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Introduction: As medical advances have significantly increased the life expectancy among older adults, the number of older patients requiring trauma care has risen proportionately. Nevertheless, it is unclear among this growing population which sociodemographic and economic factors are associated with decisions to triage and transfer to level I/II centers. This study aims to assess for any association between patient sociodemographic characteristics, triage decisions, and outcomes during acute trauma care presentations., Methods: The National Trauma Data Bank was queried for patients aged 65 and older with an injury severity score > 15 between the years 2007 to 2017. Factors associated with subsequent levels of triage on presentation were assessed using multivariate logistic regression, and associations of levels of triage with outcomes of mortality, morbidity, and hospital length of stay are examined using logistic and linear regression models., Results: Triage of 210,310 older adult trauma patients showed significant findings. American Indian patients had higher odds of being transferred to level I/II centers, while Asian, Black, and Native Hawaiian patients had lower odds of being transferred to level I/II centers when compared to Caucasian patients (P < 0.001). Regarding insurance, self-pay (uninsured) patients were less likely to be transferred to a higher level of care; however, this was also demonstrated in private insurance holders (P < 0.001). Caucasian patients had significantly higher odds of mortality, with Black patients (odds ratio [OR] 0.80 [0.75, 0.85]) and American Indian patients (OR 0.87 [0.72, 1.04]) having significantly lower odds (P < 0.001). Compared to government insurance, private insurance holders (OR 0.82 [0.80, 0.85]) also had significantly lower odds of mortality, while higher odds among self-pay were observed (OR 1.75 [1.62, 1.90]), (P < 0.001)., Conclusions: Access to insurance is associated with triage decisions involving older adults sustaining trauma, with lower access increasing mortality risk. Factors such as race and gender were less likely to be associated with triage decisions. However, due to this study's retrospective design, further prospective analysis is necessary to fully assess the decisions that influence trauma triage decisions in this patient population., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Certain cells present in mouse skin are resistant to calcium-induced terminal differentiation. It is believed that these calcium-resistant cells (CRCs) represent an early stage in the carcinogenic process, in part, because frequency increases after treatment with mutagens. The frequency of CRCs in C3H mouse skin was measured before and after treatment with certain petroleum-derived materials. One objective was to determine whether this assay could differentiate between genotoxic and nongenotoxic mouse skin carcinogens. An additional objective was to determine whether CRCs are an important factor in the tumorigenicity of petroleum middle distillates (PMDs), a class of apparently nongenotoxic mateials. Three petroleum-derived materials were tested: mineral oil (MO), a noncarcinogenic product used as the negative control; catalytically cracked clarified oil (CCCO), a highly carcinogenic and mutagenic material; and a lightly paraffinic (LRPO), a PMD which has produced tumors when repeatedly applied, but is not mutagenic and does not initiate most skin tumors. The CRC frequency was not increased by LRPO treatment; however, a statistically significant and dose-related increase was produced by CCCO. These results are consistent with observations that genotoxic, petroleum-derived liquids are capable of tumor initiation in mouse skin, whereas PMDs which are not genotoxic do not initiate skin tumors. The number of CRCs in untreated and MO-treated mice was approximately twice the tumor frequency measured in bioassays of PMDs. Thus, tumor production associated with these products could be due to promotion of preexisting, spontaneously initiated cells.

The metabolism of saturated nitriles, including acetonitrile, has been assumed to occur by a cytochrome P-450-dependent oxidation at the alpha-carbon, yielding a cyanohydrin intermediate which may spontaneously degrade to hydrogen cyanide and an aldehyde. However, results of studies in our laboratory suggest that formaldehyde is not a metabolite of acetonitrile. Since acetonitrile is structurally similar to iodomethane, a substrate for glutathione (GSH) S-transferases, we hypothesized that the metabolism of acetonitrile to cyanide might also occur by a nucleophilic substitution reaction involving GSH. The present studies were conducted to investigate these hypotheses and to further our study of the effects of acetone on acetonitrile metabolism. Female Sprague-Dawley rats were pretreated with buthionine sulfoximine BSO (4 mmol/kg ip, at -4 and -2 hr), cobalt heme (90 mumol/kg sc, at -48 hr), acetone (1960 mg/kg po, at -24 hr), or vehicle, and hepatocytes were isolated after collagenase perfusion of the liver. BSO reduced the cellular GSH content by greater than 80%, but did not appear to affect the metabolism of acetonitrile: the liberation of cyanide correlated with cytochrome P-450, and not GSH, concentrations. Cobalt heme depleted hepatocellular cytochrome P-450 (-45%) content, decreased cell yield and viability, and resulted in a marked reduction in the metabolism of acetonitrile to cyanide. Cobalt heme did not affect the recovery of sodium cyanide from hepatocyte suspensions. Pretreatment of rats with acetone resulted in a twofold increase in the metabolism of acetonitrile to cyanide. Addition of acetone in vitro inhibited acetonitrile metabolism, with an IC50 of 319 microM.(ABSTRACT TRUNCATED AT 250 WORDS)