Objective To investigate the correlation between IL‐6 ,hs‐CRP and blood lipids ,blood glucose in type 2 diabetes mel‐litus(T2DM) patients complicated with coronary heart disease .Methods 64 outpatients first diagnosed T2DM complicated with coronary heart disease were selected ,56 T2DM patients and 58 health examination were as compare from 2014 January to November in my courtyard .Interleukin‐6(IL‐6) ,high sensitivity C reactive protein(hs‐CRP) and total cholesterol(TC) ,low density lipopro‐tein‐C(LDL‐C) ,blood glucose and HbA1c were detected in 3 groups of person .Results T2DM group and T2DM complicated with coronary heart disease with fasting glucose ,HbA1c ,TC and LDL‐C was significantly higher than normal group ,the difference was statistically significant(P<0 .05);The level of IL‐6 ,hs‐CRP in patients T2DM with coronary heart disease complicated was signifi‐cantly higher than that of T2DM group ,and T2DM group was higher than that of healthy group ,the differences were statistically significant(P<0 .05) .Conclusion IL‐6 and hs‐CRP can be as a specific index to predict the disease process of T2DM complicated with coronary heart disease .

The relationship between M3 cholinergic receptor agonist (carbachol) hyperstimulation-induced pancreatic acinar cellular injury and trypsinogen activation or NF-kappaB activation in rats was studied in vitro. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, the active protease inhibitor (pefabloc), and NF-kappaB inhibitor (PDTC) in vitro. Intracellular trypsin activity was measured by using a fluorogenic substrate. The cellular injury was evaluated by measuring the leakage of LDH from pancreatic acinar cells. The results showed that as compared with control group, 10(-3) mol/L carbachol induced a significant increase of the intracellular trypsin activity and the leakage of LDH from pancreatic acinar cells. Pretreatment with 2 mmol/L pefabloc could significantly decrease the activity of trypsin and the leakage of LDH from pancreatic acinar cells (P < 0.01) following the treatment with a high concentration of carbachol (10(-3) mol/L) in vitro. The addition of 10(-2) mol/L PDTC didn't result in a significant decrease in the activity of trypsin and the leakage of LDH from pancreatic acinar cells treated with a high concentration of carbachol (10(-3) mol/L) in vitro (P > 0.05). It was concluded that intracellular trypsinogen activation is likely involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro. NF-kappaB activation may not be involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro.
Carbachol/*pharmacology ; Cholinergic Agonists/pharmacology ; NF-kappa B/*metabolism ; Pancreas/metabolism ; Pancreas/*pathology ; Rats, Wistar ; Receptor, Muscarinic M3/agonists ; Trypsinogen/*metabolism

Objective To compare the expression of mIFN-γ, replicative activities and anti-tumor activities of CNHK300-mIFN-γand Ad-mIFN-γin normal and gastric cancer cells. Methods The replicative activities of viruses in cells were measured by viral replication assay. CPE assay was used to detect the antitumor effect of viruses. The expression level of mIFN-γ in cancer cells was detected by ELISA. Results The infection of CNHK300-mIFN-γled to an obvious expression of mIFN-γin gastric cancer cells. The vector system CNHK300-mIFN-γpossessed more replicated potential than Ad-mIFN-γ, and could specifically kill most of BGC-823 cells at MOI value of 0.1, which was much better than that by the traditional adenoviral vector. Conclusion CNHK300-mIFN-γcan selectively replicate and effectively express mIFN-γ in tumor cells, and specifically kill gastric cancer cells, suggesting a splendid future as a new anticancer agent.

Objective:To evaluate the objective imaging markers of cognitive impairment in patients with end-stage renal disease by MRI intravoxel incoherent motion.Methods:A total of 40 patients with ESRD were enrolled in the Department of Nephrology, Changzhou Second Hospital Affiliated to Nanjing Medical University from January 2019 to August 2020, and 24 healthy controls were prospectively enrolled at the same time.All subjects performed with MRI scan were collected, and the slow apparent diffusion coefficient (ADC slow) of the corresponding brain regions were obtained .The cognitive function was evaluated by the Montreal cognitive assessment scale (MoCA). Two-sample t test was used to analyze the difference of ADC slow and cognitive score between the two groups.Pearson correlation analysis was performed among the cognitive function score of end-stage renal disease and ADC slow value. Results:(1) The score of the intelligence test scale in the ESRD group (23.30±1.76) was significantly lower than that of the healthy control group (27.92±1.00) ( P<0.01). The ADC slow values of bilateral frontal lobe, hippocampus, and insula brain areas (respectively(0.648±0.035), (0.633±0.043), (0.762±0.043), (0.756±0.042), (0.792±0.048), (0.776±0.054))in the ESRD group were significantly higher than those in the healthy control group ((0.600±0.039), 0.610±0.037, (0.725±0.059), (0.711±0.054), (0.740±0.063), (0.716±0.051)) ( P<0.01). (2) Pearson correlation analysis showed that the ADC slow values of bilateral insula and right hippocampus in the ESRD group were negatively correlated with MoCA scales ( r=-0.38, -0.38, -0.66, all P<0.05). Conclusion:ADC slow value in IVIM can better reflect the changes of cognitive function impairment in ESRD patients.

Objective To investigate the combined biological effects of low dose radiation,carbon monoxide,benzene and noise on rats.Methods Sixteen male SD rats were randomly divided into experiment group and control group.The experiment group was exposed to carbon monoxide,benzene,low dose radiation and noise daily,the control group was in common environment.Peripheral blood,organ index,and marrow DNA content were detected.Two-dimensional electrophoresis (2-DE) was performed on serum protein analysis.Differential expressed proteins were identified by a matrix assisted laser desorption/ionization time of flight mass spectrometry (MAIDI-TOF-MS).Results Compared to control group,the liver index,spleen index,thymus index,leukocytes,platelets count,and marrow DNA content of the experiment group were decreased significantly (t =2.732,4.141,3.053,2.211,2.668,11.592,P ＜0.05).12 altered proteins were detected and through identification,3 proteins were definite in terms of serum amyloid A-4 protein (SAA4),trichoplein keratin filament-binding protein (TCHP) and tubulin alpha-4A chain (TUBA4A).Conclusions The hematopoietic system and immune system of rats are damaged significantly with the changes of several serum protein expressions by the combined exposure of low dose radiation,carbon monoxide,benzene and noise.This study may provide new information for the mechanism of the combination effects.

The relationship between M3 cholinergic receptor agonist (carbachol) hyperstimulationinduced pancreatic acinar cellular injury and trypsinogen activation or NF-κB activation in rats was studied in vitro. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, the active protease inhibitor (pefabloc), and NF-κB inhibitor (PDTC) in vitro. Intracellular trypsin activity was measured by using a fluorogenic substrate. The cellular injury was evaluated by measuring the leakage of LDH from pancreatic acinar cells. The results showed that as compared with control group, 10-3 mol/L carbachol induced a significant increase of the intracellular trypsin activity and the leakage of LDH from pancreatic acinar cells. Pretreatment with 2 mmol/L pefabloc could significantly decrease the activity of trypsin and the leakage of LDH from pancreatic acinar cells (P ＜0.01) following the treatment with a high concentration of carbachol (10-3 mol/L) in vitro. The addition of 10-2 mol/L PDTC didn't result in a significant decrease in the activity of trypsin and the leakage of LDH from pancreatic acinar cells treated with a high concentration of carbachol (10-3 mol/L) in vitro (P＞0.05). It was concluded that intracellular trypsinogen activation is likely involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro. NF-κB activation may not be involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro.