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BackgroundAcute kidney injury (AKI) is a common complication after thoracoscopic lobectomy in high-risk patients due to insufficient intraoperative infusion. Goal-directed fluid therapy (GDFT) is an individualized fluid infusion strategy; the fluid infusion strategy is adjusted according to the patient’s fluid response. GDFT during operation can reduce the incidence of AKI after major surgery. Enhanced recovery after surgery (ERAS) protocol optimizes perioperative interventions to decrease the postoperative complications after surgery. In ERAS protocol of lobectomy, intraoperative restrictive fluid therapy is recommended. In this study, we will compare the effects of intraoperative GDFT with restrictive fluid therapy combined with an ERAS protocol on the incidence of AKI after thoracoscopic lobectomy in high-risk patients.Methods/designThis is a prospective single-center single-blind randomized controlled trial. Two hundred seventy-six patients scheduled for thoracoscopic lobectomy are randomly allocated to receive either GDFT or restrictive fluid therapy combined with an ERAS protocol at a 1:1 ratio. The primary outcome is the incidence of AKI after operation. The secondary outcomes include (1) the incidence of renal replacement therapy, (2) the length of intensive care unit stay after operation, (3) the length of hospital stay after operation, and (4) the incidence of other complications including infection, acute lung injury, pneumonia, arrhythmia, heart failure, myocardial injury after noncardiac surgery, and cardiac infarction.DiscussionThis is the first study to compare intraoperative GDFT with restrictive fluid therapy combined with an ERAS protocol on the incidence of AKI after thoracoscopic lobectomy in high-risk patients. The hypothesis is that the restrictive fluid therapy is noninferior to GDFT in reducing the incidence of AKI, but restrictive fluid therapy is simpler to apply than GDFT.Trial registrationClinicalTrials.govNCT04302467. Registered on 26 February 2020

Background The goal of this study was to review relevant randomized controlled trials in order to determine the efficacy of continuous positive airway pressure (CPAP) versus mandibular advancement device (MAD) in the treatment of obstructive sleep apnea (OSA). Methods Using appropriate keywords, we identified relevant studies using PubMed, the Cochrane Library, and Embase. Key pertinent sources in the literature were also reviewed, and all articles published through October 2019 were considered for inclusion. For each study, we used odds ratios (ORs), mean difference (MD), and 95% confidence interval (95% CI) to assess and synthesize outcomes. Results We included 14 RCTs, for a total of 249 patients in the CPAP group and 247 in the MAD group. Compared with MAD, CPAP significantly decreased apnea hypopnea index (AHI) (WMD: −7.08, 95%CI: −9.06∼-5.10) and the percentage of stage 1 and 2 after therapy (WMD: −3.728, 95%CI: −6.912∼-0.543). However, compared with MAD, CPAP significantly decreased the SF-36-social function score (WMD: −3.381, 95%CI: −6.607∼-0.154).There was no significant difference in Epworth sleepiness scale score after therapy between the two groups. Conclusion CPAP has better therapeutic efficacy in OSA patients than MAD.

OBJECTIVE The purpose of this study was to assess the fibrinolytic status after cardiopulmonary bypass in rheumatic valvular heart disease patients, and detect the associated factors of post-cardiopulmonary bypass hyperfibrinolysis. METHODS According to the fibrinolytic status after cardiopulmonary bypass, 203 rheumatic valvular heart disease patients were divided into two groups: hyperfibrinolysis group (H group, n = 78) and non-hyperfibrinolysis group (NH group, n = 125). The demographic characteristics, operative variables, and postoperative follow-ups were compared between these two groups. RESULTS The incidence of hyperfibrinolysis was 38.4% after cardiopulmonary bypass. Patients in the H group had a significant higher incidence of preoperative atrial fibrillation than patients in the NH group (92.3% vs. 55.2%, P

This study aimed to elucidate the effect of miR-1306–3p on metastasis of hepatocellular carcinoma (HCC) and potential mechanism involved. miR-1306–3p promoted migration and invasion of HCC in vivo and in vitro. Moreover, miR-1306–3p inhibited snail to enhance its expression via directly targeting FBXL5, thus inducing the epithelial-mesenchymal transition (EMT) in HCC. Intriguingly, miR-1306–3p expression was transcriptionally enhanced by FoxM1. Consistently, miR-1306–3p was upregulated in HCC compared with paracarcinoma and correlated with poor prognosis of HCC patients. Our researches suggest that miR-1306–3p is a tumor enhancer in regulating of HCC metastasis, and miR-1306–3p may be clinically utilized as a factor for the clinical diagnosis and prognosis of HCC.

BACKGROUND: The balance of oxygen delivery and consumption is essential in patients who are critically ill. Mixed venous oxygen saturation (SvO2) is a standard method to evaluate oxygen delivery and consumption during anesthesia. However, SvO2 is monitored through a pulmonary artery catheter, which is invasive. Regional cerebral oxygenation (rScO2) reflects oxygen saturation in a small region of the frontal lobes and is monitored noninvasively through near-infrared spectroscopy. In the present study, the correlation between rScO2 and SvO2 was calculated during off-pump coronary artery bypass grafting surgery to determine whether a positive correlation exists between rScO2 and SvO2. METHODS: A total of 56 subjects were consecutively enrolled in the study. Then rScO2 and SvO2 were simultaneously monitored. The parameters were recorded at 5 time points: T1, 10 min after intubation (1.0 FIO2 for 10 min); T2, 20 min after intubation (0.60 FIO2 for 10 min); T3, at the end of the revascularization of the left anterior descending artery (0.60 FIO2); T4, after protamine infusion (0.60 FIO2); and T5, 10 min after protamine infusion (1.0 FIO2 for 10 min). The correlation between rScO2 and SvO2 and the variation trend between rScO2 and SvO2 when FIO2 increased from 0.60 to 1.0 were analyzed. RESULTS: There was a significant positive correlation between rScO2 and SvO2 at these 5 time points (r2 = 0.77, 0.81, 0.70, 0.83, and 0.92, respectively). There also was a significant positive correlation between Δ rScO2 and Δ SvO2 (n = 112, r2 = 0.72, P CONCLUSIONS: There was a positive correlation between rScO2 and SvO2 during off-pump coronary artery bypass grafting surgery, and there also was a positive correlation in the variation trend between rScO2 and SvO2.

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TIGIT, an immune checkpoint molecule widely expressed on NK cells, activated T cells and Tregs, has been involved in delivering inhibitory signals through the interaction with PVR. The blockade of TIGIT/PVR interaction is a promising approach in cancer immunotherapy. Here, we unexpectedly discovered the expression of TIGIT in murine tumor cells. To elucidate the mechanism of such intrinsic expression, TIGIT knockout murine colorectal CT26 and MC38 cell lines were generated by using CRISPR/Cas9 system. Although TIGIT knockout showed no effects on proliferation and colony formation of tumor cells in vitro, the tumor growth in mice was considerably inhibited. TIGIT knockout led to the increase of IFN-γ secretion by NK and CD8+ T cells. Further, in BABL/c nude mice, CD8+ T cells depleting mice and NK cells depleting nude mice, the promotion of tumor growth was significantly diminished, suggesting that both NK cells and CD8+ T cells were involved in the tumor promoting process mediated by intrinsic TIGIT. In addition, blocking TIGIT/PVR interaction by the antibody or recombinant PVR protein could elicit anti-tumor effects by facilitating the tumor infiltration and restoring the function of CD8+ T cells, and the antibody-mediate TIGIT blockade could inhibit MC38 tumor growth through blocking TIGIT expressed on tumor cells. We therefore propose a novel TIGIT/PVR interaction mode that tumor intrinsic TIGIT delivers inhibitory signals to CD8+ T cells and NK cells by engaging with PVR.

Since there were a few articles to report the treatment of severe pulmonary vasoconstriction induced by protamine in cardiac surgery, we described the use of epoprostenol to reverse this condition. A total of 5 cases of severe pulmonary vasoconstriction induced by protamine in cardiac surgery were reviewed. The demographic, clinical data and treatment process were obtained. All the patients were followed up. Severe pulmonary vasoconstriction was occurred 4 to 10 minutes after protamine infusion. The primary sign was sudden hypotension, the pulmonary artery pressure was increased gradually, the arterial oxygen partial pressure was decreased in all the patients. Epoprostenol was infused via pulmonary artery catheter at dosage of 20 to 40 ng/kg·min in all the patients, 2 patients were underwent re-cardiac pulmonary bypass assistance. The hemodynamic instability status lasted 40 to 65 minutes respectively. All the patients were recovered uneventfully. All physicians should alert to the incidence of severe pulmonary vasoconstriction induced by protamine in cardiac surgery. Use epoprostenol through pulmonary artery catheter could treat pulmonary artery vasoconstriction effectively and safely.

The identification of novel cytotoxic T lymphocyte (CTL) epitopes is important to analysis of the involvement of CD8+ T cells in Mycobacterium tuberculosis infection as well as to the development of peptide vaccines. In this study, a novel CTL epitope from region of difference 11 encoded antigen Rv3425 was identified. Epitopes were predicted by the reversal immunology approach. Rv3425‐p118 (LIASNVAGV) was identified as having relatively strong binding affinity and stability towards the HLA‐A*0201 molecule. Peripheral blood mononuclear cells pulsed by this peptide were able to release interferon‐γ in healthy donors (HLA‐A*02+ purified protein derivative+). In cytotoxicity assays in vitro and in vivo, Rv3425‐p118 induced CTLs to specifically lyse the target cells. Therefore, this epitope could provide a subunit component for designing vaccines against Mycobacterium tuberculosis.

To study the effects of L-arginine (L-Arg) on human colon carcinoma cell line LS174 through NO pathway and the mechanism.LS174 cells were cultured in the presence of L-Arg at different concentrations for different time. MTT assay was employed to evaluate the cell proliferation, and the cell morphological changes were observed by optical and electron microscopy. The apoptosis of L-Arg-treated cells was observed by the Annexin V/PI staining. The expression levels of VEGF, COX-2, p53, bcl-2 and bax in the cells were determined using Western blotting and immunocytochemical staining.L-Arg promoted the growth of LS174 cells at a low concentration (0.125 mmol/L) and inhibited the cell growth at higher concentrations (0.5, 2, 8, and 32 mmol/L). Under electron microscope, ultrastructual changes in the cytoplasm and nuclei of LS174 cells were observed 48 h after exposure to L-Arg. Some of the cells showed morphological changes characteristic of cell apoptosis such as cell size reduction, condensation and margination of the nuclear chromatin. Low concentration of L-Arg resulted in a cell apoptosis rate of 2.29%, as compared with the rate of 2.84% in the control group; at higher concentrations, L-Arg caused significantly increased cell apoptosis rates to 26.88%, 28.95%, 63.36%, and 84.51%, respectively. In cells treated with a low concentration of L-Arg, the expressions of VEGF and COX-2 were increased as compared with those in the control cells; higher concentrations of L-Arg obviously decreased the expressions of p53 and bcl-2 and increased the expression of bax.Low-concentration L-Arg can promote the growth of LS174 cells probably by up-regulating VEGF and COX-2 protein under the influence of NO, the metabolite of L-Arg. The inhibitory effect of high concentrations of L-Arg is probably mediated by inducing cell apoptosis via NO. The mechanism of L-Arg- induced cell apoptosis may be related to the up-regulation of bax protein and the down-regulation of p53 and bcl-2 proteins.