Background/Objectives: The winter holiday season in the US, which spans mid-November to mid-January, contributes to over half of annual body weight gain. Although self-reported data has linked this weight change to both increased energy intake and reduced physical activity, objective techniques have never been used and thus the actual cause of holiday weight gain is controversial. Here, we aimed to determine changes in components of energy balance leading to the holiday weight gain. Methods: Body weight change was compared between the pre-holiday (mid-September to mid-November) and the holiday period (mid-November to early January). Total energy expenditure (TEE) was measured using doubly labeled water during holiday time (early to mid-December). Subjective (ratings) and physiological (appetite-regulating hormones) measures of appetite, eating-away-from-home frequency, and incentive salience of food pictures were also evaluated. Results: In 23 obese adults (87% female), body weight change during the holidays (0.41 ± 0.42 kg) was significantly higher (P=0.02) than the body weight change during the pre-holiday period (−0.86 kg ± 0.42 kg). The TEE was unchanged during the two periods, suggesting no role of energy expenditure on weight gain. However, participants reported lower satisfaction after a meal pre-load which was significantly correlated with increased body weight during the holiday period. An increase in number of episodes of eating at sit-down restaurants was also reported during that period. Overall, these changing behaviors were supported by a non-significant increase in energy intake (+80 kcal/day, P=0.07) observed during the study holiday period. Conclusion: We conclude that a decrease in energy expenditure does not result in the weight increase, but that an increase in food intake is the more likely cause. Our data imply that compromised internal satiety mechanisms in presence of external food cues and diet related behavioral variables during the holidays may influence this weight gain.
This study compares the utilization costs of ceftazidime therapy with those of gentamicin in combination with other antibacterial drugs. The results show that the relatively high purchase cost of ceftazidime compared to combinations is more than counterbalanced by the additional materials used for drug administration and serum antibiotic assays, even when other drugs were combined with ceftazidime. The average drug and equipment costs were 230.13 pounds for ceftazidime regimens and 253.94 pounds for gentamicin regimens. It is also shown that ceftazidime therapy is associated with a reduction in personnel time compared to gentamicin regimens. The average times per patient for administration and assay were 1 h 43 min for ceftazidime and 4 h 57 min for gentamicin regimens. We conclude that ceftazidime regimens are cheaper than gentamicin regimens when all drug and equipment costs are quantified. Moreover, the use of ceftazidime will release staff time for other purposes.
Excessive alcohol consumption is a risk factor associated with colorectal cancer; however, some epidemiological studies have reported that moderate alcohol consumption may not contribute additional risk or may provide a protective effect reducing colorectal cancer risk. Prior research highlights the importance of proliferation, differentiation, and apoptosis as parameters to consider when evaluating colonic cell growth and tumorigenesis. The present study investigated whether chronic low-to-moderate ethanol consumption altered these parameters of colonic cell growth and expression of related genes. Twenty-four nondeprived young adult (109 days old) and 24 nondeprived middle-aged (420 days old) Wistar rats were randomly assigned to an ethanol-exposed or a water control group (n = 12/group). The ethanol group was provided voluntary access to a 20% v/v ethanol solution on alternate days for 13 weeks. Colon tissues were collected for quantitative immunohistochemical analyses of cell proliferation, differentiation and apoptosis using Ki-67, goblet cell and TUNEL, respectively. Gene expression of cyclin D1 (Ccnd1), Cdk2, Cdk4, p21waf1/cip1 (Cdkn1a), E-cadherin (Cdh1) and p53 were determined by quantitative real-time polymerase chain reaction in colonic scraped mucosa. Ethanol treatment resulted in a lower cell proliferation index and proliferative zone, and lower Cdk2 expression in both age groups, as well as trends toward lower Ccnd1 and higher Cdkn1a expression. Cell differentiation was modestly but significantly reduced by ethanol treatment only in older animals. Overall, older rats showed decreases in apoptosis and gene expression of Cdk4, Cdh1, and p53 compared to younger rats, but there was no observed effect of ethanol exposure on these measures. These findings suggest that low-to-moderate ethanol consumption improves at least one notable parameter in colonic tumorigenesis (cell proliferation) and associated gene expression regardless of age, however, selectively decreased cell differentiation among older subjects.
The most important finding of the current study was that iontophoresis of acetazolamide did not significantly decrease sweat rate during exercise in the heat. Such results suggest that in past studies it was systemic dehydration, and not CA inhibition at the level of the sweat gland, that caused the reported decreased sweat rate.
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