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To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.brat.2010.07.001 Byline: Naomi Breslau (a), Edward L. Peterson (b) Abstract: reported that prior trauma alone, in the absence of PTSD, did not predict an increased PTSD risk, relative to no prior trauma. Only prior trauma that resulted in PTSD predicted an increased PTSD risk following a subsequent trauma. Recently, proposed that the effect of prior trauma might vary by type of prior trauma, a possibility not considered in Breslau et al. They report that childhood sexual or physical assault, in the absence of PTSD, increased the PTSD risk following a subsequent trauma. This report examines the PTSD effects of prior assaultive violence, using data from . The study assessed PTSD in relation to up to three events. Analysis was performed on the subset with PTSD assessment for two distinct events, the earliest trauma and a subsequent trauma (n =967), using as reference persons with no prior trauma (n =972). Neither prior assaultive violence nor other prior traumas, in the absence of PTSD, influenced the subsequent risk of PTSD. In contrast, prior PTSD increased considerably the PTSD risk of a subsequent trauma. The limitations in and in this study and future research directions are discussed. Author Affiliation: (a) Department of Epidemiology, Michigan State University, College of Human Medicine, B645 West Fee Hall, East Lansing, MI 48824, USA (b) Henry Ford Health System, Department of Biostatistics and Research Epidemiology, Detroit, MI, USA Article History: Received 1 March 2010; Revised 25 June 2010; Accepted 6 July 2010

N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) inhibits collagen production and cell proliferation in cultured rat cardiac fibroblasts, but its effect on differentiation of fibroblasts into myofibroblasts is not known. High amounts of transforming growth factor-[beta]1 (TGF-[beta]1) have been found in fibrotic cardiac tissue. TGF-[beta]1 converts fibroblasts into myofibroblasts, which produce more extracellular matrix proteins than fibroblasts. We hypothesized that 1) Ac-SDKP inhibits TGF-[beta]1-induced differentiation of fibroblasts into myofibroblasts; and 2) this effect is mediated in part by blocking phosphorylation of small-mothers-against-decapentaplegic (Smad) 2 and extracellular signal-regulated kinase (ERK) 1/2. For this study, we used human fetal cardiac fibroblasts (HCFs), which do not spontaneously become myofibroblasts when cultured at low passages. We investigated the effect of Ac-SDKP on TGF-[beta]1-induced HCF transformation into myofibroblasts, Smad2 and ERK1/2 phosphorylation, Smad7 expression, cell proliferation, and collagen production. We also investigated TGF-[beta]1 production by HCFs stimulated with endothelin-1 (ET-1). As expected, HCFs treated with TGF-[beta]1 transformed into myofibroblasts as indicated by increased expression of [alpha]-smooth muscle actin and a higher proportion of the embryonic isoform of smooth muscle myosin compared with untreated cells. TGF-[beta]1 also increased Smad2 and ERK1/2 phosphorylation but did not affect Smad7 expression. In addition. TGF-[beta]1 stimulated HCF proliferation as indicated by an increase in mitochondrial dehydrogenase activity and collagen production (hydroxyproline assay). AcSDKP significantly inhibited all of the effects of TGF-[beta]1. It also inhibited ET-l-stimulated TGF-[beta]1 production. We concluded that Ac-SDKP markedly suppresses differentiation of human cardiac fibroblasts into myofibroblasts, probably by inhibiting the TGF-[beta]/ Smad/ERK1/2 signaling pathway, and thus mediating its anti-fibrotic effects. transforming growth factor-[beta]1; human cardiac myofibroblasts; N-acetyl-seryl-aspartyl-lysyl-proline; collagen; signal transduction; fibroblast differentiation doi: 10.1152/ajpheart.00464.2009.

Several essential components of NADPH oxidase, including [p22.sup.phox], [gp91.sup.phox] (nox2) and its homologs nox1 and nox4, [p47.sup.phox], [p67.sup.phox], and rac1, are present in the vasculature. We previously reported that [p67.sup.phox] is essential for adventitial fibroblast NADPH oxidase [O.sup.-.sub.2] production. Thus we postulated that inhibition of adventitial [p67.sup.phox] activity would attenuate angioplasty-induced hyperplasia. To test this hypothesis, we treated the adventitia of carotid arteries with a control adenovirus (Ad-control), a virus expressing dominant-negative [p67.sup.phox] (Ad-p67dn), or a virus expressing a competitive peptide (gp91ds) targeting the [p47.sup.phox]-[gp91.sup.phox] interaction (Ad-gp91ds). Common carotid arteries (CCAs) from male Sprague-Dawley rats were transfected with Ad-control, Ad-p67dn, or Ad-gp91ds in pluronic gel. After 2 days, a 2-F (Fogarty) catheter was used to injure CCAs in vivo. After 14 days, CCAs were perfusion-fixed and analyzed. In 13 experiments, digital morphometry suggested a reduction of neointimal hyperplasia with Ad-p67dn compared with Ad-control; however, the reduction did not reach statistical significance (P = 0.058). In contrast, a significant reduction was achieved with Adgp91ds (P = 0.006). No changes in medial area or remodeling were observed with either treatment. Moreover, adventitial fibroblast proliferation in vitro was inhibited by Ad-gp91ds but not by Ad-p67dn, despite confirmation that Ad-p67dn inhibits NADPH oxidase in fibroblasts. These data appear to suggest that a multicomponent vascular NADPH oxidase plays a role in neointimal hyperplasia. However, inhibition of [p47.sup.phox] may be more effective than inhibition of [p67.sup.phox] at attenuating neointimal growth. NADPH oxidase; [p47.sup.phox]; adventitia; restenosis

Asthma and lead poisoning are prevalent among urban children in the United States. Lead exposure may be associated with excessive production of immunoglobulin E, possibly increasing asthma risk and contributing [...]

Objective: Odontogenic sinusitis (ODS) can cause infectious orbital, intracranial, and osseous complications. Diagnosis and management of complicated ODS have not been discussed in recent sinusitis guidelines. The purpose of this systematic review was to describe epidemiological and clinical features, as well as management strategies of complicated ODS. Data Sources: PubMed, EMBASE, and Cochrane Library. Review Methods: A systematic review was performed to describe various features of complicated ODS. All complicated ODS studies were included in qualitative analysis, but studies were only included in quantitative analysis if they reported specific patient-level data. Results: Of 1126 studies identified, 75 studies with 110 complicated ODS cases were included in qualitative analysis, and 47 studies with 62 orbital and intracranial complications were included in quantitative analyses. About 70% of complicated ODS cases were orbital complications. Only 23% of complicated ODS studies were published in otolaryngology journals. Regarding ODS-related orbital and intracranial complications, about 80% occurred in adults, and 75% were male. Complicated ODS occurred most commonly from apical periodontitis of maxillary molars. There were no relationships between sinusitis extent and orbital or intracranial complications. High rates of anaerobic and α-hemolytic streptococcal bacteria were identified in complicated ODS. Management generally included systemic antibiotics covering aerobic and anaerobic bacteria, and surgical interventions were generally performed to address both the complications (orbital and/or intracranial) and possible infectious sources (dentition and sinuses). Conclusion: ODS should be considered in all patients with infectious extrasinus complications. Multidisciplinary management between otolaryngologists, dental specialists, ophthalmologists, and neurosurgeons should be considered to optimize outcomes. [ABSTRACT FROM AUTHOR]

Young children who are exposed to two or more dogs or cats may have a lower risk of developing allergies than those who are not exposed to dogs or cats. This was the conclusion of a study of 474 children born between 1987 and 1989 who were followed until the age of 6 or 7. This conclusion supports studies showing that children who grow up with farm animals have a lower risk of asthma and other allergies.

The younger a person begins smoking, the less likely that person may be to quit. A group of 1,007 members of a Michigan health maintenance organization ranging in age from 21 to 31 responded to a survey ascertaining smoking habits. Overall, 414 persons had been daily smokers for at least a month. Of these, 34% had first smoked at age 13 or younger, 43% began smoking at between 14 and 16 years old, and 23% began at age 17 or older. Among smokers, 145 had quit and not smoked for at least one year. Only 4% of smokers from the group that started smoking youngest quit compared with 10% of smokers in the intermediate group and 14% of smokers beginning at the oldest age. Although a history of conduct problems or depression and symptoms of nicotine dependence such as failed attempts to quit or withdrawal symptoms also decreased the likelihood of quitting, age at smoking initiation remained a significant independent factor.