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Circ Res. 2003 Aug 7 [Epub ahead of print].
Respiratory Sinus Arrhythmia. Endogenous Activation of Nicotinic Receptors Mediates Respiratory Modulation of Brainstem Cardioinhibitory Parasympathetic Neurons.

Neff RA, Wang J, Baxi S, Evans C, Mendelowitz D.

Department of Pharmacology, The George Washington University, Washington, DC.

The heart rate increases during inspiration and decreases during expiration. This respiratory sinus arrhythmia (RSA) occurs by modulation of premotor cardioinhibitory parasympathetic neuron (CPN) activity. However, RSA has not been fully characterized in rats, and despite the critical role of CPNs in the generation of RSA, little is known about the mechanisms that mediate this cardiorespiratory interaction. This study demonstrates that RSA in conscious rats is similar to that in other species. The mechanism of RSA was then examined in vitro. Rhythmic inspiratory-related activity was recorded from the hypoglossal rootlet of 700- to 800- micro m medullary sections. CPNs were identified by retrograde fluorescent labeling, and neurotransmission to CPNs was examined using patch-clamp electrophysiological techniques. During inspiratory bursts, the frequency of both spontaneous gamma-aminobutyric acidergic (GABAergic) and spontaneous glycinergic synaptic events in CPNs was significantly increased. Focal application of the nicotinic antagonist dihydro-beta-erythroidine in an alpha4beta2-selective concentration (3 micro mol/L) abolished the respiratory-evoked increase in GABAergic frequency. In contrast, the increase in glycinergic frequency during inspiration was not altered by nicotinic antagonists. Prenatal nicotine exposure exaggerated the increase in GABAergic frequency during inspiration and enhanced GABAergic synaptic amplitude both between and during inspiratory events. Glycinergic synaptic frequency and amplitude were unchanged by prenatal nicotine exposure. This study establishes a neurochemical link between neurons essential for respiration and CPNs, reveals a functional role for endogenous acetylcholine release and the activation of nicotinic receptors in the generation of RSA, and demonstrates that this cardiorespiratory interaction is exaggerated in rats prenatally exposed to nicotine.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12907666&dopt=Abstract [PubMed - as supplied by publisher]

Eur J Epidemiol. 2003;18(6):487-92.
Serum cotinine as a marker of environmental tobacco smoke exposure in epidemiological studies: the experience of the MATISS project.

Seccareccia F, Zuccaro P, Pacifici R, Meli P, Pannozzo F, Freeman KM, Santaquilani A, Giampaoli S; Research Group of the MATISS Project.

Laboratory of Epidemiology and Biostatistics, Istituto Superiore di Sanita, Rome, Italy. fulviass.it

To describe serum cotinine levels in a rural Italian population and to examine its usefulness as an epidemiologic biomarker of nicotine exposure, cross-sectional data collected in 1993 for the MATISS Project (2098 men and 1352 women, aged 20-79 years) were used. The study population consisted of 977 current smokers, 882 nonsmokers reporting exposure to environmental tobacco smoke (ETS) and 1520 nonsmokers reporting no ETS exposure. Mean values of serum cotinine measured by radioimmunoassay for never smokers, ex-smokers and current smokers (including four categories of cigarette consumption), and for categories of ETS exposure in all nonsmokers were calculated. In univariate analysis, there was a positive association between self-reported nicotine exposure and serum cotinine levels in all groups. Using self-reported status as truth, sensitivity and specificity for various cotinine cutoff points were estimated to distinguish nonsmokers from smokers. The value of 15 ng/mL represented the best combined levels of sensitivity (95%) and specificity (96%). Using this cutoff point, the overall misclassification rate for self-reported nonsmokers was 2.1% and about two times greater for the more vs. the less educated. In multivariate analysis, reported ETS exposure among nonsmokers was significantly associated with serum cotinine even after adjusting for age, socio-demographic and behavioural factors, though the strength of the association was not strong. In conclusion, serum cotinine represents a reliable epidemiological marker of nicotine intake and may be helpful when studying ETS exposure. Improved information collection is needed to reduce misclassification among nonsmokers and enhance our understanding of the relationship between ETS and cotinine measures.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12908713&dopt=Abstract [PubMed - in process]

Ann Oncol. 2003 Mar;14(3):353-7.
More on the regulation of tobacco smoke: how we got here and where next.

Gray N, Kozlowski LT.

Division of Epidemiology and Biostatistics, European Institute of Oncology, Milan, Italy.

The modern cigarette is unnecessarily dangerous. Despite being lower in tar yield, and consequently in squamo-carcinogenic polyaromatic hydrocarbons such as benzo[a]pyrene, the nitrosamine yields are often higher than they need to be. Also, reductions in tar levels have not led to the consequential reductions in mortality that were anticipated several decades ago. The modern cigarette is also smoother, easier to smoke and to learn how to smoke, highly addictive and facilitates compensatory smoking. Compensatory smoking leads to excess inhalation of carcinogens and toxins in the hunt for nicotine. Its labelling is misleading in that supposedly low-yielding cigarettes may, due to compensation occurring as a result of cigarette design, lead to inhalation of much higher amounts of nicotine, carcinogens and toxins than the smoker is led to expect. Regulation of the product is needed to provide the persistent smoker with a cigarette lower in risk, accurately labelled, providing a relatively consistent and known dose of nicotine, and less likely to facilitate compensatory smoking. This will not produce a safe cigarette but should result in a reduction in harm if seriously implemented.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12598337&dopt=Abstract [PubMed - in process]

Hair loss is a problem in modern soceity. Examining the factors of hair growth may shed light on how hair loss might occur. How long can hair grow before it stops growing eventually if it does? Given that the hair growth rate is quite uniform and constant, somewhere between 0.3-0.5 millimeters per day, it's believed that the length of anagen, the growth phase, differs among individuals, and this is the major determinant to the maximum hair length. For some individuals, anagen may last ten years. Of course the length of the anagen is governed by genes, and the genetic background of the individuals. Non-genetic factors such as nutritional condition, weather, seasonal changes (hair may grow a bit faster during winter), taking medications, health condition may of course influence the rate of hair growth as well as hair loss. The shape of the hair, straight or curly, is dependent on the shape of the follicle. A circular or round hair follicle would generate straight hair, while the follicle with oval or elliptical shapes (in its cross-section) would produce a curly hair.

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