Objective To study whether G3PD modifier protein (MP) could repair tubular epidermal cell(TEC) and ameliorate renal functions in aged rats with gentamycin induced acute tubular necrosis(ATN). Methods Aged and young rats were randomly divided into 3 groups, namely aged and young normal groups, aged and young model groups and the aged and young MP groups. The animal models of acute renal failure (ARF) were induced by gentamycin (140 mg?kg -1 ?d -1 , ip?7 d). Nitric oxide (NO) concentration was determined by Cd activated cadmium reduction method, malonaldehyde(MDA) with thiobarbituric acid test, superoxide dismutase(SOD) with hydroxylamine test, serum creatinine (Scr) with picric acid method, and the renal histology was observed by light and electron microscopy. Results NO was significantly higher in the aged MP group than that in the aged model group 〔serum: (94.29?7.68)?mol/L vs (70.14?5.53)?mol/L, P

Objective To investigate the expression of the cytosolic phospholipase A2(c-PLA2),interleukin-1 beta(IL-1?),tissue inhibitor of matrix metalloproteinase-1(TMP-1) in rat brain after injury.Methods The model of traumatic brain injury originally described by Feeney was employed.The mRNA was analyzed by RT-PCR.Results The mRNA of cytosolic phospholipase A2 was increased at 2 hour and its peak was at 7 day.At 14 day,the level of cytosolic phosphalipase A2 mRNA was still in high level as compared to the control group.Likely,the enhancement expression of interleukin-1? was seen at the 1 hour and the peak time was from 5 to 8 hour.At 72 hour,it decreased to normal level.The expression of inhibitor of matrix metalloproteinase-1 was increased at the 2 hour,and the highest expression level was seen during 48 to72 hour.It came down to normal level at 14 day after injury.Conclusion The augment of the expression of the cytosolic phospholipase A2,interleukin-1? and tissue inhibitor of matrix metalloproteinase-1 following traumatic brain injury suggested that they participated in the pathogenesis of the traumatic brain injury,and may played roles in this pathophysiological process.

Objective: To study relative risk factors for diabetic nephropathy (DN). Methods: A total of 238 patients diagnosed as type 2 diabetes mellitus (DM) were enrolled in the study. According to urine microalbuminuria to urine creatinine ratio (UACR), patients were divided into pure DM group (group DM1, n=90), early diabetic nephropathy group (group DM2 , n=73) and clinical diabetic nephropathy group (group DM3 ,n=75). Clinic data of all patients were collected; Fasting blood glucose (FBG), 2h postprandial blood glucose (2hPB), blood lipids, uric acid (UA), fibrinogen (Fg) and glycosylated haemoglobin (HbA1c) were measured in all patients, and their correlations with DN were analyzed. Results: Compared with group DM1, the course of disease in DM [(7.25±6.29) years vs. (10.25±7.67) years vs. (13.53±7.82) years], levels of FBG [(8.46±2.52) mmol/L vs. (9.52±3.38) mmol/L vs. (10.82±3.30) mmol/L], 2hPB [(18.40±5.64) mmol/L vs. (20.27±5.94) mmol/L vs. (22.59±6.14) mmol/L], HbA1c [(7.96±1.65) % vs. (8.60±1.76) % vs. (9.55±2.09) %], triglyceride [TG, (1.72±0.86) mmol/L vs. (2.34±1.87) mmol/L vs. (3.16±1.85) mmol/L], Fg [(3.49±0.93) g/L vs. (3.88±1.21) g/L vs. (4.99±2.10) g/L] and UA [(295.42±52.34) μmol/L vs. (324.18±96.29) μmol/L vs. (351.23±56.88) μmol/L] significantly increased in group DM2 and group DM3 in order (P<0.01~0.001). Logistic gradual regression analysis indicated that course of DM, HbA1c, TG, Fg and UA were risk factors for DN (OR=1.008~1.910, P<0.01~0.001). Conclusion: The course of DM, blood glucose, blood lipid, uric acid and fibrinogen are risk factors of diabetic nephropathy; increased UACR reflects progress of patient’ condition in DM patients, its detection is used for diabetic prognosis and treatment.

COVID-19/genetics* ; Genome, Viral/genetics* ; Humans ; RNA, Viral/genetics* ; RNA-Seq ; SARS-CoV-2/genetics* ; Whole Genome Sequencing

SARS-CoV-2 infection causes complicated clinical manifestations with variable multi-organ injuries, however, the underlying mechanism, in particular immune responses in different organs, remains elusive. In this study, comprehensive transcriptomic alterations of 14 tissues from rhesus macaque infected with SARS-CoV-2 were analyzed. Compared to normal controls, SARS-CoV-2 infection resulted in dysregulation of genes involving diverse functions in various examined tissues/organs, with drastic transcriptomic changes in cerebral cortex and right ventricle. Intriguingly, cerebral cortex exhibited a hyperinflammatory state evidenced by significant upregulation of inflammation response-related genes. Meanwhile, expressions of coagulation, angiogenesis and fibrosis factors were also up-regulated in cerebral cortex. Based on our findings, neuropilin 1 (NRP1), a receptor of SARS-CoV-2, was significantly elevated in cerebral cortex post infection, accompanied by active immune response releasing inflammatory factors and signal transmission among tissues, which enhanced infection of the central nervous system (CNS) in a positive feedback way, leading to viral encephalitis. Overall, our study depicts a multi-tissue/organ transcriptomic landscapes of rhesus macaque with early infection of SARS-CoV-2, and provides important insights into the mechanistic basis for COVID-19-associated clinical complications.
Animals ; COVID-19/genetics* ; Macaca mulatta ; SARS-CoV-2/genetics* ; Transcriptome