Omega-3 polyunsaturated fatty acids alleviate adenine-induced chronic renal failure via regulating ROS production and TGF-ß/SMAD pathway.

The article "Omega-3 polyunsaturated fatty acids alleviate adenine-induced chronic renal failure via regulating ROS production and TGF-ß/SMAD pathway", by J. Xu, Z.-P. Feng, H.-Y. Peng, P. Fu, published in Eur Rev Med Pharmacol Sci 2018; 22 (15): 5024-5032-DOI: 10.26355/eurrev_201808_15645-PMID: 30070341, has been retracted by the authors due to input errors which occurred in the experimental data. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/15645.

Investigation on the mechanism of p38MAPK in the failure of autogenous arteriovenous fistula caused by stenosis.

The present study aimed to probe into the mechanism of p38MAPK in the failure of autogenous arteriovenous fistula (AVF) caused by stenosis. A total of 24 patients with maintenance hemodialysis and the autologous AVF as the hemodialysis route were enrolled in the present study. In the experimental group, the internal fistula operation mode was the end-to-side anastomosis, and patients were those who needed autogenous AVF repair due to the venous hyperplasia and stenosis of the internal fistula anastomosis (n = 12). The control group was composed of patients who underwent autogenous AVF surgery for the first time (n = 12). The discarded venous tissues in each group were used for immunohistochemistry and Western blot detection of ASK1, P38, and ATF-2. SPSS 17.0 and GraphPad Prism 5 software were adopted for data analysis. The measurement data were expressed as means ± standard deviations ( x ± s), and P < 0.05 was considered statistically significant. The results of immunohistochemistry staining: the expressions of ASK1, P38, and ATF-2 in the experimental group were significantly higher than those in the control group, and the differences were statistically significant (P < 0.01). The results of Western blot: the expression of P38 in the experimental group was significantly higher than that in the control group, and the difference was statistically significant (P < 0.05). There was no significant difference in the expression of ASK1 and ATF-2 between the experimental group and the control group (P > 0.05). In stenotic AVF, the expressions of ASK1, P38, and ATF-2 all significantly increased, indicating that the p38MAPK signaling pathway might be involved in the formation of venous stenosis in AVF, and the p38MAPK signaling pathway might become a therapeutic target in preventing and treating the vascular stenosis in the fistula.

Omega-3 polyunsaturated fatty acids alleviate adenine-induced chronic renal failure via regulating ROS production and TGF-ß/SMAD pathway.

OBJECTIVE: To explore the role of omega-3 polyunsaturated fatty acids (ω-3 PUFAs) in adenine-induced rat chronic renal failure and its underlying mechanism. MATERIALS AND METHODS: 30 Sprague Dawley (SD) rats were randomly assigned into three groups, namely sham group, adenine induction group (adenine group) and adenine induction + ω-3 PUFAs treatment group (ω-3 PUFAs group), with 10 rats in each group. Serum and kidney samples were collected after rats were sacrificed. Serum levels of Cr (creatinine) and BUN (urea nitrogen) were detected using commercial kits. HE (hematoxylin and eosin) staining was performed to evaluate the pathological changes of kidneys. Levels of oxidative stress indicators in rat kidney homogenate were detected by relative commercial kits, including SOD (superoxide dismutase), GSH (reduced glutathione), CAT (catalase), and T-AOC (total antioxidant capacity). Reactive oxygen species (ROS) production was also detected by immunofluorescence. Protein expressions of nuclear factor E2 related factor 2 (Nrf2) and transforming growth factor-beta (TGF-ß)/SMAD pathway-related genes were detected by Western blot. RESULTS: Serum levels of Cr and BUN in ω-3 PUFAs group were remarkably decreased compared with those of adenine group. Higher contents of SOD, GSH, CAT and T-AOC were observed in ω-3 PUFAs group compared with those of adenine group. Besides, MAD content and ROS production were lower in ω-3 PUFAs group than those of adenine group. Pathological changes of kidneys were alleviated after ω-3 PUFAs treatment. Western blot results demonstrated that ω-3 PUFAs treatment remarkably upregulates Nrf2, HO-1, NQO1, but downregulates relative genes in TGF-ß/SMAD pathway. CONCLUSIONS: ω-3 PUFAs alleviated adenine-induced chronic renal failure through enhancing antioxidant stress and inhibiting inflammatory response via regulating Nrf2 and TGF-ß/SMAD pathway.

The expression of endogenous hydrogen sulfide signal during distraction osteogenesis in a rabbit model.

The hydrogen sulfide (H2S) signal system plays an important role in bone metabolism. However, the role of endogenous H2S during distraction osteogenesis (DO) remains unclear. Sixty-two male New Zealand White rabbits were subjected to right mandibular DO. Before distraction, the animals were divided randomly into two groups: group A, 0.5mm twice/day for 10 days; group B, 1.25mm twice/day for 4 days. Plasma and distraction gap tissue were harvested to determine the H2S signal. The osteogenesis effect was also evaluated. The newly regenerated bone in group A presented a higher level of mineralization and biomechanical strength than that in group B. The bone mineralization density in group A was 1.95-fold that in group B (P=0.028), while the biomechanical strength in group A was 1.26-fold that in group B (P=0.042) at the end of the experiment. The H2S signal was detected during the whole process of DO. The relative plasma H2S concentrations in group A were noticeably higher than those in group B at the middle of distraction (P<0.001), at the end of the distraction (P=0.034), and 2 weeks after the end of distraction (P=0.002). The results suggest that the endogenous H2S signal system plays a major role during DO.

Low level of low-density lipoprotein cholesterol is related with increased hemorrhagic transformation after acute ischemic cerebral infarction.

OBJECTIVE: The prevalence of hemorrhagic transformation (HT) after acute ischemic infarction varies greatly. Risk factors of HT include ageing, severity of stroke, baseline hypertension, high NIH Stroke Scale (NIHSS) scores, hyperglycemia and cardioembolic infarction and low levels of low-density lipoprotein (LDL). We investigated the relationship between LDL, lipid profile and HT after acute ischemic infarction and suggested precautions for HT management. PATIENTS AND METHODS: Three hundred and forty-eight patients with acute infarction were included in the study. Fasting lipid profile was examined on the next morning following hospitalization. Either MRI GRE-T2*WI or CT was performed, one week after hospitalization to detect any cerebral microbleed (CMB) and hemorrhagic transformation. The lipid profiles examined included total cholesterol (TCH), triglyceride (TG), LDL and high-density lipoprotein (HDL). RESULTS: Among all the patients, HT was noted in 35 patients and non-HT in 313. As compared with non-HT group, HT group had lower levels of TCH, HDL and LDL, lower rates of leukoaraiosis and CMB, but higher scores of NIHSS, higher rates of diabetes mellitus, atrial fibrillation and urokinase thrombolysis. The multivariate binary logistic regression showed that cardioembolic infarction, infarction with undetermined etiology, high scores of NIHSS and diabetes were the risk factors of HT, while the protective factor was LDL (OR=0.654, 95% CI: 0.430-0.996, p=0.048). CONCLUSIONS: Low level of LDL is likely associated with increased HT after acute ischemic infarct, so for those patients with low level of LDL, high scores of NIHSS and cardioembolic infarction at admission, aggressive lipid- lowering treatment should be prescribed cautiously to prevent the incidence of HT.

A nucleation site and mechanism leading to epitaxial growth of diamond films

A diamond nucleation site responsible for epitaxial growth of diamond on silicon by chemical vapor deposition (CVD) is identified in high-resolution transmission electron microscopic images. Other sites in the same sample leading to polycrystalline growth, but deleterious to epitaxial CVD growth, are also described. A mechanism for the heteroepitaxial growth of diamond is suggested, in which etching of the nondiamond carbon binder exposes and removes nonadherent nanodiamond nuclei, leaving intact only those directly nucleated on the silicon substrate. This work enhances our understanding of diamond nucleation and heteroepitaxial growth and its potential applications.