热-磁-振疗法对慢性阻塞性肺疾病患者气道炎症的影响

目的观察热-磁-振疗法对慢性阻塞性肺疾病（COPD）患者气道炎症的影响，并探讨其作用机制。 方法将78例急性发作期COPD患者分为治疗组40例和对照组38例。对照组行常规治疗，治疗组在常规治疗的基础上给予热-磁-振治疗，每日1次，每次30 min。2组患者均在治疗前、后分别记录其临床症状及体征，并检测血清中肿瘤坏死因子α（TNF-α）、白介素6（IL-6）、白介素8（IL-8）、白介素13（IL-13）以及肺通气功能［1秒钟用力呼气容积占预计值百分比（FEV1.0%）和1秒钟用力呼气容积/用力肺活量百分比（FEV1.0/FVC）］。 结果治疗组治疗后其咳嗽、痰液性状、痰量及干啰音等临床症状与体征的改善明显优于对照组（P<0.05或P<0.01），TNF-α、IL-6、IL-8、IL-13均显著降低（P<0.05或P<0.01）,FEV1.0%、FEV1.0/FVC明显升高，其中治疗后FEV1.0%、FEV1.0/FVC（%）的改善治疗组优于对照组（P<0.01）。相关分析表明，TNF-α、IL-6、IL-8、IL-13均与FEV1.0%呈负相关（P<0.01）。 结论热-磁-振疗法治疗COPD具有调节炎性细胞因子分泌，减轻气道炎症，提高肺通气功能的作用。     

超短波对辅助无创通气治疗COPD伴Ⅱ型呼吸衰竭的影响

目的观察超短波对接受无创正压通气治疗慢性阻塞性肺病（COPD）伴Ⅱ型呼吸衰竭患者的影响。 方法治疗组在常规治疗及无创正压通气的基础上加用超短波治疗，微热量，每日1次，每次15 min，共15 d；对照组在常规治疗的基础上加用无创正压通气。对所有患者进行血氧饱和度监测，治疗前、后检测动脉血气分析指标动脉血氧分压（PaO2）、动脉血二氧化碳分压（PaCO2）及肺的通气功能指标：用力肺活量（FVC）、第一秒用力呼气量（FEV1.0），记录机械通气时间和住院时间。 结果治疗组总有效率为93.3%，对照组总有效率为73.3%，治疗组总有效率明显高于对照组（P<0.05）；机械通气时间治疗组为（6.2±2.6）d，对照组为（8.1±3.0）d，住院时间治疗组为（17.8±2.5）d，对照组为（19.2±3.0）d，上述指标2组比较，差异有统计学意义（P<0.05）；动脉血气分析结果治疗组明显优于对照组（P<0.05），治疗组肺功能改善明显高于对照组（P<0.05）。 结论超短波辅助无创正压通气治疗COPD伴Ⅱ型呼吸衰竭患者可提高临床疗效，减少患者机械通气时间和住院时间，改善患者缺氧状态及肺的通气功能。     

超短波并川芎嗪雾化吸入疗法对支气管哮喘细胞因子失衡的调节作用

目的探讨超短波加川芎嗪雾化吸入疗法对支气管哮喘细胞因子失衡的调节作用。 方法选取轻、中度支气管哮喘患者70例，随机分为超短波加川芎嗪雾化吸入治疗组（超短波组）36例和单纯川芎嗪雾化吸入治疗组（吸入疗法组）34例，疗程为2周。另选本院无吸烟史的健康体检者30例作为健康对照组。所有患者于入院第1天治疗前及治疗2周后进行症状体征评分，记录无症状天数、β2受体激动剂吸入量，测定肺功能指标，包括1秒钟用力呼气容积（FEV1）、最大呼气流量（PEF）。3组均抽取静脉血，采用双抗体夹心酶联免疫吸附测定法检测IL-4和IFN-γ水平。 结果与健康对照组比较，哮喘患者血清IL-4水平升高、IFN-γ水平降低，差异均有统计学意义（P<0.05）。2组患者经治疗后，临床症状评分下降，FEV1、PEF升高，血清IL-4水平、IL-4/IFN-γ比值降低，与治疗前比较，差异有统计学意义（P<0.05）；且超短波组上述各指标变化更明显，与吸入疗法组比较，差异有统计学意义（P<0.05）。2组患者IFN-γ水平虽有升高，但与治疗前比较，差异无统计学意义（P&rt;0.05）。 结论超短波加川芎嗪雾化吸入治疗支气管哮喘有较好的临床疗效，其作用机制可能与调节失衡的TH1/TH2平衡有关。     

超短波与氦-氖激光穴位照射治疗毛细支气管炎疗效观察

目的观察超短波与氦-氖激光穴位照射治疗小儿毛细支气管炎的疗效。 方法将80例急性毛细支气管炎患儿随机分为药物组、超短波组、激光组及综合组，每组20例，药物组予以药物治疗，超短波组在药物治疗的基础上加用超短波治疗，激光组在药物治疗的基础上加用氦-氖激光穴位照射治疗，综合组在药物治疗的基础上加用超短波与氦-氖激光穴位照射治疗。观察4组患儿临床症状体征消失的天数、住院天数、住院总费用以及治疗7 d后的疗效。 结果药物组临床症状和体征消失天数长于其他各组（P<0.01），而超短波组和激光组的咳嗽、肺部痰鸣音消失天数较综合组明显延长（P<0.01）；药物组住院天数较综合组和超短波组明显延长（P<0.01），药物组的住院天数比激光组长（P<0.05），药物组住院总费用高于其他各组（P<0.01）；超短波组和激光组临床症状体征消失天数、住院天数、住院总费用比较，差异无统计学意义（P&rt;0.05）；综合组、超短波组、激光组治疗7 d后的治愈率明显高于药物组，差异有统计学意义（P<0.01）。 结论应用超短波与氦-氖激光穴位照射治疗小儿毛细支气管炎，能加速病情好转，缩短住院时间，降低住院费用，提高治疗效果。     

深呼吸体操联合负荷呼吸训练对慢性阻塞性肺疾病患者肺功能的影响

目的观察深呼吸体操训练联合负荷呼吸训练对慢性阻塞性肺疾病（COPD）患者肺功能的影响。 方法共选取27例COPD患者，将其分为治疗组14例及对照组13例。对照组给予深呼吸体操训练，治疗组在此基础辅以负荷呼吸训练。于入选时及治疗60 d后对2组患者肺功能［包括最大肺活量（VC）、用力肺活量（FVC）、第1秒用力呼气容积 (FEV1)、呼气峰流速（PEF）及呼吸频率等指标］进行比较。 结果经60 d训练后，发现治疗组及对照组各项肺功能指标均较入选时明显改善（P<0.05），并且以治疗组的改善幅度相对较显著，与对照组间差异具有统计学意义（P<0.05）。 结论深呼吸体操训练联合负荷呼吸训练治疗COPD患者具有协同疗效，能进一步改善患者肺功能，促进病情缓解。     

肺俞穴经皮电神经刺激对慢性阻塞性肺疾病患者肺功能及诱导痰肿瘤坏死因子-α浓度的影响

目的观察经皮电神经刺激（TENS）肺俞穴对慢性阻塞性肺疾病（COPD）患者肺功能及诱导痰中肿瘤坏死因子-α（TNF-α）浓度的影响。 方法采用随机数字表法将30例轻、中度（肺功能Ⅰ-Ⅱ级）COPD患者分为治疗组及对照组,每组15例。治疗组患者给予肺俞穴经皮电神经刺激治疗,对照组患者则给予肺俞穴经皮神经假刺激治疗。于治疗前、治疗4周后分别对2组患者肺功能,体质指数-气流阻塞-呼吸困难-运动能力（BODE）指数及诱导痰中TNF-α浓度进行检测。 结果治疗前2组患者肺功能［包括用力肺活量(FVC)、1秒用力呼气容积(FEV1)、1秒用力呼气容积与用力肺活量比值(FEV1%)及呼气峰值流速(PEFR)］、BODE指数及诱导痰中TNF-α浓度组间差异均无统计学意义（P&rt;0.05）;分别经4周治疗后,发现治疗组FVC［（2.75±0.77）L］、FEV1［(1.77±0.50)L］、FEV1%［（73.20±7.69)%］及PEFR［(4.33±1.09)L/S］均较治疗前及对照组明显改善（P<0.05）;治疗组治疗后诱导痰中TNF-α浓度［（14.27±2.78)pg/ml］、BODE指数［（0.43±0.65)分］亦较治疗前及对照组明显下降（P<0.05）,而对照组上述指标治疗前、后均无明显变化（P&rt;0.05）。 结论肺俞穴经皮电神经刺激能缓解轻、中度COPD患者气道炎性反应,改善肺功能,降低其BODE指数,对提高患者日常生活活动能力具有重要意义。     

重复功能性磁刺激联合腹直肌电刺激对颈髓损伤患者肺通气功能的影响

目的观察重复功能性磁刺激（rFMS）联合腹直肌电刺激对中、低位颈髓损伤（CSCI）患者肺通气功能的影响。 方法共选取25例中、低位CSCI患者,采用随机数字表法将其分为治疗组及对照组。对照组给予上肢主动运动、站立训练、呼吸功能训练等综合康复治疗,治疗组在此基础上辅以rFMS及腹直肌中频电刺激。分别于治疗前、治疗3个月后对2组患者肺功能［包括最大肺活量（VC）、1秒钟用力呼气量（FEV1）、呼气峰值流速（PEF）及潮气量（VT）等指标］进行评定。 结果2组患者分别经3个月治疗后,发现治疗组VC［(3.24±0.89)L］、FEV1［(2.58±0.74)L］、PEF［(6.74±1.63)L］、VT［(394.33±96.54)ml］及对照组VC［(2.19±0.52)L］、FEV1［(2.10±0.47)L］、PEF［(5.24±1.69)L］、VT［(316.72±74.18)ml］均较治疗前明显改善（P<0.05）,并且上述指标均以治疗组患者的改善幅度较显著,与对照组间差异均具有统计学意义（P<0.05）。 结论中、低位CSCI患者在常规康复训练基础上辅以rFMS及腹直肌中频电刺激,可进一步改善通气效率,提高肺通气功能。     

呼吸训练队缓解期慢性阻塞性肺病患者肺功能的影响

目的观察呼吸训练对缓解期慢性阻塞性肺病（COPD）患者肺功能的影响。 方法将74例缓解期COPD患者随机分为对照组和治疗组,治疗组进行6个月呼吸训练,包括缩唇呼吸、腹式呼吸、呼吸操,对照组不进行呼吸训练。比较2组治疗前、后肺功能指标。 结果治疗组呼吸训练后肺活量（VC）、用力肺活量（FVC）、第一秒用力呼出量（FEV1）、用力呼气高峰流速（PEFR）、25％肺活量最大呼气流量（V25）增加,残气量（RV）、残气/肺总量％（RV/TLC）减低,与对照组比较,差异有统计学意义（均P<0.05）,与治疗前比较,差异有统计学意义（均P<0.05）。 结论呼吸训练能够改善COPD缓解期患者的肺功能。     

综合疗法治疗膝关节功能障碍疗效观察

目的观察持续被动运动（CPM）、玻璃酸钠关节腔注射、超短波和超声波治疗膝关节功能障碍的疗效。 方法60例膝关节功能障碍患者随机分为治疗组30例和对照组30例，治疗组采用CPM、玻璃酸钠注射液关节腔注射、超短波和超声波治疗，对照组仅采用超短波和超声波治疗，并分别于治疗前及治疗5周后测量关节活动度，评定疗效。 结果治疗组治疗前、后关节活动度改善优于对照组（P<0．05），且疗效优良率优于对照组（P<0．05）。 结论采用玻璃酸钠关节腔注射、CPM、超短波和超声波治疗膝关节功能障碍可有效防止关节粘连的发生，提高膝关节活动度，恢复其功能作用。     

康复干预对气道高反应性患者肺功能的影响

目的探讨康复干预对轻、中度气道高反应性患者肺功能的影响。 方法轻、中度气道高反应性患者60例,随机分为对照组30例和观察组30例,对照组采用常规药物治疗,观察组在常规药物治疗的基础上增加呼吸功能训练、适宜的有氧运动训练和心理指导等。应用肺功能仪检测2组患者治疗前和治疗2,4,8周后的用力肺活量（FVC）、第一秒用力呼气量（FEV1.0）、用力呼气50%流速（FEF50）、用力呼气中期流速（MMEF）。 结果治疗2,4,8周后,观察组的FVC实测值占预计值的百分比（FVC%）、FEV1.0实测值占预计值的百分比（FEV1.0%）、FEF50实测值占预计值的百分比（FEF50%）、MMEF实测值占预计值的百分比（MMEF%）均明显高于对照组（P<0.05）。 结论对气道高反应性患者采用呼吸功能训练等措施早期干预,可明显改善肺功能,延缓或防止发展成为慢性阻塞性肺疾病（COPD）。     

Structural determinants of the eosinophil: chemotactic activity of the acidic tetrapeptides of eosinophil chemotactic factor of anaphylaxis

The acidic tetrapeptides of ECF-A, Ala/Val-Gly-Ser-Glu, exhibit peak in vitro chemotactic activity for human eosinophils at concentrations of 3 X 10(-8) M to 10(-6) M, and rapidly deactivate eosinophils to homologous and other stimuli at concentrations as low as 10(-10) M. The analogue Leu-Gly-Ser-Glu reaches peak activity at 10(-8)M-10(-7)M, while Phe-Gly-Ser-Glu requires 10(-4)M to elicit a peak response. Although inversion of the order of glycine and serine does not alter the eosinophil chemotactic activity of the tetrapeptides, deletion of glycine increases by 10-fold the concentration required for peak chemotactic activity, indicating the critical nature of the spacing between NH2- and COOH-terminal residues. The substituent COOH-terminal tripeptide, which is only marginally chemotactic, irreversibly suppresses eosinophil chemotactic responsiveness at a concentration 10,000-fold higher than concentrations necessary for deactivation by the intact tetrapeptide. The high concentration of tripeptide required for this cell directed effect, which is assumed to be analogous to deactivation, is attributed to the absence of the NH2-terminal residue which would facilitate effective interaction with the eosinophil. A substituent NH2-terminal tripeptide and amides of the NH2-terminal amino acids, which are devoid of chemotactic and deactivating activities, reversibly inhibit the tetrapeptide stimulus in a dose- response fashion. The additional finding that the NH2-terminal tripeptide protects the eosinophil from deactivation by the intact tetrapeptide confirms that the competitive interaction is stimulus specific.     

The eosinophil enigma

Eosinophils accumulate in high numbers in the lungs of asthmatic patients. These cells have the ability to induce tissue damage, a capacity that relates to their traditional role in host defense against parasitic worms. On the other hand, eosinophils produce growth factors associated with tissue repair and remodeling, notably TGF-beta1. The relationship of these activities to lung dysfunction in asthma is highly controversial, but recent observations in humans and in animal models add spice to the debate.     

Human eosinophil heterogeneity

Summary The aim of this review is to examine some of the most important findings pointing toward human eosinophil heterogeneity. Special importance is given to cell density, surface receptors, metabolism and response to biological products or synthetic compounds.     

Enhancement of human blood eosinophil cytotoxicity by semi-purified eosinophil colony-stimulating factor(s)

Purified human blood eosinophils, when incubated in human placental conditioned medium (a source of colony-stimulating factors) [CSF]) demonstrate an enhanced ability to damage antibody- or complement- coated schistosomula. This enhancement represents a 4- to 10-fold increase of eosinophil schistosomicidal ability and a 10-fold lowering of the threshold for antibody or complement required in the killing reaction. The activity that enhances eosinophil cytotoxicity and the eosinophil colony-stimulating activity in the placental conditioned medium are eluted in the same fraction (CSF-alpha) after chromatography on Sephadex G-100 and phenyl-Sepharose columns, suggesting that these two activities might be associated with the same molecule. CSF-alpha enhances the adherence step of the killing reaction: antibody-coated larvae were frequently found covered by several layers of eosinophils in tubes containing CSF-alpha. Such a degree of adherence was rarely seen in control tubes lacking CSF-alpha. This enhancement of the eosinophil adherence is detectable 45-60 min after addition of CSF- alpha to the culture. It is not affected by washing the cells after a short time of preincubation with CSF-alpha, and it occurs in the absence of protein synthesis, whereas colony-stimulating activity requires continuous protein synthesis and ceases when CSF is removed from the culture. Finally, CSF-alpha enhances the temperature-dependent reaction that insures the irreversibility of eosinophil attachment to schistosomula. These observations suggest that eosinopoietic factors could be responsible for some of the modified properties of blood eosinophils in eosinophilic individuals.     

Cloning, expression, and characterization of the human eosinophil eotaxin receptor

Although there is a mounting body of evidence that eosinophils are recruited to sites of allergic inflammation by a number of beta- chemokines, particularly eotaxin and RANTES, the receptor that mediates these actions has not been identified. We have now cloned a G protein- coupled receptor, CC CKR3, from human eosinophils which, when stably expressed in AML14.3D10 cells bound eotaxin, MCP-3 and RANTES with Kds of 0.1, 2.7 and 3.1 nM, respectively. CC CKR3 also bound MCP-1 with lower affinity, but did not bind MIP-1 alpha or MIP-1 beta. Eotaxin, RANTES, and to a lessor extent MCP-3, but not the other chemokines, activated CC CKR3 as determined by their ability to stimulate a Ca(2+) - flux. Competition binding studies on primary eosinophils gave binding affinities for the different chemokines which were indistinguishable from those measured with CC CKR3. Since CC CKR3 is prominently expressed in eosinophils we conclude that CC CKR3 is the eosinophil eotaxin receptor. Eosinophils also express a much lower level of a second chemokine receptor, CC CKR1, which appears to be responsible for the effects of MIP-1 alpha.     

Differentiation in vitro of hybrid eosinophil/basophil granulocytes: autocrine function of an eosinophil developmental intermediate

Granulocytes with the hybrid characteristics of eosinophils and basophils have been identified in the bone marrow and peripheral blood of humans with myeloid leukemias. We now describe a technique by which such hybrid granulocytes can be developed in vitro from normal cord blood precursors cultured in the presence of recombinant human interleukin (rhIL) 3 (350 pM) and rhIL-5 (200 pM) in a plastic vessel coated with Matrigel. After 14 d in culture, 90 +/- 3% (mean +/- standard error of the mean) of the nonadherent cells cultured in the Matrigel-coated flasks contained both eosinophil and basophil granules, as indicated by staining with Wright's and Giemsa stains. Of the nonadherent cells, 93 +/- 1% contained cyanide-resistant peroxidase, and 88 +/- 2% were toluidine blue-positive, characteristic of eosinophil and basophil granules, respectively. Transmission electron micrographs showed hybrid cells containing ultrastructurally distinct eosinophil granules with developing crystalline cores and basophil granules with reticular structures. These 14-d cord blood-derived cell cultures showed strong hybridization signals for eosinophil-derived neurotoxin by RNA blot analysis and contained 78 ng histamine per 10(6) cells. When the granulocytes were removed from cytokine-containing medium and suspended without Matrigel in RPMI 1640 medium containing 10% fetal calf serum (FCS), more than 80% of the granulocytes excluded trypan blue for as long as 5 d, and 93% had developed into eosinophils at 6 d. Conditioned medium prepared over 48 h from the 14-d cell cultures (hybrid granulocytes) sustained the 4-d viability in vitro of 78% of peripheral blood eosinophils from atopic donors. In comparison, 13% survived in RPMI 1640 containing 10% FCS alone. This viability- sustaining activity was nearly completely neutralized by an anti- granulocyte/macrophage colony-stimulating factor (GM-CSF) antibody and was only minimally reduced by anti-IL-3 or IL-5. Thus, cells possessing both eosinophil and basophil granules by both histochemical and ultrastructural analysis can be developed from normal progenitors in vitro in response to eosinophilopoietic cytokines and Matrigel. Their subsequent spontaneous development into mature eosinophils suggests that hybrid granulocytes are part of a normal developmental sequence during eosinophilopoiesis. Furthermore, these hybrid granulocytes are capable of autoregulation through elaboration of GM-CSF, which sustains their viability.     

Effect of zinc and other cations on the release of the eosinophil cationic protein

The eosinophil cationic protein, ECP, is a unique eosinophil granule constituent, which is released extracellularly after exposure of the eosinophils to a non-phagocytosable surface such as complement-coated Sephadex beads. The ECP is released to some extent even in the absence of Ca2+ and Mg2+, though both these cations augment the release reaction tested alone, and an optimal release is observed only in the presence of 2 mmol/l Ca2+ and 2 mmol/l Mg2+ in the medium. Zn2+ at concentrations from 0.25-4.0 mmol/l inhibited the release of ECP in a dose-dependent fashion, with or without Ca2+ and Mg2+ in the medium. Mn2+ had dual effects, stimulating the ECP release in the absence of Mg2+ and Ca2+, and inhibiting the release in the presence of these cations. Li1+ caused minor inhibition of ECP release, but only in the absence of Ca2+ and Mg2+. The inhibitory effect of Zn2+ was immediate and reversible after washing of the cells, suggesting that the inhibition is due to interaction with the plasma membrane functions.