Menthol is the only tobacco additive promoted and advertised by the tobacco industry. Although a considerable body of research has examined the effects of menthol when it is administered alone and unburned, the effects of menthol when burned in cigarette smoke are more complex because it is administered in a matrix of more than 4,000 substances. Therefore, it is difficult to isolate potential pharmacological and toxic effects of menthol when it is administered in a smoke mixture. Menthol properties include cooling and local anesthesia, as well as effects on drug absorption and metabolism, bronchodilation and respiration changes, and electrophysiology. Subjective effects of smoothness and less harshness have been identified as reasons for menthol cigarette smoking, but findings have been inconclusive regarding the effect of menthol on carbon monoxide exposure and smoking topography parameters. Gaps in the research literature and future research areas include the following: (a) What is the role of menthol in tobacco reinforcement and addiction? (b) In the absence of nicotine, is menthol reinforcing? (c) Are the pharmacological and physiological effects of menthol mediated by a menthol-specific receptor or some other central nervous system-mediated action? (d) What are the influences of menthol and menthol metabolism on the metabolic activation and detoxification of carcinogens in tobacco smoke? and (e) Do differences exist in cigarette smoking topography in relation to the interaction of ethnicity, gender, and menthol cigarette preference? Answers to these questions will help to elucidate the function of menthol in cigarettes and its impact on smoking behavior.

Physiological events in the initial inflammatory stage of cutaneous wound healing influence subsequent stages. Proinflammatory cytokines coordinate molecular and cellular processes during the inflammatory stage. Polyunsaturated fatty acids (PUFA) alter proinflammatory cytokine production, but how this phenomenon specifically influences wound healing is not clearly understood. In the present study, effects of marine-derived ω-3 eicosapentaenoic and docosahexaenoic PUFA on proinflammatory cytokines in wound serum and time to complete healing in healthy, human skin were evaluated. We compared plasma fatty acid levels in two groups (N=30) at baseline and after 4 weeks of eicosapentaenoic/ docosahexaenoic PUFA supplements (active) or placebo (control). Eight small blisters on participants' forearms were created. Proinflammatory cytokines interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α were quantified in blister fluid at 5 and 24 hours after creation. Wound area was calculated daily. Eicosapentaenoic and docosahexaenoic plasma fatty acid levels were significantly higher in the active group. Additionally, we found significantly higher IL-1β levels in blister fluid in the active group and time to complete wound closure was somewhat longer. These results suggest that eicosapentaenoic and docosahexaenoic PUFA may increase proinflammatory cytokine production at wound sites and thus, depending on the clinical context, have noninvasive, therapeutic potential to affect cutaneous wound healing Wound healing is a complex, sequential, biological process that occurs in at least three overlapping stages, the first being inflammation.1 Molecular and cellular processes during the inflammatory stage of skin healing are initiated and amplified to a large degree by a group of protein mediators known as proinflammatory cytokines.1 ,2 Proinflammatory cytokine synthesis and activity are affected by the concentration of ω-3 polyunsaturated fatty acids (PUFA) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), obtained primarily from fish oil, in plasma, tissue and cellular membranes as well as the ω-3 to ω-6 ratio. 3 The ω-6 arachidonic acid (AA) and the ω-3 EPA are released from the phospholipid bilayer of cellular membranes in response to stimuli such as wounding and are competitively metabolized with EPA being the preferential substrate. 4, 5 A general assertion can be made that as dietary quantities of marine-derived EPA and DHA increase and are metabolized more lipid mediators known as eicosanoids result that are less biologically potent for inciting cellular responses than those from AA metabolism, which subsequently influences proinflammatory cytokine production. In addition, EPA and DHA are believed to affect the actual gene expression of proinflammatory cytokines at the level of transcription by altering cellular membrane fluidity, cell to cell signaling, mobility of cells, interaction of receptors with their agonist, membrane function such as capping, and formation of secondary signals. 4,7 The effects o...

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Objective-Laboring women are often admitted to labor units under criteria commonly associated with the onset of active phase labor, i.e., cervical dilatation of 3-5 cm in the presence of regular contractions. Beginning with these criteria through complete dilatation, this systematic review describes labor duration and cervical dilation rates among low-risk, nulliparous women with spontaneous labor onset. English (1990English ( -2008 were identified via MEDLINE and CINAHL searches. Data were abstracted and weighted 'active labor' durations (i.e., from 3-5 cm through complete dilatation) and linear dilation rates were calculated. Methods-Studies published inResults-Eighteen studies (n = 7009) reported mean 'active labor' duration. The weighted mean duration was 6.0 hrs and the calculated dilation rate was 1.2 cm/hr. These findings closely parallel those found at the median. At the statistical limits, the weighted 'active labor' duration was 13.4 hrs (mean + 2 SD) and the dilation rate was 0.6 cm/hr (mean − 2 SD).Conclusions-Nulliparous women with spontaneous labor onset have longer 'active' labors and, hence, slower dilation rates than are traditionally associated with active labor when commonly used criteria are applied as the starting point. Revision of existing active labor expectations and/or criteria used to prospectively identify active phase onset is warranted.