Exposure to Tobacco Retail Outlets and Smoking Initiation among New York City Adolescents

This study was designed to estimate the relationship between exposure to tobacco retail outlets and smoking initiation in a racially diverse urban setting. Using data from the 2011 NYC Youth Risk Behavior Survey, multivariable logistic regression analyses were conducted to estimate the exposure–initiation relationship and test for effect modification, while controlling for covariates. The predicted probability of smoking initiation from the multivariable model increased from 7.7 % for zero times a week exposed to tobacco retailers to 16.0 % for exposure seven times or more per week. The odds of initiation were significantly higher among adolescents exposed to tobacco retail outlets two times or more a week compared with those exposed less often (AOR = 1.41; 95 % CI: 1.08, 1.84). Risk-taking behavior modified the relationship between exposure and initiation, with the odds of initiation highest among those low in risk-taking (AOR = 1.78; 95 % CI: 1.14, 1.56). These results are consistent with past research, showing that frequent exposure to tobacco marketing in retail settings is associated with increased odds of initiation. Reducing exposure to tobacco retail marketing could play an important role in curtailing smoking among adolescents, especially those less prone to risk-taking.     

A 2-year review of recent Nuclear Regulatory Commission events: What errors occur in the modern brachytherapy era?

PurposeTo perform a retrospective analysis of recently reported brachytherapy errors to the Nuclear Regulatory Commission and to compare with historical trends.MethodsAll events reported in the 2-year period from January 1, 2009 to December 31, 2010 were categorized and analyzed. The 4 main areas of dose delivery were Gamma Knife radiosurgery, therapeutic radiopharmaceutical administration, high-dose-rate brachytherapy, and low-dose-rate brachytherapy. The different types of errors were wrong site, wrong dose, unintended exposure, lost or leaking source, or other. The causes of events were specified as the following: communication errors, equipment malfunction, human error, lack of training, or miscellaneous.ResultsOne hundred and forty-seven events were found in the 2-year period. This error reporting rate far surpasses previous reports. The greatest number of events reported was for low-dose-rate brachytherapy, and the most common cause of error was human error. Wrong dose was the error that occurred most often, followed by wrong site.ConclusionsVery simple treatment errors, such as wrong patient, or wrong side of patient treated, are still occurring. Newer, complex deliveries such as high-dose-rate partial breast irradiation and low-dose-rate prostate brachytherapy also had a large number of events reported in this sampling. This report can help institutions establish needs for quality assessment and quality control processes.     

MEMORY CONJUNCTION ERRORS IN YOUNGER AND OLDER ADULTS: EVENT-RELATED POTENTIAL AND NEUROPSYCHOLOGICAL DATA

In a study/recognition paradigm, new words at test were recombinations of studied syllables (e.g. BARLEY from BARTER and VALLEY), shared one syllable with studied words, or were completely new. False alarm rates followed the gradient of similarity with studied items. Event-related potentials to the three classes of false alarms were indistinguishable. False alarms elicited different brain activity than did hits, arguing against the idea that conjunction errors occur during encoding and are later retrieved liked genuine memories. In Experiment 2, with healthy older adults, neuropsychological tests sensitive to frontal lobe function predicted false alarm rate, but not hit rate. Performance on standardised memory scales sensitive to medial temporal/diencephalic function influenced the pattern of false alarm rates across the three classes of new words. The experiments suggest that false alarms to conjunction lures are not similar to true recollections, but are products of faulty monitoring at retrieval.     

Absence of PhIP adducts,p53 and Apc mutations,in rats fed a cooked beef diet containing a high level of heterocyclic amines

Meat cooked at high temperatures contains mutagens and carcinogens known as heterocyclic amines (HCA). Cooking temperature and time determine the amount of HCA produced. The present study examined the DNA of liver, colon, and stomach from rats fed a high level of HCA for 27 weeks. Male Sprague‐Dawley rats were fed a high‐fat AIN‐76A‐based diet containing 60% by weight cooked beef containing a high level of HCA, especially 2‐amino‐l‐methyl‐6‐phenylimidazo[4,5‐b]pyridine (PhIP, 72 ng/g cooked beef), the most abundant HCA in cooked meat products. At the end of 27 weeks the rats were terminated, and small portions of liver, colon, and stomach were quick‐frozen in liquid nitrogen. The DNA was isolated from the thawed tissue by phenol‐chloroform extraction, and the genomic DNA was analyzed for the presence of PhIP adducts by ³²P‐postla‐beling analysis. The DNA was also used in polymerase chain reactions to amplify the rat p53 and Apc genes, then direct dye‐terminator DNA sequencing was carried out. Results showed no PhIP adducts in any tissue. In addition, no signature p53 or Apc gene mutations were seen in colon or stomach DNA. These results indicate that the high level of HCA present in a diet of well‐cooked meat does not cause 1) persistent PhIP adducts similar to those produced by feeding pure PhIP at high doses or 2) p53 and Ape gene mutations in nontumor tissue.     

Anti-adaptors provide multiple modes for regulation of the RssB adaptor protein

RpoS, an RNA polymerase σ factor, controls the response of Escherichia coli and related bacteria to multiple stress responses. During nonstress conditions, RpoS is rapidly degraded by ClpXP, mediated by the adaptor protein RssB, a member of the response regulator family. In response to stress, RpoS degradation ceases. Small anti-adaptor proteins—IraP, IraM, and IraD, each made under a different stress condition—block RpoS degradation. RssB mutants resistant to either IraP or IraM were isolated and analyzed in vivo and in vitro. Each of the anti-adaptors is unique in its interaction with RssB and sensitivity to RssB mutants. One class of mutants defined an RssB N-terminal region close to the phosphorylation site and critical for interaction with IraP but unnecessary for IraM and IraD function. A second class, in the RssB C-terminal PP2C-like domain, led to activation of RssB function. These mutants allowed the response regulator to act in the absence of phosphorylation but did not abolish interaction with anti-adaptors. This class of mutants is broadly resistant to the anti-adaptors and bears similarity to constitutively activated mutants found in a very different PP2C protein. The mutants provide insight into how the anti-adaptors perturb RssB response regulator function and activation.