脑性瘫痪伴听力损失儿童的听力学特点及高危因素分析

目的探讨脑性瘫痪伴听力损失儿童的听力学特点及高危因素。方法对2009年1月～2010年12月诊断为脑性瘫痪的120例患儿进行听力学诊断,包括ABR、诊断型DPOAE测试,明确是否伴有听力损伤及听损伤的程度和部位,并对听力损伤的高危因素进行分析。结果 120例脑性瘫痪儿童中,双耳ABR反应阈正常82例(68.33%,82/120),其DPOAE均正常;38例(31.67%,38/120)ABR异常,其中,双耳35例,3例轻度、5例中度、3例重度、24例极重度;单耳3例,2例极重度、1例中度听力损失;23例双耳、3例单耳DPOAE未引出,与ABR检查结果一致,符合感音神经性聋诊断;12例双耳DPOAE正常,而ABR波形异常,符合蜗后聋诊断。38例听损伤脑瘫患儿的高危因素主要有高胆红素血症13例(34.21%)、窒息8例(21.05%)、早产低体重8例(21.05%),母孕期感染7例(18.42%)、伴其它新生儿疾病(先天性甲状腺机能低下症、败血症、化脓性脑膜炎、面神经麻痹等)6例(15.79%),脑瘫或耳聋家族史2例(5.26%),有两种或两种以上高危因素者11例。结论本组脑性瘫痪伴听力损失儿童以双耳极重度感音神经性聋为主,其次为双耳极重度蜗后聋,多数脑瘫伴听力损失儿童具有听力损伤高危因素。     

Migrating foreign body into the common carotid artery and internal jugular vein – A rare case

Ingested foreign bodies are a fairly common otorhinolaryngological emergencies encountered in Malaysia. The vast majority of these foreign bodies are fish bones which most commonly are impacted at the level of the cricopharynx. Rarely, however, a foreign body may migrate extraluminally and may even extrude subcutaneously. We report a rare occurrence where a fish bone not only migrated extraluminally, it was found to have migrated into the common carotid artery and the internal jugular vein and required surgical removal.     

胃黏膜肠化生的逆转性问题

胃黏膜肠化生作为胃癌前病变,与胃癌的发病存在密切联系.关于肠化生是否具有逆转性,目前尚有争议.但来自流行病学的证据显示,经过长期随访研究,肠化生可以逆转,但改变程度较小.除H pylori感染外,维生素C缺乏、胃酸减少和/或胆汁返流等亦是其发病因素.肠化生的发病机制尚处于探索阶段,H pylori毒力因子、肠道特异性转录因子、微卫星不稳定性等均参与其发病环节,但尚不能肯定肠化生是由干细胞突变引起的胃上皮细胞表型的改变.肠化生在诊断上存在诸多困难,严格的内镜评估以及正确的取检部位尤为重要.单独根除H pylori似乎不足以逆转肠化生,联合应用其他化学阻断剂以及中医药,可能是一条新的治疗途径.     

Optimizing implantable cardioverter-defibrillator treatment of rapid ventricular tachycardia: Antitachycardia pacing therapy during charging

BACKGROUND: Previous studies in implantable cardioverter-defibrillator (ICD) patients demonstrated the efficacy and safety of antitachycardia pacing (ATP) for rapid ventricular tachycardias (VT). To prevent shock delay in case of ATP failure, a new feature (ATP during charging) was developed to deliver ATP for rapid VT while charging for shock. OBJECTIVE: The purpose of this study was to determine the efficacy and safety of this new feature. METHODS: In a prospective, nonrandomized trial, patients with standard ICD indication received an EnTrust ICD. VT and ventricular fibrillation (VF) episodes were reviewed for appropriate detection, ATP success, rhythm acceleration, and related symptoms. RESULTS: In 421 implanted patients, 116 VF episodes occurred in 37 patients. Eighty-four (72%) episodes received ATP during or before charging. ATP prevented a shock in 58 (69%) of 84 episodes in 15 patients. ATP stopped significantly more monomorphic (77%) than polymorphic VTs (44%, P = .05). Five (6%) episodes accelerated after ATP but were terminated by the backup shock(s). No symptoms were related to ATP during charging. In four patients, 38 charges were saved by delivering ATP before charging. Of 98 induced VF episodes, 28% were successfully terminated by ATP versus 69% for spontaneous episodes (P <.01). CONCLUSION: Most VTs detected in the VF zone can be painlessly terminated by ATP delivered during charging, with a low risk of acceleration or symptoms. ATP before charging allows delivery of two ATP attempts before shock in the same time that would otherwise be required to deliver only one ATP plus a shock. It also offers potential battery energy savings.     

Beta-catenin is temporally regulated during normal liver development

BACKGROUND & AIMS: beta-Catenin, a key component of the Wnt pathway, plays an important role in unregulated liver growth in liver tumors, in regulated growth during liver regeneration, and in ex vivo embryonic liver cultures. METHODS: We used developing livers from several stages of gestational development to examine beta-catenin expression, protein-protein interactions, localization, and regulation in prenatal and postnatal livers. RESULTS: Microarray, Northern, and protein analyses showed peak expression of beta-catenin during early liver development at Embryonic day 10 (E10)-E12, followed by a decrease and a complete loss of normal beta-catenin (97-kilodalton species) after E16 through the remaining prenatal period. At the early stages, beta-catenin localized to the cytoplasm and nuclei of resident cells in addition to its normal membranous localization, which was seen at all later stages and in adult liver. Decreases in beta-catenin levels at E14 onward coincided with its decreased gene expression and increased degradation, as seen by an increase in serine 45/threonine 41-phosphorylated beta-catenin and its other negative regulators, such as axin, adenomatous polyposis coli gene product (APC), and glycogen synthase kinase-3 beta. Finally, we showed an intact association of E-cadherin and beta-catenin despite the loss of beta-catenin at E16-E18, owing to the presence of membrane-associated smaller-molecular-weight beta-catenin species. CONCLUSIONS: We also identified a stage-specific expression and regulation of beta-catenin during liver development that might be crucial for physiological liver development. Nuclear and cytoplasmic beta-catenin corresponded to cell proliferation in liver development. Finally, a smaller-molecular-weight species of beta-catenin might be maintaining normal interactions at the membrane.     

Therapeutic vaccination using CD4+CD25+ antigen-specific regulatory T cells

Autoimmune disease results from the dysregulation of basic tolerogenic processes designed to control self/non-self-discrimination. Approaches to treat autoimmunity have focused historically on potent immunosuppressives that block the activation and expansion of antigen-specific T cells before they differentiate into pathogenic T cell responses. These therapies are very efficient in reducing clonal expansion and altering early signaling pathways. However, once the pathogenic responses are established (i.e., autoimmunity), the interventions are less effective on activated and differentiated T cell subsets (including memory T cells) or acting in the presence of an inflammatory milieu to abort immune responses at the target tissue and systemically. Moreover, the current immunotherapies require continuous use because they do not redirect the immune system to a state of tolerance. The continuous treatment leads to long-term toxicities and can profoundly suppress protective immune responses targeted at viruses, bacteria, and other pathogens. Over the past decade, there have been tremendous advances in our understanding of the basic processes that control immune tolerance. Among the most exciting has been the identification of a professional regulatory T cell subset that has shown enormous potential in suppressing pathologic immune responses in autoimmune diseases, transplantation, and graft vs. host disease. In this review, we summarize current efforts to induce and maintain tolerance in the autoimmune diabetes setting by using therapeutic vaccination with CD4(+)CD25(+) regulatory T cells. Emphasis will be placed on approaches to exploit regulatory T cells either directly or through the use of anti-CD3 immunotherapy.     

湖南省基本消灭丝虫病后的监测

目的：探讨自1986年湖南省达到基本消灭丝虫病后该病残存传染源消长规律及传播作用。方法：应用常规方法进行病原学、蚊媒和血清学纵向、横向监测以及流动人口监测，对薄弱环节采取适当的巩固措施。结果：在55个县（市）的横向监测中，末次检出微丝蚴阳性者系于1993年，蚊媒监测已有12年未查见人体幼丝虫感染蚊。血清学（IFAT）监测，平均人群抗体阳性率从1987年的13．15％至1996年降为1．06％，与非流行区人群水平相似。5个县（市）6个纵向监测点连续10－17年的观察结果，检获的11例残存微丝蚴血症者，有10例均在1－10年内阴转，另1例至14年未阴转。蚊媒监测，2个马来丝虫病监测点均未查见幼丝虫，4个班氏丝虫病监测点于第1－3年查见幼丝虫，其自然感染率为0．38％－1．98％，第4年以后均为阴性。结论：湖南省基本消灭丝虫病后残存传染源逐年减少，丝虫病传播已被阻断。