Social comparison,competition and teacher–student relationships in junior high school classrooms predicts bullying and victimization

This cross-sectional research examines how social comparison, competition and teacher–student relationships as classroom characteristics are associated with bullying and victimization among junior high school students in grades 7 and 8 in Canada. The study tests a conceptual model of youth outcomes that highlights the importance of modeling the effects of teaching practices as proximal structural conditions at the classroom level (N = 38) that affect bullying outcomes at the individual level (N = 687). Results of Hierarchal linear modeling (HLM) revealed significant classroom-level effects in that increased social comparison, competition and teacher–student relationships were related to bullying and victimization. An interaction for teacher–student relationships and gender also emerged. These findings may guide future intervention programs for junior high schools that focus on enhancing cooperation and pro-social behavior in classrooms. The findings could also inform programs that focus on building strong relationships between students and teachers to help prevent bullying and victimization, particularly among boys.     

Predictors of Cognitive Functions in Children With Sturge–Weber Syndrome: A Longitudinal Study

BackgroundSturge–Weber syndrome is often accompanied by seizures and neurocognitive deterioration, although previous studies have suggested that early functional brain reorganization may diminish the cognitive sequelae in some children with unilateral Sturge–Weber syndrome. The “rules” governing these plasticity mechanisms are poorly understood. In this study, we evaluated longitudinal changes of cognitive functioning (intelligence quotient [IQ]) and assessed the performance of clinical, electroencephalography (EEG), and magnetic resonance imaging (MRI) variables for predicting IQ in children with Sturge–Weber syndrome.MethodsThirty-three young children (mean age: 3.3 years at baseline) with unilateral Sturge–Weber syndrome underwent MRI, scalp EEG, and neuropsychology evaluation twice, with a median follow-up of 2 years. None of the children had epilepsy surgery. Longitudinal IQ changes were calculated. Seizure variables, interictal EEG abnormalities, and extent and location of MRI brain involvement were correlated with IQ assessed at follow-up.ResultsGlobal IQ showed a highly variable course with both increases and decreases over time. Lower IQ at baseline was associated with interval IQ increase. In univariate analyses, lower outcome IQ was associated with baseline EEG abnormalities (P < 0.001), young age at seizure onset (P = 0.001), high seizure frequency (P = 0.02), and early frontal-lobe involvement on MRI (P = 0.01). In multivariate analysis, EEG abnormalities at baseline remained a robust, independent predictor of outcome IQ.ConclusionsThe early trajectory of cognitive changes in children with unilateral Sturge–Weber syndrome is highly variable; children with improving IQ likely undergo effective unimpeded functional reorganization. Early onset, frequent seizures, and interictal epileptiform abnormalities on EEG likely interfere with this process resulting in poor cognitive functions. Future studies assessing interventions should target this high-risk subgroup to optimize cognitive outcome in Sturge–Weber syndrome.     

Atypical performance patterns on Delis–Kaplan Executive Functioning System Color–Word Interference Test: Cognitive switching and learning ability in older adults

Introduction: Cognitive set shifting requires flexible application of lower level processes. The Delis–Kaplan Executive Functioning System (DKEFS) Color–Word Interference Test (CWIT) is commonly used to clinically assess cognitive set shifting. An atypical pattern of performance has been observed on the CWIT; a subset of individuals perform faster, with equal or fewer errors, on the more difficult inhibition/switching than the inhibition trial. This study seeks to explore the cognitive underpinnings of this atypical pattern. It is hypothesized that atypical patterns on CWIT will be associated with better performance on underlying cognitive measures of attention, working memory, and learning when compared to typical CWIT patterns. Method: Records from 239 clinical referrals (age: M = 68.09 years, SD = 10.62; education: M = 14.87 years, SD = 2.73) seen for a neuropsychological evaluation as part of diagnostic work up in an outpatient dementia and movement disorders clinic were sampled. The standard battery of tests included measures of attention, learning, fluency, executive functioning, and working memory. Analyses of variance (ANOVAs) were conducted to compare the cognitive performance of those with typical versus atypical CWIT patterns. Results: An atypical pattern of performance was confirmed in 23% of our sample. Analyses revealed a significant group difference in acquisition of information on both nonverbal (Brief Visuospatial Memory Test–Revised, BVMT–R total recall), F(1, 213) = 16.61, p < .001, and verbal (Hopkins Verbal Learning Test–Revised, HVLT–R total recall) learning tasks, F(1, 181) = 6.43, p < .01, and semantic fluency (Animal Naming), F(1, 232) = 7.57, p = .006, with the atypical group performing better on each task. Effect sizes were larger for nonverbal (Cohen’s d = 0.66) than verbal learning (Cohen’s d = 0.47) and semantic fluency (Cohen’s d = 0.43). Conclusions: Individuals demonstrating an atypical pattern of performance on the CWIT inhibition/switching trial also demonstrated relative strengths in semantic fluency and learning.     

Set-up and routine use of a database of 10 555 genotyped blood donors to facilitate the screening of compatible blood components for alloimmunized patients

Background and Objectives  Large-scale genotyping of blood donors for red blood cell and platelet antigens has been predicted to replace phenotyping assays in the screening of compatible blood components for alloimmunized patients. Although several genotyping platforms have been described, novel procedures and processes are needed to perform genotyping efficiently and to maximize its benefits for blood banks.
Materials and Methods  Here we describe the processes and procedures developed to introduce large-scale genotyping in our routine operations.
Results  Preliminary cost–benefit analysis indicated that genotyping must target frequent blood donors (> 3 donations/year) to be efficiently used. A custom-designed computer application was developed to manage the whole project. It selects frequent donors among recent donations, prints coded labels to identify blood samples sent to the external genotyping laboratory, and stores genotyping results. It can search for donors compatible for any combination of the 22 genotyped antigens as well as consult the current inventory for the presence of the corresponding blood components. The phenotype of recovered components is confirmed by standard serology techniques prior to shipment to hospitals.
Conclusion  Since October 2007, 10 555 blood donors have been genotyped. The database is used on a regular basis to find compatible blood components with a genotype–phenotype concordance of 99·6%.     

彩色多普勒超声在活体供肝肝移植中的应用价值

目的探讨彩色多普勒超声（CDFI）在活体供肝肝移植（LDLT）术前、术中及术后的应用价值。方法回顾性总结和分析了6例LDLT术前、术中及术后的CDFI检查结果。结果术前超声发现1例供者肝动脉过细,1例肝静脉属支过粗;术中超声未发现明显异常;术后受者超声发现l例桥血管栓塞。结论CDFI在LDLT整个肝移植过程中观察血供具有重要价值。     

长冷缺血时间对心脏移植供心超微结构的影响

 目的 观察长冷缺血时间对离体供心超微结构的影响,为临床心脏移植供体的合理利用提供资料。方法 将离体供心置于低温器官保存液（the University of Wisconsin solution,UW液）中保存,分别于冷缺血时间6、8、10、12及14 h取部分左心室心肌和冠状动脉在电镜下观察超微结构的变化。结果 供心缺血时间6 h,心肌细胞及冠状动脉内皮细胞超微结构基本正常。随着缺血时间的延长,心肌细胞及血管内皮细胞出现损伤性改变。供心缺血超过12 h,心肌肌丝断裂,心肌细胞出现局灶性坏死,血管内皮细胞完全脱落。结论 心肌超微结构的改变是衡量供心质量的重要指标。供心冷缺血时间10 h以内,心肌损伤程度较轻,供心可用于移植。缺血时间超过10 h,心肌超微结构出现不可逆损伤改变明显增多,供心将不宜用于移植。     

Insights into major facilitator superfamily domain-containing protein-2a (Mfsd2a) in physiology and pathophysiology. What do we know so far?

Major facilitator superfamily domain-containing protein-2a (Mfsd2a) which was considered as an orphan transporter has recently gained attention for its regulatory role in the maintenance of proper functioning of the blood–brain barrier. Besides the major role of Mfsd2a in maintaining the barrier function, increasing evidence has emerged with regard to the contributions of Mfsd2a to various biological processes such as transport, cell fusion, cell cycle, inflammation and regeneration, managing tumor growth, functioning of other organs with barrier functions or responses to injury. The purpose of this article is to review the different roles of Mfsd2a and its involvement in the physiological and pathophysiological processes primarily in the central nervous system and throughout the mammalian body under the lights of the current literature.     

GDF15 promotes simultaneous astrocyte remodeling and tight junction strengthening at the blood–brain barrier

Perivascular astrocyte processes (PAP) surround cerebral endothelial cells (ECs) and modulate the strengthening of tight junctions to influence blood–brain barrier (BBB) permeability. Morphologically altered astrocytes may affect barrier properties and trigger the onset of brain pathologies. However, astrocyte-dependent mediators of these events remain poorly studied. Here, we show a pharmacologically driven elevated expression and release of growth/differentiation factor 15 (GDF15) in rat primary astrocytes and cerebral PAP. GDF15 has been shown to possess trophic properties for motor neurons, prompting us to hypothesize similar effects on astrocytes. Indeed, its increased expression and release occurred simultaneously to morphological changes of astrocytes in vitro and PAP, suggesting modulatory effects of GDF15 on these cells, but also neighboring EC. Administration of recombinant GDF15 was sufficient to promote astrocyte remodeling and enhance barrier properties between ECs in vitro, whereas its pharmacogenetic abrogation prevented these effects. We validated our findings in male high anxiety-related behavior rats, an animal model of depressive-like behavior, with shrunk PAP associated with reduced expression of the junctional protein claudin-5, which were both restored by a pharmacologically induced increase in GDF15 expression. Thus, we identified GDF15 as an astrocyte-derived trigger of astrocyte process remodeling linked to enhanced tight junction strengthening at the BBB.     

D2 autoreceptor switches CB2 receptor effects on [3H]-dopamine release in the striatum

CB₂ receptors (CB₂R) are expressed in midbrain neurons. To evidence the control of dopamine release in dorsal striatum by CB₂R, we performed experiments of [³H]-dopamine release in dorsal striatal slices. We found a paradoxical increase in K⁺-induced [³H]-dopamine release by CB₂R activation with GW 833972A and JWH 133 two selective agonist. To understand the mechanism involved, we tested for a role of the D₂ autoreceptor in this effect; because in pallidal structures, the inhibitory effect of CB₁ receptors (CB₁R) on GABA release is switched to a stimulatory effect by D₂ receptors (D₂R). We found that the blockade of D₂ autoreceptors with sulpiride prevented the stimulatory effect of CB₂R activation; in fact, under this condition, CB₂R decreased dopamine release, indicating the role of the D₂ autoreceptor in the paradoxical increase. We also found that the effect occurs in nigrostriatal terminals, since lesions with 6-OH dopamine in the middle forebrain bundle prevented CB₂R effects on release. In addition, D₂–CB₂R interaction promoted cAMP accumulation, and the increase in [³H]-dopamine release was prevented by PKA blockade. D₂–CB₂R coprecipitation and proximity ligation assay studies indicated a close interaction of receptors that could participate in the observed effects. Finally, intrastriatal injection of CB₂R agonist induced contralateral turning in amphetamine-treated rats, which was prevented by sulpiride, indicating the role of the interaction in motor behavior. Thus, these data indicate that the D₂ autoreceptor switches, from inhibitory to stimulatory, the CB₂R effects on dopamine release, involving the cAMP → PKA pathway in nigrostriatal terminals.