呼吸机相关性肺炎53例临床与病原学研究

金双歧是由长双歧杆菌、保加利亚乳杆菌及嗜热链球菌组成的复合活菌制剂，其中长双歧杆菌是人体肠道中最重要的生理性细菌，在体外经过长期抗酸耐氧驯化，能经过胃酸屏障，提高稳定性；保加利亚乳酸杆菌及嗜热链球菌为双歧杆菌的生长提供了理想的厌氧环境，使双歧杆菌更易在肠道定植和繁殖。该产品采用真空包装，制成奶片可保证在保质期内有较高的活菌数，且口感好，易被儿童接受。     

腹泻Ⅲ号对抗生素相关性腹泻小鼠肠道双歧杆菌和乳杆菌的影响

本实验采用抗生素相关性腹泻模型，应用细菌学检测方法，研究了中药腹泻Ⅲ号对小鼠ＡＡＤ模型肠道双歧杆菌和乳杆菌的影响。结果表明，腹泻Ⅲ号可有效地促进小鼠以歧杆菌及乳杆菌的生长。     

应用PCR—直接测序法测定结核分支杆菌rpsL基因突变的研究

目的：了解我国结核分支杆菌耐链霉素（Ｓｔｒｅｐｔｏｍｙｃｉｎ,ＳＭ）分离株ｒｐｓＬ基因突变情况,建立快速检测结核分支杆菌耐药基因型的分子药敏试验方法。方法：通过聚合酶链反应（ＰｏｌｙｍｅｒａｓｅＣｈａｉｎＲｅａｃｔｉｏｎ,ＰＣＲ）－单链构象多态性（Ｓｉｎｇｌｅ－ｓｔｒａｎｄｅｄＣｏｎｆｏｒｍａｔｉｏｎＰｏｌｙｍｏｒｐｈｉｓｍ,ＳＳＣＰ）、ＰＣＲ－限制性片段长度多态性（ＲｅｓｔｒｉｃｔｉｏｎＦｒａｇｍｅｎｔＬｅｎｇｔｈＰｏｌｙｍｏｒｐｈｉｓｍ,ＲＦＬＰ）和ＰＣＲ－直接测序法（ＤｉｒｅｃｔＳｅｑｕｅｎｃｉｎｇ,ＤＳ）分析３８株结核分支杆菌耐ＳＭ分离株的ｒｐｓＬ基因。结果３８株耐ＳＭ分离株中,２５株ＳＳＣＰ异常、不被ＭｂｏⅡ消化、ＤＳ分析４３位密码子ＡＡＧ→ＡＧＧ突变;１株ＳＳＣＰ异常、可被ＭｂｏⅡ消化、ＤＳ分析３３位密码子ＧＴＡ→ＡＴＡ突变;１２株ＳＳＣＰ正常、可被ＭｂｏⅡ消化、ＤＳ分析未见异常;未发现８８位密码子突变。结论：大多数结核分支杆菌耐ＳＭ是由于其ｒｐｓＬ基因４３位密码子突变所致,采用ＰＣＲ－ＳＳＣＰ、ＰＣＲ－ＲＦＬＰ和ＰＣＲ－ＤＳ方法可快速测定部分结核分支杆菌ＳＭ耐药基因型。     

酪酸梭菌与婴儿型双歧杆菌对艰难梭菌的试管内生物拮抗试验的研究

本文用酪酸梭菌（Ｃｌｏｓｔｒｉｄｉｕｍｂｕｔｙｒｉｃｕｍ）和婴儿型双歧杆菌（ＢｉｆｉｄｏｂａｃｔｅｒｕｍＩｎｆａｎｔｉｓ）对艰难梭菌（Ｃｌｏｓｔｒｉｄｉｕｍｄｉｆｆｉｃｌｉｅ）进行了试管内的生物拮抗试验。将酪酸梭菌ＬＣＬ１６６株，婴儿型双歧杆菌菌ＬＣＬ１７２株及酪酸梭菌ＬＣＬ１６６株和婴儿型双歧杆菌１７２株分别与艰难菌ＬＣＬ１６６株和婴儿型双歧杆菌ＬＣＬ１７２株能明显抑制艰梭菌ＶＰＩ１０４６３株的     

双歧杆菌在国外的研究和应用

本文介绍了国外双歧杆菌的研究应用近况，试验表明双歧杆菌中改善肠道疾病及防止感染方面有一定疗效，还可能提高宿主Ｂ族维生素，建议生产中应选用人源型双歧杆菌，且以长型双歧杆菌最稳定，为确保产品质量，应控制生产条件，配伍合适的乳酸杆菌和需氧菌等，以保持双歧杆菌的活性。     

双歧杆菌,乳酸杆菌,DL—菌混合发酵液的药理学研究

研究了双歧杆菌，乳酸杆菌ＤＬ－菌发酵活菌体混合液对小鼠生长，腺体发育，耐力，应激力等作用，结果显示，用药组可显著促进幼鼠生长，提高耐力和应激力，研究了双岐杆菌，乳酸杆菌ＤＬ－菌发酵活菌体混合液对机体清除超氧阴离子的作用，结果显示，该混合液可提高小鼠血液对连苯三酚自氧化的抑制率，降低血液中丙二醛的含量，菌体与上清液的作用无显著差异。     

对环丙沙星耐药的肺炎克雷伯氏菌外膜蛋白图谱分析

为了探讨肺炎克雷伯氏菌对喹诺酮类药物的耐药机制，从临床送检标本中分离出８株耐环丙沙星的肺炎克雷伯氏菌，对其外膜蛋白进行了ＳＤＳ－ＰＡＧＥ分析。结果发现除１株菌外，其余所有耐环丙沙星的肺炎克雷伯氏菌４２ｋＤ外膜蛋白带消失，另有１株菌的２５ｋＤ外膜蛋白带也同时消失。这一结果表明，肺炎克雷伯氏菌的４２ｋＤ外膜蛋白与其对环丙沙星的通透性有关，此外膜蛋白消失是该菌对环丙沙星产生耐药性的重要原因之一     

红霉素发酵液中污染细菌的分离与鉴定及其对红霉素发酵的影响

作者从红霉素发酵污染液中分离出了４５株污染细菌，对其进行了分类鉴定，其中有３９株属于芽孢杆菌属的８个种，有５株属于微球菌属，１株为无芽孢的杆菌。利用芽孢杆菌属８个种的污染细菌进行了人为模拟污染的红霉素发酵试验，其结果表明：其中凝结芽孢杆菌、枯草芽孢杆菌、地衣芽孢杆菌、蜡状芽孢杆菌、坚强芽孢杆菌等５种芽孢杆菌对红霉素发酵有显著影响；其危害极大。短芽孢杆菌对红霉素发酵影响不大，而巨大芽孢杆菌和短小孢杆     

双歧杆菌乳剂对复发性口疮病人细胞免疫功能的影响

双歧杆菌乳剂对复发性口疮病人细胞免疫功能的影响１５０医院（河南洛阳４７１０３１）孙苗根张妙贤侯玉双歧杆菌制剂对复发性口疮（以下简称口疮）的疗效笔者曾作过报道［１］。本文重点介绍在应用双歧杆菌乳剂治疗口疮前后患者Ｔ淋巴细胞亚群（ＣＤ３、ＣＤ４、ＣＤ８）...     

甲氧西林耐药金葡球菌（MRSA）耐药机制的研究

用北京地区综合医院中分离的１９０株金葡球菌进行耐药机制研究。按照ＮＣＣＬＳ发表的ＭＲＳＡ标准，采用琼脂稀释敏感试验并以多聚酶链反应（ＰＣＲ）技术检测ｍｅｃＡ基因。１９０株金葡球菌中，８８株耐甲氧西林（ＭＩＣ≥１６ｍｇ／Ｌ），９１株耐苯唑西林（ＭＩＣ≥４ｍｇ／Ｌ），全部甲氧西林耐药金葡球菌和９８．８９％苯唑西林耐药金葡球菌为ｍｅｃＡ基因阳性。有１１株ｍｅｃＡ基因阳性金葡球菌对甲氧西林敏感，９株ｍｅｃＡ基因阳性金葡球菌对苯唑西林敏感。在８８株ＭＲＳＡ菌株中，７３．６３％为β－内酰胺酶产生菌，但克拉维酸只对低度耐药的ＭＲＳＡ菌株有影响，高度耐药的ＭＲＳＡ其ＭＩＣ值则不受克拉维酸的影响。这表明高度耐药ＭＲＳＡ所产生的β－内酰胺酶的作用还不清楚。群体分析结果发现所测试的全部菌株的耐药类型均为异质性耐药菌株。以上结果表明，我国临床分离的ＭＲＳＡ，其耐药机制主要是ｍｅｃＡ基因介异的。     

Why prescribe short-burst oxygen?

In previous reviews of domiciliary oxygen therapy, we have commented on the lack of evidence to justify use of short-burst oxygen therapy, which is expensive and can be difficult to withdraw from patients once they are established on it. For these reasons, we concluded that short-burst oxygen therapy should not be started without objective evidence of benefit for the individual patient, and its use should be under the supervision of a specialist. In February 2006, the supply process for all forms of home oxygen in England and Wales was changed, with the aim of giving patients more appropriate treatment through proper clinical assessment and correct ordering and monitoring of oxygen therapy. Here we reassess the role of short-burst oxygen therapy within these new supply arrangements.     

Bolus or slow titrated injection of midazolam prior to upper gastrointestinal endoscopy? Relative effect on oxygen saturation and prophylactic value of supplemental oxygen

A total of 131 patients undergoing upper gastrointestinal endoscopy were sedated with midazolam given as a bolus injection over 5 seconds. The oxygen saturation was continuously measured using a pulse oximeter. Supplemental oxygen was given via nasal cannulae at a rate of 3 litres per minute to 54 patients, while the remaining 77 patients only received oxygen if their oxygen saturation dropped below 85%. Both groups in the present series were compared with 3 previously published series of patients, in whom we had used intravenous midazolam as a slow titrated injection. Despite using on average only two-thirds of the dose of midazolam, following bolus injection the degree of oxygen desaturation during the endoscopic procedure was greater, and the ability of supplemental oxygen delivered via nasal cannulae to prevent hypoxia was less (P less than 0.01), than with a slow titrated injection.     

Generation of hydroxyl radicals mediated by streptozotocin in pancreatic islets of mice in vitro

Type I diabetes is considered a multifactorial autoimmune process initiated by an environmental factor. There is evidence that reactive oxygen species are involved in destructing insulin-producing beta-cells. In mice, reactive oxygen species and nitric monoxide contribute to beta-cell damage in the non-obese diabetic strain developing spontaneously diabetes and in diabetes induced with multiple low doses of streptozotocin. Previously, we found that zinc sulfate induced metallothionein in pancreatic islets, protected beta-cells against streptozotocin toxicity in vitro, and prevented diabetes induced with multiple low doses of streptozotocin. Since metallothionein is known to scavenge hydroxyl radicals in cell-free systems, we hypothesize that the protective effect of zinc sulfate results from metallothionein induction scavenging hydroxyl radicals generated by multiple low doses of streptozotocin. Therefore, we studied whether levels of hydroxyl radicals are increased by streptozotocin in isolated islets in vitro. Here, we demonstrate basal and streptozotocin-stimulated hydroxyl radicals by electron spin resonance spectroscopy in combination with hydroxyl radical-specific spin trapping in islet homogenates. Furthermore, in islet cultures, streptozotocin augmented generation of reactive oxygen species as determined by fluorescence. Of the group of reactive oxygen species, the streptozotocin-augmented generation of hydrogen peroxide was also specifically determined. We conclude that streptozotocin-mediated hydroxyl radicals and generation of reactive oxygen species may be crucial effectors in beta-cell damage.     

The effect of hyperbaric oxygen on acute experimental sulfide poisoning in the rat

In order to evaluate the efficiency of hyperbaric oxygen in experimental acute sulfide poisoning, we studied the effect of 1 ATA (atmosphere absolute) oxygen and sodium nitrite therapy. We then studied the effect of oxygen at 3 ATA alone and in combination with intraperitoneal sodium nitrite injection on rats poisoned by intraperitoneal injection of LD75 sulfide. Electroencephalogram and heart rate were continuously monitored. We also studied the effect of sodium nitrite and hyperbaric oxygen administered before the poisoning (protective effect). In our experimental set, death of untreated poisoned animals occurred within 5 min. There is a parallel between modification of the EEG pattern and apnea. Respiratory arrest always preceded cardiac arrest. Pure oxygen (1 ATA O2) is effective in preventing death in experimental sulfide poisoning. 3 ATA oxygen was significantly more effective in preventing death than 1 ATA oxygen, or sodium nitrite alone. The best therapeutic regimen was a combination of 3 ATA oxygen and sodium nitrite administration.     

Phototoxicity from nalidixic acid: oxygen dependent photohemolysis

Erythrocyte lysis photosensitized by nalidixic acid was investigated. This photohemolysis was found to be oxygen dependent. The effects of various antioxidants and hydroxyl radical scavengers on photohemolysis induced by nalidixic acid suggested a photo-oxidative step. In addition, using the oxygen quencher histidine and the deuterium oxide effect on the singlet oxygen lifetime we obtained evidence indicative of a photodynamic mechanism mediated by oxygen singlet and hydroxyl radicals. On the other hand, pre-irradiated nalidixic acid was not lytic to erythrocytes, yet photoproducts of nalidixic acid demonstrated a greater photohemolytic potential than nalidixic acid itself.     

Oxygen administration enhances memory formation in healthy young adults

Despite numerous studies indicating that transient cerebral oxygen depletion has a detrimental effect on cognition, surprisingly little research has examined the possibility of cognitive enhancement following elevated oxygen levels in healthy adults. Here, we present evidence demonstrating that oxygen administration improves memory formation. Inhalation of oxygen immediately prior to learning a word list resulted in a significant increase in mean number of words recalled 10 min later, compared to subjects who inhaled oxygen immediately prior to recall or to controls who underwent no intervention. In a second experiment, the learning-test interval was increased to 24 h and, again, only pre-learning (but not pre-test) oxygen administration resulted in significant memory facilitation. In experiment 3, inhalation of oxygen prior to learning was compared to inhalation of compressed air, oxygen (but not compressed air) resulted in a significant increase in word recall 24 h later. In no experiment did oxygen have a significant effect on any mood item measured. We interpret these data as indicating that increased availability of cerebral oxygen facilitates cognition, including memory consolidation. The implications for the psychopharmacology of cognitive enhancement are considered in the context of cholinergic systems and neural metabolism.     

早期高压氧、法舒地尔联合治疗脑梗塞临床疗效观察

目的探讨高压氧(HBO)、法舒地尔联合治疗脑梗塞的疗效。方法将98例脑梗塞的患者按随机数字表法分为3组:常规治疗组(对照组),采用常规治疗;高压氧治疗组(高压氧组),采用高压氧治疗;法舒地尔联合治疗组(联合治疗组),脑梗塞后24 h内开始行高压氧治疗及法舒地尔静脉滴注。盲法对3组患者治疗前后行神经功能缺损评分和Barthel指数(BI)进行日常生活活动能力(ADL)评分,并于治疗前后行血液流变学检测及脑梗塞程度测定,探讨治疗脑梗塞患者的疗效。结果治疗30 d后,联合治疗组患者神经功能缺损评分和Barthel指数(BI)进行日常生活活动能力(ADL)评分明显优于对照组(P<0.01),且治疗组血液粘滞度明显降低(P<0.01);早期高压氧、法舒地尔联合治疗梗塞面积小于10 cm3的脑梗塞,疗效显著较好(P<0.01),当治疗大于或等于10 cm3的脑梗塞时,疗效与对照组差异无显著性(P>0.05)。结论早期高压氧、法舒地尔联合治疗梗塞面积小于10 cm3的脑梗塞,疗效显著,可以明显促进神经功能恢复,提高患者生存、生活质量。     

The mechanism of toxic action of hyperbaric oxygenation on the mitochondria of rat-heart cells

Hyperbaric oxygenation of the whole animal was examined with respect to changes in mitochondria from heart cells. Accumulation of conjugated dienes, decrease of unsaturated fatty acids and changes in phospholipid pattern of the mitochondrial membrane indicate peroxidative damage of membrane lipids during oxygen stress. Hyperoxia induces increased activities of Superoxide dismutase, catalase and glutathione peroxidases, all enzymes protecting mitochondria from deleterious effects of reactive oxygen species. From the multiplicity of parameters related to pathophysiological effects of O₂ we inferred on increased formation rates of toxic oxygen species involving superoxide as the initial step in biological activation of O₂. The K_m for superoxide formation was 550 μM, ranging above physiological oxygen levels by a factor of 11. Thus, the mechanism by which hyperoxia might affect stimulation of superoxide formation is discussed on the basis of enhanced Michaelis-Menten kinetics due to elevated oxygen levels in the heart tissue. The onset of the membrane damage is the first event in hyperbaric O₂ toxicity. Despite a clear induction, activities of protecting enzymes seem to be ‘swamped’ by raising oxygen concentration above normal.     

DPPH and oxygen free radicals as pro-oxidant of biomolecules.

Numerous investigations exist about the alterations that oxygen free radicals can provoke on biomolecules; these modifications can be prevented and/or reversed by different antioxidants agents. On the other hand, 2,2-diphenyl-1-picrylhydrazyl radical (DPPH), a stable nitrogen synthetic radical, is used to evaluate the antioxidant capacity of medicinal herbal products; however, the structural changes that this radical provoke on the herbal active principles are not clear yet. In this work, we compared the redox reactivity of oxygen free radicals and DPPH radical on phospholipids and protein thiol groups present in rat liver microsomes. Cu2+/ascorbate was used as generator system of oxygen free radical and as antioxidant, an extract of Buddleja globosa's leaves. Cu2+/ascorbate provoked microsomal lipid peroxidation, microsomal thiols oxidation and oxygen consumption; all of these phenomena were inhibited by B. globosa extract. On the other hand, DPPH was bleached in different extension by the herbal extract and phosphatidyl choline; beside, DPPH decreased microsomal thiols content, but this phenomenon were not prevented by the herbal extract. Furthermore, DPPH did not induce oxygen consumption and neither modified the oxygen consumption induced by Cu2+/ascorbate. Distinct redox mechanisms may explain the differences between the reactivity of DPPH and oxygen free radicals on biomolecules, which is discussed.     

Synchronous delivery of oxygen and photosensitizer for alleviation of hypoxia tumor microenvironment and dramatically enhanced photodynamic therapy

Photosensitizer, proper laser irradiation, and oxygen are essential components for effective photodynamic therapy (PDT) in clinical cancer therapy. However, native hypoxic tumoral microenvironment is a major barrier hindering photodynamic reactions in vivo. Thus, we have prepared biocompatible liposomes by loading complexes of oxygen-carrier (hemoglobin, Hb) and photosensitizer (indocyanine green, ICG) for enhanced PDT against hypoxic tumor. Ideal oxygen donor Hb, which is an oxygen-carried protein in red blood cells, makes such liposome which provide stable oxygen supply. ICG, as a photosensitizer, could transfer energy from lasers to oxygen to generate cytotoxic reactive oxygen species (ROS) for treatment. The liposomes loading ICG and Hb (LIH) exhibited efficient tumor homing upon intravenous injection. As revealed by T₂-weighted magnetic resonance imaging and immunohistochemical analysis, the intratumoral hypoxia was greatly alleviated, and the level of hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in tumor was obviously down-regulated. A weak PDT efficiency was found in cells incubated in simulated hypoxia condition in vitro, while PDT effect was dramatically enhanced in LIH treated hypoxia cells under near-infrared (NIR) laser, which was mainly attributed to massive generation of ROS with sufficient oxygen supply. ROS trigger oxidative damage of tumors and induce complete suppression of tumor growth and 100% survival rate of mice, which were also in good health condition. Our work highlights a liposome-based nanomedicine that could effectively deliver oxygen to tumor and alleviate tumor hypoxia state, inducing greatly improved efficacy compared to conventional cancer PDT and demonstrates the promise of modulating unfavorable tumor microenvironment with nanotechnology to overcome limitations of cancer therapies.