4-硒硫酸酯多糖的体内抗瘤作用

目的　观察 4-硒硫酸酯多糖 (Se-carra)的体内抗瘤作用。方法　于小鼠右腋皮下接种瘤细胞 2 4h后开始给药 ,连续 10天 ,观察其抑瘤率 ;小鼠腹腔接种肿瘤细胞前或接种后连续给药 10天 ,观察动物的生存时间。结果　 4-硒硫酸酯多糖能明显抑制肿瘤细胞的生长 ,延长小鼠的生存期。结论　 4-硒硫酸酯多糖体内给药有良好的抗瘤效果 ,值得进一步研究。     

针刺对糖尿病视网膜病变免疫调节机理的研究

目的：探讨针刺治疗糖尿病视网膜病变的机理,并加以论证,为其临床应用提供理论依据。方法：选择大鼠建立糖尿病视网膜病变动物模型,分别以针刺治疗及胰岛素治疗,并设正常对照组及模型对照组,于３个月及６个月取大鼠血清及视网膜检测ＩＬ－２和ＴＮＦ及电镜检察。结果：各时段ＩＬ－２针刺及胰岛素治疗组明显高于模型对照组：ＴＮＦ明显氏于模型对照组。两与正常对照组无显性差异,针刺后电镜观察视网膜微血管病变得到改善。     

P^27的研究概况

目的：综述Ｐ＾２７的研究进展。方法：光盘检索有关献,归纳综合整理。结果：Ｐ＾２７是细胞周期的相关蛋白,Ｐ＾２７白过度表达可抑制细胞周期的进程,阻断细胞生长于Ｇ１期。结论：Ｐ＾２７是细胞周期中重要的负性调控控因子,是一种新的侯选的肿瘤抑制基因。     

黄芪灯盏花注射液对阳气虚型冠心病心率变异的影响

观察黄芪灯盏花注射液对 2 5例阳气虚型冠心病患者的心率变异性(HRV)的影响 ,并设对照组及正常人组 ,采用动态心电图含有 HRV时域分析软件进行分析。结果 :黄芪灯盏花注射液组 HRV数值明显提高 ,差异显著 (P<0 .0 5 ) ,或非常显著 (P<0 .0 1)。提示 :黄芪灯盏花注射液对冠心病患者 HRV心脏自主神经功能具有益影响。     

Pyroptosis: A road to next-generation cancer immunotherapy

The goal of cancer immunotherapy is to clear tumor cells by activating antitumor immunity, especially by mobilizing tumor-reactive CD8⁺T cells. Pyroptosis, programmed lytic cell death mediated by gasdermin (GSDM), results in the release of cellular antigens, damage-associated molecular patterns (DAMPs) and cytokines. Therefore, pyroptotic tumor cell-derived tumor antigens and DAMPs not only reverse immunosuppression of the tumor microenvironment (TME) but also enhance tumor antigen presentation by dendritic cells, leading to robust antitumor immunity. Exploring nanoparticles and other approaches to spatiotemporally control tumor pyroptosis by regulating gasdermin expression and activation is promising for next-generation immunotherapy.     

安乃近溶液鼻粘膜吸收的研究

 目的：研究安乃近溶液弄粘膜吸收规律。方法:以大鼠在体鼻循环法为实验模型,考察循环液的体积、流速等对安乃近弃枯膜吸收的影响。并在体积、流速确定的条件下,考查循环液浓度不同时,安乃近鼻粘膜吸收规律。结果:循环液体积越大,单位时间内粘膜吸收百分率越小;当流速较小时,随着流速的增加,吸收速度常数K增大,流速超过2 . 0 ml · min^-1后,K显著减小;以循环液体积为3 ml,流速2.0 ml"min^-1,考察了50,100,150,200 g·L^-1安乃近溶液弄粘膜吸收规律,表明不同浓度的安乃近鼻粘膜吸收速度为一常数。结论:安乃近溶液鼻粘膜吸收机制为被动扩散,吸收符合一级动力学,吸收速度常数K为0.022 19 min^-1 。     

Cytogenetic abnormalities related to histopathologic grade of astrocytic tumors

Cytogenetic analysis was performed on 7 lowgrade astrocytomas, 10 anaplastic astrocytomas, and 14 glioblastomas. Abnormal chromosome numbers were noted in all cases of high-grade astrocytomas but were rarely noted in low-grade astrocytomas (28%). The most consistent changes in high-grade astrocytomas were complete loss of chromosome 10 (61%), gain of chromosome 7 (56%), and loss of chromosome 17 (28%). Certain structural abnormalities, such as marker chromosomes and double minutes (33%), and the deletion and translocation of chromosomes 1 (33%) and 17 (17%), were also noted. These results indicate that changes in the number and/or structure of chromosomes with related inactivation of tumor suppressor gene or oncogene activation might play a critical role in the formation and anaplastic progression of astrocytic tumors.     

Comparison of the acute cardiotoxicity of the antimalarial drug halofantrine in vitro and in vivo in anaesthetized guinea-pigs

1. Several unrelated drugs have pro-arrhythmic activity associated with an ability to prolong the QT interval of the ECG. The aim of this work was to examine the effects of the antimalarial drug halofantrine in vivo and in vitro.
2. In anaesthetized guinea-pigs consecutive bolus doses of halofantrine (0.3, 1, 3, 10 and 30 mg kg⁻¹, i.v.) at 25 min intervals caused dose-dependent prolongation of the rate corrected QTc interval and bradycardia. The change in heart rate became significant after administration of 10 mg kg⁻¹ halofantrine (−23±9 beats min⁻¹) whereas the increase in QTc was significant with only 1 mg kg⁻¹ halofantrine (22±10 ms). It was only with the highest dose of halofantrine that the PR interval was increased (from 52±3 to 67±4 ms) and second degree atrioventricular (AV) block (type 1 Mobitz) occurred in all animals. No changes were observed in any parameters in a separate group of guinea-pigs which received vehicle (dimethylacetamide 60% propylene glycol 40%) at equivalent time points.
3. The blood concentrations of halofantrine ranged from 0.26±0.17 μM after administration of 0.3 mg kg⁻¹ to 2.79±0.87 μM after 30 mg kg⁻¹, i.v. There was a significant correlation between the blood concentrations of halofantrine and the changes in QTc interval.
4. In guinea-pig left papillary muscles the effective refractory period was increased significantly 60 min after addition of halofantrine; from 161±4 to 173±6 ms with 10 μM, 156±8 to 174±6 ms with 30 μM and 165±6 to 179±5 ms with 100 μM halofantrine. However, the vehicle (0.1% Tween 80 in DMSO; final concentration of vehicle in Krebs, 1%) also increased the effective refractory period from 164±5 to 173±6 ms. Similar results were obtained in right ventricular strips but left atrial effective refractory periods were not altered by either the vehicle or halofantrine.
5. The results of these experiments suggest that any direct effects that halofantrine may have had on the effective refractory period of cardiac muscle cannot be separated from those of the vehicle. The prolongation of QTc and consistent observation of AV block with halofantrine in anaesthetized guinea-pigs suggest that in vivo models may be more useful for further studies investigating the mechanisms underlying the cardiotoxicity of halofantrine.

     

Monitoring normal and aberrant electrocardiographic activity from an endotracheal tube: Comparison of the surface,esophageal, and tracheal electrocardiograms

Introduction. We designed an endotracheal (ET) tube with orthogonally spaced ECG cuff electrodes. This ET tube was evaluated in dogs and sheep to determine (1) whether ECGs recorded from our tube were sufficient to make accurate clinical decisions concerning heart rate and rhythm; and (2) whether metallic cuff electrodes in direct contact with the trachea could induce mucosal burn injury during episodes of defibrillation.Methods. Using experimental animals, we obtained ECGs from their tracheae and compared our findings with ECGs obtained from surface and esophageal electrodes. The electrical activity of the heart was modified by increasing the depth of anesthesia, occluding the left coronary artery, and administering beta-adrenergic drugs. Before the dogs were euthanized, they were subjected to episodes of transthoracic and intrathoracic defibrillation at energy levels of 200 to 400 J. A postmortem pathological examination of the trachea was performed to determine the incidence of mucosal burn injury.Results. Tracheal electrocardiography provided valid information on heart-rate monitoring and certain morphology profiles. The R-R, PR, QRS, and QT intervals measured from the trachea had a correlation of 1.0, 0.96, 0.83, and 0.98, respectively, when compared with the same intervals obtained from surface electrodes. Two tracheae subjected to intrathoracic defibrillation at >300 J revealed evidence of minor burn injury. Some localized epithelium loss was displayed in all tracheae; we attributed this to tracheal intubation.Conclusion. Tracheal electrocardiography may be useful in trauma patients who require intubation where injury precludes placement of chest ECG electrodes.