Late-onset and Recurrent Neonatal Group B Streptococcal Disease Associated with Breast-milk Transmission

The purpose of the study was to determine the epidemiological relationships in three unrelated cases of neonatal late-onset Group B streptococcal (GBS) disease and maternal breast-milk infection with GBS. All deliveries were by cesarean section; case 1 was at term, and cases 2 and 3 were at 32- and 33-wk gestation, respectively. Case 1 relates to a mother with clinical mastitis and recurrent GBS infection in a 20-day-old male infant. Following antibiotic therapy and cessation of breast-feeding, the infant recovered without sequelae. Case 2 refers to a mother with clinical mastitis and the occurrence of late-onset GBS disease in 5-wk-old male twins. Despite intervention, one infant died and the second became ill. Following antibiotic therapy and cessation of breast-feeding, the surviving infant recovered without sequelae. Case 3 refers to a mother with sub-clinical mastitis and late-onset GBS infection occurring in a 6-day-old female twin. Following intervention, the infant recovered but suffered a bilateral thalamic infarction resulting in developmental delay and a severe seizure disorder. Following recovery of GBS from an inapparent mastitis and cessation of breast-feeding, the second infant remained well. Blood cultures from all affected infants and maternal breast milk were positive for GBS. Epidemiological relationships between neonatal- and maternal-derived GBS isolates were confirmed by a random amplified polymorphic DNA polymerase chain reaction assay (RAPD-PCR). This study is significant in that it has demonstrated that maternal milk (in cases of either clinical or sub-clinical mastitis) can be a potential source of infection resulting in either late-onset or recurrent neonatal GBS disease.     

The upregulation of glial glutamate transporter-1 participates in the induction of brain ischemic tolerance in rats.

Glial glutamate transporter-1 (GLT-1) plays an essential role in removing glutamate from the extracellular space and maintaining the glutamate below neurotoxic level in the brain. To explore whether GLT-1 plays a role in the acquisition of brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIP), the present study was undertaken to observe in vivo changes in the expression of GLT-1 and glial fibrillary acidic protein (GFAP) in the CA1 hippocampus during the induction of BIT, and the effect of dihydrokainate (DHK), an inhibitor of GLT-1, on the acquisition of BIT in rats. Immunohistochemistry for GFAP showed that the processes of astrocytes were prolonged after a CIP 2 days before the lethal ischemic insult, which could protect pyramidal neurons in the CA1 hippocampus against delayed neuronal death induced normally by lethal ischemic insult. The prolonged processes extended into the area between the pyramidal neurons and tightly surrounded them. These changes made the pyramidal layer look like a 'shape grid'. Simultaneously, the prolonged and extended processes showed a great deal of GLT-1. Western blotting analysis showed significant upregulation of GLT-1 expression after the CIP, especially when it was administered 2 days before the subsequent lethal ischemic insult. Neuropathological evaluation by thionin staining showed that DHK dose-dependently blocked the protective role of CIP against delayed neuronal death induced normally by lethal brain ischemia. It might be concluded that the surrounding of pyramidal neurons by astrocytes and upregulation of GLT-1 induced by CIP played an important role in the acquisition of the BIT induced by CIP.     

The CLDN5 locus may be involved in the vulnerability to schizophrenia.

The present study was designed to detect three single nucleotide polymorphisms (SNPs) located on 22q11 that was thought as being of particularly importance for genetic research into schizophrenia. We recruited a total of 176 Chinese family trios of Han descent, consisting of mothers, fathers and affected offspring with schizophrenia for the genetic analysis. The transmission disequilibrium test (TDT) showed that of three SNPs, rs10314 in the 3'-untranslated region of the CLDN5 locus was associated with schizophrenia (chi(2) = 4.75, P = 0.029). The other two SNPs, rs1548359 present in the CDC45L locus centromeric of rs10314 and rs739371 in the 5'-flanking region of the CLDN5 locus, did not show such an association. The global chi-square (chi(2)) test showed that the 3-SNP haplotype system was not associated with schizophrenia although the 1-df test for individual haplotypes showed that the rs1548359(C)-rs10314(G)-rs739371(C) haplotype was excessively non-transmitted (chi(2) = 5.32, P = 0.02). Because the claudin proteins are a major component for barrier-forming tight junctions that could play a crucial role in response to changing natural, physiological and pathological conditions, the CLDN5 association with schizophrenia may be an important clue leading to look into a meeting point of genetic and environmental factors.     

双侧内囊前肢毁损术治疗难治性强迫症疗效及随访研究

目的　对难治性强迫症进行双侧内囊前肢毁损术治疗 ,评定手术疗效并进行 2年随访 ,以进一步探索脑外科手术对难治性强迫症的疗效 ,并探讨手术治疗的良好适应症。方法　对 2 8例难治性强迫症患者进行双侧内囊前肢毁损术治疗 ,并分别在手术前、手术后二周、手术后三月、手术后六月、手术后一年、手术后二年进行Y BOCS、HAMA、HAMD量表评定及术后疗效评定。结果　 (1)强迫症患者手术后各期Y BOCS评分、HAMA评分与手术前比较均下降 ,有极显著差异 (P <0 .0 0 1) ;(2 )手术后各期Y BOCS的强迫思维评分均有明显下降 (P <0 .0 0 1) ,强迫行为在手术后 1年和 2年 ,与手术前比较无明显改变 (P >0 .0 5 ) ;(3)手术后 2年的总有效率为 5 3.5 % ,明显低于手术后 3月的总有效率 (P <0 .0 1)。结论　采用双侧内囊毁损术有相当的治疗效果 ,对于难治性强迫症患者可作为一种补充治疗手段 ;手术治疗对强迫行为的长期疗效较差 ,以严重的强迫思维为主的难治性强迫症患者为手术更好的适应症。     

神经、精神因素对儿科疾病的影响

儿童时期是人生一个重要而又特殊的阶段 ,身体正处于不断的生长发育之中。神经系统尤其是脑组织是人类精神心理活动和行为的物质基础。小儿神经系统的发育尚未成熟 ,功能也不够完善和稳定 ,精神心理状态易受到周围环境、家庭、学校或社会等诸多因素的影响 ,特别是近 2 0年来我国独生子女明显增多 ,对各种情况变化缺乏足够的适应能力和承受能力 ,因此与成人相比较易发生心理行为障碍。神经、精神因素不仅对许多儿科疾病的发生、发展有着重要的影响 ,而且还可以作为主要的致病因素引起一些疾病。众所周知 ,在儿科临床上一些较常见的疾病如儿童…     

苯胺衍生物掺杂的PMMA薄膜的二次非线性光学性能的稳定性研究

具有A-π-D电子结构的苯胺衍生物掺杂的玻璃态高聚物PMMA的有机薄膜经极化取向后显示很强的二次非线性光学性能,其取向弛豫是实用化的一个有待解决的重要问题。木文通过几种苯胺衍生物以不同百分比与PMMA掺杂,用紫外-可见吸收光谱、二次谐波强度测量、动态力学粘弹谱等方法进行了取向弛豫的机理研究,结果表明分子尺寸和形状以及偶极矩的大小对取向弛豫有显著影响。