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Strabismus Wikipedia

Vaughan & Asbury's general ophthalmology (18th ed.). McGraw-Hill Medical. ... The Massachusetts Eye and Ear Infirmary illustrated manual of ophthalmology (3rd ed.).

PLA2G6, TUBB3, CHN1, OPHN1, PHOX2B, ACO2, POGZ, KAT6B, ADNP, MED13L, SPECC1L, NEDD4L, CAMTA1, DDHD2, PLXND1, SPART, NIPBL, IQSEC2, DHX30, TREX1, ERLIN2, MID2, CPLX1, SDCCAG8, GJB6, RAI1, PLK4, ATP6V0A2, SIN3A, NDUFAF3, POMT2, ZDHHC9, NDUFAF1, ABHD5, MLXIPL, POLR1D, YARS2, EXOSC3, NSDHL, SLC25A24, ALG6, CLDN16, GMPPB, NDUFAF4, TUBGCP4, FOXP1, TBL2, HIBCH, TRAF3IP1, AUTS2, TMEM98, YME1L1, MAB21L2, CTCF, SUCLA2, FIBP, CTDP1, BAZ1B, AP3D1, HERC2, AP1S2, HESX1, DPM2, DPM1, PEX11B, LARGE1, PTCH2, CDK13, CASK, AP3B1, IKBKG, KCNAB2, PEX3, PPM1D, PRSS12, AP4M1, NOG, GLRX5, MED12, POMT1, DEAF1, SLC9A6, CD96, ALG3, BCAP31, LRPPRC, PQBP1, DNM1L, MAFB, NRXN1, ARNT2, SEMA3E, ZNF592, GTF2IRD1, POLR1C, MPDU1, PIGL, PEX16, RECQL4, SLC45A2, CCDC174, ARID1A, WDR81, CHST14, STRADA, NDUFAF2, RSPRY1, UBE3B, TUBGCP6, SHANK3, PIGY, WDR73, COL25A1, CDCA7, MFRP, PUS3, MED25, NUBPL, TTI2, L2HGDH, CSPP1, SNIP1, FA2H, FKRP, RAB39B, NDUFA11, TIMMDC1, DMBX1, ALG11, KIF7, NDUFS7, TUBB2B, SLC6A19, EOGT, LAMA1, KANSL1, CHAMP1, NALCN, EBF3, UBR1, ARID2, ASXL1, ARX, B3GALNT2, A2ML1, NDUFAF6, EVC2, PROKR2, NAXE, NDUFAF5, COLEC11, RSRC2, TMEM237, FRMD4A, PACS1, PEX26, CHD7, POMGNT1, FOXRED1, SETD5, NSUN2, DLL4, NDUFB11, TMCO1, PRMT7, FGFRL1, BCL11A, INPP5K, ATP8A2, SUFU, DYNC2LI1, PIGT, WAC, PHF21A, HHAT, AGK, ERMARD, DOCK6, PORCN, SIL1, NSD1, SLC39A8, PRDM16, PIEZO2, TRAPPC11, ALX4, MPP4, HACE1, MCTP2, PCDH19, ARHGAP31, ARID1B, SHROOM4, MCOLN1, SALL4, KLHL7, NDUFA12, TMEM126B, ACOX1, CDC45, USP9X, NDUFS1, HNRNPU, HIST1H1E, GTF2I, GNB1, GNAQ, GLI1, GK, GGCX, GFPT1, GBA, GALC, GABRD, FLNA, FLII, FLI1, FGFR2, FGFR3, FGFR1, FGF14, FGD1, FKTN, HRAS, HSD17B4, HSPD1, KMT2A, NDUFB3, NDUFA10, LZTR1, NDUFA2, NDUFA1, NDP, NAGA, MYH3, TRIM37, MITF, HSPG2, MDH2, MC1R, SMAD4, LIMK1, LETM1, LAMB2, L1CAM, KRAS, RBPJ, FBN1, FANCE, FANCD2, BBS4, ERCC8, CHRNE, LYST, CHAT, CDH11, CA8, BRAF, FOXL2, BCS1L, BBS1, COX15, ATR, ATP6V1E1, ATP6V1A, RERE, ATM, ASCL1, SLC25A4, JAG1, ADSL, COX10, CRYAA, FANCC, ERCC2, FANCA, EZH2, EXT2, EVC, ERF, ERCC6, ERCC5, ERCC4, ERCC3, ELN, CTBP1, EIF2S3, DLG3, DKC1, CYB5R3, DHCR24, DHCR7, DDOST, DDB2, CTNNB1, NDUFB9, NDUFA9, NDUFS2, RMRP, TCF4, TBX15, MAP3K7, SURF1, ABCC8, STXBP1, SSR4, SOX11, SOX5, SOX3, SOX2, SOS2, SOS1, SON, SMARCE1, SMARCB1, SMARCA4, SKI, NDUFS3, SDHA, RRAS, TCF12, TCOF1, TFAP2A, NSD2, MKKS, KMT2D, SHOC2, KAT6A, BRPF1, ZBTB16, ZIC1, XPC, XPA, CLIP2, TFAP2B, BEST1, VLDLR, KDM6A, UBE3A, TYRP1, TYR, TWIST1, TGFBI, NR2F1, RPS19, SIM1, RIT1, OCA2, RFC2, PEX13, PEX12, PEX10, PEX6, PEX1, PAX6, OTX2, ORC1, OPA1, GPR143, PPP2R5D, NRAS, NOTCH1, NONO, NHS, NFIX, NDUFV2, NDUFS8, NDUFS6, NDUFS4, NDUFV1, PITX2, PEX14, PEX19, PURA, REV3L, RET, RASA2, RAP1B, RAP1A, RAF1, ALDH18A1, PEX5, PEX2, PRSS56, PTPN11, PRKAR1A, PTEN, PTCH1, MAP2K2, MAP2K1, VANGL1, VANGL2, PHOX2A, ALDH5A1, ECEL1, CRYBB1, TSHR, KIF21A, CACNA1F, ERG, GATAD2B, FRMD7, HOXB1
- Heterophoria Wikipedia
  
  Heterophoria Specialty Optometry Ophthalmology Heterophoria is an eye condition in which the directions that the eyes are pointing at rest position, when not performing binocular fusion, are not the same as each other, or, "not straight". This condition can be esophoria, where the eyes tend to cross inward in the absence of fusion; exophoria, in which they diverge; or hyperphoria, in which one eye points up or down relative to the other. Phorias are known as 'latent squint' because the tendency of the eyes to deviate is kept latent by fusion. A person with two normal eyes has single vision (usually) because of the combined use of the sensory and motor systems. The motor system acts to point both eyes at the target of interest; any offset is detected visually (and the motor system corrects it).
Motion Sickness Wikipedia

Burr (eds.). Medical Aspects of Harsh Environments. 2. Washington, D.C.: Borden Institute. pp. 1048–1083.

NLGN1, AUTS2, LINC01241, SDK1, LINC00924, CPNE4, PRDM16, LRP1B, PDZRN4, LINC01243, POU6F2, CELF2, ST18, MAP2K5, HOXD3, HOXB3, GPD2, CNR2, CNR1
- Motion Sickness Omim
  
  Although motion sickness is not likely to be mendelian, it appears to show familial aggregation. Hence, the hypothesis of Treisman (1977) is of interest. The hypothesis is based on the idea that 'motion sickness is triggered by difficulties which arise in the programming of movements of the eyes or head when the relations between the spatial frameworks...are repeatedly and unpredictably perturbed. Such perturbations may be produced by certain types of motion, or by disturbances in sensory input or motor control produced by ingested toxins.' In nature the last would be important. Emesis in response to motion is viewed by this hypothesis as an unfortunate accidental byproduct of the system to get rid of neurotoxins. Neuro - Motion sickness Inheritance - Not likely mendelian, but shows familial aggregation ▲ Close
- Motion Sickness Ghr
  
  Motion sickness is a common condition characterized by a feeling of unwellness brought on by certain kinds of movement. The usual symptoms include dizziness, pale skin (pallor), and sweating, followed by nausea and vomiting. Affected individuals may also experience rapid breathing (hyperventilation), headache, restlessness, and drowsiness. These symptoms can be triggered by many kinds of motion, particularly traveling in a car, bus, train, airplane, or boat. Amusement park rides, skiing, and virtual reality environments can also induce motion sickness.
Beckwith–wiedemann Syndrome Wikipedia

(eds.), "Beckwith-Wiedemann Syndrome", GeneReviews®, University of Washington, Seattle, PMID 20301568, retrieved 2018-11-30 ^ Ranzini, A; Daysalvatore, D; Turner, T; Smulian, J; Vintzileos, A (1997).

CDKN1C, KCNQ1, NSD1, IGF2, H19, KCNQ1OT1, H19-ICR, SPTBN1, CIB2, ICR1, RSS, CTCF, SMS, TGM1, UROD, AFP, GPC3, CALCA, GNAS, TFPI, PLAGL1, WDR20, ABCC8, IGF1R, TRPM5, TBPL1, ELN, DNMT1, CISH, CMTR1, PHPT1, NLRP2, CEND1, ZNF215, CDKN3, FRA18C, AMER1, CD81, NLRP7, ZFP57, ZACN, DEL11P13, DLK1, TYRP1, WT1, POU5F1, IGF1, SMAD3, TRPM1, MYOD1, SLC22A18, PAX6, PCNA, PLXNA2, S100A8, IGF2R, HRAS, SNRPN, SOX2, ASAH1, GTF2I, TERT, TP53, TSC1, SOX3
- Beckwith-Wiedemann Syndrome Omim
  
  A number sign (#) is used with this entry because Beckwith-Wiedemann syndrome (BWS) can be caused by mutation or deletion of imprinted genes within the chromosome 11p15.5 region. Specific genes involved include p57(KIP2) (CDKN1C; 600856), H19 (103280), and LIT1 (KCNQ1OT1; 604115). Hypermethylation and variation in the H19/IGF2-imprinting control region (ICR1; 616186) on chromosome 11p15.5, which regulates imprinted expression of H19 and IGF2 (147470), is also associated with BWS. See also Silver-Russell syndrome (SRS; 180860), which is caused by hypomethylation defects at 11p15. Description Beckwith-Wiedemann syndrome is a pediatric overgrowth disorder involving a predisposition to tumor development.
- Beckwith-Wiedemann Syndrome Gene_reviews
  
  Summary Clinical characteristics. Beckwith-Wiedemann syndrome (BWS) is a growth disorder variably characterized by neonatal hypoglycemia, macrosomia, macroglossia, hemihyperplasia, omphalocele, embryonal tumors (e.g., Wilms tumor, hepatoblastoma, neuroblastoma, and rhabdomyosarcoma), visceromegaly, adrenocortical cytomegaly, renal abnormalities (e.g., medullary dysplasia, nephrocalcinosis, medullary sponge kidney, and nephromegaly), and ear creases/pits. BWS is considered a clinical spectrum, in which affected individuals may have many of these features or may have only one or two clinical features. Early death may occur from complications of prematurity, hypoglycemia, cardiomyopathy, macroglossia, or tumors. However, the previously reported mortality of 20% is likely an overestimate given better recognition of the disorder along with enhanced treatment options. Macroglossia and macrosomia are generally present at birth but may have postnatal onset.
- Beckwith-Wiedemann Syndrome Gard
  
  Beckwith-Wiedemann syndrome (BWS) is a growth disorder that can affect several parts of the body. Babies and children are larger than normal usually until age 8, when growth slows down, resulting in an average height in adults. Symptoms may include one side or area of the body growing more than the other side (asymmetric growth or hemihyperplasia), omphalocele or other abdominal wall defect at birth, low blood sugar (hypoglycemia) in infancy, an abnormally large tongue (macroglossia), abnormally large abdominal organs, creases or pits in the skin near the ears, and kidney abnormalities. Affected children have an increased risk to develop tumors, particularly a rare form of kidney cancer called Wilms tumor, a cancer of muscle tissue called rhabdomyosarcoma, and a form of liver cancer called hepatoblastoma. Some people only have one symptom while others may have many of the symptoms.
- Beckwith-Wiedemann Syndrome Ghr
  
  Beckwith-Wiedemann syndrome is a condition that affects many parts of the body. It is classified as an overgrowth syndrome, which means that affected infants are considerably larger than normal (macrosomia) and tend to be taller than their peers during childhood. Growth begins to slow by about age 8, and adults with this condition are not unusually tall. In some children with Beckwith-Wiedemann syndrome, specific parts of the body on one side or the other may grow abnormally large, leading to an asymmetric or uneven appearance. This unusual growth pattern, which is known as hemihyperplasia, usually becomes less apparent over time.
- Beckwith-Wiedemann Syndrome Orphanet
  
  Beckwith-Wiedemann syndrome (BWS) is a genetic disorder characterized by overgrowth, tumor predisposition and congenital malformations. Clinical description Patients tend to grow at an increased rate during the 2nd half of pregnancy and in the first few years of life; adult heights are typically in the normal range. Abnormal growth may also manifest as hemihyperplasia and/or macroglossia (leading to difficulties in feeding, speech and infrequently, sleep apnea). Hypoglycemia is reported in 30-50% of neonates. A recognizable facial gestalt is common and often normalizes by adulthood. In addition to macrosomia, macroglossia, hemihyperplasia and hypoglycemia, characteristic findings may include omphalocele/umbilical hernia/diastasis recti, embryonal tumor, anterior earlobe crease(s) and posterior helical pit(s), nevus flammeus or other vascular malformations, visceromegaly involving abdominal organs, fetal adrenocortical cytomegaly (pathognomonic), renal abnormalities, positive family history, and rarely cleft palate.
Shingles Wikipedia

Epidemiology and Prevention of Vaccine-Preventable Diseases (PDF) (13 ed.). ... Essentials of Pain Medicine (3rd ed.). London: Elsevier Health Sciences. p. 358. ... Essential Microbiology for Dentistry (4th ed.). Elsevier Health Sciences. pp. 638–42. ... Burket's oral medicine (12th ed.). coco. pp. 62–65. ISBN 978-1-60795-188-9 . ^ Chai W, Ho MG-R. ... He L (ed.). "Antiviral treatment for preventing postherpetic neuralgia".

APOE, IL10, MST1, ERVK-19, CCR2, RBM45, LMLN, TMPRSS13, GAL, TRPV1, TECTA, MSMB, CCR5, MBL2, HLA-DRB1, HLA-A, ESR1, CYP17A1, CYP11A1, CPS1, ERVK-11
- Shingles Ghr
  
  Shingles (also known as herpes zoster) results from infection by the varicella zoster virus. This common virus causes chickenpox (also known as varicella), which is characterized by itchy spots on the skin that cover the whole body and usually occurs in childhood or adolescence. After the body fights the initial infection, the varicella zoster virus remains in nerve cells for the rest of a person's life. Because the virus is controlled by immune system cells called T cells, it is generally inactive (latent) and typically causes no health problems. However, in some people, the virus becomes active again (reactivates) and causes shingles.
Charcot–marie–tooth Disease Wikipedia

Muscle biopsy : a practical approach (Fourth ed.). Philadelphia: Saunders/Elsevier.

MPZ, LRSAM1, PMP22, FIG4, GDAP1, KIF1B, LMNA, SH3TC2, TRPV4, GJB1, MTMR2, NEFL, GARS, EGR2, SBF2, NDRG1, MORC2, HOXD10, FGD4, COX6A1, MFN2, DNM2, HSPB1, HSPB8, DYNC1H1, AARS, SBF1, IGHMBP2, LITAF, DNAJB2, PRX, MARS, RAB7A, INF2, PRPS1, SMN1, AIFM1, HSPB3, HINT1, MED25, KIF5A, GNB4, PLEKHG5, PDK3, MME, HK1, FBLN5, SOX10, VCP, POLG, SPTLC1, DRP2, TFG, KARS, ARHGEF10, ABCC9, SPG7, TUBB3, SIGMAR1, NEBL, ACTC1, SLC1A3, SOS1, SLC12A6, TNNI3, SPTBN2, TAZ, TTR, CSRP3, GAN, ELP1, TCAP, TTPA, TTN, CTDP1, TPM1, SPTLC2, TNNT2, BAG3, VCL, WASHC5, TNNC1, CLTCL1, ZFYVE26, SEPT9, PNPLA6, JPH2, GATAD1, PRDM12, SLC5A7, SIL1, REEP1, WNK1, TMEM43, SLC52A2, MYH14, SPG11, FBXO38, LAS1L, MYPN, SLC25A46, C12orf65, NEXN, SLC52A3, ZFYVE27, SYT2, TTBK2, RBM20, CHCHD10, COQ8A, TWNK, TDP1, BSCL2, LDB3, SCN11A, CCT5, SETX, SPART, BICD2, TRIM2, SCN9A, ATL3, SACS, ANKRD1, DHTKD1, PDLIM3, DCAF8, DHH, ATL1, SPG21, PRKAG2, MYOZ2, RETREG1, APTX, SLC52A1, SGCD, SPAST, NRAS, PEX7, GAA, LAMP2, KCNA1, DES, DMD, DNMT1, NTRK1, DSC2, DSG2, DSP, NGF, DTNA, TYMP, KCNC3, NAGLU, EMD, MYL3, MYL2, KRAS, MYH7, MYH6, MYBPC3, MTTP, L1CAM, MRE11, LAMA4, MPV17, FKTN, FGF14, PDHA1, DCTN1, JUP, CRYAB, ACTN2, RYR2, HADHA, ALDH3A2, HADHB, RIT1, HARS, ATP7A, RAF1, PTPN11, KIF1A, BRAF, CACNB4, PRNP, MAP2K2, PLN, PLP1, ITPR1, PHYH, PKP2, GLA, MAP2K1, FXN, SCN5A, CAV3, CASQ2, HRAS, PRKCG, GSTT2, RNMT, MAD2L1BP, RAB7B, MTM1, YARS, ACKR1, YARS2, HSPB2, ATP6, MCM3AP, PLEK, CANX, SMN2, JPH1, SLURP1, AARS2, MUL1, CNTF, CMTX3, AR, CBLL2, DCPS, CCL2, HDAC6, PRKN, RIEG2, SLC3A2, NTF3, TSG101, NEDD4, MAG, DGAT2, PRB4, TPR, EIF3K, SYVN1, SURF1, CDC42, CMTX2, PMP2, MBS2, PGR, CSF1, SCARB2, MTG1, SRY, PRPH, LRIG3, SOX4, APP, SLCO6A1, APOA2, APCDD1, SOD1, SNRPN, DFNA49, GSTK1, SORT1, DNM1P33, GUSBP1, PGM1, OPA1, BUD31, SMAD3, VAC14, MFN1, MBP, SMA4, FUS, RER1, GBA, DFNA7, GJB2, MYO15A, STMN1, GJB3, SUN2, GLC3B, ERBB3, ERBB2, DCTN2, SLC2A4RG, EMP3, EMP2, GJC2, MYO1A, LPAR1, NRG2, NEFH, NT3, ARHGEF2, SNURF, DNM1, TEKT3, IL17B, LOC100653061
- Charcot-Marie-Tooth Disease Gard
  
  Charcot-Marie-Tooth disease is a group of disorders that affect the peripheral nerves, the nerves running from outside the brain and spine. Defects in many different genes cause different forms of this disease. Common symptoms may include foot drop, foot deformity, loss of lower leg muscle, numbness in the foot or leg, “slapping" gait (feet hit the floor hard when walking), and weakness of the hips, legs, or feet. There is currently no cure for Charcot-Marie-Tooth disease, but physical therapy, occupational therapy, braces and other orthopedic devices, pain medication, and orthopedic surgery can help manage and improve symptoms. There are over 40 types of Charcot-Marie-Tooth disease. You can search for more information on a particular type of Charcot-Marie-Tooth disease from the GARD Home page.
Snakebite Wikipedia

Rosen's emergency medicine : concepts and clinical practice (7 ed.). Philadelphia: Mosby/Elsevier. p. 746. ... PMID 9868843. ^ a b MedlinePlus – Snake bites Archived 4 December 2010 at the Wayback Machine From Tintinalli JE, Kelen GD, Stapcynski JS, eds. Emergency Medicine: A Comprehensive Study Guide. 6th ed. New York, NY: McGraw Hill; 2004. ... Stephen P., Mackessy, ed. (2010). Handbook of Venoms and Toxins of Reptiles (2nd ed.). ... Venomous Snakes: Envenoming, Therapy (2nd ed.). Hauppauge, NY: Nova Science Publishers.
Postpartum Bleeding Wikipedia

Danforth's obstetrics and gynecology (10th ed.). Philadelphia: Lippincott Williams & Wilkins. p. 453.
Sleep Apnea Wikipedia

Sleep apnea Other names Sleep apnoea, sleep apnea syndrome Obstructive sleep apnea Pronunciation /æpˈniːə/, /ˈæpniə/ Specialty Otorhinolaryngology, sleep medicine Symptoms Pauses in breathing or periods of shallow breathing during sleep, snoring, tired during the day[1][2] Complications Heart attack, stroke, diabetes, heart failure, irregular heartbeat, obesity, motor vehicle collisions[1] Usual onset 55–60 years old[1][3] Causes Obstructive sleep apnea (OSA), central sleep apnea (CSA), mixed sleep apnea[1] Risk factors Overweight, family history, allergies, enlarged tonsils[4] Diagnostic method Overnight sleep study[5] Treatment Lifestyle changes, mouthpieces, breathing devices, surgery[1] Frequency 1–6% (adults), 2% (children)[3][6] Sleep apnea, also spelled sleep apnoea, is a sleep disorder where a person has pauses in breathing or periods of shallow breathing during sleep.[1] Each pause can last for a few seconds to a few minutes and they happen many times a night.[1] In the most common form, this follows loud snoring.[2] There may be a choking or snorting sound as breathing resumes.[1] Because the disorder disrupts normal sleep, those affected may experience sleepiness or feel tired during the day.[1] In children it may cause hyperactivity or problems in school.[2] Sleep apnea may be either obstructive sleep apnea (OSA) in which breathing is interrupted by a blockage of air flow, central sleep apnea (CSA) in which regular unconscious breath simply stops, or a combination of the two.[1] Obstructive (OSA) is the most common form.[1] Risk factors for OSA include being overweight, a family history of the condition, allergies, a small breathing airway, and enlarged tonsils.[4] Some people with sleep apnea are unaware they have the condition.[1] In many cases it is first observed by a family member.[1] Sleep apnea is often diagnosed with an overnight sleep study.[5] For a diagnosis of sleep apnea, more than five episodes per hour must occur.[7] Treatment may include lifestyle changes, mouthpieces, breathing devices, and surgery.[1] Lifestyle changes may include avoiding alcohol, losing weight, stopping smoking, and sleeping on one's side.[8] Breathing devices include the use of a CPAP machine.[8] Without treatment, sleep apnea may increase the risk of heart attack, stroke, diabetes, heart failure, irregular heartbeat, obesity, and motor vehicle collisions.[1] OSA affects 1 to 6% of adults and 2% of children.[3][6] It affects males about twice as often as females.[3][9] While people at any age can be affected, it occurs most commonly among those 55 to 60 years old.[1][3] CSA affects less than 1% of people.[10] A type of CSA was described in the German myth of Ondine's curse where the person when asleep would forget to breathe.[11] Contents 1 Signs and symptoms 2 Risk factors 3 Mechanism 4 Diagnosis 4.1 Oximetry 4.2 Classification 4.2.1 Obstructive sleep apnea 4.2.2 Central sleep apnea 4.2.3 Mixed apnea 5 Management 5.1 Continuous positive airway pressure 5.2 Weight loss 5.3 Surgery 5.3.1 Nasal obstruction 5.3.2 Pharyngeal obstruction 5.3.3 Hypopharyngeal or base of tongue obstruction 5.3.4 Multi-level surgery 5.3.5 Potential complications 5.4 Other 5.4.1 Neurostimulation 5.4.2 Medications 5.4.3 Oral appliances 5.4.4 Nasal EPAP 5.4.5 Oral pressure therapy 6 Epidemiology 7 History 7.1 Treatment 8 See also 9 References 10 External links Signs and symptoms[edit] People with sleep apnea have problems with excessive daytime sleepiness (EDS), impaired alertness, and vision problems.[12] OSA may increase risk for driving accidents and work-related accidents. ... Physician Assistant Review (4 ed.). Lippincott Williams & Wilkins. p. 40. ... Neuroscience (Sixth ed.). New York. ISBN 9781605353807 . OCLC 990257568. ^ Pendharkar, Sachin R.; Povitz, Marcus; Ayas, Najib T.; Laratta, Cheryl R. (2017-12-04). ... (ed.). "Overview – Indications and Contraindications". Medscape – Diaphragm Pacing.

BCHE, ACE, ADORA1, GHSR, S100B, ABCB1, PHOX2B, EDN1, EDNRA, IL10, IL1B, TLX3, GHRL, AHDC1, MAGEL2, SOD1, NPAP1, GPR101, PWAR1, RAI1, MKRN3-AS1, GNE, AIP, FLCN, HERC2, SNORD115-1, MKRN3, TSPYL1, PWRN1, TCF4, SNORD116-1, SNRPN, APOE, FGFR3, FGFR2, NDN, IPW, HCRT, FMR1, CYSLTR1, APP, AR, CYSLTR2, GH1, GSN, REM1, SP140, IDS, AGT, LEP, LEPR, NPPC, NPR2, IL1R2, PMP22, VEGFA, PTGS2, SLC6A4
Trachoma Wikipedia

Goldman's Cecil Medicine (24th ed.). Philadelphia: Elsevier Saunders. pp. e326–2.

TNF, IL10, HLA-A, HLA-DRB1, IL15, OR10A4, RBM45, FOXP3, LYVE1, EBI3, IL18R1, CCL2, KIR2DL3, KIR2DL2, IL17A, IL13RA2, HLA-B, IL13RA1, IL10RA, IL6, IL4, IL1RN, IL1B, IL1A, IFNG, HP, HLA-C, MIR147B
Niemann–pick Disease, Type C Wikipedia

(eds.). "Niemann–Pick Disease Type C". GeneReviews™ [Internet]. Seattle WA: University of Washington, Seattle.

NPC1, NPC2, LIPA, SMPD1, APP, PDLIM7, ABCA1, MAPT, PSMB9, FATE1, ULK1, RARRES3, SFRP1, MIR663A, MIR31, SULT1E1, TERT, MIR10B, LINC01193, TFAP2A, TNF, TOP2A, TRAF1, VEGFA, CDK10, ROBO3, BECN1, CDK5R1, OSCP1, PTPN12, CDCA5, POSTN, RASSF1, SMUG1, DDX58, AMACR, BACE1, GDE1, RTRAF, CD163, PIK3CA, PTGS2, MAP3K8, EGR1, TYMP, DAPK1, DAP, CYP2B6, CTGF, CDKN2A, FASN, CDK5, CDK4, ATP7B, ARF6, APOE, ANXA6, ERCC1, FCN2, ANXA1, IL12A, ABCB1, MNAT1, MMP1, MICE, LDLR, KDR, IL1A, FGF2, IGFBP6, IFNG, HLA-A, HDAC2, GCHFR, FN1, UPK3B
- Niemann-Pick Disease, Type C2 Omim
  
  A number sign (#) is used with this entry because Niemann-Pick disease type C2 (NPC2) is caused by homozygous mutation in the NPC2 gene (601015) on chromosome 14q24. Description Niemann-Pick type C (NPC) disease is an autosomal recessive lipid storage disorder characterized by progressive neurodegeneration. Approximately 95% of cases are caused by mutations in the NPC1 gene (607623), referred to as type C1 (257220); 5% are caused by mutations in the NPC2 gene (601015), referred to as type C2. The clinical manifestations of types C1 (257220) and C2 are similar because the respective genes are both involved in egress of lipids, particularly cholesterol, from late endosomes or lysosomes (summary by Vance, 2006). Clinical Features Vanier et al. (1996) reported 5 patients with NPC2.
- Niemann-Pick Disease Type C Gene_reviews
  
  Summary Clinical characteristics. Niemann-Pick disease type C (NPC) is a lipid storage disease that can present in infants, children, or adults. Neonates can present with ascites and severe liver disease from infiltration of the liver and/or respiratory failure from infiltration of the lungs. Other infants, without liver or pulmonary disease, have hypotonia and developmental delay. The classic presentation occurs in mid-to-late childhood with the insidious onset of ataxia, vertical supranuclear gaze palsy (VSGP), and dementia. Dystonia and seizures are common. Dysarthria and dysphagia eventually become disabling, making oral feeding impossible; death usually occurs in the late second or third decade from aspiration pneumonia.
- Niemann-Pick Disease Type C Orphanet
  
  Niemann-Pick disease type C (NP-C) is a lysosomal lipid storage disease (see this term) characterized by variable clinical signs, depending on the age of onset, such as prolonged unexplained neonatal jaundice or cholestasis, isolated unexplained splenomegaly, and progressive, often severe neurological symptoms such as cognitive decline, cerebellar ataxia, vertical supranuclear gaze palsy (VSPG), dysarthria, dysphagia, dystonia, seizures, gelastic cataplexy, and psychiatric disorders.
- Niemann-Pick Disease, Type C1 Omim
  
  A number sign (#) is used with this entry because Niemann-Pick disease type C1 and Niemann-Pick disease type D, also known as the Nova Scotian type, are caused by homozygous or compound heterozygous mutation in the NPC1 gene (607623) on chromosome 18q11. Description Niemann-Pick type C (NPC) disease is an autosomal recessive lipid storage disorder characterized by progressive neurodegeneration. Approximately 95% of cases are caused by mutations in the NPC1 gene, referred to as type C1; 5% are caused by mutations in the NPC2 gene (601015), referred to as type C2 (607625). The clinical manifestations of types C1 and C2 are similar because the respective genes are both involved in egress of lipids, particularly cholesterol, from late endosomes or lysosomes (summary by Vance, 2006). Historically, Crocker (1961) delineated 4 types of Niemann-Pick disease: the classic infantile form (type A; 257200), the visceral form (type B; 607616), the subacute or juvenile form (type C), and the Nova Scotian variant (type D).
Developmental Coordination Disorder Wikipedia

In Packiam Alloway T, Gathercole SE (eds.). Working Memory and Neurodevelopmental Disorders. ... Lin C (ed.). "Psychometric assessment of the French European Developmental Coordination Disorder Questionnaire (DCDQ-FE)". ... Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. pp. 74–7.

FGFR2, OGG1, PTEN, AKAP5, DISC1, SHANK1, CLN6, CAMKMT, DCD
Gastroesophageal Reflux Disease Wikipedia

. ^ Patient information: Barrett's esophagus, archived from the original on 9 September 2017 ^ Mills, S (ed.) 2009.Sternberg's Diagnostic Pathology. 5th Edition.

CXCL8, PTGS2, TAC1, ABAT, TP63, HLA-DRB1, PHOX2B, NSD2, SMC1A, LTBP4, PPM1D, KCNAB2, ELP1, SMC3, TFAP2A, SLC6A5, NRXN1, ADAMTS2, GABBR2, SEMA3E, PIEZO1, TECPR2, ARNT2, FAM13A, TSPYL1, TERC, TERT, NPHS1, ORC4, PARN, POLG, PYCR1, ALDH18A1, RAD21, RET, RPL10, SALL1, SCN9A, SFTPC, ABCA3, SLC6A3, SNRPB, SSR4, CDKL5, STXBP1, MAP3K7, TCF4, GPHN, SLC9A6, DEAF1, SLC46A1, PRDM16, WNK1, RHBDF2, UBA5, KIAA0319L, STN1, MCEE, SHANK3, DPP9, AMER1, SMG9, ASXL1, FLCN, EBF3, NALCN, CHAMP1, NEXMIF, MYMK, SFTPA1, MUC5B, SHROOM4, KLHL7, RAI1, AFF4, CPLX1, NTNG1, IQSEC2, POGZ, ATP11A, PIGN, ORC6, NIPBL, FBXL4, RRM2B, HDAC8, MLXIPL, RTEL1, FGFRL1, RETREG1, SAMD9, TRMT10C, RNF125, SETD5, CHD7, ORC1, SKI, SFTPA2, GABRD, CAV1, CDC6, CCR6, COL1A1, COL1A2, HNRNPH2, COL5A1, HIVEP2, COL5A2, GLRB, GLRA1, COL13A1, CTBP1, KIF1A, CTGF, FMR1, FLNA, FLII, FOXG1, CYP2C19, EXT2, ELN, DDC, DDOST, DHCR7, TYMP, BRAF, HRAS, DSP, ASPA, MEIS2, LETM1, ATP7A, LBR, MID1, KMT2A, MECP2, RERE, LAMA2, ASCL1, IRF5, ATRX, ATP12A, ATP4A, CDX2, IL1B, F2RL1, TRPV1, EGF, COX2, MMP1, CCL26, NR1I2, IL1RN, CCND1, GNB3, CALCA, SLC52A1, HIF1AN, COL3A1, ADRB2, APOA4, COPD, PWAR1, CAPN14, FOXP1, MIR223, DKK4, ACE, MIR21, CCK, CRNN, CYP3A4, CDX1, MIR203A, ATP2A3, ISYNA1, CYLD, SLC52A2, NOX5, CTSZ, CTSW, CTSK, PERP, TRPV4, NQO1, GER, MIR142, NGF, EFNB2, TLR4, HSPA4, HSPB1, HSPB2, HTR2A, IGF1R, TACR1, IL6, IL13, SPARC, IL18, SCNN1D, MDM2, SAFB, S100A8, MGMT, MAP2K2, MAP2K1, MMP3, PIK3CA, PAX2, MMP12, P2RX7, SLC22A18, MUC1, MUC4, THBS1, TNFRSF1A, DKK1, TOP2B, EGFR, NES, AGR2, ERCC2, RAMP1, F2R, NOS2, FOXC2, FLG, SLC4A7, FLT1, ASIC3, GABRA6, HSPB3, BECN1, GDNF, GUCY2C, BAG6, XRCC3, XRCC1, EZR, VEGFA, TYMS, TSC2, TP53, FASN
- Gastroesophageal Reflux Omim
  
  Description Gastroesophageal reflux (GER) is characterized by the retrograde movement of stomach contents into the esophagus. In its most severe form, GER results in extensive tissue damage caused by acid reflux. In adolescents and adults, and even infrequently in children, chronic GER is associated with the risk of developing Barrett metaplasia (614266), a premalignant lesion of the esophageal mucosa (Hu et al., 2000). In turn, Barrett metaplasia is correlated with the development of adenocarcinoma of the esophagus (see 614266), estimated as the fifth most prevalent neoplasia in the Western world (Lagergren et al., 1999). Mapping To identify a genetic locus that cosegregates with a severe pediatric GER phenotype in families with multiple affected members, Hu et al. (2000) performed a genomewide scan using microsatellite markers spaced at an average interval of 8 cM.
Aspirin Exacerbated Respiratory Disease Wikipedia

. ^ Mendelsohn D, Jeremic G, Wright ED, Rotenberg BW (March 2011). "Revision rates after endoscopic sinus surgery: a recurrence analysis".

PTGER2, TBX21
Progressive Supranuclear Palsy Wikipedia

Bradley's neurology in clinical practice (Sixth ed.). Philadelphia: Elsevier Saunders. p. 1778.

MAPT, STX6, MOBP, EIF2AK3, TRA2B, SRSF2, SLCO1A2, CD8B, IRF4, APOE, LRRK2, C9orf72, STH, CSF2, LAMC2, ATXN2, PRKN, TARDBP, TGM2, TH, DCTN1, GRN, GFAP, SLC25A38, MIR132, TPO, UBB, VEGFA, NF1P1, SPECC1, UBASH3B, SNCAIP, ROCK2, TREM2, RIDA, NPC2, YWHAQ, PSPC1, BPIFA2, MINK1, SMUG1, ANXA6, TGM1, STXBP3, BDNF, RUNX1T1, CDK5, CDR1, CRHR1, MTOR, FUS, GBA, GSTM1, IRS1, MSMB, NGF, NOS1, NPC1, NSF, NR4A2, PIN1, PSPN, PSPH, REG1A, ROCK1, SPG7, SPP1, ATXN2-AS
- Supranuclear Palsy, Progressive, 3 Omim
  
  For a phenotypic description and a discussion of genetic heterogeneity of progressive supranuclear palsy (PSP), see PSNP1 (601104). Mapping Using a pooling-based genomewide association study of more than 500,000 SNPs in 288 patients with PSP and 344 age- and sex-matched controls, Melquist et al. (2007) identified candidate SNPs with large differences in allelic frequency by ranking all SNPs by their probe-intensity difference between cohorts. The MAPT H1 haplotype (see 157140) was strongly detected by this approach as was a second major locus (PSNP3) on chromosome 11p12-p11 that showed evidence of association at allelic (p less than 0.001), genotypic (p less than 0.001), and haplotypic (p less than 0.0001) levels and was narrowed to a single haplotype block containing the DNA damage-binding protein-2 (DDB2; 600811) and lysosomal acid phosphatase-2 (ACP2; 171650) genes. Since DNA damage and lysosomal dysfunction have been implicated in aging and neurodegenerative processes, Melquist et al. (2007) considered both genes to be viable candidates for conferring risk of disease.
- Supranuclear Palsy, Progressive, 1 Omim
  
  A number sign (#) is used with this entry because of evidence that progressive supranuclear palsy-1 (PSNP1) is caused by heterozygous mutation in the gene encoding microtubule-associated protein tau (MAPT; 157140) on chromosome 17q21. Description Progressive supranuclear palsy (PSP) is the second most frequent cause of degenerative parkinsonism. In addition to parkinsonism, the clinical symptoms include early postural instability, supranuclear gaze palsy, and cognitive decline. Neuropathologically, the disorder is characterized by abundant neurofibrillary tangles, which differ in both distribution and composition from those associated with Alzheimer disease. In progressive supranuclear palsy, the tangles are primarily localized to subcortical regions and are found in both neurons and glia, whereas in Alzheimer disease they are more widespread, largely cortical, and limited to neurons.
- Progressive Supranuclear Palsy Ghr
  
  Progressive supranuclear palsy is a brain disorder that affects movement, vision, speech, and thinking ability (cognition). The signs and symptoms of this disorder usually become apparent in mid- to late adulthood, most often in a person's 60s. Most people with progressive supranuclear palsy survive 5 to 9 years after the disease first appears, although a few affected individuals have lived for more than a decade. Loss of balance and frequent falls are the most common early signs of progressive supranuclear palsy. Affected individuals have problems with walking, including poor coordination and an unsteady, lurching gait.
- Supranuclear Palsy, Progressive, 2 Omim
  
  For a phenotypic description and a discussion of genetic heterogeneity of progressive supranuclear palsy (PSP), see PSNP1 (601104). Clinical Features De Yebenes et al. (1995) studied a 5-generation Spanish family in which progressive supranuclear palsy was transmitted as an autosomal dominant trait. The proband had the classic presentation of this disorder beginning with axial rigidity, slowness of movement, and gait difficulty. Over the course of 2 years he progressed to complete vertical gaze palsy, axial dystonia, and retrocollis, as well as generalized severe akinesia. Postmortem examination demonstrated neuronal loss and atrophy of the brainstem, cerebellum, and diencephalon.
- Parkinson-Dementia Syndrome Omim
  
  A number sign (#) is used with this entry because of evidence that a form of atypical supranuclear palsy is caused by mutation in the microtubule-associated protein tau gene (MAPT; 157140). Clinical Features Mata et al. (1983) described 2 brothers and a sister with a 'new' Parkinson-dementia syndrome. The disorder, characterized also by ophthalmoparesis and pyramidal signs, came on in the third decade and progressed for several years. Kyphoscoliosis was present in all 3 sibs. Examination of the brain in the sister, who died at age 31 years, showed neurofibrillary degeneration of the hippocampus, basal ganglia and brainstem nuclei. The parents were not related. The authors suggested that the disorder most closely resembled the Parkinson-dementia complex of Guam (105500) but could be distinguished by the lack of Chamorro descent (a dubious argument) and the earlier age of onset.
- Classic Progressive Supranuclear Palsy Syndrome Orphanet
  
  Classical progressive supranuclear palsy, also known as Richardson's syndrome, is the most common clinical variant of progressive supranuclear palsy (PSP; see this term), a rare late-onset neurodegenerative disease characterized by postural instability, progressive rigidity, supranuclear gaze palsy and mild dementia. Epidemiology The prevalence is conservatively estimated at about 1/16,600. Clinical description PSP usually manifests during the sixth or seventh decade of life with postural instability and falls, slowing of vertical saccadic eye movements and cognitive slowing. Progressively patients develop other eye abnormalities (dry and red eyes, blurred vision, spontaneous involuntary eyelid closure, photophobia), a dysexecutive cognitive syndrome with impulsivity, problems in speech (slow speech) and a supranuclear gaze palsy and difficulties in swallowing. The disease is characterized neuropathologically by gliosis with astrocytic plaques, accumulation of tau-immunoreactive neurofibrillary tangles and neuronal loss in specific brain areas, especially in the subthalamic nucleus and the substantia nigra.
- Progressive Supranuclear Palsy Gard
  
  Progressive supranuclear palsy (PSP) is a degenerative neurologic disease due to damage to nerve cells in the brain. Signs and symptoms vary but may include loss of balance; blurring of vision; problems controlling eye movement; changes in mood, behavior and judgment; cognitive decline; and slowing and slurred speech. PSP is often misdiagnosed as Parkinson disease due to similar symptoms. Onset is usually after age 60 but may occur earlier. Most cases of PSP appear to be sporadic, but familial cases have been reported. Some cases have been found to be caused by a mutation in the MAPT gene, and other genetic factors are being studied.
- Progressive Supranuclear Palsy Orphanet
  
  A rare late-onset neurodegenerative disease characterized by supranuclear gaze palsy, postural instability, progressive rigidity, and mild dementia. Epidemiology Prevalence is conservatively estimated at about 1/16,600. Clinical description PSP usually manifests during the sixth or seventh decade of life. Five clinical variants have been described with clinicopathological correlations: Classical PSP (Richardson's syndrome), and four atypical variants of PSP including PSP-Parkinsonism (PSP-P), PSP-Pure akinesia with gait freezing (PSP-PAGF), PSP-corticobasal syndrome (PSP-CBS), and PSP-progressive non fluent aphasia (PSP-PNFA) (see these terms). Richardson's syndrome is the most common clinical variant and manifests with a lurching gait, falls due to postural instability, cognitive impairment and slowing of vertical saccadic eye movements.
Peripheral Artery Disease Wikipedia

. ^ a b c d e f g h Harrison's principles of internal medicine (20 ed.). ... Creager, Mark A., Beckman, Joshua A., Loscalzo, Joseph. (2nd ed.). Philadelphia, PA: Elsevier/Saunders. 2013. ... (Fifty-eighth ed.). New York, N.Y. ISBN 9781260117431 . OCLC 1048597590. ^ a b c Peripheral Arterial Disease at Merck Manual of Diagnosis and Therapy Professional Edition. ... Fowkes, Gerry (ed.). "Angioplasty (versus non surgical management) for intermittent claudication".

BMP8A, BMP2, CNOT4, PAQR8, WWOX, CNNM1, VEGFA, ZYG11B, LRRTM4, TLR10, UTRN, PPP2R2C, UGDH, OSBPL10, RBFOX1, PPP4R2, MTHFD1L, NSMCE1, VIT, UBAC2, PPIEL, ATXN2, HGF, APOB, MTHFR, F2, ACE, LPA, IL6, TNF, THBS1, LIPC, CCL2, TLR4, CRP, HIF1A, LPL, PADI4, P2RY12, DHX40, NOS3, APOE, ANGPT1, PON1, RENBP, CXCL12, RAP2A, SELENOP, SSAV1, EIF2AK2, TCF7L2, NAT2, ADAMTS7, TLR2, TNFRSF1B, PCSK9, PRSS55, SLC35G1, TRIM63, SPZ1, ANTXR1, SPRTN, AGGF1, UGT1A1, WDTC1, PPARGC1A, YBX3, AAAS, WRN, CRISP2, PRH2, MPO, PON3, PECAM1, CYBA, CX3CR1, CS, COX8A, CHRNB4, CHRNA3, CHI3L1, SCARB1, CD36, CD34, CD14, CASR, BLM, CCND1, ATF3, APP, APOH, APOA1, ANGPT2, AGTR1, AGT, JAG1, ADD1, CYP1A2, CYP2B6, CYP2C19, FOXO1, NPY, ABO, MMP2, LDLR, IPO5, JAK2, IL10, CXCL8, GNB3, FLT1, FGF2, DPP4, FGF1, FGB, FAP, F12, F8, F7, F5, F3, EEF1A2, EDN1, AAA1
Hypoplastic Left Heart Syndrome Wikipedia

Williams Obstetrics (24 ed.). New York, NY: McGraw-Hill Education. ^ Galindo, A., Nieto, O., Villagrá, S., Grañeras, A., Herraiz, I., & Mendoza, A. (2009).

NKX2-5, GJA1, SAP130, PCDHA13, PCDHA9, FOXF1, TBX5, NR2F2, SYNPR, PKD1L2, MYH7B, ARHGAP31, CCDC22, MGAT4A, WASHC5, WT1, SYNPR-AS1, DTNA, NOTCH1, HAND1, MYH6, PROX1, FOXL1, APOE, CAMK4, JAM3, CAMK2G, EDN1, ETS1, MCTP2, FOXC2, FOXP1, S100B, LBX1, FXN, TNNT2, PLN, ADRB1, TBX2, ADCY5
- Critical Congenital Heart Disease Ghr
  
  Critical congenital heart disease (CCHD) is a term that refers to a group of serious heart defects that are present from birth. These abnormalities result from problems with the formation of one or more parts of the heart during the early stages of embryonic development. CCHD prevents the heart from pumping blood effectively or reduces the amount of oxygen in the blood. As a result, organs and tissues throughout the body do not receive enough oxygen, which can lead to organ damage and life-threatening complications. Individuals with CCHD usually require surgery soon after birth. Although babies with CCHD may appear healthy for the first few hours or days of life, signs and symptoms soon become apparent.
- Hypoplastic Left Heart Syndrome 2 Omim
  
  A number sign (#) is used with this entry because of evidence that hypoplastic left heart syndrome (HLHS2) is caused by heterozygous mutation in the NKX2-5 gene (600584) on chromosome 5q35.1. Description Hypoplastic left heart syndrome results from defective development of the aorta proximal to the entrance of the ductus arteriosus and hypoplasia of the left ventricle and mitral valve. As a result of the abnormal circulation, the ductus arteriosus and foramen ovale are patent and the right atrium, right ventricle, and pulmonary artery are enlarged (Brekke, 1953). For a discussion of genetic heterogeneity of hypoplastic left heart syndrome, see HLHS1 (241550). Molecular Genetics In 1 (1%) of 80 patients with hypoplastic left heart syndrome, McElhinney et al. (2003) identified heterozygosity for a missense mutation in the NKX2-5 gene (R25C; 600584.0004).
- Hypoplastic Left Heart Syndrome 1 Omim
  
  A number sign (#) is used with this entry because of evidence that hypoplastic left heart syndrome-1 (HLHS1) is caused by mutation in the GJA1 gene (121014) on chromosome 6q22. Description Hypoplastic left heart syndrome results from defective development of the aorta proximal to the entrance of the ductus arteriosus and hypoplasia of the left ventricle and mitral valve. As a result of the abnormal circulation, the ductus arteriosus and foramen ovale are patent and the right atrium, right ventricle, and pulmonary artery are enlarged (Brekke, 1953). Genetic Heterogeneity of Hypoplastic Left Heart Syndrome Hypoplastic left heart syndrome-2 (HLHS2; 614435) is caused by mutation in the NKX2-5 gene (600584) on chromosome 5q35.1. Somatic mutations in the HAND1 gene (602406) have been identified in tissue samples from patients with HLHS.
- Hypoplastic Left Heart Syndrome Orphanet
  
  A rare, congenital, non-syndromic, heart malformation characterized by under development of the left-sided cardiac structures (including left ventricle, ascending aorta, aortic arch, and mitral and/or aortic valve) such that the left heart is unable to provide adequate systemic cardiac output. Epidemiology Hypoplastic left heart syndrome (HLHS) has been reported to occur in 1/3,500 to 12,500 live births. A male to female predominance ratio of 1.5:1 is observed. Clinical description Newborn infants with HLHS are generally born at full term. Initially appearing healthy, they are dependent upon the patent ductus arteriosus (PDA) for systemic blood flow. As the PDA closes, systemic perfusion decreases, resulting in hypoxemia, acidosis, and cardiogenic shock.
- Hypoplastic Left Heart Syndrome Gard
  
  Hypoplastic left heart syndrome (HLHS) is a heart condition present from birth (congenital heart defect). In HLHS, the heart's left side (including the aorta, aortic valve, left ventricle and mitral valve) is underdeveloped. At birth, oxygen-rich blood bypasses the underdeveloped left side of the heart, going through openings between the left and right side that normally close a few days after birth (the patent ductus arteriosus and the patent foramen ovale). The right side of the heart then pumps blood to the lungs and the body. Therefore, there may be no symptoms for a few days. However, when these openings close, oxygen-rich blood cannot easily get to the rest of the body.
Takotsubo Cardiomyopathy Wikipedia

(Fifty-sixth ed.). New York. ISBN 978-1259585111 . OCLC 957316517. ^ Akashi YJ, Nakazawa K, Sakakibara M, Miyake F, Koike H, Sasaka K (2003).

ADRB1, ADRB2, CTRL, ESR1, ESR2, FMR1, GRK5, LPA, SERPINE1, VWF, BAG3, FSD1, FSD1L
- Tako-Tsubo Cardiomyopathy Orphanet
  
  A rare cardiac disease characterized by acute occurrence of heart failure after an emotional or physical trigger however, recovery of the wall motion abnormalities are observed within months. Symptoms are similar to acute coronary syndrome (ACS). Epidemiology Takotsubo syndrome (TTS) is found in about 1-3% of all patients with symptoms of ACS; however, the prevalence is likely underestimated. Around 90% of TTS patients are women, typically postmenopausal but male and younger patients are diagnosed increasingly due to raised awareness of the syndrome. Clinical description In the acute phase, clinical presentation, electrocardiography (ECG) and cardiac biomarkers are similar to those of ACS. Typical symptoms are acute chest pain or dyspnea. Further symptoms can arise from complications of TTS, e.g. heart failure, cardiogenic shock, or cardiac arrest.
Alopecia Areata Wikipedia

Lookingbill and Marks' Principles of Dermatology (4th ed.). Elsevier Inc.

IL2RA, CTLA4, IKZF4, STX17, CXCL9, PRDX5, CXCL10, RAET1L, ULBP3, CXCR3, CLEC16A, PTPN22, TRPS1, KDM5C, C6orf10, LINC01254, ACOXL, ATXN2, MAGI3, ERBB3, MALRD1, SLC16A12, HR, AIRE, IL1RN, ICAM1, IL1A, IL1B, FLG, TNF, HLA-DRB1, HLA-DQB1, HLA-C, GZMB, NFE2L2, MED25, FCRL3, FCGR1B, SPATA5, FCGR1A, CD40, FASLG, MCHR2, IFNG, FOXP3, NOS3, ICOSLG, PSIP1, MCRS1, IL13, TRAF1, TLR1, TGFB1, FAS, SLC3A2, MX1, NOTCH4, TRBV20OR9-2
Inflammatory Bowel Disease Wikipedia

(ed.). "Inflammatory Bowel Disease Health Center". WebMD. Retrieved 14 October 2014. ^ Lu DG, Ji XQ, Liu X, Li HJ, Zhang CQ (January 2014). ... PMID 15563659. ^ a b c Agabegi ED, Agabegi SS (2008). "Inflammatory bowel disease (IBD)".

IL10, TNF, TNFSF15, NOD2, ATG16L1, IRGM, IL23R, CARD9, IL18RAP, STAT3, PLCG2, IL6, MUC19, PTGS2, ICAM1, PTPN22, APC, SLC11A1, IL2RA, TGFB1, DEFA5, APC2, SFRP2, SFRP1, ITGA4, INAVA, VNN1, SLAMF8, ITGB8, ITGAL, CUL2, RASSF1, IL2, XBP1, ESR2, RUNX3, MUC2, CD40LG, NFIL3, SLC6A14, SLC22A4, IGF2, KLKB1, NOS2, IL21, PTPN2, F5, MST1, STAT4, IL18R1, IL27, SMAD3, ZMIZ1, TNFRSF6B, NUDT15, TYK2, ITLN1, IL1RL1, MAP3K8, FERMT1, WAS, RORC, FCGR2A, NR5A2, LRRK2, TRAF3IP2, FADS2, SH2B3, KSR1, IL1A, NR1I2, BSN, SKAP2, OSMR, IL1B, DLG5, HPS1, IBD2, TM9SF4, IFNG, IFNGR2, LITAF, LPXN, PLAU, GPR65, LPP, PLA2G4A, RIT1, ATXN2, ABCB1, NOTCH1, NFKB1, NFATC1, TLR4, TPMT, CUL1, IRF6, UBE2L3, PRKCB, WIPF1, IL17A, CXCL8, SYN3, IL1RN, SCAMP3, SBNO2, NOD1, NDFIP1, FAM171B, DENND1B, AMZ1, PUS10, HORMAD2, LACC1, CCDC26, GALM, ZNF831, SNX20, CDYL2, ZNF300, PYGO2, ZGPAT, MAML2, KIAA1109, TSPAN14, IPMK, BTBD8, UBAC2, LINC00598, KCCAT333, LINC00824, CRTC3-AS1, C5orf66, RTEL1-TNFRSF6B, SPATA48, LINC00484, TRAF3IP2-AS1, DUPD1, MIR3936HG, C5orf56, C10orf55, FLJ31356, TEX41, GRID2IP, C17orf67, DUSP16, CPEB4, RGS14, SEMA6D, IMPG2, IL22, FOXP1, ACAD8, SH2B1, PNKD, SPDEF, TBC1D9, TAB2, PLA2R1, HGFAC, PARK7, ATXN2L, SP140, CDC37, CIT, CD226, IBD5, TUBD1, IL23A, BACH2, ANKRD55, FTO, CRTC3, ERAP2, IFIH1, TMBIM1, THADA, SLAIN2, HDAC7, ERGIC1, CDC42SE2, BANK1, INTS11, CDKAL1, TET2, SUFU, HLA-DQA1, TAB2-AS1, CREM, GPR18, GALC, ADCY7, DNMT3B, CD6, GPR183, GPR35, CELSR3, FUT2, FEN1, EPHB4, GNA12, CD28, ETS1, PTK2B, CCND3, GCKR, DAP, CAMK2A, ADCY3, IL17D, HLA-DRB1, FOXP3, IL4, TP53, SMAD7, PPARG, SLC22A5, IBD3, IL12B, TIMP1, NKX2-3, IL17C, ITPA, MYO9B, TAC1, VDR, CSF2, IL10RA, IL33, CLDN2, SLC15A1, TG, CD14, TLR2, IL18, CCL20, NR3C1, MMP1, GSTT1, IL13, MTHFR, TREM1, KRT8, HLA-B, CCR5, IL17F, STAT6, TLR5, MLH1, GH1, IRF5, XIAP, LCN2, IL16, FCGR3A, JAK2, TACR1, MIF, FGF7, NPSR1, DEFB4A, IL37, REG1A, SETD2, HMGB1, IL15, DUOX2, CRP, CCL2, MUC1, HPGDS, CTLA4, IBD6, NLRP3, COX2, GSTM1, F2, TCF4, PRDM1, BPI, GSTK1, CD44, S100A12, S100A9, PLA2G1B, SLCO6A1, CCL5, FCGR3B, CD40, MMP2, MMP9, MMP3, MIR146A, PHB, GP2, SIRT1, AGR2, IL11, AHR, VEGFA, HNF4A, F2RL1, CCR6, ISG20, MIR21, DMBT1, AGT, CARD8, MICA, HIF1A, CUZD1, DECR1, TFF3, CCL26, DSG2, NOX1, PANX1, RAG2, EBI3, FGF2, TLR6, RAC1, CD1D, CASP1, REG4, S100A8, PROC, MAPK8, MAPK1, CYBB, FHIT, PRH2, IL24, PON2, PON1, NLRP1, ACE, IL32, TRBV20OR9-2, EDN1, CD68, MUC13, BTNL2, TCF7L2, MYDGF, CHI3L1, TTC7A, TLR3, MTOR, AICDA, TNFRSF1A, CMA1, SPP1, LRBA, SLC52A1, CNR1, IL19, VDAC1, CXCL12, SDC1, CXCR4, ENTPD1, ERAP1, CLEC7A, ULK1, IL25, TNFSF14, ADAM15, ENO1, CFTR, S100B, NAT2, CYP3A4, MIR155, NM, HSPA4, MYLK, BCL2, MUC5AC, DEFB4B, CD24, GBP1, CCND1, ARSA, MMP13, ADORA3, IGFBP3, CXCR3, IL1R1, MEP1A, MEFV, IL2RB, APOA4, IL6ST, IL7, MIR135B, CXCR2, KRAS, IL10RB, GLB1, CXCL10, IRF4, HSPA1B, MIR31, HT, PAK1, NR4A1, LINC-ROR, HMOX1, HLA-C, RBM45, HP, SLC11A2, HGF, HSPA1A, MAST3, CPOX, POP5, CRNKL1, TNFRSF12A, F11R, TLR8, TLR7, EXOSC1, ATF6, ACP1, CRK, NPS, CLDN4, MIR425, BW16, NR0B1, CUX1, KLRK1, PADI4, MIR346, VN1R17P, MIR34C, AFTPH, CNR2, LOC105369230, ALB, DEFB103A, UGT1A1, TERF2IP, CYP2D6, CBX3, KIF21B, TREM2, EIM, GPR166P, TLR9, DUOX1, CBSL, ACHE, KLF6, COX8A, SCART1, AGER, IL21R, REXO2, B3GAT1, CRX, PSC, CBR3-AS1, MAPK14, RNU1-1, FGF20, OCLN, POLDIP2, CHMP2B, IBD4, CSF2RA, CSF3, KLRC4-KLRK1, RNF19A, CSF3R, TFIP11, TMEFF2, LY96, LPAR3, SLC39A14, MIR1246, IBD21, VENTX, ACTB, CTGF, AMACR, PILRA, MIR595, MUC5B, SNX10, CD274, CCR2, C1GALT1C1, MIR665, MCTS1, TRIB2, MPRIP, MCAT, CMM, ADORA2B, ADAMDEC1, TPSD1, RABGEF1, MRGPRX3, MARCH1, EIF2A, CBS, ZFP90, IL34, BMI1, CCNE1, PNPLA3, COMMD1, CFB, GPBAR1, BDKRB2, ELOVL7, BCL3, MORC4, MMP28, CD19, NDRG4, OXER1, BCL11B, FNDC4, IBD8, MLKL, FGD2, GPRC6A, UNC5CL, DCLRE1C, MAP1LC3B, NRG4, MRGPRX1, BMP7, IL22RA2, FCRL3, NXPE1, TIRAP, SLC15A4, DBA2, C4B, PRRT2, CAVIN3, C3, EGLN3, EGLN2, TSPO, REEP6, G6PC3, CAMP, BRCA1, CAST, SCLT1, GPR151, SLC2A14, RSPO3, TRIM63, CASR, CBR1, CD36, MAGI3, MIR301A, TEPP, FAM20C, CHGA, SERPINA13P, TRIM39, ASAH2, ANXA1, IL17REL, ALPI, ALOX5, LANCL2, DEFB103B, IL26, LINC01194, AMBRA1, MIR10A, MIR122, CLCN5, MIR132, MIR150, MRGPRX4, MIR200B, MIR223, CCR3, ANKZF1, MIR224, IL31, IBD7, IFNL2, LINC01193, CD47, SLC28A3, CCDC88B, SLC22A23, PROK2, IGAN1, ARRB2, PGP, CD69, LGR6, TRPV4, AREG, CELIAC2, CXCL16, FAS, ZNF410, APOE, HAMP, CDKN1A, CDKN1B, ARMH1, CDX2, TMEM173, RTN4, RSPO2, MAGT1, GUCY2C, DBP, CD160, NFE2L2, GABPA, ACKR1, NFKBIA, NGF, NOS3, FTL, NTRK1, NTS, NTSR1, TNFRSF11B, OPRM1, OSM, P2RX5, P2RX7, NELL1, NCF4, NCF2, MRC1, FOXO4, MMP7, MMP12, MMP14, MPO, MPZ, COX1, NCAM1, RNR1, GAPDH, MUC4, MUC6, MYD88, CEACAM6, PAEP, SERPINE1, PAPPA, FGFR2, PRKAB1, PSAP, PSMD7, PTCH1, PTGER4, PTGS1, PTPN11, PRKAA1, PTPRC, PTPRH, PTPRS, RAC2, RAP1A, RARRES2, PRKAA2, PRH1, PC, FPR2, PDCD1, PDGFB, PDZK1, PGA5, SLC25A3, PKM, PLAT, PRF1, FLG, FOXO1, PLG, PMP22, PON3, POU2F1, MLN, MIP, MICE, GPR3, IFNA1, IFNA13, IFNAR1, GPER1, IGF1, IGF1R, GNAO1, IDUA, GNAI2, IL3, IL4R, IL6R, GLI3, IL9, IFI16, IDH2, IL12A, HPRT1, HLA-A, HLA-DPB1, GSTM2, HLA-DQB1, HLA-DQB2, HLA-G, HSD11B2, IDH1, HSPA2, HSP90AA1, IAPP, ICA1, GRN, ICAM3, GLI1, IL15RA, MICB, LTB, LEP, LGALS1, LGALS2, LGALS3, LPL, LTA, LTBR, L1CAM, LYZ, GC, SMAD5, MBL2, CIITA, CD99, RPSA, KRT18, IMPDH1, GCY, IDO1, IRF1, GHSR, GDF1, ITGAX, ITGB2, JAK1, KRT1, JAK3, KCNA3, KCNN4, KLK1, KAT2A, KNG1, REL, REG1B, RNASE3, CD163, PSTPIP1, CLDN1, EEF1A2, EEF1A1, ARHGEF2, GPR55, SLIT2, EGF, SLC9A3R1, PLAA, COX5A, GRAP2, NTN1, ABCG2, SOCS3, MTMR3, ARHGEF6, RIPK1, ERF, ERBB4, STX2, IKBKG, TP63, MBTPS1, TNFRSF14, GZMB, RIPK2, EMD, ELK4, EGR1, PER3, EGFR, AIM2, ATN1, STK24, HPSE, AHSA1, DLD, CORIN, CERS1, DEFB1, IQGAP2, LILRB1, LANCL1, EBNA1BP2, IMMT, SDS, LILRB4, RIPK3, DEFA6, IPO8, DMRT1, TBPL1, DPP4, PTGES, CLOCK, PDIA4, DRD2, MAGI2, SLC23A1, NR1H4, POP7, DNMT1, PTPRU, ARPC2, LRPPRC, NAMPT, RABEPK, DHX16, PLA2G6, RNU1-4, SOD1, SLC9A1, SLC9A3, SLC16A1, SLC22A1, ACACA, SOAT1, ST14, SFTPD, FCGR1A, STAT5A, STATH, SULT1E1, TACR2, ADAM17, SLC6A4, FCN1, TCF21, CCL7, FER, RPLP0, RPLP2, S100A1, S100A10, SAA1, CCL11, FCN2, CCL14, CCL15, CXCL11, CXCL5, CX3CL1, SELENOP, TBP, TCOF1, FZD4, VIPR1, TNFSF4, TNFRSF4, UBC, F2R, VCAM1, EZR, TRPV1, TRAF6, WNT1, ESR1, LST1, AIMP2, BAS, ERN1, TUFM, HSP90B1, PRDX2, FAT1, TEK, TERF2, TERT, TFF1, TFF2, TGFA, TGFB2, ACSL1, TIAL1, TIMP2, TLR1, FASN, TNFRSF1B, TPI1, SPHK1
Dupuytren's Contracture Wikipedia

[citation needed] Notable cases[edit] Bill Frindall, who had a finger amputated.[61] Margaret Thatcher[62] Misha Dichter[63] Prince Joachim of Denmark[64] Ronald Reagan[62] Bill Nighy[65] Tim Herron[66] John Elway[67] See also[edit] Knuckle pads References[edit] ^ Fitzpatrick's dermatology in general medicine (6 ed.).

MMP14, LINC01592, BOP1, DDR2, NEDD4, RAB31, ITGA11, EIF3E, TIMP2, ATL1, EPDR1, EBF2, ZC3H12D, DUXA, YAP1, WNT2, AIMP2, SQSTM1, GRAP2, RNF19A, POLDIP2, AHSA1, POSTN, THY1, CCT7, ACTA2, TGFB2, IL1A, CRK, MAPK14, EGF, EGFR, FGF2, GAPDH, HFE, HLA-DRB1, IL1B, TGFB1, MB, MMP2, RNR2, MAPK1, SFRP4, SMN1, SMN2, KLF6, TGFA