Objective Extracorporeal membrane oxygenation is a cardiopulmonary supportive therapy. Since 2004, our institution has adopted venoarterial ECMO for adult patients who otherwise could not be weaned from cardiopulmonary bypass and patients experiencing postcardiotomy cardiogenic shock and/or pulmonary dysfunction unresponsive to conventional treatment algorithms. In this study, we reviewed our experience with ECMO support and tried to identify measurable values which might predict in-hospital mortality. Methods From January 2004 through December 2008, 50 of 21,298 adult patients received VA ECMO. We retrospectively analyzed clinical records of these 50 consecutive patients. Demographics, preoperative measurements, clinical characteristics at the time of ECMO implantation, ECMO related complications and in-hospital mortality were collected. Logistic regression analyses were performed to investigate predictors of mortality. A p value ≤0. 05 was accepted as significant. Results Mean ECMO duration was ( 110 ± 17 ) hours. 38 patients were weaned from ECMO and 33 patients survived upon discharge. The overall survival was 66%. In univariate analyses, duration of ECMO support, receiving cardiopulmonary resuscitation prior to ECMO setup, ECMO setup in ICU, pre-ECMO plasma lactate level, infection, lower limbs ischemia, renal failure, experiencing at least one ECMO related complications were all associated with in-hospital death. In a multiple logistic regression adjusted for other factors mentioned above, blood lactate level before initiation of ECMO was a risk factor associated with in-hospital mortality (OR 1. 27 95% CI 1. 042-1. 542 ). To evaluate the utility of pre-ECMO lactate in predicting mortality, a conventional receiver operating characteristic curve was produced. Sensitivity and specificity were optimal at a cut-off point of 12.6 mmol/L, with an AUC of 0. 752. The positive and negative predictive values were 73.3% and 83.9% respectively. Conclusion ECMO is a justifiable alternative treatment for postoperative refractory cardiac and pulmonary dysfunction which could rescue more than 60 percent of otherwise fatal patients. Patients with pre-ECMO lactate above 12.6mmol/L are at higher risks for in-hospital death. Evidence based therapy for this group of high risk patients is needed.

Objective: To analyze variations of TYR and P genes among 14 patients with clinically diagnosed oculocutaneous albinism. Methods: Potential variations of the TYR and P genes were detected by Sanger sequencing. Novel variations were predicted with bioinformatics software including SIFT and PolyPhen-2. Results: No variation was found in the TYR gene, while 9 types of variations were found in the P gene among the 14 patients, which included c. 803-3C>G (7/26), c. 1327G>A (p.Val443Ile) (5/26), c. 632C>T (p.Pro211Leu) (4/26), c. 1832T>C (p.Leu611Pro) (3/26), c. 1349C>A (p.Thr450Lys) (2/26), c. 2363C>T (p.Ser788Leu) (2/26), c. 2228C>T (p.Pro743Leu) (1/26), c. 1525A>G(p.Thr509Ala) (1/26), and c. 1349C>T(p.Thr450Met) (1/26). Only 1 heterozygous variation was detected in 2 families. c. 2363C>T (p.Ser788Leu), c. 1832T>C (p.Leu611Pro) and c. 1525A>G (p.Thr509Ala) were not reported previously and predicted as "harmful" to the protein function. Conclusion The main type of ocular albinism is oculocutaneous albinism type Ⅱ in Liuzhou region, where the most common variations of the P gene were c. 803-3C>G and c. 1327G>A (p.Val443Ile). Above finding has enriched the variation spectrum of the P gene.

Background: An excess of thyroid hormones in Graves’ disease (GD) has profound effects on systemic energy metabolism that are currently partially understood. In this study, we aimed to provide a comprehensive understanding of the metabolite changes that occur when patients with GD transition from hyperthyroidism to euthyroidism with methimazole treatment. Methods: Eighteen patients (mean age, 38.6±14.7 years; 66.7% female) with newly diagnosed or relapsed GD attending the endocrinology outpatient clinics in a single institution were recruited between January 2019 and July 2020. All subjects were treated with methimazole to achieve euthyroidism. We explored metabolomics by performing liquid chromatography-mass spectrometry analysis of plasma samples of these patients and then performed multivariate statistical analysis of the metabolomics data. Results: Two hundred metabolites were measured before and after 12 weeks of methimazole treatment in patients with GD. The levels of 61 metabolites, including palmitic acid (C16:0) and oleic acid (C18:1), were elevated in methimazole-naïve patients with GD, and these levels were decreased by methimazole treatment. The levels of another 15 metabolites, including glycine and creatinine, were increased after recovery of euthyroidism upon methimazole treatment in patients with GD. Pathway analysis of metabolomics data showed that hyperthyroidism was closely related to aminoacyl-transfer ribonucleic acid biosynthesis and branched-chain amino acid biosynthesis pathways. Conclusion In this study, significant variations of plasma metabolomic patterns that occur during the transition from hyperthyroidism to euthyroidism were detected in patients with GD via untargeted metabolomics analysis.

AIM: To investigate the effect of Shenqi fuzheng injection (SFI) on tumor immunity and its preliminary molecular mechanism. METHODS: The animal model of low glucose tumor microenvironment was established by B16-PKM2-OE; the level of interleukin-2(IL-2) and interferon-γ(IFN-γ), CD40L and transforming growth factor-β1(TGF-β1) were detected by ELISA kit; the expressions of glucose transporter-1 (Glut-1) and key enzymes of glycolysis ( HK, PFK and PK ) in CD4

AIM: To investigate the function and mechanism of quercetin (Que) in anti-fibrosis in vitro and in vivo from the perspective of interfering with the glycolysis of renal interstitial fibroblasts. METHODS: ln vivo experiments, mice were administered in groups, kidneys were dissected, weighed and examined histopathologically and biochemically; ln vitro experiments, rat normal renal fibroblasts (NRK-49F cells) were treated with different reagents, proteins were extracted, and NRK-49F cell activation indicators such as α-smooth muscle actin (α-SMA) were detected by protein immunoblotting (Western Blot). The expression of the proteins, such as proliferating cell nuclear antigen (PCNA), was examined by protein immunoblotting (Western Blot), and the effect of Que on glucose uptake in NRK-49F cells induced by transforming growth factor-β (TGF-β1) and epidermal growth factor (EGF) was examined by fluorescence assay; the lactate content of cells in different experimental groups was examined by lactate assay kit; the effect of Que on glucose uptake in NRK-49F cells induced by TGF-β1 and EGF was examined by fluorescence quantitative PCR. EGF-induced mRNA of hexokinase (HK2), phosphofruc-tokinase 1 (PFK1) and muscle pyruvate kinase isozyme 2 (PKM2), key enzymes of glycolysis in NRK-49F cells. RESULTS: Compared with the UUO group, the morphological structures of kidney tissues in the Que administration group were all alleviated to different degrees, which were related to the inhibition of glycolysis, and the serum levels of urea nitrogen (BUN) and blood creatinine (Scr) in mice showed a significant downward trend; lactate production and glucose uptake in NRK-49F cells were gradually reduced, and Que affected TGF-β1 and EGF-induced RIF of mRNA levels of key enzymes of glycolysis gradually decreased and were associated with PKM2. CONCLUSION: Que inhibits PKM2 enzyme activity and glycolysis in NRK-49F cells and reduces TGF-β1-induced myofibroblast activation.

Ulcerative colitis （UC） is one of the chronic refractory inflammatory bowel diseases characterized by abdominal pain， diarrhea， and mucus， pus and blood in the stool. In recent years， with changes in human life style and improvements of the diagnosis， the incidence and prevalence of UC have been increasing. The pathogenesis of UC is closely related to intestinal mucosal immune dysfunction， intestinal flora disturbance， and abnormal bile acid secretion. Patients with UC have abnormal bile acid secretion and intestinal flora imbalance. A large number of studies have found that abnormal bile acid secretion inhibits immune function， affects signal transduction， and destroys the intestinal mucosal barrier. Intestinal flora disturbance has an important impact on the occurrence and development of inflammation， immune homeostasis， and stress. Bile acids indirectly or directly affect the structure and function of intestinal flora， and at the same time， they produce secondary bile acids under the modification of intestinal flora， entering the liver through enterohepatic circulation. Therefore， the complex dialogue mechanism of bile acid-intestinal flora axis is closely related to the occurrence and development of UC. Based on the basic theory of traditional Chinese medicine（TCM） and clinical research， it is found that emotion is an important factor that induces this disease， spleen and stomach weakness is the root of the disease， and liver depression and spleen deficiency are the key pathogenesis of UC. Combined with modern medicine and molecular biology research， it is believed that abnormal secretion of bile acids is a microscopic manifestation of liver depression in TCM， and intestinal flora disturbance is the biological basis of spleen deficiency. In the pathogenesis of UC， the imbalanced bile acid-intestinal flora axis is consistent with the pathogenesis of liver depression and spleen in TCM. The exploration of the biological connotation of the pathogenesis of UC with liver depression and spleen deficiency from the perspective of bile acid-intestinal flora axis can better explain the scientific nature of its pathogenesis， which provides new clinical solutions and reliable references for studying the pathogenesis of UC with liver depression and spleen deficiency and finding representative prescriptions to prevent and treat this disease.

BACKGROUND: Chemotherapy is a common treatment for advanced hepatocellular carcinoma, but the effect is not satisfactory. The study aimed to retrospectively evaluate the effects of adding all-trans-retinoic acid (ATRA) to infusional fluorouracil, leucovorin, and oxaliplatin (FOLFOX4) for advanced hepatocellular carcinoma (HCC). METHODS: We extracted the data of patients with advanced HCC who underwent systemic chemotherapy using FOLFOX4 or ATRA plus FOLFOX4 at the Eastern Hepatobiliary Surgery Hospital, First Hospital of Jilin University, and Zhejiang Sian International Hospital and retrospectively compared for overall survival. The Cox proportional hazards model was used to calculate the hazard ratios for overall survival and disease progression after controlling for age, sex, and disease stage. RESULTS: From July 2013 to July 2018, 111 patients with HCC were included in this study. The median survival duration was 14.8 months in the ATRA plus FOLFOX4 group and 8.2 months in the FOLFOX4 only group ( P  < 0.001). The ATRA plus FOLFOX4 group had a significantly longer median time to progression compared with the FOLFOX4 group (3.6 months vs. 1.8 months, P  < 0.001). Hazard ratios for overall survival and disease progression were 0.465 (95% confidence interval: 0.298-0.726; P  = 0.001) and 0.474 (0.314-0.717; P  < 0.001) after adjusting for potential confounders, respectively. CONCLUSION ATRA plus FOLFOX4 significantly improves the overall survival and time to disease progression in patients with advanced HCC.
Humans ; Carcinoma, Hepatocellular/drug therapy* ; Retrospective Studies ; Liver Neoplasms/pathology* ; Oxaliplatin/therapeutic use* ; Fluorouracil/adverse effects* ; Disease Progression ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use* ; Leucovorin/adverse effects* ; Colorectal Neoplasms/drug therapy*