The human major histocompatibility complex class Ib molecule HLA-E binds signal sequence-derived peptides with primary anchor residues at positions 2 and 9

Human histocompatibility leukocyte antigen E (HLA-E) and mouse major histocompatibility complex (MHC) class Ib antigen, Qa-1, share the same substitutions at two normally conserved positions 143 and 147, which are likely to affect binding of the C terminus of peptides. Qa-1 is able to bind a peptide derived from the leader sequence of H-2 D and H-2 L molecules. We developed a peptide binding assay in vitro to compare the binding specificity of HLA-E with the mouse MHC class Ib molecule Qa-1. We demonstrate that HLA-E binds, although poorly, the peptide which binds to Qa-1 and that it also binds nonamer signal sequence-derived peptides from human MHC class I molecules. Using alanine and glycine substitutions, we could define primary anchor residues at positions 2 and 9 and secondary anchor residues at position 7 and possibly 3.     

Brain serotonin transporter binding in non-depressed patients with Parkinson's disease

Early post-mortem data suggest that damage to brain serotonin neurones might play a role in some features (e.g., depression) of Parkinson's disease (PD). However, it is not known whether such damage is a typical characteristic of living patients with PD or whether the changes are regionally widespread. To address this question we measured, by positron emission tomography imaging, levels of the brain serotonin transporter (SERT), a marker for serotonin neurones, as inferred from binding of [¹¹C]-3-amino-4-(2-dimethylaminomethyl-phenylsulfanyl)-benzonitrile (DASB), a second generation SERT radioligand, in subcortical and cerebral cortical brain areas of clinically advanced non-depressed (confirmed by structured psychiatric interview) patients with PD. SERT binding levels in PD were lower than those in controls in all examined brain areas, with the changes statistically significant in orbitofrontal cortex (−22%), caudate (−30%), putamen (−26%), and midbrain (−29%). However, only a slight non-significant reduction (−7%) was observed in dorsolateral pre-frontal cortex, an area implicated in major depression. Our imaging data suggests that a modest, regionally widespread loss of brain serotonergic innervation might be a common feature of advanced PD. Further investigation will be required to establish whether SERT binding is more or less decreased in those patients with PD who also have major depressive disorder.     

颞肌筋膜瓣与全厚皮片移植修复下睑凹陷性畸形

目的探讨颞筋膜瓣或颞肌筋膜瓣与自体全厚皮片移植,在下睑凹陷性瘢痕畸形修复中的应用效果。方法设计以颞浅动脉为蒂的颞筋膜瓣,对伴眶下壁骨缺损者同时行以颞浅、深动脉为蒂的颞肌筋膜瓣,并取耳后全厚皮片移植联合矫正下睑凹陷性畸形。结果8例患者,术后组织瓣及皮片成活良好,凹陷处填充效果满意。随访6个月至1年,睑外翻矫正,瘢痕不显,颞部供区毛发生长良好。结论应用颞筋膜瓣或颞肌筋膜瓣与全厚皮片移植,联合矫正下睑凹陷性畸形的方法,具有操作简便,且无明显的供区损害的特点,是修复下睑凹陷性瘢痕畸形较理想的方法。     

阿米替林合并认知疗法治疗精神分裂症后抑郁的对照研究

目的　评价阿米替林合并认知疗法对精神分裂症后抑郁的治疗效果。方法　将符合CCMD 3诊断标准的 86例精神分裂症后抑郁患者随机分为治疗组和对照组 ,治疗组给予阿米替林合并认知治疗 ,对照组织给予阿米替林治疗 ,疗程 12周。采用汉密尔顿抑郁量表 (HAMD)、简明精神病量表(BPRS)、阴性症状量表 (SANS)评定临床疗效 ,采用副反应量表 (TESS)评定副反应。结果　在治疗的 4、8、12周末 ,HAMD评分治疗组优于对照组 ,显效率分别为 83 95 %和 6 1 90 % (u =5 .83,P <0 0 5 )。结论　阿米替林与认知治疗组结合治疗精神分裂症后抑郁疗效好于单用阿米替林治疗。     

Depressive Symptoms and Associated Factors in Children With Attention Deficit Hyperactivity Disorder

PROBLEM: To compare depressive symptoms in children with attention deficit hyperactivity disorder (ADHD) to those in healthy children, and to explore the influence of individual and family factors on level of depression. METHODS: Individual interviews with 68 children, ages 7 to 12 years, in order to complete the Children's Depression Inventory. FINDINGS: Children with ADHD reported significantly more depressive symptoms than did children without ADHD; 14.7% of children with ADHD reached the threshold of a 19 point score, which suggests clinical depression. No significant effects of individual and family factors on level of depression were found. CONCLUSIONS: Children with ADHD are more inclined to experience depressive symptoms than are healthy children. To plan appropriate interventions, nurses evaluating and working with children with ADHD should always consider a possible coexistence of depressive symptoms.     

Activity-dependent Decay of Early LTP Revealed by Dual EPSP Recording in Hippocampal Slices from Young Rats

The early maintenance of long-term potentiation (LTP) was studied in the CA1 region of hippocampal slices from 12- to 18-day-old rats in a low-magnesium solution (0.1 mM). The α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and N-methyl-D-aspartate (NMDA) receptor-mediated components of the field excitatory postsynaptic potential were estimated in parallel using early and late measurements of the composite potential. At the normal test stimulus frequency of 0.1 Hz, LTP was seen initially as a predominant increase in the AMPA component, but converted, via a substantial decay of this component and a gradual growth of the NMDA component, into nearly equal changes of the two components. Interrupting the test stimulation for 10 min, changing the test stimulus frequency to 1/60 Hz after LTP induction, or using a test stimulus frequency of 1/60 Hz during the entire experiment significantly reduced the decay of the potentiation of the AMPA component while enhancing the potentiation of the NMDA one. The ratio between the magnitudes of the two excitatory postsynaptic potential (EPSP) components showed a decaying time course that was independent of the manipulations used. Application of the NMDA antagonist D(-)-2-amino-5-phosphonopentanoic acid (50μM) after LTP induction stabilized the LTP of the AMPA component until washout was started. On the other hand, the phosphatase inhibitor okadaic acid (1 μM) resulted in decay of the potentiation of both EPSP components back to around baseline and altered the time course of the ratio between the components. Our results show that the early maintenance of LTP is controlled in an activity-dependent and NMDA-dependent manner. This process accelerates the decay of LTP of both AMPA and NMDA components in parallel, suggesting that it is similar to homosynaptic long-term depression, although it operates at the normal test stimulus frequency. The data support a scenario in which LTP ensues as a selective AMPA receptor modification and subsequently converts to another modification, possibly a presynaptic one.