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44; 95% CI 0.22-0.90). Meanwhile, octreotide was shown to have the highest probability ranking the best to improve initial hemostasis (mean rank =1.8) and carries a lowest risk of adverse events (9.1%) and serious adverse events (0.0%) compared to other drugs. Conclusions Balanced with curative effect and tolerability, octreotide may be the preferred vasoactive drug facilitating endoscopy. 2019 Annals of Translational Medicine. All rights reserved.Background The world-wide prevalence of carbapenem-resistant Klebsiella pneumoniae (CRKP) poses a threat to the public health. The objective of this study was to determine the epidemiological and molecular patterns of KPC-producing Klebsiella pneumoniae (K. pneumoniae) clinical isolates. Methods In this study, a total of 82 non-duplicated CRKP isolates were analyzed for the prevalence of resistant determinants including carbapenemase, extended spectrum β-lactamase (ESBLs), and AmpC as well as integrons and cassette regions by polymerase chain reaction (PCR) and DNA sequencing. The genetic relatedness was investigated by pulsed field gel electrophoresis (PFGE) and multi-locus sequencing typing (MLST). Results Overall, bla KPC-2 (n=75) was the predominant carbapenemase gene, followed by high prevalence of bla SHV (92.7%) and bla CTX-M (90.2%). PFGE and MLST analysis revealed that 65 out of 68 KPC-2-producing CRKP belonged to the ST11 clone and were distributed mainly in the department of neurology ICU. Moreover, first report on clonal dissemination of KPC-2-producing CRKP ST48 clone and NDM-5-producing CRKP ST337 clone was also identified. Class I integron were detected in 17 (20.7%) of 82 isolates with aadA2 being the most common cassette. And a novel cassette array of integron, aac(6')-II-bla CARB/PSE-1 was identified. Conclusions All in all, KPC-2-producing CRKP ST11 and ST48 clone were widely disseminated in multiple departments of our hospital, which triggers the need for active surveillance and implementation of infection control measures. 2019 Annals of Translational Medicine. All rights reserved.Background Fast and reliable biomarkers are needed to distinguish whether individuals were exposed or not to radiation and assess radiation dose, and to predict the severity of radiation damage in a large-scale radiation accident. Serum amyloid A1 (SAA1) is a protein induced by multiple factors including inflammatory. Therefore, this study aimed at exploring the role of SAA1 in the radiation dose estimation and lethality prediction after radiation. Methods C57BL/6J female mice were exposed to total body irradiation (TBI) at different doses and time points and amifostine, a drug used to reduce the side effects of radiotherapy, was injected before irradiation. Patients with nasopharyngeal carcinoma subjected to radiotherapy were used as the irradiation model in humans. Results A moderate SAA1 increase was observed at 6 hours in serum samples from irradiated mice at all doses used, with a peak at 12 hours, then decreased to day 3 after exposure. selleck inhibitor A second SAA1 increase was observed from day 5 to 7, which was associated to subsequent lethality. Treatment with amifostine before irradiation could prevent mice death and inhibit the second SAA1 increase. SAA1 increase after radiation was confirmed in human serum of nasopharyngeal carcinoma patients after radiotherapy. Conclusions Serum SAA1 levels could represent a biomarker for radiation dose estimation and its second increase might be a useful lethality indicator after radiation in a mouse model. 2019 Annals of Translational Medicine. All rights reserved.Background Heart-protecting musk pill (HMP), derived from Chinese herbal medicines, has been found to possess protective roles against atherosclerosis-related cardiovascular diseases (CVDs), however, the anti-atherosclerotic mechanisms of HMP are still unclear. Here, we investigated the effects of HMP on alleviating atherosclerotic lesion severity in mice and explored the molecular mechanisms. Methods Apolipoprotein E-deficient mice were fed western-type diet supplemented with HMP (25 mg/kg/day) or normal saline gavage for 20 weeks. Then histopathological staining was performed to assess the atheromatous plaque burden. Biochemical kits were used to detect levels of lipid profiles. Moreover, effector factors associated with lipid metabolism in liver and intestinal tissues were investigated by western blot and real-time PCR assays. Levels of signal molecules participating in the mitochondrial-mediated apoptosis pathway were detected by Western blot. Results We found that HMP notably reduced atherosclerotic lesiConclusions Altogether, our study indicates that HMP plays anti-atherosclerotic roles via regulating lipid metabolism and improving vascular intimal injury. 2019 Annals of Translational Medicine. All rights reserved.Background Ulcerative colitis (UC) is an inflammatory bowel disease (IBD) that causes long-lasting inflammation and ulcers in the human digestive tract. The repair role of TLR4 in the intestinal epithelium is still unknown. Methods By comparing to wild-type (WT) mice, Toll-like receptor 4 (TLR4)-knockout mice (TLR4-KO) were used as dextran sulfate sodium (DSS)-induced colitis models to explore the role of TLR4 signaling in intestinal injury. High-throughput RNA-Seq, RT-qPCR and ELISA were performed to screen and verify key differences in gut genes between WT and TLR4-KO mice. Functional study of core dysregulated factors was performed in intestinal cell lines. Results We found that DSS-induced intestinal injury was aggravated by LPS (TLR4 agonist) and TLR4-KO. When compared to WT mice, IL6, CCL2, CSF3, IL11, Ccnb1, Ccnd1 and TNF-α significantly decreased and Fas and FasL have increased in the gut of TLR4-KO mice. IL6, CCL2, CSF3, Fas and FasL have all increased in CT-26 cells treated with LPS. Combined with the above data and KEGG enrichment, it can be assumed that TLR4-KO might aggravate DSS-induced intestinal damage by attenuating cell cycle, cytokine-cytokine receptor interaction, and Toll-like receptor signaling pathway, and enhancing the apoptosis pathway. In the functional study of core dysregulated factors, it was found that LPS, IL6, IL11, CSF3, CCL2, S100A8, S100A9 and Mmp3 have improved viability of colon cancer cell lines and decreased apoptosis rate of mouse colon cancer cells when these were treated with DSS. However, Jo-2 (Fas agonistic monoclonal antibody) played the opposite role in colon cancer cells treated with DSS. Conclusions TLR4 had a repairing effect on DSS-induced intestinal damage and it up-regulate IL6, CCL2 and CSF3. Fas and FasL enhanced DSS-induced colon injury in mice, but might have little to do with TLR4 signaling. 2019 Annals of Translational Medicine. All rights reserved.