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A facile liquid-phase exfoliation method to prepare few-layer FeOCl nanosheets in acetonitrile by ultrasonication is reported. The detailed exfoliation mechanism and generated products were investigated by combining first-principle calculations and experimental approaches. The similar cleavage energies of FeOCl (340 mJ m(-2) ) and graphite (320 mJ m(-2) ) confirm the experimental exfoliation feasibility. As a Fenton reagent, FeOCl nanosheets showed outstanding properties in the catalytic degradation of phenol in water at room temperature, under neutral pH conditions, and with sunlight irradiation. Apart from the increased surface area of the nanosheets, the surface state change of the nanosheets also plays a key role in improving the catalytic performance. The changes of charge density, density of states (DOS), and valence state of Fe atoms in the exfoliated FeOCl nanosheets versus plates illustrated that surface atomistic relationships made the few-layer nanosheets higher activity, indicating the exfoliation process of the FeOCl nanosheets also brought about surface state changes., (© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Objective: To evaluate the clinical effects of Yuleshu oral mixture combined with conventional therapy on chronic prostatitis., Methods: Eighty-eight patients with chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) were equally randomized to a control and an experimental group to receive conventional therapy (oral antibiotics, alpha blockers, proprietary Chinese medicine for activating blood circulation and massage of the prostate) and conventional therapy combined with Yuleshu oral mixture respectively. Before and after treatment, the severity of symptoms and sexual function of the patients were evaluated using NIH-CPSI and IIEF-5, their anxiety, depression and other emotional problems assessed with Hamilton Depression Rating Scale (HAMD) and Hamilton Anxiety Scale (HAMA), and the results subjected to statistical analysis., Results: Both the experimental and control groups showed significant improvement in prostatitis symptoms and sexual function after treatment as compared with the baseline (P < 0.01), even more significant in the former than in the latter group, especially in pain symptoms (7.89 +/- 2.82 vs 10.41 +/- 2.55, P < 0.01). Before and after treatment, the HAMA and HAMD score had no significant difference in the control, but there was significant difference in the experimental group. The experimental group exhibited remarkably higher scores after than before treatment on HAMA (24.30 +/- 5.07 vs 13.80 +/- 3.62, P < 0.01) and HAMD (23.81 +/- 5.01 vs 16.23 +/- 5.93, P < 0.01), but not the control group (P > 0.05)., Conclusion: Yuleshu oral mixture can effectively relieve anxiety, depression and other psychological problems in CP/CPPS patients, and improve their clinical symptoms as well. Therefore, it is an effective drug for chronic prostatitis.

Background: Transforming growth factor-β1 (TGF-β1) is known to be a key fibrogenic cytokine in a number of chronic fibrotic diseases, including chronic allograft nephropathy. We examined the effects of inhibition of TGF-β1 expression by RNA interference on renal allograft fibrosis, and explored the mechanisms responsible for these effects., Methods: A Sprague-Dawley-to-Wistar rat model of accelerated kidney transplant fibrosis was used. Sixty recipient adult Wistar rats were randomly divided into four groups: group J (sham-operated group), group T (plasmid-transfected group), group H (control plasmid group), and group Y (transplant only group). Rats in group T were transfected with 200 µg of TGF-β1 short hairpin RNA (shRNA). Reverse transcription-polymerase chain reaction and Western blotting were used to examine the expression of TGF-β1, Smad3/7, E-cadherin, and type I collagen. The distribution of type I collagen was measured by immunohistochemistry. The pathologic changes and extent of fibrosis were assessed by hematoxylin and eosin and Masson staining. E-cadherin and α-smooth muscle actin immunohistochemical staining were used to label tubular epithelial cells and fibroblasts, respectively., Results: Plasmid transfection significantly inhibited the expression of TGF-β1, as well as that of its target gene, type I collagen (P < 0.05 and P < 0.01, respectively). In addition, the degree of fibrosis was mild, and its development was delayed in plasmid-transfected rats. In contrast, TGF-β1-shRNA transfection maintained the expression of E-cadherin in tubular epithelial cells while it inhibited the transformation from epithelial cells to fibroblasts. Blood urea nitrogen and serum creatinine were lower in the plasmid group than in the control groups (P < 0.05 and P < 0.01, respectively)., Conclusions: This study suggests that transfection of a TGF-β1-shRNA plasmid could inhibit the fibrosis of renal allografts. The mechanism may be associated with the downregulation of Smad3 and upregulation of Smad7, resulting in suppressed epithelial-myofibroblast transdifferentiation and extracellular matrix synthesis.

Objective: To investigate the effects of shRNA-transforming growth factor (TGF)-beta1 plasmid upon epithelial-myofibroblast transdifferentiation of renal allograft in rats., Methods: Divided the Wistar rats into 4 groups: Group J (sham-operated group), T (plasmid group), H (vacant plasmid group) and Y (simply transplantation group). The SD to Wistar rat transplant kidney-sclerosis accelerated model was constructed and transfected with the plasmid based on hydromechanics. Transplanted kidneys were collected at Months 1, 2 and 3 post-transplantation. The gene transcriptional levels of TGF-beta1 and E-cadherin were detected by RT-PCR and the protein variation of E-cadherin was examined by Western blotting. The pathological changes and infiltrated inflammatory cells were assessed by HE staining and the immunohistochemical staining of E-cadherin and alpha-SMA used to label epithelial cells and fibroblast in order to exhibit cell transdifferentiation., Results: Compared with Group H and Y, the mRNA transcription of TGF-beta1 was obviously inhibited in the Group T: at Month 3, the TGF-beta1 mRNA of Group T is 0.73 +/- 0.08, significantly lower than Group H and Y (0.92 +/- 0.07 and 0.95 +/- 0.04, both P < 0.01); the expression of E-cadherin was maintained at a high level: at the Month 3, the E-cadherin mRNA of Group T is 0.39 +/- 0.11, significantly higher than Group H and Y (0.15 +/- 0.07, and 0.17 +/- 0.06, both P < 0.01); the E-cadherin protein of Group T is 0.38 +/- 0.08, significantly higher than group H and Y (0.15 +/- 0.07 and 0.15 +/- 0.07, both P < 0.01); epithelial cells were much more and fibroblast was much less than that of Group H and Y; there were also less infiltrated chronic inflammatory cells and extracellular matrix deposition in the Group T., Conclusion: The shRNA-TGF-beta1 plasmid can inhibit the epithelial-myofibroblast transdifferentiation of renal allograft in rats. The mechanisms may be associated with its effects of down-regulating TGF-beta1 and up-regulating E-cadherin.

Objective: To isolate and purify exosomes derived from human bladder transitional cell carcinoma T24 cells, analyze the morphology and protein composition, and investigate the antitumor effect of specific cytotoxic T lymphocytes induced by exosomes., Methods: Exosomes were isolated and purified by ultrafiltration and sucrose gradient centrifugation, and characterized by electron microscopy and Western blot. Dendritic cells were amplified and purified from peripheral blood and pulsed with exosomes. Then they were co-cultured with T cells, and divided into 3 groups: exosome-pulsed DC group, unplused DC group and control group. Alamar-Blue assay was used to evaluate the specific cytolytic activity., Results: The exosomes were in size about 30 approximately 90 nm saucer-shaped membranous vesicles. HSP70, ICAM-1 and CK20 were detected by Western blot. The CTL induced by DC pulsed with exosomes had significant cytolytic activity (P < 0.01)., Conclusion: The exosomes derived from T24 cells are loaded with immunoprotein HSP70 and ICAM-1, and DC pulsed with exosomes can promote the anti-tumor effect of CTLs in vitro.