292例胎儿生长受限相关危险因素分析

目的 探讨胎儿生长受限（FGR）发生的相关因素，达到早发现、早诊断、早治疗，预防FGR的合并症及并发症。方法 对292例FGR病例进行回顾性分析。结果292例中母体因素87例（29．8％），胎儿因素18例（6．2％），胎盘因素17例（5．8％），脐带因素58例（19．9％），无明确原因112例（38．0％）；阴道分娩组新生儿窒息24例，占41．4％，剖宫产组新生儿窒息24例，占10．3％，两组分娩方式差异有统计学意义。结论 FGR的主要病因是母体因素，及时恰当地治疗妊娠合并症和并发症，适当放宽剖宫产指征，有利于降低FGR的后遗症。     

胎儿生长受限的相关因素及分娩方式与新生儿结局关系的分析

目的：探讨胎儿生长受限（FGR）发生的相关因素,以期早发现、早诊断、早治疗,改善新生儿预后。方法：对175例FGR患者进行回顾性分析。结果：175例中母体因素52例（29.7%）,胎儿因素11例（6.3%）,胎盘因素10例（5.7%）,脐带因素35例（20.0%）,无明确原因67例（38.3%）。阴道分娩组新生儿窒息17例,占39.5%,剖宫产组新生儿窒息14例,占10.6%,两组分娩方式比较,差异有统计学意义。结论：FGR的主要病因是母体因素,及时恰当地治疗妊娠合并症及并发症,适当放宽剖宫产指征,有利于改善FGR患儿的预后。     

胎儿生长受限相关因素分析

目的探讨胎儿生长受限发生的相关因素。方法回顾性分析59例胎儿生长受限患者的临床资料。结果 59例患者中母体因素28例,占47.4%。胎儿因素8例,占13.6%。胎盘因素6例,占10.2%。脐带因素17例,占28.8%。阴道分娩33例。急症剖宫产15例。选择性剖宫产11例。结论胎儿生长受限的主要病因是母体因素,孕期进行及时恰当地治疗,选择恰当的分娩时机和分娩方式,有利于减少胎儿窘迫和新生儿窒息的发生。     

110例胎儿生长受限主要因素分析

目的 探讨胎儿生长受限(FGR)发生的母体因素.方法 对足月胎儿生长受限110例临床资料进行回顾性分析.结果 110例胎儿生长受限母体因素54例(占49%),为FGR发生的最主要病因,其次为脐带因素,约40例(占36.6%),脐带因素组发生胎儿宫内窘迫18例(占45%),而母体因素组发生胎儿宫内窘迫仅为12例(占22.2%),两组比较差异有统计学意义(P＜0.005).结论 胎儿生长受限的主要病因是母体因素,以妊娠高血压为首要因素(48%),但在本组中因感染性疾病引发FGR病例数为15例(13.6%),且其中12例(11%)发生胎儿宫内窘迫;其次为脐带因素.因脐带因素发生胎儿宫内窘迫的几率高于母体因素,而母体因素中以感染性疾病发生胎儿宫内窘迫率稍高.因此基层医院在孕期或临产过程中发现胎儿生长发育受限迹象,并且考虑脐带因素或感染性疾病可能,应适当放宽剖宫产指征,以降低新生儿窒息的几率,减少后遗症的发生.     

胎儿窘迫200例临床分析

目的探讨引起胎儿窘迫的各种原因,选择合适的分娩方式以降低剖宫产率、减少新生儿窒息。方法对我院200例发生胎儿窘迫孕产妇的临床资料进行回顾性分析。结果 引起胎儿窘迫的原因依次无为脐带因素、羊水因素、母体因素、胎盘因素、产力异常、过期妊娠,经阴道分娩的新生儿发生窒息明显高于剖宫产术,差异有统计学意义(P<0.05)。结论胎儿窘迫受多种因素影响,是新生儿窒息和围生儿死亡的重要原因,加强妊娠晚期胎儿窘迫早期诊断,选择恰当分娩方式终止妊娠,适时助产,适当放宽剖宫产指征,以降低新生儿窒息、围生儿的并发症及病死率。     

76例新生儿窒息原因分析

目的探索新生儿窒息相关因素,为降低新生儿窒息发生率提供科学依据.方法对2004年1月至2005年12月在本院出生的符合新生儿窒息诊断标准的76例患儿进行回顾性分析.结果脐带因素30例,占39.47%,胎儿宫内窘迫18例,占23.68%,羊水少5例,占6.58%,早破膜5例,占6.58%,胎位异常4例,占5.26%,其母妊娠高血压综合征3例,占3.95%,胎盘因素3例,占3.95%,继发宫缩无力2例,占2.63%,过期妊娠2例,占2.63%,早产2例,占2.63%,双胎妊娠2例,占2.63%.新生儿窒息与分娩方式有关,阴道助产发生率最高(52.38%),剖宫产次之(5.84%),自然分娩发生率最低(3.44%).结论做好孕期系统管理,恰当、适时选择分娩方式,加强产科、儿科医务人员技术培训,熟练掌握新生儿窒息复苏技术,是降低新生儿窒息发生率的有效措施.     

头位妊娠脐带绕颈的处置

脐带是维系胎儿生命的重要通道,一旦血运受阻,将对胎儿造成危害。脐带异常是新生儿窒息的首要原因。头位妊娠脐带绕颈在脐带未被拉紧及受压时,脐血流通畅,胎儿宫内状况良好。当出现胎儿窘迫时,选择适当的分娩方式极为重要,原则上应使胎儿尽快脱离母体。本研究就309例头位妊娠脐带绕颈分娩的临床资料进行分析,探讨不同分娩方式对新生儿的影响,以达到降低胎儿窘迫、新生儿窒息及病死率的目的。1临床资料双鸭山市人民医院2005年1月至2007年6月头位妊娠分娩1446例,新生儿出生时发现脐带绕颈者309例,其发生率为21·37%。309例中75例于临产前或产程初期因有剖宫产指征行选择性剖宫产术;另234例中,128例自然分娩,未发生胎儿窘迫,106例在产程中发生胎儿窘迫(45·30%)。309例中发生新生儿窒息35例,发生率11·33%,新生儿死亡1例,病死率0·32%。2讨论脐带是维系胎儿生命的重要通道,一旦血运受阻,将对胎儿造成危害。脐带异常是新生儿窒息的首位原因,约22%的新生儿窒息、25%的重度新生儿窒息、20%的新生儿死亡是由脐带因素引起。脐带因素中最常见的是脐带绕颈,占脐带异常的79·25%。头位妊娠脐带绕颈在孕晚期或分...     

新生儿窒息的产科原因分析

目的 对新生儿窒息的产科原因进行分析,探讨有效的防治措施.方法 回顾性分析该院2010年10月-2012年10月产科分娩后出现的窒息新生儿58例的临床资料,对其窒息相关性因素进行综合分析.结果 导致新生儿窒息因素主要包括母体因素、胎儿因素及分娩方式.其中母体妊娠合并症或并发症、前置胎盘、胎盘早剥、脐带因素及胎儿生长受限是主要产科因素.剖宫产新生儿窒息发生率高于阴道分娩,差异有统计学意义（P〈0.05）.结论 导致新生儿窒息因素是多方面的,加强围生期保健、产前及产时胎儿监护,及时发现导致新生儿窒息的危险因素并进行有效防治对于降低新生儿窒息有着重要临床作用.     

新生儿窒息产科因素分析

目的从产科角度探讨新生儿窒息发生的相关因素,提出干预措施.方法对2003年1月～2004年12月江门市新会区妇幼保健院199例新生儿窒息的产科原因进行分析.结果脐带因素、胎儿窘迫为主要原因,分别占28.64%、26.13%,胎儿、分娩、母体、胎盘因素次之.结论做好系统围生育期保健,及早发现及治疗高危妊娠.加强胎儿胎盘功能监测,及早发现异常,及时处理.密切产程中胎儿的监护,综合分析可能发生新生儿窒息的高危因素适时正确选择分娩方式是降低新生儿窒息和病死率的关键措施.     

263例脐带缠绕临床分析

目的探讨脐带缠绕的分娩方式及与新生儿窒息的关系。方法将住院头位妊娠产前诊断脐带绕颈者,产前及产时使用胎儿电子监护仪行外监护,及时发现胎儿宫内窘迫,适时终止妊娠等作回顾性分析。结果脐带缠绕仍以自然分娩占大多数,随着脐带绕颈周数增多,剖宫产术及阴道助产术比例增高,新生儿窒息所占比例增高。急诊剖宫产术组的新生儿窒息明显大于选择性剖宫产术组,两组比较差异有非常显著性(P<0.01)。结论脐带缠绕分娩方式仍以正常分娩多见,次为剖宫产分娩,对于脐带绕颈2周或以上者,尽可能选择剖宫产术,以避免母婴严重并发症。     

Nachweis einiger Heilmittel in der Kniegelenksynovialflüssigkeit

Zusammenfassung Mittels Gaschromatographie und Dünschichtchromatographie wiesen die Autoren 11 Substanzen nach, welche durch Injektion oder nach Verabreichung per os in die Kniegelenksynovialflüssigkeit eindrangen. In ihrer Aufstellung konnten sie eine direkte Beziehung zwischen Struktur sowie chemischphysikalischen Eigenschaften der Substanz und ihrer Fähigkeit, aus dem Blut in die Kniegelenksynovialflüssigkeit einzudringen, nicht nachweisen, außer der Tatsache, daß Substanzen mit starker Affinität zu Eiweißstoffen erst in höheren Dosen nachweisbar waren.     

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.     

Emerging drugs for epilepsy

Epilepsy affects ≤ 1% of the world's population. Antiepileptic drugs (AEDs) are the mainstay of treatment, although more than a third of patients are not rendered seizure free with existing medications. Uncontrolled epilepsy is associated with increased mortality and physical injuries, and a range of psychosocial morbidities, posing a substantial economic burden on individuals and society. Limitations of the present AEDs include suboptimal efficacy and their association with a host of adverse reactions. Continued efforts are being made in drug development to overcome these shortcomings employing a range of strategies, including modification of the structure of existing drugs, targeting novel molecular substrates and non-mechanism-based drug screening of compounds in traditional and newer animal models. This article reviews the need for new treatments and discusses some of the emerging compounds that have entered clinical development. The ultimate goal is to develop novel agents that can prevent the occurrence of seizures and the progression of epilepsy in at risk individuals.     

盐酸达泊西汀中甲磺酸甲酯、甲磺酸乙酯及甲磺酸异丙酯的顶空毛细管GC-ECD法测定

建立了衍生化顶空毛细管气相色谱-电子捕获检测器(ECD)法测定盐酸达泊西汀中的甲磺酸甲酯(MMS)、甲磺酸乙酯(EMS)和甲磺酸异丙酯(IMS).应用碘化钠衍生技术,使用PW-5毛细管柱,载气为氮气,ECD检测,程序升温.MMS、EMS和IMS分别在0.03～0.30、0.05～0.50和0.05～0.50 μg/ml浓度范围内线性关系良好,平均回收率分别为63.5％、100.3％和96.2％,最低检测限分别为0.30、0.50和0.50 ng/ml.     

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.