Psychological distress among migrant groups in Australia: results from the 2015 National Health Survey

Social Psychiatry and Psychiatric Epidemiology - To understand the relationship between migration and psychological distress, we (a) calculated the prevalence of psychological distress in specific...     

BMP2 Regulation of CXCL12 Cellular,Temporal, and Spatial Expression Is Essential During Fracture Repair

The cellular and humoral responses that orchestrate fracture healing are still elusive. Here we report that bone morphogenic protein 2 (BMP2)‐dependent fracture healing occurs through a tight control of chemokine C‐X‐C motif‐ligand‐12 (CXCL12) cellular, spatial, and temporal expression. We found that the fracture repair process elicited an early site‐specific response of CXCL12⁺‐BMP2⁺ endosteal cells and osteocytes that was not present in unfractured bones and gradually decreased as healing progressed. Absence of a full complement of BMP2 in mesenchyme osteoprogenitors (BMP2^cKO/+) prevented healing and led to a dysregulated temporal and cellular upregulation of CXCL12 expression associated with a deranged angiogenic response. Healing was rescued when BMP2^cKO/+ mice were systemically treated with AMD3100, an antagonist of CXCR4 and agonist for CXCR7 both receptors for CXCL12. We further found that mesenchymal stromal cells (MSCs), capable of delivering BMP2 at the endosteal site, restored fracture healing when transplanted into BMP2^cKO/+ mice by rectifying the CXCL12 expression pattern. Our in vitro studies showed that in isolated endosteal cells, BMP2, while inducing osteoblastic differentiation, stimulated expression of pericyte markers that was coupled with a decrease in CXCL12. Furthermore, in isolated BMP2^cKO/cKO endosteal cells, high expression levels of CXCL12 inhibited osteoblastic differentiation that was restored by AMD3100 treatment or coculture with BMP2‐expressing MSCs that led to an upregulation of pericyte markers while decreasing platelet endothelial cell adhesion molecule (PECAM). Taken together, our studies show that following fracture, a CXCL12⁺‐BMP2⁺ perivascular cell population is recruited along the endosteum, then a timely increase of BMP2 leads to downregulation of CXCL12 that is essential to determine the fate of the CXCL12⁺‐BMP2⁺ to osteogenesis while departing their supportive role to angiogenesis. Our findings have far‐reaching implications for understanding mechanisms regulating the selective recruitment of distinct cells into the repairing niches and the development of novel pharmacological (by targeting BMP2/CXCL12) and cellular (MSCs, endosteal cells) interventions to promote fracture healing. © 2015 American Society for Bone and Mineral Research.     

The Impact of Intimate Partner Violence Exposure in Adolescence and Emerging Adulthood: A Developmental Psychopathology Approach

Despite increased attention on parental intimate partner violence (IPV) exposure, a relative paucity of research has examined the developmental consequences of this traumatic experience within a life span approach. The aim of the present study was to examine how parental IPV exposure may relate to mental health during the transition from adolescence to emerging adulthood. Furthermore, we examined whether the impact of parental IPV exposure was unique from more commonly studied maltreatment experiences, specifically neglect and physical abuse. A large, racially and ethnically diverse sample (N_baseline = 1,042; 56% female; M_age = 15.1, SD = 0.79; 31.4% Hispanic, 29.4% White, 27.9% African American, 3.6% Asian, 7.7% biracial or other) of adolescents completed a baseline assessment for parental physical IPV exposure and maltreatment as well as measures for symptoms of depression, posttraumatic stress, and substance use, annually for 6 consecutive years. Mixed-level modeling was used to examine how parental IPV exposure was uniquely associated with different patterns of mental health across developmental epochs. Findings demonstrated a multifaceted relation with mental health. For internalizing symptoms, the effect was pronounced during adolescence, and neglect increased the risk for depression symptomatology. Meanwhile, parental-IPV-exposed adolescents were at increasing risk for substance use as they aged into adulthood. Symptom levels and trajectories were independent and distinct from maltreatment experiences. This study helps illuminate parental IPV exposure’s unique influence on well-being during vulnerable developmental periods. It also calls attention to the importance of developing suitable intervention/prevention programs to target this vulnerable population.     

Polymorphisms in P2X4R and CAMKK2 may affect TNFα production: Implications for a role in HIV-associated sensory neuropathy

Polymorphisms in P2X4R and CAMKK2 associate with susceptibility to HIV-associated sensory neuropathy (HIV-SN) – a condition likely mediated by TNFα. As single nucleotide polymorphisms (SNPs) and haplotypes of CAMKK2, and a neighbouring gene P2X4R, mark susceptibility to HIV-SN in South Africans living with HIV, we examined the relationship between P2X4R and CAMKK2 genotypes and TNFα production. Peripheral blood mononuclear cells from 129 healthy donors were stimulated with killed Escherichia coli, and concentrations of soluble TNFα were assessed. Their DNA was genotyped for 22 SNPs in P2X4R and CAMKK2. Three SNPs within P2X4R and two SNPs within CAMKK2 influenced concentrations of TNFα, but these SNP did not associate with risk for HIV-SN. This incongruence may reflect differences in P2X4R haplotypes present in Africans and Europeans. However some CAMKK2 haplotypes were found in both populations, so CAMKK2 polymorphisms may impact upon HIV-SN via effects of the protein on pathways other than TNFα.     

红细胞输注前的质量标准

现行红细胞输注规则主要规定红细胞采集量和输注时存活红细胞的比例,即450ml的采集量,输注时24h平均体内的存活率至少75%。其他还限制了游离血红蛋白的含量,通常不超过红细胞总量的1．0%。特殊需求的红细胞产品又有额外的要求。每单位少白细胞的红细胞的残余白细胞不超过1×10~6。     

Effectiveness of a prospective physician self-audit transfusion- monitoring system

BACKGROUND: The purpose of this study was to search for a more effective transfusion-monitoring system than the existing system of retrospective peer review. STUDY DESIGN AND METHODS: This research used a study-control, preintervention and postintervention design, to evaluate the effectiveness of a prospective physician self-audit transfusion-monitoring system that functioned without the direct involvement of transfusion service physicians. This research also evaluated the effectiveness of issuing to physicians a memo with transfusion guidelines. Three process indicators were used to assess physician behavior at various stages of the blood-ordering process: 1) the number of crossmatches ordered per admission, 2) the transfusion-to- crossmatch ratio, and 3) the number of blood units returned to the laboratory after physician self-auditing. The study used two outcome indicators to reflect overall blood utilization: 1) the percentage of patients who received red cell transfusions and 2) the number of blood units transfused per recipient each month. RESULTS: The prospective physician self-audit system implemented at the study hospital did not reverse physician transfusion decisions, and the process of issuing to physicians a memo with transfusion guidelines at the control hospital failed to reduce blood usage. However, a transient reduction in blood utilization was observed at the study hospital. CONCLUSION: The reduction was hypothesized to be due to a Hawthorne effect, in which observed behavior is affected by the subject's awareness of the research study.     

自体干细胞移植治疗老年心肌梗死后心力衰竭

目的：实验以移植后3个月、6个月时间超声心动图客观指标评估了自体干细胞冠状动脉内移植治疗老龄心肌梗死后心力衰竭的效果和安全性。方法：选择2004—06／2006—06江苏省苏北人民医院心内科自愿接受干细胞移植的7例心肌梗死后心力衰竭患者，平均年龄69岁，心功能Ⅲ-Ⅳ级，左室射血分数〈50％。药物治疗基础上加用自体干细胞冠状动脉内移植治疗的方法，其中2例骨髓干细胞在体外扩增后获得，5例经粒细胞集落刺激因子皮下注射动员自体骨髓干细胞后分离外周血获得干细胞悬液。将采集的干细胞悬液经0ver-the-wire球囊导管中心腔注入梗死相关动脉。观察自体干细胞动员，培养，采集和回输过程中的不良反应。在移植前、移植后3月、6月应用超声心动图评价左室形态和心功能变化，室壁运动积分指数及6min步行距离。结果：7例患者均进入结果分析。移植3个月后，心功能得到改善，超声心动图检查左室收缩期内径及射血分数变化不大，6min步行距离有所提高，但差异无显著性（P〉0．05）。移植6个月后，患者心功能明显改善，超声心动图检查左室收缩期内径及射血分数和室壁运动积分均有明显提高（P〈0．05），6min步行距离也有明显提高（P〈0．05）。整个过程中未出现严重并发症。结论：自体干细胞冠状动脉内移植治疗老龄心肌梗死后心力衰竭，6个月时超声心动图客观指标评估能够改善患者心功能，且安全。     

Beta-cell dysfunction in classic transient neonatal diabetes is characterized by impaired insulin response to glucose but normal response to glucagon

OBJECTIVE: To investigate beta-cell function and the long-term health of four case subjects presenting with chromosome 6-associated transient neonatal diabetes (TND). RESEARCH DESIGN AND METHODS: Two unrelated case subjects presenting with paternal uniparental isodisomy of chromosome 6 (UPD6) and two siblings with a paternally inherited duplication of 6q24 were studied. Three case subjects presented with neonatal diabetes that recurred at 4-17 years, while diabetes was incidentally discovered in the other case subject at 14 years of age. beta-Cell function was investigated after diabetes relapse by means of an oral glucose tolerance test (OGTT), an intravenous glucose tolerance test (IVGTT), and glucagon tests. The quantitative insulin sensitivity check index (QUICKI) was calculated from fasting blood samples as an estimate of insulin sensitivity. RESULTS: beta-Cell function was investigated at diabetes relapse in two case subjects: the insulin response to both an OGTT and IVGTT was low, whereas the basal levels of C-peptide were normal. No evidence of insulin resistance was found. Residual beta-cell function was further explored by a glucagon test in all subjects at the age of 16-28 years and was found to be normal. Final height was within the normal percentiles, whereas one case, who had been poorly controlled since puberty, presented with diabetes-related microvascular complications. CONCLUSIONS: In patients with chromosome 6-associated TND, the beta-cell is preserved and able to secrete insulin through the stimulatory G protein pathway while exhibiting a specific defect of insulin secretion after glucose stimulation. This form of diabetes can be managed with insulin or diet, although new therapeutic agents (glucagon-like synthetic analogs) may prove useful in the future. Lack of treatment leads to long-lasting hyperglycemia without the risk of ketoacidosis but associated with microangiopathy in adult life.