对《伤寒杂病论》亡血家禁汗之辨析

《伤寒杂病论》亡血家见于发汗禁忌的条文中而未提及治则治法,文章试从原文、注解及辨证论治等方面进行阐述。

艾迪注射液对晚期肺癌患者外周血淋巴细胞凋亡及Treg细胞的影响研究

目的:观测艾迪注射液对晚期肺癌患者外周血淋巴细胞凋亡及Treg细胞的动态变化,探讨其对晚期肺癌患者免疫功能的影响。方法:收集2004年7月～2011年9月晚期肺癌患者86例,随机分为艾迪治疗组52例,非艾迪治疗组34例,并以健康志愿者作为对照组。以流式细胞术动态检测各试验组在使用艾迪15 d、30 d、60 d的外周血单个核细胞(PBMC)中淋巴细胞凋亡率及Treg细胞(CD4+CD25+T cell)数量的变化。结果:肺癌患者外周血中淋巴细胞凋亡率明显高于对照组及艾迪治疗组。经艾迪治疗后的肺癌患者淋巴细胞凋亡率明显下调。肺癌患者外周血中CD4+CD25+T细胞的数量明显高于对照组及艾迪治疗组,艾迪注射液治疗后肺癌患者外周血中CD4+CD25+T细胞的数量可明显下调。结论:艾迪注射液能降低晚期肺癌患者外周血淋巴细胞凋亡率。下调CD4+CD25+T细胞的数量,可能有改善晚期肺癌患者免疫状态的作用。

《高注金匮要略》“忘血”释疑

清代高学山在其学术著作《高注金匮要略》一书中《血痹虚劳病脉症治第六》篇中多次使用"忘血"一词,而《金匮要略》原文及后人对本书批注或校订时均写作"亡血"。就这种文字上的差异及高氏所谓"忘血"的含义予以分析,得出"忘血"与"亡血"辞异义同,并非高学山使用有误的结论。

Pinacidil reduces neuronal apoptosis following cerebral ischemia-reperfusion in rats through both mitochondrial and death-receptor signal pathways

Objective To investigate effect of pinacidil, an ATP sensitive potassium channel （KATP） opener, on the neuronal apoptosis and its signaling transduction mechanism following focal cerebral ischemia-reperfusion in rats. Methods One hundred male Wistar rats were randomly divided into four groups： A, sham-operated group; B, ischemia-reperfusion group; C, KATe opener treatment group; and D, KATe opener and blocker treatment group. The middle cerebral artery occlusion （MCAO） model was established by using the intraluminal suture occlusion method, neuronal apoptosis was determined by TUNEL staining, and expressions of caspase-8, caspase-9 and caspase-3 mRNA were detected by in situ hybridization. Results （1） The numbers of apoptotic neurons at 12 h, 24 h, 48 h, and 72 h were significantly less in group C than in groups B and D （P 〈 0.01 or P 〈 0.05）; and there was no difference between groups B and D at all time points （P 〉 0.05）. （2） The expressions of caspase-3 mRNA and caspase-8 mRNA at all times and the expressions of caspase-9 mRNA at 12 h, 24 h, 48 h, 72 h were significantly lower in group C than in groups B and D （P 〈 0.01 or P 〈 0.05）; and there were no differences between groups B and D at all time points （P 〉 0.05）. Conclusions KATP opener can significantly decrease the neuronal apoptosis and the expressions of caspase-3, caspase-8 and caspase-9 mRNAs following cerebral ischemiareperfusion. The neuronal apoptosis may be decreased by the inhibition of both mitochondrial and death-receptor signal pathways.

《伤寒论》“家”字注

《伤寒论》中“家”字约用10次之多,但其含义不尽一致。有的认为“凡家字皆指宿疾而言”,有的则归纳为15种含义。如将“家”字集中起来对比、归纳,则可以发现这些“家”字有一个共同的特点。

Correlation of free radical level and apoptosis after intracerebral hemorrhage in rats

Objective To investigate the correlation of perihematomal free radical level and neuronal apoptosis following the intracerebral hemorrhage （ICH）. Methods Animals were randomly divided into 4 groups： sham operation group, model group, 1 mg/kg edaravone group, and 3 mg/kg edaravone group. Each group was then divided into seven subgroups, in which the rats were correspondingly killed at 6 h, 12 h, 24 h, 48 h, 72 h, 7 d or 14 d （n = 1 in each subgroup of the sham group, and n = 6 in each subgroup of the other 3 groups）. By Horseley-Clarke technique, autoblood （80 μL） were administered into the left caudate putamen of SD rats in a double administration-withdrawal way. Rats in the sham group were needled in but not administered with autoblood. The ICH model was then evaluated by Bederson＇s scale. Around the hematoma, the levels of malonaldehyde （MDA） and hydroxyl radical were tested by spectrophotometer, and the process of apoptosis was tested by terminal deoxynucleofidyltransferase-mediated dUTP-biotin nick end labeling （TUNEL） method. Results （1） ICH significantly increased the levels of MDA and hydroxyl radicals. Significant differences in MDA and hydroxyl radical contents were observed among the four groups. （2） In the sham group, a small number of TUNEL-positive cells were found. In the other three groups, the TUNEL-positive cells were observed at 6 h, increased significantly at 24 h, and reached peak level at 3 d, then fell profoundly at 7 d, but remained detectable at 14 d. （3） The positive correlation existed between apoptosis and free radical level （r = 0.2003）, and existed between apoptosis and MDA content （r = 0.6563） in the brain. Conclusion Post-hemorrhagic apoptosis was related to the production of free radicals, indicating that the elevated free radicals following the ICH could induce neuron and glial cell apoptosis.

Inhibitory Effect of Oridonin on the Proliferation of NB4 Cells and Its Mechanism

Objective: To investigate the anti-proliferation e?ect of oridonin on leukemic NB4 cells and its mechanism. Methods: NB4 cells in culture medium in vitro were given di?erent concentrations of oridonin. The inhibitory rate of the cells were measured by MTT assay, cell apoptotic rate was detected by ?ow cytometry(FCM), morphology of cell apoptosis was observed by hoechst 33258 ?uorescence staining , and the activity of telomerase was detected using TRAP-PCR-ELISA before and after apoptosis occurred. Results: Oridonin (over 8 μmol/L) could decrease the telomerase activity, inhibit the growth of NB4 cells and induce apoptosis signi?cantly in a time- and dose-dependent manner. Marked morphological changes of cell apoptosis were observed by hoechst 33258 ?uorescence staining especially after the cells treated by oridonin for 48–60 h. Conclusion: Oridonin could inhibit the proliferation and induce the apoptosis of NB4 cells in vitro. One of the mechanisms may be the decrease of the telomerase activity of NB4 cells.

桂枝加龙骨牡蛎汤临床运用举偶

桂枝加龙骨牡蛎汤为仲景方,见于《金匮要略》,主治＂男子失精,女子梦交＂,巳为医家所共知。然就笔者十余年来临床运用本方,不仅可治＂失精梦交＂,并对遗尿、盗汗、自汗、乳泣、亡血等证,均有卓效。

"En avancant…" ; réflexions sur le profil conceptuel des Illuminations

La poésie de Rimbaud et surtout le recueil des Illuminations, ont un attrait universel. On le volt bien ces jours-ci àl’occasion de ce colloque à l’Université de Wuhan. Cet attrait ne s’explique pas seulement, semble-t-il, par les enseignements qu’on y trouve concernant l’époque historique mouvementée clans laquelle vivait Rimbaud, ni par les reflets qui éelairent certains épisodes de sa

Effect of Activation-induced Cell Death of Peripheral Blood Mononuclear cells in Patients with Condyloma Acuminatum

Objective: To investigate the effect of activation-induced cell death (AICD) on cellular immune function in the condyloma acuminatum(CA). Methods: Peripheral blood mononuclear cells (PBMC) were isolated from normal healthy individuals (control group) and patients with CA. PBMC were cultured with PHA-P for 48h in vitro. Apoptosis of the PBMC was detected by flow cytometry. Supernatant cytokines (IL-2 and IL-10) were assayed by ELISA. Results: The rate of PBMC apoptosis in both CA group and control group in fresh PBMC was very low and similar in both groups(P>0.05). The rate of PBMC apoptosis within the CA group was noticeably increased compared to that of the control (P<0.001)af-ter PBMC were cultured for 48h. The level of IL-2 was significantly lower in the CA group than in the control group (P<0.001), The level of IL-10 was significantly higher in the CA group compared to thecontrol group(P<0.001). Conclusion: Study results indicate that AICD may affect cellular mediated immune function and play an important role in the pathogenesis of CA.

Mechanisms of lysosomal proteases participating in cerebral ischemia-induced neuronal death

There are three different types of cell death, including apoptosis （Type I）, autophagic cell death （Type II）, and necrosis （Type III）. Ischemic neuronal death influences stroke development and progression. Lysosomes are important organelles having an acidic milieu to maintain cellular metabolism by degrading unneeded extra- and intracellular substances. Lysosomal enzymes, including cathepsins and some lipid hydrolases, when secreted following rupture of the lysosomal membrane, can be very harmful to their environment, which results in pathological destruction of cellular structures. Since lysosomes contain catalytic enzymes for degrading proteins, carbohydrates and lipids, it seems natural that they should participate in cellular death and dismantling. In this review, we discuss the recent developments in ischemic neuronal death, and present the possible molecular mechanisms that the lysosomal enzymes participate in the three different types of cell death in ischemic brain damage. Moreover, the research related to the selective cathepsin inhibitors may provide a novel therapeutic target for treating stroke and promoting recovery.

Inhibition of Telomerase with hTERT Antisense Increases Susceptibility of Leukemic Cells to CDDP-induced Apoptosis

Objective: To investigated the e?ect of inhibition of telomerase with hTERT antisense on leukemic cells (HL-60 and K562) to CDDP-induced apoptosis. Methods: Antisense phosphorothioate oligodeoxynucleotide (AS PS-ODN) was synthesized and puri?ed. Telomerase activity was detected by Telomerase PCR ELASA kit and cell apoptosis was observed by morphological method and determined by ?owcytometry. Results: AS PS-ODN could signi?cantly inhibit telomerase activity by down regulat- ing the hTERT expression, and increase the susceptibility of leukemic cells to CDDP-induced apoptosis. Conclusion: Inhibition of telomerase with hTERT antisense can increases the susceptibility of leukemic cells to CDDP-induced apoptosis.

Genistein inhibits invasive potential of human hepatocellular carcinoma by altering cell cycle, apoptosis, and angiogenesis

AIM： To study the in vitro and in vivo inhibitory effects of genistein on invasive potential of Bel 7402 hepatocellular carcinoma （HCC） cells and to explore the underlying mechanism. METHODS： Bel 7402 HCC cells were exposed to genistein. The invasive activity of tumor cells was assayed in transwell cell culture chamber, p125^FAK expression and cell cycle were evaluated by a functional assay. Cell apoptosis analysis was performed with TUNEL method. In addition, bilateral subrenal capsule xenograft transplantation of HCC was performed in 10 nude mice. Genistein was injected and the invasion of HCC into the renal parenchyma was observed. Nicrovessels with immunohistochemical staining were detected. RESULTS： Genistein significantly inhibited the growth of Bel 7402 cells, the inhibitory rate of tumor cells was 26 -42%. The invasive potential of Bel 7402 cells in vitro was significantly inhibited, the inhibitory rate was 11- 28%. Genistein caused G2/M cell cycle arrest, S phase decreased significantly. The occurrence of apoptosis in genistein group increased significantly. The expression of p125^FAK in 5 μg/mL genistein group （15.26±0.16%） and 10 μg/mL genistein group （12.89±0.36%） was significantly lower than that in the control group （19.75± 1.12%, P〈0.05）. Tumor growth in genistein-treated nude mice was significantly retarded in comparison to control mice, the inhibitory rate of tumor growth was about 20%. Genistein also significantly inhibited the invasion of Bel 7402 cells into the renal parenchyma of nude mice with xenograft transplant. The positive unit value of microvessels in genistein-treated group （10.422 ±0.807） was significantly lower than that in control group （22.330 ± 5.696, P〈 0.01）. CONCLUSION： Genistein can effectively inhibit the invasive potential of Bel 7402 HCC cells by altering cell cycle, apoptosis and angiogenesis, inhibition of focal adhesion kinase may play a significant role in this process.

Inhibitive effects of anti-oxidative vitamins on mannitol-induced apoptosis of vascular endothelial cells

Objective: Study blood vessel injury and gene expression indicating vascular endothelial cell apoptosis induced by mannitol with and without administration of anti-oxidative vitamins. Methods: Healthy rabbits were randomly divided into four groups. Mannitol was injected into the vein of the rabbit ear in each animal. Pre-treatment prior to mannitol injection was per- formed with normal saline (group B), vitamin C (group C) and vitamin E (group D). Blood vessel injury was assessed under electron and light microscopy. In a second experiment, cell culture specimen of human umbilical vein endothelial cells were treated with mannitol. Pre-treatment was done with normal saline (sample B), vitamin C (sample C) and vitamin E (sample D). Total RNA was extracted with the original single step procedure, followed by hybridisation and analysis of gene expression. Results: In the animal experiment, serious blood vessel injury was seen in group A and group B. Group D showed light injury only, and normal tissue without pathological changes was seen in group C. Of all 330 apoptosis-related genes analysed in human cell culture specimen, no significant difference was seen after pre-treatment with normal saline, compared with the gene chip without pre-treatment. On the gene chip pre-treated with vitamin C, 45 apoptosis genes were down-regulated and 34 anti-apoptosis genes were up-regulated. Pre-treatment with vitamin E resulted in the down-regulation of 3 apoptosis genes. Conclusion: Vitamin C can protect vascular endothelial cells from mannitol-induced injury.

Neuroprotective Effects of Bushen Decoction Against Glutamate-Induced Neurotoxicity in PC12 Cells

Aim The enhanced effect of Bushen (Kidney-tonifying) decoction (BS) oncultured PC12 cell proliferation and its antagonistic action on neurotoxicity induced by glutamatewere investigated by serum pharmacological method of the Chinese material medica (CMM) in vitro.Methods The effect of BS on cultured PC12 cell activity and its antagonistic action on neurotoxicityinduced by glutamate was observed by MTT method. Flow cytometry and fluorescence microscopetechniques were employed to observe the antagonistic effect of BS on early period apoptosis of PC12cells induced by glutamate. Results The serum with BS was able to enhance activity of PC12 cells andexert antagonistic effect on glutamate-induced neurotoxicity. Meanwhile, these beneficial effectsproduced by BS were found to be the strongest in 20% concentration of in serum BS. Moreover, it caninhibit apoptosis of PC12 cells induced by glutamate , which occurs in the early period. ConclusionBS may exert a potential neuroprotective effect.

Experimental Study on Apoptosis in Leukemia Cells Induced by Econazole

To investigate apoptosis in mouse leukemia cell (WEHI-3) induced by Econazoleand its mechanism. Methods: Apoptosis induced by Econazole was examined by flow cytometry. Freecalcium ([Ca^(2+])i) was determined by Fura-2 fluorescein load technique. The protein was isolatedfrom endoplasmic reticulum of WEHI-3 cells, and then the expression of caspase-12 and caspase-7 wasdetected by Western blot. Results: WEHI-3 cells exhibited typical change of apoptosis when they weretreated by Econazole. [Ca^(2+)]i was significantly higher in Econazole-treated group than incontrol group. The expression of caspase-12 and caspase-7 was increased with the increase ofEconazole concentration. Conclusion: Caspase-12 may play a key role in WEHI-3 apoptosis induced byEconazole.

The apoptosis in various stages of infantile hemangioma

Objective: To detect the apoptosis in various stages of infantile hemangioma. Methods:Total 52 samples of infantile hemangioma (including 8 fresh samples) were included in this study. Agarose gel electrophoresis, transmission electron microscopy(TEM) and in situ TdT mediated dUTP-biotin nick end labeling(TUNEL) staining were used to observe the apoptosis. H-E staining was used to analyze the number of cells,the number and area of microvessels in hemangiomas. Results: The typical “ladder” occurred in the DNA electrophoresis of the hemangioma tissue in the late proferating stage. Many apoptotic cells were found in infantile hemangiomas with TEM. TUNEL staining identified that there were apoptotic cells througout the pathologic evolution of infantile hemangioma and the AI(%) was the highest in the late proferating stage. There existed close relationship between the AI(%) and the total number of cells in hemangioma. Conclusion: The decrease of cells resulted from the apoptosis may be the major cause of the spontaneous involution of infantile hemangioma.

PI 3-kinase pathway is responsible for antiapoptotic effects of atrial natriuretic peptide in rat liver transplantation

AIM： To investigate the in vivo effect of atrial natriuretic peptide （ANP） and its signaling pathway during orthotopic rat liver transplantation.METHODS： Rats were infused with NaCI, ANP （5 μg/ kg）, wortmannin （WH, 16μg/kg）, or a combination of both for 20 min. Livers were stored in UW solution （4℃） for 24 h, transplanted and reperfused. Apoptosis was examined by caspase-3 activity and TUNEL staining. Phosphorylation of Akt and Bad was visualized by Western blotting and phospho-Akt-localization by confocal microscopy.RESULTS： ANP-pretreatment decreased caspase-3 activity and TUNELopositive cells after cold ischemia, indicating antiapoptotic effects of ANP in vivo. The an- tiapoptotic signaling of ANP was most likely caused by phosphorylation of Akt and Bad, since pretreatment with PI 3-kinase inhibitor WM abrogated the ANP-induced reduction of caspase-3 activity. Interestingly, analysis of liver tissue by confocal microscopy showed translocation of phosphorylated Akt to the plasma membrane of hepa- tocytes evoked by ANP.CONCLUSION： ANP activates the PI-3-kinase pathway in the liver in vivo leading to phosphorylation of Bad an event triggering antiapoptotic signaling cascade in ischemic liver.