To compare the clinical efficacy and safety of robotic-assisted liver resection (RLR) and laparoscopic liver resection (LLR) by the means of meta-analytical techniques. We searched PubMed, Cochrane library, Embase and Web of Science databases, collecting randomized or non-randomized studies about robotic-assisted and laparoscopic liver resections. The searching cutoff date was 2017/6/30, all the data obtained were statistically analyzed using RevMan5.3 software recommended by Cochrane Collaboration. A total of thirteen articles, involving 938 patients were enrolled in meta-analysis. Among them, 435 cases underwent RLR, and 503 cases underwent LLR. Compared with LLR, the RLR had longer operative time [MD=65.49, 95%CI (42.00, 88.98) P＜0.00001＝more intraoperative blood loss [MD=69.88, 95%CI (27.11, 112.65) P=0.001] and a higher cost [MD=4.24, 95%CI (3.08, 5.39) P＜0.00001＝. There were no significant differences between the two groups in transfusion rate, complication rate, conversion rate, the R1 resection rate and hospital stay. In the subgroup analysis of surgery after 2010, a lower conversion rate was observed in RLR, other clinical outcomes are comparable between RLR and LLR. In the subgroup analysis of minor hepatectomy, RLR is still associated with longer operative time, but there is no difference in other outcomes. In the subgroup analysis of left hemihepatectomy or left lateral hepatectomy, RLR is associated with more blood loss. Although RLR associated with Longer operative time and more intraoperative blood loss, it displays the same safety and effectiveness as LLR for hepatectomies. And the high cost is still a major hindrance for the widely application of robotic surgery.

Macrophages are critical myeloid cells with the hallmark of phenotypic heterogeneity and functional plasticity. Macrophages phenotypes are commonly described as classically-activated M1 and alternatively-activated M2 macrophages which play an essential role in the tissues homeostasis and diseases pathogenesis. Alternations of macrophage polarization and function states require precise regulation of target-gene expression. Emerging data demonstrate that epigenetic mechanisms and transcriptional factors are becoming increasingly appreciated in the orchestration of macrophage polarization in response to local environmental signals. This review is to focus on the advanced concepts of epigenetics changes involved with the macrophage polarization, including microRNAs, DNA methylation and histone modification, which are responsible for the altered cellular signaling and signature genes expression during M1 or M2 polarization. Eventually, the persistent investigation and understanding of epigenetic mechanisms in tissue macrophage polarization and function will enhance the potential to develop novel therapeutic targets for various diseases.

Background Invasive candidiasis (IC) is the most common invasive fungal infection. The epidemiology of IC in hospitalized patients has been widely investigated in many metropolitan cities; however, little information from medium and small cities is known. Methods A 5-year retrospective study was carried out to analyze the prevalence, species distribution, antifungal susceptibility, risk factors and mortality of inpatients with invasive Candida infection in a regional tertiary teaching hospital in Southwest China. Results A total of 243 inpatients with invasive Candida infection during the five-year study period were identified, with a mean annual incidence of 0.41 cases per 1000 admissions and a 30-day mortality rate of 12.3%. The species distributions of Candida albicans, Candida glabrata, Candida tropicalis, Candida krusei, Candida parapsilosis and other Candida species was 45.3, 30.0, 15.2, 4.9, 2.1 and 2.5%, respectively. The total resistance rates of fluconazole (FCA), itraconazole (ITR) and voriconazole (VRC) were 18.6, 23.1 and 18.5%, respectively. Respiratory dysfunction, pulmonary infection, cardiovascular disease, chronic/acute renal failure, mechanical ventilation, abdominal surgery, intensive care in adults, septic shock and IC due to C. albicans were associated with 30-day mortality (P < 0.05) according to the univariate analyses. Respiratory dysfunction [odds ratio (OR), 9.80; 95% confidence interval (CI), 3.24–29.63; P < 0.001] and IC due to C. albicans (OR, 3.35; 95% CI, 1.13–9.92; P = 0.029) were the independent predictors of 30-day mortality. Conclusions This report shows that the incidence and mortality rates are lower and that the resistance rates to azoles are higher in medium and small cities than in large cities and that the species distributions and risk factors in medium and small cities are different from those in large cities in China. It is necessary to conduct epidemiological surveillance in medium and small cities to provide reference data for the surveillance of inpatients with IC infections.

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The inflammatory response in acute pancreatitis (AP) is associated with acinar-to-dendritic cell transition. The CD4+ T-cell-mediated adaptive immune response is necessary for pancreatic inflammatory damage. However, the effect of acinar-to-dendritic cell transition on the CD4+ T-cell response and the regulatory mechanism remain undefined. A mouse animal model of AP was established by repeated intraperitoneal injection of CAE. The mTOR inhibitor rapamycin was administered before AP induction. Primary acinar cells were isolated and co-incubated with subsets of differentiated CD4+ T cells. The expression of DC-SIGN was also assessed in pancreatic tissues from human AP patients. We found acinar cells expressed DC-SIGN and displayed the phenotype of dendritic cells (DCs), which promoted the differentiation of naive CD4+ T cells into CD4+/IFN-γ+ Th1 and CD4+/IL-17A+ Th17 cells in pancreatic tissues during AP. DC-SIGN was the target gene of Myc. The mTOR inhibitor rapamycin inhibited AP-induced DC-SIGN expression, CD4+ Th1/Th17 cell differentiation and the pro-inflammatory response via Myc. Acinar cells expressed DC-SIGN in pancreatic tissues of human patients with AP. In conclusion, acinar-to-dendritic cell transition is implicated in the CD4+ T-cell immune response via mTOR-Myc-DC-SIGN axis, which might be an effective target for the prevention of local pancreatic inflammation in AP.

Background While hospital-acquired influenza A results in an additional cost burden and considerable mortality in patients, its risk factors are unknown. We aimed to describe the characteristics of patients vulnerable to hospital-acquired influenza A and to identify its risk factors to assist clinicians control hospital-acquired infections and reduce the burden of treatment. Methods A case-control study was conducted among hospitalized patients aged ≥18 years at a tertiary level teaching hospital during the 2018–2019 influenza A season. Patient data were retrieved from hospital-based electronic medical records. Hospital-acquired influenza A was defined as a case of influenza A diagnosed 7 days or more after admission, in a patient with no evidence of influenza A infection on admission. The controls without influenza A were selected among patients exposed to the same setting and time period. We identified risk factors using conditional logistic regression and described the characteristics of hospital-acquired influenza A by comparing the clinical data of infected patients and the controls. Results Of the 412 hospitalized patients with influenza A from all the departments in the study hospital, 93 (22.6%) cases were classified as hospital-acquired. The most common comorbidities of the 93 cases were hypertension (41.9%), coronary heart disease (21.5%), and cerebrovascular disease (20.4%). Before the onset of hospital-acquired influenza A, patients presented more lymphocytopenia (51.6% vs 35.5%, P = 0.027), hypoalbuminemia (78.5% vs 57.0%, P = 0.002), and pleural effusion (26.9% vs 9.7%, P = 0.002) than the matched controls. Infected patients also had longer hospital stays (18 days vs 14 days, P = 0.002), and higher mortality rates (10.8% vs 2.2%, P = 0.017) than the matched controls. Lymphocytopenia (odds ratio [OR]: 3.11; 95% confidence interval [CI]: 1.24–7.80; P = 0.016), hypoalbuminemia (OR: 2.24; 95% CI: 1.10–4.57; P = 0.027), and pleural effusion (OR: 3.09; 95% CI: 1.26–7.58; P = 0.014) were independently associated with hospital-acquired influenza A. Conclusions Lymphocytopenia, hypoalbuminemia and pleural effusion are independent risk factors that can help identify patients at high risk of hospital-acquired influenza A, which can extend hospital stay and is associated with a high mortality.

α-Mangostin (MG) is a versatile bioactive compound isolated from mangosteen and possesses significant pharmacokinetic shortages. To augment the potential clinical efficacy, MG-loaded self-microemulsion (MG-SME) was designed and prepared in this study, and its potential as a drug loading system was evaluated based on the pharmacokinetic performance and tissue distribution feature. The formula of MG-SME was optimized by an orthogonal test under the guidance of ternary phase diagram, and the prepared MG-SME was characterized by encapsulation efficiency, size distribution, and morphology. Optimized high performance liquid chromatography method was employed to determine concentrations of MG and characterize the pharmacokinetic and tissue distribution features of MG in rodents. It was found that diluted MG-SME was characterized as spherical particles with a mean diameter of 24.6 nm and an encapsulation efficiency of 87.26%. The delivery system enhanced the area under the curve of MG by 4.75 times and increased the distribution in lymphatic organs. These findings suggested that SME as a nano-sized delivery system efficiently promoted the digestive tract absorption of MG and modified its distribution in tissues. The targeting feature and high oral bioavailability of MG-SME promised a good clinical efficacy, especially for immune diseases.

The concept of macrophage polarization is defined in terms of macrophage phenotypic heterogeneity and functional diversity. Cytokines signals are thought to be required for the polarization of macrophage populations toward different phenotypes at different stages in development, homeostasis and disease. The suppressors of cytokine signaling family of proteins contribute to the magnitude and duration of cytokines signaling, which ultimately control the subtle adjustment of the balance between divergent macrophage phenotypes. This review highlights the specific roles and mechanisms of various cytokines family and their negative regulators link to the macrophage polarization programs. Eventually, breakthrough in the identification of these molecules will provide the novel therapeutic approaches for a host of diseases by targeting macrophage phenotypic shift.