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The article discusses the consolidation of archival materials from the U.S. National Archives in St. Louis, Missouri and the U.S. National Personnel Records Center (NPRC) and the opening of an archival facility in St. Louis to house the records. Particular focus is given to the individual and national importance of these military records and to the efforts of archival staff to retrieve information for patrons. Public programs and storage and research areas in the building are also discussed.

This community-based project examined the interpersonal and system influences on smoking practices and exposure to cigarette smoke that place young pregnant and parenting First Nations women and their children at risk. The aim was to work with the community using this information to develop meaningful strategies to support tobacco reduction and reduce exposure to second-hand smoke. Ethnographic methods informed by decolonizing approaches were used to study smoking practices and exposure within the context of six First Nations rural reserve villages in the Gitxsan territory in North-Western British Columbia. Data were collected through individual interviews with key community members, individual and group interviews with women, men, youth and older people, including Elders, and participant observation. Older people, including grandparents and Elders expressed great interest in being more involved in their communities, particularly with youth. Other community members, especially mothers, saw such older people as important in diminishing the tobacco exposure problem, with ideas for their involvement ranging from role modeling non-smoking or respectful smoking to teaching cultural traditions. Elders in First Nations communities represent a culturally-relevant resource for health that is currently underused. Communities might draw upon their wisdom and influence to decrease tobacco exposure and promote community health in other ways. This offers a concrete, practical strategy in response to widespread calls for supporting the culture of Aboriginal people as part of health promotion. Ce projet communautaire portait sur les influences interpersonnelles et systémiques qui exposent les jeunes femmes enceintes et les jeunes mères des Premières nations et leurs enfants au tabagisme et à la fumée de cigarette. Le but était d’utiliser ces informations en élaborant, avec la collaboration de la communauté, des stratégies concrètes pour réduire le tabagisme et l’exposition à la fumée secondaire. Nous avons employé des méthodes ethnographiques étayées par des approches de décolonisation pour étudier le tabagisme et l’exposition à la fumée de cigarette dans six villages situés dans des réserves rurales des Premières nations sur le territoire gitksan (Nord-Ouest de la Colombie-Britannique). Les données ont été recueillies au moyen d’entretiens individuels avec des membres influents des communautés, d’entretiens individuels et collectifs avec des femmes, des hommes, des jeunes et des personnes âgées (y compris des anciens) et par l’observation des participants. Les personnes âgées, dont les grands-parents et les anciens, étaient vivement intéressées à s’impliquer davantage dans leur communauté, particulièrement auprès des jeunes. Les autres résidents, surtout les mères, considéraient les personnes âgées comme étant importantes pour réduire le problème d’exposition au tabac et avaient des idées pour les impliquer (en étant des exemples de non-fumeurs pour les jeunes ou en leur enseignant le respect du tabac ou d’autres traditions culturelles). Les anciens des communautés des Premières nations sont une ressource de santé culturellement significative encore sous-utilisée. Les communautés pourraient faire appel à leur sagesse et à leur influence pour réduire l’exposition au tabac et promouvoir la santé communautaire de diverses façons. Ce serait une stratégie concrète et pratique pour répondre aux appels généralisés en faveur de l’intégration de la culture des peuples autochtones dans la promotion de la santé.

Methoxyacetaldehyde, an Intermediate Metabolite of 2-Methoxyethanol, Is Immonosuppressive in the Rat. Smialowicz, R. J., Riddle, M. M., and Williams, W. C. (1993). Fundam. Appl. Toxicol.21, 1-7.

The article explores on how social media provides easy and convenient access to historical information in the U.S. It notes that the National Archives at St. Louis, Missouri's National Personnel Records Center (NPRC) has joined the social media explosion as part of the agency's attempt to open its doors to the on-line world in August 2010. It stresses the ample advantages afforded by social media sites which can be used as teaching tools to increase civic and historical literacy.

A simple, achiral monoamine sigma-1 (σ1) receptor selective ligand (σ2Kiσ1Ki>2000) is described, which could replace the chiral (+)-pentazocine or dextrallorphan as a σ1masking agent in σ2binding assays.

The article reports that the National Personnel Records Center (NPRC) of the U.S. National Archives and Records Administration (NARA) will move a large number of records to a new location in St. Louis, Missouri. Types of personnel records being relocated are related to military service and federal civilian employees.

ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.

Oral dosing of adult male F344 rats with the glycol ether 2-methoxyethanol (ME) or its principal metabolite 2-methoxyacetic acid (MAA) results in the suppression of the primary plaque-forming cell (PFC) response to trinitrophenyl-lipopolysaccharide (TNP-LPS). In the present study, the PFC response to TNP-LPS was used to evaluate the immunotoxic potential of ethylene glycol (EG) as well as the glycol ethers 2-methoxyethyl acetate (MEA), 2-(2-methoxyethoxy) ethanol, bis(2-meth- oxyethyl) ether, 2-ethoxyethanol and its principal metabolite 2-ethoxyacetic acid, 2-ethoxyethyl acetate, and 2-butoxyethanol relative to ME and MAA. Rats were immunized with TNP-LPS and then exposed 4 and 28 hr later to 50, 100, 200, or 400 mg/kg of glycol ether or EG. Three days following immunization, the PFC response to TNP-LPS was determined. In addition to ME and MAA, only MEA, which was as effective as ME, suppressed the PFC response to TNP-LPS. Concomitant administration of the alcohol dehydrogenase inhibitor 4-methylpyrazole with ME or MEA prevented suppression of the PFC response by these glycol ethers. These results indicate that of the chemicals tested only ME, MEA, and MAA are immunosup pressive, and that oxidative metabolism via alcohol dehydrogenase is necessary for ME- and MEA-suppression of the response to TNP-LPS.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental contaminant that produces adverse effects on the immune system of experimental animals. In this study, the effect that TCDD has on the antibody plaque-forming cell (PFC) response to the T cell-independent (TI) antigen trinitrophenyl-lipopolysaccharide (TNP-LPS) was compared in adult female B6C3F1 mice and F344 rats. Mice or rats were given a single intraperitoneal injection of TCDD at doses ranging from 1 to 30 μg/kg, 7 days prior to immunization with TNP-LPS by intravenous injection. Three days later body, spleen, thymus, and liver weights were measured and the PFC response to TNP-LPS was determined. Thymus weights were decreased at 10 and 30 μg TCDD/kg, whereas spleen weights were decreased and liver weights increased in mice dosed at 3,10, and 30 μg/kg. Mice dosed at 10 and 30 μg TCDD/kg had suppressed PFC responses and serum hemagglutination liters. In rats, thymus weights were decreased and liver weights increased at 3, 10, and 30 μg TCDD/kg; however, the PFC response and serum hemagglutination titers to TNP-LPS were suppressed only at 30 μg/kg TCDD. TCDD did not affect splenic lymphocyte subsets evaluated by flow cytometry. These results indicate that TCDD suppresses the TI antibody response to TNP-LPS in both B6C3F1 mice and F344 rats, with mice more sensitive to suppression by TCDD than rats.

2-Methoxyethanol (ME) is metabolized to 2-methoxyacetic acid (MAA) via the intermediate metabolite methoxyacetaldehyde (MAAD). Both ME and MAA have been shown in this laboratory to be immunosuppressive in rats following oral dosing. In this study, the plaque-forming cell (PFC) response to trinitrophenyl-lipopolysaccharide (TNP-LPS) was used to determine if MAAD is immunosuppressive in rats. Rats pretreated with the aldehyde dehydrogenase inhibitors disulfiram (2 mmol/kg) or cyanamide (0.48 mmol/kg) followed by oral dosing with ME (2.64 mmol/kg) resulted in suppressed PFC responses equivalent to the suppressed responses of rats dosed with ME alone. Rats pretreated with disulfiram and then dosed with 2.64 mmol/kg 2-methoxyethyl acetate (MEA), also resulted in suppressed PFC responses similar to that of MEA alone. In contrast, coadministration of the alcohol dehydrogenase inhibitor 4-methylpyrazole (1.2 mmol/kg) with ME or MEA blocked suppression of the PFC response following exposure to ME or MEA alone. Oral dosing with equimolar (2.64 mmol/kg) concentrations of ME, MAA, or MAAD resulted in equivalent suppression of the TNP-LPS PFC response. Rats exposed to either disulfiram or cyanamide and MAAD also resulted in suppression of the PFC response. These results indicate that metabolism of ME to either MAAD or MAA is required for immunosuppression, and that these two metabolites are equipotent immunosuppressants in the rat.