The time is now - a call to action for gender equality in global health leadership.

Gender equality is considered paramount to the success of the Sustainable Development Goals and incorporated into global health programming and delivery, but there is great gender disparity within global health leadership and an absence of women at the highest levels of decision making. This perspective piece outlines the current gaps and challenges, highlighting the lack of data and unanswered questions regarding possible solutions, as well as the activity of Women in Global Health and efforts to directly address the inequity and lack of female leaders. We conclude with an agenda and tangible next steps of action for promoting women's leadership in health as a means to promote the global goals of achieving gender equality and catalyzing change.

The role of women's leadership and gender equity in leadership and health system strengthening.

Gender equity is imperative to the attainment of healthy lives and wellbeing of all, and promoting gender equity in leadership in the health sector is an important part of this endeavour. This empirical research examines gender and leadership in the health sector, pooling learning from three complementary data sources: literature review, quantitative analysis of gender and leadership positions in global health organisations and qualitative life histories with health workers in Cambodia, Kenya and Zimbabwe. The findings highlight gender biases in leadership in global health, with women underrepresented. Gender roles, relations, norms and expectations shape progression and leadership at multiple levels. Increasing women's leadership within global health is an opportunity to further health system resilience and system responsiveness. We conclude with an agenda and tangible next steps of action for promoting women's leadership in health as a means to promote the global goals of achieving gender equity.

Cotinine levels in Southeast Asian smokers.

Understanding the contribution of race to factors associated with cigarette smoking and nicotine metabolism is essential for the characterization of patterns of tobacco use, nicotine dependence and incidence of tobacco-related diseases. This paper reports an investigation of cotinine levels among Southeast Asian smokers in two separate studies. Study 1 included 327 male and female smokers who participated in community-based interviews where smoking history information was obtained and a saliva continine sample was collected. Results indicated that subjects smoked an average of 11.2 cigarettes/day, with men reporting significantly higher consumption rates as compared to women (p < 0.0001). Subjects' mean cotinine level was 65 ng/ml with an average cotinine/cigarette ratio of 8.2. In Study 2, plasma and saliva cotinine in six Southeast Asian adult smokers were measured during 2 days of smoking followed by 6 days of abstinence. On day 1, mean plasma and saliva continine levels were 268 and 235 ng/ml, respectively. After 6 days of abstinence, mean levels had dropped to 12 ng/ml for plasma and 8 ng/ml in saliva. On average, it required at least 4.7 days for saliva continine levels to reach < 14 ng/ml. Mean cotinine concentrations during smoking differed in these two separate studies. Implications of these findings are discussed and future research recommendations are presented.

The effect of chronic administration of nicotine on antinociception, opioid receptor binding and met-enkelphalin levels in rats.

The effect of chronic nicotine administration on (1) antinociception; (2) opioid receptor binding; and (3) met-enkelphalin levels in discrete brain regions in rats was investigated. Male and female Sprague-Dawley rats were treated with nicotine 0.3 mg/kg, 0.1 mg/kg, or saline three times a day subcutaneously during a 14-day protocol. Antinociception was measured by hotplate (HP) test on days 1, 2, 7, 10 and 14. After completion of the protocol, mu-opioid receptors were analyzed by [3H]-DAMGO binding studies and met-enkelphalin levels were determined by radioimmunoassay. Results indicated that hot-plate latency increased during the first 2 days of nicotine administration for male and female rats who were treated with 0.3 mg/kg nicotine. There was an up-regulation of mu-receptors (increased Bmax) in the striatum of rats treated with 0.3 mg/kg nicotine, compared to 0. 1 mg/kg nicotine and saline groups. An interaction effect of group by gender was noted. After 14 days of chronic nicotine administration, met-enkelphalin levels were significantly lower in striatum and midbrain of animals treated with 0.3 mg/kg nicotine, as compared to controls. These results suggest that chronic nicotine administration, in doses representative of human smoking, produces antinociception initially, and is accompanied by an upregulation of micro-opioid receptors in the striatum of rats. In addition, nicotine-induced tolerance to antinociception may be associated with a decrease in met-enkelphalin level over a period of time.

Naltrexone administration affects ad libitum smoking behavior.

Endogenous opioid peptides have been implicated in the reinforcement of smoking and opioid antagonists have been examined to determine their role in smoking behavior. To date, the relationship between smoking behavior and chronic opiate antagonist administration during ad libitum smoking has not been investigated. The purpose of this study was to examine the relationships between naltrexone, an opiate antagonist administered orally, and smoking behavior and mood states during ad libitum smoking. A repeated measures experimental design was used. Normal adult male and female volunteers, admitted to the Clinical Research Center, were randomly assigned to naltrexone-treated (n = 22) or placebo-control (n = 21) groups in a double-blind manner. Day 1 was considered acclimation to the unit and day 2 was baseline, or pre-drug administration. On days 3, 4, and 5, subjects received 50 mg naltrexone or a placebo at 0700 and 1600 hours. Plasma nicotine and expired air carbon monoxide levels were measured daily at 1900 hours. Number of cigarettes smoked, mood states, withdrawal symptomatology and self-reported satisfaction with smoking were also quantified daily. Results indicated that plasma nicotine levels (P = 0.005), number of cigarettes smoked daily (P = 0.003) and self-reported satisfaction with smoking (P = 0.043) were significantly lower among those treated with naltrexone, compared to the placebo-control group. Expired air carbon monoxide levels did not differ between the two groups. In addition, mood states and withdrawal symptoms did not differ between groups. These findings suggest that endogenous opioid peptides influence specific smoking behavior variables.

Misclassification of smoking status among Southeast Asian adult immigrants.

A total of 1,403 Southeast Asian adult immigrant males (n = 783) and females (n = 620) from Cambodia, Laos, and Vietnam who currently resided in Central Ohio were interviewed to determine the self-reported smoking prevalence among them, and underwent biochemical confirmation of their smoking status. Variables having to do with the subjects' sociodemography, acculturation, and smoking history that were related to the misclassification of smoking status were also investigated. Self-reported current smoking rates were 40.9% and 5.6% for males and females, respectively. After verification of the subjects' smoking status by saliva cotinine assay (smoker status > or = 14 ng/ml), the rates of smoking were found to be greater, at 43.7% for males and 14.8% for females. Years of education, self-reported smoking status, country of origin, and method of healthcare payment were significant predictors of misclassification. These findings suggest that the prevalence of smoking is higher among Southeast Asian adult females than has been previously reported. Variables that predict misclassification with regard to smoking status are presented, and their implications for clinicians and researchers are discussed.

Preproenkephalin mRNA and methionine-enkephalin content are increased in mouse striatum after treatment with nicotine.

A single dose of nicotine increased methionine-enkephalin (Met-Enk) immunoreactivity in the striatum of mice in a time-dependent manner. Met-Enk content reached maximum by approximately 1 h after nicotine and returned to control values by 6 h. The response to nicotine was blocked by pretreating animals with the nicotinic receptor antagonist mecamylamine. In contrast, pretreating mice with the muscarinic receptor antagonist atropine or the dopamine receptor antagonist haloperidol did not block the response. A single dose of nicotine also increased mRNA for the precursor peptide preproenkephalin (PPE). The increase of PPE mRNA preceded that of Met-Enk and reached a maximum by approximately 30 min after nicotine. PPE mRNA levels returned to near normal by approximately 3 h and increased again by 6 h after nicotine. Daily administration of nicotine for 14 days increased Met-Enk content and PPE mRNA in the striatum of mice as well. Taken together, our results suggest that nicotinic receptors modulate Met-Enk content and PPE mRNA in the mouse striatum.

Changes in succinate dehydrogenase activity of rats after intraventricular injections of GABA, muscimol and picrotoxin.

Effects of intraventricular injections of GABA, and a GABA agonist, muscimol and an antagonist, picrotoxin on succinate dehydrogenase (SDH) enzyme activity in plasma and a few hypothalamic nuclei of brain of rats have been investigated using biochemical, histochemical and cytophotometric techniques. Results show that SDH decreased by GABA and muscimol treatment, and increased after picrotoxin injection. From the above findings, it is apparent that GABA, muscimol and picrotoxin influence SDH activity of plasma and hypothalamic nuclei.

Butyrylcholinesterase fluctuation in male albino rats with intracerebroventricular injection of gamma aminobutyric acid, muscimol, and picrotoxin.

The effects of intracerebroventricular injection of gamma-Aminobutyric acid, muscimol, or picrotoxin have been studied on butyrylcholinesterase (BuChE) activities in the serum and several hypothalamic nuclei using biochemical, histochemical, and cytophotometric techniques, respectively. The blood samples were withdrawn from indwelling catheters in jugular vein 1, 15, 30, 45, 60, 90, and 120 min after injection of the drugs. Biochemical estimations demonstrated a significant inhibition of BuChE after GABA and muscimol injections, whereas a pronounced stimulation of BuChE was observed after injection of picrotoxin. The peak changes were observed within 30 min of drug injection. Cytophotometric studies have appeared to dovetail the biochemical findings. Only a marginal decrease was observed after injection of GABA in all nuclei, while muscimol induced a very conspicuous decrease of BuChE. On the contrary, intracerebroventricularly administered picrotoxin markedly increased the levels of BuChE activity. Thus it could be concluded that probably GABA and muscimol along with picrotoxin appear to alter BuChE.

Qualitative and quantitative changes in monoamine oxidase activity after acute third ventricle treatment of GABA, muscimol, and picrotoxin in rat.

The effect of acute IIIrd ventricle injection of GABA, muscimol, and picrotoxin on the activity of monoamine oxidase (MAO) has been investigated in serum and a few hypothalamic nuclei of the rat brain using biochemical, histochemical, and cytophotometric techniques. Biochemical estimation demonstrated a significant reduction in MAO enzyme activity after GABA and muscimol injection, whereas picrotoxin produced pronounced increase in the enzyme activity. Histochemical and cytophotometric studies confirmed the biochemical findings. Even in brain, GABA and muscimol inhibited and picrotoxin stimulated the MAO activity. From the above findings, it may be concluded that GABA, muscimol, and picrotoxin regulate the MAO activity, possible mechanisms for which are being discussed.

Effect of chronic intracerebroventricular morphine to feeding responses in male rats.

Stainless steel cannulae were implanted stereotaxically in the third ventricle of male albino rats. The rats were fed with natural food pellets and water ad lib. After seven days of cannulation, daily body weight, food intake and water intake were recorded for the first five days, which was considered the preinjection control. Then increased and repetitive injections of morphine sulphate were administered intracerebroventricularly (ICV) in dosage of 30 micrograms/2 microliter, 45 micrograms/3 microliter, 60 micrograms/4 microliter, 75 micrograms/5 microliter, 90 micrograms/6 microliter and 105 micrograms/7 microliter on each following day respectively. In a separate set of experiments, the blood glucose levels were measured in animals injected with morphine to a dose corresponding to 15 micrograms/1 microliter, 30 micrograms/2 microliter, 45 micrograms/3 microliter, 60 micrograms/4 microliter and 75 micrograms/5 microliter on days 1, 2, 3, 4 and 5 respectively. Statistically significant (p less than 0.001) decreases in the body weight, food intake, water intake and increase in blood glucose were observed. The inferences derived from the above observations for the possible involvement and interaction of opioids in the regulation of feeding mechanisms have been discussed.