PubMed · 8749460
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A Kato, K Suzuki, S Sato. 1995. [Hepatic encephalopathy].. https://pubmed.ncbi.nlm.nih.gov/8749460/
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BACKGROUND: Ischemic heart disease (IHD) is the leading cause of morbidity and mortality. Branched-chain amino acids (BCAAs) are associated with higher IHD risk, but the underlying biological pathways remain unclear. OBJECTIVES: This study aims to explore these pathways using 2-step proteome-wide Mendelian randomization. METHODS: We examined the associations between genetic proxies for BCAAs and 2922 proteins in the United Kingdom Biobank Pharma Proteomics Project, supplemented by a meta-analysis with data from deCODE to identify proteins associated with BCAAs. Next, we tested their effects on IHD risk using Coronary Artery Disease Genome-wide Replication and Meta-analysis plus Coronary Artery Disease Genetics Consortium (122,733 cases and 424,528 controls) and replicated in FinnGen (31,640 cases and 187,152 controls). We conducted sensitivity analyses using genetic instruments from deCODE. Proteins associated with IHD risk and, in a consistent direction, with genetically predicted BCAAs were considered potential mediators. RESULTS: Genetic proxies for BCAAs were associated with 40 proteins. Among these, 6 proteins showed consistent evidence of mediation, including complement C1s subcomponent, coagulation factor II, granulin, proprotein convertase subtilisin/kexin type 9, sex hormone-binding globulin, and V-set and transmembrane domain-containing protein 2-like. These proteins are involved in inflammation, coagulation, lipid metabolism, and cellular stress response. All associations were robust across different analytical methods and replicated in independent datasets. Mediation analysis showed that these proteins accounted for 6.5% to 32.1% of the association between BCAAs and IHD risk. CONCLUSIONS: This study identified 6 proteins that potentially link BCAAs to IHD, implicating pathways related to inflammation, coagulation, lipid metabolism, and cellular stress responses. To our knowledge, these findings provide novel mechanistic insights into the BCAA-IHD relationship and highlight potential protein targets for future prevention and intervention strategies.
BACKGROUND: A combined colorectal and hepatic resection is considered too risky by many surgeons owing to the high risk of postoperative septic complications. The aim of the present study was to investigate the effects of hepatic resection on the healing of left-sided colonic anastomoses in rats on postoperative day 7. MATERIAL AND METHODS: Fifty-four Sprague-Dawley rats were block-randomized into three groups. In each group, 1 cm of the left side of the colon was resected and anastomosed. Additionally, 40 or 70% of the liver was resected in group 2 and 3, respectively. Rats were killed on postoperative day 7. The abdominal cavity was inspected for the presence of complications. The bursting pressure and hydroxyproline content of the anastomoses were measured. RESULTS: The total number of complications was significantly higher in group 3 than in group 2. Anastomotic bursting pressure and hydroxyproline content did not differ significantly among the groups. CONCLUSIONS: Increasing the extent of simultaneous hepatic resection did not significantly affect the healing of left-sided colonic anastomoses in rats on postoperative day 7, although there was a tendency towards lower bursting pressure paralleling the extent of liver resection. Excessive hepatic resection with colectomy may increase postoperative complications.
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