Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

First rate collaboration between clinicians and research scientists in a multiplicity of fields have brought new hope to patients with cystic fibrosis (CF). The gene, mutations of which give rise to the disease, has been exhaustively mapped, and the functional defects are becoming steadily clearer. Diagnosis is continually being improved and simplified. Neonatal screening has been introduced in many countries and has yielded good results. Promising new advances in treatment include inhalatory DNase (deoxyribonuclease), lung and liver transplantation, UDCA (ursodeoxycholic acid) against cirrhosis, and in vitro fertilisation for men with CF. Pseudomonas species are being combatted more and more effectively with new antibiotics, with immunoglobulins (IgY) for prophylaxis, and possibly new vaccines to come. Future treatment strategies, designed to correct anomalies of cellular biology, are already undergoing clinical trials, and gene therapy using a variety of vectors is undergoing phase-1 trials. A definitive cure remains a realistic hope.
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PMID:[Further clarification of functional issues in cystic fibrosis. Current research and future prospects]. 1047 96

Nonalcoholic steatohepatitis (NASH) is a progressive, inflammatory form of fatty liver disease. It is the most rapidly rising risk factor for the development of hepatocellular carcinoma (HCC), which can arise in NASH with or without cirrhosis. The inflammatory signals promoting the progression of NASH to HCC remain largely unknown. The propensity of neutrophils to expel decondensed chromatin embedded with inflammatory proteins, known as neutrophil extracellular traps (NETs), has been shown to be important in chronic inflammatory conditions and in cancer progression. In this study, we asked whether NET formation occurs in NASH and contributes to the progression of HCC. We found elevated levels of a NET marker in serum of patients with NASH. In livers from STAM mice (NASH induced by neonatal streptozotocin and high-fat diet), early neutrophil infiltration and NET formation were seen, followed by an influx of monocyte-derived macrophages, production of inflammatory cytokines, and progression of HCC. Inhibiting NET formation, through treatment with deoxyribonuclease (DNase) or using mice knocked out for peptidyl arginine deaminase type IV (PAD4-/- ), did not affect the development of a fatty liver but altered the consequent pattern of liver inflammation, which ultimately resulted in decreased tumor growth. Mechanistically, we found that commonly elevated free fatty acids stimulate NET formation in vitro.
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PMID:Neutrophil extracellular traps promote inflammation and development of hepatocellular carcinoma in nonalcoholic steatohepatitis. 2963 32