Objective To study the effect of chitosan-pCrmA nanoparticles on the apoptosis of chondrocytes induced by interleukin-1 beta (IL-1β).Methods Chitosan-pDNA nanoparticles were prepared and characterized.The transfection efficiency of chitosan-mediated pIRES2-EGFP was evaluated using fluorescence microscope.The cytotoxicity of chitosan-pIRES2-EGFP nanoparticles in primary rabbit chondrocytes was analyzed by MTT assay.The expression of chitosan-mediated pCrmA in primary rabbit chondrocytes was verified by Western blotting.The effect of chitosan-mediated CrmA on chondrocytes apoptosis induced by IL-1β were analyzed by TUNEL assay.One-way ANOVA was used to analysis.Results The size of chitosan-pDNA nanoparticles was 50 nm.The pDNA release of chitosan-pDNA nanoparticles appeared as biphasic release at pH 2.0 and pH 7.4 buffer.The expression of CrmA in rabbit primary chondrocytes mediated by chitosan could be detected.The chitosan-pIRES2-EGFP nanoparticles had no cytotoxicity.The apoptosis rate of chondrocytes in the chitosan-pCrmA nanoparticles treated group was significantly lower than that of the chitosan treated group (P＜0.05) and PBS group (P＜0.01).Conclsion Chitosan is an effective non-viral gene transfer vector.The CrmA mediated by chitosan can significantly inhibit chondrocytes apoptosis induced by IL-1β,suggesting that chitosan-pCrmA nanoparticles may be the treatment of osteoarthrifis.

Misdiagnosis and missed diagnosis are common in forensic appraisal of orbital fracture. Now imaging technology is very important for studying the forensic features of orbital fracture and evaluating the degree of injury. This article reviews the classification, pathogenesis and imaging diagnosis of orbital fracture. It may do some help to forensic appraisal of orbital fracture.
Forensic Medicine ; Humans ; Magnetic Resonance Imaging ; Orbital Fractures/diagnosis* ; Tomography, X-Ray Computed

Objective To investigate drug resistance mechanism of aminoglycoside-resistant Acinetobacter baumannii by detecting 16S rRNA methylase gene and three common genes of aminoglycoside-modifying enzymes in Acinetobacter baumannii infected patients at EICU. Methods The 48 Acinetobacter baumannii strains were collected,and antimicrobial susceptibility tests were performed by VITEK automicroscan. The MIC was detected by 2-fold agar dilution method,and genes were analyzed by polymerase chain reaction( PCR) . Results Among 48 strains,28 were highly resistant to aminoglycosides and 20 showed lower resistances. The 16S rRNA armA,APH(3')-I,ANT(3'')-Ia,AAC(6')-Ib genes were detected in 71. 43%,60. 71%,82. 14%, and 53. 57%of the 28 highly resistant strains,but only present in 0. 00%,0. 05%,0. 05%,and 0. 05%of the low-resistant isolates(P<0. 01). Conclusion The aminoglycoside-modifying enzymes and 16S rRNA methylase were frequently found in Acinetobacter baumannii clinical isolates,which is closely related to the high-level resistance to aminoglycoside antibiotics.

OBJECTIVE To determine the functional role of hydrogen sulfide (H2S) in protecting against mitochondrial dysfunction in heart failure through the inhibition of Ca2 +/calmodulin-dependent protein kinaseⅡ (CaMKⅡ) using wild type and CSE knockout mouse models. METHODS Continuous subcutaneous injection isoprenaline (7.5 mg·kg-1·d-1), once a day for 4 weeks to induce heart failure in Male C57BL/6 (6-8 weeks old) mice and CSE-/- mice. 150 μmol·L-1 H2O2 was used to induce oxidative stress in H9c2 cells. Echocardiograph was used to detect cardiac parameters. H&E stain and Masson stain was to observation histopathological changes. Western blot was used to detect protein expression and activity. The siRNA was used to silence protein expression. HPLC was used to detect H2S level. Biotin assay was used to detect the level of S- sulfhydration protein. RESULTS Treatment with S-propyl-L-cysteine (SPRC) or sodium hydrosulfide (NaHS), modulators of blood H2S levels, attenuated the development of heart failure in animals, reduced lipid peroxidation, and preserved mitochondrial function. The inhibition CaMKⅡ phosphorylation by SPRC and NaHS as demonstrated using both in vivo and in vitro models corresponded with the cardioprotective effects of these compounds. Interestingly, CaMKⅡ activity was found to be elevated in CSE-/- mice as compared to wild type animals and the phosphorylation status of CaMKⅡ appeared to relate to the severity of heart failure. Importantly, in wild type mice SPRC was found to promote S-sulfhydration of CaMKII leading to reduced activity of this protein however, in CSE-/- mice S-sulfhydration was abolished following SPRC treatment. CONCLUSION A novel mechanism depicting a role of S-sulfhydration in the regulation of CaMKⅡ is presented. SPRC mediated S-sulfhydration of CaMKII was found to inhibit CaMKⅡ activity and to preserve cardiovascular homeostasis.

OBJECTIVE To determine the functional role of hydrogen sulfide (H2S) in protecting against mitochondrial dysfunction in heart failure through the inhibition of Ca2 +/calmodulin-dependent protein kinaseⅡ (CaMKⅡ) using wild type and CSE knockout mouse models. METHODS Continuous subcutaneous injection isoprenaline (7.5 mg·kg-1 per day), once a day for 4 weeks to induce heart failure in male C57BL/6 (6-8 weeks old) mice and CSE-/- mice. 150 μmol·L-1 H2O2 was used to induce oxidative stress in H9c2 cells. Echocardiograph was used to detect cardiac parameters. H&E stain and Masson stain was to observation histopathological changes. Western blot was used to detect protein expression and activity. The siRNA was used to silence protein expression. HPLC was used to detect H2S level. Biotin assay was used to detect the level of S-sulfhydration protein. RESULTS Treatment with S-propyl-L-cysteine (SPRC) or sodium hydrosulfide (NaHS), modulators of blood H2S levels, attenuated the development of heart failure in animals, reduced lipid peroxidation, and preserved mitochondrial function. The inhibition CaMKⅡ phosphorylation by SPRC and NaHS as demonstrated using both in vivo and in vitro models corresponded with the cardioprotective effects of these compounds. Interestingly, CaMKⅡ activity was found to be elevated in CSE-/- mice as compared to wild type animals and the phosphorylation status of CaMK Ⅱ appeared to relate to the severity of heart failure. Importantly, in wild type mice SPRC was found to promote S-sulfhydration of CaMKⅡ leading to reduced activity of this protein however, in CSE-/- mice S-sulfhydration was abolished following SPRC treatment. CONCLUSION A novel mechanism depicting a role of S-sulfhydration in the regulation of CaMKⅡ is presented. SPRC mediated S-sulfhydration of CaMKⅡ was found to inhibit CaMKⅡ activity and to preserve cardiovascular homeostasis.

To observe the protective effects of drug-contained serum of Lingqi Huangban Granule (LQHBG), a compound traditional Chinese herbal medicine, on oxidative stress-induced injury in rabbit retinal pigment epithelial (RPE) cells in vitro.

Objective The aim of the study is to explore the sexual life situation of adult males with continuous ambulatory peritoneal dialysis (CAPD).Methods Data of experience about sexual life of 12 male CAPD patients was collected using in-depth interview and were analyzed with category approach.Results Five themes were sublimated:declined sexual desire,decreased self-confidence to get and to maintain an erection,restraint of sexual life,changes in sexual and marriage satisfaction,and urgent desire for sexual knowledge.Conclusions There are varying degrees of sexual dysfunction in adult male CAPD patients.Nurses should pay attention to and supply the education of sexual knowledge.

Objective To express a recombinant protein TFPR1 ( the functional region of the snake venom proteins from Trimeresurus flavoviridis) in Pichia pastoris expression system. Methods The target gene was codon-optimized and synthesized according to the sequence of the conserved structural do-main of triflin and then cloned into the Pichia pastoris expression vector pPICZαA to construct the recombi-nant expression plasmid pPICZαA-TFPR1. The recombinant plasmid pPICZαA-TFPR1 was electroporated into the yeast strain X33. The transformed strains carrying expression plasmid were screened out with Zeocin and then induced by methanol to express the recombinant protein TFPR1. ELISA was performed for the screening of positive clones. SDS-PAGE and Western blot were used for further identification of the ex-pressed products. Results The recombinant plasmid pPICZαA-TFPR1 was successfully constructed. The recombinant protein TFPR1 was expressed in a secreted form at a molecular weight of 16×103. Conclusion The recombinant protein TFPR1 was successfully expressed in Pichia pastoris expression system, which laid a foundation for further researches on its biological function and application as an adjuvant.

AIMTo evaluate androgen receptor (AR) expression in clinically localized prostate cancer (PCa).

METHODSSpecimens were studied from 232 patients who underwent radical prostatectomy for clinically localized prostatic adenocarcinoma without neoadjuvant hormonal therapy or chemotherapy at our institution between November 2001 and June 2005. Immunohistochemical study was performed using an anti-human AR monoclonal antibody AR441. The mean AR density in the hot spots of different histological areas within the same sections were compared and the correlation of malignant epithelial AR density with clinicopathological parameters such as Gleason score, tumor, nodes and metastases (TNM) stage and pre-treatment prostate-specific antigen (PSA) value was assessed.

RESULTSAR immunoreactivity was almost exclusively nuclear and was observed in tumor cells, non-neoplastic glandular epithelial cells and a proportion of peritumoral and interglandular stromal cells. Mean percentage of AR-positive epithelial cells was significantly higher in cancer tissues than that in normal prostate tissues (mean +/- SD, 90.0% +/- 9.3% vs. 85.3 +/- ?9.7%, P < 0.001). The histological score yielded similar results. The percentage of AR immunoreactive prostatic cancer nuclei and histological score were not correlated with existing parameters such as Gleason score, tumor, nodes and metastases stage and pre-treatment PSA value in this surgically treated cohort.

CONCLUSIONThe results of the present study suggest that there may be limited clinical use for determining AR expression (if evaluated in hot spots) in men with localized PCa.

Adenocarcinoma ; genetics ; pathology ; surgery ; Aged ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Neoplasm Metastasis ; Neoplasm Staging ; Paraffin Embedding ; Prostate-Specific Antigen ; analysis ; metabolism ; Prostatectomy ; Prostatic Neoplasms ; genetics ; pathology ; surgery ; Receptors, Androgen ; biosynthesis ; genetics

Objective To investigate the causes,consequences and management of injuries to the draining veins after embolization of brain arteriovenous malformations(BAVMs)with ?-n-butyl cyanoacrylate (NBCA).Methods The angiographic imaging data of 189 BAVMs patients who underwent NBCA embolization were studied retrospectively.The status of the draining veins before and after NBCA embolization was observed and compared.The intracerebral hemorrhage(ICH)complications and their relation to their angiographic features were analyzed.Results Twenty-three patients out of 189 patients showed injuries to the draining venous system,including 10 low-grade injury,6 moderate injury,and 7 high- grade injury.Six patients suffered from ICH after embolization,of whom 4 patients were due to injuries of the draining veins(2 moderate and 2 high-grade).In the 3 months follow-up evaluation of 4 patients with ICH, one died,one was in vegetative state,and the other two patients suffered from residual severe or minor (1 patient for each)permanent neurological deficits.Conclusion Our findings suggest that injury of the draining veins is the major cause of ICH and may lead to serious consequences after embolization of BAVMs with NBCA.