Objective:To analyze the influencing factors of short-term prognosis, and construct a 30-day mortality risk prediction model for patients with cardiogenic shock in Xinjiang region with nomogram.Methods:The clinical data of 295 patients with cardiogenic shock from 2013 to 2019 in the First Affiliated Hospital of Xinjiang Medical University were retrospectively analyzed. Univariate and multivariate Logistic regression were used to analyze the risk factors for 30-day death in patients with cardiogenic shock, the nomogram was used to construct a prediction model for the risk of death in patients with cardiogenic shock, and the consistency coefficient and receiver operating characteristic (ROC) curve were used to evaluate the model.Results:Among 295 patients, 182 died at 30 d (death group) and 113 survived (survival group). There were statistical differences in gender, age, ICU time, systolic blood pressure, white blood cell, neutrophil count, red blood cell distribution width (RDW), prothrombin time, potassium, blood glucose, serum creatinine, total bilirubin, bicarbonate, base excess, lactic acid, brain natriuretic peptide precursor (NT-proBNP), cardiac troponin I (cTnI) and the percentage of respiratory failure, liver disease, kidney disease between death group and survival group ( P<0.01 or<0.05). Multivariate Logistic regression analysis results showed that NT-proBNP, prothrombin time, cTnI, lactic acid and systolic blood pressure were independent risk factors of death in patients with cardiogenic shock ( OR = 1.00, 1.10, 1.30, 1.29 and 1.04; 95% CI 1.00 to 1.00, 1.01 to 1.18, 1.00 to 1.68, 1.01 to 1.65 and 1.02 to 1.07; P<0.01 or<0.05). The independent factors obtained from multivariate analysis were combined with clinical practice, Akaike information criterion (AIC) analysis was conducted to select modeling variables, and the variables included in the nomogram model were NT-proBNP, prothrombin time, cTnI and lactic acid. After 500 times of internal Bootstrap self-sampling verification of the nomogram model, the C index was 0.805, area under the curve was 0.846, and the optimum threshold value was 0.486, with a sensitivity of 78.6% and a specificity of 83.1%. Conclusions:NT-proBNP, prothrombin time, cTnI and lactic acid are the related influencing factors for the short-term prognosis of patients with cardiogenic shock, and the related nomogram prediction model is constructed, which has guiding significance for the early intervention of cardiogenic shock.

Objective To evaluate the safety and efficacy of intra-arterial infusion neoadiuvant chemotherapy in local advanced bladder cancer. Methods Nineteen cases with T2-T4a bladder cancer were enrolled in this study.Intra-arterial infusion chemotherapy with Gemcitabine and Cisplatin (GC)were performed for 1 to 3 cycles before radical cystectomy.Postoperative values of hematological parameters,maximum diameter of tumors,TNM(tumor,node and metastasis)stages and pathological grades were compared with preoperative parameters of the same case. Results Compared to the values before GC chemotherapy,WBC count showed no significant change post-operative,(6.63±2.58)×109/L vs(5.12±2.91)×109/L(P=0.13);RBC(4.41+0.52)×1012/L vs(3.92±0.42)×1012/L(P=0.00)and platelet count(220.50±59.86)×109/L vs(157.05±56.72)×109/L(P=0.001)showed significant decrease;ALT did not show significant decrease(20.00±8.31 vs 26.88±17.04 U/L,P=0.08);Creatltme also showed no significant change(95.82±14.57 vs 88.04±17.76μmol/L,P=0.06);Maximum diameter of tumors decreased significantly(3.72±1.23 vs 2.80±1.29 cm,P=0.02).Compared with clinical TNM stages,pathological TNM stages demonstrated significant decrease in 9 cases;While cell differentiation did not show decrease. Conclusions Intra-arterial infusion with GC regimen can reduce tumor size,decrease TNM stages,while not causing significant adverse impact to radical cystectomy.Bladder-spare treatment is an option for chemotherapy-sensitive cases.

Objective To investigate the relationship between dyslipidemia and nephrolithiasis in a population-based study.Methods All participants were investigated by questionnaires,physical examinations and laboratory tests including liver and renal function,lipid profile,serum fasting glucose,glycosylated hemoglobin.Nephrolithiasis was diagnosed by kidney Bultrasonography.Subjects with estimated glomerular filtration rate (eGFR) ＜ 60 ml · min-1 · (1.73 m2)-1were excluded.Results 10 316 individuals were enrolled with an average age of (54.88 ± 10.27) years (range 17-88 years) and the ratio of male to female 1:1.12.The prevalence of nephrolithiasis was 5.6％,3.7％ and 7.8％ for whole population,women and men,respectively.In women,only eGFR in stone group was significantly lower than that in non-stone group (P ＜ 0.05).However,participants in stone group were significantly older (P ＜ 0.05),of higher blood pressure (P ＜ 0.01),higher serum uric acid (P ＜ 0.01),worse renal function (serum creatinine,P ＜ 0.05;eGFR,P ＜ 0.01),and higher low-density lipoprotein (LDL) (P ＜ 0.05),compared with those in non-stone group in men.Logistic regression analysis showed that only eGFR (P ＜ 0.05) was the independent influential factor for kidney stones in women;In men,LDL was an independent influential factor for nephrolithiasis with a hazard ratio of 1.149 (95％CI 1.003-1.317,P ＜ 0.05),except for mean blood pressure and eGFR.After being divided into normal group,borderline high group and high LDL group according to the LDL level,with the increase of LDL,the prevalence of nephrolithiasis was significantly increased by 7.3％,8.3％ and 10.6％ in men respectively.There was no significant relationship between total cholesterol,triglyceride,high-density lipoprotein and nephrolithiasis.Conclusions Dyslipidemia is associated with nephrolithiasis in men,and high LDL cholesterol is an independent risk factor for nephrolithiasis.Clinical lipid testing not only helps to reduce the risk of atherosclerotic disease,but also reduces the risk of kidney stones.

Objective:To explore the association between urinary stone disease (USD) and peripheral arterial disease (PAD).Methods:The study was based on the cross-sectional chronic diseases survey performed in Pinggu district, Beijing from March to May, 2014. All subjects completed a questionnaire, physical examination, renal ultrasound examination to detect USD, ankle-brachial index (ABI) examination to detect PAD (defined as ABI<0.9 on either side of the body), and brachial-ankle pulse wave velocity (baPWV) measurement to estimate arterial stiffness. Blood and first morning urine sample were detected for serum creatinine, blood glucose and so on.Results:There were 10 281 participants included in this study. Among these participants, the prevalences of USD and PAD were 5.66% and 3.95%, respectively. Compared with non-stone participants, the persistent USD formers had a higher prevalence of PAD (8.26% vs 3.90%, P<0.001) and baPWV [(16.3±3.5) m/s vs (15.5±3.2) m/s, P<0.001]. Even after adjusting the confounding factors, the persistent USD formers also had a 2.066-fold increased risk of PAD ( OR=2.066, 95% CI 1.276-3.343, P=0.003). In the subgroup analysis, persistent USD patients in older participants who were≥60 years old, women, chronic kidney disease, and central obesity had a significantly increased risk of PAD. Conclusions:In the present population, persistent USD is positively associated with a high risk of PAD and increased arterial stiffness. Patients with persistent USD should be screened for vascular diseases.

Objective : To explore the impact of high glucose ( HG) intervention on immune escape of pancreatic cancer cells and its molecular mechanisms． Methods : PANC-1 cells were treated with different concentrations of glucose (0，7. 5，15，30 mmol / L) for 24 h to establish high glucose intervention PANC-1 cells．miR-429 mimics and its negative control ( mimics NC) were transfected into PANC-1 cells，which were divided into control group，HG group，HG + mimics NC group，HG + mimics group，HG + mimics + oe-NC group，and HG + mimics + oe-ZEB1 group．Flow cytometry was utilized to measure the expression level of cell surface molecule PD-L1 ; qRT-PCR was used to detect the expression levels of miR-429 and ZEB1 mRNA in cells ; Western blot was used to detect the ex- pression level of ZEB1 protein in cells．The above-mentioned PANC-1 cells from each group were co-cultured with CD8 + T cells to establish a co-culture system，and CCK-8 was used to assess cell proliferation activity ; apoptosis levels of cells were measured using flow cytometry ; lactate dehydrogenase ( LDH) release assay was used to detect the killing effect of CD8 + T cells on PANC-1 cells ; dual-luciferase reporter system was used to validate the target- regulatory relationship between miR-429 and ZEB1 . Results : HG could promote the expression of cell surface mole- cules PD-L1 and ZEB1 in PANC-1 cells (P＜0. 05) ，inhibit the expression of miR-429，and exhibit concentration dependence．Overexpression of miR-429 could significantly suppress the expression of cell surface molecule PD-L1 induced by HG in PANC-1 cells，while overexpression of ZEB1 could reverse the inhibitory effect of miR-429 over- expression on the expression of cell surface molecule PD-L1 induced by HG．After establishing a co-culture system with CD8 + T cells，compared with the control group，the proliferation activity of PANC-1 cells in the HG group sig- nificantly increased，and the apoptosis rate and cytotoxicity significantly decreased (P＜0. 05) ．Compared with the HG + mimics NC group，the proliferation activity of PANC-1 cells in the HG + mimics group significantly decreased， and the apoptosis level and cytotoxicity significantly increased (P＜0. 05) ．Compared with the HG + mimics group， the proliferation activity of PANC-1 cells in the HG + mimics + oe-ZEB1 group significantly increased，and the apop- tosis rate and cytotoxicity significantly decreased (P ＜0. 05 ) ．Dual luciferase reporter gene assay confirmed that miR-429 negatively regulated ZEB1． Conclusion High glucose promotes immune escape of PANC-1 cells by down- regulating the expression level of miR-429，negatively regulating the expression of ZEB1 mRNA，and increasing the expression level of cell surface molecule PD-L1 in PANC-1 cells.