Peripheral Nerve and Transgene Cells Transplantation in the Treatment of Experimental Neuropathy of SD Rats

Purpose: To observe whether optic nerve can regenerate by peripheral nerve transplantation and GDNF gene transfer.Methods: Optic nerve was transected about 2 mm posterior to the eye to establish experimental models of optic neuropathy. Sciatic nerve was sutured to the sheath of injury optic nerve by a 10 - 0 nylon, pcDNA3-GDNF was smeared to the joint and injected to the vitreous cavity. The regenerated retinal ganglion cells axons were observed by HRP. The retina and optic nerve were observed by pathohistological methods.Results: Some retinal ganglion cells with regenerated axons could be seen a week after transplantation with large cell bodies. The cells could be identified by HRP. The regenerated nerve fibers grew to the transplanted sciatic nerve. Then the number of retinal ganglion cells with regenerated axons increased with time going. Only a few regenerated retinal ganglion cells could be seen two months after transplantation. The large retinal ganglion cells were seen to have plenty of cytoplasm     

NEUROTROPISM TO TISSUE SPECI FICITY IN NERVE REGENERATION EXPERIMENTAL STUDV ON SCIATIC NERVES OF RAT

Using the left sciatic nerves of 44 rats we studied neurotropism in nerve regeneration. The proximal and distal cut ends of the nerves were separately introduced into the ends of a specially designed silastic Y- or cross-shaped tube. Either the distal stump or a cut end of the Achilles tendon was inserted into the other ends of the tube, or was left empty. The distance between the tissue ends, nerve-to-nerve or nerve-to-tendon, was 4 mm. Four weeks later, neurofibers sprung out from the proximal stump and grew towards the distal nerve end instead of the tendon end or the vacant channel of the tube. This finding suggests that neurotropic factors may influence the direction of growth of the newly formed neurofibers. This paper discusses the mechanism of neurotropism, the effect of the distance between the cut ends of the nerve, and the choice of the silastic material.     

甲状旁腺激素对系膜细胞合成分泌纤连蛋白的影响

在慢性肾病早期,血清甲状旁腺激素(PTH)水平即已显著增高。增高的PTH对大部分组织脏器,都有负性影响,而当行甲状旁腺切除降低PTH水平后,其异常的指标可以得到明显的改善。PTH是一种新型的尿毒症毒素已为学者们所共识。我们曾证实,系膜细胞上也存在PTH受体,PTH与受体结合后,能显著促进系膜细胞的增殖,并刺激系膜细胞合成与分泌TGF-β[1]。为进一步探讨     

胸椎椎体上皮样血管内皮瘤一例

患者女,22岁.反复腰背部酸痛2年,病初疼痛呈间歇性,后呈持续性.体检:腰椎前屈、后伸、侧弯均受限.T12、L1棘突压痛、叩击痛,右侧腰背肌压痛.     

不同剂量猪肺表面活性物质对大鼠油酸型急性肺损伤疗效的影响

目的 探讨不同剂量猪肺表面活性物质（PPS）混悬液对油酸致大鼠急性肺损伤（ALI）的治疗作用及量-效关系。方法56只SD大鼠按随机数字表法分为假手术组、油酸模型组和5个不同剂量PPS治疗组。静脉注入油酸诱发大鼠ALI，30min后治疗组和模型组经气管分别滴入50、80、100、150和200mg／kg PPS和等量生理盐水。实验过程中计数大鼠呼吸频率，测定动脉血气。4h后处死，计算大鼠存活率，观察肺组织形态学改变，并检测肺系数、支气管肺泡灌洗液（BALF）中总蛋白含量和血浆肿瘤坏死因子-α（TNF-α）的浓度。结果与模型组比较，PPS50mg／kg组有减慢呼吸频率、短时间内提高动脉血氧分压（PaO2）的作用，但是并不能明显改善肺损伤；PPS80～200mg／kg组除改善呼吸功能外，大鼠肺毛细血管通透性、肺出血、肺水肿、血浆TNF-α浓度以及大鼠死亡率也均明显降低（P均〈0．05）。显示高剂量PPS（150～200mg／kg）在减轻炎症反应和肺损伤方面具有更好的效果。结论单独应用PPS能明显改善早期油酸型ALI大鼠的呼吸功能，≥80mg／kg的PPS有明显减轻肺损伤的作用，而各剂量之间无量-效关系。     

Does the consumption of green tea reduce the risk of lung cancer among smokers?

Experimental and epidemiological studies were reviewed to assess whether the consumption of green tea could reduce the risk of lung cancer in smokers. Articles published since 1990 were located by searching electronic databases PubMed, Ovid and Science Direct, using keywords 'lung cancer', 'tea' and 'smoking' without any restriction on language. After relevant articles had been located, further papers were obtained from their reference lists. Evidence from experimental studies (in vitro animal and human trials) suggested that regular intake of green tea may be protective against tobacco carcinogens. However, the mechanism behind the protective effect is only partly understood. In most of the epidemiological studies reviewed, the green tea exposure was within 5 years of the interview or follow-up, which would coincide with the induction period and latent period of lung cancer. Longer term studies are thus needed to further quantify the cancer risk. There is some evidence suggesting regular intake of green tea at high level (>3 cups per day) may reduce the risk of smokers developing lung cancer. Improvement in measuring green tea intake is required in order to confirm the evidence from epidemiological studies.     

脂联素对体外培养肝细胞乙醛氧化酶1分泌的影响

目的探讨脂联素（Apm）对体外培养人肝脏细胞乙醛氧化酶1（AOX1）分泌的影响。方法采用基因芯片、逆转录．聚合酶链反应（RT-PCR）分析AOX1 mRNA的表达，用免疫印迹试验分析Apm、5-氨基咪唑4-氨基甲酰胺（AICAR）、二甲双胍、非诺贝特酸（FBA）、棕榈酸及瘦素对体外培养细胞分泌AOX1的影响及AOX1在大鼠脂肪肝中的表达情况。结果Apm、FBA能降低人肝细胞中AOX1 mRNA及其蛋白质的水平，而二甲双胍、AICAR、棕榈酸及瘦素对AOX1的表达没有明显影响。FBA能降低AOX1活性达35％，而二甲双胍对其活性基本没有影响。大鼠脂肪肝肝细胞中Apm分泌明显减少，AOX1的表达明显增多。结论AOX1与肝脏脂肪化有关，Apm能抑制体外培养的人肝脏细胞分泌AOX1。     

Protective Effect of Ginsenoside Rd on Lipopolysaccharide‑Induced Acute Lung Injury through its Anti‑Inflammatory and Anti‑Oxidative Activity

Background: Inflammation and oxidation stress are key factors in the mechanism of acute lung injury(ALI). Therefore, suppression of the inflammatory response and oxidative stress could be a potential strategy to treat lipopolysaccharide(LPS)-induced ALI. Ginsenoside Rd(Rd), a natural Ginseng extract, alleviates inflammation and oxidative stress in several diseases such as Alzheimer's disease and cerebral ischemia, but its effect on ALI is still unclear. Aims and Objectives: To explore the protective effect of Rd on LPS-induced ALI and explored associated mechanisms. Materials and Methods: Mice were divided into five groups: A sham-operated group, a LPS-induced ALI group, and three LPS groups pretreated with Rd doses of 20, 40, and 80 mg/kg, respectively. The pathological changes of lung, collagen deposition, pulmonary edema, inflammatory cytokine, oxidative stress and the expression levels of TLR4 and NF-κB were detected. Results: The oral administration of Rd dose dependently attenuated histopathologic changes in the lung, lung edema, pulmonary collagen deposition, protein concentration in bronchoalveolar lavage fluid(BALF), myeloperoxidase(MPO) activity, and inflammatory cell infiltration. In addition, Rd suppressed the LPS-induced inflammatory cytokines tumor necrosis factor-α, interleukin(IL)-6, and IL-1 β in BALF. The productions of oxidative stress-related enzymes(catalase, superoxide dismutase, and glutathione peroxidase) in lung tissue were significantly upregulated by Rd administration. However, malondialdehyde and pulmonary MPO activity was reduced in the Rd-pretreated groups when compared with LPS-induced ALI group. Rd treatment also dose dependently suppressed LPS-induced NF-κB activation and TLR4 expression. Conclusion: Overall, these findings provide evidence that Rd pretreatment inhibits LPS-induced ALI through anti-inflammatory and antioxidative actions, suggesting that it could be a promising protective drug for LPS-induced ALI.     

Sex Hormones and Androgen Receptor：Risk Factors of Coronary Heart Disease in Elderly Men

Objective To investigate the variation of sex hormone and its receptor level in elderly male patients with coronary heart disease （CHD） and to evaluate the correlations between CHD and sex hormone as well as sex hormone receptor. Methods Altogether 139 male CHD patients （CHD group） aged 60-92 years and 400 healthy men （control group） aged 60-90 years were included in this cross sectional study. The plasma concentrations of dehydroepiandrosterone sulfate （DHEAS）,total testosterone （TT）,free testosterone （FT）,estradiol （E2）,sex hormone binding globulin （SHBG）,luteinizing hormone （LH）,and follicle-stimulating hormone （FSH） were measured. The androgen receptor （AR） was tested by flow cytometry. Correlations between CHD and levels of sex hormones and AR were analyzed. Results Compared with the control group,the levels of DHEAS,TT,FT,SHBG,and the fluorescence intensity of AR in the CHD group significantly reduced （P0.05）,while the levels of FSH and E2 significantly increased （P0.01）. Age was negatively correlated with TT （r=-0.28,P=0.00） and FT （r=-0.17,P=0.01）,while it was positively correlated with SHBG （r=0.14,P=0.04） and E2 （r=0.33,P=0.00）. AR fluorescence intensity was negatively correlated with systolic blood pressure （r=-0.12,P=0.01）. Binary logistic regression analysis showed that TT,SHBG,and AR were all negatively correlated with CHD （P0.05）. Conclusions Elderly male patients with CHD are found to have low levels of DHEAS,TT,FT,SHBG,and AR,while high concentrations of E2 and FSH. Low levels of TT and SHBG may be the potential risk factors of CHD in elderly men.     

Synthesis and evaluation of a new series of tri-, di-, and mono-N-alkylcarbamylphloroglucinols as bulky inhibitors of acetylcholinesterase

1,3,5-Tri-N-alkylcarbamylphloroglucinols (1-4) are synthesized as a new series of bulky inhibitors of acetylcholinesterase that may block the catalytic triad, the anionic substrate binding site, and the entrance of the enzyme simultaneously. Among three series of phloroglucinol-derived carbamates, tridentate inhibitors 1,3,5-tri-N-alkylcarbamylphloroglucinols (1-4), bidentate inhibitors 3,5-di-N-n-alkylcarbamyloxyphenols (5-8), and monodentate inhibitors 5-N-n-alkylcarbamyloxyresorcinols (9-12), tridentate inhibitors 1-4 are the most potent inhibitors of mouse acetylcholinesterase. When different n-alkylcarbamyl substituents in tridentate inhibitors 1-4 are compared, n-octylcarbamate 1 is the most potent inhibitor of the enzyme. All inhibitors 1-12 are characterized as the pseudo substrate inhibitors of acetylcholinesterase. Thus, tridentate inhibitors 1-4 are supposed to be hydrolyzed to bidentate inhibitors 5-8 after the enzyme catalysis. Subsequently, bidentate inhibitors 5-8 and monodentate inhibitors 9-12 are supposed to yield monodentate inhibitors 9-12 and phloroglucinol, respectively, after the enzyme catalysis. This means that tridentate inhibitors 1-4 may act as long period inhibitors of the enzyme. Therefore, inhibitors 1-4 may be considered as a new methodology to develop the long-acting drug for Alzheimer's disease. Automated dockings of inhibitor 1 into the X-ray crystal structure of acetylcholinesterase suggest that the most suitable configuration of inhibitor 1 to the enzyme binding is the (1,3,5)- (cis,trans,trans)-tricarbamate rotamer. The cis-carbamyl moiety of this rotamer does not bind into the acetyl group binding site of the enzyme but stretches out itself to the entrance. The other two trans-carbmayl moieties of this rotamer bulkily block the tryptophan 86 residue of the enzyme.