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OBJECTIVES: The popularity of snuff especially among adolescents is rising. The association between long-term snuff use and oral cancer discovered in epidemiological studies has prompted a variety of preventive measures to be taken to reduce snuff use and prevent adoption of the habit. In this study, the effect of a recent (I March, 1995) snuff sales ban introduced in Finland was investigated. Further, the rates of smoking, snuff use, alcohol use and drug experimenting were investigated before the introduction of the ban to characterize the study population.
DESIGN AND SUBJECTS: Two questionnaire studies were carried out. The first was carried out 3 months prior to the ban in 1994 and the second 9 months after the ban in 1995 in a senior high school population in southwestern Finland. The participants were 793 students (aged 15–22 years) in the first survey and 545 students (aged 16–23) in the second. Associations between variables were analyzed using cross-tabulation and stepwise logistic regression. The effects of the ban were determined on the basis of direct questions in the second questionnaire relating to the snuff sales ban.
RESULTS: Snuff was used by 9% of the students participating in the first study. The results of the second questionnaire indicate that the implementation of the snuff sales ban reduced the rate of snuff use by 1% in the study population. The majority of the snuff users (76%) reported that they had maintained their snuff habit. Of those reporting that they were snuff users before implementation of the snuff sales ban, 12% had switched to smoking and 5% to drugs.
CONCLUSIONS: The results of the present study suggest that the snuff sales ban in this population with a high rate of snuff use had little effect on snuff use rates and may have some short-term negative consequences as some snuff users switch to other substitutes, such as smoking, with known adverse health effects.  相似文献   
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Monitoring of inspired oxygen concentration during anesthesia with nitrous oxide is becoming accepted as essential. This type of monitoring demands accurate monitors that respond rapidly. We evaluated two such devices for their response patterns to rapid changes in oxygen concentration, a galvanic or “fuel cell” unit and a polarographic device. Data were stored after analog-to-digital conversion. The response patterns to stepwise changes in nitrous oxide and oxygen mixtures were recorded at flow rates ranging from 2 to 10 L/min. Both units responded accurately to all changes in the absolute oxygen concentration; the polarographic unit was, on average, twice as fast. Responsiveness to nitrous oxide was low (<0.4% at 100% nitrous oxide), and the stability of the signals was good. The 90% response time (T90) was consistent for any stepwise increase or decrease in oxygen concentration between 0, 21, 33, 50, and 100%. After a step change from 0 to 100% oxygen at a gas flow rate of 10 L/min, the T90 was 5.8 seconds in the polarographic device and 11.4 seconds in the galvanic device (p<0.01). After a decrease from 100 to 0% oxygen, the T90 was 0.6 second longer in both monitors. Comparing flow rates of 2 L/min with 10 L/min, the T90 was delayed by 1.1 and 2.3 seconds for an increase, and by 1.4 and 2.9 seconds for a decrease in oxygen concentration. Experimental data suggest that both sensors respond adequately during routine clinical use. The faster response of the polarographic device is probably of limited clinical relevance, but it may aid in calibration.  相似文献   
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The purpose of the present study was to characterize adenosine receptors in human atrial and ventricular myocardium. In isolated electrically driven preparations, adenosine produced "direct" negative inotropic effects in atrial myocardium (AT). In ventricular myocardium (VE), it only had negative inotropic properties when force of contraction had been stimulated with isoprenaline ("indirect" effect), but it has no inotropic effect alone. The adenosine receptor antagonist 8-phenyltheophylline antagonized the "direct" and "indirect" effects; these findings indicated that both effects were mediated by adenosine receptors. In cardiac membranes from human AT and VE, adenosine receptors were characterized with [3H]-8-cyclopentyl-1,3-dipropylxanthine (DPCPX) binding. The effects of agonists R-(-)-N6-phenylisopropyladenosine (R-PIA), S-(+)-N6-phenylisopropyladenosine (S-PIA), and 5'-(N-ethylcarboxamido) adenosine (NECA) and the effects of guanine nucleotides [Gpp(NH)p] were studied also. The antagonist affinities as judged from the apparent affinity, Kd, of [3H]DPCPX were similar in AT (2.2 nmol/l; 95% confidence limits, 1.4-3.7) and VE (1.8 nmol/l; 95% confidence limits, 1.0-3.0). The number of adenosine receptors was 1.7 times greater in AT (26.9 +/- 2.33 fmol/mg protein; n = 5) than in VE (16.2 +/- 2.3 fmol/mg protein; n = 5). High and low affinity states of adenosine receptors evaluated with the influence of Gpp(NH)p on agonist competition with R-PIA were similar in AT or VE. The rank orders of potency for agonists (R-PIA greater than S-PIA greater than NECA) and antagonists (DPCPX greater than 8-phenyltheophylline greater than theophylline) were characteristic for the A1 receptor subtype. It is concluded that A1 adenosine receptors exist in the human myocardium. Since binding properties were similar in AT and VE, the same A1 adenosine receptor probably couples to different effectors in a similar guanine nucleotide-dependent way. [3H]DPCPX is the first radiolabeled antagonist ligand that allows detection of A1 adenosine receptors and their coupling in the human myocardium.  相似文献   
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Cerebral blood flow is a finely tuned process dependent on coordinated changes in arterial tone. These changes are strongly tied to smooth muscle membrane potential and inwardly rectifying K+ (KIR) channels are thought to be a key determinant. To elucidate the role of KIR2.1 in cerebral arterial tone development, this study examined the electrical and functional properties of cells, vessels and living tissue from tamoxifen-induced smooth muscle cell (SMC)-specific KIR2.1 knockout mice. Patch-clamp electrophysiology revealed a robust Ba2+-sensitive inwardly rectifying K+ current in cerebral arterial myocytes irrespective of KIR2.1 knockout. Immunolabeling clarified that KIR2.1 expression was low in SMCs while KIR2.2 labeling was remarkably abundant at the membrane. In alignment with these observations, pressure myography revealed that the myogenic response and K+-induced dilation were intact in cerebral arteries post knockout. At the whole organ level, this translated to a maintenance of brain perfusion in SMC KIR2.1−/− mice, as assessed with arterial spin-labeling MRI. We confirmed these findings in superior epigastric arteries and implicated KIR2.2 as more functionally relevant in SMCs. Together, these results suggest that subunits other than KIR2.1 play a significant role in setting native current in SMCs and driving arterial tone.  相似文献   
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