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Xuanwei City (formerly known as Xuanwei County) locates in the northeastern of Yunnan Province and is rich in coal, iron, copper and other mines, especially the smoky (bituminous) coal. Unfortunately, the lung cancer morbidity and mortality rates in this region are among China's highest, with a clear upward trend from the mid-1970s to mid-2000s. In 2004-2005, the crude death rate of lung cancer was 91.3 per 100,000 in the whole Xuanwei City, while that for Laibin Town in this city was 241.14 per 100,000. The epidemiologic distribution (clustering patterns by population, time, and space) of lung cancer in Xuanwei has some special features, e.g., high incidence in rural areas, high incidence in females, and an early age peak in lung cancer deaths. The main factor that associates with a high rate of lung cancer incidence was found to be indoor air pollution caused by the indoor burning of smoky coal. To a certain extent, genetic defects are also associated with the high incidence of lung cancer in Xuanwei. Taken together, lung cancer in this smoky coal combustion region is a unique model for environmental factor-related human cancer, and the current studies indicate that abandoning the use of smoky coal is the key to diminish lung cancer morbidity and mortality.

The objective of this paper is to review and describe the main neuropharmacological changes caused by the chronic use of alcohol and those observed during its withdrawal period. The results show international data referring to the involvement of monoamine systems, neurotransmitters and calcium channels in both neuroadaptation and tolerance to alcohol effects and withdrawal. Relevant studies showing the participation of other systems in those mechanisms, as opioids and other substances, are also shown. The article reinforces the importance, for both physicians and researchers, of an always growing understanding of alcohol central mechanisms of action. This understanding is necessary to new pharmacological options to alcohol harm reduction as well as to alcohol withdrawal treatment.

Alcoholism is associated with a higher incidence of smoking. In addition to the stimulatory effects of both ethanol and nicotine on the mesolimbic reward pathway, nicotine's ability to counteract some of the adverse effects of ethanol (e.g. ataxia) may be a powerful incentive for alcohol consumers to increase their tobacco (nicotine) intake. The cerebellum is believed to play an important role in ethanol-induced ataxia. In this study, we sought to test the hypothesis that nicotine would protect against toxic effects of ethanol in primary cultures of cerebellar granule cells. Moreover, it was postulated that the effects of nicotine would be mediated through nicotinic receptors. Primary cultures of cerebellar granule cells were prepared from 20-day embryos obtained from timed-pregnant Sprague Dawley rats. Cells were cultured for 10 days and were then exposed for 3 days to various concentrations of ethanol with and without pretreatment with nicotine and nicotinic antagonists. Cellular toxicity was evaluated by measuring the lactate dehydrogenase level. Administration of ethanol (10-100 mM) resulted in a dose-dependent toxicity. Pretreatment with nicotine 1-20 micro M resulted in a dose-dependent protection against ethanol-induced toxicity. The effects of nicotine were blocked by pretreatment with nicotinic antagonists such as mecamylamine 1-20 micro M, dihydro-beta-erythroidine 1.0 nM-1.0 micro M and methyllycaconitine 5 nM-5 micro M in a dose-dependent manner. Thus, ethanol-induced cytotoxicity in primary cultures of cerebellar granule cells is blocked by pretreatment with nicotine. The effects of nicotine, in turn, may be blocked by nicotinic antagonists, implicating both high and low affinity nicotinic receptors in mediating the actions of nicotine. The exact mechanism of ethanol-induced toxicity and/or neuroprotection through activation of nicotinic receptors in this paradigm remains to be elucidated. The neuroprotective effect of nicotine against ethanol-induced toxicity in cerebellar neurons may be a contributing factor to the high incidence of smoking among alcoholics.

Background: The consumption of significant amounts of alcohol (ethanol, EtOH) may markedly increase serum triglyceride levels. This study describes a significant increase in fasting serum triglyceride (TG) levels in adult male rats whose mothers consumed EtOH. The hypertriglyceridemia occurred although the offspring never directly consumed EtOH and had consumed only rat chow for the preceding 14 months. Furthermore, both male and female adult offspring had an additional, significant increase in TG levels if their mothers consumed EtOH and experienced stress (restraint) during the pregnancy.Methods: Harlan‐derived Sprague Dawley® female rats were dosed during pregnancy with EtOH via a liquid diet, and their offspring were compared with offspring of mothers who were either fed ad libitum or pair‐fed the liquid diet without EtOH. At birth, the offspring of EtOH mothers exhibited no visible abnormalities except reduced weight, and all offspring were surrogate fostered within 48 hr of birth to mothers who had consumed commercial rat chow throughout their pregnancy. After weaning, all offspring consumed only commercial rat chow, and they were examined over the next 14 months for changes in triglyceride homeostasis as a function of maternal alcohol intake.Results: Adult male offspring of mothers that consumed EtOH during their pregnancy had significant increases in fasting serum triglycerides associated with an increase in the very low density lipoprotein serum fraction. Acute administration of insulin to the offspring of all maternal dietary groups resulted in a rapid clearing of the serum triglycerides, and there were no differences in basal or heparin‐releasable lipoprotein lipase activity between any of the progeny. Castration of the male offspring of EtOH‐treated mothers prevented the development of elevated TG levels. Administration of testosterone to littermate female offspring increased circulating TG levels compared with testosterone‐treated offspring of pair‐fed mothers. EtOH‐consuming mothers who also underwent five periods of restraint‐induced stress (approximately 10 min each session) produced offspring whose fasting serum TG levels were higher than those whose mothers consumed EtOH but experienced no restraint or who experienced restraint but no EtOH. Maternal stress significantly reduced lipoprotein lipase activity in some offspring treatment groups, but the changes did not correspond to changes in the serum TG levels of the offspring. That is, maternal restraint‐induced stress was associated with a loss of heparin‐releasable lipoprotein lipase activity by male progeny from pair‐fed and EtOH‐fed mothers and the female offspring of ad libitum‐fed and EtOH‐fed mothers.Conclusions: Although serum triglycerides increased with age in all offspring, the increase was much more pronounced in the progeny of mothers who consumed EtOH during their pregnancy. The hypertriglyceridemia was significantly more pronounced in the male offspring and in female offspring treated with testosterone. Castration of male offspring inhibited the hypertriglyceridemia development, which suggests that male sex hormones may play a role in the development of this condition. Maternal EtOH consumption coupled with maternal restraint‐induced stress significantly increased the level of hypertriglyceridemia in both male and female offspring compared with offspring whose mothers experienced restraint but no EtOH or EtOH with no restraint. If this study models the human condition, the results could represent an unrecognized risk factor in a number of adult disease states hypothesized to be associated with hypertriglyceridemia, such as cardiovascular disease, hypertension, and diabetes.

We studied the peculiarities of the participation of ERK1/2 and р38 in regulation of various types of progenitor cells of the nervous tissue under conditions of ethanol-induced neurodegeneration modeled in vitro and in vivo. The stimulating role of these signaling molecules in the realization of the growth potential of intact multipotent neural stem cells and committed neuronal precursors (clonogenic PSA-NCAM+ cells) was demonstrated. In vitro exposure to neurotoxic doses of ethanol led to the loss of the specified role of ERK1/2 and p38 in the cell cycle regulation. Inversion of the role of both studied MAP-kinases in determining the proliferation status of neural stem cells after long-term administration of ethanol to experimental animals was revealed. In committed neuronal precursors, this inversion (inhibition of mitotic activity instead of activation) was revealed only for ERK1/2. In mice exposed to chronic alcoholization, ERK1/2 no longer participated in the process of specialization of both types of regeneration-competent cells of the nerve tissue. The revealed fundamental difference between the functions of ERK1/2 and p38 in the cell cycle regulation in neural stem cells and committed neuronal precursors under optimal conditions and during ethanol-induced neurodegeneration does not allow drawing definite conclusions about the prospect of using modifiers of their activity for the therapy for alcohol-related CNS pathologies.

The association between alcohol and blood glucose levels, and whether it is modified by other variables, was examined in a cross-sectional survey of 5518 staff aged 40-65 years at worksites in Auckland and Tokoroa, New Zealand. Diabetes was determined by oral glucose-tolerance tests using 1999 WHO criteria. Usual alcohol intake in the previous 3 months, measured by food frequency questionnaire, was related positively with fasting triglycerides and high-density-lipoprotein (HDL)-cholesterol, and unrelated with fasting glucose, but had an approximate U-shaped relationship with 2-h glucose, which varied from an adjusted mean (S.E.) of 5.62 (0.08) mmol/l in non-drinkers, down to 5.34 (0.08) mmol/l in light alcohol drinkers (alcohol or =20 g per day). Adjusting further for triglycerides increased the mean difference in 2-h glucose for all drinking categories compared with non-drinkers, particularly for heavy drinkers (> or =20 g per day), from -0.22 (S.E. = 0.10) to -0.37 (0.10) mmol/l. The confounding effect of triglycerides suggests alcohol may affect the diabetes risk by a mechanism related to the triglyceride metabolism, which in heavy drinkers may counteract the protective effect of improved insulin sensitivity, resulting in the U-shaped relationship between alcohol and diabetes described in previous studies.

An ethanolic herbal extract residue was prepared from the seeds of premature fruits of Terminalia arjuna Linn. Different concentrations of it were tested against 1 x 10⁶ million Dalton's Lymphoma Ascites (DLA) tumour cells. At a 200 μg/ml concentration it registered 90% toxicity. Then its effect on the lifespan of mice with DLA tumour cells was studied. At high and low dosages of 50 and 10 mg. b. wt. kg-1 of herbal extract residue, it exhibited 87.5% and 60.4% increase in the lifespan, respectively. Blood parameters such as percentage Hb, RBC and WBC counts were conducted with tail vein blood samples. Hb and RBC counts of treated mice were higher than that of tumour bearing mice, while WBC counts were lower. This is a good index of tumour recovery. Further studies were carried out on mice with solid tumours to record volumes, along with a lifespan study. Low dosage of the herbal extract residue was able to control the tumour volume 35.1% and 32.9% increase in the lifespan was noted both at high and low dosages, respectively.

Indoor air pollution in developing countries is a public health problem deserving of urgent attention. The aim of this study was to assess indoor second‐hand smoke (SHS) exposure via PM2.5 (fine particles with diameter ≤ 2.5 μm) level measurements in several public venues in Kuwait. The PM2.5 mean, median, and interquartile range (IQR) values for nonsmoking areas were; respectively, 28, 24, 32 μg/m3 while the corresponding values for smoking areas were 274, 222, 288 μg/m3 in the absence of water pipe usage and 1434, 1001, 964 μg/m3 in the presence of water pipes, respectively. Differences among the three tested venues (nonsmoking, smoking with and without water pipes) were statistically significant (F = 330.7, P < 0.001). The air quality index (AQI) results showed that nonsmoking areas were mostly classified as either “Good” or “Moderate” whereas the classification in smoking areas varied between “Moderate” to “Hazardous.” Adverse health outcomes from exposure to PM2.5 were also evaluated. The estimated lifetime lung cancer and cardiopulmonary risks in nonsmoking area were 4 × 10−3 and 3 × 10−3, respectively. In smoking areas, the risks were more than sixfold and 30‐fold increases of cancer and cardiopulmonary relative to nonsmoking areas without and with water pipes, respectively. In smoking venues, the relative ratio values were 1.26 and 1.16 with no water pipe and 1.86 and 1.51 when water pipe usage was observed, for lung cancer and cardiopulmonary mortality, respectively. These values reveal that people, especially the young and elderly, occupying or visiting these venues are susceptible to lung cancer and cardiopulmonary mortality. © 2018 American Institute of Chemical Engineers Environ Prog, 38:e13096, 2019

To determine the relationship among helmet use, alcohol use, and ethnicity in people killed on motorcycles.Retrospective review of all motorcycle fatalities in New Mexico from 1984 through 1988.Office of the Medical Investigator, State of New Mexico.All decedents of motorcycle crashes in New Mexico from 1984 through 1988.Review of all autopsies, medical investigator reports, traffic fatality reports, and toxicological studies on fatally injured motorcyclists.Nine of the helmeted drivers (18%) were legally intoxicated compared with 67 of the nonhelmeted drivers (51%) (chi 2 = 15.7, P less than .0001); 42 of the white nonHispanic decedents (37%), ten of Hispanic decedents (12%), and none of the Native-American decedents were wearing helmets. The head and neck region was the most severely injured body region in 42 of the nonhelmeted cases (84%) and in eight of the helmeted cases (50%) (Fisher's exact test, P less than .02).There is an association between nonuse of helmets and alcohol intoxication in fatally injured motorcyclists in New Mexico. Strategies for preventing motorcycle fatalities should address alcohol abuse and ethnicity in conjunction with helmet use.