The Genetic Privacy Act and commentary

The Genetic Privacy Act is a proposal for federal legislation. The Act is based on the premise that genetic information is different from other types of personal information in ways that require special protection. Therefore, to effectively protect genetic privacy unauthorized collection and analysis of individually identifiable DNA must be prohibited. As a result, the premise of the Act is that no stranger should have or control identifiable DNA samples or genetic information about an individual unless that individual specifically authorizes the collection of DNA samples for the purpose of genetic analysis, authorized the creation of that private information, and has access to and control over the dissemination of that information

Chinese ‘low-tar’ cigarettes do not deliver lower levels of nicotine and carcinogens

BackgroundLow-tar cigarette smoking is gaining popularity in China. The China National Tobacco Corporation (CNTC) promotes low-tar cigarettes as safer than regular cigarettes.MethodsA total of 543 male smokers smoking cigarettes with different tar yields (15 mg, regular cigarettes, 10-13 mg low-tar cigarettes and < 10 mg low-tar cigarettes) were recruited in Shanghai, China, who then completed a questionnaire on smoking behaviour and provided a urine sample for analysis of the nicotine metabolites cotinine and trans-3'-hydroxycotinine. A total of 177 urine samples were selected at random for the analysis of the carcinogens polycyclic aromatic hydrocarbon metabolites (PAHs) (1-hydroxypyrene, naphthols, hydroxyfluorenes and hydroxyphenanthrenes) and the tobacco specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-butanone (NNK) metabolites, 4-(methylnitrosamino)-1-(3-pyridyl)-butanol (NNAL) and NNAL-glucuronide. Values were normalised by creatinine to correct for possible distortions introduced by dilution or concentration of the urine.ResultsSmokers of low-tar cigarettes smoked fewer cigarettes per day (p=0.001) compared to smokers of regular cigarettes. Despite this lower reported consumption, levels of cotinine, trans-3'-hydroxycotinine and PAHs in urine of people smoking low-tar cigarettes were not correlated with nominal tar delivery of the cigarettes they smoked. Urine concentrations of NNAL were higher in smokers of lower tar than higher tar cigarettes.ConclusionsChinese low-tar cigarettes do not deliver lower doses of nicotine and carcinogens than regular cigarettes, therefore it is unlikely that there would be any reduction in harm. CNTC's promotion of low-tar cigarettes as 'less harmful' is a violation of the World Health Organization Framework Convention on Tobacco Control, which China ratified in 2005

972-107 L-Arginine Decreases Infarct Size in Rats Exposed to Environmental Tobacco Smoke

We previously showed that environmental tobacco smoke (ETS) increased myocardial infarct size in a rat model of ischemia and reperfusion. If reduced reperfusion was caused by endothelial cell damage and increased vascular tone, we postulated that L-arginine (ARG) would increase nitric oxide and better protect the heart. 60 rats were randomly divided into 4 groups: ETS or Control (C) with and without ARG (2.25% ARG in drinking water). The ETS groups were exposed (4 Marlboro cigarettes per 15 minutes. 6 hours a day) for 6 weeks. During ETS-exposure, average air nicotine, carbon monoxide and total particulate concentrations were 1304 μg/m3, 78 ppm and 31 mg/m3, respectively. After 6 weeks, all rats were subjected to 35 min LAD occlusion (0) and 120 min reperfusion, with hemodynamic monitoring via the carotid artery. Aortic rings were harvested to evaluate vascular reactivity. Infarct size (infarct mass/risk area x 100%) decreased significantly in the ETS with ARG group compared to the ETS without ARG group. There were no significant differences among groups in heart rate (HR), systolic pressure (SP), and rate pressure product. Tlere were positive correlations between infarct size and heart rates from baseline to reperfusion 120 min (r = 0.4-0.6. p = 0.01-0.001). There was no relationship between vascular reactivity and infarct size.GroupNo. of RatsInf/LV (%)Inf/RA (%)0-35’HR (beats/m)0-35'SP (mmHg)Max Relax (%)C1125±351±6408±11120±784±11C+ ARG1025±252±3415±10103±11112±15ETS1034±464±6427±16108±8128±16ETS + ARG1122±3*42±6*410±17106±10127±18Values are Means±SEM*p<0.05, p values from two-way ANOVAConclusionL-arginine decreases myocardial infarct size after ischemia and reperfusion in ETS-exposed rats. This effect does not appear to be secondary to alterations in hemodynamics

Synaptophysin and postsynaptic density protein 95 in the human prefrontal cortex from mid-gestation into early adulthood

Previous studies of postnatal synaptic development in human frontal cortex have shown that synaptic density rises after birth, reaches a plateau in childhood and then decreases to adult levels by late adolescence. A similar pattern has been seen in nonhuman primate cortex. These earlier studies in human cortex are limited, however, by significant age gaps in study subjects at critical inflection points of the developmental curve. Additionally, it is unclear if synaptic development occurs in different patterns in different cortical layers in prefrontal cortex (PFC). The purpose of this study was to examine synaptic density in human PFC across development by measuring two synaptic marker proteins: synaptophysin (presynaptic), and postsynaptic density-95 (PSD-95; postsynaptic). Western blotting was used to assess the relative levels of synaptophysin and PSD-95 in dorsolateral PFC of 42 subjects, distributed in age from 18 weeks gestation to 25 years. In addition, synaptophysin immunoreactivity was examined in each layer of areas 9 and 46 of PFC in 24 subjects, ranging in age from 0.1 to 25 years. Synaptophysin levels slowly increased from birth until age 5 and then increased more rapidly to peak in late childhood around age 10. Synaptophysin subsequently decreased until the adult level was reached by mid-adolescence, around age 16. PSD-95 levels increased postnatally to reach a stable plateau by early childhood with a slight reduction in late adolescence and early adulthood. The pattern of synaptophysin immunoreactivity seen with immunohistochemistry was similar to the Western experiments but the changes across age were more subtle, with little change by layer within and across age. The developmental patterns exhibited by these synaptic marker proteins expand upon previous studies of developmental synaptic changes in human frontal cortex; synaptic density increases steadily from birth to late childhood, then decreases in early adolescence to reach adult levels by late adolescence

The Tobacco Industry’s Role in the 16 Cities Study of Secondhand Tobacco Smoke: Do the Data Support the Stated Conclusions?

BACKGROUND: Since 1996, the tobacco industry has used the 16 Cities Study conclusions that workplace secondhand tobacco smoke (SHS) exposures are lower than home exposures to argue that workplace and other smoking restrictions are unnecessary. OBJECTIVES: Our goal was to determine the origins and objectives of the 16 Cities Study through analysis of internal tobacco industry documents and regulatory agency and court records, and to evaluate the validity of the study’s conclusions. RESULTS: The tobacco industry’s purpose in conducting the 16 Cities Study was to develop data showing that workplace SHS exposures were negligible, using these data to stop smoking restrictions by the U.S. Occupational Safety and Health Administration. The extensive involvement of R.J. Reynolds Tobacco Company and the tobacco industry’s Center for Indoor Air Research in controlling the study was not fully disclosed. The study’s definition of “smoking workplace” included workplaces where smoking was restricted to designated areas or where no smoking was observed. This definition substantially reduced the study’s reported average SHS concentrations in “smoking workplaces” because SHS levels in unrestricted smoking workplaces are much greater than in workplaces with designated smoking areas or where no smoking occurred. Stratifying the data by home smoking status and comparing exposures by workplace smoking status, however, indicates that smoke-free workplaces would halve the total SHS exposure of those living with smokers and virtually eliminate SHS exposure for most others. CONCLUSIONS: Data in the 16 Cities Study reveal that smoke-free workplaces would dramatically reduce total SHS exposure, providing significant worker and public health benefits

Pro-apoptotic Par-4 and dopamine D2 receptor in temporal cortex in schizophrenia, bipolar disorder and major depression

Although the etiology of schizophrenia remains unknown, diverse neuropathological evidence suggests a disorder of synaptic connectivity. Apoptosis is a form of cell death that helps determine synaptic circuitry during neurodevelopment and altered regulation of apoptosis has been implicated in schizophrenia. Prostate apoptosis response-4 (Par-4) is an upstream regulator of apoptosis preferentially localized to synapses. Brain Par-4 levels are upregulated in response to pro-apoptotic stimuli in rodent models and in patients with classic neurodegenerative diseases. Recently, Par-4 was also found to form a complex with the dopamine D2 receptor (D2DR) in competition with the calcium-binding protein calmodulin, implicating Par-4 as an important regulatory component in normal dopamine signaling. Interestingly, mutant mice with disrupted Par-4/D2DR interaction demonstrated depressive-like behaviors, suggesting a potential role for Par-4 in both depression and schizophrenia. In this study, Par-4, D2DR and calmodulin protein levels were measured using semiquantitative Western blotting in postmortem temporal cortex in subjects with schizophrenia, major depression and bipolar disorder. Compared to normal controls, mean Par-4 levels appeared slightly lower in schizophrenia and bipolar disorder. However, in major depression, Par-4 was decreased by 67% compared to normal controls. No differences were found between any groups for calmodulin or for the D2DR 48 kDa band. The D2DR 98 kDa band was lower by 50% in the schizophrenia compared to control groups. Changes in the Par-4/D2DR signaling pathway represent a novel mechanism that may link apoptotic and dopamine signaling pathways in major depression and schizophrenia