论卫生船舶在登陆作战中的配置

在大规模登陆作战中需要大量的卫生船舶实施各种保障,因此必须对卫生船舶进行合理的配置,保证其既能有效地完成保障任务,又能避免重叠配置造成浪费．卫生船舶的配置应与指挥关系、保障任务战时分类相适应,具体配置时按医院船、卫生运输船、卫生救护艇的保障要求配置,并可根据保障任务的变化进行相应的调整．     

微波和磁疗治疗膝关节骨性关节炎300例

1临床资料①对象:本组骨性关节炎患者300(男130,女170)例,年龄36～78(56±1.0)岁,病程1 mo～10 a,其中左膝120例,右膝112例,双膝68例.临床表现为关节疼痛、僵直、活动受限,偶尔会关节肿胀、关节腔积液.X线表现为关节间隙变窄,关节软骨下骨质致密,骨密度增高,骨小梁有断裂,髁间嵴变尖及髌骨后缘和外侧缘增生形成骨刺[1].     

Validity of silver, chitosan, and curcumin nanoparticles as anti-Giardia agents

This study was carried out to evaluate the anti parasitic potential of silver, chitosan, and curcumin nanoparticles as anti-Giardia agents. Non-treated infected control rats were inoculated with Giardia lamblia cysts in a dose of 2?×?10(5) cysts/rat. Experimental group was infected then treated with curcumin, curcumin nanoparticles, chitosan, chitosan nanoparticles, and silver nanoparticles as single or combined therapy. The number of Giardia cysts in stools and trophozoites in intestinal sections were detected. Toxicity of nanoparticles was evaluated by comparing hematological and histopathological parameters of the normal control group and treated non-infected control group. The amount of silver was also measured in the liver, kidney, small intestine, lung, and brain of rats treated with silver nanoparticles. The number of the parasites in stool and small intestinal sections decreased in treated infected rats compared with infected non-treated ones. The effect in the single therapy was better with nanoparticles, and the best effect was detected in nano-silver. The combined therapy gave better results than single. Combination between nanoparticles was better than the combination of nano-forms and native chitosan and curcumin. The best effect was detected in combinations of nano-silver and nano-chitosan but with no full eradication. In conclusion, the highest effect and complete cure was gained by combining the three nano-forms. The parasite was successfully eradicated from stool and intestine. None of the treatments exhibited any toxicity. Accumulated silver in different organs was within the safe limits.     

Investigation of brain-derived neurotrophic factor (BDNF) gene expression in hypothalamus of obese rats: Modulation by omega-3 fatty acids

Purpose: The aim of this study was investigating the effect of omega-3 fatty acids (ω-3 FAs) on brain-derived neurotrophic factor (BDNF) gene expression, using in vivo and in vitro models, to unravel the potential mechanisms of polyunsaturated fatty acids use in obesity.

Materials and methods: Twenty-nine Sprague-Dawley rats were divided into three groups; lean controls fed normal chow diet for 14 weeks, obese controls fed 60% of their diet as saturated fats for 14 weeks, and ω-3 FAs-treated rats fed 60% saturated fat diet for 14 weeks with concomitant oral administration of 400?mg/kg/day ω-3 FAs, mainly docosahexaenoic acid and EPA, from week 12 to week 14. For the in vitro experiment, hypothalamic cells from six obese rats were cultured in the presence of different concentrations of ω-3 FAs to determine its direct effect on BDNF expression.

Results: In vivo results showed that obesity has negative effect on BDNF gene expression in rat hypothalamus that was reversed by administration of ω-3 FAs. Obese rats showed hypercholesterolemia, hypertriglyceridemia, normoinsulinemia, hyperglycemia and hyperleptinemia. Treatment with ω-3 FAs showed significant decrease in serum total cholesterol and TAG. Also serum glucose level and HOMA index were decreased significantly. In vitro results demonstrated the increase in BDNF expression by ω-3 FAs in a dose-dependent manner.

Conclusions: Obesity causes down-regulation of BDNF gene expression that can be reversed by ω-3 FAs treatment, making them an interesting treatment approach for obesity and metabolic disease.     

Exacerbation by nicotine of the cyclosporine A-induced impairment of beta-adrenoceptor-mediated renal vasodilation in rats

Nicotine is implicated in smoking-related renovascular impairment and worsening of existing nephropathies. In the present study, we investigated whether nicotine aggravates the deleterious effect of the immunosuppressant drug cyclosporine A (CsA) on renal vasodilation induced by the beta-adrenoceptor agonist isoprenaline. Bolus isoprenaline (0.03-8.0 micromol) elicited dose-dependent vasodilation of phenylephrine-preconstricted perfused kidneys that was attenuated by infusion at 5 mL/min of nicotine (5 x 10(-4) mol/L) or CsA (2 micromol/L). Further, chronic administration of nicotine (0.4 mg/kg per day) or CsA (20 mg/kg per day) for 3 weeks reduced isoprenaline-induced vasodilation and elevated plasma urea and creatinine concentrations, effects that were magnified when both nicotine and CsA were administered concurrently. The role of endothelial and smooth muscle signalling in the acute nicotine/CsA renovascular interaction was investigated. Vasodilation caused by 0.25 micromol isoprenaline was attenuated by 6 micromol/L propranolol and 10 mmol/L tetraethylammonium (TEA), potentiated by 100 micromol/L hexamethonium and 7 micromol/L diclophenac, and virtually abolished in 80 mmol/L KCl-preconstricted tissues. N(G)-Nitro-L-arginine (L-NNA; 200 micromol/L), methylene blue (10 micromol/L), 3-[(3-cholamidopropyl)-dimethyl-ammonio]-1-propane-sulphonate (CHAPS; 0.2% for 30 s), nifedipine (750 nmol/L), atropine (1 micromol/L) and SQ22536 (an adenylyl cyclase inhibitor; 3 x 10(-5) mol/L) had no effect on isoprenaline responses. Nicotine (5 x 10(-4) mol/L) reduced isoprenaline-induced vasodilation and this effect was potentiated by concurrent CsA (2 micromol/L) infusion. Nicotine-induced impairment of the vasodilator response to isoprenaline was reduced by hexamethonium and potentiated by L-NNA, methylene blue, CHAPS and nifedipine. Alternatively, CsA exacerbation of the nicotine-isoprenaline interaction was abolished by propranolol, L-NNA, methylene blue, CHAPS, L-arginine, TEA and nifedipine. 5. In summary, nicotine and CsA produce additive impairment of kidney function and beta-adrenoceptor-mediated renovascular control, nitric oxide (NO)-cGMP signalling tonically restrains nicotine-induced impairment of isoprenaline vasodilation and the endothelial NO-K+ pathway modulates the aggravating effect of CsA on nicotine-isoprenaline interactions.     

Preparation and distribution of 5-fluorouracil 125I sodium alginate-bovine serum albumin nanoparticles

ＮＴＲＯＤＵＣＴＩＯＮＮａｎｏｐａｒｔｉｃｌｅ（ＮＰ）ｉｓａｎｃｏｌｏｉｄａｌｄｉｓｐｅｒｓｉｏｎｓｙｓｔｅｍ,ｗｉｔｈｄｉａｍｅｔｅｒｓｒａｎｇｉｎｇｆｒｏｍ１０ｎｍｔｏ１０００ｎｍ．Ｔｈｅｐａｒｔｉｃｌｅｓｅｘｉｓｔｍａｉｎｌｙｉｎｔｈｅｏｒｇａ...     

靶向化疗:基因治疗研究的新热点

１原文要点作者应用逆转录病毒感染法将目的基因Ｇ１ＣＥＡＣＤＮａ及ｐＣＤ２分别转导入高分泌ＣＥＡ的大肠癌细胞系（Ｌｏｖｏ）中,再分别接种到裸鼠皮下,成瘤后腹腔给予５ＦＣ（５００ｍｇ／ｋｇ·ｄ）治疗,疗程４０ｄ,结果显示含Ｇ１ＣＥＡＣＤＮａ及ｐＣＤ２逆...