CAT 评分对评估慢性阻塞性肺疾病病情及急性加重诊断的意义

目的探讨CAT评分对于反映COPD患者病情及评估急性加重的意义。方法选取88例COPD—AE患者,分别于住院时及出院前进行CAT评分,并于住院后行肺功能检测,比较稳定期及急性加重期CAT分值差异,比较低CAT评分组及高评分组FEV1％pred及急性加重频率的区别,观察稳定期CAT值与FEV1％pred及此前1年内急性加重次数的相关性。结果急性加重期COPD患者CAT评分显著高于稳定期（P〈0．05）。高CAT评分组FEV．％pred明显低于低CAT评分组,1年内急性加重次数多于低CAT评分组（P〈0．05）。稳定期CAT评分与FEV1％pred无明显相关性（P〉O．05）,但与此前1年内急性加重次数呈正相关（r=0．72,P〈0．05）。结论结合CAT评分可更好反映COPD疾病全貌,CAT评分可增加COPD—AE诊断的客观性。     

健康教育及早期康复训练对脑梗死患者康复的疗效观察

目的：探讨健康教育及早期康复训练对急性脑梗死患者康复的效果,为临床康复方案的制定提供参考。方法选取急性脑梗死患者124例,采用数字表法随机分为观察组和对照组各62例。对照组采用急性脑梗死常规治疗方案进行干预,观察组在对照组干预方案的基础上,采用健康教育以及早期康复训练。比较两组患者成功戒烟、戒酒的比例,比较两组患者能够合理调整饮食结构、积极配合康复训练的比例,比两组患者干预前后的简式 Fugl-Meyer 评测法（FMA）和 Barthel 指数积分的评估结果。结果观察组成功戒烟的比例为80．65％、成功戒酒的比例为78．95％,均显著高于对照组的40．00％、41．18％（χ2＝10．554、3．914,均P ＜0．05）;观察组能够合理调整饮食结构的比例为77．42％、积极配合康复训练的比例为67．74％,均显著高于对照组的40．32％、35．48％（χ2＝17．619、11．657,均 P ＜0．05）;两组患者干预后的 FMA 评分和 Barthel 积分指数均显著高于干预前（均 P ＜0．05）,观察组干预后的 FMA 评分为（68．92±25．83）分、Barthel 积分指数为（56．81±16．03）,均显著高于对照组的（50．26±24．37）分、（41．49±14．52）（t ＝2．975、2．582,均 P ＜0．05）。结论健康教育和早期康复训练能够帮助急性脑梗死患者纠正不良生活习惯,提高患者治疗的依从性,促进患者肢体运动功能和日常生活活动能力的改善。     

慢性阻塞性肺疾病患者对疾病认知与治疗情况的调查

目的研究慢性阻塞性肺疾病（COPD）患者对疾病的认知及治疗情况。方法2012年7月-2013年9月期间入住本院的365例COPD患者进行调查,内容包括患者对疾病的认识,稳定期的用药情况、家庭氧疗及康复锻炼等。结果曾被告知为COPD的患者仅为6例（1．6％）;342例患者从未做过肺功能检查（93．7％）。COPD患者从未用药的为191例（52．3％）,家庭氧疗36例（9．9％）,康复锻炼的12例（3．3％）,家庭无创呼吸机应用1例（0.3％）。结论COPD患者对疾病的认知情况差,治疗不规范。加强对COPD患者的健康宣教,进一步提高基层医院医生对COPD的诊治水平是今后重要的工作。     

舒利迭对慢性阻塞性肺疾病稳定期患者的肺功能及生活质量的影响

目的探讨舒利迭对稳定期慢性阻塞性肺疾病（COPD）患者的肺功能改善生活质量的影响。方法将稳定期COPD患者103例随机分成治疗组51例和对照组52例,两组患者在治疗前以及治疗后6周（第43d）治疗12周（第85d）分别测定肺功能。6min步行距离,圣—乔治问卷（SGRQ总评分）,CAT量表等参数。治疗组在常规治疗基础上吸入舒利迭,每天早晚各1次,每次1吸,对照组只给予常规治疗,不吸入舒利迭。结果治疗后6周、12周,治疗组患者肺功能中FEV1、FEV1%与对照组比较显著改善[1.68＋0.13 VS 1.12＋0.14;1.81＋0.18 VS 1.07＋0.15 P〈0.05]。6min步行距离大幅度提高[464＋15 VS 312＋20 P〈0.05]圣—乔治问卷（SGRQ总评分）CAT量表分值均显著减少,[40.9＋0.69 VS 4.37＋0.97;16＋21VS 24＋18 P〈0.05]。结论长期规范吸入舒利迭可改善中、重度COPD患者的肺功能,并且能提高患者的生活质量;此疗法值得临床进一步推广应用。     

健康教育在慢性阻塞性肺疾病稳定期中应用的效果评价

目的观察规范健康教育在慢性阻塞性肺疾病（COPD）稳定期中应用的效果。方法将94例住院的COPD稳定期患者分为观察组46例和对照组48例。两组患者均采用COPD常规治疗,在此基础上,观察组患者采用规范的健康教育,比较两组患者COPD相关知识掌握情况、患者满意度、出院后氧疗、吸入用药、呼吸功能锻炼的依从性及平均急性发作次数。结果观察组患者COPD相关知识掌握情况、患者满意度、出院后氧疗、吸入用药、呼吸功能锻炼的依从性明显高于对照组,平均急性发作次数低于对照组。结论规范健康教育有利于患者COPD相关知识的掌握,可减少急性发作次数,改善肺功能,提高自觉用药及康复锻炼的依从性。     

不同时期 COPD 患者肺康复时间依从性的比较及影响因素分析

目的 探讨慢性阻塞性肺疾病（COPD）患者不同时期进行肺康复治疗的时间依从性差异及其影响因素。方法 连续选取 2013 年 6 月—2015 年 5 月天津市胸科医院呼吸与危重症科因 COPD 急性加重住院患者, 最终到达观察终点 304 例, 随机分为稳定期康复组（178 例）及急性加重期康复组（126 例）; 根据所有患者实际完成康复时间是否大于计划康复时间的 70%判定依从性, 并据此分为依从性好组（115 例）及依从性差组（189 例）。 分别比较稳定期康复组及急性加重期康复组实际完成康复时间、达到依从性好的患者比例及退出率, 比较依从性好组及依从性差组的一般临床资料, 在肺康复结束后, 采用 Logistic 回归分析影响肺康复依从性的因素。 结果 稳定期康复组实际完成康复时间、达到依从性好的患者比例均高于急性加重期康复组（ [ 5 641.5±1 080.1）min vs.（4 426.5±1 046.8）min, 46.7% vs. 25.4%）], 稳定期康复组退出率 10.6%（21/199）低于急性加重期康复组的退出率 26.7%（46/172）; 依从性好的患者家庭月收入水平、6 分钟内步行距离（6MWD）高于依从性差组, 年龄、吸烟者比例、呼吸困难评分（MRC 评分）及 COPD 评估测量（CAT）评分低于依从性差组（均 P < 0.05）。 Logistic 回归分析结果显示年龄大、吸烟、MRC 评分高、CAT 评分高是肺康复依从性差的危险因素, 月收入≥3 000 元、6MWD 长是保护因素。 结论 COPD 患者整体肺康复时间依从性较差, 年龄低、不吸烟、收入水平高、生活质量及健康状况好的患者肺康复时间依从性佳。     

联合吸入布地奈德／福莫特罗和噻托溴铵在治疗中重度稳定期慢性阻塞性肺疾病中的临床疗效研究

目的研究布地奈德／福英特罗联合吸入噻托溴铵对中重度慢性阻塞性肺疾病（COPD）稳定期患者的疗效。方法选取128例中重度COPD稳定期患者为研究对象,将其随机分为两组（各64例）,对照组吸入布地奈德／福英特罗,观察组吸入布地奈德／福莫特罗联合噻托溴铵,疗程6个月,测定患者治疗前后圣乔治呼吸问卷评分（SGRQ）、6min步行距离（6MWT）和肺功能情况（FEVl,FEVI／FVC％,FEV,占预计值％）并进行比较分析。结果两组患者在SGRQ、6MWT及肺功能方面较治疗前均明显改善（P〈0．05）,观察组各项指标较对照组改善更明显（P〈0．05）。结论布地奈德／福莫特罗联合吸八噻托溴铵在治疗中重度稳定期COPD患者临床疗效较单独吸入布地奈德／福莫特罗疗效好。     

慢性阻塞性肺病稳定期患者外周血Th17/Treg失衡情况及与预后的关系

目的：观察慢性阻塞性肺病（chronic obstructive pulmonary disease,COPD）稳定期患者外周血中Th17与Treg细胞的水平.方法：选取本院2010年1月-2012年12月间确诊的40例COPD稳定期患者,选取同期40例健康体检健康人群作为对照组,收集两组人群的外周血后采用流式细胞术检测各个人群Th17与Treg细胞亚群的比例,采用ELISA法检测血清中的IL-17、TGF-β水平,采用RT-PCR检测转录因子RORγT与Foxp3 mRNA水平.结果：COPD稳定期患者外周血中Th17比例为（3.14±0.31）％,显著高于对照组人群的（1.23±0.24）％,差异有统计学意义（P＜0.05）;COPD稳定期患者外周血中Treg比例为（6.27±0.32）％,显著高于对照组人群的（3.43±0.32）％,差异有统计学意义（P＜0.01）;COPD稳定期患者外周血中IL-17水平为（89.36±4.13） pg/mL,显著高于对照组的（30.35±2.53） pg/mL,差异有统计学意义（P＜0.05）;COPD稳定期患者外周血中TGF-β水平为（681.45±41.65） pg/mL,显著高于对照组人群的（519.36±30.43） pg/mL,差异有统计学意义（P＜0.01）;COPD稳定期患者外周血转录因子Foxp3与RORγT mRNA水平均显著高于对照组人群,差异有统计学意义（均P＜0.01）.COPD稳定期患者Th17、Treg比例高水平的住院天数和病死率均高于对应低水平亚组（P＜0.05）.结论：Th17、Treg细胞及IL-17、TGF-β水平在COPD稳定期患者外周血表达增加,且转录因子Foxp3与RORγT mRNA水平表达增加,提示其与COPD患者的预后有关,其外周血中Th17与Treg细胞的不平衡可能参与了COPD发病和病程的进展.     

呼吸康复治疗对缓解期慢性阻塞性肺疾病疗效观察

目的：观察呼吸康复治疗对于缓解期慢性阻塞性肺疾病（chronic obstructive pulmonary disease，COPD）的疗效。方法：COPD患者60例，随机分为两组，其中30例患者为对照组，给予药物治疗；30例患者为观察组，在对照组的基础上给予呼吸康复治疗，电话随访确保康复治疗依从性。3个月后对患者临床症状、活动耐力、健康相关生活质量进行评价。结果：观察组的咳嗽、呼吸困难症状改善率分别为70．0％、73．3％，均明显高于对照组的40．0％、46．7％（P〈0．05）；经过康复治疗，观察组（480．6±58．7）m，显著高于康复前（356．8±43．5）in，P〈0．05，差异具有统计学意义。对照组康复前与康复后活动耐力无差异，P〉0．05。观察组患者康复后生存质量评分显著低于对照组，P〈0．05。结论：COPD缓解期进行呼吸康复治疗，可以明显缓解临床症状，提高活动耐力及健康相关生活质量，值得临床推广。     

稳定期慢性阻塞性肺疾病病人生存质量影响因素分析

目的 探讨分析影响稳定期慢性阻塞性肺疾病(COPD)病人生存质量的因素并提出改进策略.方法 选取2019年6—7月在南京鼓楼医院药学门诊就诊的COPD病人120例,采用调查问卷方式收集其一般资料及COPD评估测试(CAT)评分、Morisky用药依从性问卷(MMAS-8)评分,通过欧洲五维健康量表计算健康效用值,对量表与因素进行单因素分析及多元线性回归分析.结果 共发放120份问卷,有效回收115份,单因素分析结果显示用药种类越多["≤2"比"3～5"比">5":(0.747±0.225)比(0.733±0.178)比(0.604±0.268)]、CAT评分越高["轻"比"中"比"严重"比"非常严重":(0.833±0.138)比(0.753±0.168)比(0.610±0.267)比(0.536±0.220)],效用值越低(P<0.05),病人的生存质量越差;而多元线性回归分析显示吸烟(β=-0.186)、CAT评分(β=-0.009)、MMAS-8评分(β=0.030)为COPD病人生存质量的影响因素(P<0.05).结论 吸烟、CAT评分为COPD病人生存质量的危险因素,MMAS-8评分为其保护因素.药师可通过开设药物治疗管理门诊,帮助COPD病人戒烟、提高疾病知识、解决药物相关问题等,从而改善病人生存质量.     

Synthesis,Cytotoxicity and Antileishmanial Activity of Some N-(2-(indol-3-yl)ethyl)-7-chloroquinolin-4-amines

We report herein the condensation of 4,7-dichloroquinoline (1) with tryptamine (2) and D-tryptophan methyl ester (3) . Hydrolysis of the methyl ester adduct (5) yielded the free acid (6) . The compounds were evaluated in vitro for activity against four different species of Leishmania promastigote forms and for cytotoxic activity against Kb and Vero cells. Compound (5) showed good activity against the Leishmania species tested, while all three compounds displayed moderate activity in both Kb and Vero cells.     

Lung disease and PKCs

The lung offers a rich opportunity for development of therapeutic strategies focused on isozymes of protein kinase C (PKCs). PKCs are important in many cellular responses in the lung, and existing therapies for pulmonary disorders are inadequate. The lung poses unique challenges as it interfaces with air and blood, contains a pulmonary and systemic circulation, and consists of many cell types. Key structures are bronchial and pulmonary vessels, branching airways, and distal air sacs defined by alveolar walls containing capillaries and interstitial space. The cellular composition of each vessel, airway, and alveolar wall is heterogeneous. Injurious environmental stimuli signal through PKCs and cause a variety of disorders. Edema formation and pulmonary hypertension (PHTN) result from derangements in endothelial, smooth muscle (SM), and/or adventitial fibroblast cell phenotype. Asthma, chronic obstructive pulmonary disease (COPD), and lung cancer are characterized by distinctive pathological changes in airway epithelial, SM, and mucous-generating cells. Acute and chronic pneumonitis and fibrosis occur in the alveolar space and interstitium with type 2 pneumocytes and interstitial fibroblasts/myofibroblasts playing a prominent role. At each site, inflammatory, immune, and vascular progenitor cells contribute to the injury and repair process. Many strategies have been used to investigate PKCs in lung injury. Isolated organ preparations and whole animal studies are powerful approaches especially when genetically engineered mice are used. More analysis of PKC isozymes in normal and diseased human lung tissue and cells is needed to complement this work. Since opposing or counter-regulatory effects of selected PKCs in the same cell or tissue have been found, it may be desirable to target more than one PKC isozyme and potentially in different directions. Because multiple signaling pathways contribute to the key cellular responses important in lung biology, therapeutic strategies targeting PKCs may be more effective if combined with inhibitors of other pathways for additive or synergistic effect. Mechanisms that regulate PKC activity, including phosphorylation and interaction with isozyme-specific binding proteins, are also potential therapeutic targets. Key isotypes of PKC involved in lung pathophysiology are summarized and current and evolving therapeutic approaches to target them are identified.     

Gender-related symptoms and correlates of alcohol dependence among men and women with a lifetime diagnosis of alcohol use disorders

This study explored gender-related symptoms and correlates of alcohol dependence in a crosssectional study of 150 men and 150 women with a lifetime diagnosis of alcohol use disorders (AUD). Participants were recruited in equal numbers from treatment settings, correctional centres and the general community. Standardized measures were used to determine participants' use of substances, history of psychiatric disorders and psychosocial stress, their sensation seeking and family history of substance use and mental health disorders. Multivariate analyses were used to detect patterns of variables associated with gender and the lifetime severity of AUD. Men had a longer history of severe AUD than women. Women had similar levels of alcohol dependence and medical and psychological sequelae as men, despite 6 fewer years of AUD. More women than men had a history of severe psychosocial stress, severe dependence on other substances and antecedent mental health problems, especially mood and anxiety disorders. There were differences in family history of alcohol-related problems approximating same-gender aggregation. The severity of a lifetime AUD was predicted by its earlier age at onset and the occurrence of other disorders, especially anxiety, among both men and women. The limitations in the generalizability of these findings due to sample idiosyncrasies are discussed.     

Biochemical and molecular characterisation of cubozoan protein toxins

Class Cubozoa includes several species of box jellyfish that are harmful to humans. The venoms of box jellyfish are stored and discharged by nematocysts and contain a variety of bioactive proteins that are cytolytic, cytotoxic, inflammatory or lethal. Although cubozoan venoms generally share similar biological activities, the diverse range and severity of effects caused by different species indicate that their venoms vary in protein composition, activity and potency. To date, few individual venom proteins have been thoroughly characterised, however, accumulating evidence suggests that cubozoan jellyfish produce at least one group of homologous bioactive proteins that are labile, basic, haemolytic and similar in molecular mass (42-46 kDa). The novel box jellyfish toxins are also potentially lethal and the cause of cutaneous pain, inflammation and necrosis, similar to that observed in envenomed humans. Secondary structure analysis and remote protein homology predictions suggest that the box jellyfish toxins may act as α-pore-forming toxins. However, more research is required to elucidate their structures and investigate their mechanism(s) of action. The biological, biochemical and molecular characteristics of cubozoan venoms and their bioactive protein components are reviewed, with particular focus on cubozoan cytolysins and the newly emerging family of box jellyfish toxins.     

Dose tolerability of chronically inhaled voriconazole solution in rodents

Invasive pulmonary aspergillosis (IPA) is a fungal disease of the lung associated with high mortality rates in immunosuppressed patients despite treatment. Targeted drug delivery of aqueous voriconazole solutions has been shown in previous studies to produce high tissue and plasma drug concentrations as well as improved survival in a murine model of IPA. In the present study, rats were exposed to 20 min nebulizations of normal saline (control group) or aerosolized aqueous solutions of voriconazole at 15.625 mg (low dose group) or 31.25 mg (high dose group). Peak voriconazole concentrations in rat lung tissue and plasma after 3 days of twice daily dosing in the high dose group were 0.85 ± 0.63 μg/g wet lung weight and 0.58 ± 0.30 μg/mL, with low dose group lung and plasma concentrations of 0.38 ± 0.01 μg/g wet lung weight and 0.09 ± 0.06 μg/mL, respectively. Trough plasma concentrations were low but demonstrated some drug accumulation over 21 days of inhaled voriconazole administered twice daily. Following multiple inhaled doses, statistically significant but clinically irrelevant abnormalities in laboratory values were observed. Histopathology also revealed an increase in the number of alveolar macrophages but without inflammation or ulceration of the airway, interstitial changes, or edema. Inhaled voriconazole was well tolerated in a rat model of drug inhalation.