Nonepileptic seizures treatment workshop summary

In May 2005, an international, interdisciplinary group of researchers gathered in Bethesda, MD, USA, for a workshop to discuss the development of treatments for patients with nonepileptic seizures (NES). Specific subgroup topics that were covered included: pediatric NES; presenting the diagnosis of NES, outcome measures for NES trials; classification of NES subtypes; and pharmacological treatment approaches and psychotherapies. The intent was to develop specific research strategies that can be expanded to involve a large segment of the epilepsy and psychiatric treatment communities. Various projects have resulted from the workshop, including the initial development of a prospective randomized clinical trial for NES.     

Improving surveillance of intimate partner violence by use of multiple data sources

BACKGROUND: Intimate partner violence (IPV) is a significant public health problem in the United States. Estimates of incidence and prevalence vary widely, depending on the data source used. Combining information from different sources can enhance our understanding of IPV. METHODS: In this paper, we used 1998 data from the Rhode Island (RI) Department of Health Violence Against Women Public Health Surveillance System to describe the prevalence of IPV reported to police, the demographic characteristics and help-seeking efforts of women reporting IPV, and characteristics of IPV incidents. We used data from the 1998 RI Department of Health Behavioral Risk Factor Surveillance System survey to examine associations between health care use and health outcomes of victims and nonvictims of IPV, and to explore the correlates of IPV. We also discuss the use of both narrow and broad definitions of IPV. RESULTS: Our findings show that the definition of IPV and the source used to identify IPV victims can produce a markedly different picture of IPV victims, and that combining information from different data sources can enhance our understanding of IPV. An important finding for health care providers is that IPV victims do not appear to be significantly different from nonvictims in their access to and utilization of routine health care, and that more than 60% of victims at highest risk for injury reported seeing a health care provider because of IPV. CONCLUSIONS: Our findings underscore the importance of health care providers addressing IPV and its consequences among their patients.     

Defining MC1R Regulation in Human Melanocytes by Its Agonist α-Melanocortin and Antagonists Agouti Signaling Protein and β-Defensin 3

The melanocortin 1 receptor (MC1R), a G(s) protein-coupled receptor, has an important role in human pigmentation. We investigated the regulation of expression and activity of the MC1R in primary human melanocyte cultures. Human β-defensin 3 (HBD3) acted as an antagonist for MC1R, inhibiting the α-melanocortin (α-melanocyte-stimulating hormone (α-MSH))-induced increase in the activities of adenylate cyclase and tyrosinase, the rate-limiting enzyme for melanogenesis. α-Melanocortin and forskolin, which activate adenylate cyclase, and 12-O-tetradecanoylphorbol-13-acetate, which activates protein kinase C, increased, whereas exposure to UV radiation reduced, MC1R gene and membrane protein expression. Brief treatment with α-MSH resulted in MC1R desensitization, whereas continuous treatment up to 3?hours caused a steady rise in cAMP, suggesting receptor recycling. Pretreatment with agouti signaling protein or HBD3 prohibited responsiveness to α-MSH, but not forskolin, suggesting receptor desensitization by these antagonists. Melanocytes from different donors expressed different levels of the G protein-coupled receptor kinases (GRKs) 2, 3, 5, and 6, as well as β-arrestin 1. Therefore, in addition to the MC1R genotype, regulation of MC1R expression and activity is expected to affect human pigmentation and the responses to UV.     

Evaluation of postpartum blood loss after misoprostol-induced labour

Objective  To objectively evaluate postpartum blood loss after successful misoprostol induction and compare it with blood loss after oxytocin induction of labour.
Design  Prospective randomised study.
Setting  Labour ward in university maternity hospital.
Population  A total of 150 women up to third parity with completed 40 weeks of singleton normal pregnancy, average size cephalic fetus.
Methods  Cases were randomised between oxytocin induction and misoprostol induction. Blood was collected in suction set and measured in the delivery room starting after delivery of the fetus and was evaluated by pad weighing in the following 6 hours. Pre- and postdelivery haematocrit were measured and difference between the two values was assessed and analysed.
Main outcome measures  Success of induction, induction delivery interval, postpartum blood loss, and difference between pre- and postdelivery haematocrit.
Results  Induced labour was significantly faster with misoprostol induction ( P < 0.001). Blood loss and haematocrit difference was significantly greater in the misoprostol group than in oxytocin group ( P < 0.02 and 0.001, respectively). Blood loss in both groups was significantly correlated with higher initial Bishop score ( P < 0.001 and 0.024, respectively) and short labour duration ( P < 0.0002 and 0.0001, respectively).
Conclusions  Misoprostol induction is associated with increased blood loss especially when used in women with high Bishop score; therefore, it is better reserved for cases requiring cervical ripening.     

Is MSH2 a breast cancer susceptibility gene?

Mutations in the DNA mismatch repair gene MSH2 lead to increased replication error and microsatellite instability and account for a substantial proportion of hereditary non-polyposis colorectal cancer (Lynch syndrome). A recent international collaborative genome-wide linkage scan (GWS) for breast cancer susceptibility loci found some evidence for there being a breast cancer susceptibility gene in a genomic region on chromosome 2p close to MSH2. We sought to investigate the possibility that mutations in MSH2 might explain the multiple cases of breast cancer in some families that were included in the international GWS. DNA samples from the affected probands of 59 multiple-case breast cancer families, many of whom gave LOD scores >0.5 in the MSH2 region, were screened for large genomic alterations in MSH2 via the Multiplex Ligation-dependant Probe Amplification (MLPA) assay and for coding region mutations via exonic sequencing. Several of the families also contained cases of colorectal cancer in addition to breast cancer and had been included in the GWS that had identified a positive LOD score on chromosome 2p. Using MLPA, c.1236C > T was identified in one proband but this variant was not predicted to create an alternate acceptor/donor site within exon 7 MSH2 using in silico analyses. A c.1734T > C was identified in a second proband via exonic sequencing but testing of the variant in other family members did not support segregation of this variant with disease. Extensive screening of 59 multiple-case breast cancer families did not identify any coding region mutations or larger genomic alterations in MSH2 that might implicate MSH2 as a breast cancer susceptibility gene.