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Objective@#To analyze non-alcoholic steatohepatitis (NASH)-related differentially expressed genes (DEGs) by bioinformatics methods to find key pathways and potential therapeutic targets for NASH.@*Methods@#GSE61260 chip was downloaded from the public microarray database and liver biopsy samples from 24 NASH cases and 38 healthy controls were included. The Limma software package in R language was used to screen DEGs under the condition of difference multiple > 1.5 and adj. P < 0.05. The clusterProfiler software package was used for GO analysis and KEGG analysis. The STRING online database was used for protein-protein interaction analysis, and the L1000 and DrugBank databases were used for drug prediction.@*Results@#Compared with healthy control group, 857 DEGs were screened out in NASH group including 167 up-regulated genes and 690 down-regulated genes. GO analysis showed that DEGs were mainly involved in inflammation and cholesterol metabolism. KEGG analysis showed that DEGs were mainly enriched in PPAR, non-alcoholic fatty liver disease, oxidative phosphorylation and other signaling pathways. Among them, eight genes of ACSL4, CYP7A1, FABP4, FABP5, lipoprotein lipase, ME1, OLR1 and PLIN1 were enriched in PPAR signaling pathway, and 165 interaction nodes were formed with 47 DEGs-encoded proteins. Lipoprotein lipase interacted with 21 DEGs, and its up-regulated expression had improved lipid metabolism, insulin resistance and anti-inflammatory effects. Four drugs (gemfibrozil, bezafibrate, omega-3 carboxylic acid and glycyrrhizic acid) were screened by L1000 and DrugBank to activate lipoprotein lipase. Presently, these four drugs are clinically used to treat hypertriglyceridemia or to improve inflammation. In this regard, we speculated that the pharmacological effects of these four drugs had improved NASH by activating lipoprotein lipase to promote liver lipid metabolism and alleviate inflammation.@*Conclusion@#PPAR signaling pathway is closely associated to the occurrence and development of NASH, and thereby lipoprotein lipase agonist is a new attempt to treat NASH.
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Nonalcoholic fatty liver disease (NAFLD) includes nonalcoholic simple fatty liver, nonalcoholic steatohepatitis, liver cirrhosis, and liver cancer and is the most common liver disease in the world. The complex pathogenesis of NAFLD is a major concern among researchers. CD36 is a transmembrane glycoprotein that takes up fatty acid and binds to oxidized low-density lipoprotein in the liver, and therefore, it is involved in the development and progression of NAFLD. With reference to the latest research findings, this article reviews the association between CD36 and NAFLD and the role of CD36.
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<p><b>OBJECTIVE</b>To assess the clinical value ofprocalcitonin in cirrhotic patients with severe infection by comparing the serum procalcitonin levels in those patients with and without liver cirrhosis when suffering from sepsis.</p><p><b>METHODS</b>A total of 225 septic patients were included in the study,including 91 patients without hepatopathy, 80 patients with cirrhosis, and 54 patients with chronic liver disease. The serum procalcitonin level was measured in all patients and statistically assessed for correlation with relevant clinical biochemistry indicators. The t-test, ANOVA test, Mann-Whitney U test, chi-square test and Spearman's correlation analysis were used for statistical analyses.</p><p><b>RESULTS</b>The patients with cirrhosis showed significantly lower serum procalcitonin levels (0.84 (0.32-3.44) ng/ml) than the patients with no hepatopathy (2.17 (0.70-9.18) ng/ml) or the patients with chronic liver disease (2.12 (0.33-13.61) ng/ml) (both P less than 0.05); the patients in the no hepatopathy group and the chronic liver disease group showed statistically similar levels of serum procalcitonin (P=0.616). The patients with cirrhosis of Child-Pugh grade C showed significantly higher level of serum procalcitonin (1.25 (0.54-4.61) ng/ml) than those patients with Child-Pugh grade B (0.33 (0.14-1.31) ng/ml; P=0.026), suggesting that patients with Child-Pugh C stage cirrhosis may be more susceptible to gram-negative bacterial infection. In the cirrhosis group,serum procalcitonin level was positively correlated with white blood cell (WBC) count (r=0.312) and percentage of neutrophils (N%) (r=0.228) (both P less than 0.05). Correlation analysis of the no hepatopathy group and the chronic liver disease group showed no correlation between serum procalcitonin level and either WBC or N%.</p><p><b>CONCLUSION</b>Under the sepsis condition, cirrhotic patients have lower serum procalcitonin level than patients without cirrhosis, and the serum procalcitonin level is positively correlated with WBC count and N%.</p>
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Humans , Calcitonin , Calcitonin Gene-Related Peptide , Liver Cirrhosis , Protein Precursors , SepsisABSTRACT
Objective To obtain a reliable estimate of the risk of H. pylori infection in causing pancreatic cancer ,by perform‐ing a M eta‐analysis of the existing observational studies evaluating the association .Methods Observational studies comparing the prevalence of H. pylori infection in patients with pancreatic cancer and healthy controls were identified through systematic search in the Medline ,EMBASE ,the Cochrane ,PubMed ,VIP database .H. pylori infection was confirmed by serological testing using an anti‐gen‐specific enzyme‐linked immunosorbent assay .Pooled adjusted odds ratios (AOR) and associated 95% confidence intervals (CI) were obtained by using a Dersimonian and Laird random‐effects model .Results Six studies involving a total of 2 335 patients met our eligibility criteria .A significant association between H. pylori seropositivity and development of pancreatic cancer (AOR=1 .38 , 95% CI:1 .08-1 .75 ;P=0 .009) was seen .No significant association had been seen on pooled analysis of the three studies assessing the relationship between CagA positivity and pancreatic cancer (AOR=1 .14 ,95% CI:0 .66-1 .97 ,P=0 .639) .Conclusion The da‐ta suggests an association between infection with H. pylori and the development of pancreatic cancer .Further research is needed to confirm our findings .
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Objective To investigate the distribution of Leptotrombidium deliense among different small mammal hosts in some areas of Yunnan province. Methods A field survey was carried out in some counties of Yunnan province and the small mammal hosts were captured, using mouse cages and traps with baits. Chigger mites on the surface of two auricles were scraped off by a bistoury, and then preserved in 70% ethanol. Every specimen of the chigger mites on the slides was finally identified into species under a microscope. Some conventional statistical methods were adopted to calculate all the collected chigger mite species and the constituent ratios of Leptotrombidium deliense in different areas and on different hosts, together with its prevalence and mean abundance on different hosts. Results A total of 10 222 small mammal hosts were captured from 19 counties and identified as 11 families, 34 genera and 62 species in 5 orders, and 92 990 individuals of chigger mites were collected from the body surface of these small mammal hosts. All the collected chigger mites were identified as 3 subfamilies, 22 genera, and 225 species. Meanwhile, Leptotrombidium deliensee only accounted for 1.659% of the total. The host specificity of Leptotrombidium deliense was very low and 1544 individuals of Leptotrombidium deliense collected from 8518 small mammal hosts belonged to 6 families, 13 genera and 19 species in 3 orders. Our results showed that Leptotrombidium delienses were mainly collected from Insectivora and Rodentia. Leptotrombidium deliense had long been considered as the dominant species of chigger mites and the main vector of tsutsugamushi disease in Yunnan province of China, but our results seemed not thoroughly supporting this point of view. Conclusion Traditionally, Leptotrombidium deliense was the dominant species and the main vectors of scrub typhus in Yunnan province. However, based on our results, the above view might be true in some local places and the composition of chigger mites and the main vector of tautsugamushi disease might be different in regions and habitats in Yunnan province.