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目的探讨肠神经系统在大鼠重症急性胰腺炎肠动力紊乱时的变化以及柴芍承气汤对大鼠肠道肌间神经丛内一氧化氮合成酶（nNOS）神经元表达的影响。方法将30只SD大鼠随机分为3组：假手术组、模型组、柴芍承气汤组（CSCQD组）;模型组和CSCQD组经胰胆管逆行注射质量浓度为50 g/L的牛磺胆酸钠建立大鼠SAP模型后,分别给予生理盐水和CSCQD药液。测定大鼠的胃肠传递时间,HE染色光镜下观察胰腺的病理变化,用双重免疫荧光染色法观察回肠及结肠肌间神经丛NOS神经元的变化。结果与模型组相比,CSCQD组传递指数（TI）明显升高（P〈0.05）,胰腺组织病理损害明显减轻（P〈0.05）,NOS神经元占总神经元的百分比明显降低（P〈0.05）。结论CSCQD通过逆转肠神经系统NOS神经元的可塑性变化,改善SAP大鼠的肠动力,同时减轻了胰腺的病理损伤。

目的 探讨内皮型一氧化氮合成酶（eNOS)在肺动脉高压的发生、发展及肺血管重建中的作用。方法 经心动超声及多普勒检查，确定为单纯室间隔缺损患者10例为对照组；室间隔缺损合并肺动脉高压患者共30例，为实验组。体外循环建立前取右肺中叶少许肺组织，福尔马林固定，石蜡包埋，SP法免疫组织化学染色，并进行灰度扫描。以管壁厚度占血管外径的百分比（WT％）、管壁面积占血管总面积的百分比（WA％）反映肺血管壁的增厚程度。方差分析进行组间差异比较。结果 先心病患者随肺动脉压力的增高，肺组织eNOS表达呈下降趋势，而肺小血管形态发生明显改变，WT％、WA％明显增高（P＜0.01)。eNOS的表达与肺高压程度、肺血管形态学改变之间存在负相关性(P<0.01)。结论 先心病肺高压的eNOS含量低下，造成内源性一氧化氮（NO）生成减少，在肺动脉高压的发生、发展及肺血管重建中起一定作用。

The effect of Cuscuta chinensis extract on the rabbit penile corpus cavernosum （PCC） was evaluated in the present study. Penises obtained from healthy male New Zealand white rabbits （2.5-3.0 kg） were precontracted with phenylephrine （Phe, 10 pmol I^-1） and then treated with various concentrations of Cuscuta chinensis extract （1, 2, 3, 4 and 5 mg ml^-1）. The change in penile tension was recorded, and cyclic nucleotides in the PCC were measured by radioimmunoassay （RIA）. The interaction between Cuscuta chinensis and sildenafil was also evaluated. The result indicated that the PCC relaxation induced by Cuscuta chinensis extract was concentration-dependent. Pre-treatment with an nitric oxide synthase （NOS） inhibitor （No〉 nitro-L-arginine-methyl ester, L-NAME）, a guanylyl cyclase inhibitor （1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-l-one, ODQ）, or a protein kinase A inhibitor （KT 5720） did not completely inhibit the relaxation. Incubation of penile cavernous tissue with the Cuscuta chinensis extract significantly increased cyclic guanosine monophosphate （cGMP） and cyclic adenosine monophosphate （cAMP） in the PCC. Moreover, the Cuscuta chinensis extract significantly enhanced sildenafil-induced PCC relaxation. In conclusion, the Cuscuta chinensis extract exerts a relaxing effect on penile cavernous tissue in part by activating the NO-cGMP pathway, and it may improve erectile dysfunction （ED）, which does not completely respond to sildenafil citrate.

Oncogenic H-Ras G12V and its variants have been shown to inhibit muscle differentiation. However, the role of proto-oncogenic Ras （c-Ras） in muscle differentiation remains unclear. The active GTP-bound form of Ras has been known to associate with diverse effectors including Raf, phosphatidylinositol 3-kinase （PI3K）, RaI-GDS, and other molecules to transmit downstream signals. We hypothesize that c-Ras may stimulate muscle differentiation by selectively activating PI3K, an important mediator for muscle differentiation. In our experiments, inhibition of c-Ras by farnesyltransferase inhibitors and a dominant negative form of H-Ras （Ras S17N） suppressed muscle differentiation. Consistently, individual knockdown of H-Ras, K-Ras, and N-Ras by siRNAs all blocked muscle differentiation. Interestingly, we found that c-Ras preferentially interacts with PI3K rather than its major binding partner c-Raf, during myogenic differentiation, with total c-Ras activity remaining unchanged. PI3K and its downstream myogenic pathway, the Nox2/NF-kB/inducible nitric oxide synthase （iNOS） pathway, were found to be suppressed by inhibition of c-Ras activity during differentiation. Furthermore, expression of a constitutively active form of PI3K completely rescued the differentiation block and reactivated the Nox2/NF-kB/iNOS pathway in c-Ras-inhibited cells. On the ba- sis of our results, we conclude that contrary to oncogenic Ras, proto-oncogenic H-Ras, K-Ras, and N-Ras are directly involved in the promotion of muscle differentiation via PI3K and its downstream signaling pathways. In addition, PI3K pathway activation is associated with a concurrent suppression of the otherwise predominantly activated Raf/ Mek/Erk pathway.

Dibutyltin dilaurate functions as a stabilizer for polyvinyl chloride. In this study, experimental rats were intragastrically administered 5, 10, or 20 mg/kg dibutyltin dilaurate to model sub-chronic poisoning. After exposure, our results showed the activities of superoxide dismutase and glutathione peroxidase decreased in rat brain tissue, while the malondialdehyde and nitric oxide content, as well as nitric oxide synthase activity in rat brain tissue increased. The cell cycle in the right parietal cortex was disordered and the rate of apoptosis increased. DNA damage was aggravated in the cerebral cortex, and the ultrastructure of the right parietal cortex tissues was altered. The above changes became more apparent with exposure to increasing doses of dibutyltin dilaurate. Our experimental findings confirmed the neurotoxicity of dibutyltin dilaurate in rat brain tissues, and demonstrated that the poisoning was dose-dependent.

The precise aetiology of benign prostatic hyperplasia （BPH） remains unclear; however, it is known that immunological inflammatory processes have a role in the pathogenesis of BPH initiation and progression. Nitric oxide synthase 2 （NOS2） inducible expression is closely correlated with prostatic disease, including prostate cancer and BPH. The aim of this study was to investigate the relationship between NOS2 polymorphisms and BPH. With a cohort of 205 controls and 229 BPH subjects, we genotyped three single nucleotide polymorphisms （SNPs） in the NOS2 gene, including rs2779248 （promoter, -278 T/C）, rs 10459953 （5＇-untranslated region） and rs2297518 （exon 16, missense, Ser608Leu）, using direct sequencing and restriction fragment length polymorphism. The genotypic and allelic frequencies between control and BPH subjects were compared, and the associations among the BPH subjects were analyzed. SNPStats, SNPAnalyzer and HelixTree programmes were used to analyze SNPs. There was no association on SNPs between control and BPH subjects. When BPH subjects were analyzed, there was no association on SNPs between the low and high prostate-specific antigen groups. However, one SNP （rs 10459953, odds ratio [OR] = 0.44, 95% confidence interval [CI] = 0.29-0.65, P 〈 0.0001, in codominant model; OR = 0.23, 95% CI = 0.12-0.46, P 〈 0.0001, in dominant model; and OR = 0.46, 95% CI = 0.24-0.86, P = 0.015, in recessive model） was associated with prostatic volume in BPH. We detected a strong association in genotype frequencies of NOS2 SNP （rs10459953） between subjects with small and large prostatic volume in BPH. The result suggests that NOS2 may be associated with prostatic volume in BPH.

A rat model of middle cerebral artery permanent occlusion was established using the modified Longa method. Successfully established model animals were treated by blood-letting puncture at twelve Jing-Well points of the hand, and/or by injecting mannitol into the caudal vein twice daily. Brain tissue was collected at 24, 48 and 72 hours after modeling, and blood was collected through the retinal vein before Evans blue was injected, approximately 1 hour prior to harvesting of brain tissue. Results showed that Evans blue leakage into brain tissue and serum nitric oxide synthase activity were significantly increased in model rats. Treatment with blood-letting punctures at twelve Jing-Well points of the hand and/or injection of mannitol into the caudal vein reduced the amount of Evans blue leakage into the brain tissue and serum nitric oxide synthase activity to varying degrees. There was no significant difference between single treatment and combined treatment. Experimental findings indicate that blood-letting punctures at twelve Jing-Well points of the hand can decrease blood-brain barrier permeability and serum nitric oxide synthase activity in rats following middle cerebral artery occlusion, and its effect is similar to that of mannitol injection alone and Jing-Well points plus mannitol injection.