013). Retrieved 1/28, 2015, from http://www.orpha.net/consor/cgi-bin/OC_Exp.php? ... Retrieved 2019-11-05 . ^ a b c d e Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy. (2011). Retrieved 1/28, 2015 ^ a b Devaraddi, Navalli; Jayalakshmi, G.; Mutalik, Narayan R. (2018-01-01).
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Dacryocystocele
Wikipedia
Other regions around the world should take consideration of this study in order to treat dacryocystocele effectively in their regions. [3] References [ edit ] ^ a b c "Dacryocystitis : Symptoms, Diagnosis and Management" . AIMU . 28 February 2017. ^ a b c Taylor, Roger S.; Ashurst, John V. (26 June 2020). ... Acta Otorhinolaryngologica Italica . 28 (6): 298–301. PMC 2689544 . PMID 19205594 .
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Arthrogryposis, Distal, Type 2a
Omim
Molecular Genetics Toydemir et al. (2006) screened 28 FSS probands (7 familial and 21 sporadic) for mutations in genes that encode myosin heavy chains. They found a mutation in the MYH3 gene in 26 of 28 FSS cases, including 12 with an R672H (160720.0001) mutation, 8 with an R672C (160720.0002) mutation, 3 with a de novo missense mutation not involving arg672, and 3 with a T178I (160720.0003) mutation that was also found in 2 patients with DA2B.
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Cutis Marmorata Telangiectatica Congenita
Wikipedia
"Orphanet: Cutis marmorata telangiectatica congenita" . www.orpha.net . Retrieved 28 April 2019 . ^ "OMIM Entry – 219250 – CUTIS MARMORATA TELANGIECTATICA CONGENITA; CMTC" . omim.org . ... Dermatologica. 1981;163(5):408-12. ^ Vascular Lesions and Congenital Nevi in the Newborn. UpToDate viewed on 03-28-2008 [ permanent dead link ] . ^ doctor/3295 at Who Named It?
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Distal Renal Tubular Acidosis
Wikipedia
"The Excretion of Acid in Renal Disease". QJM . 28 (110): 259–313. PMID 13658353 . ^ Walsh SB, Shirley DG, Wrong OM, Unwin RJ (2007). ... PMID 1340779 . ^ "What Ailed Tiny Tim" . Time . 1992-12-28 . Retrieved 2010-05-22 . ^ Morris RC, Sebastian A (2002).SLC4A1, ATP6V0A4, ATP6V1B1, WDR72, SLC4A4, CA2, GATA3, OSGEP, EPHA3, NCOA7, MRGPRF, SLC26A7, VAX2, RBFOX2, ALB, SLC26A4, AMH, GYPB, GYPA, FOXI1, CANX, ATP6AP1, GYPE
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Macular Dystrophy, Vitelliform, 3
Omim
To assess the frequency of peripherin/RDS mutations in the clinically heterogeneous group of adult-onset vitelliform macular dystrophies (AVMD), Felbor et al. (1997) analyzed the entire coding region of the gene in 28 unrelated German AVMD patients. They identified 5 novel mutations, including 2 presumed null mutations (see, e.g., 179605.0014 and 179605.0015). Thus, 5 (18%) of 28 AVMD patients carried point mutations in the RDS gene, suggesting that it is frequently involved in the pathogenesis of this macular disorder.
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Oculopharyngeal Muscular Dystrophy
Wikipedia
Genetics Home Reference . Retrieved 2016-05-28 . ^ a b "OMIM Entry - * 602279 - POLYADENYLATE-BINDING PROTEIN, NUCLEAR, 1; PABPN1" . www.omim.org . Retrieved 2016-05-29 . ^ https://www.ncbi.nlm.nih.gov/gene/8106 "PABPN1 poly(A) binding protein, nuclear 1 [ Homo sapiens (human) ]"]11 OCT 2014. ^ a b "Oculopharyngeal muscular dystrophy" (PDF) . Retrieved 28 May 2016 . ^ "OMIM Entry - # 164300 - OCULOPHARYNGEAL MUSCULAR DYSTROPHY; OPMD" . www.omim.org .PABPN1, LRP12, NUTM2B-AS1, GCG, PABPC1P2, BCL2L2-PABPN1, NRL, PABPC1, SACS, TNNT3, TARDBP, SIRT1, SYNM, SIRT2, OPTN, DNAJB6, GCA, BCL2, TGM2, CTNNB1, PRKAB1, PRKAA2, PRKAA1, PAX7, MLF1, LTBP3, IL6, DNAJA1, HNRNPA2B1, HNRNPA1, MSTN, FKBP1A, SOD1
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Progeria
Wikipedia
A study that compared HGPS patient cells with the skin cells from young and elderly normal human subjects found similar defects in the HGPS and elderly cells, including down-regulation of certain nuclear proteins, increased DNA damage, and demethylation of histone , leading to reduced heterochromatin . [27] Nematodes over their lifespan show progressive lamin changes comparable to HGPS in all cells but neurons and gametes . [28] These studies suggest that lamin A defects are associated with normal aging . [27] [29] Diagnosis [ edit ] Skin changes, abnormal growth, and loss of hair occur. ... S2CID 2459118 . ^ LMNA Archived 2015-12-28 at the Wayback Machine At Genes Archived 2015-12-22 at the Wayback Machine At Genetics Home Reference Archived 2019-02-04 at the Wayback Machine ^ De Sandre-Giovannoli, A.; Bernard, R; Cau, P; Navarro, C; Amiel, J; Boccaccio, I; Lyonnet, S; Stewart, CL; Munnich, A; Le Merrer, M; Lévy, N (27 June 2003). ... Archived from the original on 2017-03-28 . Retrieved 2020-05-22 . ^ a b "Learning About Progeria" . genome.gov. ... Retrieved 17 March 2008 . ^ a b "Progeria Research Foundation | The PRF Diagnostic Testing Program" . Archived from the original on 28 August 2016 . Retrieved 16 November 2011 . ^ "FDA Approves First Drug For Rare, Rapid-Aging Genetic Disorder" . ... Archived from the original on 2 December 2013 . Retrieved 28 November 2013 . ^ "In loving memory of those children who have passed away since The Progeria Research Foundation was formed in 1999" .
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Cornelia De Lange Syndrome 1
Omim
Hyperactivity was the most frequent sign associated with GER, present in 23 (85%) of the 28 patients. A spectrum of endocrinopathies may be seen in patients with BDLS (Schwartz et al., 1990). ... Selicorni et al. (2009) performed echocardiographic evaluation of 87 consecutive Italian patients referred with a diagnosis of Brachmann-de Lange syndrome and identified a cardiac anomaly in 29 (33.3%) of the patients, including 28 with a structural anomaly and 1 with isolated nonobstructive CMH (see 192600). Of the 28 patients with a structural anomaly, 12 (42.9%) had an isolated defect, including 10 (36%) with pulmonary stenosis and 8 (28.6%) with an isolated left-to-right shunt. The single most common lesion was valvular pulmonary stenosis, which was present in 11 (39%) of 28 patients. Isolated late-onset mild to moderate mitral or tricuspid valve regurgitation was detected at follow-up examination in 4 patients (14.3%) older than 10 years, who had a previously normal examination and electrocardiogram. ... Genotype/Phenotype Correlations Yan et al. (2006) identified 13 different NIPBL mutations, including 11 novel mutations, in 13 (46%) of 28 Polish patients with a clinical diagnosis of CDLS.NIPBL, RAD21, HDAC8, SMC3, SMC1A, BRD4, KMT2A, SETD5, PDS5A, ATR, LZTR1, SOS1, RIT1, RAF1, PTPN11, KRAS, CENPJ, CEP63, GPT, CREBBP, ESCO2, NAALADL2, TNKS, MAU2, PHIP, EPS15L1, GALNT14, DYM, GSC, ANKRD11, AFF4, ARSD, PDS5B, STAG2, CTCF, STAG1, CHRD, SHOX2, MYC, HDAC2, GRM1, GH1, FOXF1, EP300, DDX11, CRABP2, CARS1, NIPBL-DT
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Vitiligo
Wikipedia
It tends to affect areas of skin that are associated with dorsal roots from the spinal cord and is most often unilateral. [1] [24] It is much more stable/static in course and its association with autoimmune diseases appears to be weaker than that of generalized vitiligo. [24] SV does not improve with topical therapies or UV light, however surgical treatments such as cellular grafting can be effective. [10] Differential diagnosis [ edit ] Chemical leukoderma is a similar condition due to multiple exposures to chemicals. [25] Vitiligo however is a risk factor. [25] Triggers may include inflammatory skin conditions, burns, intralesional steroid injections and abrasions. [26] Other conditions with similar symptoms include the following: Pityriasis alba Tuberculoid leprosy Postinflammatory hypopigmentation Tinea versicolor [23] Halo nevus Albinism Piebaldism [23] Idiopathic guttate hypomelanosis [23] Progressive macular hypomelanosis [23] Primary adrenal insufficiency Treatment [ edit ] There is no cure for vitiligo but several treatment options are available. [1] The best evidence is for applied steroids and the combination of ultraviolet light in combination with creams. [27] Due to the higher risks of skin cancer, the United Kingdom's National Health Service suggests phototherapy be used only if primary treatments are ineffective. [28] Lesions located on the hands, feet, and joints are the most difficult to repigment; those on the face are easiest to return to the natural skin color as the skin is thinner in nature. [1] Immune mediators [ edit ] Topical preparations of immune suppressing medications including glucocorticoids (such as 0.05% clobetasol or 0.10% betamethasone) and calcineurin inhibitors (such as tacrolimus or pimecrolimus ) are considered to be first-line vitiligo treatments. [1] Phototherapy [ edit ] Phototherapy is considered a second-line treatment for vitiligo. [1] Exposing the skin to light from UVB lamps is the most common treatment for vitiligo. ... Because of the high doses of UVA and psoralen, PUVA may cause side effects such as sunburn-type reactions or skin freckling. [28] Narrowband ultraviolet B (NBUVB) phototherapy lacks the side-effects caused by psoralens and is as effective as PUVA. [1] As with PUVA, treatment is carried out twice weekly in a clinic or every day at home, and there is no need to use psoralen. [28] Longer treatment is often recommended, and at least 6 months may be required for effects to phototherapy. [31] NBUVB phototherapy appears better than PUVA therapy with the most effective response on the face and neck. [31] With respect to improved repigmentation: topical calcineurin inhibitors plus phototherapy are better than phototherapy alone, [32] hydrocortisone plus laser light is better than laser light alone, gingko biloba is better than placebo , and oral mini-pulse of prednisolone (OMP) plus NB-UVB is better than OMP alone. [8] Skin camouflage [ edit ] In mild cases, vitiligo patches can be hidden with makeup or other cosmetic camouflage solutions. ... Depigmentation takes about a year to complete. [28] History [ edit ] Descriptions of a disease believed to be vitiligo date back to a passage in the medical text Ebers Papyrus c. 1500 BCE in ancient Egypt . ... Seminars in Cutaneous Medicine and Surgery . 28 (2): 86–92. doi : 10.1016/j.sder.2009.04.008 .
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Epilepsy
Wikipedia
An example of this type is the absence seizure , which presents as a decreased level of consciousness and usually lasts about 10 seconds. [2] [25] Focal seizures are often preceded by certain experiences, known as auras . [26] They include sensory (visual, hearing, or smell), psychic, autonomic, and motor phenomena. [2] Jerking activity may start in a specific muscle group and spread to surrounding muscle groups in which case it is known as a Jacksonian march . [27] Automatisms may occur, which are non-consciously-generated activities and mostly simple repetitive movements like smacking of the lips or more complex activities such as attempts to pick up something. [27] There are six main types of generalized seizures: tonic-clonic , tonic , clonic , myoclonic , absence and atonic seizures . [28] They all involve loss of consciousness and typically happen without warning. ... These include depression , anxiety , obsessive–compulsive disorder (OCD), [40] and migraine . [41] Attention deficit hyperactivity disorder affects three to five times more children with epilepsy than children without the condition. [42] ADHD and epilepsy have significant consequences on a child's behavioral, learning, and social development. [43] Epilepsy is also more common in children with autism . [44] Causes [ edit ] See also: Causes of seizures Epilepsy can have both genetic and acquired causes, with interaction of these factors in many cases. [45] Established acquired causes include serious brain trauma, stroke, tumours and problems in the brain as a result of a previous infection . [45] In about 60% of cases the cause is unknown. [24] [29] Epilepsies caused by genetic , congenital , or developmental conditions are more common among younger people, while brain tumors and strokes are more likely in older people. [24] Seizures may also occur as a consequence of other health problems; [28] if they occur right around a specific cause, such as a stroke, head injury, toxic ingestion or metabolic problem, they are known as acute symptomatic seizures and are in the broader classification of seizure-related disorders rather than epilepsy itself. [46] [47] Genetics [ edit ] Genetics is believed to be involved in the majority of cases, either directly or indirectly. [13] Some epilepsies are due to a single gene defect (1–2%); most are due to the interaction of multiple genes and environmental factors. [13] Each of the single gene defects is rare, with more than 200 in all described. [48] Most genes involved affect ion channels , either directly or indirectly. [45] These include genes for ion channels themselves, enzymes , GABA , and G protein-coupled receptors . [31] In identical twins , if one is affected there is a 50–60% chance that the other will also be affected. [13] In non-identical twins the risk is 15%. [13] These risks are greater in those with generalized rather than focal seizures. [13] If both twins are affected, most of the time they have the same epileptic syndrome (70–90%). [13] Other close relatives of a person with epilepsy have a risk five times that of the general population. [49] Between 1 and 10% of those with Down syndrome and 90% of those with Angelman syndrome have epilepsy. [49] Acquired [ edit ] Epilepsy may occur as a result of a number of other conditions including tumors, strokes , head trauma, previous infections of the central nervous system , genetic abnormalities, and as a result of brain damage around the time of birth. [28] [29] Of those with brain tumors, almost 30% have epilepsy, making them the cause of about 4% of cases. [49] The risk is greatest for tumors in the temporal lobe and those that grow slowly. [49] Other mass lesions such as cerebral cavernous malformations and arteriovenous malformations have risks as high as 40–60%. [49] Of those who have had a stroke, 2–4% develop epilepsy. [49] In the United Kingdom strokes account for 15% of cases and it is believed to be the cause in 30% of the elderly. [24] [49] Between 6 and 20% of epilepsy is believed to be due to head trauma. [49] Mild brain injury increases the risk about two-fold while severe brain injury increases the risk seven-fold. [49] In those who have experienced a high-powered gunshot wound to the head, the risk is about 50%. [49] Some evidence links epilepsy and celiac disease and non-celiac gluten sensitivity , while other evidence does not. ... Seizure threshold is lowered in epilepsy. [59] In epileptic seizures a group of neurons begin firing in an abnormal, excessive, [24] and synchronized manner. [2] This results in a wave of depolarization known as a paroxysmal depolarizing shift . [62] Normally, after an excitatory neuron fires it becomes more resistant to firing for a period of time. [2] This is due in part to the effect of inhibitory neurons, electrical changes within the excitatory neuron, and the negative effects of adenosine . [2] Focal seizures begin in one hemisphere of the brain while generalized seizures begin in both hemispheres. [28] Some types of seizures may change brain structure, while others appear to have little effect. [63] Gliosis , neuronal loss, and atrophy of specific areas of the brain are linked to epilepsy but it is unclear if epilepsy causes these changes or if these changes result in epilepsy. [63] Diagnosis [ edit ] An EEG can aid in locating the focus of the epileptic seizure. ... Identifying an epilepsy syndrome is useful as it helps determine the underlying causes as well as what anti-seizure medication should be tried. [28] [70] The ability to categorize a case of epilepsy into a specific syndrome occurs more often with children since the onset of seizures is commonly early. [47] Less serious examples are benign rolandic epilepsy (2.8 per 100,000), childhood absence epilepsy (0.8 per 100,000) and juvenile myoclonic epilepsy (0.7 per 100,000). [47] Severe syndromes with diffuse brain dysfunction caused, at least partly, by some aspect of epilepsy, are also referred to as epileptic encephalopathies. ... Melatonin , as of 2016 [update] , is insufficiently supported by evidence. [125] The trials were of poor methodological quality and it was not possible to draw any definitive conclusions. [125] Prognosis [ edit ] Deaths due to epilepsy per million persons in 2012 0–7 8–10 11–13 14–17 18–21 22–28 29–37 38–67 68–100 101–232 Epilepsy cannot usually be cured, but medication can control seizures effectively in about 70% of cases. [7] Of those with generalized seizures, more than 80% can be well controlled with medications while this is true in only 50% of people with focal seizures. [5] One predictor of long-term outcome is the number of seizures that occur in the first six months. [24] Other factors increasing the risk of a poor outcome include little response to the initial treatment, generalized seizures, a family history of epilepsy, psychiatric problems, and waves on the EEG representing generalized epileptiform activity. [126] In the developing world, 75% of people are either untreated or not appropriately treated. [29] In Africa, 90% do not get treatment. [29] This is partly related to appropriate medications not being available or being too expensive. [29] Mortality [ edit ] People with epilepsy are at an increased risk of death. [127] This increase is between 1.6 and 4.1 fold greater than that of the general population. [128] The greatest increase in mortality from epilepsy is among the elderly. [128] Those with epilepsy due to an unknown cause have little increased risk. [128] Mortality is often related to: the underlying cause of the seizures, status epilepticus , suicide , trauma , and sudden unexpected death in epilepsy (SUDEP). [127] Death from status epilepticus is primarily due to an underlying problem rather than missing doses of medications. [127] The risk of suicide is between 2 and 6 times higher in those with epilepsy; [129] [130] the cause of this is unclear. [129] SUDEP appears to be partly related to the frequency of generalized tonic-clonic seizures [131] and accounts for about 15% of epilepsy-related deaths; [126] it is unclear how to decrease its risk. [131] In the United Kingdom, it is estimated that 40–60% of deaths are possibly preventable. [24] In the developing world, many deaths are due to untreated epilepsy leading to falls or status epilepticus. [18] Epidemiology [ edit ] Epilepsy is one of the most common serious neurological disorders [132] affecting about 39 million people as of 2015 [update] . [8] It affects 1% of the population by age 20 and 3% of the population by age 75. [16] It is more common in males than females with the overall difference being small. [18] [47] Most of those with the disorder (80%) are in low income populations [133] or the developing world . [29] The estimated prevalence of active epilepsy (as of 2012 [update] ) is in the range 3–10 per 1,000, with active epilepsy defined as someone with epilepsy who has had a least one unprovoked seizure in the last five years. [47] [134] Epilepsy begins each year in 40–70 per 100,000 in developed countries and 80–140 per 100,000 in developing countries. [29] Poverty is a risk and includes both being from a poor country and being poor relative to others within one's country. [18] In the developed world epilepsy most commonly starts either in the young or in the old. [18] In the developing world its onset is more common in older children and young adults due to the higher rates of trauma and infectious diseases. [18] In developed countries the number of cases a year has decreased in children and increased among the elderly between the 1970s and 2003. [134] This has been attributed partly to better survival following strokes in the elderly. [47] History [ edit ] See also: On the Sacred Disease Hippocrates, 17th century engraving by Peter Paul Rubens of an antique bust The oldest medical records show that epilepsy has been affecting people at least since the beginning of recorded history. [135] Throughout ancient history , the disease was thought to be a spiritual condition. [135] The world's oldest description of an epileptic seizure comes from a text in Akkadian (a language used in ancient Mesopotamia ) and was written around 2000 BC. [22] The person described in the text was diagnosed as being under the influence of a moon god, and underwent an exorcism . [22] Epileptic seizures are listed in the Code of Hammurabi (c. 1790 BC) as reason for which a purchased slave may be returned for a refund, [22] and the Edwin Smith Papyrus (c. 1700 BC) describes cases of individuals with epileptic convulsions. [22] The oldest known detailed record of the disease itself is in the Sakikku , a Babylonian cuneiform medical text from 1067–1046 BC. [135] This text gives signs and symptoms, details treatment and likely outcomes, [22] and describes many features of the different seizure types. [135] As the Babylonians had no biomedical understanding of the nature of disease, they attributed the seizures to possession by evil spirits and called for treating the condition through spiritual means. [135] Around 900 BC, Punarvasu Atreya described epilepsy as loss of consciousness; [136] this definition was carried forward into the Ayurvedic text of Charaka Samhita (about 400 BC). [137] The ancient Greeks had contradictory views of the disease.SCN8A, GRIN2B, SLC12A5, PCDH19, ABCB1, SLC6A1, CACNA2D2, SCN1A, SCN2A, NPY, POLG, SLC1A2, PRRT2, KCNQ2, CDKL5, STXBP1, TSC1, TSC2, CHD2, CNTNAP2, MECP2, BDNF, GABRG2, GFAP, GRIN2A, HCN1, GABRB3, SYNGAP1, IQSEC2, GNAO1, SMC1A, MEF2C, AKT1, SCN9A, SLC12A2, FOXG1, POMC, UBE3A, SLC1A1, GABRB2, GRM1, SLC35A2, KCNH1, ALB, FLNA, STX1B, DNM1, EEF1A2, WDR45, KDM5C, TGFB1, NEXMIF, HNRNPU, SLC4A10, FGFR3, CACNB4, SLC1A3, FOS, DDX3X, NPY2R, KCNAB2, PIGH, CHRM2, GPX1, KCND2, STAMBP, PURA, FOSB, KCNH5, EIF2S3, DYRK1A, GLUD1, PCDH12, RARS2, ZDHHC9, ALG13, RAB39B, LMAN2L, ARID1B, ASXL3, TANC2, SLC5A6, SPARCL1, CERT1, L2HGDH, SETD1A, EIF2A, SELENOW, TXNRD1, AGMO, SNAP25, ASTN1, LGI1, CHRM1, GAD2, ACTG1, PIGQ, P2RX4, IL1B, IL6, ILK, AUTS2, ANKRD11, ADRA2A, ERN1, FOLR1, VDAC2, VDAC1, KCNT2, EARS2, OPRD1, OPRM1, P2RX2, TNF, KCNA1, GRIA1, SYN2, ALDH5A1, NR1I2, MAPT, GAPDH, CDYL, SIRT1, S100B, RGS4, GRM8, RELA, CAMK2D, TH, PPIA, CAPN1, HES1, NF2, MIF, SLCO1A2, C1QA, SLC2A1, BDKRB1, BECN1, BSN, BDKRB2, BCL2L2, ATP1A2, BMP4, SLC13A5, ATP1A3, MTR, CPA6, CAMSAP2, TBCK, WDR37, HDAC9, TSHR, CHRM3, COTL1, LINC02109, KCNJ10, DIAPH1, AMPD2, SCN1A-AS1, PIK3CA, TUBA3E, C12orf57, BBS1, P2RX7, ARX, TBC1D9, EFHC1, HMGB1, TSEN15, KCNQ3, HTC2, PTPN23, IQCM, MTHFR, CACNA1A, CEP128, MTOR, DMBX1, EPHB1, SYT2, COX3, PCDHB4, HLA-B, INO80, SCN3A, SEC24D, DEPDC5, DCX, KCNT1, UBE4A, TBC1D24, GRIA2, SV2A, GAD1, CHRNA4, OLFML3, C9orf92, ABCC2, MATN4, KMT2E, APOE, CRAMP1, ZDHHC24, BCO2, PTPRD, PEX5, OTUD6B, PTGS2, MAST4, LINC00558, ARFGEF2, CYP2C9, CYP2C19, UGT2B7, PIK3CB, PIK3CG, KCNJ11, GABRA1, PIK3CD, SCN1B, GLUL, SYN1, TLR4, FMR1, PVALB, ADK, NRXN1, HSPA4, ABCG2, PTEN, IL1A, MIR146A, MIR134, IDH1, SRPX2, NFE2L2, KCNMA1, PTPN4, PAFAH1B1, GRM2, SLC12A3, RBFOX1, WWOX, ARSD, GABBR1, ARHGEF9, EPHX1, LRP2, MCF2L, TSPO, CSTB, ABCB6, GPHN, TESC, GJA1, TAC1, KCNH2, MALAT1, REST, HIF1A, RELN, PRNP, FOXP2, COX2, MMP9, PRICKLE1, LETM1, LEP, SOD2, MTCO2P12, CLCN2, DMD, CYP3A5, BRAF, CNR1, MBD5, UGT1A4, GABRD, TPP1, GRM5, VEGFA, GAL, AZGP1, UGT1A6, PNPO, IL10, LGI2, MAPK1, KCNQ1, ALDH7A1, GABPA, TWNK, CRP, FAM20C, CYP3A4, MIR21, MIR155, PCDH10, SMUG1, GRIN1, EPHB2, SZT2, HCN2, KCNA2, ZEB2, ABCC1, PLPBP, NEDD4L, ACHE, KCNB1, PCMT1, LTBP3, RASGRF1, CLN8, REN, CYP2D6, EPO, CYP2C18, RBFOX3, PPP3CA, PTH, PSEN1, SHANK3, DLG4, EGR1, MYD88, APP, AGER, PLCG1, NHS, NTRK2, AQP4, ADGRV1, CHRNA2, CYP2B6, PIGN, HCAR1, CACNA1H, CHRNA7, PANX1, CDK5, PPIG, CD34, CLCN4, PLCB1, CACNA2D1, CASP3, CAMK4, FARS2, RALBP1, TNFSF14, NPRL3, CCL2, SRF, VARS2, CSF2, SLC6A4, SLC6A8, SOX2, SPAST, STAT3, EPM2A, CREB1, TFPI, BAD, VDR, VIM, VIP, LAMC2, RPS19, GSK3B, GRIK2, GRM7, GRIA3, KCND3, C20orf181, GRM3, GABRA2, MIR145, MIR132, MIR106B, GRM4, KCNQ4, WAS, SYNJ1, PLXNA1, VRK2, CELF4, GRIK1, SGCE, RGMA, SLC6A12, CSF1R, NARS2, FGF13, CACNA1G, CHRNB2, APOBEC1, ADGRG1, SMS, BACE1, IL17A, SLC22A1, GCG, CMA1, PDGFB, FRRS1L, PDPK1, KIF4A, SLC6A3, KCNQ5, PHF6, PIGA, SLA2, FGF12, IL4, SPDEF, SLC16A1, PART1, MIR196B, HSP90AA1, CDH1, PRL, IDH2, KLHL1, BRD2, RORA, RORB, RPL10, MCTS1, HSP90AB1, BCL2, GLRA3, FN1, ACSM3, GJD2, NUFIP2, CLU, SCN2B, CTSD, SHROOM4, SCN5A, NR3C1, SGSM3, IGF1, PTGS1, DECR1, PDXP, SUCLA2, MIR187, SYCE1L, ADAM23, SLC4A3, IGHE, DBH, MAGEE1, CLCN1, TUBA1A, SLC17A6, TRPV4, HPGDS, JRK, GABRA6, MCAT, PAK3, ZFYVE9, NRG1, COX1, SAMD12, MARS1, MDM4, CNKSR2, CALCA, MEF2A, UCA1, CALB2, TCF4, GSTM1, TAT, SETD1B, TMTC3, CALB1, TAP1, STRADA, SIK1, SYT1, MSH3, MAP6, MARCHF1, KCNC1, ATP7A, TP53, KCNK3, LIAS, ESR1, TRPM2, ADAM10, KNG1, TLR3, TK2, TOMM40, ADORA1, THBS1, COMT, TUBB2A, COX8A, HCA1, ADAM22, GSTM2, CYFIP1, GRIN2D, SYP, NGF, ALPL, SCARB2, CLOCK, DBA2, FCMTE2, SPTAN1, SRI, PTGES, UCHL1, GNAQ, SST, GDNF, SOD1, IDO1, JAG1, TLE5, TRNK, FAME3, ABCC5, OTX1, DRD2, KCNK9, SOS1, CACNA1D, MVP, STX1A, SNCA, TSPEAR, BCHE, PIK3R4, NANS, KCNIP3, DUOX1, RMDN1, KCNK10, DUOX2, BCL11A, PTOV1, IER3IP1, NDUFA13, SLC45A1, TLR7, CCR2, EJM2, BBS4, SUCO, ISYNA1, FCMTE1, LGSN, ATL1, EXOSC3, PIGT, OPN1MW2, NHLRC1, UBQLN1, PACS2, EMC1, POGZ, CIC, PSC, MAPK8IP3, PMPCA, RHOBTB2, CACNA1S, CACNA1E, SIRT3, SMG6, SATB2, CUX2, PPR1, MICA, SYNM, PUM2, CRTC1, KDM1A, SV2C, ARHGEF15, NTNG1, ABCA1, AP3M2, SLC27A4, GTF2A1L, STON1, ZWINT, ABCA2, OPN1MW3, PSIP1, PGR-AS1, KLK8, ABR, SLCO2B1, PARK7, GABARAP, SYNPO, PHLDA1, CACNA1C, CACNA1B, ALG6, CNTN6, FECD2, SMOX, FOXD3, SIGLEC7, LAT, SND1, FOXP1, ACADS, BCL9, SLC35A3, APEX2, BHLHE22, DESI1, REM1, SETD2, ZDHHC8, MIR147B, EEF2K, NPTN, ELP4, GREM1, PHGDH, BRD4, ZFYVE26, RBFOX2, ATP6V0A2, LINC01672, ECT, SLC7A11, FTX, FTSJ1, MIR1183, SHC2, PRDX5, DCAF13, CAPN5, PARS2, BNIP3, BCS1L, TREM2, RNASE12, TMCO1, MIR181C, PIGM, TRMT10A, ANXA1, CADPS2, ANK2, AMT, ASIC2, ALOX15, ABCD1, AGTR2, NLRP3, MIR155HG, TNFRSF13C, NUS1, AGTR1, GRIN3B, NIPA1, SEZ6, HSPB6, TIMM50, ZNF804A, KCNH7, UQCC2, MIR16-1, MIR15A, TMX1, NIPA2, CCM2, APLP1, SNX25, APBA2, NKX6-2, SLC25A21, NTNG2, SPZ1, TMEM25, SLC7A3, MIR149, WDR73, CNTNAP4, CHRFAM7A, SLC44A3, MIR141, AFM, ADCYAP1, ADORA2A, CALHM1, NPAS4, NEAT1, KANSL1, PIGW, ELFN1, SLC9A9, STON1-GTF2A1L, SLC35F1, CELIAC5, CPP, ADARB1, TGM6, ACP1, COL6A4P1, ADA, ZACN, ACR, BRAT1, ACMSD, PWAR1, MPLKIP, SLC32A1, TRPM6, RSS, OR2AG1, ADRA2B, ADRA1D, MIR125A, RMDN2, ZSCAN25, KCTD7, SLC35G1, LGI4, PRICKLE2, KCNV2, PARP1, PRSS55, C9orf72, COL18A1, SRCIN1, MIR597, TARS2, SCN3B, ATP6V1A, ACTB, ANKH, TARP, PANX2, SLC2A4RG, ATM, MIR323A, COQ8A, MIR34C, MIR30A, SLC17A7, ATF3, ZFHX3, TIGAR, GOPC, CHMP1B, ASCL1, ERMARD, MIR378A, MIR499A, CNNM2, UGT1A9, ATRX, MIR421, UGT1A3, PDP1, LEPROT, FBLIM1, MIR542, ATP6V1B2, PACS1, RMDN3, RHOT1, CHDH, FOXRED1, CHD7, MT1XP1, SYBU, MIR487A, MIR27A, ABHD6, ASAH1, MIR183, GORASP1, MICAL1, P2RY12, NDRG4, WNK1, WNK3, LRFN4, TRPM8, FTO, IRF2BPL, SLC52A2, HSPBAP1, TBL1XR1, SLC25A22, AQP1, APRT, TRPM3, SPG11, NSD1, ABCG4, ARSA, EHMT2, PHOX2A, HECW2, AR, SORCS2, NLGN2, MIR23A, AQP6, MIR212, MIR211, NAPB, MIR206, MIR203A, CACHD1, TRIB3, CREBZF, MIR200C, PRM3, GAS5, FASTK, GHRH, PNPLA6, DRD4, NRAS, NSF, NT5E, NTF3, NTRK1, NUP98, NR4A2, ODC1, OPHN1, OPRK1, CCN3, OPRL1, DPYSL3, DPYSL2, P4HB, DPP4, PAM, PAX3, PAX6, PCDH7, DSCAM, ECM1, PDHA1, RNR1, MOG, MPO, MST1, EGR3, CYTB, MTHFD1, EGFR, ND6, EFNB3, MTRR, NOS3, MUSK, NEFL, NEUROD1, EEF2, EEF1B2P2, NFKB1, NGFR, NNMT, NONO, PCP4, PDYN, ELAVL2, PTCH1, PRKCD, PRKG2, MAPK8, MAPK10, PRODH, PROS1, PRS, DDIT3, TAS2R38, ACE, PRKCA, PTHLH, DAPK1, DAP, DAG1, CYP19A1, PVT1, QARS1, MOK, RAN, PRKCB, PTPA, CFP, PLA2G4A, DXO, PHEX, SERPINB6, DNMT3A, DNAH8, DLX2, DLX1, PITX2, PLA2G1B, PLAT, PPP1CB, PLAU, PLN, PLP1, DLG3, POU2F1, PPARA, PPARG, MED1, DHCR24, ALDH6A1, MMP3, RET, HSPB1, GABRA4, HIP1, HK1, HLA-A, GABRA3, HNF4A, HOXD@, FYN, FOSL2, HSPB2, HCRT, HSPG2, HTR1A, HTR2A, ICAM1, AFF2, IDS, IFNG, IGFALS, RBPJ, HDAC2, HCLS1, IL1RN, FFAR1, GLI3, GLO1, GLP1R, GLRA1, GLRA2, GLRB, GFER, GLUD2, OPN1MW, GRK5, GSTT1, GC, GAP43, GRIA4, GRIK4, GALR1, GABRR2, GRIN2C, GABRA5, CXCL1, FGFR1, IL2, MMP2, LPL, KRT10, LAIR1, LAMB1, EPRS1, LEPR, LIFR, LMNA, LNPEP, LPA, CAPRIN1, KRAS, ME2, EPHA3, ENO2, MFAP1, MGAT1, ELN, KMT2A, MLLT3, FOXO4, KRT5, KIF22, IL2RB, PTK2B, CXCR2, IL13, FEB1, INS, INSR, ITGA5, JUN, JUNB, JUND, FABP7, KIF5C, F9, F2R, KCNJ6, F2, EXT1, KCNK2, ESR2, ERBB4, KIF5A, RARRES2, RPS27A, CPLX1, PDLIM7, SLC28A1, SCAF11, ARHGEF2, SLC16A7, SLC33A1, HACD1, CHI3L1, MSC, CDX2, SLC9A3R2, GJB2, KL, NRXN3, ADIPOQ, CDK1, CD68, HOMER1, PICK1, ABCG1, CD38, AIFM1, HSPB3, CD36, KCNK5, GEMIN2, DGKE, DEGS1, KHSRP, TNFSF11, NPFF, RTCA, RNASET2, AKR1C3, NAPA, WASL, CLC, DPM2, NRP2, AP2M1, CFLAR, CISH, PHOX2B, TOP3B, AP3D1, RAPGEF2, HDAC4, CUL4B, CASP8, LAMC3, CACNG2, TUBA1B, TUBB3, RACK1, HAX1, FST, CAP1, DEAF1, ARFGEF1, MARCHF6, SORBS1, NPRL2, CAMKK2, TNFSF13B, GNB5, OGA, RAI1, CHL1, NES, MMDK, BCKDK, KEAP1, HCN4, DNAJC6, ELMO1, GAB2, MAGI2, FIG4, SV2B, KRIT1, SLC12A6, AKT3, RUNX2, CNKSR1, DNM1L, ABCC9, PQBP1, CAT, ARPC2, ATP6AP2, DHRS9, TNK2, CASP9, SEMA7A, RECK, RYR2, CRIP1, SLC6A13, SLC8A1, SLC8A3, SLC9A1, SLC12A1, SLC18A2, SLC18A3, SLC20A2, CRIP2, ABAT, SLC6A9, SOX11, SP1, SSTR1, CREBBP, VAMP2, CPT1A, CPA1, CP, TACR1, SLC6A11, SLC5A2, TCF3, CUX1, S100A10, TSPAN31, SC5D, CYP1A2, CYP1A1, CYBB, CX3CR1, SCN4A, SCN7A, SCNN1D, CSNK1E, CTNND2, SGK1, SH3GL2, SHBG, SHMT1, ST3GAL3, CTNNB1, CTAA1, CSNK2B, CNTN2, TCOF1, PLA2G6, CLTC, UGT1A, PLK3, UGT2B15, UGT8, NR1H2, UROD, VARS1, VCAM1, VCP, BEST1, UCP2, TRPV1, YWHAG, KCNAB1, BAG6, CCDC6, KMT2D, ST8SIA2, SLC7A5, CLCN7, CNN3, UBTF, TERT, TPO, TFCP2, TGIF1, NKX2-1, TLE4, COL4A5, TRAPPC10, COL4A1, TNFRSF1B, TP73, CRISP2, CNP, TRAF1, TRH, TRIO, TRPC5, COL2A1, COL1A1, CNR2, TUBG1, UBC, A1BG
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Abortion In Poland
Wikipedia
U.S. News & World Report . Retrieved 28 October 2020 . ^ Abortion Policies: A Global Review . ... Retrieved 24 October 2020 . ^ Hloušek, Vít; Kopeček, Lubomír (2010), Origin, Ideology and Transformation of Political Parties: East-Central and Western Europe Compared , Ashgate, p. 196 ^ Nodsieck, Wolfram, "Poland" , Parties and Elections in Europe , retrieved 28 March 2012 ^ "Sejm rejects citizens' initiative to ban abortion" . ... Retrieved 6 July 2015 . ^ "Central and Eastern Europe | Final Topline | Religious Belief and National Belonging in Central and Eastern Europe" (PDF) . Pew Research Center . Retrieved 28 October 2020 . ^ Zakolska, Olga (18 August 2020). ... Retrieved 31 October 2020 . ^ a b Hirvonen, Ewa (28 November 2017). "Polish Abortion Tourism" (PDF) . ... "As Poland mulls new abortion bill, women head to Germany" . CNN . Retrieved 28 October 2020 . ^ Cocotas, Alex (30 November 2017).
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Pornography Addiction
Wikipedia
Specifically, the World Health Organization (WHO) wrote: "Based on the limited current data, it would therefore seem premature to include [pornography viewing] in ICD-11." [24] Introductory psychology textbook authors Coon, Mitterer and Martini, passingly mentioning NoFap , speak of pornography as a "supernormal stimulus" but use the model of compulsion rather than addiction. [25] Treatment [ edit ] Cognitive-behavioral therapy has been suggested as a possible effective treatment for pornography addiction based on its success with internet addicts , though no clinical trials have been performed to assess effectiveness among pornography addicts as of 2012. [26] Acceptance and commitment therapy has also been shown to be a potentially effective treatment for problematic internet pornography viewing. [5] Online pornography [ edit ] See also: Internet addiction disorder § Internet addiction and pornography Some clinicians and support organizations recommend voluntary use of Internet content-control software , internet monitoring , or both, to manage online pornography use. [27] [28] [29] Sex researcher Alvin Cooper and colleagues suggested several reasons for using filters as a therapeutic measure, including curbing accessibility that facilitates problematic behavior and encouraging clients to develop coping and relapse prevention strategies. [27] Cognitive therapist Mary Anne Layden suggested that filters may be useful in maintaining environmental control. [29] Internet behavior researcher David Delmonico stated that, despite their limitations, filters may serve as a "frontline of protection." [28] Medications [ edit ] See also: Behavioral addiction § Treatment Studies of those with non-paraphilic expressions of hypersexuality have hypothesized that various mood disorders, as defined in the DSM, may occur more frequently in sexually compulsive men. [30] [31] [32] Compulsive sexual behavior has been treated with antidepressants including SSRIs and serotonin-norepinephrine reuptake inhibitors, naltrexone , a medication used to inhibit reward mechanisms in opiate or alcohol addictions, other mood-stabilizers, and anti-androgens . ... May 27, 2014. Archived from the original on May 28, 2014. ^ ABC News (2016-02-25). "Terry Crews Says Porn Addiction Nearly Ruined His Life" . ... v=5kvzamjQW9M ^ "Hot Girls Wanted" . ^ Corriston, Michele (December 28, 2014). "Chris Rock & Wife Malaak Compton-Rock Split" . People . Retrieved December 28, 2014 . ^ Bitette, Nicole (August 23, 2016).
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Allergic Bronchopulmonary Aspergillosis
Wikipedia
There are challenges involved in long-term therapy with corticosteroids—which can induce severe immune dysfunction when used chronically, as well as metabolic disorders—and approaches have been developed to manage ABPA alongside potential adverse effects from corticosteroids. [27] [28] The most commonly described technique, known as sparing, involves using an antifungal agent to clear spores from airways adjacent to corticosteroid therapy. ... Newer triazole drugs—such as posaconazole or voriconazole —have not yet been studied in-depth through clinical trials in this context. [27] [28] Whilst the benefits of using corticosteroids in the short term are notable, and improve quality of life scores, there are cases of ABPA converting to invasive aspergillosis whilst undergoing corticosteroid treatment. ... Metabolic disorders, such as diabetes mellitus and osteoporosis , can also be induced. [27] [28] In order to mitigate these risks, corticosteroid doses are decreased biweekly assuming no further progression of disease after each reduction. ... The exception to this rule is patients who are diagnosed with advanced ABPA; in this case, removing corticosteroids almost always results in exacerbation and these patients are continued on low-dose corticosteroids (preferably on an alternate-day schedule). [27] [28] Serum IgE can be used to guide treatment, and levels are checked every 6–8 weeks after steroid treatment commences, followed by every 8 weeks for one year. ... Chest X-ray or CT scans are performed after 1–2 months of treatment to ensure infiltrates are resolving. [27] [28] Epidemiology [ edit ] There are limited national and international studies into the burden of ABPA, made more difficult by a non-standardized diagnostic criteria.
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Abortion In Missouri
Wikipedia
Nick Schroer . [25] On January 30, 2019, HB 126 was referred to the Children and Families Committee, and on February 12, 2019, a public hearing on the bill was completed. [26] On February 21, 2018, HB 126 was voted out of committee to the full House with the recommendation that it "do pass." [27] [28] On February 27, 2019, HB 126 was passed out of the Missouri House and was sent to the state Senate. [29] Missouri's House Speaker Elijah Haahr has said he supports the “heartbeat bill” calling it a top priority for the 2019 session. [30] [31] When asked if he would sign a fetal heartbeat bill, Governor Mike Parson said, "I’ve been pro-life my entire career, and I support that all the time." [32] At the time the bill passed, only 25% of the state legislators were female. [33] In March 2019, Missouri Family Health Council was the state's only Title X administrator. ... Only about 10% of their operations were related to abortion services. [20] On May 28, 2019, the sole remaining abortion clinic in Missouri announced it would likely be shutting down by the end of the week as the state pulled its operating license. ... The rules committee met Thursday morning. ^ Associated Press (February 28, 2019). "MO House passes fetal heartbeat bill; legislation moves to the Senate" . ABC 7 - KHQA . Retrieved February 28, 2019 . ^ Ballentine, Summer (February 14, 2019). ... Retrieved 2019-05-23 . ^ "Missouri's last abortion clinic says it may lose its license this week" . www.cbsnews.com . Retrieved 2019-05-28 . ^ a b c "Text-Only NPR.org: Missouri's Last Abortion Provider Wins Reprieve, As Judge Rules Against State" . text.npr.org .
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Hpv-Positive Oropharyngeal Cancer
Wikipedia
Phenotypic variants include basaloid squamous carcinoma , a high grade form ( see Chung Fig. 35-3(C) [28] and illustration here). They are most commonly non-keratinising. ... This suggests that the oncogenic alterations produced by the virus are spatially limited rather than related to a field defect. [29] [28] [30] Anatomy [ edit ] Anatomy of oropharynx and surrounding structures The oropharynx , at the back of the mouth , forms a circle and includes the base of the tongue (posterior third) below, the tonsils on each side, and the soft palate above, together with the walls of the pharynx , including the anterior epiglottis , epiglottic valleculae and branchial cleft at its base. ... Relative to HPV-OPC, the oncogenic molecular progression of HPV+OPC is poorly understood. [28] The two main viral oncoproteins of the high risk HPV types are E6 and E7. ... They bind to and inactivate the best known of these mechanisms, the tumor suppressor proteins p53 and retinoblastoma protein pRB (pRb) leading to genomic instability and then cell cycle deregulation ( see Chung et al., 2016 Fig. 35.2). [28] Further, yet to be elicited, mechanisms are required for the final steps of malignant transformation of HPV infected cells. [28] HPV- and HPV+OPC are distinguishable at the molecular level. ... [e] [133] [132] IMRT has a two-year disease free survival between 82 and 90%, and a two-year disease specific survival up to 97% for stage I and II. [134] [135] Reported toxicities include dry mouth ( xerostomia ) from salivary gland damage, 18% (grade 2); [f] difficulty swallowing ( dysphagia ) from damage to the constrictor muscles, larynx and oesophageal sphincter, 15% (grade 2); subclinical aspiration up to 50% (reported incidence of aspiration pneumonia approximately 14%); hypothyroidism 28–38% at three years (may be up to 55% depending on amount of the thyroid gland exposed to over 45 Gy radiation; esophageal stenosis 5%; osteonecrosis of the mandible 2.5%; and need for a gastrostomy tube to be placed at some point during or up to one year after treatment 4% (up to 16% with longer follow up). [12] [137] [135] [138] [139] Concerns have been expressed regarding excessive short and long term toxicity, especially dysphagia and xerostomia, [140] [141] [142] and hence whether standard doses expose patients with better prognoses are being exposed to overtreatment and unnecessary side effects. [143] [89] Dosimetry [ edit ] The probability of xerostomia at one year increases by 5% for every 1Gy increase in dose to the parotid gland .
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Arthritis
Wikipedia
Best Practice & Research. Clinical Rheumatology . 28 (3): 353–66. doi : 10.1016/j.berh.2014.08.002 . PMID 25481420 . ^ Richette P, Bardin T (January 2010). "Gout". Lancet . 375 (9711): 318–28. doi : 10.1016/S0140-6736(09)60883-7 . ... "Osteoarthritis" . Acta Medica Portuguesa . 28 (1): 99–106. doi : 10.20344/amp.5477 . ... "Physical therapy is effective for patients with osteoarthritis of the knee: a randomized controlled clinical trial (2001)" . J. Rheumatol . 28 (1): 156–64. PMID 11196518 . ^ "The Role of Occupational Therapy in Providing Assistive Technology Devices and Services" . www.aota.org . 2018 . ... "Medical Devices Active Licence Listing (MDALL)" . aem . Retrieved 2020-03-28 . ^ "Juvenile idiopathic arthritis: MedlinePlus Medical Encyclopedia" . medlineplus.gov .COPA, IL17A, ZFP36, CD69, HP, COL2A1, CNR2, MMP2, MEFV, TLR4, HLA-B, HLA-DRB1, IL10, NLRP3, NOD2, PTPN22, TNFRSF1A, CTLA4, BTK, CCR6, IL23R, PRG4, WAS, STAT4, CCN2, FCGR2A, SPP1, HLA-C, MMP14, IFIH1, BLNK, CCR1, FAS, HGD, NLRC4, LRBA, RAG2, TCF3, ASAH1, IRF5, IRAK1, HNF4A, MMP13, ABCG8, IL18, ASF1A, IFNG, IL12B, GP1BB, IL12A, RNF168, MYH14, LEMD3, PRKCD, IL4, JMJD1C, PRTN3, PSMB4, PSMB9, RNASEH2B, CD79B, CD79A, CXCL8, GJB2, GLA, PTGS2, RAG1, IL6, COL4A1, COL4A2, FOXP3, COMT, COX2, LRRC8A, MVK, SH3KBP1, MMP9, IL1RN, IL1B, RBM45, IL1A, RPS19, DNASE1L3, DNASE1, NLRP12, OCRL, IGLL1, IGHM, ABCG5, IL23A, FCGR2B, ERAP1, HJV, LBR, SAMHD1, CRP, PIK3R1, ADA2, RNASEH2C, TREX1, CPT2, RREB1, NCOA5, C1R, C1QA, RNASEH2A, TBX1, HNF1B, MLX, TF, TFR2, ATP7B, ARVCF, TNF, RASGRP1, HIRA, FASLG, SEC24C, UFD1, VEGFA, WIPF1, AGA, NCF1, KLRC4, LOH19CR1, PSTPIP1, ADAR, TNFSF11, HOXD10, IL12A-AS1, MTCO2P12, HPGD, C4A, GPI, CASP10, CAV1, UBAC2, CFI, SLCO2A1, CCL2, STAT3, GJB6, IL22, TNFSF13B, TNFRSF1B, MMP3, HSPD1, GRN, MAPK1, VIP, CCR5, MAPK14, CRYGD, IL2, MIR146A, MIR155, JAK2, NFKB1, PTGES, AIMP2, TLR2, CXCL12, ITGAM, IL2RA, CYBB, CXCL10, POLDIP2, SIRT1, IL34, PIK3CG, C5AR1, TRBV20OR9-2, CCR2, AHR, GRAP2, HOXC6, AHSA1, COMP, CRK, RNF19A, TEK, ALB, CSF2, SERPINA1, ESR1, IFNA1, MYDGF, FN1, HFE, CDH11, MMP1, ACAN, F2RL1, TNFSF15, ZAP70, NR1I2, PADI4, TP53, CTSK, PDCD1, DKK1, OSM, TNFRSF11B, FGF2, ISG20, CRH, ADAMTS12, NOS2, NM, IFNA13, MBL2, HSPA14, ADIPOQ, IL1F10, C5, IL17D, HLA-DQA1, TREM1, SLC52A1, IL32, FSTL1, IL9, CD40, ADAMTS7, ACR, S100A8, LEP, CTHRC1, LGALS1, PIK3CB, BCL2, PGF, HMGB1, THBD, TGFB1, PIK3CA, CCN1, NR4A2, PIK3CD, SMUG1, PLA2G1B, LTB4R, PLG, IGF1, TSLP, TLR3, CD28, CCL5, LGALS3, CXCR4, ALOX5, ANGPT1, MIF, TM7SF2, IL27, ICAM1, MTX1, CD274, IL17B, HSPA4, IFNB1, HSPA5, ACKR3, MRAP, IL15, IL6R, ANKH, PRL, PTEN, PTGS1, RELA, SAA1, CCL3, RIPK3, NFAT5, CXCR6, SYT1, ADAM17, TIMP1, TRAF6, TRPV1, KHSRP, AOC3, SOCS3, TNFSF10, SPHK1, MAPK8, PPARG, POMC, MMP17, CXCR2, ITGB2, KLKB1, TLR9, LIF, LYZ, TLR7, MAP3K5, MPO, PRDX5, IL20, NFATC1, NGF, ACAD8, SERPINE1, HSD11B1, PLA2G2A, PLA2G4A, CD248, CCN6, FOXO3, ENO1, CD44, AKT1, ALOX15, CSF1, FCGR3A, ANGPT2, NR3C1, GORASP1, BMP2, CD40LG, GLB1, BDNF, WNK1, IL33, B2M, TSPO, AGBL2, DECR1, CTSS, ELANE, IL21, EGFR, S1PR1, ACTB, VPS51, HMOX1, S100A9, MOK, ADAMTS5, RAC1, BTG3, SAA2, VSIG4, CAT, NCR3, KRIT1, MS4A1, RARRES2, CD38, PADI2, S100B, CD14, S100A1, HPX, CD74, HTRA1, ATN1, DPP4, C5AR2, HT, DHODH, OPRM1, P2RX7, PAH, CTSB, PF4, CTNNB1, ABCB1, CSF3, CR2, CPOX, COX8A, COL1A2, IL17RA, SH3BP4, CHRM3, SH3BP2, CHI3L1, CTSC, PROS1, MASP1, PRKCA, SSTR4, SLC11A1, ADRA2B, VIL1, VIM, ANK1, ADAMTS4, WNT5A, ABCG2, COX5A, AGER, ASIC3, MSC, TAM, LPAR2, VCAM1, PDCD5, ADRA1A, PLA2G10, TRAP, ADA, RIPK1, TNFSF13, TNFRSF14, RIPK2, TNFRSF11A, LINC02605, VDR, MIR34A, CYSLTR1, BRAF, CALCA, SOAT1, PDPN, TRIM21, TAC1, C3, MAP3K7, CNTN2, TBCA, BSG, BRS3, NOD1, TYRO3, KLF2, TIMP3, NAMPT, AXL, TLR5, TNFAIP3, TNFAIP6, ARG1, NR2C2, MIR29A, TNFRSF4, TSC22D3, PTX3, ESR2, GZMA, CIITA, SUCNR1, MOG, KRTAP5-9, GATA3, RHBDF2, EPHB2, SOST, MMP10, LOX, RNPC3, GAS6, IL11, DBA2, FRZB, LTB4R2, COL18A1, FCGR3B, FOXM1, GPSM3, IL7, LGALS9, GPR42, DCXR, KITLG, CXCL9, ORAI1, IL25, RETN, IL13, SPHK2, FPR2, NR4A1, TRPV2, FOS, HLA-DRB3, KRT20, CD46, TNC, SMAD7, HLA-DQB1, FAP, BANK1, HRH4, KDR, SIRT6, HLA-A, FLT3LG, MACIR, COX1, EDNRA, KNG1, ITGA2, IL3, MTHFR, STEAP4, KIR3DL1, MIR145, WDR26, CCDC134, MIR143, WASF2, MIR147A, MIR142, SLC40A1, GDF11, GPATCH2, ANP32B, RTL1, GPR101, IL17RD, FCRL4, BATF, MIRLET7B, SEMA4D, MERTK, TMEM147, TXNDC5, YAP1, RASGRP2, NDEL1, MIR106B, ADI1, MIR107, MIR10A, MIR140, TNIP1, LANCL1, SPRY2, LGR4, RABEPK, MIR149, KEAP1, STAB2, TSL, NIF3L1, KLF4, CCL28, CD83, LGR6, H2AC19, ARHGEF2, CXCL16, SLC16A3, MEPE, SLC16A4, PIGQ, PSTPIP2, LYPD8, MUC3B, CCRL2, CADM3, RAB4B-EGLN2, TRPA1, WASF1, TIMELESS, PERCC1, SLC12A9, SQSTM1, SEMA6A, ST3GAL5, ITGBL1, MIR337, MIR182, SLC52A2, MIR196A2, LRPPRC, MIR20A, CAMKMT, ENAM, SH2D3A, MIR223, SH2D3C, MIR27A, ELMO1, CLEC2A, MIR29B2, PRDX6, PARD3, MIR93, CDCP1, MIR17HG, CLEC7A, VN1R17P, ADAMTS3, SEMA4A, CRLF2, GPR166P, AIM2, SRR, MIR148B, PROCR, LINC01193, ILDR2, PWAR1, CLEC4E, PTPRVP, FBXO32, C1QTNF6, ANGPTL4, COMMD1, C1QTNF3, PLB1, GPBAR1, PLEKHO1, BTLA, CMC1, SUMF2, SPAAR, SLC5A12, CLEC12A, OXER1, PANX1, IDO2, CLEC5A, PSORS1C1, PRRT2, DNAJB1P1, LPAR3, CABIN1, BRD4, EGLN3, ERAL1, LRG1, CXCL13, AATF, IL19, ICOS, OSCAR, ADGRE2, CD209, TBK1, EHD2, PYCARD, TRBC1, SLCO6A1, TRBV7-9, GPR151, TRBV16, MUC17, HPGDS, MRGPRX4, MRGPRX3, IL17C, SIGLEC9, IL37, SIRPA, BBC3, SIGLEC7, OR2AG1, LACC1, IL21R, HAVCR1, SLURP1, UNC13D, SATB2, ICOSLG, SYVN1, PSIP1, NEAT1, ARMH1, AGBL3, CDC42EP1, CD160, RCAN3, UBASH3A, CNTRL, CPP, EBNA1BP2, IRGM, RALBP1, MALT1, TUBGCP2, H3P44, TAGAP, PADI6, GSTK1, JAM3, CYTL1, TXNIP, IVNS1ABP, MALAT1, TRIM3, EGLN1, SPZ1, TMEM60, WNT3A, SIRT2, RHOBTB2, PRSS55, SMG1, EGLN2, DNER, GP6, UCMA, GPRC6A, SPESP1, WDFY3, ZBTB38, NPNT, CARD8, WIF1, NLRP1, PHB2, TLR8, TNFRSF12A, GADD45GIP1, CD300A, MRGPRX1, CHP1, DCTN3, POLG2, COPD, IFNL1, MLKL, A1BG, IQGAP1, IDO1, FCGRT, FCN1, FGF1, FGFR1, FGFR3, FGG, FHL2, FOXO1, FOLH1, FOSB, FOSL2, MTOR, FUT1, ACKR1, GABPA, GCH1, GCY, MSTN, GEM, FCGR1A, FCER1G, FAT1, EFNB2, DNMT1, DNMT3B, DRD2, DUSP7, DVL2, LPAR1, S1PR3, PHC1, EMD, PTK2B, EREG, ERG, ESRRB, ETS1, F2R, F2RL2, F3, FAAH, GFER, GH1, GHSR, IGFBP3, HLA-DRB4, HLA-G, HPRT1, HSD11B2, HSP90AA1, DNAJB1, IFNAR1, IGF1R, IGFBP5, HLA-DOA, IGH, IK, IKBKB, IL1R1, IL2RB, IL6ST, IL7R, CXCR1, HLA-DPB1, HK1, CBLIF, CXCL2, GJA1, GJA8, GOLGA4, CCR10, CXCR3, MCHR1, GPER1, CXCL1, GRP, HIP1, GSN, GTS, GUSB, GYS1, HAS1, HCLS1, HGF, HIF1A, DYNC1H1, DMP1, DES, BCKDHA, ARG2, ARNTL, ARRB1, ARRB2, ART1, ASS1, ATF3, ATP4A, BCL2A1, AQP4, CFB, CXCR5, BMI1, BMP6, BTF3P11, C4B, C6, C7, AR, AQP1, CALCR, GRK2, ABCF1, ACACA, ACLY, ACP5, ACP3, ADAM10, ADORA1, ADORA2A, GRK3, APOE, JAG1, AGT, AMELX, ANG, AOC2, APC, APOA1, APOB, CA9, CALM1, ACE, COL1A1, CISH, CLTC, CMD1B, CCR7, ACKR2, CMKLR1, CNN2, CNTN1, CORT, CECR, CPB1, CRYAB, CSF1R, CSF3R, CTSL, CUX1, CYP2B6, CD55, CHI3L2, CEBPB, CALM2, CD27, CALM3, CALR, CAMP, CAPG, CASP1, CASP8, RUNX2, CD22, CD80, CDKN2A, ENTPD1, CD59, ADGRE5, CDA, CDC25B, CDC42, CDK9, CDKN1A, IL10RA, INSR, TNFRSF10A, IRF1, SOD1, SOD2, SOD3, SPR, SPRR2A, STAT1, STAT6, SYK, TAP2, TAT, TBP, TBX5, TBX3, TRA, TRB, TGFB2, TGFBR1, TGM2, TH, FSCN1, SLN, SLC22A4, CCL17, RORA, RPL23A, S100A7, S100A12, SAA3P, SCN10A, CCL7, CCL8, CCL21, SLC22A2, CXCL6, CX3CL1, SDC4, SELL, SETMAR, SFRP1, SFTPD, SLC4A1, THBS1, TIA1, TIE1, NR0B2, SLC25A16, FOSL1, GDF5, UBL4A, FZD4, H2AC18, H2AC20, PLA2G6, CUL4B, LST1, PIK3R3, PIR, TP63, MARCO, HYAL2, TNFRSF25, TNFSF14, TNFRSF6B, ARHGEF5, DEK, TIMP2, TWIST1, TIMP4, TLR1, TNP1, CRISP2, TRAF1, TRAF2, HSP90B2P, TRPC5, TNFSF4, IL1R2, TXN, UBE2D3, UQCRFS1, VIPR2, VWF, YY1, YWHAZ, ZNF7, RGS1, RELB, REL, MUC5AC, MMP8, MMP12, MPP1, MRC1, MSI1, RNR2, MUC1, MUC3A, MYC, FOXO4, GADD45B, NCF2, NEDD9, NELL1, NFE2L2, NFIL3, NFKBIA, NFKBIL1, MME, MECP2, NOS1, LAG3, ITGAE, ITGAL, ITGAX, JAK1, JUN, JUNB, JUND, KLRC2, LAIR1, MDM4, RPSA, LIFR, LTA, LTB, MAZ, MC4R, MCAM, MDK, NHS, NOTCH1, RDX, MAP2K6, PPP1R1A, PPP3CA, SRGN, PRKCB, PRKCH, PRKD1, MAPK9, MAP2K3, MAP2K7, PPBP, PROC, PSMD7, PSMD12, PTHLH, PTH1R, PTPN11, PTPRJ, A2M, PPM1A, PPARD, NOTCH2, PAEP, NPPA, NRAS, NRGN, NT5E, ODC1, OLR1, P2RX3, P4HB, ENPP1, POU2AF1, ENPP2, PECAM1, SERPINF1, SERPINA4, PIP, PLAU, PLD1, PLTP, H3P28
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Cholecystitis
Wikipedia
Open arrow points to stones in the GB Acute cholecystitis with gallbladder wall thickening, a large gallstone, and a large gallbladder Play media Significant gallbladder wall thickening [28] Play media Significant gallbladder wall thickening [28] Histopathology [ edit ] Histopathology is indicated if preoperative imaging and/or gross examination gives a suspicion of gallbladder cancer . [29] Gross examination of gallbladder carcinoma, with a prominent nodule. ... November 2013. Archived from the original on 28 July 2016 . Retrieved 27 July 2016 . ^ a b c d e f g h i j Ansaloni, L (2016). "2016 WSES guidelines on acute calculous cholecystitis" . ... "Correlation among clinical, laboratory, and hepatobiliary scanning findings in patients with suspected acute cholecystitis". Annals of Emergency Medicine . 28 (3): 267–72. doi : 10.1016/s0196-0644(96)70024-0 . ... S2CID 8792764 . ^ a b "Cholecystitis" . Mayo Clinic . Mayo Clinic. 28 August 2014. Archived from the original on 25 November 2014 .ABCB4, ACVRL1, F5, PSAP, SMAD4, JAK2, HK1, GPI, GDF2, TPI1, PKLR, PNPLA2, ENG, BPGM, ARSA, ALDOA, TP53, GCG, CHDH, CXCL16, RCBTB1, ABCG8, SSBP2, MUC16, EHMT1, IL33, WIF1, BTBD8, GOLGA6A, GGTLC5P, GGTLC3, GGT2, OPN1MW2, GGTLC4P, TBC1D9, ADAM17, SLC9A3R1, GPT, RUNX3, CMM, CTLA4, ESR1, OPN1MW, GGT1, GLP1R, MYBL2, GLP2R, ABCB1, S100A8, AGA, TRAF3, VEGFA, PSCA, CLDN2, OPN1MW3
