Are quit attempts among U.S. female nurses who smoke different from female smokers in the general population? An analysis of the 2006/2007 tobacco use supplement to the current population survey

<p>Abstract</p> <p>Background</p> <p>Smoking is a significant women's health issue. Examining smoking behaviors among occupational groups with a high prevalence of women may reveal the culture of smoking behavior and quit efforts of female smokers. The purpose of this study was to examine how smoking and quitting characteristics (i.e., ever and recent quit attempts) among females in the occupation of nursing are similar or different to those of women in the general population.</p> <p>Methods</p> <p>Cross-sectional data from the Tobacco Use Supplement of the Current Population Survey 2006/2007 were used to compare smoking behaviors of nurses (n = 2, 566) to those of non-healthcare professional women (n = 93, 717). Smoking characteristics included years of smoking, number of cigarettes, and time to first cigarette with smoking within the first 30 minutes as an indicator of nicotine dependence. Logistic regression models using replicate weights were used to determine correlates of ever and previous 12 months quit attempts.</p> <p>Results</p> <p>Nurses had a lower smoking prevalence than other women (12.1% vs 16.6%, <it>p </it>< 0.0001); were more likely to have ever made a quit attempt (77% vs 68%, <it>p </it>= 0.0002); but not in the previous 12 months (42% vs 43%, <it>p </it>= 0.77). Among those who ever made a quit attempt, nurses who smoked within 30 minutes of waking, were more likely to have made a quit attempt compared to other women (OR = 3.1, 95% CI: 1.9, 5.1). When considering quit attempts within the last 12 months, nurses whose first cigarette was after 30 minutes of waking were less likely to have made a quit attempt compared to other females (OR = 0.69, 95% CI: 0.49, 0.98). There were no other significant differences in ever/recent quitting.</p> <p>Conclusions</p> <p>Smoking prevalence among female nurses was lower than among women who were not in healthcare occupations, as expected. The lack of difference in recent quit efforts among female nurses as compared to other female smokers has not been previously reported. The link between lower level of nicotine dependence, as reflected by the longer time to first cigarette, and lower quit attempts among nurses needs further exploration.</p

X-linked Angelman-like syndrome caused by Slc9a6 knockout in mice exhibits evidence of endosomal–lysosomal dysfunction

Mutations in solute carrier family 9 isoform 6 on chromosome Xq26.3 encoding sodium–hydrogen exchanger 6, a protein mainly expressed in early and recycling endosomes are known to cause a complex and slowly progressive degenerative human neurological disease. Three resulting phenotypes have so far been reported: an X-linked Angelman syndrome-like condition, Christianson syndrome and corticobasal degeneration with tau deposition, with each characterized by severe intellectual disability, epilepsy, autistic behaviour and ataxia. Hypothesizing that a sodium–hydrogen exchanger 6 deficiency would most likely disrupt the endosomal–lysosomal system of neurons, we examined Slc9a6 knockout mice with tissue staining and related techniques commonly used to study lysosomal storage disorders. As a result, we found that sodium–hydrogen exchanger 6 depletion leads to abnormal accumulation of GM2 ganglioside and unesterified cholesterol within late endosomes and lysosomes of neurons in selective brain regions, most notably the basolateral nuclei of the amygdala, the CA3 and CA4 regions and dentate gyrus of the hippocampus and some areas of cerebral cortex. In these select neuronal populations, histochemical staining for β-hexosaminidase activity, a lysosomal enzyme involved in the degradation of GM2 ganglioside, was undetectable. Neuroaxonal dystrophy similar to that observed in lysosomal disease was observed in the cerebellum and was accompanied by a marked and progressive loss of Purkinje cells, particularly in those lacking the expression of Zebrin II. On behavioural testing, Slc9a6 knockout mice displayed a discrete clinical phenotype attributable to motor hyperactivity and cerebellar dysfunction. Importantly, these findings show that sodium–hydrogen exchanger 6 loss of function in the Slc9a6-targeted mouse model leads to compromise of endosomal–lysosomal function similar to lysosomal disease and to conspicuous neuronal abnormalities in specific brain regions, which in concert could provide a unified explanation for the cellular and clinical phenotypes in humans with SLC9A6 mutations

Models of Traumatic Cerebellar Injury

Traumatic brain injury (TBI) is a major cause of morbidity and mortality worldwide. Studies of human TBI demonstrate that the cerebellum is sometimes affected even when the initial mechanical insult is directed to the cerebral cortex. Some of the components of TBI, including ataxia, postural instability, tremor, impairments in balance and fine motor skills, and even cognitive deficits, may be attributed in part to cerebellar damage. Animal models of TBI have begun to explore the vulnerability of the cerebellum. In this paper, we review the clinical presentation, pathogenesis, and putative mechanisms underlying cerebellar damage with an emphasis on experimental models that have been used to further elucidate this poorly understood but important aspect of TBI. Animal models of indirect (supratentorial) trauma to the cerebellum, including fluid percussion, controlled cortical impact, weight drop impact acceleration, and rotational acceleration injuries, are considered. In addition, we describe models that produce direct trauma to the cerebellum as well as those that reproduce specific components of TBI including axotomy, stab injury, in vitro stretch injury, and excitotoxicity. Overall, these models reveal robust characteristics of cerebellar damage including regionally specific Purkinje cell injury or loss, activation of glia in a distinct spatial pattern, and traumatic axonal injury. Further research is needed to better understand the mechanisms underlying the pathogenesis of cerebellar trauma, and the experimental models discussed here offer an important first step toward achieving that objective

Real life impact of educating nurses in tobacco cessation intervention

Introduction Nurses, when educated in tobacco cessation interventions, are well positioned to address smoking with their patients achieving a long-time quit rate of approximately 10%, according to the literature. Methods Together in partnership with the International Society of Nurses in Cancer Care and University of California in Los Angeles, USA, and the Society for Treatment of Tobacco Dependence, Czech Republic, an international project funded by Bristol-Myers Squibb Foundation “The Eastern Europe Nurses‘ Centre of Excellence in Tobacco Control – Developing Nurse Champions for Tobacco Dependence Treatment” (EE-COE) involves six Eastern European countries (CZ, HU, MD, RO, SI, SK). The EE-COE offers to nurses various educational activities in tobacco control, i.e. train of trainer workshops, short seminars, or online e-learning. Through these methods positively evaluated in previous projects, thousands of nurses have already been educated. Results Results from EE-COE 2016 five country 3-month post-training online surveys, a total of 507 trained nurses estimated that they offered cessation intervention to 850 to 1239 patients a week (minimum / maximum weekly estimates, respectively), a mean of 1,044 patients per week. Assuming a 10% long-term quit rate from nurses’ intervention, we estimated that 104 patients quit tobacco use per week, or 5,408 ex-smokers per year in five countries alone. Simplified calculation of investment into nurses’ education translated to $63 USD spent per ex-smoker. Conclusion Investment into nurses‘ education in tobacco control knowledge and skills is an effective approach with substantial impact on patients quitting smoking, improved patient health, in addition to health care cost savings