Objective:To investigate the influence of α cells and glucagon-like peptide l (GLP-1) in the function of β cells (INS-1 cells) in the rats,and to elucidate the possible mechanism of α cells and INS-1 cells transplantation in influencing hypoglycemia.Methods:The proliferation abilities of INS-1 cells after treated with 10％,20％ and 30％ islet α-cell conditioned medium and 0.03,0.30,3.00,30.0 mg · L-1 of GLP-1 were analyzed by MTT assay.The levels of insulin secretion of INS-1 cells after treated with 10％,20％,30％ α cells,α-cell conditioned medium and different concentrations of GLP-1 were analyzed by enzyme linked immunosorbent assay (ELISA).The concentrations of Ca2+ in INS-1 cells after treated with high glucose and GLP-1 were analyzed by laser confocal microscope.The expression levels of insulin protein after treated with different concentrations of islet α-cell conditioned medium and different concentrations of GLP-1 were detected by Western blotting methed.After the INS-1 cells,the mixture of INS-1 cells and α cells were transplanted into the left renal capsule of the nude mice,the blood glucose levels and the kidney morphology were observed.The levels of insulin/glucagon in the transplanted cells were detected by immunohistochemistry.Results:Compared with control group,both of α-cell conditioned media and GLP-1 promoted the INS-1 cell proliferation and insulin secretion (P ＜ 0.05).The laser confocal microscope results revealed that GLP-1 stimulated the increased intracellular Ca2+ concentration in INS-1 cells (P＜ 0.05).Compared with control group,there was no significant difference in the expression levels of insulin protein in the insulin-1 cells after treated with islet α cell conditioned medium and GLP-1 (P＞0.05).Compared with pre transplantation,the blood glucose level in the transplanted INS-1 cells was significantly decreased at 35 d after renal capsul trasplantation (P＜0.05),and even hypoglycemia presented renal capsular in the diabetic nude mice;the transplantation site was obviously swollen.However,the levels of blood glucose had no change of the diabetic rats after transplated with the mixture of INS-1 and α cells (P＜0.05).The expression of insulin and glucagon in the INS-1 transplanted cells were found by immunohistochemistry staining.Conclusion:Pancreatic islet α cells and their secretions can promote the INS-1 cell proliferation and insulin secretion,and the mixture of INS-1 cells and α cells transplanted under the renal capsule of the diabetic nude mice can reduce the hypoglycemic effect of INS-1 cell transplantation which might be related to the INS-1 cells that can express both of insulin and glucagon genes.

Objective:To investigate the correlation between serum uric acid level and heart rate variability (HRV) in patients with acute ischemic stroke.Methods:Patients with acute ischemic stroke admitted to the Department of Neurology, the First Affiliated Hospital of Nanjing Medical University from July 2017 to July 2019 were enrolled retrospectively. They were divided into 4 groups (Q1, Q2, Q3, and Q4) according to the sex-specific serum uric acid quartiles. The demographic data, baseline clinical data, laboratory indicators and HRV recorded by 24-h dynamic electrocardiogram in each group were compared. The independent correlation between HRV time domain parameters RR (normal-to-normal, NN) interval standard deviation (standard deviation of the NN intervals, SDNN), RR interval mean standard deviation (standard deviation of the average NN intervals, SDANN) and serum uric acid level was analyzed through multiple linear regression model.Results:A total of 141 patients were enrolled in the study, including 100 males (70.92%), aged 61.55±12.92 years. The median baseline National Institutes of Health Stroke Scale (NIHSS) score was 2 (interquartile range: 1-4), and the serum uric acid level was 302.87±73.48 μmol/L. There were significant differences in the NIHSS score ( P<0.034), the proportion of patients with hypertension ( P=0.015), the estimated glomerular filtration rate ( P<0.001), and the HRV time domain parameters (all P<0.001) between each quartile group. The proportion of patients with low HRV (SDNN <100 ms) in the lowest serum uric acid level quartile group was significantly higher than that in other quartile groups ( P<0.05). Multiple linear regression analysis showed that serum uric acid levels were significantly and positively correlated with SDNN (standardized β=0.321, P<0.001) and SDANN (standardized β=0.266, P=0.001). Conclusions:The low level of serum uric acid in patients with acute ischemic stroke indicates that HRV is low, which may suggest that the mechanism of oxidative stress is involved in the decrease of HRV in patients with acute ischemic stroke.

Objective:To investigate the neutrophil to lymphocyte ratio (NLR) and clinical manifestations, imaging manifestations and plasma D-dimer in cerebral venous sinus thrombosis (CVST) patients with headache as the first symptom.Methods:CVST inpatients with headache as the first symptom admitted to the First Affiliated Hospital of Nanjing Medical University from January 2012 to December 2019 were enrolled retrospectively as case group. In the same period, patients with similar headache symptoms and healthy subjects were included consecutively as control group. The differences of demographic data, biochemical indexes, blood routine indexes and plasma D-dimer were compared among the three groups. Multivariate logistic regression analysis was used to identify the independent correlation between NLR and plasma D-dimer and CVST with headache as the first symptom. According to the median NLR, patients with CVST were divided into low NLR group and high NLR group, and the differences in clinical manifestations, imaging manifestations and plasma D-dimer were compared between the two groups. Multiple linear regression analysis was used to determine the independent correlation between the reciprocal of NLR and plasma D-dimer and clinical features. Results:A total of 51 CVST inpatients with headache as the first symptom, 54 headache controls and 53 healthy controls were included in the study. There were significant differences in triglyceride ( P=0.002), fasting blood glucose ( P=0.044), serum albumin ( P=0.013), uric acid ( P=0.010), plasma D-dimer ( P<0.001), proportion of D-dimer negative patients ( P<0.001), mean corpuscular volume ( P=0.015), white blood cell count ( P<0.001), neutrophil count ( P<0.001), lymphocyte count ( P=0.005), monocyte count ( P=0.004), mean platelet volume ( P=0.010), platelet distribution width ( P=0.029), NLR ( P<0.001) and lymphocyte to monocyte ratio ( P<0.001) among the three groups. Post-hoc analysis showed that plasma D-dimer and NLR in the case group were significantly higher than those in the two control groups (all P<0.001). Multivariate logistic regression analysis with the headache control group and the healthy control group as references showed that NLR and plasma D-dimer were significantly and independently correlated with CVST with headache as the first symptom (all P<0.05). According to the median NLR (4.817 6), the case group was divided into low NLR group and high NLR group. The comparison showed that the onset time ( P=0.041), the proportion of patients with headache as the only symptom ( P=0.016) and the proportion of plasma D-dimer negative patients ( P=0.002) in the low NLR group were significantly higher than those of the high NLR group, and the proportion of patients with headache complicated with disturbance of consciousness ( P=0.032), plasma D-dimer ( P<0.001) and fasting blood glucose ( P<0.001) were significantly lower than those in the high NLR group. With the reciprocal of NLR as the dependent variable, multiple linear regression analysis showed that the reciprocal of NLR was independently negatively correlated with plasma D-dimer ( R=-0.521, P<0.001), and independently positively correlated with headache as the only symptom ( R=0.280, P=0.049). Conclusions:NLR was significantly increased in CVST patients with headache as the first symptom. It might help early diagnosis and clinical feature prediction of CVST patients.