The Quality and Quantity of Lower Genital Tract Research Across Multiple Journals.

OBJECTIVE: This study aimed to determine the quantity and quality of lower genital tract disease (LGTD) research by topic published across a variety of gynecology and dermatology journals. METHODS: Authors accessed all articles that were rejected (1,111, 59.5%) and accepted (755, 40.5%) by the Journal of Lower Genital Tract Disease ( JLGTD ) from 2008 to 2020. Studies were categorized by key topic: Cervix, Human Papillomavirus, Vulva, Vagina, Anal, and Other. Studies were further subcategorized based on methodology. These data were compared with all LGTD publications from 2018 to 2020 in 4 other widely recognized journals ( Obstetrics and Gynecology , The British Journal of Obstetrics and Gynaecology , JAMA Dermatology , and the British Journal of Dermatology ). RESULTS: Most JLGTD -accepted submissions were related to the cervix (298/755, 39.5%) and vulva (189/755, 25.0%). Rates of acceptance were similar across all key topic areas. Only 3.2% of publications in the other 4 journals (92/2,932) were related to LGTD topics. Across all 5 journals, vulva studies were most commonly case reports/case series (82/218, 37.6%), with a low prevalence of systematic reviews/meta-analyses (4/218 1.8%). In comparison, cervix studies had the highest number of systematic reviews/meta-analyses (14/317, 4.4%) and the lowest number of case reports (14/317, 4.4%). CONCLUSIONS: Vulvar research is of lower quality compared with cervix research published across 5 journals. Comparing accepted versus rejected articles in JLGTD , there is no publication bias against vulva topics noted; rather, the overall research quality in vulva is lower than that of cervical disease. This is a call to action for higher quality vulvar research.

Diet-regulated behavior: FVB/N mice fed a lean diet exhibit increased nocturnal bouts of aggression between littermates.

The hyperactive FVB/N inbred mouse strain is widely used for transgenic research applications, although rarely for behavioral studies. These mice have visual impairments via retinal degeneration, but are considered highly intelligent and rely largely on olfaction. While investigating diet-induced obesity in autotaxin transgenic FVB/N mice, we observed an increase in the necessity for male, but not female, cage separations. Based on the observations, we hypothesized that feeding FVB/N mice a lean diet increases nocturnal bouts of aggression between male littermates. The diets of adult littermates were switched from normal chow to either ad libitum high-fat (45% fat) or lean (10% fat) matched diets for 27 weeks, whereby the mice reached an average of 43 g versus 35 g, respectively. Then, cage separations due to nocturnal bouts of aggression became mandatory, even though littermates peacefully cohabitated for 10-16 weeks previously. Since the data was of an unusual nature, it required uncommon statistical methods to be engendered to evaluate whether and where significance existed. Therefore, utilizing the randomization and population models, we established a methodology and postulated that either testosterone, the autotaxin transgene or diet alteration was the causal factor. Statistical evaluation demonstrated a significant correlation between cage separations and aggressive behavior associated with the lean-diet-fed mice, not autotaxin. Biochemical data did not appear to explain the behavior. In contrast, energy metabolism highlighted differences between the groups of normally hyperactive mice by diet. This characteristic makes FVB/N male mice unsuitable subjects for long-term studies with lean-diet modifications.

Maternal diet-induced obesity alters muscle mitochondrial function in offspring without changing insulin sensitivity.

In utero overnutrition can predispose offspring to metabolic disease. Although the mechanisms are unclear, increased oxidative stress accelerating cellular aging has been shown to play a role. Mitochondria are the main site of reactive oxygen species (ROS) production in most cell types. Levels of ROS and the risk for oxidative damage are dictated by the balance between ROS production and antioxidant defense mechanisms. Originally considered as toxic species, physiologic levels of ROS are now known to be essential cell signaling molecules. Using a model of maternal overnutrition in C57BL6N mice, we investigate the mechanisms involved in the development of insulin resistance (IR) in muscle. In red and white gastrocnemius muscles of offspring, we are the first to report characteristics of oxidative phosphorylation, H2O2 production, activity of mitoflashes, and electron transport chain supercomplex formation. Results demonstrate altered mitochondrial function with reduced response to glucose in offspring of mice fed a high-fat and high-sucrose diet, increases in mitochondrial leak respiration, and a reduction in ROS production in red gastrocnemius in response to palmitoyl carnitine. We also demonstrate differences in supercomplex formation between red and white gastrocnemius, which may be integral to fiber-type specialization. We conclude that in this model of maternal overnutrition, mitochondrial alterations occur before the development of IR.-McMurray, F., MacFarlane, M., Kim, K., Patten, D. A., Wei-LaPierre, L., Fullerton, M. D., Harper, M. E. Maternal diet-induced obesity alters muscle mitochondrial function in offspring without changing insulin sensitivity.