Is smoking a risk factor for AMD?

This article is concerned specifically with the possible links between smoking and age related macular degeneration (AMD). It reviews the epidemiological and physiological evidence that smoking may be a risk factor for AMD, and describes the possible mechanisms by which smoking might contribute to the development of AMD.

AMD and smoking: an update

This article provides an update to a previous publication on this topic and includes the results of new epidemiological and physiological experiments which have implicated smoking as an important cause of AMD.

Retinal and systemic vascular function in health and disease: the effect of smoking and coronary artery disease

The purpose of the following studies was to explore the effect of systemic vascular and endothelial dysfunction upon the ocular circulation and functionality of the retina. There are 6 principal sections to the present work. Retinal vessel activity in smokers and non-smokers: the principal findings of this work were: chronic smoking affects retinal vessel motion at baseline and during stimulation with flickering light; chronic smoking leads to a vaso-constrictory shift in retinal arteriolar reactivity to flicker; retinal arteriolar elasticity is decreased in chronic smokers. The effect of acute smoking on retinal vessel dynamics in smokers and non-smokers: the principal finding of this work was that retinal reactivity in chronic smokers is blunted when exposed to clicker light provocation immediately after smoking one cigarette. Ocular blood flow in coronary artery disease: The principal findings of this work were: retrobulbar and retinal blood flow is preserved in CAD patients, despite a change pulse wave transmission; arterial retinal response to flickering light provocation is significantly delayed in CAD patients; retinal venular diameters are significantly dilated in CAD patients. Autonomic nervous system function and peripheral circulation in CAD: The principal findings in this work were: CAD patients demonstrate a sympathetic overdrive during a 24 period; a delay in peripheral vascular reactivity (nail-fold capillaries) as observed in patients suffering from CAD could be caused by either arteriosclerotic changes of the vascular walls or due to systemic haemodynamic changes. Visual function in CAD: The principal findings in this work were: overall visual function in CAD patients is preserved, despite a decrease in contrast sensitivity; applying a filtering technique selecting those with greater coefficient of variance which in turn represents a decrease in reliability, some patients appear to have an impaired visual function as assessed using FDT visual field evaluation. Multiple functional, structural and biochemical vascular endothelial dysfunctions in patients suffering from CAD: relationships and possible implications: The principal findings of this work were: BMI significantly correlated with vWF (a marker of endothelial function) in CAD patients. Retinal vascular reactivity showed a significant correlation with peripheral reactivity parameters in controls which lacked in the CAD group and could reflect a loss in vascular endothelial integrity; visual field parameters as assessed by frequency doubling technology were strongly related with systemic vascular elasticity (ambulatory arterial stiffness index) in controls but not CAD patients.

Classification of Smoking Cessation Status Using Various Data Mining Methods

AMS Subj. Classification: 62P10, 62H30, 68T01

Regulation as country-specific (dis-)advantage:smoking bans and the location of foreign direct investment in the tobacco industry

This paper seeks to examine the relationship between smoking bans and the propensity of tobacco firms to engage in foreign direct investment (FDI). Using international business theory based on the firm-specific advantage/country-specific advantage (FSA/CSA) matrix, the authors show that, contrary to what one may expect, smoking bans at home are an important institutional intervention, reducing the propensity for firms to engage in FDI, even to countries without a ban themselves.

Prenatal augmented auditory stimulation and visual system development: Effects of timing on intersensory organization

This study investigated the effects of augmented prenatal auditory stimulation on postnatal visual responsivity and neural organization in bobwhite quail (Colinus virginianus). I delivered conspecific embryonic vocalizations before, during, or after the development of a multisensory, midbrain audiovisual area, the optic tectum. Postnatal simultaneous choice tests revealed that hatchlings receiving augmented auditory stimulation during optic tectum development as embryos failed to show species-typical visual preferences for a conspecific maternal hen 72 hours after hatching. Auditory simultaneous choice tests showed no hatchlings had deficits in auditory function in any of the groups, indicating deficits were specific to visual function. ZENK protein expression confirmed differences in the amount of neural plasticity in multiple neuroanatomical regions of birds receiving stimulation during optic tecturn development, compared to unmanipulated birds. The results of these experiments support the notion that the timing of augmented prenatal auditory stimulation relative to optic tectum development can impact postnatal perceptual organization in an enduring way.^

The role of temporal synchrony in the facilitation of perceptual learning during prenatal development

This study explored the critical features of temporal synchrony for the facilitation of prenatal perceptual learning with respect to unimodal stimulation using an animal model, the bobwhite quail. The following related hypotheses were examined: (1) the availability of temporal synchrony is a critical feature to facilitate prenatal perceptual learning, (2) a single temporally synchronous note is sufficient to facilitate prenatal perceptual learning, with respect to unimodal stimulation, and (3) in situations where embryos are exposed to a single temporally synchronous note, facilitated perceptual learning, with respect to unimodal stimulation, will be optimal when the temporally synchronous note occurs at the onset of the stimulation bout. To assess these hypotheses, two experiments were conducted in which quail embryos were exposed to various audio-visual configurations of a bobwhite maternal call and tested at 24 hr after hatching for evidence of facilitated prenatal perceptual learning with respect to unimodal stimulation. Experiment 1 explored if intermodal equivalence was sufficient to facilitate prenatal perceptual learning with respect to unimodal stimulation. A Bimodal Sequential Temporal Equivalence (BSTE) condition was created that provided embryos with sequential auditory and visual stimulation in which the same amodal properties (rate, duration, rhythm) were made available across modalities. Experiment 2 assessed: (a) whether a limited number of temporally synchronous notes are sufficient for facilitated prenatal perceptual learning with respect to unimodal stimulation, and (b) whether there is a relationship between timing of occurrence of a temporally synchronous note and the facilitation of prenatal perceptual learning. Results revealed that prenatal exposure to BSTE was not sufficient to facilitate perceptual learning. In contrast, a maternal call that contained a single temporally synchronous note was sufficient to facilitate embryos’ prenatal perceptual learning with respect to unimodal stimulation. Furthermore, the most salient prenatal condition was that which contained the synchronous note at the onset of the call burst. Embryos’ prenatal perceptual learning of the call was four times faster in this condition than when exposed to a unimodal call. Taken together, bobwhite quail embryos’ remarkable sensitivity to temporal synchrony suggests that this amodal property plays a key role in attention and learning during prenatal development.

Impact of a cognitive-behavioral weight control program on body weight, diet quality, and smoking cessation in weight-concerned female smokers

Many people use smoking as a weight control mechanism and do not want to quit because they fear weight gain. These weight-concerned smokers tend to be female, are significantly less likely to stop smoking, are less likely to join smoking cessation programs, and will relapse more often than smokers who are not weight-concerned. Research suggests that a woman’s confidence in her ability to control her weight after quitting relates positively with her intention to quit smoking. Likewise, success in smoking cessation has been associated with increased self-efficacy for weight control. It has been shown that success in changing one negative health behavior may trigger success in changing another, causing a synergistic effect. Recently research has focused on interventions for weight-concerned smokers who are ready to quit smoking. The present study investigated the effect of a cognitive based weight control program on self-efficacy for weight control and the effect on smoking behavior for a group of female weight concerned smokers. Two hundred and sixteen subjects who wanted to lose weight but who were not ready to quit smoking were recruited to participate in a 12-week, cognitive-behavioral weight control program consisting of twelve one-hour sessions. Subjects were randomly assigned to either (1) the weight-control program (intervention group), or (2) the control group. Results of this study demonstrated that subjects in the intervention group increased self-efficacy for weight control, which was associated with improved healthy eating index scores, weight loss, increased self-efficacy for quitting smoking, a decrease in number of cigarettes smoked and triggered positive movement in stage of change towards smoking cessation compared to the control subjects. For these subjects, positive changes in self-efficacy for one behavior (weight control) appeared to have a positive effect on their readiness to change another health behavior (smoking cessation). Further study of the psychological variables that influence weight-concerned female smokers’ decisions to initiate changes in these behaviors and their ability to maintain those changes are warranted.

Prenatal environmental exposure and neurodevelopmentally important gene expression in malformed brain tissue from pediatric intractable epilepsy patients

The primary objective of this proposal was to determine whether mitochondrial oxidative stress and variation in a particular mtDNA lineage contribute to the risk of developing cortical dysplasia and are potential contributing factors in epileptogenesis in children. The occurrence of epilepsy in children is highly associated with malformations of cortical development (MCD). It appears that MCD might arise from developmental errors due to environmental exposures in combination with inherited variation in response to environmental exposures and mitochondrial function. Therefore, it is postulated that variation in a particular mtDNA lineage of children contributes to the effects of mitochondrial DNA damage on MCD phenotype. Quantitative PCR and dot blot were used to examine mitochondrial oxidative damage and single nucleotide polymorphism (SNP) in the mitochondrial genome in brain tissue from 48 pediatric intractable epilepsy patients from Miami Children’s Hospital and 11 control samples from NICHD Brain and Tissue Bank for Developmental Disorders. Epilepsy patients showed higher mtDNA copy number compared to normal health subjects (controls). Oxidative mtDNA damage was lower in non-neoplastic but higher in neoplastic epilepsy patients compared to controls. There was a trend of lower mtDNA oxidative damage in the non-neoplastic (MCD) patients compared to controls, yet, the reverse was observed in neoplastic (MCD and Non-MCD) epilepsy patients. The presence of mtDNA SNP and haplogroups did not show any statistically significant relationships with epilepsy phenotypes. However, SNPs G9804A and G9952A were found in higher frequencies in epilepsy samples. Logistic regression analysis showed no relationship between mtDNA oxidative stress, mtDNA copy number, mitochondrial haplogroups and SNP variations with epilepsy in pediatric patients. The levels of mtDNA copy number and oxidative mtDNA damage and the SNPs G9952A and T10010C predicted neoplastic epilepsy, however, this was not significant due to a small sample size of pediatric subjects. Findings of this study indicate that an increase in mtDNA content may be compensatory mechanisms for defective mitochondria in intractable epilepsy and brain tumor. Further validation of these findings related to mitochondrial genotypes and mitochondrial dysfunction in pediatric epilepsy and MCD may lay the ground for the development of new therapies and prevention strategies during embryogenesis.