-
Head And Neck Cancer
Wikipedia
Smokeless tobacco is a cause of oral cancer and oropharyngeal cancer . [27] Cigar smoking is also an important risk factor for oral cancer. [28] Other environmental carcinogens suspected of being potential causes of head and neck cancer include occupational exposures such as nickel ore refining , exposure to textile fibers, and woodworking. ... National Cancer Institute . 22 November 2019 . Retrieved 28 November 2019 . ^ a b c d e f g World Cancer Report 2014 . ... PMID 24369209 . ^ "Throat cancer | Head and neck cancers | Cancer Research UK" . www.cancerresearchuk.org . Retrieved 28 November 2019 . ^ a b c d e f g h Ridge JA, Glisson BS, Lango MN, et al.EGFR, TP53, PIK3CA, FGFR2, BCL2L1, ERBB3, RARB, XRCC3, RAD51, BAP1, TGFA, GRP, PIK3CB, APOBEC3B, STAT6, VEGFA, FGFR1, FAT1, ERBB2, PRAME, UROD, TYMS, GPX1, MAL, DPYD, CYLD, BCL2, MAPK1, AREG, CEBPA, CSF3, MAPK3, CDC73, NAA25, HELQ, FOXE1, ADH7, MINPP1, ADH1B, HABP2, IL6, PTGS2, AHR, RRM2, XRCC1, IL13, PTGS1, CCND1, CA9, CYP1A1, STAT3, S100A2, TCF21, ICAM5, STAT5B, SDHC, TNF, STAT5A, NAT2, TP53BP1, VIM, HOTAIRM1, MTRNR2L12, MIR210, MIR204, MIR148A, ABCC10, MRPL11, ING3, CYCS, TLR7, ING4, TMEM97, BBC3, HPSE, ROBO1, DLGAP1, IFITM1, GJB6, MSH2, RAD17, MAPK6, GJB2, FGFR4, EPOR, EPO, EPHB3, EPAS1, EIF4E, EGF, DSG3, DDIT3, CYP1B1, CD44, CD4, BRAF, BRCA1, BMI1, B2M, AR, ALDH1A1, GNAS, GSTM1, GSTP1, MKI67, PCYT1A, FURIN, NOS2, NME1, MTRR, MTR, ABCC1, MLH1, MET, HIF1A, KDR, IL13RA2, IL2RA, IGFBP3, IGF1R, IGF1, HLCS, HLA-C, CERNA3
-
Separation Anxiety Disorder
Wikipedia
In many cases, there are no signs during childhood. [28] [29] Behavioral inhibition (BI) plays a large role in many anxiety disorders, SAD included. ... "The origins of attachment theory: John Bowlby and Mary Ainsworth". Developmental Psychology . 28 (5): 759–775. doi : 10.1037/0012-1649.28.5.759 . ^ Mychailyszyn, Matthew P.; Mendez, Julia L.; Kendall, Philip C. (2010). ... Journal of Abnormal Child Psychology . 28 (2): 205–211. doi : 10.1023/A:1005179032470 .
-
Anthrax
Wikipedia
Exposure [ edit ] The spores of anthrax are able to survive in harsh conditions for decades or even centuries. [26] Such spores can be found on all continents, including Antarctica. [27] Disturbed grave sites of infected animals have been known to cause infection after 70 years. [28] Historically, inhalational anthrax was called woolsorters' disease because it was an occupational hazard for people who sorted wool . ... Archived from the original on 2 January 2016. ^ "Injection Anthrax | Anthrax | CDC" . www.cdc.gov . 28 January 2019 . Retrieved 16 September 2020 . ^ a b Anthrax - Chapter 4 - 2020 Yellow Book | Travelers' Health | CDC .ANTXR2, ANTXR1, BRAF, MAP2K1, NLRP1, VWF, ITIH4, CAP1, ADAMTS13, IMMT, KIF1C, SORBS1, ACTB, HACD1, CNTNAP1, PPIP5K2, VEGFA, TLR4, YWHAZ, BRD4, UBR2, SET, PADI4, ZDHHC5, FBXO8, GAL, PGPEP1, NLRC4, NOD2, FBRS, ARAP3, PAGR1, PLB1, SREBF2, SELP, SELPLG, LCN2, BAK1, BMP1, CALR, CASP1, COL11A2, CTAA1, EPHB2, ERBB2, NR5A1, GAST, GALNS, IL1B, STT3A, LGALS1, PARP1, LNPEP, LRP6, LRP5, NR4A2, PAEP, PRDX1, SERPINB6, PLA2G1B, PLG, PRCP, MAPK1, MAP2K3, ROS1, HNP1
-
Chronic Fatigue Syndrome
Wikipedia
Sensitivity to pain increases after exertion, which is opposite to the normal pattern. [27] Onset [ edit ] Gradual or sudden onset of the illness may occur, and studies have mixed results as to which occurs more frequently. [2] : 158 : 181 Physical functioning [ edit ] The functional capacity of individuals with CFS varies greatly. [28] Some persons with CFS lead relatively normal lives; others are totally bed-ridden and unable to care for themselves. [29] For the majority of persons with CFS, work, school, and family activities are significantly reduced for extended periods of time. [30] The severity of symptoms and disability is the same regardless of gender, [31] and many experience strongly disabling chronic pain . [32] Persons report critical reductions in levels of physical activity. [33] Also, a reduction in the complexity of activity has been observed. [34] Reported impairment is comparable to other fatiguing medical conditions [35] including late-stage AIDS , [36] lupus , rheumatoid arthritis , chronic obstructive pulmonary disease (COPD), and end-stage kidney disease . [37] [ failed verification ] CFS affects a person's functional status and well-being more than major medical conditions such as multiple sclerosis, congestive heart failure, or type II diabetes mellitus. [38] [39] Often, courses of remission and relapse of symptoms occur, which make the illness difficult to manage. ... Björn Sigurðsson disapproved of the name, stating that the illness is rarely benign, doesn't always cause muscle pain, and is possibly never encephalomyelitic. [137] The syndrome appeared in sporadic as well as epidemic cases. [141] In 1969, benign myalgic encephalomyelitis appeared as an entry to the International Classification of Diseases under Diseases of the nervous system. [142] In 1986, Ramsay published the first diagnostic criteria for ME, in which the condition was characterized by: 1) muscle fatiguability in which, even after minimal physical effort, 3 or more days elapse before full muscle power is restored; 2) extraordinary variability or fluctuation of symptoms, even in the course of one day; and 3) chronicity. [143] By 1988, the continued work of Ramsay had demonstrated that, although the disease rarely resulted in mortality, it was often severely disabling. [2] : 28–29 Because of this, Ramsay proposed that the prefix "benign" be dropped. [139] [144] [145] Chronic fatigue syndrome [ edit ] In the mid-1980s, two large outbreaks of an illness that resembled mononucleosis drew national attention in the United States.FURIN, NR3C1, RNASEL, NTRK3, ETV6, TNF, TRPM3, IL10, COMT, SLC6A4, TGFB1, NHS, NOS2, TPH2, HTR2A, APRT, MFAP1, HLA-DRB1, PTGS2, EIF2AK2, SERPINA6, HPSE, MTA2, MASP2, GDF15, ADIPOQ, ASIC3, TRPA1, TRBV20OR9-2, VIP, TRPM2, PLAU, SULT1E1, TH, PRKCD, REN, ACTB, TMED2, TPPP, ERVK-18, CD24, MIR330, MIR99B, MIR30C2, MIR30C1, MIR150, MIR143, MIR126, COPD, EMX2OS, NRSN1, EMB, RBM45, NLRP3, IL17F, SIGLEC12, FANCM, KRT20, REM1, SESN1, DISC1, B3GAT1, CHP1, PSIP1, PF4, NFE2L2, OAS2, NPAS2, GABPA, FLNA, FCN1, PTK2B, ESR2, ELANE, DUT, ACE, DBI, CTSB, CPT2, MAP3K8, CD69, CD38, MS4A1, CD14, CD9, CD6, BLM, CFB, AVP, ATR, AMPD1, GCH1, GDNF, GRIK2, IL2, ADCYAP1, MYOG, MUC1, RNR2, MBL2, LTA, KLRC2, KIR3DS1, IL18, IL6, IL1B, HTT, IL1A, IGHG3, IFNB1, IFNA13, IFNA1, HTR7, HTR1A, HLA-DQB1, HLA-DQA1, CFH, H3P19
-
Refusal Of Work
Wikipedia
It was founded in 1993 by Tom Hodgkinson and Gavin Pretor-Pinney with the intention of exploring alternative ways of working and living. [28] Refusal of work in practice [ edit ] "Slackers" [ edit ] The term slacker is commonly used to refer to a person who avoids work (especially British English), or (primarily in North American English) an educated person who is viewed as an underachiever . [29] [30] While use of the term slacker dates back to about 1790 or 1898 depending on the source, it gained some recognition during the British Gezira Scheme , when Sudanese labourers protested their relative powerlessness by working lethargically, a form of protest known as 'slacking'. [31] The term achieved a boost in popularity after its use in the films Back to the Future and Slacker . [29] [32] NEET [ edit ] NEET is an acronym for the government classification for people currently "Not in Employment , Education or Training ". ... Globetrotter.berkeley.edu . Retrieved 2010-06-28 . ^ a b "From wage slaves to wage workers: cultural opportunity structures and the evolution of the wage demands of the Knights of Labor and the American Federation of Labor, 1880–1900. ... Archived from the original on 2009-06-30 . Retrieved 2010-06-28 . ^ "The Bolsheviks and Workers Control" . www.spunk.org . ^ Full text of Cannibals All!
-
Anxiety Disorder
Wikipedia
Common symptoms include hypervigilance , flashbacks , avoidant behaviors, anxiety, anger and depression. [28] In addition, individuals may experience sleep disturbances. [29] People who suffer from PTSD often try to detach themselves from their friends and family, and have difficultly maintaining these close relationships.There are a number of treatments that form the basis of the care plan for those suffering with PTSD. ... Archived from the original on 10 June 2012 . Retrieved 28 March 2013 . ^ a b c d National Collaborating Centre for Mental Health, (UK) (2006). ... ISBN 978-1-57230-446-8 . ^ Lindsay, S.J.E.; Powell, Graham E., eds. (28 July 1998). The Handbook of Clinical Adult Psychology (2nd ed.). ... Archived from the original on 8 May 2016 . Retrieved 28 April 2016 . ^ "Anxiety disorders – Symptoms and causes" .
-
Neurogenic Claudication
Wikipedia
NSAIDs and prostaglandin-based medications control inflammation at sites of nerve damage or pressure by inhibiting cyclooxygenase activity, and reducing the production of prostaglandins , a key contributor of inflammation. [24] [25] By reducing inflammation, less pressure is put on the nerve roots, decreasing pain, and providing relief for NC patients. [26] Gabapentin aims to reduce pain and provide relief by altering the normal functioning of neurotransmitters that induce a sensation of pain and discomfort. [27] However, the exact mechanism of Gabapentin’s functioning in the body is not completely understood and current knowledge is based on experimental studies that target the nervous system. [28] Methylcobalamin is another medication that targets the nervous system to reduce pain and provide NC patients with temporary pain-relief. ... "Lumbar Stenosis: A Recent Update by Review of Literature" . Asian Spine Journal . 9 (5): 818–28. doi : 10.4184/asj.2015.9.5.818 . ... PMID 23886845 . ^ Kuritzky L, Samraj GP (2012-11-28). "Nonsteroidal anti-inflammatory drugs in the treatment of low back pain" .
-
Birth Defect
Wikipedia
These birth defects and behavioral disorders were found in cases of both long- and short-term paternal alcohol ingestion. [24] [25] In the same animal study, paternal alcohol exposure was correlated with a significant difference in organ size and the increased risk of the offspring displaying ventricular septal defects at birth. [25] Toxic substances [ edit ] Further information: Developmental toxicity , Drugs in pregnancy , and Environmental toxins and fetal development Substances whose toxicity can cause congenital disorders are called teratogens , and include certain pharmaceutical and recreational drugs in pregnancy , as well as many environmental toxins in pregnancy . [26] A review published in 2010 identified six main teratogenic mechanisms associated with medication use: folate antagonism , neural crest cell disruption, endocrine disruption , oxidative stress , vascular disruption, and specific receptor- or enzyme-mediated teratogenesis. [27] An estimated 10% of all birth defects are caused by prenatal exposure to a teratogenic agent. [28] These exposures include medication or drug exposures, maternal infections and diseases, and environmental and occupational exposures. ... It is hypothesized that this may be due to environmental exposures or lifestyle choices. [76] Research has found that there is a correlation between advanced paternal age and risk of birth defects such as limb anomalies , syndromes involving multiple systems, and Down syndrome . [60] [29] [77] Recent studies have concluded that 5-9% of Down syndrome cases are due to paternal effects, but these findings are controversial. [60] [61] [29] [78] There is concrete evidence that advanced paternal age is associated with the increased likelihood that a mother will have a miscarriage or that fetal death will occur. [60] Unknown [ edit ] Although significant progress has been made in identifying the etiology of some birth defects, approximately 65% have no known or identifiable cause. [28] These are referred to as sporadic, a term that implies an unknown cause, random occurrence regardless of maternal living conditions, [79] and a low recurrence risk for future children.
-
Rhabdomyolysis
Wikipedia
In 2012, the United States military reported 402 cases. [26] Another group at increased risk is firefighters. [27] [28] History [ edit ] Investigations of people injured in collapsed buildings during the Blitz of London led to numerous discoveries in the mechanisms underlying kidney impairment in rhabdomyolysis.ACADM, CYP2C8, INS, AMPD1, HMOX1, HAVCR1, ALAS1, CPT2, RYR1, FKRP, TRAPPC2L, STRN4, DBNL, PGK1, TANGO2, TSFM, SLC12A3, SCN4A, ANO5, RYR2, POLG, LDHA, PGAM2, PFKM, ACADVL, HADHB, HADHA, GABRA3, CLCNKB, SLC25A20, CACNA1S, BCS1L, ATP5F1D, AHCY, KCNJ18, CKM
-
Cognitive Inertia
Wikipedia
Despite Polaroid's large research and development into the digital market, their inability to refocus their strategy to hardware sales instead of film eventually led to their collapse. [28] Scenario planning has been one suggestion to combat cognitive inertia when it comes to making strategic decisions to improve business.
-
Hypovolemic Shock
Wikipedia
Elderly patients are more likely to experience hypovolemic shock due to fluid losses as they have a less physiologic reserve . [4] Hypovolemia secondary to diarrhea / dehydration is thought to be predominant in low-income countries. [13] See also [ edit ] Adipsia Anemia Cardiac index Heart murmur References [ edit ] ^ a b "Hypovolemic shock: MedlinePlus Medical Encyclopedia" . MedlinePlus . 2019-01-28 . Retrieved 2019-02-21 . ^ a b McGee, Steven (2018).
-
Mosquito-Borne Disease
Wikipedia
Twenty-seven (27) sub-Saharan African countries have reported Anopheles vector resistance to pyrethroid insecticides. [28] Indoor spraying of insecticides is another prevention method widely used to control mosquito vectors.
-
Terminal Illness
Wikipedia
Initial screening measures include: blood tests, pregnancy tests, serologic tests, urinalysis, drug screening, imaging, and physical exams. [27] [28] [29] For patients who are interested in liver transplantation, only patients with acute liver failure have the highest priority over patients with only cirrhosis. [30] Acute liver failure patients will present with worsening symptoms of somnolence or confusion (hepatic encephalopathy) and thinner blood (increased INR) due to the liver's inability to make clotting factors. [31] Some patients could experience portal hypertension, hemorrhages, and abdominal swelling (ascites). ... "Evidence on the cost and cost-effectiveness of palliative care: A literature review". Palliative Medicine . 28 (2): 130–150. doi : 10.1177/0269216313493466 . ... "Retrospective studies of end-of-life resource utilization and costs in cancer care using health administrative data: A systematic review". Palliative Medicine . 28 (10): 1167–1196. doi : 10.1177/0269216314533813 . ... "The effects of advance care planning on end-of-life care: A systematic review". Palliative Medicine . 28 (8): 1000–1025. doi : 10.1177/0269216314526272 .
-
Repressed Memory
Wikipedia
Loftus and Guyer also found evidence that, following her initial "recall" of the abuse during therapy at age six, Doe had talked about the abuse during the eleven years in between the sessions of therapy, indicating that even if abuse had really occurred, memory for the abuse had not been repressed. [17] [18] More generally, in addition to the problem of false memories, this case highlights the critical dependence of repression-claims cases on the ability of individuals to recall whether or not they had previously been able to recall a traumatic event; as McNally has noted, people are notoriously poor at making that kind of judgment. [9] An argument that has been made against the validity of the phenomenon of repressed memories is that there is little (if any) discussion in the historical literature prior to the 1800s of phenomena that would qualify as examples of memory repression or dissociative amnesia. [19] In response to Pope's 2006 claim that no such examples exist, Ross Cheit , a political scientist at Brown University , cited the case of Nina , a 1786 opera by the French composer Nicolas Dalayrac , in which the heroine, having forgotten that she saw her lover apparently killed in a duel, waits for him daily. [20] Pope claims that even this single fictional description does not clearly meet all criteria for evidence of memory repression, as opposed to other phenomena of normal memory. [21] Despite the claims by proponents of the reality of memory repression that any evidence of the forgetting of a seemingly traumatic event qualifies as evidence of repression, research indicates that memories of child sexual abuse and other traumatic incidents may sometimes be forgotten through normal mechanisms of memory. [22] [23] Evidence of the spontaneous recovery of traumatic memories has been shown, [24] [25] [26] and recovered memories of traumatic childhood abuse have been corroborated; [27] however, forgetting trauma does not necessarily imply that the trauma was repressed. [22] One situation in which the seeming forgetting, and later recovery, of a "traumatic" experience is particularly likely to occur is when the experience was not interpreted as traumatic when it first occurred, but then, later in life, was reinterpreted as an instance of early trauma. [22] Thus, although Sheflin and Brown claimed that a total of 25 studies on amnesia for child sexual abuse exist and that they demonstrate amnesia in their study subpopulations, an editorial in the British Medical Journal concludes, in reference to the Sheflin and Brown findings, that "on critical examination, the scientific evidence for repression crumbles." [28] [29] Authenticity [ edit ] Memories can be accurate, but they are not always accurate.
-
Brain Tumor
Wikipedia
Mutations and deletions of tumor suppressor genes , such as P53 , are thought to be the cause of some forms of brain tumor. [26] Inherited conditions, such as Von Hippel–Lindau disease , tuberous sclerosis , multiple endocrine neoplasia , and neurofibromatosis type 2 carry a high risk for the development of brain tumors. [1] [27] [28] People with celiac disease have a slightly increased risk of developing brain tumors. [29] Smoking has been suggested to increase the risk but evidence remains unclear. [30] Although studies have not shown any link between cell phone or mobile phone radiation and the occurrence of brain tumors, [31] the World Health Organization has classified mobile phone radiation on the IARC scale into Group 2B – possibly carcinogenic. [32] The claim that cell phone usage may cause brain cancer is likely based on epidemiological studies which observed a slight increase in glioma risk among heavy users of wireless and cordless phones. ... No results have yet been published. [89] Non-invasive detection [ edit ] Efforts to detect signs of brain tumors in the blood are in the early stages of development as of 2019. [90] See also [ edit ] List of brain tumor cases References [ edit ] ^ a b c d e f g h i j k l m n o p q "Adult Brain Tumors Treatment" . NCI . 28 February 2014. Archived from the original on 5 July 2014 .TP53, ALK, BRAF, IDH1, PTEN, EGFR, CTNNB1, VEGFA, CDKN2A, MGMT, CDK4, CCND1, SOX2, IL2, SPP1, YAP1, HRAS, PON1, S100B, PCNA, TGM2, SIRT1, PTCH1, SOD2, CYP2C9, RELA, NRARP, IQGAP2, FJX1, ITGB2, TGFBR2, SMO, HES5, IQGAP1, EML4, DTX2, DLL1, AMOT, DAPK1, PIK3CA, IDH2, APC, H3-3A, NRAS, FLI1, POLE, PIK3CB, ERBB2, POLD1, PIK3R1, MTOR, TNF, PROM1, PIK3CG, SMARCB1, PIK3CD, PTPN11, CD44, EGF, ATM, ABCB1, MIR21, CXCR4, GFAP, DMBT1, NES, STAT3, PDPN, SMUG1, AQP4, IL13, CXCL12, TERT, AKT1, BCL2, RAF1, NR2E1, TNC, HIF1A, ABCG2, OLIG2, NTRK1, NOTCH1, BMI1, MYC, HPGDS, TFRC, GSTT1, MET, CD46, MMP9, CDKN2B, PLAU, PDCD1, SST, SLC2A1, NRP1, H3P10, TBC1D9, CASP3, MMP2, IL6, BDNF, GSTM1, NF1, GSTP1, MSH6, OSM, MYCN, NF2, KNG1, KRAS, RTEL1, CD274, MSH2, CSF2, KDR, ACKR3, DSC3, TF, ANXA2, SLCO6A1, L3MBTL2, GSTK1, MMP14, IFNB1, TYMS, LOC110806263, CCL2, SERPINE1, TNFSF10, NOTCH2, PGR, IFNG, FLT3LG, CXADR, ZHX2, CDKN1A, L3MBTL1, IGFBP2, ING1, LCN2, HSPA4, HGF, RAC1, PAEP, MDM2, H3-3B, FGFR1, FHIT, ESRRB, FN1, ERCC1, FOLH1, NOS2, NAP1L1, GH1, PMS2, MTHFR, GLI1, ABCC1, FGF2, PRKAR1A, REST, SPARC, IGF2, LINC01194, LGR5, ALOX5, COL18A1, PPP1R2C, APEX1, LGI1, APOE, GDF15, CAV1, MELK, CASR, NR1I3, OPTN, SLC12A9, TRIM13, CA9, ARR3, TSPO, PYCARD, AHR, ALB, ATRX, SLC12A2, IGF1R, CXADRP1, HOTAIR, KLF6, SPG7, H3C9P, MRC1, MSI1, TTYH1, MIR326, IL4, MKI67, MSH3, MLH1, P2RX5-TAX1BP3, C20orf181, FOXP3, IL1B, MIB1, TMED7, TMED7-TICAM2, MNAT1, NT5C3A, MIR10B, MIR137, LRP1, KIT, TICAM2, GADL1, INSR, L1CAM, LAMC2, ZAR1, LIF, MIR155, MAPT, CXCL8, CABYR, AZIN2, MTDH, MDM4, IDO1, IL13RA2, LIN28A, MIR34A, MIR17HG, LRRC4, SAI1, CBX5, PLXND1, TAM, SLC7A5, AD5, TFPI2, XRCC3, XRCC1, VIM, PKM, PHLDA2, TPMT, TPM3, TLR2, PPARG, TFAM, TEK, ADAM17, PTGDS, PTGS2, PTN, SOX10, SOAT1, SNCA, SLC2A3, SCT, SAT1, SERPINI1, AXIN1, TMEFF1, P2RX1, P2RX2, DKK1, HPSE, NFKBIA, S100A4, ZBTB18, APC2, NPY, CEBPZ, ABCB6, MVP, P2RX3, PECAM1, P2RX4, P2RX5, P2RX7, P2RY1, P2RY2, P2RX6, TNFRSF10B, ADAM23, PSMG1, PDGFRA, ENPP1, NGF, NAT2, IGF1, EPO, CTSL, CYP1A1, CYP2D6, DHCR24, DNMT3B, DUSP2, E2F1, EPHB2, EPOR, GLS, ERBB4, ERCC2, ESR1, EZH2, EFEMP1, FLT1, FUS, SLC37A4, CSPG4, VCAN, CDK2, CD47, ACTB, ACYP2, ADCYAP1R1, PARP1, JAG1, ALAD, ANG, ANGPT1, AQP9, STS, AXL, ADGRB1, BMP4, CA2, CALCR, CASP9, CCND2, GJA1, RB1, ICAM1, LAMB1, BCL6, WIF1, CHEK2, PDCD10, BRS3, SBNO2, BRCA1, IL12A, EPB41L3, SEC14L2, BCL2A1, MAPK8IP3, SULF1, SYNM, BAX, ADGRB3, TRAM1, MACF1, RASSF1, IL1RAPL1, TBC1D8, PTPRT, CAMKK2, CXCR6, DCTN6, KLF9, BST2, CYSLTR1, SEPTIN9, BSG, FGL2, PPARGC1A, MMP24, LYVE1, SUB1, IMMT, IL24, ADAMTS13, ADAMTS8, SUZ12, CASP14, HSPA14, EHD3, NXT1, ASAH1, IAPP, RMC1, NOP53, BICRA, ERVW-1, ADGRE2, NOX4, ADGRB2, DELEC1, TRAT1, ARSA, TMED5, ARG2, GAL, ING4, EGFL7, DNAJC15, ASCL1, ATF4, TMEM97, PATZ1, CORO1C, HSPBP1, SLC7A11, IL10RA, QPCT, TPSG1, PRDX5, PART1, ZNF521, IL10, PHGDH, AVP, GNL3, HAVCR1, LAT, ATR, IGF2BP1, BUB1B, TRIM3, TRIP10, PCSK7, LPAR2, OSMR, CCK, MTA2, CRLF1, CACNA2D2, SOCS6, SLIT2, MXD4, SLC9A3R1, NMT2, NTN1, RUNX3, GSTO1, ONECUT2, MAGED1, RUNX1, SLC6A5, CCNB1, SOCS3, HSPB3, URI1, TNFSF14, CD40LG, CD38, CD164, TNFRSF6B, FADD, DLK1, CD34, CD80, CD2, IL18, TSC22D1, APLN, CACNA1I, TIMELESS, H3C7, GOSR1, CYTIP, SH3PXD2A, NET1, CCNO, AKR1A1, TUBB3, PRG3, NDRG1, PIAS3, CA4, VAV3, GPNMB, IL12B, NXF1, CRTAP, KAT5, ZNRD2, SPTLC1, MRPL28, POMT1, CA12, DDR1, EIF5B, HTC2, FAM131B, RB1CC1, SPATA2, CAT, LRIG2, SV2A, HSPD1, CASP8, CASP2, DNM1L, TSPAN1, LRPPRC, CAPZB, BCAP31, CALR, TRIM28, LHFPL2, LEF1, NIN, LAMB2, IFI27, LIN28B, C1QTNF8, C17orf97, ADRA1A, MIR106A, MIR106B, MIR107, MIR10A, MIR125A, PLK5, MIR129-2, MIR132, MIR134, ADM, MIR144, MIR145, MIR146A, MIR149, ADRA2B, AFM, IDUA, GEN1, ZNF513, ALCAM, RSS, SIRPA, MGAT5B, IL2RG, GPHA2, HTRA4, ALKBH3, IL27, EBF3, ALRH, BTBD8, AKT2, APLNR, NANOS1, CXorf66, ADH1A, MIR191, MIR203A, CCR2, ESRG, ADAM8, CCN1, RAB6C-AS1, CD24, IFNA2, ACHE, RPL17-C18orf32, COMMD3-BMI1, ABO, ERVK-20, CERNA3, ABCA4, MNS16A, H3P9, H3P23, H3P24, MIR671, MIR92B, MIR205, PRB2, RBPJ, MIR25, MIR296, ADCYAP1, ADARB2, EIF2AK4, LOC441204, ADARB1, XRCC6P5, ADAR, MIR338, MIR367, MIR520G, MIR504, POU5F1P3, POU5F1P4, ADAM10, UHMK1, OLIG1, ARL4D, CD248, MEG3, DEPDC1, AP5M1, SULF2, BCCIP, CHPT1, IL6ST, AQP1, RTN4, CYGB, DANCR, FASLG, AICDA, SLC12A5, FAS, KIAA1549, MARK4, SUGP1, FBXW7, ADI1, P3H2, SBNO1, THEG, TNFRSF12A, DCDC2, RTRAF, HSPB11, SUFU, AREG, TLR9, NLGN3, KRT20, L1TD1, BCAS3, BCOR, PID1, PRPF38B, MSTO1, SMG8, NGB, RXFP1, ERVK-6, ID4, PITPNM3, MXD3, ARHGAP24, PLVAP, SESN2, ANCR, FSD1L, DTNBP1, PCBD2, BRMS1L, NKX6-2, PHF5A, GFM1, PYGO2, AMBP, ALOX15, ALDH1A3, SPRY4, TSGA10, KLK3, CD276, MMP25, GORASP1, NT5DC2, PINK1, RTN4R, MARCKSL1, WNK1, WNK2, FSD1, TMEM43, ZNF329, APAF1, L2HGDH, DHDDS, WLS, PDGFD, WNT10A, ABCC3, B3GALNT1, PEA15, ABCB4, PDK1, HSPA1A, PDPK1, ETV5, SERPINF1, PGK1, ETS1, HSPA1B, ERCC5, FGF13, KCNA10, ANOS1, ERBB3, JAK2, ITGB8, EPHX1, ITGB3, PLG, PDGFRB, F3, PDGFB, PDE4A, FGF5, FEN1, FECH, FDPS, P4HA1, P4HB, PA2G4, PEBP1, HRG, FASN, PAK1, PAM, PAX5, PCBD1, PTK2B, PCYT1A, FABP3, PLXNA2, PML, EPHB1, PROX1, PSEN1, PSMD9, PSMD10, PTBP1, EGR1, EDNRB, EDNRA, HSPA5, ITGAV, ATN1, PTPRA, PVR, NECTIN1, RAB3A, ITGAM, RAC2, RAC3, KLK6, PROP1, POLB, MAP2K7, EPAS1, ENO2, EMP1, POU5F1, PPARD, EMD, PPIA, PPP2R2C, EIF4E, PRKCA, PRKDC, PRKG2, MAPK1, MAPK8, MAPK9, MAPK10, MAP2K1, FGF9, FHL2, RALGDS, GPR42, MCAM, MCL1, MCM3, HFE, MDK, HBD, HBA2, HBA1, CD99, OTC, MIF, GPR34, LPAR4, MAP3K10, KMT2A, GNS, GNA12, GLUL, MBP, MATN1, MATK, MAS1, LAMC1, LAMP1, HMGA1, RPSA, LBR, HMGB1, LDHA, LEP, LGALS3, HLA-G, LIG4, LMNA, LPA, HLA-C, SMAD3, MAOA, HLA-A, LAMA4, MPST, GLI3, NM, NOS1, TLX1, FRZB, FXN, FLT3, NPC1, NPM1, KIF11, NT5E, NTF3, FLNB, NTRK2, NTRK3, OGN, OMG, OPCML, FOXO1, NMT1, FUT4, GLI2, G6PD, MS, GLG1, GLB1, HNRNPA2B1, GHSR, MXI1, MYB, GFRA1, GFPT1, MYL2, GDNF, NCAM1, SEPTIN2, NELL1, GAPDH, KRT5, NFE2L2, DMD, RASA1, EIF3A, TXN, TOP1, CLIC1, TP73, CLU, CHGA, TSC2, CHEK1, TTF1, CECR, TDO2, TYR, TYRP1, SUMO1, VDR, CDKN1B, CDK9, VIP, WAS, CNTF, CLDN5, TM7SF2, COL11A2, CST6, TERF1, INHA, HSPB2, CSNK2A2, TFPI, CSNK1D, TGFA, TGFB1, CRYAB, CPOX, TIMP1, TIMP2, NKX2-1, TK1, MAP3K8, TLR4, WNT5A, WNT2B, WT1, ADGRE5, TRRAP, CD74, H3C1, H3C4, H3C3, H3C6, H3C11, H3C8, H3C12, H3C10, H3C2, ENC1, CD70, CD48, USO1, IMPDH2, TNKS, USP11, IGF2R, CDK6, HMGA2, CDK5, XRCC4, ZIC1, CNBP, ZNF131, ZNF207, DNALI1, PAX8, HSP90AA1, CDH11, ARHGEF5, PSCA, MLLT10, ADAM12, RASSF7, CDH1, YEATS4, TEAD4, TRBV20OR9-2, ABCA2, SHH, DCX, CCL3, CCL14, SDCBP, DCR, SEL1L, SELL, SEMA3F, PMEL, TCF12, SIM2, SKIL, DCN, DCC, SLC5A5, SLC6A2, SLC6A8, SLC7A1, DDX3X, ATXN1, SATB1, DES, RBBP4, RBBP7, RBP3, DIO2, REN, DIAPH2, RET, RHO, RNASE3, ROS1, RPL17, RPL35A, RPS15A, NQO1, ITGAE, ACSM3, CFD, DBI, SLCO1A2, SNAI2, CTSB, SSX4, STAT1, CTLA4, STAT5A, STAT5B, SULT1E1, AURKA, STK11, SULT1A1, ABCC8, SUV39H1, SYT1, CSTA, TAT, TCF4, TCF7L2, ZEB1, SSTR4, SRC, DAG1, HSPB1, SMN1, SMN2, CYP19A1, SMS, CYP17A1, CYP2E1, ITGA5, SOD3, CYP2A7, SOX4, SOX5, SOX9, CYP1B1, SP100, IRF7, CUX1, SPOCK1, CDC20
-
Gynecomastia
Wikipedia
(a) With flutamide; (b) after discontinuation of flutamide. [24] More than 90% of cases of gynecomastia with nonsteroidal antiandrogens including flutamide are mild to moderate. [25] [26] About 10–25% of cases are estimated to result from the use of medications, known as nonphysiologic gynecomastia. [10] [17] Medications known to cause gynecomastia include cimetidine , ketoconazole , gonadotropin-releasing hormone analogues , human growth hormone , human chorionic gonadotropin , 5α-reductase inhibitors such as finasteride and dutasteride , certain estrogens used for prostate cancer , and antiandrogens such as bicalutamide , flutamide, and spironolactone . [7] [10] [27] [28] Medications that are probably associated with gynecomastia include calcium channel blockers such as verapamil , amlodipine , and nifedipine ; risperidone , olanzapine , anabolic steroids , [10] [29] alcohol , opioids , efavirenz , alkylating agents , and omeprazole . [10] [30] Certain components of personal skin care products such as lavender essential oil [31] or tea tree oil and certain dietary supplements such as dong quai and Tribulus terrestris have been associated with gynecomastia. [17] Chronic disease [ edit ] People with kidney failure are often malnourished, which may contribute to gynecomastia development.PRL, CYP19A1, AR, HSD17B3, STK11, LEPR, PHF6, LEP, SRY, ALMS1, AIP, SPRY4, FGF17, HESX1, KISS1R, LAS1L, CUL4B, WT1, NR0B1, SLCO2A1, TACR3, SOX9, SEMA3E, SOX10, TAC3, VAMP7, HS6ST1, SRA1, SDHC, SLC52A2, WDR11, POLR3B, CHD7, SLC29A3, RBM28, COQ8A, IL17RD, RNF216, WWOX, DMRT3, ZBTB20, NSMF, FLRT3, PROK2, CDH23, ZFPM2, SMCHD1, POLR3A, PNPLA6, SEC23B, SEMA3A, SDHD, PIK3CA, SDHB, CYP21A2, PTEN, NR5A1, SH3PXD2B, FMR1, FGFR1, FGF8, DUSP6, DCC, CYP17A1, GNRHR, CYP11B1, CYP11A1, FEZF1, CYB5A, KLLN, AXL, AKT2, AKT1, GNRH1, GATA4, CCDC141, ANOS1, HDAC8, MEN1, MAP3K1, SLC52A3, PROKR2, LHB, HFE, KISS1, ERMARD, ITGA3, INSR, HSD3B2, HPGD, RSPO1, ESR1, HTC2, CGB3, CGA, CGB8, CGB5, TICAM2, IS1, AGRP, PARPBP, MECP2, BRCA2, CYP3A4, ESR2, FOLH1, GPER1, HOXD10, KIT, LHCGR, NR3C2, TMED7, PGR, SHBG, VEGFA, TP63, ARTN, EDIL3, TRAM1, SMUG1, TMED7-TICAM2
-
Craniosynostosis
Wikipedia
Several research groups have found evidence that these environmental factors are responsible for an increase in the risk of craniosynostosis, likely through effects on fibroblast growth factor receptor genes. [28] [29] [30] [31] [32] On the other hand, a recent evaluation of valproic acid (an anti-epilepticum), which has been implicated as a causative agent, has shown no association with craniosynostosis. [33] Certain medication (like amine-containing drugs) can increase the risk of craniosynostosis when taken during pregnancy, these are so-called teratogenic factors. [29] [32] Hormonal factors [ edit ] Hyperthyroid induced craniosynostosis is a hormone mediated premature closure. [34] It is thought that the bone matures faster due to high levels of thyroid hormone . [34] Genetic factors [ edit ] In 6 to 11% of the children born with coronal synostosis, more often involving the bilateral cases than unilateral, other members of the family have been reported that were also born with the same condition. [35] This finding is highly suggestive of a genetic cause, which has possibly been found in the fibroblast growth factor receptor 3 (FGFR3) and TWIST genes. [35] Fibroblast growth factor and fibroblast growth factor receptors regulate fetal bone growth and are expressed in cranial sutures during pregnancy. [6] The transcription factor gene TWIST is thought to decrease the function of FGFR, thus also indirectly regulating fetal bone growth. [6] A relation between the mutations in these genes and craniosynostosis is therefore possible. ... "Assessment of quality of continuous intracranial pressure recordings in children". Pediatric Neurosurgery . 42 (1): 28–34. doi : 10.1159/000089506 . PMID 16357498 .FGFR2, FGFR1, MSX2, NELL1, TWIST1, EFNB1, TCF12, ERF, SMAD6, ZIC1, ALX4, WDR35, ZNF462, IFT122, RUNX2, BMP2, BBS9, MN1, FREM1, EZH2, AXIN2, FGFR3, GLI3, CDC45, RAB23, POR, CYP26B1, IL11RA, FLNA, PHEX, SMO, TNFSF11, STAT3, RSPRY1, LRP5, ATR, FBN1, PTEN, SNX10, LIG4, ORC6, CENPJ, WDR19, SETD2, RTTN, PSAT1, IL6, FLNB, HNRNPK, GMNN, IFT52, H3-3A, GTF2E2, GRIN2B, LEMD3, MAGEL2, NSUN2, DONSON, PRKAR1A, SPECC1L, CEP152, SLC12A6, NR1I3, MED12, ADAMTS3, RBBP8, SKI, SON, SPG7, KAT6A, MAP3K7, RNF113A, TGFBR1, TGFBR2, TNF, TRPS1, TAS2R38, MASP1, HUWE1, ENPP1, NFIX, TLK2, NPR2, PLK4, ORC4, PCNT, COLEC10, GPC6, TCIRG1, APC2, TRAIP, TRIM13, PPP1CB, PPP3CA, ORC1, SLC35A2, ERCC3, DPH1, CXADR, COLEC11, SLC2A10, CDT1, ATRIP, DMP1, COL10A1, CLCN7, ERCC2, CENPE, CDH11, GNPTAB, CDC6, CD19, NSD1, ARR3, ESCO2, AKT1, ALPL, CXADRP1, MEGF8, SCARF2, GTF2H5, FAT4, MPLKIP, CCBE1, IFT43, CASR, B3GLCT, SLC39A8, POSTN, IL4, MMP9, IL13, IFNG, MUC5AC, SCGB1A1, IL10, IL17A, IL5, RNASE3, CFTR, TLR9, CAMP, CXCL8, PDGFRA, S100A7, S100A8, JAG1, TSLP, IL1B, IL1A, ZMYND10, SPINK5, KRAS, PTGDS, SIRT1, SLC26A4, ABCB1, AHSA1, NDRG1, IFIH1, HLA-DRB1, HMGB1, TNFRSF11B, NT5E, NM, GJA1, MMRN1, CHI3L1, GJB2, OSM, BDNF, MAPK1, KMT2D, AHR, TLR2, DEFB4B, MUC5B, AIMP2, SPP1, EGFR, SHOC2, SNAI1, S100A12, EFNA4, S100A9, NOG, RECQL4, MYDGF, GRAP2, FGF4, FGF8, GPC3, FGF9, CLC, IL2, CRP, CRK, IL22, CSF2, LAMB1, MAPK14, HPGDS, RNF19A, IGF1R, CYP2B6, DEFB4A, POLDIP2, HGF, CYP26A1, IL19, IL6ST, LYZ, KAT6B, IL25, MMP1, PRKRA, MIR150, KCNQ5, PLA2G10, SMC1A, MMP23A, DUOX1, NR1I2, MIR146A, TP63, IL1RL2, ALX1, TRPA1, IL1RL1, TLR7, BPIFA1, CAMKMT, BCL11B, RGS21, SFTPA1, SLC25A24, PGA3, LOC102724971, LOC102723407, UVRAG, VCAM1, TAS2R13, TRPV4, MIR4492, VDR, VIM, TRPV1, OCLN, VWF, GATAD2B, SFTPA2, NOX4, IRAK4, CRLF2, DUOX2, PGA4, SCARA3, MAP1LC3B, CPP, FNDC3B, IL37, CHD7, AGO2, PLA2G2D, B3GAT3, SOX6, KHDRBS1, POLD3, PARS2, SLC52A1, CYSLTR1, CARTPT, GFM1, GJB6, MORF4, CKAP4, PART1, NUDT6, PTGDR2, PPP1R9B, BCL2L12, FGFRL1, TINAGL1, MXD3, CCL26, TFG, IFNL3, TAS2R20, FGFBP1, IGHV3-69-1, MED13L, RAB14, IGHV3OR16-7, CST8, SGSM3, RASD1, ADAMDEC1, RBM45, CST9, LRRK2, SCGB3A2, LRPPRC, NLRP3, SPRY1, AHDC1, GLCCI1, NOD2, IL33, AGER, TNNI3, CYP11B1, FGF2, FES, FCGR3A, ACSL3, F3, F2RL1, ERBB2, EPHA1, EGR2, EGF, DUSP4, DSG3, RCAN1, DPP4, DNASE1, DNAH5, DMBT1, DLX5, DDX5, FGF3, FGF14, FGFR4, GRK5, HSD11B1, HOXD13, HLA-DQB1, HLA-DQA1, MNX1, H2AX, GZMB, CXCL1, GPC1, GAD2, GNB3, GNAS, GLP1R, GLI1, GJB1, GH1, GDF2, GATA3, CYP24A1, CTLA4, IGF1, CCN2, CCND1, BAX, AZGP1, ATP4A, ATP12A, ARSA, ARG2, ARG1, AQP5, AOAH, ANXA7, ANXA6, ANK1, ALX3, ALOX15, ALOX5AP, ALOX5, AGTR1, AGT, BCL2, TNFRSF17, BGLAP, CD8A, CSTA, CST3, CST1, CPB2, COL17A1, CFL1, CD52, CD34, KRIT1, BMP6, SERPINH1, CAV1, CASP3, CALM3, CALM2, CALM1, CAD, BMPR1A, HSPA4, IGH, TLR3, PIK3CG, SCN4A, RPE65, ROS1, REN, RAF1, PTPRO, PTPN11, PTH2R, PTGS2, PTGER4, KLK6, MAPK8, PRG2, POMC, PRRX1, PLG, PLAT, PLA2G2A, PLA2G1B, CCL5, CCL18, CCL21, SPARC, TGFB2, TGFA, TFF1, TAPBP, TAP2, TAP1, SPRR2A, SPRR1B, SMN2, CCL25, SMN1, SIPA1, SFTPD, SFTPB, SFRP4, SDC1, CXCL5, CXCL6, PIN1, PIK3CD, IGHD, PIK3CB, LMX1B, LMNA, LDLR, LCN2, LBP, L1CAM, KCNMA1, JAK1, ITGA3, IRS1, IRF6, CXCL10, TNFRSF9, IL15, IL11, IL9R, IL9, IL6R, IHH, LRPAP1, LTF, CD180, NOS3, PIK3CA, PGA5, PCDH1, PRDX1, OMP, NTRK1, NPPC, NPY, NOS1, SMAD3, NHS, NGF, NFKBIA, MYB, MUC7, COX2, MRC1, MET, MTCO2P12
-
Anesthesia Awareness
Wikipedia
Thus, the incidence is 0.2% in general surgery, about 0.4% during caesarean section, between 1 and 2% during cardiac surgery and between 10% and 40% for anesthesia of the traumatized. [28] [29] [30] [31] [32] [33] [34] [35] [36] The majority of these do not feel pain although around one third did, in a range of experience from a sore throat due to the endotracheal tube, to traumatic pain at the incision site.
-
Delayed Sleep Phase Disorder
Wikipedia
DSPD tends to run in families, [26] and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene [27] [28] and CRY1 gene. [3] There have been several documented cases of DSPD and non-24-hour sleep–wake disorder developing after traumatic head injury . [29] [30] There have been cases of DSPD developing into non-24-hour sleep–wake disorder, a severe and debilitating disorder in which the individual sleeps later each day. [5] Diagnosis [ edit ] A sleep diary with nighttime at the top and the weekend in the middle, to better notice trends DSPD is diagnosed by a clinical interview, actigraphic monitoring, and/or a sleep diary kept by the patient for at least two weeks. ... "Phase-dependent treatment of delayed sleep phase syndrome with melatonin" . Sleep . 28 (10): 1271–8. doi : 10.1093/sleep/28.10.1271 .
-
Mold Health Issues
Wikipedia
Several studies and reviews have suggested that childhood exposure to dampness and mold might contribute to the development of asthma. [22] [23] [24] [25] For example, residents of homes with mold are at an elevated risk for both respiratory infections and bronchitis. [26] When mold spores are inhaled by an immunocompromised individual, some mold spores may begin to grow on living tissue, [27] attaching to cells along the respiratory tract and causing further problems. [28] [29] Generally, when this occurs, the illness is an epiphenomenon and not the primary pathology. ... PMID 12857779 . ^ "Mold – General Information – Basic Facts" . www.cdc.gov . 2019-10-28 . Retrieved 2019-11-19 . ^ "Agriculture" .
