Celecoxib induces functional recovery after intracerebral hemorrhage with reduction of brain edema and perihematomal cell death.

The selective cyclooxygenase-2 (COX-2) inhibitor has been reported to have antiinflammatory, neuroprotective, and antioxidant effects in ischemia models. In this study, the authors examined whether a selective COX-2 inhibitor (celecoxib) reduces cerebral inflammation and edema after intracerebral hemorrhage (ICH), and whether functional recovery is sustained with longer treatment. ICH was induced using collagenase in adult rats. Celecoxib (10 or 20 mg/kg) was administered intraperitoneally 20 minutes, 6 hours, and 24 hours after ICH and then daily thereafter. Seventy-two hours after ICH induction, the rats were killed for histologic assessment and measurement of brain edema and prostaglandin E2. Behavioral tests were performed before and 1, 7, 14, 21, and 28 days after ICH. The brain water content of celecoxib-treated rats decreased both in lesioned and nonlesioned hemispheres in a dose-dependent manner. Compared with the ICH-only group, the number of TUNEL-positive, myeloperoxidase-positive, or OX42-positive cells was decreased in the periphery of hematoma and brain prostaglandin E2 level was reduced in the celecoxib-treated group. Celecoxib-treated rats recovered better by the behavioral tests at 7 days after ICH throughout the 28-day period, and the earlier the drug was administered, the better the functional recovery. Evidence of similar effects in an autologous blood-injected model showed that direct collagenase toxicity was not the major cause of inflammation or cell death. These data suggest that celecoxib treatment after ICH reduces prostaglandin E2 production, brain edema, inflammation, and perihematomal cell death in the perihematomal zone and induces better functional recovery.     

Effects of cocaine, exercise, and resting conditions on plasma corticosterone and catecholamine concentrations in the rat

Cocaine and exercise are both known as stressors, but little is known about the combined effects of these two treatments. In this study, rats under the influence of cocaine (12.5 mg/kg, intraperitoneally [IP]) or saline were exposed to a variety of resting conditions, as well as exercise (running, 26 m/min, 10% grade, for 30 minutes), to evaluate the amount of stress imposed by these conditions as determined by the changes in the plasma concentrations of corticosterone (C) and catecholamines (norepinephrine [NE], epinephrine [E], dopamine [DA]). After injection of saline, resting near the operating treadmill for 30 minutes caused the concentration of C to increase from 0.07 +/- 0.03 to 0.30 +/- 0.05 microgram/mL (P less than .05), compared to the increase to only 0.15 +/- 0.04 micrograms/mL after resting in a cage. This increase due to proximity to the treadmill subsided after 50 minutes. After cocaine, the 30-minute resting values were 0.70 +/- 0.15 (treadmill) and 0.55 +/- 0.13 (cage) (P less than .05), and did not subside after 50 minutes. Cocaine also increased levels of E, NE, and DA above those in saline under all rest conditions. With exercise, the value for C in saline increased to 0.61 +/- 0.18, but, in cocaine, the value went to 0.93 +/- 0.05 (P less than .05). The concentrations of E (946 +/- 74 v 603 +/- 101 pg/mL, cocaine v saline) and NE (1,027 +/- 102 v 440 +/- 153, cocaine v saline) during exercise also were exaggerated by cocaine treatment (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)     

IMMUNOREGULATORY EFFECT OF PANAXATRIOL GINSENOSIDE ON IMMUNE FUNCTIONS IN BONE MARROW SUPPRESSED MICE

The effect of Panaxatriol Ginsenoside (PTGS) on Immune functions in bone marrow suppressed mice induced by injection of cyclophosphamide (CY) has been studied. Bone marrow suppressed mice were made by injection of CY (150 mg/kg) parenterally. Subcutaneous injection of PTGS three days earlier partially restored the number and the activity of bone marrow cells, significantly enhanced the production of IL-1, IL- 3 and IL- 6 like substances and promoted the reactivity of murlne spleen cells to Con-A In bone marrow suppressed mice.     

Immunoregulatory effects of phospholipase A2 (PLA2) on the proliferation of human lymphocytes

Extracellular phospholipase A2 (PLA2) is a proinflammatory enzyme found especially in the inflammatory exudate to modulate blood flow to areas of antigen stimulation. In this study we found that PLA2 exerted a biphasic effect on the proliferation of phytohemagglutinin (PHA)-stimulated human mononuclear cells (PHA MNC). At low concentrations range from 0.001 to 1 U/ml, PLA2 enhanced the proliferation of PHA MNC (maximal increase was 37.0 +/- 5.67%). Conversely, at concentrations over 10 U/ml, PLA2 markedly suppressed the PHA-induced MNC proliferation (maximal decrease was 88.86 +/- 2.89%). PLA2 was non-toxic to lymphocytes after three days culture, unless the concentration was higher than 100 U/ml. The membrane polarization of PHA-stimulated lymphocytes was also increased by PLA2 at a low concentration. In addition, PLA2 displayed a similar effect on the proliferation of streptokinase-streptodornase (SK/SD) or allogeneic cell stimulated lymphocytes. The change of lymphocyte proliferation by PLA2, was parallel to the change of percentage of helper T cells. Furthermore--a CD4-rich population was proved more susceptible to PLA2 effect than a CD8-rich population. Para-bromophenacyl bromide (pBPB), an irreversible inhibitor of PLA2, abrogated the biphasic effect of PLA2 on PHA MNC proliferation. These results suggest that PLA2 plays a regulatory role on immune reactions by modulating the percentage of helper T cells.     

冠心病行为模式与心理状态的相关性探讨

目的为探讨Ａ型行为在冠心病（ＣｏｒｏｎａｒｙＨｅａｒｔＤｉｓｅａｓｅ，ＣＨＤ）中的作用及与心理状态的相关性。方法对１１４例ＣＨＤ及３７例非ＣＨＤ应用心理测验方法对照调查。结果发现Ａ型行为的人易患ＣＨＤ。ＣＨＤＡ型行为者在焦虑、抑郁、人际关系、认识、敌对性症状因子分较ＣＨＤ非Ａ型行为者有明显增高。ＣＨＤ非Ａ型行为者也具有一些特有的心理症状。结论ＣＨＤ病人的行为模式与病后的某些心理表现呈正相关。     

白血病患者血浆和外周血白细胞内维生素变化

检测４５例正常人和４４例不同病期白血病血浆和外周血白细胞内维生素Ａ、Ｅ、Ｃ、Ｂ１２和β－胡罗卜素、叶酸浓度。结果表明，初治白血病患者血浆维生素Ａ、β－胡罗卜素降低（Ｐ＜０．０１），未缓期解者血浆β－胡罗卜素和叶酸低于正常（Ｐ＜０．０１和Ｐ＜０．０５）。在初治和未缓解期患者的外周血白细胞内，维生素Ｅ、Ｃ、Ｂ１２和β－胡罗卜素均显著降低（Ｐ＜０．０１～０．００１）。而且，外周血白细胞内维生素代谢异常比血浆更为显著。提示维生素含量变化对于解释病因，预测疗效及估计预后有一定的价值。     

滥用药物与生命质量退化的伦理思考

本文从生命质量的内涵入手,分析了滥用药物的直接和间接、近期和远期的危害,通过论证得出了滥用药物必将引起人类生命质量退化的结论.以期从一个新的认识度唤起人们对滥用药物问题的重视、并由此引出了一些对医学目的以及滥用药物控制措施的思考.     

常见肿瘤患者血清维生素A,E,C水平

本文报告２６０例恶性肿瘤患者血清维生素Ａ、Ｅ、Ｃ水平的测定结果。发现除慢性白血病外，蓁７种恶性肿瘤患者血清维生素Ａ水平平均显著低于健康人（Ｐ＜０．０１）；急性白血，肝癌、食管癌患者血清维生素Ｅ水平显著低于健康人（Ｐ＜０．０５）；急性粒细胞白血病、急性单核细胞白血病、肝癌患者血维生素Ｃ水平显著低于健康人（Ｐ＜０．０１）。本研究工作为维生素Ａ、Ｅ、Ｃ药物在肿瘤临床上的应用提供了参考。     

烧伤后检测血儿茶酚胺类、血糖及血胰岛素的临床意义

我们对３０例住院病人用荧光分光光度法测定了不同烧伤时间、不同烧伤指数（ＢＩ）血儿茶酚胺类（ＣＡ）释放量，以期了解病人的应激状况，同时测血糖（ＢＳ）和用放射免疫法测血胰岛素（ＳＩ）。结果表明烧伤后ＣＡ类释放是持续性的，且有休克和感染两个高峰（Ｐ＜０．０５，Ｐ＜０．０１）；ＣＡ类释放主要是去甲肾上腺素（ＮＥ）的持续性增加，是正常量的两倍以上。休克期ＣＡ类释放如不增加，脓毒症阶段肾上腺素（Ｅ）与去甲肾上腺素从高值骤然下降，且低于休克期。提示：交感－肾上腺系统已处于衰竭状态，死亡似不可避免，而胰岛素分泌正常或相对不足。因此我们认为，ＣＡ类释放增加、糖原异生、胰岛β细胞分泌受抑制，是烧伤后全过程内分泌变化的主要原因。扩容纠酸、早期切痂预防感染以及使用抗ＣＡ类药物是防治的主要措施。