喀喇昆仑山不同海拔高度肺通气功能测验

1987年7月作者于喀喇昆仑山海拔1410、3700、4300、5100、5200、5380m对291名健康青年做了几项肺通气功能测验,结果如下。 被测者生于平原,年龄17～28岁,均进入高原1个月,已基本习服。仪器为美国ES-800肺功能仪,室温20℃,每人重复测试2～3次,仪器自动选择最佳参数。     

便携式脑循环功能分析仪的研制

介绍了一种结构新颖的便携式脑循环功能分析仪的基本原理、参数算法和仪器设计方法。该仪器动用超声多普勒、超声脉冲和臂式自动血压模块检测颈动脉血流速度、血管管径及肱动脉舒张压和收缩压。根据血液动力学原理建立了简化的脑血管动力学参数计算方法,可获得人体颈动脉系统外周阻力、动态阻力、临界压力及搏动指数等反映脑循环功能状况的动力学参数。该仪器结构精巧、操作便捷、指标敏感,适用于各级医院、医疗机构,特别是基层医院和社区康复中心对脑血管病进行早期诊断。     

微机化动态光度法细胞力学分析仪研究药物对红细胞膜的作用

介绍了一种新型的微机化动态流光度法细胞力学参数分析仪,它能自动测量静态红细胞参数(RF)、膜硬度、(S)半松弛时间、(t50%)和细胞粘度(VP)等微力学参数,来描述细胞力学特性.对仪器的灵敏度、精确度和重复性,对Triton、水杨酸钠.ROK、TRE、DUS、EGb761等药物对于红细胞力学性质的作用分别进行了研究,证明了本仪器对药理作用研究具有重要价值,并认为该仪器在今后临床检验中有广泛的应用价值.     

基于声门下嗓音源的肺胸系统声传递特征研究

本文根据嗓音－－呼吸系统生理及生物物理原理,提出了传导语音产生及在下声道和肺胸系统传播的物理模型,在胸前颈下V型槽处记录传导语音并利用复倒谱技术提取声门下噪音源,可以看出它非常有效地提取了声门下嗓音源,根据所提出的模型、提取的声门下噪声源和胸壁记录的传导语音,研究肺胸系统的声传递特征,从结果可以看出该方法是研究肺胸系统声传递特征函数的一种有效方法。     

呼吸力学参数的强迫振荡识别方法及其应用

呼吸力学参数包括呼吸气体的压力、流率、胸肺系统的顺应性、气道阻力、惯性阻力以及呼吸功等。测量这些参数可进一步从生物力学角度分析呼吸过程,在理论上与实际上均有一定意义。例如,测量胸内压、各级气道阻力、肺顺应性等,有助于深入了解肺内气体的传输和分布问题;定量研究气道阻力或肺顺应性的改变,对于阐明慢性阻塞性肺疾病(COPD)     

自动组织脱水机控制程序的编制与应用

自动组织脱水机 (Automated Tissue Processor)是为组织学标本的固定、脱水、透明及浸蜡所设计的一种全自动化处理仪器 ,集微机和机械为一体 ,采用全封闭的编程处理过程。此类仪器另设计有温度、真空压力循环、搅拌等参数 ,比机械式脱水机和手工脱水方法更能满足多种组织处理要求。为了使组织标本在整个过程中达到最优化的处理及考虑到实施质量控制 ,我们经过一个时期不断摸索 ,建立了一套适应日常外检工作需要的操作程序 ,介绍如下 :仪器的构成和参数我科采用 10 5 0型自动组织脱水机 ,该机可选择十道试剂和三道石蜡 ,可设置 1.脱水时间 …     

一种微生物生长动态的研究仪器Biotran Ⅲ的用法

微生物生长动态的重要参数是细胞群体中细胞数目、形态和大小的变化。这些参数的测量虽很重要,但由于实验费时、费力,且有操作人员主观上的误差,从而影响了我国这方面研究工作的开展。最近由美国引入一批自动计数及求积的仪器——Biotran Ⅲ,是New Brunswich Scientific Co.Ine.生产的,该仪器能自动计数菌落,而且在与显微镜或其它图象放大仪联用时,     

Hippo信号通路在肺发育、再生和疾病中的功能

哺乳动物肺对于血液与外部环境之间的气体交换至关重要。而肺相关的疾病是现代人死亡的主要原因之一。肺的发育、再生和相关疾病的研究对临床治疗具有重要的指导作用。研究发现,Hippo信号通路参与细胞增殖与分化的调控、器官大小的控制,以及机械力的感应和传递。Hippo信号通路中的核心转录调控分子YAP/TAZ在肺部的多种细胞中均有表达,其表达及定位的变化在肺发育与再生中发挥着重要的调控作用。本文主要介绍了Hippo信号通路在肺生长发育中的功能及其与肺纤维化、肺癌的关系,并从肺泡力学和肺泡相关免疫两个角度对Hippo信号通路潜在的功能进行了展望。     

基于生理征象变化的心理测试技术研究进展

本文从心理测试技术的起源和早期应用入手,介绍了心理状态与皮肤电、心率、脉搏、血压、呼吸、眼动等生理指标的关系,阐述了心理变化与生理征象变化之间的密切关系,揭示了心理测试技术的生理学依据.通过分阶段对萌芽期、近代、现代和当代心理测试仪器的设计思路和原理介绍,结合对典型的机械式、电子式和多元化测试仪器的功能,较为充分的展示了心理测试技术的研究进展及其在测试仪器改进上的体现.文章还介绍了基于脑电信号、事件相关电位、功能磁共振成像、核磁共振、皮肤温度、语音次声波等生理参数设计的正处于研发阶段的新型测试仪,并展望了心理测试技术发展和应用前景.     

昆虫振动信号监听、记录和重放技术

由固体介质(寄主植株)传递的振动信号是区别于空气传播鸣声的另一类昆虫声信号。本文介绍了笔者用以监听、记录和重放昆虫振动信号的仪器和有关技术。     

The lung lamellar body as a functioning membrane in protein-catalyzed phosphatidylcholine transfer

Lung lamellar bodies and liver mitochondria were used to demonstrate that soluble phospholipid transfer proteins from lung transfer phosphatidylcholine to both of these acceptors. The initial rate of transfer to lung lamellar bodies is about half that of the rate of transfer to the liver mitochondria when both acceptor membranes are present at saturating concentrations. Phosphatidylcholine unilamellar vesicles were used to demonstrate that the fatty acyl composition of the membrane phosphatidylcholine is a significant determinant of the rate of phosphatidylcholine transfer catalyzed by these proteins. The lamellar bodies have a unique phosphatidylcholine composition, and these studies suggest that this is an important factor in determining the lower initial rate of transfer to lamellar bodies. The studies have also characterized two phospholipid transfer proteins in rat lung in terms of isoelectric point. Isoelectric points for the two proteins which transfer phosphatidylcholine were found to be 5.6 ± 0.08 and 6.2 ± 0.03.     

Intratracheal gene transfer of tissue factor pathway inhibitor attenuates pulmonary fibrosis

Activation of the coagulation system and increased expression of tissue factor (TF) in pulmonary fibrosis associated with acute and chronic lung injury have been previously documented. In the present study, we evaluated the effect of TF inhibition with intratracheal gene transfer of tissue factor pathway inhibitor (TFPI), a potent and highly specific endogenous inhibitor of TF-dependent coagulation activation, in a rat model of bleomycin-induced lung fibrosis. Significant lung fibrotic changes as assessed by histologic findings and hydroxyproline content, and increased procoagulant activity and thrombin generation in bronchoalveolar lavage fluid were detected in rats after intratracheal injection of bleomycin. Intratracheal administration of an adenovirus vector expressing TFPI significantly decreased bleomycin-induced procoagulant and thrombin generation resulting in a strong inhibition of pulmonary fibrosis. TFPI-overexpression in the lung was associated with a significant reduction in gene expression of the connective tissue growth factor, a potent profibrotic growth factor. This is the first report showing that direct inhibition of TF-mediated coagulation activation abrogates bleomycin-induced pulmonary fibrosis.     

Inhibition of endotoxin-induced lung inflammation by interleukin-10 gene transfer in mice

Interleukin (IL)-10 is an anti-inflammatory cytokine that has great potential for use in the treatment of inflammatory and immune illnesses. In this study, gene transfer was used to induce IL-10 transgene expression in murine lungs for treatment of endotoxin-induced lung inflammation. Gene transfer was performed with a cytomegalovirus (CMV)-IL-10 plasmid with the aid of the liposomal agents LipofectAMINE and N-[1-(2,3-dioleoyl)propyl]-N,N, N-trimethylammonium methylsulfate (DOTAP). Administration of the endotoxin caused a marked increase in lung inflammation as indicated by increased tumor necrosis factor (TNF)-alpha release and neutrophil count. Pretreatment of the mice with IL-10 plasmid with and without LipofectAMINE had no inhibitory effect on lung inflammation and IL-10 transgene expression. LipofectAMINE by itself induced lung inflammation, an effect that was not observed with DOTAP. IL-10 plasmid when codelivered with DOTAP expressed biologically active IL-10 protein and caused a reduction in endotoxin-induced inflammation. Transgene expression was observed as early as 3 h after administration, peaked at 12 h, and declined thereafter. We conclude that IL-10 gene transfer is a feasible approach for the treatment of lung inflammation.     

Protection against hyperoxia by serum from endotoxin treated rats: absence of superoxide dismutase induction

Endotoxin greatly reduces lung injury and pleural effusions in adult rats exposed to normobaric hyperoxia (greater than 98% oxygen for 60 hours). This study reports that serum from endotoxin treated donor rats protects serum recipients against hyperoxic lung injury without altering lung superoxide dismutase (SOD) activity. Rats pretreated with endotoxin alone were protected and exhibited an increase in lung SOD activity as previously reported by others. Protection by serum was not due to the transfer of residual endotoxin or SOD. These results show that protection from oxygen toxicity can occur in rats without an increase in lung SOD and suggest that a serum factor may be involved.     

Pulmonary Function after Lymphography

The effects of lymphography on ventilatory function and gas transfer factor were studied in nine patients. Serial measurements made up to one month showed no change in the forced expiratory volume in one second or vital capacity. A small but reversible fall in transfer factor was found. The greatest reduction was at 24 or 48 hours. It was concluded that patients with normal lungs are unlikely to encounter difficulties but that patients with severe lung disease require careful assessment before lymphography.     

Protein arginine methyltransferase 5 is essential for growth of lung cancer cells

PRMT5 (protein arginine methyltransferase 5) is an enzyme that catalyses transfer of methyl groups from S-adenosyl methionine to the arginine residues of histones or non-histone proteins and is involved in a variety of cellular processes. Although it is highly expressed in some tumours, its direct role in cancer growth has not been fully investigated. In the present study, in human lung tissue samples we found that PRMT5 was highly expressed in lung cancer cells, whereas its expression was not detectable in benign lung tissues. Silencing PRMT5 expression strongly inhibited proliferation of lung adenocarcinoma A549 cells in tissue culture, and silencing PRMT5 expression in A549 cells also abolished growth of lung A549 xenografts in mice. In vitro and in vivo studies showed that the cell growth arrest induced by loss of PRMT5 expression was partially attributable to down-regulation of fibroblast growth factor receptor signalling. These results suggest that PRMT5 and its methyltransferase activity is essential for proliferation of lung cancer cells and may serve as a novel target for the treatment of lung cancer.     

Gene transfer of hepatocyte growth factor by electroporation reduces bleomycin-induced lung fibrosis

Abnormal alveolar wound repair contributes to the development of pulmonary fibrosis after lung injury. Hepatocyte growth factor (HGF) is a potent mitogenic factor for alveolar epithelial cells and may therefore improve alveolar epithelial repair in vitro and in vivo. We hypothesized that HGF could increase alveolar epithelial repair in vitro and improve pulmonary fibrosis in vivo. Alveolar wound repair in vitro was determined using an epithelial wound repair model with HGF-transfected A549 alveolar epithelial cells. Electroporation-mediated, nonviral gene transfer of HGF in vivo was performed 7 days after bleomycin-induced lung injury in the rat. Alveolar epithelial repair in vitro was increased after transfection of wounded epithelial monolayers with a plasmid encoding human HGF, pCikhHGF [human HGF (hHGF) gene expressed from the cytomegalovirus (CMV) immediate-early promoter and enhancer] compared with medium control. Electroporation-mediated in vivo HGF gene transfer using pCikhHGF 7 days after intratracheal bleomycin reduced pulmonary fibrosis as assessed by histology and hydroxyproline determination 14 days after bleomycin compared with controls treated with the same vector not containing the HGF sequence (pCik). Lung epithelial cell proliferation was increased and apoptosis reduced in hHGF-treated lungs compared with controls, suggesting increased alveolar epithelial repair in vivo. In addition, profibrotic transforming growth factor-beta1 (TGF-beta1) was decreased in hHGF-treated lungs, indicating an involvement of TGF-beta1 in hHGF-induced reduction of lung fibrosis. In conclusion, electroporation-mediated gene transfer of hHGF decreases bleomycin-induced pulmonary fibrosis, possibly by increasing alveolar epithelial cell proliferation and reducing apoptosis, resulting in improved alveolar wound repair.     

Cell-specific expression of human HGF by alveolar type II cells induces remodeling of septal wall tissue in the lung: a morphometric study

Hepatocyte growth factor (HGF) is involved in development and regeneration of the lungs. Human HGF, which was expressed specifically by alveolar epithelial type II cells after gene transfer, attenuated the bleomycin-induced pulmonary fibrosis in an animal model. As there are also regions that appear morphologically unaffected in fibrosis, the effects of this gene transfer to normal lungs is of interest. In vitro studies showed that HGF inhibits the formation of the basal lamina by cultured alveolar epithelial cells. Thus we hypothesized that, in the healthy lung, cell-specific expression of HGF induces a remodeling within septal walls. Electroporation of a plasmid of human HGF gene controlled by the surfactant protein C promoter was applied for targeted gene transfer. Using design-based stereology at light and electron microscopic level, structural alterations were analyzed and compared with a control group. HGF gene transfer increased the volume of distal air spaces, as well as the surface area of the alveolar epithelium. The volume of septal walls, as well as the number of alveoli, was unchanged. Volumes per lung of collagen and elastic fibers were unaltered, but a marked reduction of the volume of residual extracellular matrix (all components other than collagen and elastic fibers) and interstitial cells was found. A correlation between the volumes of residual extracellular matrix and distal air spaces, as well as total surface area of alveolar epithelium, could be established. Cell-specific expression of HGF leads to a remodeling of the connective tissue within the septal walls in the healthy lung, which is associated with more pronounced stretching of distal air spaces at a given hydrostatic pressure during instillation fixation.     

Lung Function in Patients Receiving Busulphan

An attempt was made to achieve earlier detection of busulphan lung (fibrosing alveolitis) and to determine its incidence by means of serial studies during life, including measurement of the gas transfer factor. Twenty-three patients were investigated over an average period of nearly two years of busulphan treatment. One case of busulphan lung was detected and subsequently confirmed at necropsy, but in the remainder there was no clinical, radiological, or physiological evidence of fibrosing alveolitis. It is concluded that the development of fibrosing alveolitis may be related to individual genetic or immunological factors rather than to busulphan dosage.     

Chemokine expression in Th1 cell-induced lung injury: prominence of IFN-gamma-inducible chemokines

Proinflammatory responses generated by T helper type 1 (Th1) cells may contribute significantly to immune-mediated lung injury. We describe a murine model of Th1 cell-induced lung injury in which adoptive transfer of alloreactive Th1 cells produces pulmonary inflammation characterized by mononuclear cell vasculitis, alveolitis, and interstitial pneumonitis. To investigate the link between activation of Th1 cells in the lung and inflammatory cell recruitment, we characterized cytokine and chemokine mRNA expression in Th1 cells activated in vitro and in lung tissue after adoptive transfer of Th1 cells. Activated Th1 cells per se express mRNA for interferon (IFN)-gamma and several members of the tumor necrosis factor family as well as the C-C chemokine receptor-5 ligands regulated on activation normal T cells expressed and secreted and macrophage inflammatory protein-1alpha and -1beta. Additional chemokine genes were induced in the lung after Th1 cell administration, most notably IFN-gamma-inducible protein (IP-10) and monokine induced by IFN-gamma (MIG). Remarkable increases in IP-10- and MIG-immunoreactive proteins were present in inflammatory foci lung and identified in macrophages, endothelium, bronchial epithelium, and alveolar structures. The findings suggest that IFN-gamma-inducible chemokines are an important mechanism for amplifying inflammation initiated by Th1 cells in the lung.