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Objective: To investigate the efficacy and safety of cold snare endoscopic mucosal resection (CS-EMR) and hot snare endoscopic mucosal resection (HS-EMR) for colorectal polyps with diameters of 6–9...

Yan Guo, Hua-Ming Li, Wei-Qin Zhu, Zhen Li Department of Gastroenterology, Hangzhou Third People’s Hospital, Hangzhou, 310009, People’s Republic of ChinaCorrespondence: Yan GuoDepartment of Gastroenterology Hangzhou Third People’s Hospital, No. 38 West Lake Road, Shangcheng District, Hangzhou, 310009, People’s Republic of ChinaTel +86 571 87823158Fax +86 571 87814481Email yanguodr1@163.comObjective: To investigate the role of Helicobacter pylori (HP) eradication in chronic spontaneous urticaria (CSU) treatment.Methods: Retrospective analysis was performed on the clinical data of 522 patients with CSU who underwent a HP breath test in Hangzhou Third People’s Hospital between January 2018 and December 2019. The CSU-HP(+) group consisted of patients with CSU and HP infection, who were treated with antihistamines combined with HP eradication therapy. The CSU-HP(-) group consisted of patients with CSU alone, who were treated with antihistamines. Propensity score matching (PSM) analysis, using the nearest neighbor matching method on a 1:1 basis, was performed to ensure the characteristics of the CSU-HP(+) and CSU-HP(-) groups were similar. Factors, including age, gender, white blood cells, red blood cells, platelets, alanine transaminase, creatinine, immunoglobulin E, and pre-treatment urticaria activity score (UAS), were matched to obtain a balanced cohort of patients in each group. Therapeutic effects were compared after matching. t-tests, &KHgr;2 test, and McNemar’s test were used for comparison between the two groups before and after matching.Results: Patients in the CSU-HP(+) group reported significantly more gastrointestinal symptoms than those in the CSU-HP(-) group. UAS scores in the second week of treatment were significantly different between the two groups. After 3 months, the recurrence rate in the CSU-HP(+) group was lower than in the CSU-HP(-) group.Conclusion: Eradication of HP infection in patients with CSU helps relieve gastrointestinal symptoms, improves the therapeutic effect of CSU within 2 weeks, and reduces the recurrence rate 3 months after treatment.Keywords: chronic urticaria, chronic spontaneous urticaria, Helicobacter pylori, eradication therapy

Introduction: Previous studies showed that high density lipoprotein (HDL) can stimulate angiogenesis. However, the mechanisms by which HDL promotes angiogenesis remains unclear. Hypothesize: HDL may promote angiogenesis by regulating miRNAs expression. Methods: HDL was isolated from healthy subjects. Human umbilical vein endothelial cells (HUVECs) were cultured with vehicle or HDL (100 μg/ml), and the differential miRNAs expression were indentified by miRNA array and verified by qRT-PCR. HUVECs were treated with vehicle or HDL (100 μg/ml) with or without miRNAs mimic, endothelial cells proliferation, migration and tube formation were detected. The production of nitric oxide(NO) was measured. The expression and phosphorylation of endothelial nitric oxide synthase (eNOS) was determined. Results: The miRNAs profile of HDL-treated HUVECs is significantly different from control group. HDL significantly downregulated miR-24-3p expression. HDL significantly promoted HUVECs proliferation, migration and tube formation. HDL also significantly stimulated NO production and up-regulated the expression and phosphorylation of eNOS. However, HDL did not stimulated HUVECs proliferation, migration, tube formation and NO production as well as the expression and phosphorylation of eNOS after pretreated with miR-24-3p mimic. Conclusions: HDL can promote angiogenesis by suppressing miR-24-3p expression.

Simvastatin treatment is cardioprotective in patients undergoing noncoronary artery cardiac surgery. However, the mechanisms by which simvastatin treatment protects the myocardium under these conditions are not fully understood. Seventy patients undergoing noncoronary cardiac surgery, 35 from a simvastatin treatment group and 35 from a control treatment group, were enrolled in our clinical study. Simvastatin (20 mg/d) was administered preoperatively for 5-7 days. Myocardial tissue biopsies were taken before and after surgery. Apoptosis was detected by TUNEL staining. The expressions of Bcl-2 and Bak in myocardial tissue were detected by immunoblotting. The expressions of miRNA and Bcl-2 mRNA were detected by quantitative real-time polymerase chain reaction assays. Cardiomyocytes were isolated from rat and cultured cells. MiR-15a-5p mimic was transfected into cardiomyocytes, and the Bcl-2 was detected by immunoblotting. TUNEL staining showed significantly less myocardial apoptosis in the simvastatin treatment group when compared with the control treatment group. Protein expression of Bcl-2 was increased in the simvastatin treatment group before surgery, and Bak expression was increased in the control treatment group after surgery. Further comparisons showed that Bcl-2/Bak ratios were reduced in the control treatment group but were not significantly changed in the simvastatin treatment group after surgery. Furthermore, microarray assays revealed that miR-15a-5p was significantly decreased by simvastatin treatment. This was validated by quantitative real-time polymerase chain reaction analysis. MiR-15a-5p was predicted to target Bcl-2 mRNA at nucleotide positions 2529-2536. This was validated by luciferase binding assays. Coincident with the change in miR-15a-5p, the mRNA expression of Bcl-2 was increased in the simvastatin treatment group. MiR-15a-5p mimic significantly inhibited Bcl-2 expression in cardiomyocytes. Our findings strongly suggest that simvastatin treatment preoperatively protected the myocardium in patients undergoing noncoronary artery cardiac surgery, at least in part, by inhibiting apoptosis via suppressing miR-15a-5p expression, leading to increasing expression of Bcl-2 and decreasing expression of Bak.

Acute pancreatitis is rarely associated with drugs. Acetaminophen overdose is a well-known cause of hepatic toxicity, but drug-induced pancreatitis is rarely reported, especially after mild overdose. A 32-year-old woman presented with nausea and vomiting for 12 h, but no abdominal pain following an overdose of eight Tylenol tablets containing acetaminophen (325 mg acetaminophen per tablet). Laboratory results on admission showed abnormal amylase and lipase levels but completely normal liver function. Magnetic resonance cholangiopancreatography revealed mild swelling of the pancreas without fluid collection around the pancreas. The patient complained of severe abdominal pain five days after admission when attempting to drink water and liquids. Eight days after admission, fluid around the pancreas was observed by computed tomography. The patient was subsequently diagnosed with acetaminophen-induced acute pancreatitis after exclusion of common causes. Routine treatment for pancreatitis and N-acetylcysteine were administered to prevent disease progression. The patient was discharged in good condition.

Objective To report drug-induced oesophageal ulceration in adult patients treated with doxycycline for acne vulgaris. Methods This retrospective case series included data from adult patients treated with oral doxycycline therapy for acne vulgaris, who had presented with oesophageal ulceration at the Third People’s Hospital of Hangzhou between June 2016 and December 2017, and whose diagnosis was confirmed by gastroscopy. Clinicodemographic data were analysed, including symptom onset, endoscopy results, that were assessed for classic features of oesophageal ulceration. Patients were questioned regarding medication intake. Results A total of 12 patients were included (mean age, 23.50 ± 3.20 years), eight (66.67%) of whom were female. Based on history of medication and endoscopic findings, these patients were diagnosed with doxycycline-induced oesophageal ulceration. Most patients were found to have taken the medication at bedtime, just before lying down, and/or with insufficient water. Conclusion Doxycycline may cause oesophageal irritation when not taken with sufficient water, or taken just before lying down to sleep. Prescribing physicians should be aware of these issues, and instruct patients as to the correct method for intake of doxycycline.

Endothelial dysfunction is an early stage of atherosclerosis. We recently have shown that 25-hydroxycholesterol found in atherosclerotic lesions could impair endothelial function and vasodilation by uncoupling and inhibiting endothelial nitric oxide synthase (eNOS). 1-Palmitoyl-2-(5-oxovaleroyl)-sn-glycero-3-phosphocholine (POVPC), the oxidation product of oxidized low-density lipoprotein, is another proinflammatory lipid and has also been found in atherosclerotic lesions. However, whether POVPC promotes atherosclerosis like 25-hydroxycholesterol remains unclear. The purpose of this study was to explore the effects of POVPC on endothelial function and vasodilation. Human umbilical vein endothelial cells (HUVECs) were incubated with POVPC. Endothelial cell proliferation, migration and tube formation were measured. Nitric oxide (NO) production and superoxide anion generation (O2-) were determined. The expression and phosphorylation of endothelial nitric oxide synthase (eNOS), AKT, PKC-βII and P70S6K as well as the association of eNOS and heat shock protein 90 (HSP90) were detected by immunoblotting and immunoprecipitation. Endothelial cell apoptosis was monitored by TUNEL staining. The expression of Bcl-2, Bax, and Cleaved Caspase 3 were detected by immunoblotting. Finally, aortic ring from C57BL6 mice were isolated and treated with POVPC and the endothelium-dependent vasodilation was evaluated. POVPC significantly inhibited HUVECs proliferation, migration, tube formation, decreased NO production but increased O2- generation. POVPC inhibited the phosphorylation of Akt and eNOS at Ser1177, increased activation of PKC-βII, P70S6K and the phosphorylation of eNOS at Thr495, reduced the association of HSP90 with eNOS. Meanwhile, POVPC induced endothelial cell apoptosis by inhibiting Bcl-2 expression, increasing Bax and cleaved caspase-3 expressions as well as caspase-3 activity and impaired endothelium-dependent vasodilation. These data demonstrated that POVPC impaired endothelial function by uncoupling and inhibiting eNOS as well as by inducing endothelial cell apoptosis. Therefore, POVPC may play an important role in the development of atherosclerosis and may be considered as a potential therapeutic target for atherosclerosis.

Increased evidence has showed that normal high density lipoprotein (HDL) could convert to dysfunctional HDL in diseases states including coronary artery disease (CAD), which regulated vascular endothelial cell function differently. Long non-coding RNAs (lncRNAs) play an extensive role in various important biological processes including endothelial cell function. However, whether lncRNAs are involved in the regulation of HDL metabolism and HDL-induced changes of vascular endothelial function remains unclear. Cultured human umbilical vein endothelial cells (HUVECs) were treated with HDL from healthy subjects and patients with CAD and hypercholesterolemia for 24 h, then the cells were collected for lncRNA-Seq and the expressions of lncRNAs, genes and mRNAs were identified. The bioinformatic analysis was used to evaluate the relationship among lncRNAs, encoding genes and miRNAs. HDL from healthy subjects and patients with CAD and hypercholesterolemia leaded to different expressions of lncRNAs, genes and mRNAs, and further analysis suggested that the differentially expressed lncRNAs played an important role in the regulation of vascular endothelial function. Thus, HDL from patients with CAD and hypercholesterolemia could cause abnormal expression of lncRNAs in vascular endothelial cells to affect vascular function.

Background We previously demonstrated that endothelial microparticles (EMPs) are increased in mitral valve diseases and impair valvular endothelial cell function. Perioperative systemic inflammation is an important risk factor and complication of cardiac surgery. In this study, we investigate whether EMPs increase in congenital heart diseases to promote inflammation and endothelial dysfunction. Methods The level of plasma EMPs in 20 patients with atrial septal defect (ASD), 23 patients with ventricular septal defect (VSD), and 30 healthy subjects were analyzed by flow cytometry. EMPs generated from human umbilical vascular endothelial cells (HUVECs) were injected into C57BL6 mice, or cultured with HUVECs without or with siRNAs targeting P38 MAPK. The expression and/or phosphorylation of endothelial nitric oxide synthase (eNOS), P38 MAPK, and caveolin-1 in mouse heart and/or in cultured HUVECs were determined. We evaluated generation of nitric oxide (NO) in mouse hearts, and levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in cultured HUVECs and in mice. Results EMPs were significantly elevated in patients with ASD and VSD, especially in those with pulmonary hypertension when compared with controls. EMPs increased caveolin-1 expression and P38 MAPK phosphorylation and decreased eNOS phosphorylation and NO production in mouse hearts. EMPs stimulated P38 MAPK expression, TNF-α and IL-6 production, which were all inhibited by siRNAs targeting P38 MAPK in cultured HUVECs. Conclusions EMPs were increased in adult patients with congenital heart diseases and may contribute to increased inflammation leading to endothelial dysfunction via P38 MAPK-dependent pathways. This novel data provides a potential therapeutic target to address important complications of surgery of congenial heart disease. Electronic supplementary material The online version of this article (doi:10.1186/s12967-016-1087-2) contains supplementary material, which is available to authorized users.

Background Surveillance data for rabies in Guangxi Province in China showed that human rabies cases have gradually increased since 1996. Objective To evaluate the epidemiology of rabies at the molecular level and provide suggestions for effective prevention of rabies in Guangxi. Study design Since 2000, 1569 brains from suspected rabid animals were collected from different areas of Guangxi. Rabies virus was isolated from 42 samples. RT-PCR was used to amplify a 455 nucleotide segment of the 3′-terminal of the N gene. The sequencing data from that segment was used for phylogenetic analysis. Results Nucleotide homology comparisons and phylogenetic tree analysis based on this sequence indicated that all the rabies virus isolates from Guangxi belonged to genotype 1 and could be divided into four groups. Groups I, II and IV included 23, 10 and 8 isolates, respectively. These had nucleotide homologies of 97.1–100%, 98.2–100% and 99.1–99.6%, respectively. Only the GXN119 strain belonged to group III. Group I had two group-specific mutations: T90N and E110D. Group II had one group-specific mutation of T42S. Conclusions This study showed that rabies virus isolates from Guangxi have a close genetic relationship and topographical distribution.

Acetylation of highly stereoregular syndiotactic polystyrene has been accomplished in a heterogeneous process by using carbon disulfide as the dispersing medium, and acetyl chloride and anhydrous aluminium chloride as acetylating agent and catalyst, respectively. The acetylation reaction can be well controlled and carried out to a high degree of acetylation. The resultant polymer was characterized by FTIR and NMR spectroscopy. The incorporation of acetyl groups into syndiotactic polystyrene was found to have an effect on the thermal properties of these new materials. The degree of crystallinity was decreased by the presence of acetyl groups, while the glass transition temperature increased. Copyright © 2004 Society of Chemical Industry

We describe the isolation of Laribacter hongkongensis in Hangzhou City, People's Republic of China. One strain of bacterium, named LHHZ242, had many of the same phenotypic and genotypic characteristics as Laribacter hongkongensis described in previous publications. This discovery proves that Laribacter hongkongensis is also associated with community-acquired gastroenteritis outside Hong Kong.