阿奇霉素治疗细菌性感染的临床疗效

目的:评价注射用阿奇霉素治疗细菌性感染的有效性及安全性。方法:60例呼吸系统和泌尿系统细菌感染性疾病患者随机分为治疗组和对照组,每组30例,治疗组静滴阿奇霉素250 mg,qd,疗程5 d。对照组静滴头孢噻肟钠2 g,qd,疗程7d。结果:治疗组与对照组治疗细菌感染性疾病的有效率分别为90.0%与80.0%,两组比较无统计学差异(P>0.05);细菌清除率分别为89.3%与62.1%,两组比较有统计学差异(P<0.05);不良反应发生率均为6.7%。结论:注射用阿奇霉素治疗细菌性感染疗效高、安全性好。     

3-苯基乳酸的研究进展

介绍了3-苯基乳酸的结构、制备、手性拆分等的研究现状，并阐述了其抑菌、药理作用及在医药、化工等领域的应用。     

鼻泰治疗变应性鼻炎的实验研究

鼻泰为治疗变应性鼻炎的中药滴鼻剂。实验表明，该药可抑制大鼠肥大细胞脱颗粒，抑制小鼠皮肤被动过敏反应，抑制实验性变应性鼻炎家兔的鼻粘膜炎症反应并减少其Ｐ物质水平。     

云南山楂叶化学成分的研究

目的：研究云南山楂叶化学成分。方法：云南山楂叶分别经乙醇和水提取，聚酰胺柱和硅胶柱层析，光谱分析鉴定。结果：分离鉴定了６个化合物，为芦丁，金丝桃甙，牡荆素，熊果酸，胡萝卜甙及二十九烷醇。结论：均为首次从云南山楂叶中分得。     

内镜下治疗食管平滑肌瘤12例

[目的]探讨内镜下治疗食省平滑肌瘤的可行性。[方法]应用内镜直视下单纯套扎方法后高频电换电切技术对12例食管平滑肌瘤患者进行切瘤治疗。[结果]12例中10例完整切除（83．33％）。2例失败。术后1例并发出血，无穿孔发生。[结论]内镜下治疗平滑肌瘤安全可行，适应证以直径小于2cm的粘膜层平滑肌瘤为宜。     

塞来昔布诱导SGC-7901人胃癌细胞凋亡及其影响端粒酶活性的实验研究

目的探讨选择性环氧化酶-2（COX-2）抑制剂塞来昔布对SGC-7901人胃癌细胞生长、端粒酶活性，细胞凋亡及相关基因的影响，研究其抗肿瘤的作用机制。方法终浓度为100、200及300μmol／L的塞来昔布作用于SGC-7901人胃癌细胞后，采用MTT比色法测定细胞的生长抑制率，采用半定量-TRAP银染法检测端粒酶活性，流式细胞仪检测细胞周期、细胞凋亡率及bcl-2表达水平变化。结果不同浓度的塞来昔布对SGC-7901人胃癌细胞均有抑制作用，抑制率与对照组相比，差异均有显著性（P〈0．05）；流式细胞学检测到凋亡峰，细胞阻滞于G0／G1期。同时它也显著抑制胃癌细胞的端粒酶活性，其抑制作用呈时间-剂量依赖性，且端粒酶活性的降低与bcl-2表达水平下降有关。结论塞来昔布能抑制胃癌细胞的增殖，诱导细胞凋亡，降低端粒酶活性，其作用机制与bcl-2表达水平下降有关，此可能是COX-2抑制剂抗肿瘤的机制之一。     

基于BP神经网络的半夏、生姜、甘草三泻心汤配伍研究

目的:探讨不同BP(BackPropagation,BP)算法的人工神经网络在半夏泻心汤、生姜泻心汤、甘草泻心汤配伍中的应用,并应用所建模型探讨三复方药味与剂量的配伍规律。方法:应用均匀设计对药味及剂量进行分组,测定不同组别对正常大鼠胃粘液的影响。应用MATLAB6.5进行编程,选用BP神经网络来拟合实验数据,比较831、881、8121三种拓扑结构、不同BP算法对网络模型拟合效果的影响,建立基于BP神经网络的三方对胃粘液含量影响的预测模型。结果:拓扑结构为881、算法为改进BP算法的神经网络模型可以很好的拟合学习过的样本,并对未学习过的样本有较好的预测能力,其中采用动量法和学习速率自适应调整两种策略相结合的改良BP算法的网络拟合预测效果最佳。应用模型分析可以看出,每种药物剂量变化及不同药物组合对胃粘液分泌的影响不尽相同,如辛开组合具有促进胃粘液分泌的作用,苦降组合、甘补组合具有抑制胃粘液分泌的作用。结论:以半夏、甘草、生姜泻心汤为研究模板,提出的复方类方配伍规律研究模式:“优化拆方实验设计-人工智能数据挖掘-复方类方知识发现”,将为复杂复方的研究提供借鉴。     

许树化学成分研究

目的研究许树Clerodendrum inerme的化学成分。方法利用硅胶柱色谱进行分离和纯化,通过光谱分析鉴定结构。结果分离到8个化合物,鉴定为木栓酮(friedelin,Ⅰ)、豆甾醇(stigmasterol,Ⅱ)、白桦酸(betulinicacid,Ⅲ)、金合欢素(acacetin,Ⅲ)、丁香酸(syringicacid,Ⅳ)、对甲氧基苯甲酸(Ⅴ)、芹菜素(apigenin,Ⅵ)和胡萝卜苷(daucosterol,Ⅶ)。结论化合物Ⅱ、Ⅲ、Ⅳ、Ⅳ、Ⅶ为首次从该植物中分离得到。     

Role of CYP2C9 and its variants (CYP2C9*3 and CYP2C9*13) in the metabolism of lornoxicam in humans.

CYP2C9 is an important member of the cytochrome P450 enzyme superfamily with some 12 CYP2C9 alleles (*1-*12) being previously reported. Recently, we identified a new CYP2C9 allele with a Leu90Pro mutation in a Chinese poor metabolizer of lornoxicam [Si D, Guo Y, Zhang Y, Yang L, Zhou H, and Zhong D (2004) Pharmacogenetics 14:465-469]. The new allele, designated CYP2C9*13, was found to occur in approximately 2% of the Chinese population. To examine enzymatic activity of the CYP2C9*13 allele, kinetic parameters for lornoxicam 5'-hydroxylation were determined in COS-7 cells transiently transfected with pcDNA3.1 plasmids carrying wild-type CYP2C9*1, variant CYP2C9*3, and CYP2C9*13 cDNA. The protein levels of cDNA-expressed CYP2C9*3 and *13 in postmitochondrial supernatant (S9) from transfected cells were lower than those from wild-type CYP2C9*1. Mean values of Km and Vmax for CYP2C9*1, *3, and *13 were 1.24, 1.61, and 2.79 microM and 0.83, 0.28, and 0.22 pmol/min/pmol, respectively. Intrinsic clearance values (Vmax/Km) for variant CYP2C9*3 and CYP2C9*13 on the basis of CYP2C9 protein levels were separately decreased to 28% and 12% compared with wild type. In a subsequent clinical study, the AUC of lornoxicam was increased by 1.9-fold and its oral clearance (CL/F) decreased by 44% in three CYP2C9*1/*13 subjects, compared with CYP2C9*1/*1 individuals. This suggests that the CYP2C9*13 allele is associated with decreased enzymatic activity both in vitro and in vivo.     

A serum factor enhances production of nitric oxide and tumor necrosis factor-alpha from cultured microglia

The pathological activation of microglia has been implicated in ischemic neuronal damage and some neurodegenerative diseases; however, the mechanism of microglial activation is not well understood. Previously, we showed that a serum factor, albumin, increased O(2)(-) production by cultured microglia (Si et al., 1997, Glia 21: 413-418). In the present study, we found that serum also enhanced lipopolysaccharide (LPS)-induced production of nitric oxide and tumor necrosis factor-alpha, which are other important neurotoxins released by activated microglia. In the presence of 0.1% normal rat serum, the half-effective concentration for LPS decreased from 300 to 1 ng/ml. The factor seemed to be a relatively high-molecular-weight protein because the factor was retained after a molecular sieve (50 kDa) membrane separation. The factor was labile to trypsinization and heat treatment at 72 degrees C for 5 min but was stable at 56 degrees C for 60 min. Several purified serum proteins including albumin could not mimic the enhancing effect of serum. Acute-phase serum showed a potent enhancing effect at a 10 times lower concentration than the normal serum. By gel filtration chromatography, the enhancing effect observed was a single peak at about 60 kDa. These results suggest that some serum protein infiltrates into brain parenchyma after blood-brain barrier disruption and such protein may result in neuronal damage by activating microglia to release neurotoxins in some central nervous system diseases.