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BACKGROUND Acute pancreatitis is the leading cause of hospitalization for acute gastrointestinal disease worldwide. The effects of probiotics in mild acute pancreatitis have not been studied. We hypothesized that the administration of probiotics may accelerate the recovery of intestinal function and shorten the length of hospital stay (LOS) in patients with mild pancreatitis. AIM To investigate the value of probiotics in reducing the LOS in patients with mild acute pancreatitis. METHODS We conducted a double-blind randomized clinical trial to evaluate the effects of probiotics administered to patients with mild acute pancreatitis at a tertiary medical center. The patients were given probiotics capsules (a mixed preparation of Bacillus subtilis and Enterococcus faecium) or placebo. The primary study endpoint was the LOS. The secondary endpoints included time to abdominal pain relief, recurrent abdominal pain, and time to successful oral feeding. RESULTS A total of 128 patients were included, with 64 patients in each arm. The severity of illness and the etiological distribution of disease were similar in the two groups. There was a significant reduction in the LOS in the probiotics treatment group vs the placebo group (5.36 ± 0.15 vs 6.02 ± 0.17 d, P < 0.05). The probiotics group was associated with a shorter time to abdominal pain relief and time to successful oral feeding (P < 0.01 for both) than the placebo group. No statistical difference was found in recurrent abdominal pain between the two groups. CONCLUSION The study results showed that the administration of probiotics capsules is associated with a shorter duration of hospitalization in patients with mild acute pancreatitis.

The factors associated with anti-N-methyl-D-aspartate (NMDA) receptor encephalitis relapse are yet to be elucidated.To investigate the factors associated with relapse and prognosis of anti-NMDA receptor encephalitis.This retrospective study included patients diagnosed with anti-NMDA receptor encephalitis admitted to the First Affiliated Hospital of Zhengzhou University from January 2013 to October 2019. The clinical features, auxiliary examinations, treatment regimens, and follow-up were recorded. The outcomes were relapse and 2-year disease prognosis.A total of 160 patients were included. Consequently, 6 (5%) deaths, 34 (25.4%) relapses, and 19 (15.2%) patients had a poor prognosis (modified Rankin score (mRS) ≥3) were recorded. The multivariable analyses showed that age (p = .011), abnormal magnetic resonance imaging (MRI) (p = .019), glucocorticoid pulse (p = .009), and intracranial pressure (p = .023) were independently associated with the relapse, while age (p = .030) and central hypoventilation (p = .020) were independently associated with a poor prognosis at 2 years.Glucocorticoid pulse therapy reduces the relapse of anti-NMDA receptor encephalitis. Age, abnormal MRI, and intracranial pressure are risk factors for relapse, while age and central hypoventilation are independently associated with poor prognosis.

Vascular invasion (VI) in hepatocellular carcinoma (HCC) is an important clinical parameter to predict survival. In this study, we collected microRNA (miRNA) expression data from HCC patients using The Cancer Genome Atlas database and identified a novel miRNA signature associated with VI. First, we categorized HCC patients into groups with or without VI (VI+ and VI-). We identified three miRNAs (miRNA-210, miRNA-10b, and miRNA-9-1) that were associated with VI according to a Kaplan-Meier analysis. This three-miRNA signature exhibited good predictive ability for VI in patients with HCC according to a receiver operating characteristic curve analysis at 1, 3, and 5 years. Patients with HCC with a high risk score exhibited a trend toward worse outcomes as determined by multivariable Cox regression and stratified analyses. This three-miRNA signature provides an accurate prediction of VI and can be used as an independent prognostic indicator for predicting VI in HCC patients.

We hypothesized that the adipose-derived mesenchymal stem cells (ADMSCs), which secrete high amounts of soluble molecules, such as soluble tumor necrosis factor receptor 1 (sTNFR1), may ameliorate sepsis-induced acute lung injury (ALI). A total of 120 male adult Sprague-Dawley rats were separated into four groups: the sham control (SC), sepsis induced by cecal ligation and puncture (CLP), CLP-ADMSCs, and CLP-sTNFR1 small interfering RNA (siRNA) groups; CLP groups underwent CLP and then received 1 × 106 ADMSCs with or without knockdown of sTNFR1 intravenously at 1 hr after surgery. Rats were killed at 3, 6, 24, and 48 hr after the SC or CLP procedures. 5-Ethynyl-2'-deoxyuridine-labeled ADMSCs extensively colonized the lungs at 6, 24, and 72 hr after injection. The lung wet/dry (W/D) weight ratios in the CLP group were higher than those in SC group; however, ADMSCs ameliorated the W/D weight ratios following CLP, and this effect was abolished by sTNFR1 siRNA treatment. The levels of serum sTNFR1 and interleukin-10 (IL-10) were higher in the CLP-ADMSCs group and lower in the SC group than in other groups; interestingly, these levels were higher in CLP and CLP-sTNFR1 siRNA groups than in SC group. Tumor necrosis factor-α and IL-6 levels increased significantly after CLP, and ADMSCs could alleviate these changes, but the effect was weakened by sTNFR1 siRNA treatment. The lung cell apoptosis and edema levels were consistent with IL-6 levels among all groups. Therapeutically administered ADMSCs secrete sTNFR1, which most likely protects against ALI in septic rats by ameliorating inflammation and lung edema.

The polymyxins are important antimicrobial agents against antibiotic-resistant gram-negative bacilli. In 2020, the Clinical and Laboratory Standards Institute modified the clinical breakpoints for polymyxin susceptibility test by eliminating the "susceptible" interpretive category, only reporting intermediate (≤2 mg/L) and resistant (≥4 mg/L). However, the European Committee on Antimicrobial Susceptibility Testing recommended the use of clinical breakpoints of ≤2 mg/L as susceptible and2 mg/L as resistant. The first-line laboratorians and clinicians in China have been perplexed by the inconsistence of international polymyxin clinical breakpoints and discouraged by the difficulty of conducting polymyxin susceptibility testing. Therefore, it is urgently needed to make it clear for the laboratorians in China to know how to accurately carry out polymyxin susceptibility testing and standardize the interpretation of susceptibility testing results. To this end, the experts from relevant fields were convened to formulate this consensus statement on the testing and clinical interpretation of polymyxin susceptibility. Relevant recommendations are proposed accordingly for laboratorians and clinicians to streamline their daily work.

Supplemental Digital Content is available in the text, Thrombotic thrombocytopenic purpura (TTP) is a life-threatening disease, and its mortality rate is 10% to 20%. However, there are currently only a few markers to predict the prognosis in patients with TTP. We aimed to identify several clinical indices and laboratory parameters for predicting the prognosis of TTP at admission. A single-centre observational cohort study that included patients with TTP from the First Affiliated Hospital of Zhengzhou University in China was conducted from January 1, 2012 to November 30, 2018. The primary outcome was prognosis, including in-hospital mortality, major thromboembolic events, or failure to achieve remission at discharge. We used the random forest method to identify the best set of predictors. Eighty-seven patients with TTP were identified, of whom 12 died during the treatment. The total number of patients within-hospital mortality, major thromboembolic events, and failure to achieve remission at discharge was 58. The machine learning method showed that the D-dimer level was the strongest predictor of the primary outcome. Receiver operating characteristic (ROC) analysis demonstrated that the sensitivity and specificity of the D-dimer level alone for identifying high-risk patients were 78% and 81%, respectively, with an optimum diagnostic cut-off value of 770 ng/mL. The area under the ROC curve (AUC) was 0.80, and the 95% confidence interval (CI) was 0.70 to 0.90. This study found that the D-dimer level exhibited a good predictive ability for prognosis in patients with TTP. These findings may aid in the development of new and intensive treatment strategies to achieve remission among high-risk patients. However, external validation is necessary to confirm the generalizability of our approach across populations and treatment practices.

Background Adipocyte fatty acid–binding protein (FABP4) is an adipokine that plays an important role in development of cardiovascular and metabolic diseases. The aim of this study was to assess the 3-month prognostic value of serum levels of FABP4 in Chinese patients with aneurysmal subarachnoid hemorrhage (aSAH) on hospital admission. Methods This was a prospective observational study from a stroke treatment center in Zhengzhou, China. From October 2016 to May 2018, patients with aSAH who were hospitalized within 24 h were included. In addition, 202 age- and gender-matched healthy volunteers were assigned to the healthy control group. At admission, serum levels of FABP4 were measured, and patients’ characteristics, Hunt–Hess grade, and modified Fisher grade evaluated. At 3-month follow-up, functional outcome (Glasgow Outcome Scale score; dichotomized as poor [score 1–3] or good [score 4–5]) and all-cause mortality were recorded. Univariate and multivariate logistic regression models were used to investigate the association of FABP4 with the two endpoints. Results A total of 418 patients with aSAH were included in this study. The median age was 58 years (interquartile range, 49–66 years), and 57.9% were women. FABP4 serum levels were related to Hunt–Hess score (r[Spearman] = 0.381; P P P = 0.001) and 5% (odds ratio 1.05, 95% CI, 1.01–1.12; P = 0.003), respectively. Receiver operating characteristics to predict functional outcome and mortality were significantly different between conventional risk factors (difference area under the curve 0.024, 95% CI 0.018–0.032) and FABP4 plus conventional risk factors (area under the curve 0.015, 95%CI 0.011–0.020). After FABP4 was added to the existing risk factors, mortality was better reclassified and was associated with the net reclassification improvement statistic (P = 0.009), while poor outcome was better reclassified and associated with both the integrated discrimination improvement and net reclassification improvement statistics (P Conclusions Elevated serum FABP4 levels were related to poor outcome and mortality in a cohort of patients with aSAH.

Disorders of bile acids (BAs) are closely related to the development of liver and intestinal diseases, including acute pancreatitis (AP). However, the mechanism underlying the involvement of BAs in AP development remains unclear. We used intraperitoneal injection of cerulein to construct AP mouse models. These mice had significantly reduced tauroursodeoxycholic acid (TUDCA) and an imbalance of intestinal microbiota, based on 16S rDNA gene sequencing. To explore the role of AP-induced intestinal microbiota changes in the development of AP, we transplanted stool obtained from AP mice to antibiotic-treated, microbiota-depleted healthy mice. Microbiota-depleted mice presented injury to the intestinal barrier function and pancreas. Additionally, microbiota depletion reduced AP-associated pancreatic injury. This indicated that the gut microbiota may worsen AP. As TUDCA was deficient in AP mice, we gavaged AP mice with it, and evaluated subsequent expression changes in the bile acid signaling receptors farnesoid-x-receptor (FXR) and its target gene fibroblast growth factor (FGF) 15. These were downregulated, and pancreatic and intestinal barrier function injury were mitigated. Similar results were found in microbiota-depleted AP without BA treatment. However, we did not observe further downregulation of the FXR signaling pathway in microbiota-depleted AP mice given TUDCA, indicating that improvement of pancreatitis by TUDCA may be associated with gut microbiota. Our analysis of changes to the gut microbiota in AP indicated that Lactobacilli may be the key contributors. Taken together, our study shows that supplementation with BAs could improve bile acid-FXR-FGF15 signaling, and reduce pancreatic and intestinal injury, and that this effect may be associated with the gut microbiota.

Background Prenatal lipopolysaccharide (LPS) exposure causes hypertension in rat offspring through an unknown mechanism. Here, we investigated the role of the intrarenal renin-angiotensin system (RAS) in hypertension induced by prenatal LPS exposure and also explored whether adipose tissue-derived mesenchymal stem cells (ADSCs) can ameliorate the effects of prenatal LPS exposure in rat offspring. Methods Sixty-four pregnant rats were randomly divided into 4 groups (n = 16 in each), namely, a control group and an LPS group, which were intraperitoneally injected with vehicle and 0.79 mg/kg LPS, respectively, on the 8th, 10th, and 12th days of gestation; an ADSCs group, which was intravenously injected with 1.8 × 107 ADSCs on the 8th, 10th, and 12th days of gestation; and an LPS + ADSCs group, which received a combination of the treatments administered to the LPS and ADSCs groups. Results Prenatal LPS exposure increased blood pressure, Ang II expression, Ang II-positive, monocyte and lymphocyte, apoptotic cells in the kidney, and induced renal histological changes in offspring; however, the LPS and control groups did not differ significantly with respect to plasma renin activity levels, Ang II levels, or renal function. ADSCs treatment attenuated the blood pressure and also ameliorated the other effects of LPS-treated adult offspring. Conclusions Prenatal exposure to LPS activates the intrarenal RAS but not the circulating RAS and thus induces increases in blood pressure in adult offspring; however, ADSCs treatment attenuates the blood pressure increases resulting from LPS exposure and also ameliorates the other phenotypic changes induced by LPS treatment by inhibiting intrarenal RAS activation.

Background Despite significant progress in drug treatment, the prognosis of patients with advanced pulmonary arterial hypertension (PAH) remains extremely poor. Many preclinical studies have reported the efficacy of stem cell (SC) therapy for PAH; however, this approach remains controversial. The aim of this systematic review and meta-analysis is to assess the potential efficacy of SC therapy for PAH. Methods The Medline, EMBASE, Cochrane Library, and Web of Science databases were searched from inception to August 12, 2018. Preclinical studies that evaluated the use of SC therapy for PAH were included. The primary outcome was pulmonary haemodynamics, as assessed by measurement of the right ventricular systolic pressure (RVSP), mean pulmonary arterial pressure (mPAP), and/or mean right ventricle pressure (mRVP). The secondary outcomes included the weight ratio of the right ventricle to the left ventricle plus septum (RV/LV+S), the right ventricle to body weight ratio (RV/BW), the percentage of pulmonary arteriole area index (WA), and/or the percentage of medial wall thickness of the pulmonary arteriole (WT). The quality of outcomes was evaluated using the SYstematic Review Centre for Laboratory animal Experimentation (SYRCLE) bias risk tool. The inverse-variance method with random-effects modelling was used to calculate pooled weighted mean differences (WMDs) and 95% CIs. Statistical analysis was performed with STATA 14.0. Results Twenty-eight eligible articles (722 animals) were included. SC therapy reduced the pooled WMDs (95% CIs) of RVSP, mPAP, mRVP, RV/LV+S, RV/BW, WA, and WT for animals with PAH, with values of − 14.12 (− 14.63, − 13.61), − 11.86 (− 12.35, − 11.36), − 17.33 (− 18.10, − 16.56), − 0.10 (− 0.10, − 0.09), 0.23 (0.21, 0.24), − 13.66 (− 15.71, − 11.62), and − 7.96 (− 7.99, − 7.93), respectively. Conclusions SC therapy is effective for PAH in preclinical studies. These results may help to standardise preclinical animal studies and provide a theoretical basis for clinical trial design in the future. Systematic review registration PROSPERO (http://www.crd.york.ac.uk/PROSPERO). Electronic supplementary material The online version of this article (10.1186/s13287-019-1162-8) contains supplementary material, which is available to authorized users.

Background/Objectives Carbonic anhydrase 1 (CA1)/kininogen and selenoprotein W (SelW)/14-3-3η signal transduction orchestrate oxidative stress, which can also be regulated by nitric oxide (NO). The mutated caveolin-1 (Cav-1F92A) gene may enhance NO production. This study explored the effect of Cav-1F92A-modified rat bone marrow mesenchymal stem cells (rBMSC/Cav-1F92A) on oxidative stress regulation through CA1/kininogen and SelW/14-3-3η signal transduction in a rat model of monocrotaline- (MCT-) induced pulmonary arterial hypertension (PAH). Method PAH was induced in rats through the subcutaneous injection of MCT. Next, rBMSC/Vector (negative control), rBMSC/Cav-1, rBMSC/Cav-1F92A, or rBMSC/Cav-1F92A+L-NAME were administered to the rats. Changes in pulmonary hemodynamic and vascular morphometry and oxidative stress levels were evaluated. CA1/kininogen and SelW/14-3-3η signal transduction, endothelial nitric oxide synthase (eNOS) dimerization, and eNOS/NO/sGC/cGMP pathway changes were determined through real-time polymerase chain reaction, Western blot, or immunohistochemical analyses. Results In MCT-induced PAH rats, rBMSC/Cav-1F92A treatment reduced right ventricular systolic pressure, vascular stenosis, and oxidative stress; downregulated CA1/kininogen signal transduction; upregulated SelW/14-3-3η signal transduction; and reactivated the NO pathway. Conclusions In a rat model of MCT-induced PAH, rBMSC/Cav-1F92A reduced oxidative stress by regulating CA1/kininogen and SelW/14-3-3η signal transduction.

Background/Objectives. Carbonic anhydrase 1 (CA1)/kininogen and selenoprotein W (SelW)/14-3-3η signal transduction orchestrate oxidative stress, which can also be regulated by nitric oxide (NO). The mutated caveolin-1 (Cav-1F92A) gene may enhance NO production. This study explored the effect of Cav-1F92A-modified rat bone marrow mesenchymal stem cells (rBMSC/Cav-1F92A) on oxidative stress regulation through CA1/kininogen and SelW/14-3-3η signal transduction in a rat model of monocrotaline- (MCT-) induced pulmonary arterial hypertension (PAH). Method. PAH was induced in rats through the subcutaneous injection of MCT. Next, rBMSC/Vector (negative control), rBMSC/Cav-1, rBMSC/Cav-1F92A, or rBMSC/Cav-1F92A+L-NAME were administered to the rats. Changes in pulmonary hemodynamic and vascular morphometry and oxidative stress levels were evaluated. CA1/kininogen and SelW/14-3-3η signal transduction, endothelial nitric oxide synthase (eNOS) dimerization, and eNOS/NO/sGC/cGMP pathway changes were determined through real-time polymerase chain reaction, Western blot, or immunohistochemical analyses. Results. In MCT-induced PAH rats, rBMSC/Cav-1F92A treatment reduced right ventricular systolic pressure, vascular stenosis, and oxidative stress; downregulated CA1/kininogen signal transduction; upregulated SelW/14-3-3η signal transduction; and reactivated the NO pathway. Conclusions. In a rat model of MCT-induced PAH, rBMSC/Cav-1F92A reduced oxidative stress by regulating CA1/kininogen and SelW/14-3-3η signal transduction.

BACKGROUND: There are conflicting results regarding whether corticosteroids have better efficacy than placebo in acute respiratory distress syndrome (ARDS) patients. Therefore, we aim to further evaluate the efficacy and safety of corticosteroids in adult ARDS patients. METHODS: The databases, including Medline, EMBASE, and Cochrane Central Register of Controlled Trials (CENTRAL) in the Cochrane Library, were searched from their inception to May 2, 2020. Randomized controlled trials (RCTs) and observational cohort studies were selected to assess the use of corticosteroids in adult ARDS patients. The quality of the results was judged by the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) methodology. The inverse-variance method with random or fixed effects modeling was used to compute pooled odds ratio (OR), standardized mean difference (SMD), and their 95% confidence interval (CI). RESULTS: Eight eligible RCTs and six cohort studies were included. The use of corticosteroids was associated with reduced mortality (OR 0.57, 95% CI 0.43–0.76, I2=35.1%, P=0.148) in ARDS patients, and the result was confirmed in the included cohort studies (OR 0.51, 95% CI 0.27–0.95, I2=66.7%, P=0.010). The subgroup analysis stratified by the initiation time and duration of corticosteroid use showed that early ARDS and prolonged corticosteroid use had significant survival benefits in the RCTs. The low-dose corticosteroid use was also associated with significantly more ventilator-free days and a reduced rate of new infections in ARDS patients. CONCLUSIONS: The low-dose corticosteroid therapy may be safe and reduce mortality, especially in patients with prolonged treatment and early ARDS.

OBJECTIVE To study the effect of nurse-led counselling on the anxiety symptoms and the quality of life following percutaneous coronary intervention for stable coronary artery disease. DESIGN Randomised control trial. SETTING Rural and remote China. PARTICIPANTS Rural and remote patients were consecutively recruited from a medical centre located in China between January and December 2014. INTERVENTIONS The control group received standard pre-procedure information from a ward nurse on the processes of the hospitalisation and percutaneous coronary intervention, and post-procedural care. The intervention group received a structured 30-minute counselling session the day before and 24 hours after the percutaneous coronary intervention, by nurse consultants with qualifications in psychological therapies and counselling. The health outcomes were assessed by a SF-12 scale and the Seattle Angina Questionnaire at 6 and 12 months after percutaneous coronary intervention. The anxiety and depression symptoms were evaluated by a Zung anxiety and depression questionnaire. MAIN OUTCOME MEASURES Cardiac outcomes, quality of life and mental health status. RESULTS Eighty patients were randomly divided into control (n = 40) and intervention groups (n = 40). There was a significant increase in the scores of the three domains of Seattle Angina Questionnaire 12 months after percutaneous coronary intervention in the intervention group (P

Background The ProCESS, ARISE, and ProMISe trials have failed to show that early goal-directed therapy (EGDT) reduces mortality in patients with severe sepsis and septic shock. Although lactate-guided therapy (LGT) has been shown to result in significantly lower mortality, its use remains controversial. Therefore, we performed a meta-analysis to evaluate EGDT vs. LGT or usual care (UC) in adult patients with severe sepsis and septic shock. Methods Relevant randomized controlled trials published from January 1, 2001 to March 30, 2017 were identified in PubMed, EMBASE, Web of Science, and the Cochrane Library. The primary outcome was mortality; secondary outcomes included red cell transfusions, dobutamine use, vasopressor infusion, and mechanical ventilation support within the first 6 h and Acute Physiology and Chronic Health Evaluation II (APACHE II) score. Results Sixteen studies enrolling 5968 patients with 2956 in EGDT, 2547 in UC, and 465 in LGT were included in this meta-analysis. Compared with UC, EGDT was associated with a lower mortality (10 trials; RR 0.85, 95% CI 0.74–0.97, P = 0.01), and this difference was more pronounced in the subgroup of UC patients with mortality > 30%. In addition, EGDT patients received more red cell transfusions, dobutamine, and vasopressor infusions within the first 6 h. Compared with LGT, EGDT was associated with higher mortality (6 trials; RR 1.42, 95% CI 1.19–1.70, P = 0.0001) with no heterogeneity (P = 0.727, I2 = 0%). Conclusion EGDT seems to reduce mortality in adult patients with severe sepsis and septic shock, and the benefit may primarily be attributed to red cell transfusions, dobutamine administration, and vasopressor infusions within the first 6 h. However, LGT may result in a greater mortality benefit than EGDT. Electronic supplementary material The online version of this article (10.1186/s12967-018-1700-7) contains supplementary material, which is available to authorized users.

Background Despite the fact that recent evidence from meta-analysis of randomized trials indicates an increase in mortality, perioperative treatment with β-blockers is still widely advocated. We therefore performed a meta-analysis of cohort studies to evaluate the effects of perioperative β-blockers on mortality in patients undergoing non-cardiac surgery in the real world scenarios. Methods We searched PubMed and Embase from the inception to April 2014 for cohort studies, assessing the effect of perioperative β-blockers on mortality in patients undergoing non-cardiac surgery. Adjusted relative risk (RR) with 95% confidence interval (CI) was pooled using random effect models. Results Eight cohort studies with a total of 470,059 participants (180,441 patients in the β-blocker group and 289,618 patients in the control group) were included in this meta-analysis. Perioperative β-blockers were not associated with a reduced risk of mortality (RR=0.88, 95% CI, 0.75 to 1.04), postoperation myocardial infarction (RR=1.30, 95% CI, 0.76 to 2.23), and postoperation stroke (RR=1.17, 95% CI, 0.53 to 2.57). However, in subgroup analysis of mortality, taking β-blockers on the day of surgery caused statistically significant increase in mortality of 91% (RR=1.91, 95% CI, 1.01 to 3.62). Conclusions In the real world scenarios, for patients undergoing non-cardiac surgery, the routine use of β-blockers does not seem to reduce the risk of death. Moreover, those who are taking β-blockers on the day of surgery may have an increased risk of postoperative mortality. However, these results should be interpreted with caution because of the significant heterogeneity across the studies.

To describe the clinical features and management of thallium poisoning in patients with delayed hospital admission.Fourteen patients (median age 36 years) were admitted 9-19 days after ingesting food poisoned with thallium. Clinical and laboratory data, including blood and urine thallium concentrations, were collected. Patients were treated with oral Prussian blue, a chelating agent sodium dimercaptosulfonate, and hemodialysis.All patients experienced a triad of symptoms of acute gastrointestinal upset, painful combined polyneuropathy, and hair loss after consuming poisoned food. Fatigue and skin pigmentation were observed in all patients. Abnormal liver function tests were found in 6 (42.9%) and delirium and coma were identified in 4 (28.6%). Two weeks after the poisoning, the blood and urine thallium concentration ranged from 219.0 to 1414.4 μg/L (median: 535.3) and 956.5 to 11285.0 μg/L (median: 7460.0), respectively. One patient (7.1%) with a previous history of pulmonary fibrosis died of respiratory failure in hospital. Symptoms were improved and blood or urine thallium levels were normalized in the remaining 13 patients before discharge. After a 6.5 ± 1-month follow-up, 1 patient (7.1%) developed deep venous thrombosis in the left lower limb. In another patient (7.1%), numbness in the lower limbs remained.Acute thallium poisoning is commonly manifested by gastrointestinal upset, painful polyneuropathy, and significant hair loss. Treatment strategies included Prussian blue and hemodialysis, which were associated with a good outcome in this case series.

Background: Bilirubin is a potent antioxidant and previous studies have reported the relationship between low serum bilirubin concentration and atherosclerosis. Objective: To evaluate the prognostic value of serum total bilirubin (STB) in patients with angina pectoris undergoing percutaneous coronary intervention (PCI). Methods: In total of 1419 patients (931 men, mean age 60.9±10.5 years) with angina pectoris who had undergone successfully percutaneous coronary intervention (PCI) were included in this study. Patients were divided into 2 groups according to the median baseline STB (0.49 mg/dL in this cohort), which was measured before the PCI. Patients with a STB ≥0.49 mg/dL were classified into the high STB group and those with a STB

Corticosteroids are an option in the treatment of community-acquired pneumonia (CAP). However, the benefits and adverse effects of corticosteroids, especially in severe CAP, have not been well assessed.PubMed, Embase, and Cochrane library databases from inception to May 2015 were searched. Randomized controlled trials (RCTs) and cohort studies that evaluated use of corticosteroids in adult patients with CAP were included. The quality of outcomes was evaluated using Grading of Recommendations Assessment, Development and Evaluation methodology. The Mantel-Haenszel method with random-effects modeling was used to calculate pooled relative risks (RRs) and 95% CIs.Nine eligible RCTs (1,667 patients) and six cohort studies (4,095 patients) were identified. The mean corticosteroid dose and treatment duration were 30 mg/day methylprednisolone for 7 days. Corticosteroids did not have a statistically significant effect on mortality (RR, 0.72; 95% CI, 0.43-1.21; evidence rank, low) in patients with CAP and patients with severe CAP (RCTs: RR, 0.72; 95% CI, 0.43-1.21; evidence rank, low; cohort studies: RR, 1.00; 95% CI, 0.86-1.17 ). Corticosteroids treatment was associated with a decreased risk of ARDS (RR, 0.21; 95% CI, 0.08-0.59) and may reduce lengths of hospital and ICU stay, duration of IV antibiotic treatment, and time to clinical stability. Corticosteroids were not associated with increased rates of adverse events.Short-term treatment with corticosteroids is safe and may reduce the risk of ARDS, shortening the length of the disease in patients with CAP.

Introduction Vitamin D deficiency is common in critically ill patients, and was reported to be associated with adverse outcomes. However, the effect of vitamin D deficiency on mortality in critically ill patients remains unclear. Methods We searched PubMed and EMBASE from the inception to July 2014 for cohort studies to assess the effect of vitamin D deficiency on the incidence of mortality in critically ill patients. Mortality-specific odds ratio (OR) with 95% confidence interval (CI) were pooled with a random- or fixed-effect models when appropriate. Results Seven cohort studies with a total of 4,204 participants including 1,679 cases of vitamin D deficiency were included in this meta-analysis. Vitamin D deficiency was significantly associated with an increased hospital mortality (OR 1.76; 95% CI, 1.38 to 2.24; P

Objective: The objective of this article is to explore the role of imidapril on pulmonary hypertension induced by low ambient temperature in broiler chickens. Materials and methods: Ninety chickens were randomly divided into three groups ( n = 30): a control group, a low-temperature group and an imidapril group. Chickens in the low-temperature group and imidapril group were exposed to low ambient temperature from 14 days of age until 45 days of age; chickens in the imidapril group were gavaged with imidapril 3 mg/kg once daily for 30 days. The pulmonary arterial pressure, main pulmonary arterial diameter and pulmonary arterial wall thickness were measured, and lung tissue ACE, ACE2 mRNA expression, proliferating cell nuclear antigen (PCNA)-positive cells and Ang II, Ang (1-7) concentration were evaluated. Results: The pulmonary arterial pressure was higher, the main pulmonary arterial diameter was wider and the pulmonary arterial wall was thicker in the low-temperature group than those in the control group and the imidapril group. ACE mRNA and PCNA-positive cells increased significantly in the low-temperature group compared with the control group and imidapril group; lung tissue Ang II concentration in the low-temperature group was higher, but Ang (1-7) content was lower than that in the control group and imidapril group. Conclusion: Imidapril provides a protective effect on pulmonary hypertension induced by low ambient temperature in broiler chickens.

Background The impact of pre-existing diabetes on the development of acute lung injury/acute respiratory distress syndrome (ALI/ARDS) in critically ill patients remains unclear. We performed a meta-analysis of cohort studies to evaluate the risk of ALI/ARDS in critically ill patients with and without pre-existing diabetes. Materials and Methods We searched PubMed and Embase from the inception to September 2013 for cohort studies assessing the effect of pre-existing diabetes on ALI/ARDS occurrence. Pooled odds ratio (OR) with 95% confidence interval (CI) was calculated using random- or fixed-effect models when appropriate. Results Seven cohort studies with a total of 12,794 participants and 2,937 cases of pre-existing diabetes, and 2,457 cases of ALI/ARDS were included in the meta-analysis. A fixed-effects model meta-analysis showed that pre-existing diabetes was associated with a reduced risk of ALI/ARDS (OR 0.66; 95% CI, 0.55–0.80; p

Background MiRNA primarily acts to repress gene expression at the post-transcriptional level through imperfect complementarity of its 5′ region to the “seed site” in the 3′ untranslated region of target mRNAs, with its “3′–supplementary site” and “center site” also playing important roles under certain circumstances. The aim of this study was to test if artificial miRNA mimics (miR-Mimics) that are designed to target the “centered sites” without “seed sites” complementarity are able to repress gene expression as natural miRNAs. Methods We designed miR-Mimics carrying centered-site matches (CS–miR-Mimics) or seed-site matches (SS–miR-Mimics) and siRNA to two antiapoptotic genes BCL2 and AKT1. We tested the gene targeting of these constructs using real-time RT-PCR and Western blot to quantify mRNA and protein levels of BCL2 and AKT1, respectively, luciferase reporter gene assay to investigate the interaction between miR-Mimics and their target sites, and cell survival assay to study the functional outcomes of the miR-Mimics. Results We found that CS-miR-Mimic, SS-miR-Mimic and siRNA, all down regulated the mRNA and protein levels of their cognate target BCL2 or AKT1 in a concentration-dependent manner. Luciferase reporter gene assay further confirmed the functional interactions of CS–miR-Mimic, SS-miR-Mimic and siRNA with their target sites. We then observed that the miR-Mimics and siRNAs were all able to induce cell death, as indicated by the reduced survival rate of cells. Conclusions We have provided evidence for the feasibility of CS–miR-Mimics for post-transcriptional repression of genes, which can be designed to have reduced numbers of seed type off-target sites compared to the number of target sites from an average endogenous seed–site miRNA. CS–miR-Mimics may be a novel approach for miRNA research requiring miRNA gain-of-function.

This study explored the effect of imidapril on the right ventricular remodeling induced by low ambient temperature in broiler chickens. Twenty-four broiler chickens were randomly divided into 3 groups (n = 8), including the control group, low temperature group, and imidapril group. Chickens in the control group were raised at normal temperature, whereas chickens in the low temperature group and imidapril group were exposed to low ambient temperature (12 to 18°C) from 14 d of age until 45 d of age. At the same time, chickens in the imidapril group were gavaged with imidapril at 3 mg/kg once daily for 30 d. The thickness of the right ventricular wall was observed with echocardiography. The BW and wet lung weight as well as weight of right and left ventricles and ventricular septum were measured. Both wet lung weight index and right ventricular hypertrophy index were calculated. Pulmonary arterial systolic pressure was assessed according to echocardiography. The expression of ACE and ACE2 mRNA in the right ventricular myocardial tissue was quantified by real-time PCR. Proliferating cell nuclear antigen-positive cells were detected by immunohistostaining. The concentration of angiotensin (Ang) II and Ang (1–7) in the right ventricular myocardial tissue was measured with ELISA. The results showed that right ventricular hypertrophy index, wet lung weight index, pulmonary arterial systolic pressure, expression of ACE mRNA in the right ventricular tissue, Ang II concentration, and the thickness of the right ventricular wall in the low temperature group increased significantly compared with those in the control group and imidapril group. The ACE2 mRNA expression increased 36%, whereas Ang (1–7) concentration decreased significantly in the low temperature group compared with that in the control group and imidapril group. In conclusion, imidapril inhibits right ventricular remodeling induced by low ambient temperature in broiler chickens.

To decrease acute myocardial infarction (AMI) and incidence of other cardiovascular event after drug-eluting stent (DES) implantation, so as to prevent non-acute stent thrombosis.Patients who had undergone percutaneous coronary intervention with DES from January 2005 to September 2008 were enrolled. All patients were randomly assigned into two groups with different treatment protocols for anti-thrombosis. The patients in control group were treated with aspirin and clopidogrel for anti-thrombosis (double anti-treatment), while those in observation group were treated with tirofiban and warfarin on top of basic treatment with double anti-thromotic drugs. The latter group of patients received warfarin in addition for 6 months, with the international normalized ratio (INR) maintained at 1.5-2.0. The patients in both groups were followed up at 1-3 months after the treatment, and the deadline was October 2012. Stent thrombosis was assessed by the definition of Dublin for Academic Research Consortium. The main ending point indexes were main adverse cardiac and cerebral events (MACCE), and the secondary ending point indexes were incidence of bleeding and other adverse events.A total of 505 consecutive patients treated with DES implantation were enrolled, 245 in the observation group while 260 in the control. The rates of MACCE at 1- 48 months after operation in observational group were significantly lower than those in control group (1 month: 0.41% vs. 3.08%, 2-6 months: 0 vs. 2.31%, 7-12 months: 0.82% vs. 4.23%, 13-24 months: 1.22% vs. 8.85%, 25- 48 months: 2.04% vs. 12.31%, all P0.05). Cardiac death (13-24 months: 0.41% vs. 3.08%, 25-48 months: 0.82% vs. 4.23%), non-lethal acute myocardial infarction unrelated with target vessels (25-48 months: 0.41% vs. 3.08%), and rates of revascularization of target vessels (13-24 months: 0.41% vs. 3.08%, 25-48 months: 0.82% vs. 4.23%) in observation group were significantly lower than those in the control group (all P0.05). The rates of sub-acute stent thrombosis, late stent thrombosis, and very late stent thrombosis in observation group were significantly lower than those in control group (0 vs. 2.31%, 0.82% vs. 4.23%, 1.63% vs. 8.46%, all P0.05). The rate of bleeding in observational group was a litter higher than control group (3.27% vs. 1.54%, P=0.167) and no severe bleeding occurred. Other severe adverse events were not found in both groups.The results indicate that tirofiban and warfarin combined with aspirin and clopidogrel could reduce the rates of MACCE and bleeding, and it could prevent non-acute stent thrombosis safely and effectively after percutaneous coronary intervention with DES.

Purpose: Lipoprotein-associated phospholipase A2 (Lp-PLA2) is involved in the pathogenesis of atherosclerosis, especially in advanced plaques. In the present study, the abilities of darapladib, a selective Lp-PLA2 inhibitor, and lentivirus-mediated Lp-PLA2 silencing on inflammation and atherosclerosis in apolipoprotein E-deficient mice were compared. Methods: Apolipoprotein E-deficient mice were fed on a high-fat diet and a constrictive collar was placed around the left carotid artery to induce plaque formation. The mice were randomly divided into control, negative control (NC), darapladib and RNA interference (RNAi) groups. Eight weeks after surgery, lentivirus-mediated RNAi construct or darapladib were used to decrease the expression of Lp-PLA2. Plaques were collected five weeks later for histological analysis. Inflammatory gene expression in the atherosclerotic lesions were then determined at the mRNA and protein level. Results: The expression of pro-inflammatory cytokines was significantly reduced in the treatment group, compared to nontreatment group, whereas the plasma concentration of anti-inflammatory cytokines increased markedly. Moreover, our results demonstrated a significant reduction in plaque lipid content, as well as a rise in collagen content following Lp-PLA2 inhibition. Interestingly, when comparing the two methods of Lp-PLA2 inhibition, animals treated with Lp-PLA2 RNAi were found to exhibit lower plaque areas and enhanced improvement of plaque stability as compared with animals treated with darapladib. Darapladib had no attenuating effect on atherosclerotic plaque area. These therapeutic effects were independent of plasma lipoprotein levels. Conclusions: Lp-PLA2 inhibition by darapladib or lentivirus-mediated RNAi ameliorated inflammation and atherosclerosis in apolipoprotein E-deficient mice. The effect was more prominent in the RNAi group.

Background Intra-aortic balloon pumps (IABP) have generally been used for patients undergoing high-risk mechanical coronary revascularization. However, there is still insufficient evidence to determine whether they can improve outcomes in reperfusion therapy patients, mainly by percutaneous coronary intervention (PCI) with stenting or coronary artery bypass graft (CABG). This study was designed to determine the difference between high-risk mechanical coronary revascularization with and without IABPs on mortality, by performing a meta-analysis on randomized controlled trials of the current era. Methods Pubmed and Embase databases were searched from inception to May 2015. Unpublished data were obtained from the investigators. Randomized clinical trials of IABP and non-IABP in high-risk coronary revascularization procedures (PCI or CABG) were included. In the case of PCI procedures, stents should be used in more than 80% of patients. Numbers of events at the short-term and long-term follow-up were extracted. Results A total of 12 randomized trials enrolling 2155 patients were included. IABPs did not significantly decrease short-term mortality (relative risk (RR) 0.66; 95% CI, 0.42–1.01), or long-term mortality (RR 0.79; 95% CI, 0.47–1.35), with low heterogeneity across the studies. The findings remained stable in patients with acute myocardial infarction with or without cardiogenic shock. But in high-risk CABG patients, IABP was associated with reduced mortality (71 events in 846 patients; RR 0.40; 95%CI 0.25–0.67). Conclusion In patients undergoing high-risk coronary revascularization, IABP did not significantly decrease mortality. But high-risk CABG patients may be benefit from IABP. Rigorous criteria should be applied to the use of IABPs.

This study was designed to evaluate the value of plasma cystatin C in predicting adverse cardiac events after percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS).A total of 605 patients (404 male, mean age 60.4 ± 10.6 years) with ACS underwent successful PCI. Patients were divided into 4 groups according to the level of cystatin C, which was measured before the PCI: Q1 (1.02 mg/L), Q2 (1.02-1.16 mg/L), Q3 (1.17-1.34 mg/L), and Q4 (≥1.35 mg/L).After a follow-up of 14.3 ± 1.7 months, the incidence of mortality, nonfatal myocardial infarction, and target lesion revascularization in the Q2, Q3, and Q4 groups was higher than in the Q1 group (P.001). The incidence of heart failure in the Q3 and Q4 groups was higher than in the Q1 group (P.05). Multivariate Cox regression analysis showed that cystatin C elevation was an independent predictor of major adverse cardiac events. The cumulative survival rate of the Q3 and Q4 groups was lower than in the Q1 group (P .001).High plasma cystatin C concentration is an independent predictor of major adverse cardiac events in patients with ACS treated with PCI.

AIM: To investigate the relationship between salt intake and salty taste and risk of gastric cancer. METHODS: A 1:2 matched hospital based case-control study including 300 patients with gastric cancer and 600 cancer-free subjects as controls. Subjects were interviewed with a structured questionnaire containing 80 items, which elicited information on dietary, lifestyle habits, smoking and drinking histories. Subjects were tested for salt taste sensitivity threshold (STST) using concentrated saline solutions (0.22-58.4 g/L). Conditional logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (95% CI). RESULTS: Alcohol and tobacco consumption increased the risk of gastric cancer [OR (95% CI) was 2.27 (1.27-4.04) for alcohol and 2.41 (1.51-3.87) for tobacco]. A protective effect was observed in frequent consumption of fresh vegetable and fruit [OR (95% CI) was 0.92 (0.58-0.98) for fresh vegetable and 0.87 (0.67-0.93) for fruit]. Strong association was found between STST ≥ 5 and gastric cancer [OR = 5.71 (3.18-6.72)]. Increased STST score was significantly associated with salted food intake and salty taste preference (P < 0.05). CONCLUSION: A high STST score is strongly associated with gastric cancer risk. STST can be used to evaluate an inherited characteristic of salt preference, and it is a simple index to verify the salt intake in clinic.

This study was designed to investigate the effect of atorvastatin on the serum levels of tumor necrosis factor alpha (TNF-α) and interleukin-1beta (IL-1β) following acute pulmonary embolism (PE). Forty New Zealand white rabbits were divided into control and atorvastatin groups. Acute PE was created by injection of autologous blood clots into the femoral vein. Enzyme-linked immunosorbent assay was used to measure TNF-α and IL-1β. At baseline, there was no significant difference in serum TNF-α (10.6 ± 1.3 versus 11.2 ± 1.9 pg/mL; P.05) or IL-1β (8.2 ± 1.0 versus 8.6 ± 0.9 pg/mL; P.05) between the control group and the atorvastatin group. In both groups, there was a significant increase in the serum TNF-α and IL-1β following acute PE. However, the levels of serum TNF-α and IL-1β in the atorvastatin group was significantly lower than in the control group following PE (P.01). The authors conclude that acute PE is associated with a significant increase in serum proinflammatory factors TNF-α and IL-1β. Pretreatment with atorvastatin diminished the increase in TNF-α and IL-1β.

This study was designed to describe the characteristics, diagnostic and therapeutic methods of abdominal cocoon. Twelve patients with abdominal cocoon were surgically treated. The clinical findings from these patients were analyzed. All patients presented with acute complete intestinal obstruction, and 10 had a previous history of abdominal mass. In nine patients, the whole or part of the small intestines were covered by an ash gray, dense and tough fibrous membrane. The capsule was surgically excised, and the adhesion was released. Partial resection of the small intestines was performed. In the other three patients, the small intestines were only partially covered by a membrane, and there was an extensive adhesion of intestinal tract, forming a large mass which could not be relieved by surgical lysis. Intestinal tube was put in, and fistulation procedures were performed. All patients recovered fully after the surgery.There are four types of surgical findings in abdominal cocoon. The most common type is that the small intestines are fully covered by a thick white membrane, causing intestinal obstruction. Surgical excision of the membrane and the release of adhesion is the treatment of choice.