Analysis of causes of graft loss in 135 kidney transplant recipients / 南方医科大学学报

OBJECTIVE@#To investigate the causes of graft loss in kidney transplant recipients.@*METHODS@#We retrospectively analyzed the clinical data of 135 recipients with graft loss after renal transplantation in the Eighth Medical Center of Chinese PLA General Hospital from January 1, 2002 to January 1, 2022.@*RESULTS@#A total of 135 kidney transplant recipients experienced graft failure. The causes of graft loss included graft rejection (70 cases, 51.8%), death of the recipients with functional graft (37 cases, 27.4%), surgical complications (12 cases, 8.9%), drug toxicity (4 cases, 3.0%), carbapenem-resistant Klebsiella pneumoniae infection (4 cases, 3.0%), polyoma BK virus-related nephropathy (3 cases, 2.2%), primary nonfunctioning kidney (2 cases, 1.5%), recurrence of primary disease (2 cases, 1.5%), and prerenal acute renal failure (1 case, 0.7%).@*CONCLUSION@#The main cause of graft loss after renal transplantation is graft rejection, and the secondary cause is death of the recipient with functional graft, and other reasons can be rare.

Carbendazim affects testicular development and spermatogenic function in rats / 中华男科学杂志

<p><b>OBJECTIVE</b>To explore the effects of carbendazim on the testicular development and spermatogenic function of male rats and its action mechanism.</p><p><b>METHODS</b>Forty clean-grade impubic male Wistar rats were equally randomized into a low-dose, a medium-dose, a high-dose and a control group, treated respectively with carbendazim at 20, 100 and 200 mg/kg (bw) and Tween-80 solution, all by oral gavage once a day for 80 days. After treatment, the rats were weighed, their testes and epididymides immediately excised, their morphological changes observed and the weights of the right testis and epididymis obtained. Sperm motility and counts in the left cauda epididymis were determined. Histopathological changes, cell apoptosis and the expression of Bcl-2/Bax in the testis were detected by HE staining, TUNEL and immunohistochemical SABC method.</p><p><b>RESULTS</b>The medium- and high-dose groups showed obviously atrophic testes and epididymides, marked histopathological abnormality of the testis, reduced weight of the right testis and epididymis, and decreased sperm motility and counts in the left cauda epididymis (P < 0.01). With the increasing dose of carbendazim, the apoptosis rate and Bax expression were significantly raised, while the expression of Bcl-2 significantly decreased (P < 0.05, P < 0.01).</p><p><b>CONCLUSION</b>Carbendazim affects the testicular development and spermatogenic function of male rats, and the mechanism may involve cell apoptosis induced by down-regulation of Bcl-2 and up-regulation of Bax.</p>

Effects of Benzimidazole on Spermatogenesis Function and Enzymatic Activity in Testis of Rats / 环境与健康杂志

Objective To explore the effects of benzirnidazole on spermatogenesis function and enzymatic activity in testis of male rats.Methods 40 male Wistar rats,clean degree,were randomly divided into four groups,10 in each.The rats in the low- dose group (20 mg/kg),the moderate-dose group (100 mg/kg) and the high-dose (200 mg/kg) were treated with benzimidazole at different doses by garage,once a day for 80 consecutive days.Simultaneously,the rats control group were treated with the equivalent volume of distilled water and tween-80.In the end of the experiment,the rats were weighed,the testis and epididymides were immediately excised and weighed,the appearance was observed,and the viscera coefficients of the bilateral testis and epididymides were calculated.The number and motility of sperms in the tail of epididymis,the activity of some enzymes (LDH, ACP,SDH,G-6-PDH) of testis were tested.Results The testis and epididymides in the control group and the low-dose group were pink,large,smooth and plump,but they were mauve,small,obviously atrophic in the moderate-dose group and the high-dose group. The viscera coefficient of the testis and epididymides,the number and motility of sperms in the tail of epididymis were significantly decreased in the moderate-dose group and the high-dose group (P

Brain impairment induced by oral intake of lead and its effects on expression of Hoxa9 Gen in Rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To observe effects of oral intake of lead on the expression of Hoxa9 gen and the ability of learning and memory and explore the the toxic molecular mechanisms of lead.</p><p><b>METHODS</b>Thirty male Wistar rats were chosen and randomly divided into the low lead dosage group, the high lead dosage group and the control group, 10 rats in each group. The low lead dosage group and the high lead dosage group were given respectively 0.06%, 0.2% lead acetate orally while the control group was given distilled water orally. The Y-maze test was used to measure the ability of learning and memory, the graphite heat atomic absorption spectrum method to determine the lead concentration in blood and brain, and the in situ hybridization (ISH) method to determine the expression of Hoxa9 mRNA in brain.</p><p><b>RESULTS</b>(1) The number of electric shocks of the lead poisoned rats were significantly increased over time. The number of electric shocks of the lead poisoning rats was much higher than that of the control group (P < 0.01) (at the end of the experiment, the low lead dosage group: 31.8 +/- 2.26; the high lead dosage group: 37.3 +/- 1.70; the control group: 18.4 +/- 1.51). (2) The brain of the lead poisoned rats including the hippocampus, the cerebellum and the cerebral cortex were significantly atrophic and the apoptosis and necrosis occurred in the cells of the brain. Purkinje's cells in the cerebellum showed significant necrosis and disappearance. The structure of brain in rats of the control group demonstrated no atrophy. (3) The expression of Hoxa9 mRNA in the lead poisoned rats was significantly decreased compared with the control group. There were few Hoxa9 positive cells in the brain of the lead poisoned rats, but many of them were observed in the control group.</p><p><b>CONCLUSION</b>Lead may inhibit the expression of Hoxa9 and induce atrophy and necrosis of brain, which gives rise to a damage of learning and memory.</p>