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Objective: To investigate the clinic value of nasal trachea cannula under the guidance of fibrobronchoscope to establish artificial airway.

目的:探讨纤维支气管镜引导下经鼻气管插管建立人工气道的临床价值。

When used carburization and tempering, filling baskets should be designed according to different parts of horizontal

当用于渗碳及回火时,装料筐设计应根据不同工件设计横向和纵向气道,使碳势气氛和热风能均匀通过工件每一点,使工件渗碳层或回火均匀。

AIM: To explore the mechanism of signal cascades in cigarette smoke-induced mucous hypersecretion.

目的:探讨香烟对气道黏液分泌的影响及其信号转导机制。

The blood pressure of.1 of pathology physiology mechanism that SAS causes CVD breathes time-out to be able to bring about airframe in elevatory Morpheus anoxic, sympathetic is excessive and excited, element of serous catechu phenolic amine, kidney and hemal endodermis element are elevatory, bring about hemal easy of hemal convulsion; to shrink the function is disorder, can make blood-vessel flowing flesh happening reframes and fleshy, systemic blood-vessel obstruction adds element of the kidney when; is chronic and anoxic, system of hemal and nervous element is activationed, bring about blood pressure to lift. Obstruction of way of energy of life of patient of OSAS of disease of blood of 1.2 low oxygen increases, cause air current to interrupt, breath pauses, at the same time airframe gets used to low oxygen environment gradually, breathing centre drops to low oxygen and sensitivity of disease of blood of tall carbonic acid, breath suspends a frequency increasing, farther aggravating airframe is anoxic. 1.3 heads are self-adjusting the function drops normal person changes quickly in systematic circulation blood pressure when, the head can be passed adjust independently functional generation protects effect, make change of cerebral blood flow not big.

SAS诱发CVD的病理生理机制。1血压升高睡眠中呼吸暂停可导致机体缺氧,交感神经过度兴奋,血浆儿茶酚胺、肾素以及血管内皮素升高,导致血管痉挛;血管舒缩功能紊乱,可使血管平滑肌发生重构和肥厚,全身血管阻力增加;慢性缺氧时肾素—血管紧张素系统被激活,导致血压升高。1.2低氧血症OSAS患者气道阻力增加,造成气流中断、呼吸暂停,同时机体逐渐适应低氧环境,呼吸中枢对低氧和高碳酸血症敏感性下降,呼吸暂停次数增加,进一步加重机体缺氧。1.3脑自动调节功能下降正常人在体循环血压快速变化时,脑可通过自主调节功能产生保护效应,使脑血流量变化不大。

of characteristic line is applied to the software.

该软件所采用的数理模型为气体动力学中的特征线方法,主要研究从气道段至缸内这一段的流动。

Because chronic obstructive inflammation of airway severely influences the ventilation and exchange function of COPD patients, The motor ability of patients is limited .Despnoea and fatigue limit patients to sedentary,because of this, skeletal muscle began to analosis,oxygen uptaking capacity of skeletal muscle descends,and concentration of chondriosome degrades.Function limitation of skeletal muscle causes oxygen needs increase,so vicious cycle emerges,and further to restrict patient's respiratory and motor function.

由于气道的慢性炎症性阻塞,严重影响了慢阻肺患者的通气及换气功能,使得患者的运动能力明显受限,因喘息和疲劳而限制了患者的运动能力,使患者出现久坐,由此出现骨骼肌的萎缩,骨骼肌摄氧能力下降,线粒体氧浓度降低,骨骼肌的功能受限又会引起通气量不足,进而引起低氧血症和高碳酸血症,使患者的摄氧需求增加,由此出现恶性循环,进一步制约了患者的呼吸和运动功能。2001年正式提出肺康复作为中重度COPD患者稳定期非药物治疗的首选管理方案。

、Increased activation of NF-κB might be the basis for chronicity of airway inflammation in asthma.

肺组织NF-κB过度激活可能是哮喘慢性气道炎症持续存在的基础

Bronchial asthma is a chronicity airway inflammation disease.

支气管哮喘是一种慢性气道炎症性疾病。

By measuring changes of Plasma levels of GMP-140, GP lib/III a and D-dimer in patients with OSAS before and after the institution of nasal continuous positive airway pressure, we want to study whether plate activation and enhance coagulability, fibrinolytic activation occur and play a role in prevalence ofcerebrovascular and cardiovascular events in patients with OSAS and the association with hypoxemia, if so, whether therapy with nCPAP alters this effect.

我们通过检测OSAS患者血浆α-颗粒膜蛋白(GMP-140)、血小板膜糖蛋白Ⅱb/Ⅲa和D-二聚体的变化,了解OSAS患者体内是否也存在血小板活化、凝血激活和继发纤溶亢进及其与低氧血症的关系,进一步从分子生物学角度探讨血小板活化、凝血激活和继发纤溶亢进在OSAS发生发展中的作用及经鼻持续气道正压通气对其影响。

At the same time, the content of reactive oxygen species in the lung tissues was assessed with chemical colorimetry.

结果mt组大鼠气道反应性及balf中炎性细胞数明显低于哮喘组,差异有显著性(p<0.05)。

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Lugalbanda was a god and shepherd king of Uruk where he was worshipped for over a thousand years.

Lugalbanda 是神和被崇拜了一千年多 Uruk古埃及喜克索王朝国王。

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