关注甲型H1N1流感

2009年3月在墨西哥出现一种新型流感病毒,因这种新型流感病毒与北美猪流感病毒基因节段极其相似,曾被称为"猪流感",后由世界卫生组织、联合国粮农组织和世界动物卫生组织将其更名为2009 A(H1N1)流感,我国相应命名为甲型H1N1流感.这次疫情可谓"来势汹汹",在不到1个月的时间内迅速蔓延到全球,其传播速度之快前所未有.     

甲型H1N1流感的研究进展

甲型H1N1流感病毒是人流感病毒基因、禽流感病毒基因和猪流感病毒基因混合的重配株,其造成的疫情来势凶猛,引起世界各国的广泛关注.为了早发现、早诊断、早治疗及有效地预防甲型H1N1流感,本文综述了甲型H1N1流感病毒的特点、流行病学、致人发病的机制、甲型H1N1流感患者的临床表现、实验室检查及有效的治疗和预防措施.     

儿童甲型H1N1流感临床特点

<正>甲型H1N1流感是由流感病毒H1N1亚型引起的急性呼吸道传染病。其临床特点与流感病毒的亚型及其变异有关,也与人体的免疫状况和当时的流行情况有关。2009年3月北美发生猪流感,世界卫生组织于2009-04-30宣布不再使用猪流感一词,开始使用甲型H1N1流感。它具有起病急、传染性强、流行广泛、传播迅速的特点。儿童感     

1�����򲡻���Ѫ����Ƥ�غ�Ѫ���Լ�Ѫ�Ѳ����ӵļ�⼰������׵��׵Ĺ�ϵ

目的观察1型糖尿病患儿血管内皮损害标志物—内皮素(ET)和血管性假血友病因子(von Wille-brand因子,vWF)的变化,分析其与尿白蛋白排泄率(UAER)的关系,从而筛查出更敏感的早期诊断糖尿病肾病(DN)的指标。方法收集1998-06—2005-06在山东省立医院就诊的4~18岁1型糖尿病患儿40例,根据UAER分为正常白蛋白尿组(A组)25例和微量白蛋白尿组(B组)15例,同时以年龄、性别、身高1∶1匹配的健康儿童作为对照组,分别检测其血糖(FBG)、糖化血红蛋白(HbA1c)、血浆ET和vWF的变化,并分析其相关性。结果与正常对照组比较,1型糖尿病患者血浆ET-1和vWF、HbA1c明显增高,尤其是微量白蛋白尿组升高更明显(均P<0·01),血浆ET-1和vWF与UAER、HbA1c均呈正相关。结论1型糖尿病患儿在出现白蛋白尿前已存在血管内皮功能异常,其白蛋白排泄与血管内皮功能障碍程度有一定相关性。血浆ET-1、vWF检测可作为早期筛查糖尿病肾病的可靠指标。     

������ȩ��ת��ø1A1 G71Rͻ��������Ǫ�6����������øȱ�ݶ�������������Ũ�ȵ�Ӱ��

目的探讨葡萄糖醛酸转移酶1A1(UGT1A1)基因G71R突变、葡萄糖-6-磷酸脱氢酶(G6PD)缺陷对新生儿生后前3d胆红素浓度的影响.方法测定81例新生儿脐血的G6PD活性及G71R基因型,分组比较生后前3d光疗前胆红素值的组间差异.用等位基因特异性寡核苷酸探针点杂交法(ASO)确定G71R基因型.结果在G71R野生型新生儿中,G6PD缺乏组与G6PD正常组相比,生后前3d胆红素值间无统计学差异.G6PD正常新生儿中,G71R突变纯合子或杂合子的新生儿生后前3d胆红素浓度与G71R正常野生型新生儿相比无统计学差异.G6PD缺陷新生儿中,同时合并有G71R突变纯合子或杂合子的新生儿组生后第2天、第3天胆红素浓度高于G71R正常野生型新生儿组.结论G6PD缺乏与G71R基因突变并存加重新生儿黄疸程度.     

����H1N1 ������֢����12���ٴ����Ϸ���

目的探讨甲型H1N1流感患儿的临床特点及治疗。方法对2009-11-04—2009-12-24桂林市人民医院收治的12例甲型H1N1流感重症患儿的临床资料进行回顾性分析。结果12例患儿均有发热,其中10例以呼吸道症状起病,如咽痛、咳嗽、咳痰等流感样症状;1例以消化系统症状(腹泻)起病;1例以神经系统症状起病;2例伴明显喘憋、呼吸困难;3例双肺闻及痰鸣音、湿啰音,2例闻及喘鸣音。12例患儿白细胞计数增高4例,降低3例;中性粒细胞比例增高4例,降低4例;淋巴细胞比例增高4例,降低2例;血小板计数降低1例,增高1例。6例丙氨酸转移酶(ALT)增高,7例天冬氨酸转移酶(AST)增高,7例乳酸脱氢酶(LDH)增高,7例肌酸激酶(CK)增高,3例肌酸激酶同工酶(CK-MB)增高。随着患儿病情好转,白细胞、肝功、心肌酶恢复正常。结论甲型H1N1流感重症患儿多以呼吸道症状发病,主要靶器官是肺,常合并细菌、支原体感染,出现各种并发症累及多脏器功能。以神经系统症状起病患儿进展迅速、病情凶险。     

LINE1-ORF1p过表达对肾母细胞瘤细胞WT_CLS1增殖的影响

目的 制备LINE1-ORF1p多克隆抗体，研究LINE1-ORF1p过表达对肾母细胞瘤细胞WT_CLS1增殖的影响。方法 利用基因工程方法原核表达LINE1-ORF1p，免疫家兔制备多克隆抗体。间接ELISA法检测抗体效价，通过Western blot及免疫组化方法检测抗体对LINE1-ORF1p的特异性识别能力。构建真核表达载体pEGFP-N1-LINE1-ORF1，转染WT_CLS1细胞，通过Western blot和qRT-PCR检测LINE1-ORF1蛋白和基因的表达情况，采用细胞增殖实验和平板克隆形成实验检测LINE1-ORF1p对WT_CLS1细胞增殖及肿瘤细胞克隆形成的影响。结果 制备的LINE1-ORF1p抗体效价 > 1：16 000，能对细胞及肿瘤组织内LINE1-ORF1p特异识别。转染pEGFP-N1-LINE1-ORF1的WT_CLS1细胞，其LINE1-ORF1的mRNA及蛋白水平显著增高（P < 0.05），细胞增殖能力和克隆形成能力都显著增强（P < 0.05）。结论 LINE1-ORF1p可以促进肾母细胞瘤细胞的生长和肿瘤细胞克隆形成，可能参与肾母细胞瘤的发病机制。     

��ͯ2009����H1N1���������ϵͳ����֢����

??Objective??To describe the clinical characteristics of neurologic complications associated with 2009 influenza A ??H1N1?? infection in children. Methods??A prospective study of 150 children confirmed 2009 influenza A ??H1N1?? infection in Shenzhen Children Hospital from November 4, 2009, to January 19, 2010 was conducted. The clinical features and outcome of the patients with neurologic complications were analyzed. Results??The incidence rate of neurologic complications associated with 2009 influenza A ??H1N1?? infection was 14% of the hospitalized patients. 18??85.7%?? patients were diagnosed as encephalopathy??2??9.5%?? patients were diagnosed as seizures??1??4.7%?? patient was diagnosed as encephalitis. 14 were male, 7 were female?? the median age was 5 years. 12??57%?? patients were admitted to an ICU, 6??28.5%?? required mechanical ntilation. 17??80.9%?? patients were fully recovered and discharged, three ??14%?? died from severe encephalopathy. Conclusion??The incidence rate of neurologic complications associated with 2009 influenza was high, severe encephalopathy canlead to death. This result should attract a great deal of attention as 2009 influenza A ??H1N1?? pandemic continues.     

2009 H1N1 Influenza Pandemic

The 2009 H1N1 influenza pandemic took health care workers worldwide by surprise. Early in the course of the pandemic it was determined that children and pregnant women were at high risk of increased morbidity and mortality from the novel influenza virus. The Centers for Disease Control and Prevention and state and local public health officials quickly rallied to develop treatment guidelines for the new strain of influenza A, including emergency approvals for off-label use of some antiviral drugs. Prevention of the spread of influenza via vaccination and environmental controls is critical to the health of children. The 2009 H1N1 influenza virus emerged too late to be included in the 2009/2010 seasonal influenza vaccine, so production of a monovalent vaccine was set in motion. Five months from when the first cases of novel H1N1 appeared in Mexico and the United States, a vaccine was being distributed to high-risk patients. Looking ahead to the 2010/2011 influenza season, it is difficult to predict 2009 H1N1 activity. The 2010/2011 seasonal influenza vaccine will include the 2009 H1N1 strain, so it is critical to get all children vaccinated early in the flu season.     

MRI in H1N1 Encephalitis

Novel influenza A (H1N1) virus has been largely associated with respiratory complications. The exact frequency of neurological complications is not known, but are more common in children. There are very few reports of MRI findings in H1N1 encephalitis and none from India. The authors report MRI findings in an infant with H1N1 encephalitis. The diagnosis was made based on history, viral serological tests and imaging findings.     

Glycogenoses type 1b and 1c

In type 1 glycogen storage diseases, glucose-6-phosphatase may be present but associated with impaired transport of glucose-6-phosphate (type 1b) or inorganic phosphate (type 1c) through microsomal membranes. The type 1c is very rare (2 published cases). The more frequent type 1b presents all the clinical manifestations of type 1a and specific signs: recurrent stomatitis, frequent infections, chronic inflammatory bowel disease secondary to neutropenia and neutrophil dysfunction. Glucose-6-phosphatase activity is low when measured on fresh liver tissue, but is restored after detergent treatment. A good metabolic control does not influence neutropenia and its consequences.     

COL1A1基因启动子区突变(-106C>T)对其表达的影响

目的 探讨COL1A1基因启动子区突变(-106C>T)对其表达的影响.方法 PCR扩增正常人COL1A1基因转录起始点上游-1024～+36 bp的启动子序列,片段长度为1060 bp.经T/A克隆,连接酶切位点,再连接到PGL3一basic载体,得到野生型的PGL3-COL1A1表达载体.再采用定点突变的方法,把-106位碱基的C突变成T,再连接到PGL3-basic载体,构建突变型的PGL3-COL1AI表达载体.用上述两种表达载体及PGL3一basic分别瞬时转染NIH 3T3细胞.细胞培养48hA,测定各组细胞表达的荧光素酶的相对活性.以明确COL1A1启动子区-106位碱基C＞T突变对基因转录调控的影响.结果 经琼脂糖凝胶及基因测序鉴定,证实载体构建成功.荧光素酶活性测定结果显示,在转染野生型PGL3一COL1A1表达载体的细胞组,荧光素酶的相对活性为3.8665,为阴性对照组(PGL3-basic)的4.8倍;转染突变型PGL3-COL1A1表达载体的细胞组.荧光素酶的相对活性为1.3917,为阴性对照组的1.7倍.COL1A1基因动子-106位碱基C>T突变后,其转录活性较野生型降低了64%.结论 COL1A1基因启动子区-106C>T突变可以在转录水平抑制该基因的表达.     

Spontaneous pneumomediastinum in H1N1 infection

Spontaneous pneumomediastinum is an uncommon pediatric emergency which usually occurs secondary to bronchial asthma in children. We report a case of spontaneous pneumomediastinum in a 7 year child following Swine Flu (H1N1) infection.     

尿苷二磷酸葡萄糖醛酸转移酶1A1基因与新生儿黄疸

尿苷二磷酸葡萄糖醛酸转移酶（UGT）是胆红素结合的关键酶,此酶的缺陷使胆红素不能与葡萄糖醛酸结合形成结合胆红素,使非结合胆红素在体内堆积,导致Crigler—Najjiar综合征（包括Ⅰ型、Ⅱ型）和Gilbert综合征。CN—Ⅰ型患儿由于高度缺乏UGT,生后1～2d即出现严重黄疸,血清间接胆红素可达256．5～595．0μnaol／L,苯巴比妥治疗无效,需换血与光疗结合,常见短期内出现胆红素脑病,多在新生儿期和婴儿期死亡,属常染色体隐性遗传。CN—Ⅱ型为UGT活性缺陷,但并非完全缺乏,可表现为新生儿期较轻的黄疸,但也可发生严重的高胆红素血症和核黄疸。血清间接胆红素浓度一般在85—340μmol／L,苯巴比妥治疗有效,属常染色体显性遗传。Gilbert综合征为一种轻度的慢性高间接胆红素血症,系由肝脏摄取胆红素缺陷和UGT活性降低所致,通常于青春期才症状明显,给苯巴比妥能降低总胆红素值,是一种常染色体显性遗传病。