Cuatro cuestiones axiológicas de la epidemiología social para el monitoreo de la desigualdad en salud / Four axiological considerations in social epidemiology for the monitoring of health inequality

A medida que las agendas contemporáneas más relevantes de la salud pública mundial y regional se van alineando en sus componentes conceptuales y emerge más explícitamente el rol medular de la equidad como su principio constitutivo, va creciendo también el reconocimiento del valor estratégico del monitoreo de desigualdades sociales en salud como el instrumento por excelencia de la inteligencia sanitaria para juzgar objetivamente el progreso hacia la equidad en salud, pero también para dar cuenta de la acción sobre los determinantes sociales de la salud, el avance hacia el alcance progresivo de la universalidad en salud y el éxito de iniciativas intersectoriales con enfoque de salud en todas las políticas. Estas transformaciones acontecen en el marco de una cada vez más evidente transición paradigmática de la salud pública. Este ensayo plantea cuatro consideraciones axiológicas inherentes a-y esenciales para-la conceptualization e instrumentación de la medición y monitoreo de las desigualdades en salud: la ecoepidemiología como era emergente en la salud pública contemporánea, los determinantes de la salud como modelo de causalidad y núcleo del nuevo enfoque paradigmático, la relación entre jerarquía social y salud para entender el gradiente en salud, y la necesidad práctica de una clasificación socioeconómica para capturar la dimensión social de la determinación de la salud. Se plantea que estas cuatro cuestiones valorativas otorgan coherencia y racionalidad epidemiológicas al proceso de medición y monitoreo de las desigualdades en la salud y, por extensión, a la formulación de propuestas de política sanitaria en pro de la equidad.

As the conceptual components of the most important contemporary public health agendas at the global and regional levels are brought into alignment and as it becomes more clearly understood that equity is a constitutive principle of these agendas, there is also a growing awareness of the strategic value of monitoring social inequalities in health. This is the health intelligence tool par excellence, not only for objectively assessing progress towards achieving health equity, but also for reporting action on the social determinants of health, progress towards the attainment of health for all, and the success of intersectoral efforts that take a "health in all policies" approach. These transformations are taking place in the context of an increasingly evident paradigm shift in public health. This essay presents four axiological considerations inherent to-and essential for -conceptualizing and implementing ways to measure and monitor health inequalities: ecoepidemiology as an emerging field in contemporary public health; the determinants of health as the causal model and core of the new paradigm; the relationship between the social hierarchy and health to understand the health gradient; and the practical need for a socioeconomic classification system that captures the social dimension in the determinants of health. The essay argues that these four axiological considerations lend epidemiologic coherence and rationality to the process of measuring and monitoring health inequalities and, by extension, to the development of pro-equity health policy proposals.

Effects of arecoline and nicotine on the expression of hTERT in oral keratinocytes / 中华口腔医学杂志

<p><b>OBJECTIVE</b>To investigate the effects of arecoline and nicotine on the expression of human telomerase reverse transcriptase (hTERT) mRNA and protein in cultured normal human oral keratinocytes (KC).</p><p><b>METHODS</b>The experiments were divided into arecoline group, arecoline/nicotine group and control group. The hTERT mRNA and protein expression of KC was examined by reverse transcription polymerase chain reaction (RT-PCR) and Western blot.</p><p><b>RESULTS</b>Arecoline could induce the hTERT mRNA and protein expression of KC in a dose dependent manner, the hTERT mRNA and protein expression of KC was higher in 0.030, 0.060, 0.090 g/L arecoline group than control group (P < 0.001). Nicotine (0.025 g/L) increased hTERT mRNA and protein expression of KC induced by arecoline.</p><p><b>CONCLUSIONS</b>Arecoline could increase the expression of hTERT mRNA and protein in oral keratinocytes. Nicotine had a synergistic effect on arecoline. hTERT over-expression induced by arecoline and nicotine may play an important role in the malignant transformation of oral submucous fibrosis.</p>

Injury of mouse brain mitochondria induced by cigarette smoke extract and effect of vitamin C on it in vitro / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the toxicity of cigarette smoke extract (CSE) and nicotine on mouse brain mitochondria as well as the protective effect of vitamin C in vitro.</p><p><b>METHOD</b>Mouse brain mitochondria in vitro was incubated with CSE or nicotine in the absence or presence of vitamin C for 60 minutes, and the changes of mitochondrial function and structure were measured.</p><p><b>RESULTS</b>CSE inhibited mitochondrial ATPase and cytochrome C oxidase activities in a dose-dependent manner. However, no significant changes in the peroxidation indices were observed when mitochondrial respiratory enzymes activity was inhibited, and protection of mitochondria from CSE-induced injury by vitamin C was not displayed in vitro. The effect of CSE on mouse brain mitochondria swelling response to calcium stimulation was dependent on calcium concentrations. CSE inhibited swelling of mitochondria at 6.5 mumol/L Ca2+, but promoted swelling response at 250 mumol/L Ca2+. Nicotine, the major component of cigarette smoke, showed no significant damage in mouse brain mitochondria in vitro. The CSE treatment induced mitochondrial inner membrane damage and vacuolization of the matrix, whereas the outer mitochondrial membrane appeared to be preserved.</p><p><b>CONCLUSION</b>The toxic effect of CSE on brain mitochondria may be due to its direct action on enzymatic activity rather than through oxygen free radical injury. Nicotine is not the responsible component for the toxicity of CSE to brain mitochondria.</p>

Relationship between mood improvement and sleep changes with acute nicotine administration in non-smoking major depressed patients

BACKGROUND: Acute administration of nicotine patches produced rapid eye movement sleep (REM) increases in non-smoking major depressed patients as well as clinical improvement in mood. Antidepressant effect was also observed after four continuous days of nicotine administration. The main goal of the present study was to observe the relationship between changes in REM sleep variables and mood in non-smoking major depressed patients. METHOD: Fifteen major depressed patients (DSM-III-R) were studied under the following sleep laboratory conditions: habituation, two all-night polysomnography recordings, the first one was baseline and the second one was nicotine patch (17.5 mg) night. Patients should had a HAMD-21 punctuation equal or above 18 points for to be admitted in the study. A short HAMD (10 items), and side effect scale was used daily during the two recording nights. RESULTS: A significant increase in REM sleep time and reduction in sleep stage II was observed when patients were on nicotine patches. Ten patients improved (reduction of 30 in the HAMD of 10 items), the morning after nicotine. All of them also increased REM sleep time above their baseline. Eight patients from the one with significant improvement had a short REM sleep latency below 60 minutes at baseline. CONCLUSIONS: The hypersensitivity of the cholinergic system may be related to the REM sleep enhancement effect observed in some of the patients when received nicotine and also related to the clinical improvement. The role of the acetylcholine in depression could be explored with the administration of transdermal nicotine patches.