卡孕栓联合催产素在防治剖宫产产后出血中的效果评价

目的:评价卡孕栓联合催产素在防治剖宫产产后出血中的临床效果.方法:将我院收治的140例行剖宫产的产妇随机分为观察组和对照组各70例,对照组于胎儿娩出后给予子宫壁肌注催产素10U及静脉滴注催产素20U;观察组在此基础上给予舌下含服卡孕栓1mg(2枚).记录两组用后的血压改变,术中出血量、产后2h及24h出血量,比较两组产后不良反应发生率.结果:两组用药前后SBP及DBP均无显著改变(P＞0.05)且两组用药后SBP及DBP组间比较差异也无统计学意义(P＞0.01);观察组术中出血量、产后2h及24h出血量均显著低于对照组(P＜0.05),两组均无产妇发生产后出血;观察组不良反应发生率17.14％与对照组不良反应发生率11.43％无显著差异(P＞0.05).结论:卡孕栓联合催产素可有效减少剖宫产产妇术中及产后出血量,用药方便、安全性高,值得临床推广.     

益母草注射液联合卡孕栓预防产后出血128例

目的观察益母草注射液联合卡孕栓预防产后出血的疗效。方法将256例产妇随机分为治疗组和对照组,各128例,治疗组在胎儿娩出后立即肌肉注射益母草注射液20 U,立即肛门置入卡孕栓1 mg;对照组在胎儿娩出后立即肌肉注射益母草注射液20 U。比较两组产后2 h出血量、第三产程时间及不良反应发生情况。结果两组产后2 h出血量、第三产程时间比较,差异有统计学意义(P<0.05)。治疗组产后2 h总出血量不低于400 mL有4例,对照组20例,两组比较差异有统计学意义(P<0.05)。对照组无不良反应,治疗组出现恶心1例,寒战2例。结论益母草注射液联合卡孕栓预防产后出血服用方法简便、安全、不良反应小,适合临床推广。     

卡孕栓舌下含服和直肠给药联合缩宫素防治高危出血产妇剖宫产产后出血的临床疗效对比

目的：比较卡孕栓舌下含服和直肠给药联合缩宫素防治高危出血产妇剖宫产产后出血的临床疗效。方法选择2014年1月—2015年1月江阴市南闸医院收治的高位出血因素产妇70例,采用随机数字表法将其分为观察组与对照组,各35例。对照组产妇术毕肛塞卡孕栓1mg;观察组产妇在胎儿取出前3min舌下含服卡孕栓1mg。观察两组产妇出血情况（术中出血量、产后2h出血量、产后24h出血量）,术前、术后6、24h平均动脉压（ MAP）、心率（HR）变化情况及不良反应（恶心、呕吐、腹泻）发生情况。结果观察组产妇术中出血量、产后2h出血量和产后24h出血量少于对照组,差异有统计学意义（ P﹤0.05）;术前、术后6、24h两组产妇MAP、HR比较,差异无统计学意义（P﹥0.05）;两组产妇不良反应发生率比较,差异无统计学意义（P﹥0.05）。结论卡孕栓舌下含服联合缩宫素防治高危出血产妇剖宫产产后出血的临床疗效好于直肠给药,且给药方便,不良反应小。     

卡孕栓联合催产素预防剖宫产产后出血的临床效果分析

目的：探讨卡孕栓联合催产素预防剖宫产产后出血的临床效果。方法行剖宫产产妇192例,分为对照组和观察组,其中对照组92例仅采用催产素防治产后出血,另100例观察组采用卡孕栓联合催产素防治产后出血,对比两组临床效果。结果观察组产后2、24 h出血量均较对照组明显减少(P<0.05);观察组产后出血发生例数明显低于对照组(P<0.05)。结论卡孕栓联合催产素能产生强有力的子宫收缩,减少产后出血,是一种安全高效的预防剖宫产产后出血的方法。     

直肠填塞卡孕栓预防剖宫产产后出血的临床观察

目的:观察直肠填塞卡孕栓预防剖宫产产后出血的临床效果。方法:随机将160例拟施行剖宫产手术的孕妇分为观察组和对照组各80例,观察组剖宫产术中胎儿娩出后30min内经直肠置入卡孕栓1mg;对照组宫体注射催产素20U,同时静脉滴注催产素20U。结果:术后2h、24h的平均出血量观察组明显少于对照组(P<0.05);产后出血率观察组优于对照组(P<0.05),差异有统计学意义;2组用药前后血压变化比较,差异无统计学意义(P>0.05)。结论:直肠填塞卡孕栓预防剖宫产产后出血效果良好,且用药方法简单、安全。     

卡孕栓联合催产素预防剖宫产产后出血的临床观察

目的探讨卡孕栓联合催产素预防剖宫产产后出血的疗效观察。方法回顾性分析我院2011年7月至2013年9月320例行剖宫产术产妇资料,根据患者用药方式分为观察组及对照组,各160例,对照组胎儿娩出后宫体注射催产素,观察组在注射催产素的同时阴道置入卡孕栓,术后连用2 d,比较两组患者术中及术后出血量,记录患者用药不良反应。结果观察组患者术中及术后出血量均低于对照组,两组患者比较差异有统计学意义(P<0.05);两组患者用药不良反应比较无明显差异,无统计学意义(P>0.05)。结论卡孕栓能有效促进子宫收缩,预防产后出血,不增加用药不良反应,具有方便、安全、快速的特点。     

舌下含服卡前列甲酯栓预防剖宫产妇产后出血疗效观察

目的：观察舌下含服卡前列甲酯栓预防剖宫产妇产后出血的有效性和安全性。方法：存在出血高危因素的剖宫产妇62例随机分为观察组与对照组各31例,观察组于第二产程末胎头娩出前,舌下含服卡前列甲酯栓1 mg;对照组在胎儿娩出后静注催产素20 u。观察两组患者术中、术后2 h出血量和总出血量,用药前后血压变化,及治疗期间药品不良反应发生情况。结果：观察组术中、术后2 h及总出血量均明显低于对照组（P〈0.05）;两组治疗前后的收缩压及舒张压变化比较,差异均无统计学意义（P〉0.05）。治疗后观察组不良反应发生率9.7%,对照组未见不良反应发生。结论：舌下含服卡前列甲酯栓可明显减少出血高危因素产妇剖宫产术中、术后出血量,且安全性较高。     

卡孕栓联合催产素预防产后出血的临床疗效观察

目的：探讨卡孕栓联合催产素预防产后出血的临床疗效。方法选取灵丘县人民医院2010年5月—2013年3月收治的100例产妇,随机分为观察组和对照组,每组50例。对照组在胎儿娩出后给予催产素治疗,观察组在胎儿娩出后给予卡孕栓联合催产素治疗,比较两组产妇产后2、24h出血量、第三产程持续时间、不良反应发生情况。结果观察组产妇产后2、24h出血量均少于对照组,第三产程时间短于对照组,差异有统计学意义（ P<0.01）;两组均无严重不良反应发生,观察组产妇用药前后心率、血压比较,差异无统计学意义（ P>0.05）。结论卡孕栓联合催产素预防产后出血的疗效确切,不良反应少。     

卡孕栓与缩宫素联用对高危妊娠剖宫产患者术中术后出血的临床疗效评价

目的：评价卡孕栓与缩宫素联用预防高危妊娠剖宫产患者术中和术后出血的临床疗效。方法：将医院收治行剖宫产的120例产妇分为实验组和对照组,各60例;两组患者均在胎儿娩出后与胎盘娩出前均予注射2.5~5.0 U缩宫素;实验组患者在切开腹膜时予产妇舌下含服卡孕栓1 mg,术后经直肠置入1 mg卡孕栓;对照组患者除注射缩宫素外不使用其他药物;比较两组产妇术中平均出血量、产后24 h出血量、术后6 h血压及不良反应的发生情况。结果：实验组产妇术中平均出血量及产后24 h出血量均低于对照组（P〈0.05）;两组产妇术后6 h血压监测结果比较（P〉0.05）;实验组产妇予卡孕栓后7例出现轻微不良反应,均无需特殊处理后自动恢复,无感染发生,对照组未发生不良反应;两组比较其差异无统计学意义（P〉0.05）;两组产妇术后泌乳量经比较无统计学意义（P〉0.05）。结论：卡孕栓与缩宫素联用能有效预防高危妊娠剖宫产术中术后出血,且对产妇血压无明显影响。     

卡孕栓与缩宫素联合应用预防剖宫产后出血的临床观察

目的:观察小剂量卡孕栓与缩宫素联合应用预防剖宫产后出血的疗效.方法:82例剖宫产产妇,随机分为观察组和对照组,观察组在胎儿娩出后给予卡孕栓0.5 mg +缩宫素10 U,对照组给予缩宫素20 U,比较产后2 h、24 h、72 h的出血总量、产后出血发生率、血压变化和副反应.结果:两组产妇在产后2 h、24 h、72 h出血总量均有显著性差异(P＜0.05),观察组产后出血发生率明显较低(P＜0.05),不良反应发生率较低(P＜0.05),对血压影响不大.结论:小剂量卡孕栓与缩宫素联合应用可减少产后出血,并减少不良反应发生,对患者血压无明显影响.     

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.