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  • Pancreatic Neuroendocrine Tumor Wikipedia
    PanNETs are a type of neuroendocrine tumor , representing about one third of gastroenteropancreatic neuroendocrine tumors (GEP-NETs). Many PanNETs are benign , while some are malignant . ... However, morphological imaging alone is not sufficient for a definite diagnosis [14] [16] On biopsy , immunohistochemistry is generally positive for chromogranin and synaptophysin . [17] Genetic testing thereof typically shows altered MEN1 and DAXX / ATRX . [17] Staging [ edit ] The 2010 WHO classification of tumors of the digestive system grades all the neuroendocrine tumors into three categories, based on their degree of cellular differentiation (from well-differentiated "NET G1" through to poorly-differentiated "NET G3"). ... Combinations of several medicines have been used, such as doxorubicin with streptozocin and fluorouracil (5-FU) [12] and capecitabine with temozolomide. [ citation needed ] Although marginally effective in well-differentiated PETs, cisplatin with etoposide has some activity in poorly differentiated neuroendocrine cancers (PDNECs), [12] particularly if the PDNEC has an extremely high Ki-67 score of over 50%. [8] : 30 Several targeted therapy agents have been approved in PanNETs by the FDA based on improved progression-free survival (PFS): everolimus (Afinitor) is labeled for treatment of progressive neuroendocrine tumors of pancreatic origin in patients with unresectable, locally advanced or metastatic disease. [20] [21] The safety and effectiveness of everolimus in carcinoid tumors have not been established. [20] [21] sunitinib (Sutent) is labeled for treatment of progressive, well-differentiated pancreatic neuroendocrine tumors in patients with unresectable locally advanced or metastatic disease. [22] [23] Sutent also has approval from the European Commission for the treatment of 'unresectable or metastatic, well-differentiated pancreatic neuroendocrine tumors with disease progression in adults'. [24] A phase III study of sunitinib treatment in well differentiated pNET that had worsened within the past 12 months (either advanced or metastatic disease) showed that sunitinib treatment improved progression-free survival (11.4 months vs. 5.5 months), overall survival , and the objective response rate (9.3% vs. 0.0%) when compared with placebo. [25] Genetics [ edit ] Pancreatic neuroendocrine tumors may arise in the context of multiple endocrine neoplasia type 1 , Von Hippel–Lindau disease , neurofibromatosis type 1 (NF-1) or tuberose sclerosis (TSC) [26] [27] Analysis of somatic DNA mutations in well-differentiated pancreatic neuroendocrine tumors identified four important findings: [28] [6] as expected, the genes mutated in NETs, MEN1 , ATRX , DAXX , TSC2 , PTEN and PIK3CA , [28] are different from the mutated genes previously found in pancreatic adenocarcinoma . [29] [30] one in six well-differentiated pancreatic NETs have mutations in mTOR pathway genes, such as TSC2 , PTEN and PIK3CA . [28] The sequencing discovery might allow selection of which NETs would benefit from mTOR inhibition such as with everolimus , but this awaits validation in a clinical trial . mutations affecting a new cancer pathway involving ATRX and DAXX genes were found in about 40% of pancreatic NETs. [28] The proteins encoded by ATRX and DAXX participate in chromatin remodeling of telomeres ; [31] these mutations are associated with a telomerase -independent maintenance mechanism termed ALT (alternative lengthening of telomeres) that results in abnormally long telomeric ends of chromosomes . [31] ATRX / DAXX and MEN1 mutations were associated with a better prognosis . [28] References [ edit ] ^ Burns WR, Edil BH (March 2012).
    MEN1, ATRX, DAXX, ELK3, TP53, EPHB1, SLC6A2, CEACAM5, CEACAM7, UQCRFS1, DHDDS, CHPT1, RALBP1, CIB1, SEMA4D, RIPK1, CXCR4, VEGFA, TTR, GNA12, TSC2, TFE3, CDKN1B, PSG2, POMC, MYCN, CEACAM3, GRN, MUC16
  • Estrogen And Neurodegenerative Diseases Wikipedia
    In addition, estrogen deprivation is likely to initiate or enhance degenerative changes caused by oxidative stress , and to reduce the brain's ability to maintain synaptic connectivity and cholinergic integrity leading to the cognitive decline seen in aged and disease-afflicted individuals. [5] There is sufficient evidence that estradiol is a powerful neuroprotectant which might have use against AD, stroke and Parkinson's disease both in women and men. [5] Estrogen and Alzheimer's disease [ edit ] This figure shows how APP cleavage produces toxic Abeta in Alzheimer's disease. Amyloid plaques formed by amyloid-β (Aβ) deposition and neurofibrillary tangles formed by tau protein phosphorylation are dominant physiological features of Alzheimer's disease. Amyloid precursor protein (APP) proteolysis is fundamental for production of Aβ peptides implicated in AD pathology. [6] By using a cell line that contains high levels of estrogen receptors, scientists found that treatment with physiological concentrations of 17 beta-estradiol is associated with accumulation in the conditioned medium of an amino-terminal cleavage product of APP (soluble APP or protease nexin-2), indicative of non-amyloidogenic processing. [7] Estrogen and Parkinson's disease [ edit ] Recommendations on the use of postmenopausal hormonal replacement therapy in women with Parkinson's disease or those genetically at risk. [8] But another group of scientists found a positive association between estrogen use and lower symptom severity in women with early PD not yet taking L-dopa . [9] Estrogen and Huntington's disease [ edit ] Huntington's disease (HD) is a polyglutamine disorder based on an expanded CAG triplet repeat [10] leading to cerebral and striatal neurodegeneration. [11] Potential sex differences concerning the age of onset and the course of the disease are poorly defined, as the difficulties of matching female and male HD patients regarding their CAG repeat lengths limit comparability. [12] Estrogen and Amyotrophic lateral sclerosis [ edit ] ALS occurs more commonly in men than in women, and women get the disease later in life compared to men. [13] This suggested the possible protective role of estrogen in ALS. ... "Octyl Gallate Markedly Promotes Anti-amyloidogenic Processing of APP through Estrogen Receptor-Mediated ADAM10 Activation" .
  • Photoinhibition Wikipedia
    In 1966, Jones and Kok measured the action spectrum of photoinhibition and found that ultraviolet light is highly photoinhibitory. [2] The visible-light part of the action spectrum was found to have a peak in the red-light region, suggesting that chlorophylls act as photoreceptors of photoinhibition. ... Thus, the redox state of Quinone A is no longer active and there is, again, no change in the concentration of carbon dioxide in the intracellular airspaces of the leaf. All these factors work to have a net decrease of stomatal conductance. ... Photoinhibition damages PSII at the same rate whether the leaf stalk is in water or lincomycin, but, in the “leaf stalk in water” sample, repair is so rapid that no net decrease in (F V /F M ) occurs Photoinhibition can be measured from isolated thylakoid membranes or their subfractions, or from intact cyanobacterial cells by measuring the light-saturated rate of oxygen evolution in the presence of an artificial electron acceptor ( quinones and dichlorophenol-indophenol have been used). ... Ecology of photoinhibition [ edit ] Photoinhibition may cause coral bleaching . [27] See also [ edit ] Anthocyanin Chlorophyll Kautsky effect Light reaction Photosynthetic reaction centre Photosynthesis References [ edit ] ^ Kok B (1956). "On the inhibition of photosynthesis by intense light". Biochimica et Biophysica Acta . 21 (2): 234–244. doi : 10.1016/0006-3002(56)90003-8 . PMID 13363902 . ^ Jones LW, Kok B (1966). "Photoinhibition of Chloroplast Reactions.
  • Dowling-Degos Disease Gard
    Dowling-Degos disease is characterized by a lacy or net-like (reticulate) pattern of abnormally dark skin coloring (hyperpigmentation) in the body's folds and creases.
    ADAM10, KRT5, POFUT1, POGLUT1, ADAR
    • Reticulate Acropigmentation Of Kitamura Omim
      A number sign (#) is used with this entry because of evidence that reticulate acropigmentation of Kitamura (RAK) is caused by heterozygous mutation in the ADAM10 gene (602192) on chromosome 15q21. Description Reticulate acropigmentation of Kitamura (RAK) is a rare pigmentary disorder that usually shows an autosomal dominant pattern of inheritance with high penetrance. Typical features include reticulate, slightly depressed, sharply demarcated brown macules without hypopigmentation, affecting the dorsa of the hands and feet in the first or second decade of life. The macules gradually darken and extend to the proximal regions of the extremities; progression of the eruptions stops in middle age. The increased pigmentation is found on the flexor aspects of the wrists, neck, patella, and olecranon.
    • Reticulate Acropigmentation Of Kitamura Wikipedia
      Reticulate acropigmentation of Kitamura Other names RAK [1] Specialty Dermatology Reticulate acropigmentation of Kitamura consists of linear palmar pits and pigmented macules 1 to 4 mm in diameter on the volar and dorsal aspects of the hands and feet, usually inherited in an autosomal-dominant fashion. [2] : 856 [3] [4] Contents 1 Genetics 2 See also 3 References 4 External links Genetics [ edit ] This condition is associated with mutations in the a disintegrin and metalloproteinase domain-containing protein 10 ( ADAM10 ) gene. This association was first shown in 2013. See also [ edit ] Skin lesion List of cutaneous conditions References [ edit ] ^ RESERVED, INSERM US14-- ALL RIGHTS. "Orphanet: Reticulate acropigmentation of Kitamura" . www.orpha.net . Retrieved 23 April 2019 . ^ James, William; Berger, Timothy; Elston, Dirk (2005). Andrews' Diseases of the Skin: Clinical Dermatology . (10th ed.). Saunders.
    • Reticulate Acropigmentation Of Kitamura Orphanet
      A rare, genetic, hyperpigmentation of the skin disease characterized by childhood to adulthood-onset of reticulate, slightly depressed, sharply demarcated, brown, macular skin lesions without hypopigmentation, affecting the dorsa of the hands and feet, and, occasionally, progressing to involve limbs, neck, forehead and/or trunk. Interrupted dermatoglyphics and palmoplantar pits may be additionally observed. Histologically, hyperpigmented lesions show slightly elongated and thinned rete ridges, mild hyperkeratosis without parakeratosis and absence of incontinentia pigmenti.
  • Azotemia, Familial Omim
    Furthermore, urea is reabsorbed actively by the tubule; this process is apparently brought into play particularly in states of low protein intake. Net reabsorption might be due to exaggerated active reabsorption or to deficient secretion.
  • Microvasculature Remodeling Wikipedia
    What makes vessels grow with exercise training? J App Physiol 97: 1119–28, 2004. This cardiovascular system article is a stub .
  • Isolated Atrial Amyloidosis Wikipedia
    Retrieved 17 November 2010 . v t e Amyloidosis Common amyloid forming proteins AA ATTR Aβ2M AL Aβ / APP AIAPP ACal APro AANF ACys ABri Systemic amyloidosis AL amyloidosis AA amyloidosis Aβ2M/Haemodialysis-associated AGel/Finnish type AA/Familial Mediterranean fever ATTR/Transthyretin-related hereditary Organ-limited amyloidosis Heart AANF/Isolated atrial Brain Familial amyloid neuropathy ACys+ABri/Cerebral amyloid angiopathy Aβ/Alzheimer's disease Kidney AApoA1+AFib+ALys/Familial renal Skin Primary cutaneous amyloidosis Amyloid purpura Endocrine Thyroid ACal/Medullary thyroid cancer Pituitary APro/Prolactinoma Pancreas AIAPP/Insulinoma AIAPP/Diabetes mellitus type 2
  • Al Amyloidosis Wikipedia
    British Journal of Haematology . 140 (4): 365–377. doi : 10.1111/j.1365-2141.2007.06936.x . ... External links [ edit ] Classification D ICD - 10 : E85 ICD - 9-CM : 277.3 OMIM : 254500 MeSH : C531616 DiseasesDB : 315 External resources MedlinePlus : 000533 eMedicine : med/3363 v t e Amyloidosis Common amyloid forming proteins AA ATTR Aβ2M AL Aβ / APP AIAPP ACal APro AANF ACys ABri Systemic amyloidosis AL amyloidosis AA amyloidosis Aβ2M/Haemodialysis-associated AGel/Finnish type AA/Familial Mediterranean fever ATTR/Transthyretin-related hereditary Organ-limited amyloidosis Heart AANF/Isolated atrial Brain Familial amyloid neuropathy ACys+ABri/Cerebral amyloid angiopathy Aβ/Alzheimer's disease Kidney AApoA1+AFib+ALys/Familial renal Skin Primary cutaneous amyloidosis Amyloid purpura Endocrine Thyroid ACal/Medullary thyroid cancer Pituitary APro/Prolactinoma Pancreas AIAPP/Insulinoma AIAPP/Diabetes mellitus type 2 v t e Immunoproliferative immunoglobulin disorders PCDs / PP Plasmacytoma Multiple myeloma ( Plasma cell leukemia ) MGUS IgM ( Macroglobulinemia / Waldenström's macroglobulinemia ) heavy chain ( Heavy chain disease ) light chain ( Primary amyloidosis ) Other hypergammaglobulinemia Cryoglobulinemia
    CCND1, LINC02343, CBX7, LINC00457, SMARCD3, TTR, DNAH11, CD38, SCT, GDF15, NPPB, SPP1, IGKV2-29, MIR34A, SMN1, SMN2, ST2, TNF, BMS1P20, KRT20, IGKV1-8, BABAM2, GLIPR1, WDHD1, MAGEC2, SLC1A4, PLXNB2, IGKV3D-15, IGKV1D-8, IGKV3-20, PRAME, ALB, SDC1, FGA, BCR, PRDM1, CAT, MS4A1, CDA, CDH1, CRP, CSF3, CYP1B1, DDT, ETFA, GSN, FAS, IGKV@, LGALS3, LGALS4, MDK, MMP1, MMP2, MUC1, MYD88, NCAM1, PFDN5, RPS27A, SAA1
    • Multiple Myeloma Medlineplus
      Multiple myeloma is a cancer that develops in the bone marrow , the spongy tissue found in the center of most bones. The bone marrow produces red blood cells, which carry oxygen throughout the body; white blood cells, which form the body's defenses (immune system); and platelets, which are necessary for blood clotting . Multiple myeloma is characterized by abnormalities in plasma cells, a type of white blood cell. These abnormal cells multiply out of control, increasing from about one percent of cells in the bone marrow to the majority of bone marrow cells. The abnormal cells form tumors within the bone, causing bone pain and an increased risk of fractures.
    • Al Amyloidosis Orphanet
      A plasma cell disorder characterized by the aggregation and deposition of insoluble amyloid fibrils derived from misfolding of monoclonal immunoglobulin light chains usually produced by a plasma cell tumor. It usually presents as primary systemic amyloidosis (PSA) with multiple organ involvement and less frequently as primary localized amyloidosis (PLA) restricted to a single organ.
    • Al Amyloidosis Gard
      AL amyloidosisis the most common form of amyloidosis, a group of disorders in which an abnormal protein called amyloid builds up in tissues and organs. The signs and symptoms of AL amyloidosis vary among patients because the build up may occur in the tongue, intestines, muscles, joints, nerves, skin, ligaments, heart, liver, spleen, or kidneys. To diagnose AL amyloidosis, healthcare professionals use blood or urine tests to identify signs of amyloid protein and a biopsy to confirm the diagnosis. Treatment may include chemotherapy directed at the abnormal plasma cells, stem cell transplantation , or other treatments based on which symptoms have developed.
    • Primary Systemic Amyloidosis Orphanet
      Primary systemic amyloidosis (PSA) is a form of AL amyloidosis (see this term) caused by the aggregation and deposition of insoluble amyloid fibrils derived from misfolded monoclonal immunoglobulin light chains usually produced by a plasma cell tumor (see this term) and characterized by multiple organ involvement.
  • Amyloidosis Orphanet
    A vast group of diseases defined by the presence of insoluble protein deposits in tissues. Amyloidoses are classified according to clinical signs and biochemical type of amyloid protein involved. Clinical description Most amyloidoses are multisystemic, 'generalize' or 'diffuse'. Mainly affected are the kidneys, heart, GI tract, liver, skin, peripheral nerves and eyes, but any organ can be affected. Progression is usually severe, as affected organs are destroyed. There are a few forms of localized amylosis.
    TTR, PSEN1, GSN, APP, ACHE, APOE, HMOX1, APOC3, ZDHHC13, APOC2, TNFRSF1A, CCND1, POLA1, B2M, BCHE, BDNF, NLRP3, PRNP, OSMR, CASP3, MME, CSF2, CST3, SAA2, MEFV, MAPT, LYZ, LIG4, LAMC2, IL6, IL1B, TREM2, IDE, BACE1, IAPP, SAA1, GFAP, APCS, TNF, AGER, SNCA, APOA1, NEFL, TGFBI, CLU, ADAM10, IL1A, SUCLA2, DPYD, IL4, NGF, NFE2L2, APOA2, LPAL2, ABCB1, BECN1, PPARG, NRGN, TARDBP, BIN1, BCL2, TLR4, MMP9, ABCA7, CTSD, DCLRE1B, LRP1, TYROBP, SIRT1, TGFB1, LECT2, CHI3L1, MOK, RELN, PSEN2, S100A9, TSPO, LEP, CTSB, SOD1, SYP, ALOX5, KHDRBS1, DLG4, MCIDAS, CAT, CRP, IGF1, FGA, SMUG1, NUP62, DCTN4, HP, S100B, GTF2H1, GSK3B, SOD2, AQP4, CHRNA4, VEGFA, PIK3CD, ABCB6, CDK5, PLG, SQSTM1, PIK3CG, PIK3CB, MAPK3, ITM2B, PIK3CA, SORL1, IL10, LPA, VSNL1, ROS1, RXRA, PTPRC, EGR1, PARP1, ALB, CD40, STS, TLR2, PLD3, CD36, GABPA, HTT, SDC1, PYCARD, SH2D1A, LINC01672, ACE, MAPK8, CNR2, MAP3K5, CYP46A1, TSHZ1, CD55, PINK1, SERPINA3, ADIPOQ, GRM5, HTRA1, MAPK1, TRPC6, DYSF, TYRP1, RNR2, UBQLN1, QPCT, NCAM1, NFIB, MMP2, HLA-DRB1, NFIA, HCRT, PPARA, HDAC3, UCHL1, ABCG1, MAP2, PTGS2, PPARGC1A, PDB1, LDLR, NFIC, LBP, TXN, DKK1, INSR, SYNM, NCSTN, IL17A, IL13, GH1, P2RX7, RBP4, IL1RN, MFAP1, PDE5A, NFIX, A2M, CD40LG, FYN, NGB, DDIT3, CRYAB, CD38, APLP2, C4BPA, MIR200A, ARG1, ESCO1, EPO, DDR1, CYLD, CALCA, FCGRT, FAP, DECR1, LRRK2, APRT, CR1, GCG, DYRK1A, CHRM3, GDNF, ECE1, EDN1, ACTB, DRD1, IGAN1, TNMD, CHAT, DPYSL2, BAX, MFT2, PCSK9, GCSAM, LRRTM3, STOX1, CDK5R1, SUMO4, GOLGA6A, OSTN, ANO5, LOC390714, ARHGEF7, DUOX2, CD163, UBR1, FSIP1, SV2A, SNAP91, MAGI2, ZEB2, KEAP1, UCN3, TOMM20, PCLAF, CLSTN3, HDAC9, CD109, ACTRT1, CARTPT, MAD2L1BP, BCAR1, GDF15, TRIM69, TMC4, GRAP2, TICAM1, RMDN2, DAB2IP, CRADD, MSC, SLC2A12, RAB11A, MIR137, MIR107, RIPK1, VWF, DEFB103A, VTN, DNM1P33, LOC643387, SCFV, VIP, SFTPA1, VDR, VCAM1, UTRN, NR1H2, C20orf181, BACE1-AS, OCLN, TYRO3, MICA, TMX2-CTNND1, LOC102723407, LOC102724971, LINC02210-CRHR1, UPK3B, HSP90B2P, TRAF6, LOC105379528, WNT1, XBP1, XK, AGPS, MIR132, URI1, WDR1, EIF3A, MIR15B, MIR181C, UNC5C, DENR, DEGS1, MIR29A, MIR29B1, CST7, LRP8, ULK1, AXIN1, PICALM, MIR29C, BAS, FXR1, PSCA, AIMP2, TFEB, PLA2G7, NPHS2, DBA2, PPIF, DGCR2, RAB21, TP53, HSPA14, DCDC2, GDE1, DUOX1, GSAP, DAPK2, TLR9, TREM1, QPCTL, DDAH1, ODAM, SLC25A38, RMDN3, RCBTB1, SYBU, SIRT3, USE1, DEFB103B, CRTC1, CTNNBL1, ARC, SLC17A7, ARL6IP1, TBC1D9, PRDX5, BACE2, RNF19A, ADIPOR1, SNX12, EEF2K, SNX8, FLVCR1, TMEM176B, F11R, IGKV2-29, IGKV3-20, ASCC1, PRLH, GAL, IGKV1D-8, SH2B1, IGKV3D-15, IGHV3-69-1, IGHV3OR16-7, APH1A, HTRA2, VPS4A, RMDN1, HSPB8, POLDIP2, SDF4, CHMP2B, KIF1B, SHANK2, HDAC5, ATF6, GPNMB, OLFM1, PRMT5, PHF6, RTN3, COL25A1, LILRB2, CALCOCO2, MFSD2A, ABI2, NAV3, CHRFAM7A, BMF, NLRP12, BMS1P20, OPTN, PRRT2, MBL3P, NR1H3, DNM1L, CDCA5, SH2D3C, TOM1, BCL2L11, PDCD6IP, CIB1, MAP1LC3B, KAT5, FERMT2, NLGN1, NLRP1, HPS5, CENPK, KLK8, WDHD1, TPPP, ABCG4, RIPK3, HHIP, SDS, STIP1, SLC8B1, CLEC7A, UBE2Z, EDAR, CARD14, MMEL1, CLDN16, PAGR1, TXNIP, EHMT1, AHSA1, ATG7, TPSG1, PPP3R1, CLDN5, EREG, NR5A1, MTOR, FPR1, FN1, FOXO1, FGF2, FCN2, EFEMP1, FAT1, FANCD2, F10, F3, ESR2, ESR1, EPHB2, TLR5, EPHA3, EPHA1, ELN, SERPINB1, EHHADH, E2F1, DUSP6, DPP4, DPEP1, DNMT3A, DNMT1, DNM1, DLX4, DLG2, GAST, FUS, G6PD, GALNS, HSPA9, HSPA4, HSF1, HSD11B1, FOXA2, NR4A1, HMGB1, HMBS, HLA-DMA, NRG1, HFE, HDAC2, GSK3A, CXCL2, GRM3, GRM2, GRIN2B, GRIN1, GRN, GRIA1, GPX1, GNA12, GEM, GDF2, GCHFR, GC, GATA6, GAS6, GAPDH, DES, DCX, DCN, C1QB, C1QBP, BSG, BRCA2, BGN, BCR, TNFRSF17, AVP, ATF4, SERPINC1, ARSA, ABCC6, FAS, APOA4, APLP1, BIRC3, APBB2, APAF1, ANXA5, ANXA1, ALOX15, ALOX12, AKT1, AIF1, AGTR1, AGT, ACAN, ACAT1, ABCA4, ABCA1, C1QA, C1QC, CYBB, C3, CTNND1, CSF3, CSE1L, MAPK14, CRMP1, CRK, CRHR1, CRH, CPB2, COL11A2, CLCN3, CHIT1, AKR1C4, CETN1, CEBPA, CDR1, CD74, CD68, CD33, CD19, CD14, RUNX1T1, CAV1, CASR, CASP1, CAMK2G, CAMK4, CACNA1C, C4BPB, HSP90AA1, HSPD1, HSPG2, MAPK12, S100A8, S100A6, SORT1, S100A1, RPL29, RHD, RET, RARB, PVALB, PTX3, PTGS1, MAP2K6, MAP2K1, PRKCB, PRKCA, PPY, PTPA, PPID, PPARD, POR, POLB, PMP22, PLK1, PLA2G4A, PITX3, PIN1, SERPINB9, SERPINB6, SLC25A3, SAA4, ATXN7, PAWR, SCD, TIMP1, TGFBR2, PRDX2, TAT, SYT1, SYN1, VAMP1, STK11, ST13, SST, TRIM21, SPRR2A, SPP1, SOAT1, SNCG, SMN2, SMN1, SLC6A3, SLC5A5, SLC1A3, PMEL, SH3GL2, SGCG, SRSF2, SEMG1, SELPLG, CXCL12, CCL5, SCT, SERPINF1, REG3A, HTR1B, MAZ, MAOA, MAG, TACSTD2, LTB, LNPEP, LMNB1, LIMK1, LCN2, LAIR1, KRAS, KLC1, KNG1, KIR3DL1, ITIH4, ITGAM, IRS1, PDX1, INS, CXCL10, ING1, IL18, IL12A, CXCR2, CXCL8, IL2, IFNG, IFNB1, ID2, HTR2A, MATN1, MBL2, SERPINE1, MBP, PAEP, P2RY2, P2RX4, OCA2, NTRK2, YBX1, SLC11A2, NPTX1, NPPA, NPC1, NPY, NOTCH1, NOS3, NFKB1, NEFH, NCF2, NAGLU, MYOC, COX1, MT3, ABCC1, MPZ, MPV17, MNAT1, MMP3, AFF1, MFGE8, DNAJB9, CHST6, H3P40
    • Amyloidosis Wikipedia
      Contains immunoglobulin light-chains (λ,κ) derived from plasma cells. 254500 AA SAA Serum amyloid A protein (SAA) is an acute-phase reactant that is produced in times of inflammation. Aβ β amyloid / APP Found in Alzheimer disease brain lesions. 605714 ALECT2 LECT2 In LECT2 amyloidosis , the LECT2 protein deposits in the kidneys and various other tissues but only kidneys show signs or symptoms; these are typical those of kidney failure. [22] ATTR transthyretin Transthyretin is a protein that is mainly formed in the liver that transports thyroxine and retinol binding protein. [7] A mutant form of a normal serum protein that is deposited in the genetically determined familial amyloid polyneuropathies . ... External links [ edit ] Classification D ICD - 10 : E85 ICD - 9-CM : 277.3 MeSH : D000686 DiseasesDB : 633 External resources eMedicine : med/3377 Patient UK : Amyloidosis Amyloidosis at Curlie v t e Amyloidosis Common amyloid forming proteins AA ATTR Aβ2M AL Aβ / APP AIAPP ACal APro AANF ACys ABri Systemic amyloidosis AL amyloidosis AA amyloidosis Aβ2M/Haemodialysis-associated AGel/Finnish type AA/Familial Mediterranean fever ATTR/Transthyretin-related hereditary Organ-limited amyloidosis Heart AANF/Isolated atrial Brain Familial amyloid neuropathy ACys+ABri/Cerebral amyloid angiopathy Aβ/Alzheimer's disease Kidney AApoA1+AFib+ALys/Familial renal Skin Primary cutaneous amyloidosis Amyloid purpura Endocrine Thyroid ACal/Medullary thyroid cancer Pituitary APro/Prolactinoma Pancreas AIAPP/Insulinoma AIAPP/Diabetes mellitus type 2 Authority control NDL : 00569790
    • Amyloidosis Mayo_clinic
      Overview Amyloidosis (am-uh-loi-DO-sis) is a rare disease that occurs when a protein called amyloid builds up in organs. This amyloid buildup can make the organs not work properly. Organs that may be affected include the heart, kidneys, liver, spleen, nervous system and digestive tract. Some types of amyloidosis occur with other diseases. These types may improve with treatment of the other diseases. Some types of amyloidosis may lead to life-threatening organ failure. Treatments may include chemotherapy with strong drugs used to treat cancer.
  • Insulinoma Gard
    Insulinoma is a type of pancreatic neuroendocrine tumor (pancreatic NET), which refers to a group of rare tumors that form in the hormone-making cells of the pancreas.
    MEN1, RPS15, CDKN2B, CDKN2C, IAPP, GCG, CDKN1B, CDKN1A, SST, FOXM1, GLP1R, PDX1, INS, IL1B, RIT2, PTPRN2, GAD1, EHMT1, IGF2, ZGLP1, CDKN2A, SLC30A8, SLC30A10, GCK, SSTR2, FFAR1, YY1, LEP, DPP4, INSM1, MNX1, HSPD1, GAD2, SLC2A2, CASR, RALBP1, RIPK1, PDHX, BTC, UQCRFS1, TP53, TGM2, SSTR5, CDKN1C, INSR, ABCC8, SLC6A2, SSTR4, SSTR3, WFS1, NIT1, SERPINA1, PTPRN, GIP, GCKR, CORO1A, H3P47, PRL, H3P10, ERBB2, GAST, EGR1, ELK3, CALCA, CASP3, EPHB1, G6PC, DLK1, CCN5, SQSTM1, PTTG1, GCM2, LHX2, KL, MAPK8IP1, INSL5, IRS2, ZNRD2, KHDRBS1, DCTN6, LILRB1, FASTK, CCND1, PDIA5, FAS, ATF6, KDM1A, PDZD2, BCL2, BRCA1, TNKS, PLA2G6, HNF1A, TCF19, TGFA, TGFB1, CASP8, THBD, TKT, TSPAN7, TPD52, TRP-AGG2-5, TRPC1, EIPR1, TXN, TYRP1, UCP2, VDR, CACNA1D, BRAF, STAB1, ERP44, NUP62, KCNH4, CAT, KCNH8, GPR119, STOML3, AKT1, HCAR2, GOLGA6A, TICAM2, HES3, MIR107, MIR144, MIR155, MIR204, MIR21, MIR375, INS-IGF2, ADSS2, TMED7-TICAM2, ECT, LINC02210-CRHR1, H3P23, ADM, SLC22A12, TXNDC5, TRABD, RCBTB1, FGF21, MCAT, MCTS1, TMED7, ADIPOR1, DCTN4, CDKAL1, SLC25A38, BANK1, MEG3, ZC3H12A, APOC2, SOX6, SELENOS, IGSF9, SEMA6A, HAMP, G6PC2, PDIA2, ANGPT2, SYP, STAT5A, STC1, STAT5B, KCNJ1, KCNJ6, KRT8, KRT16, KRT19, DECR1, LEPR, LGALS3, LMO2, EPCAM, SMAD2, SMAD3, SMAD4, MAPT, MC2R, MDK, RAB8A, CUX1, MET, CIITA, MLH1, EGF, EGFR, INPPL1, HK1, MTOR, FGF13, GNA12, GPD2, FBN1, GRN, GSK3B, GSR, GTF2H1, ESR2, ELK1, HLA-DQB1, HMGN2, HNF4A, EPHB2, IFI27, IGFBP1, IGFBP2, IL4, IL10, MRC1, NCAM1, NEDD4, SLC2A1, RAP1A, REG1A, CPE, CMA1, S100A8, SCT, CCL2, CXCL12, SDHD, CHGA, RAB3A, CDKN2D, SLC16A1, SNX1, CDC42, CDK1, CCND3, CCNC, CCK, STAT1, RANBP2, CR2, NF1, PIK3CG, NFE2L1, CTSB, NME1, OPA1, PAX4, PAX6, PCSK1, ENPP1, CTNNB1, PKD1, CRHR1, POLD1, MAPK1, MAPK3, MAPK8, ADCYAP1, PRSS1, PSEN2, PSMD9, PTEN, ACO2
    • Insulinoma Wikipedia
      Insulinoma Pathology of pancreatic endocrine tumor (insulinoma). Specialty Oncology An insulinoma is a tumor of the pancreas that is derived from beta cells and secretes insulin . It is a rare form of a neuroendocrine tumor . Most insulinomas are benign in that they grow exclusively at their origin within the pancreas, but a minority metastasize . Insulinomas are one of the functional pancreatic neuroendocrine tumor (PNET) group ("functional" because it increases production of insulin). [1] In the Medical Subject Headings classification, insulinoma is the only subtype of "islet cell adenoma". [2] Beta cells secrete insulin in response to increases in blood glucose . The resulting increase in insulin acts to lower blood glucose back to normal levels, at which point further secretion of insulin is stopped. In contrast, the secretion of insulin by insulinomas is not properly regulated by glucose, and the tumors continue to secrete insulin causing glucose levels to fall further than normal.
    • Insulinoma Orphanet
      Insulinoma is the most common type of functioning pancreatic neuroendocrine tumor (see this term) characterized most commonly by a solitary, small pancreatic lesion that causes hyperinsulinemic hypoglycemia. Epidemiology The incidence in the general population is 1/1,000,000-1/250,000 (but higher in autopsy studies). There is a slight female predominance. It is the most common endogenous cause of hyperinsulinemic hypoglycemia. Malignant insulinoma has an incidence 0.01/100,000 in Europe. Clinical description Insulinoma can present at any age but the median age of diagnosis is in the 5th decade of life. It manifests with various autonomic and neuroglycopenic symptoms such as tremor, palpitations, weakness, diaphoresis, hyperphagia, visual disturbances, confusion, behavioral and personality changes, seizures and coma.
  • Sneddon Syndrome Gard
    It is primarily characterized by livedo reticularis (net-like patterns of discoloration on the skin) and neurological abnormalities.
    ADA2, ADA, ARSA
    • Sneddon Syndrome Omim
      A number sign (#) is used with this entry because of evidence that Sneddon syndrome (SNDNS) is caused by compound heterozygous mutation in the CECR1 gene (ADA2; 607575) on chromosome 22q11. One such family has been reported. Mutation in the ADA2 gene can also cause vasculitis, autoinflammation, immunodeficiency, and hematologic defects syndrome (VAIHS; 615688), which shows earlier onset. Description Sneddon syndrome is a noninflammatory arteriopathy characterized by onset of livedo reticularis in the second decade and onset of cerebrovascular disease in early adulthood (summary by Bras et al., 2014). Livedo reticularis occurs also with polyarteritis nodosa, systemic lupus erythematosus, and central thrombocythemia, any one of which may be accompanied by cerebrovascular accidents (Bruyn et al., 1987). Clinical Features Sneddon (1965) described 6 patients (5 females, 1 male), varying in age from 20 to 48 years, who had association of livedo reticularis with cerebrovascular accident.
    • Sneddon's Syndrome Wikipedia
      Sneddon syndrome Other names Ehrmann-Sneddon syndrome, Livedo racemosa-cerebrovascular accident syndrome, Livedo reticularis-cerebrovascular accident syndrome [1] This condition is inherited in an autosomal recessive manner [2] Specialty Rheumatology Sneddon's syndrome [1] is a form of arteriopathy characterized by several symptoms, including: Severe, transient neurological symptoms or stroke Livedo reticularis , or livedo racemosa Contents 1 Signs and symptoms 2 Pathogenesis 3 Diagnosis 4 Treatment 5 Epidemiology 6 History 7 See also 8 References 9 Further reading 10 External links Signs and symptoms [ edit ] Sneddon's syndrome generally manifests with stroke or severe, transient neurological symptoms, and a skin rash ( livedo reticularis ). Livedo reticularis appears as a bluish-purple, netlike mottling of the skin. Sneddon's syndrome may instead present with livedo racemosa , which involves larger, less organized patches of bluish-purple mottling of the skin. Both are generally found first in the extremities, both worsen in cold and either may occur without Sneddon's Syndrome or any other systemic disease. [ citation needed ] Sneddon's Syndrome can be characterized by: transient amnesia , transient aphasia , palsy , headaches , hypertension, transient ischemic attacks (TIA), stroke , [3] coronary disease and dementia. [4] The skin manifestations may precede the neurologic symptoms by years. [3] Pathogenesis [ edit ] Sneddon's syndrome is a progressive, noninflammatory arteriopathy leading to the characteristic skin condition and to cerebrovascular problems, including stroke, transient ischemic attack (TIA), severe but transient neurological symptoms thought to be caused by cerebral vasospasm, coronary disease and early-onset dementia. Progressive compromise of arterial linings in Sneddon's produces clotting, for which high-dose warfarin is most commonly prescribed, and can also cause the development of systemic arterial plaque when cholesterol levels are normal. [ citation needed ] Diagnosis [ edit ] There are no diagnostic tests on which all Sneddon's patients will have abnormal results, although brain MRI and skin biopsy are often abnormal.
    • Adenosine Deaminase 2 Deficiency Medlineplus
      Signs and symptoms that can occur with ADA2 deficiency include fevers that are intermittent, meaning they come and go; areas of net-like, mottled skin discoloration called livedo racemosa; an enlarged liver and spleen (hepatosplenomegaly); and recurrent strokes affecting structures deep in the brain that can start in the first few years of life.
    • Sneddon Syndrome Orphanet
      Clinical description The mean age of onset of neurological symptoms is 39 years, though the livedo is generally observed up to 10 years earlier and sometimes since childhood. Livedo racemosa is a persistent net-like violaceous-cyanotic, mottled discoloration of the skin affecting primarily the legs and arms, but also involving the buttocks and the trunk, and that is exacerbated by cold or pregnancy.
  • Heredofamilial Amyloidosis Wikipedia
    ISBN 978-1-4160-2999-1 . v t e Amyloidosis Common amyloid forming proteins AA ATTR Aβ2M AL Aβ / APP AIAPP ACal APro AANF ACys ABri Systemic amyloidosis AL amyloidosis AA amyloidosis Aβ2M/Haemodialysis-associated AGel/Finnish type AA/Familial Mediterranean fever ATTR/Transthyretin-related hereditary Organ-limited amyloidosis Heart AANF/Isolated atrial Brain Familial amyloid neuropathy ACys+ABri/Cerebral amyloid angiopathy Aβ/Alzheimer's disease Kidney AApoA1+AFib+ALys/Familial renal Skin Primary cutaneous amyloidosis Amyloid purpura Endocrine Thyroid ACal/Medullary thyroid cancer Pituitary APro/Prolactinoma Pancreas AIAPP/Insulinoma AIAPP/Diabetes mellitus type 2 This cutaneous condition article is a stub .
    TTR, FGA, RET, GSN, APOA1, LYZ, ITM2B, EPO, CST3, FAP, ACTB, NLRP3, GGTLC1, HAMP, FURIN, PRNP, PMP22, APOA2, LOC102724197
    • Hereditary Amyloidosis Gard
      Hereditary amyloidosis refers to a group of inherited conditions that make up one of the subtypes of amyloidosis . Hereditary amyloidosis is characterized by the deposit of an abnormal protein called amyloid in multiple organs of the body where it should not be, which causes disruption of organ tissue structure and function. In hereditary amyloidosis, amyloid deposits most often occur in tissues of the heart, kidneys, and nervous system. While symptoms of hereditary amyloidosis may appear in childhood, most individuals do not experience symptoms until adulthood. There are many types of hereditary amyloidosis associated with different gene mutations and abnormal proteins.
  • Secondary Systemic Amyloidosis Wikipedia
    ISBN 978-1-4160-2999-1 . v t e Amyloidosis Common amyloid forming proteins AA ATTR Aβ2M AL Aβ / APP AIAPP ACal APro AANF ACys ABri Systemic amyloidosis AL amyloidosis AA amyloidosis Aβ2M/Haemodialysis-associated AGel/Finnish type AA/Familial Mediterranean fever ATTR/Transthyretin-related hereditary Organ-limited amyloidosis Heart AANF/Isolated atrial Brain Familial amyloid neuropathy ACys+ABri/Cerebral amyloid angiopathy Aβ/Alzheimer's disease Kidney AApoA1+AFib+ALys/Familial renal Skin Primary cutaneous amyloidosis Amyloid purpura Endocrine Thyroid ACal/Medullary thyroid cancer Pituitary APro/Prolactinoma Pancreas AIAPP/Insulinoma AIAPP/Diabetes mellitus type 2 This cutaneous condition article is a stub .
  • Secondary Cutaneous Amyloidosis Wikipedia
    ISBN 978-1-4160-2999-1 . v t e Amyloidosis Common amyloid forming proteins AA ATTR Aβ2M AL Aβ / APP AIAPP ACal APro AANF ACys ABri Systemic amyloidosis AL amyloidosis AA amyloidosis Aβ2M/Haemodialysis-associated AGel/Finnish type AA/Familial Mediterranean fever ATTR/Transthyretin-related hereditary Organ-limited amyloidosis Heart AANF/Isolated atrial Brain Familial amyloid neuropathy ACys+ABri/Cerebral amyloid angiopathy Aβ/Alzheimer's disease Kidney AApoA1+AFib+ALys/Familial renal Skin Primary cutaneous amyloidosis Amyloid purpura Endocrine Thyroid ACal/Medullary thyroid cancer Pituitary APro/Prolactinoma Pancreas AIAPP/Insulinoma AIAPP/Diabetes mellitus type 2 This cutaneous condition article is a stub .
  • Leukoencephalopathy Wikipedia
    Leukoencephalopathy ( leukodystrophy -like diseases) is all of the brain white matter diseases, whether their molecular cause is known or not. [1] It can refer specifically to any of these diseases: Progressive multifocal leukoencephalopathy Toxic leukoencephalopathy Leukoencephalopathy with vanishing white matter Leukoencephalopathy with neuroaxonal spheroids Reversible posterior leukoencephalopathy syndrome Megalencephalic leukoencephalopathy with subcortical cysts . It can also refer to gene MLC1 or Megalencephalic leukoencephalopathy with subcortical cysts 1 , a human gene related to the former disease. Hypertensive leukoencephalopathy The classification of leukoencephalopathies is a matter of debate. Some authors divide leukoencephalopathies into hereditary disorders and acquired disorders. The hereditary demyelinating disorders are then classified according to the localization of the underlying metabolic defect, and they include the leukodystrophies when myelin growth is the underlying problem.
    CSF1R, COL4A1, TYMP, SCP2, SPP1, APP, TCN2, RHOA, MTHFR, MTR, DPYD, DARS2, BDNF, CDKN1B, NOTCH3, EIF2B2, EIF2B1, EIF2B4, CLCN2, DARS1, POLG, EIF2B5, SNORD118, RPIA, NDUFS1, NDUFAF3, HTRA1, L2HGDH, VPS11, GJC2, CLN6, TYROBP, COA8, NUBPL, EARS2, NAXE, NDUFV1, PLAA, NFE2L2, SAMHD1, NDUFS8, NDUFS6, NDUFS4, MRPS22, NDUFS3, NDUFS2, NDUFV2, TACO1, SCN8A, SCO1, YME1L1, PMPCB, AIFM1, NDUFAF1, RRM2B, TREX1, EIF2B3, NDUFB10, NDUFB11, TMEM70, FASTKD2, FOXRED1, TIMMDC1, KMT2E, NDUFAF4, TMEM126B, NDUFB9, MARS2, CTC1, PET100, AUH, NDUFS7, COX6B1, COX8A, COX10, B3GALNT2, NDUFA11, COX20, NDUFAF2, HMGCL, COX14, LAMB1, HIBCH, COLGALT1, ND2, TRNS1, ND3, NDUFAF5, NDUFA1, NDUFA6, TRNN, ND1, NDUFB3, AARS2, MLC1, EIF2S2, HEPACAM, SDHAF1, RNASET2, TUBB4A, ABCB6, LGALS14, GFAP, APOE, WARS2, CSF2, DEAF1, NFU1, PSEN1, LAMA2, KARS1, ISCA2, COA7, KCNT1, POLR3B, NOTCH2NLC, DDX59, SLC2A4RG, SHANK3, SLC26A5, GGCT, ACBD5, LYRM7, SLC5A8, RMND1, GLRX5, TREM2, MTFMT, IBA57, HIKESHI, SLC13A3, AARS1, SZT2, MS, MOG, MBP, MANBA, KIF5A, IL6, IFNG, IFNB1, HMGB1, HMBS, GJA1, GFPT1, FMR1, EIF2S3, EIF2S1, EEF1A1, EDN1, SARDH, CST3, COL4A2, CLCN1, C1QBP, ALDH3A2, ABCD1, JAG1, ADORA2A, MPV17, COX2, POLR3A, MYL2, SDS, MYL9, SCO2, FIG4, ARHGEF2, DEGS1, CUL4B, VEGFA, TUFM, TLR2, SURF1, ACTA2, SORD, SLC16A2, SLC2A1, SDHB, CCL5, PTGS2, PRPS1, PLP1, PDGFB, PAFAH1B1, NEFL, NDUFB8, NDUFA2, MTCO2P12
  • Mosquito Bites Mayo_clinic
    Avoid and exclude mosquitoes Limit exposure to mosquitoes by: Repairing any tears in the screens on windows, doors and camping gear Using mosquito netting over strollers and cribs Using mosquito netting when sleeping outdoors Selecting self-care products that don't have scents Use insect repellent Use insect repellent when mosquitoes are active. ... Some sporting goods stores sell clothing pretreated with permethrin. Don't wash bed nets or set them in sunlight, as this breaks down permethrin.
  • Clanging Wikipedia
    . ^ Spitzer, Manfred (1999). The mind within the net: Models of learning, thinking, and acting .
  • Occupational Hearing Loss Wikipedia
    Relationship between noise exposure levels and duration of allowable exposure at that level for NIOSH and OSHA The NIOSH Sound Level Meter app Sound level meters and dosimeters are two types of devices that are used to measure sound levels in the workplace. ... Some recent studies suggest that some smartphone applications may be able to measure noise as precisely as a Type 2 SLM. [15] [16] Although most smartphone sound measurement apps are not accurate enough to be used for legally required measurements, the NIOSH Sound Level Meter app met the requirements of IEC 61672/ANSI S1.4 Sound Level Meter Standards (Electroacoustics - Sound Level Meters - Part 3: Periodic Tests). [17] Ototoxic chemical exposure [ edit ] Chemically-induced hearing loss (CIHL) is a potential result of occupational exposures. ... "Evaluation of smartphone sound measurement applications (apps) using external microphones-A follow-up study" . ... "Smartphone-based sound level measurement apps: Evaluation of compliance with international sound level meter standards".
  • Organ-Limited Amyloidosis Wikipedia
    External links [ edit ] Classification D ICD - 10 : E85.4 ICD - 9-CM : 277.3 v t e Amyloidosis Common amyloid forming proteins AA ATTR Aβ2M AL Aβ / APP AIAPP ACal APro AANF ACys ABri Systemic amyloidosis AL amyloidosis AA amyloidosis Aβ2M/Haemodialysis-associated AGel/Finnish type AA/Familial Mediterranean fever ATTR/Transthyretin-related hereditary Organ-limited amyloidosis Heart AANF/Isolated atrial Brain Familial amyloid neuropathy ACys+ABri/Cerebral amyloid angiopathy Aβ/Alzheimer's disease Kidney AApoA1+AFib+ALys/Familial renal Skin Primary cutaneous amyloidosis Amyloid purpura Endocrine Thyroid ACal/Medullary thyroid cancer Pituitary APro/Prolactinoma Pancreas AIAPP/Insulinoma AIAPP/Diabetes mellitus type 2
  • Chronic Hallucinatory Psychosis Wikipedia
    Others, again, might be swept into the widespread net of dementia praecox . This state of affairs cannot be regarded as satisfactory, for they are not truly cases of melancholia, paranoia, dementia praecox or any other described affection.
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