Sepsis is a systemic inflammatory response syndrome caused by infection,and further development can lead to septic shock and multiple organ dysfunction syndrome.Clinical research of sepsis morbidity and mortality is a hot topic in this field.Subcellular related studies in recent years show that mitochondrial damage plays a very important role in the development of sepsis,especially septic shock.Mitochondria are highly dynamic organelles in the cell.They continue to merge and divide within cells,forming a dynamic equilibrium network structure.In sepsis,imbalance of mitochondrial fusion and fission leads to disorders of the intracellular molecules,cells,and organs.This article reviews the progress in the investigation of mitochondrial fusion and fission in the pathogenesis of sepsis.

Objective To study the change of the eonnxin43 expression in the heart of diabetic mellitus rats. Methods STZ-in-dueed diabetic mellitus in rats were developed. The expression of connexin43 in the heart was detected by immunohistochemistry and image analysis, and the heart function was observed by electrophysiolograph and echocardiogram. Results During the course of diabetic mellitus, the expression of connexin43 in the heart of diabetic rats decreased respectively in the 12th week and 24th week (P<0.01). The values of dp/dtmax and + dp/dtmax in group DM in the 12th week and 24th week were lower than that in normal control group respectively (P<0.01), and the LVEF were also decreased (12w P<0.05,24w P<0.01). The analysis of correlation showed that the expression of con-nexin43 in heart were positively correlated with heart function (P<0.05) . Conclusion The expression of Connexin43 evidently de-creased in the hearts of diabetic rats and it is positively correlated with the heart function.

The brain-gut axis is an important pathway for the interaction between the central nervous system and the gastrointestinal tract. Ischemic stroke can promote the imbalance and displacement of intestinal flora, and the intestinal flora and its metabolites in turn can affect the occurrence, development and outcome of ischemic stroke. This article reviews the related literature on ischemic stroke and intestinal flora, in order to review the relationship between the two and related mechanisms, and to prospect the stroke treatment of targeting intestinal flora.

Objective:To understand the urinary iodine external quality control assessment results of county-level iodine deficiency disorders laboratories in Liaoning Province.Methods:The numbers of county-level iodine deficiency disorders laboratories which participated in the national urinary iodine external quality control assessment in Liaoning Province from 2016 to 2019 were 19, 33, 39 and 56, respectively. The urinary iodine external quality control assessment results were statistically analyzed with the Z score method (qualified: │Z│≤2; basically qualified: 2 <│Z│ < 3; unqualified: │Z│≥3). The percentage of laboratories participating in the assessment and the qualified rate were calculated.Results:From 2016 to 2019, the percentage of county-level iodine deficiency disorders laboratories in Liaoning Province that participated in the national urinary iodine external quality control assessment increased year by year, which were 19.79% (19/96), 34.38% (33/96), 40.63% (39/96) and 58.33% (56/96), respectively. The qualified rates were 89.47% (17/19), 84.85% (28/33), 100.00% (39/39) and 100.00% (56/56), respectively.Conclusion:From 2016 to 2019, the percentage and detection capacity of county-level iodine deficiency disorders laboratories in Liaoning Province that participated in the national urinary iodine external quality control assessment have been improved.

Insulin sensitivity,β-cell function and serum high-sensitivity C-reactive protein (hs-CRP)levels were observed in obese and non-obese normoglycemic first-degree relatives of type 2 diabetic patients (FDR). The results showed that there existed insulin resistance,β-cell dysfunction and increased serum hs-CRP level in obese FDR of type 2 diabetic patients. Moreover, insulin resistance and increased CRP level were positively related to waist circumference.

Objective To evaluate the mechanism of reduction of protection induced by hypoxic postconditioning (HPO) in diabetic myocardiocytes subjected to hypoxia-reoxygenation (H/R),and the relationship with DJ-1 expression.Methods H9c2 cells cultured in normal culture atmosphere were randomly divided into 6 groups (n=36 each) using a random number table:control group (group C),group H/R,group HPO,plasmid carrying DJ-1 gene transfection group (group D),plasmid carrying DJ-1 gene transfection + H/R group (group DH),and plasmid carrying DJ-1 gene transfection + H/R + HPO group (group DHH).H/R was induced by 4 h of hypoxia followed by 2 h of reoxygenation.H9c2 cells were cultured in high glucose culture medium (30 mmol/L) for 48 h in C,H/R and HPO groups.H/R model was established in H/R and HPO groups.HPO was induced by 3 cycles of 5 min reoxygenation and 5 min hypoxia before the onset of reoxygenation in group HPO.In D,DH and DHH groups,the plasmid carrying DJ-1 gene (pEX-2-EGFP-DJ-1) was transfected into the cells,and then the cells were cultured in high glucose culture medium and subjected to H/R and HPO,respectively.At 2 h of reoxygenation,the cell survival rate was measured using the cell counting kit-8 assay,and the level of lactate dehydrogenase (LDH) in the supernatant was detected by enzyme-linked immunosorbent assay,the autophagosomes were examined with a transmission electron microscope,and the expression of DJ-1 and p62 and ratio of microtubule-associated protein 1 light chain 3 Ⅱ / Ⅰ (LC3 Ⅱ / Ⅰ) in cells were detected by Western blot.Results Compared with group C,the cell survival rate and DJ-1 expression were significantly decreased,and the LDH activity was significantly increased in H/R and HPO groups (P＜0.01).There was no significant difference in the parameters mentioned above between H/R and HPO groups (P＞0.05).Compared with group D,the cell survival rate was significantly decreased,and the LDH activity was significantly increased in group DH (P＜0.01).Compared with group DH,the cell survival rate,the number of autophagosomes and LC3 Ⅱ / Ⅰ ratio were significantly increased,and the LDH activity and p62 expression were significantly decreased in group DHH (P＜0.01).There was no significant difference in the parameters mentioned above between H/R and DH groups (P＞0.05).Conclusion The mechanism of reduction of protection induced by HPO in diabetic myocardiocytes subjected to H/R is related to high glucose-induced inhibition of DJ-1 expression and decrease in autophagy.

10.3969/j.issn.1000-3606.2013.06.002

Objective To investigate the effect of ischemic postconditioning (IPO) on renal injury induced by intestinal ischemia-reperfusion (I/R) and the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) in mice.Methods Thirty-six healthy male C57BL/6J mice,aged 9-12 weeks,were randomly divided into 3 groups ( n =12 each):sham operation group ( S group),I/R group,and IPO + I/R group ( group IPO).Intestinal I/R was produced by occlusion of superior mesenteric artery for 45 min followed by 2 h reperfusion.The mice underwent 3 cycles of 30 s reperfusion and 30 s ischemia at the end of 45 min ischemia before 2 h reperfusion.Blood samples were collected from carotid artery at 2 h of reperfusion and then the mice were sacrificed.The kidney was removed for microscopic examination.The pathological changes of the kidney were scored.The concentrations of serum blood urea nitrogen (BUN),creatinine (Cr) and neutrophil gelatinase-associated lipocalin (NGAL)were detected.The expression of Nrf2 and heme oxygenase- 1 ( HO- 1 ),superoxide dismutase (SOD) activity,and the content of malondialdehyde (MDA),TNF-α,IL-6 and IL-10 were determined in renal tissues.Results The concentrations of serum BUN,Cr and NGAL,MDA content and the expression of Nrf2 and HO- 1 were significantly higher,SOD activity was significantly lower,and the pathological score was significantly higher in group I/R that in group S ( P ＜ 0.05).The concentrations of serum BUN,Cr and NGAL and MDA content were significantly lower,the expression of Nrf2 and HO-1 and SOD activity were significantly higher,and the pathological score was significantly lower in group IPO that in group I/R ( P ＜0.05).There was no significant difference in the content of TNF-αα,IL-6 and IL-10 among all groups(P＞0.05).Conclusion IPO can alleviate the renal injury induced by intestinal I/R through promoting the expression of Nrf2 and up-regulating the expression of HO-1 in mice.

Objective To evaluate the effect of tert-butylhydroquinone ( t-BHQ) on DJ-1∕nuclear factor erythroid 2-related factor 2 (Nrf2) pathway during renal ischemia-reperfusion (I∕R) in diabetic rats. Methods Forty SPF healthy adult male Sprague-Dawley rats, weighing 200-220 g, were divided into 4 groups (n＝10 each) using a random number table method: control group (group C), diabetes mellitus group (group D), diabetes mellitus plus renal I∕R group (I∕R group) and t-BHQ group (group T). Diabe-tes mellitus was induced by intraperitoneal streptozotocin 60 mg∕kg and confirmed by fasting blood glucose level＞16. 7 mmol∕L 72 h later. t-BHQ 50 mg∕kg was intraperitoneally injected in 3 times at an interval of 8 h starting from 24 h before surgery in group T, while the equal volume of normal saline was given instead in D and I∕R groups. Blood samples were collected from the apex of the heart at 24 h of reperfusion for deter-mination of serum creatinine (Cr), cystatin C (Cys C) and β2-microglobulin (β2-MG) concentrations. The rats were then sacrificed, and kidneys were removed for determination of pathological changes of kidneys (with a light microscope) and for detection of the expression of DJ-1, Nrf2 and heme oxygenase-1 (HO-1) in renal tissues (by Western blot). Results Compared with group C, the concentrations of serum Cr, Cys C and β2-MG and pathological scores were significantly increased, and the expression of DJ-1, Nrf2 and HO-1 was up-regulated in D, I∕R and T groups ( P＜0. 05). Compared with group D and group I∕R, the concentrations of serum Cr, Cys C and β2-MG and pathological scores were significantly decreased, and the expression of DJ-1, Nrf2 and HO-1 was up-regulated in group T ( P＜0. 05). Conclusion t-BHQ can at- tenuate renal I∕R injury by activating DJ-1∕Nrf2 pathway in diabetic rats.