“
“Objective: Research shows a significant association between eating disorders (ED) and substance use disorders (SUD). The objective of this study is to examine the prevalence, chronology, and possibility of shared familial risk between SUD and ED symptomatology.\n\nMethod: CK0238273 Subjects included 1,206 monozygotic and 877 dizygotic adult female twins. ED symptomatology included anorexia (AN) and bulimia nervosa (BN) diagnosis, symptoms associated with diagnostic criteria, and BN symptom count. SOD included alcohol, illicit drug, and caffeine abuse/dependence. Generalized estimated equation modeling was used to examine phenotypic associations, and Choleksy

decompositions were used to delineate the contribution of genes and environment to comorbidity.\n\nResults: There were no significant differences between

SOD prevalence in women with AN and BN. Women with BN reported BN preceded SOD development while the reverse was true for AN. Twin analyses showed possible familial overlap between BN symptomatology and all SOD examined.\n\nDiscussion: Results suggest an important difference in the chronology of EDs and SUDs. Women with BN may be turning to substances to dampen bulimic Sapitinib urges. Women with AN may be engaging in substance use initially in an effort to lose weight. Results also suggest familial factors contribute to the comorbidity between BN and SOD. (C) 2010 by Wiley Periodicals, Inc.”
“The effects of hepatocyte growth factor (HGF) on barrier functions were investigated by a blood-brain barrier (BBB) in vitro model comprising a primary culture of rat brain capillary endothelial cells (RBEC). In order to examine the response of the peripheral endothelial cells to HGF, human umbilical vascular endothelial cells (HUVEC) and

human dermal microvascular endothelial cells (HMVEC) were also treated with HGF. HGF decreased the permeability of RBEC to sodium fluorescein and Evans blue albumin, and dose-dependently increased transendothelial electrical resistance (TEER) in RBEC. HGF altered the immunochemical staining pattern of F-actin bands and made ZO-1 GS-7977 DNA Damage inhibitor staining more distinct on the linear cell borders in RBEC. In contrast, HGF increased sodium fluorescein and Evans blue albumin permeability in HMVEC and HUVEC, and decreased TEER in HMVEC. In HMVEC, HGF reduced cortical actin bands and increased stress fiber density, and increased the zipper-like appearance of ZO-1 staining. Western blot analysis showed that HGF significantly increased the amount of ZO-1 and VE-cadherin. HGF seems to act on the BBB to strengthen BBB integrity. These findings indicated that cytoskeletal rearrangement and cell-cell adhesion, such as through VE-cadherin and ZO-1, are candidate mechanisms for the influence of HGF on the BBB. The possibility that HGF has therapeutic significance in protecting the BBB from damage needs to be considered. (c) 2013 Elsevier Inc. All rights reserved.