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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.

In the present study, it was found that intraperitoneal (i.p.) pre-injection of N(G)-nitro-L-arginine methyl ester (L-NAME) significantly influenced the endomorphin-1 (EM-1) and endomorphin-2 (EM-2) induced antinociception. These effects could be inhibited or reversed by L-Arg or naloxone. Our results suggest that the modulatory effect of NO system on the mu-receptor evoked analgesia is different between the two mu receptor subtypes.