Factors affecting the risk of non-proliferative diabetic retinopathy among patients with type 2 diabetic mellitus / 预防医学

Objective@#To investigate the factors affecting the development of non-proliferative diabetic retinopathy (NPDR) among patients with type 2 diabetic mellitus (T2DM), so as to provide insights into manangement of NPDR.@*Methods@#T2DM patients without obvious eye discomfort at ages of 18 years and older admitted to Department of Endocrinology, Jining No. 1 People's Hospital during the period from December 2019 to May 2021 were enrolled. Participants' demographics, smoking, alcohol consumption, medical history of diabetes and use of medicines were collected, and the height, weight and blood pressure were measured. The levels of glycosylated hemoglobin (HbA1c), fasting blood glucose, blood C-peptide, lipid and creatinine were tested, and retinopathy was examined with a non-mydriatic fundus camera. The factors affecting the development of NPDR were identified among T2DM patients using a multivariable logistic regression model.@*Results@#A total of 486 T2DM patients were enrolled, including 354 men (72.84%), with a median age of 48.00 (15.25) years, and median diabetes duration of 35.00 (104.25) months. The prevalence of NPDR was 19.34% among the participants. multivariable logistic regression analysis identified an educational level of senior high school and above (OR=0.546, 95%CI: 0.325-0.918), duration of diabetes (OR=1.008, 95%CI: 1.005-1.012), HbA1c (OR=1.183, 95%CI: 1.034-1.354) and use of non-sulfonylurea insulin secretagogues (OR=1.859, 95%CI: 1.082-3.196) as factors affecting the risk of NPDR among T2DM patients.@*Conclusion@#A high risk of NPDR is found among T2DM patients with a low educational level, long duration of diabetes, poor HbA1c control and use of non-sulfonylurea insulin secretagogues.

Performance effect of rabbit carotid artery treated with decellularization and photo-oxidation / 中南大学学报(医学版)

OBJECTIVE@#To analyze and discuss the feasibility of rabbit carotid artery treated with decellularization and photo-oxidation.@*METHODS@#Sixty vascular slices of rabbit carotid artery were divided into a fresh group, a cryopreservation group, a glutaraldehyde group, and a decellularization plus photo-oxidation group 15 in each group. To evaluate the physical properties of all the rabbit carotid arteries by testing heat-shrinking temperature, tensile stress and the max elongation of each group. Then by buliding subcutaneous embedding model in SD rats we evaluated the biological stability and the anti-calcification function property of the above rabbit carotid arteries, and the detection means included HE stain, atomic absorption spectrometry and Von-Kossa calcium salt stain.@*RESULTS@#The heat-shrinking temperature, tensile stress and the max elongation in the cryopreservation group were lower or shorter than those of the other groups and the difference had statistical significance (P<0.05). Although the heat-shrinking temperature and the tensile stress in the decellularization plus photo-oxidation group were lower or shorter than those in the glutaraldehyde group (P<0.05), the max elongation in the decellularization plus photo-oxidation group was much longer than that in the glutaraldehyde group (P<0.05). The rabbit carotid artery treated with decellularization plus photo-oxidation showed lower immunogenicity and better biological stability and better anti-calcification property compared with the other groups.@*CONCLUSION@#Decellularization associated with photo-oxidation is a suitable and novel protocol for small caliber artery allograft with a diameter of less than 6 mm which is unbreakable to mechanical properties and conducive to biological stability, which has a broad prospect.

The mechanism of cardiac protection of Hsp27 against cardiac dysfunction during endotoxema in mice / 中华急诊医学杂志

Objective To investigate the cardiac protection of Hsp27 against endotoxic cardiac depression mediated by activation of PI3K/Akt pathway and the suppression of NFκB-mediated inflammatory response in mice. Method (1) Transgenic mice with cardiac specific overexpression of Hsp27 (Hsp27 Tg) and wild littermate controls (WT) were given 10 mg/kg LPS injected intraperitoneally to induce endotoxemia, (2) The cardiac function measurement in mice was performed by using echocardiography 6 hours after LPS treatment (n = 6), (3) The activity of PBK/Akt pathway was evaluated by Western blot for [hosphor-Akt (p-Akt) and phosphor-Gsk-3β (p-Gsk-3β) one hour after LPS administration ( n = 4)], (4) Activity of inflammatory response was evaluated by protein degradation of IκBα (n = 4), (5) The apoptosis of myocardial cells was determined by TUNEL assay on the paraffin section of cardiac tissue 24 hours after LPS exposure (n = 4). Results (1) Hsp27 attenuated cardiac dysfunction significantly following LPS treatment. Compared with the primary value, LPS induced the depression of cardiac function both in WT rats and Hsp27Tg rats. However, the cardiac dysfunction was attenuated significantly in Hsp27Tg rats compared with that in WT rats ( P < 0.01 or 0.05) . (2) Hsp27 attenuated IκBα degradation after LPS administration. Compared with the primary value, LPS led to LκBα degradation by (72.92 + 9.20) % in WT rats and by (41.43 + 24.10) % in Hsp27Tg rats. The overexpression of Hsp27 lessened the IκBα degradation significantly (P < 0.05). The similar results were obtained in rat myocardial cell culture of experiments. (3) Hsp27 enhanced the activation of PI3K/Akt signaling following LPS exposure. One hour after LPS administration, the relative levels of p-Akt and p-GSK-30 were (3.11 + 0.83) and (3.19 + 1.04), respectively in WT rats, and (5.13 + 0.73) and (5.71 + 1.20) in Hsp27Tg rats, respectively. Compared with WT rats, the levels of p-Akt and p-GSK-3β were significantly higher in Hsp27Tg rats (P < 0.05). (4) The Hsp27 lessened LPS-induced the apopto-sis of myocardial cells. Twenty-four hours after LPS treatment, the percentages of myocardial cell apoptosis were (6.46+ 1.74)% in WT rats and (2.88 + 0.91)% in Hsp27Tg rats. Compared with WT rats, LPS-induced apoptosis in myocardial cells was significantly decreased in Hsp27Tg rats (P < 0.01). Conclusions The overexpression ofHsp27 attenuates cardiac dysfunction significantly during endotoxemia, and the mechanisms may be attributed to the activation of PDK/Akt signaling pathway.

Effect of heat shock protein 27 on the cardiac dysfunction induced by endotoxemia / 中华急诊医学杂志

Objective To study the effects of heat shock proetin 27(Hsp27)on the cardiac dysfunction induced by endotoxemia.Method All experiments were performed in the geriatric lab of the First Affiliated Hospital Of Nanjing Medical University,and in the Animal Model Center of Nanjing University.The genotyping of the transgenic mice with cardiac-specific overexpression of Hsp27(Hsp27 Tg)was assayed by PCR and the expression of Hsp27 was determined by western blot.Hsp27 Tg and its wild type littermates(WT)were intraperitoneally injected with LPS(10 mg/kg),and 24 hours later,cardiac function was measured by echocardiography(n=6/group).The accumulated mice mortality was recorded within 70 hous after intraperitoneal injection of LPS(20mg/kg)(n=37/WT,n=27/Hsp27Tg).The NF-kB activity for cardiac-tissue samples was analyzed by electrophoretic mobility shift assay(ENSA)and for cell culture samples by dual-reporter gene assay(n=4/group).The comparison of multiple groups was performed by one-way analysis of variance(ANOVA),and comparison of two groups was performed by Scheffe-test.Survival curves were analyzed by the log-rank test.P＜0.05 wns considered to be significant.Results The high expression of Hsp27 exhibited in myocardium of Hsp27 Tg,whereas not in myocardium of WT.LPS significantly reduced the cardiac function both in Hsp27 Tg and WT.However,compaled with LPS-treated WT,cardiac function was more significantly improved as evidenced by the increases of EF by 27.33%and FS by 37.09%(P＜0.01 or P＜0.05).Seventy hours after LPS injection,the mortality was 11.11% in Hsp27 Tg and 37.84% in WT.Compared with WT,the survival rate of Hsp27 Tg significantly increased(P＜0.05).The NF-kB activation was significantly inhibited by Hsp27(P＜0.01 or P＜0.05).Conclusions The high cardiac-specific expression of Hsp27 significantly inhibits cardiac dysfunction induced by endotoxemia,and at the same time improve the survival rate.The mechanism may be connected with Hsp27 downregulating NF-kB-activation induced by LPS.