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Premise: While some studies have found leaf variegation to reduce photosynthetic capacity, others showed that it can increase photosynthesis. Thus, what maintains variegation remains an open question. Two primary hypotheses-the anti-herbivory and abiotic heterogeneity hypotheses-have been posited, yet little empirical research explicitly investigates the maintenance of naturally occurring variegation., Methods: We used field surveys, image analysis, and climatic associations to explore the anti-herbivory and abiotic heterogeneity hypotheses in 21 populations of Hexastylis heterophylla and H. shuttleworthii, both polymorphic for leaf variegation. We measured the frequency of variegated individuals, variegation intensity, and herbivory for each morph, assessed abiotic correlates with variegation, and measured photosynthetic efficiency., Results: We found a strong elevational cline in leaf variegation strongly linked with abiotic heterogeneity; variegation was more common in lower-elevation populations characterized by higher temperatures, UV-B exposure, seasonal light change, and drier, more basic soils. Variegated and nonvariegated individuals experienced similar levels of herbivory. Morphs had similar photosynthetic quantum yields. However, nonvariegated leaves experienced more nonphotochemical quenching, an indication of photoinhibition, and had higher surface temperatures under high light., Conclusions: Our results suggest that variegation may serve as an adaptation to high temperatures and light conditions and can reduce photoinhibition in certain environmental contexts. Thus, abiotic factors can maintain variegation in wild populations and shape geographic clines in variegation., (© 2024 The Author(s). American Journal of Botany published by Wiley Periodicals LLC on behalf of Botanical Society of America.)

While developments in gynecologic health research continue advancing, relatively few groups specifically focus on vaginal tissue research for areas like wound healing, device development, and/or drug toxicity. Currently, there is no standardized animal or tissue model that mimics the full complexity of the human vagina. Certain practical factors such as appropriate size and anatomy, costs, and tissue environment vary across species and moreover fail to emulate all aspects of the human vagina. Thus, investigators are tasked with compromising specific properties of the vaginal environment as it relates to human physiology to suit their particular scientific question. Our review aims to facilitate the appropriate selection of a model aptly addressing a particular study by discussing pertinent vaginal characteristics of conventional animal and tissue models. In this review, we first cover common laboratory animals studied in vaginal research-mouse, rat, rabbit, minipig, and sheep-as well as human, with respect to the estrus cycle and related hormones, basic reproductive anatomy, the composition of vaginal layers, developmental epithelial origin, and microflora. In light of these relevant comparative metrics, we discuss potential selection criteria for choosing an appropriate animal vaginal model. Finally, we allude to the exciting prospects of increasing biomimicry for in vitro applications to provide a framework for investigators to model, interpret, and predict human vaginal health.

Pigmentation affords resistance to abiotic stressors, and thus can respond adaptively or plastically to drought and extreme temperatures associated with global change. Plants frequently display variability in flower coloration that is underlain by anthocyanin pigmentation. While anthocyanin polymorphisms impact plant-animal interactions, they also impact reproductive performance under abiotic stress. We used descriptions of flower colour from over 1900 herbarium records representing 12 North American species spanning 124 years to test whether anthocyanin-based flower colour has responded to global change. Based on demonstrated abiotic associations with performance of anthocyanin colour morphs, we predicted pigmentation would increase in species experiencing increased aridity, but decline in those experiencing larger increases in temperature. We found that the frequency of reports of pigmented morphs increased temporally in some taxa but displayed subtle declines in others. Pigmentation was negatively associated with temperature and positively associated with vapour pressure deficit (a metric of aridity) across taxa. Species experiencing larger temperature increases over time displayed reductions in pigmentation, while those experiencing increases in aridity displayed increases in pigmentation. Change in anthocyanin-based floral colour was thus linked with climatic change. Altered flower coloration has the strong potential to impact plant-animal interactions and overall plant reproductive performance.

We hypothesized that endogenous CCK reduces food intake by activating the dorsal vagal complex (DVC) and the myenteric neurons of the gut. To test this hypothesis, adult rats were given camostat mesilate; a nonnutrient releaser of endogenous CCK, by orogastric gavage, and Fos-like immunoreactivity (Fos-LI) was quantified in the DVC and the myenteric plexus. The results for endogenous CCK were compared with those for exogenous CCK-8. Exogenous CCK-8 reduced food intake and stimulated Fos-LI in the DVC and in myenteric neurons of the duodenum and jejunum. In comparison, endogenous CCK reduced food intake and increased DVC Fos-LI but did not increase Fos-LI in the myenteric plexus. Similar to CCK-8, devazepide, a specific CCK(1) receptor antagonist, and not L365,260, a specific CCK(2) receptor antagonist, attenuated the reduction of food intake by camostat. In addition, Fos-LI in the DVC in response to both exogenous CCK-8 and camostat administration was significantly attenuated by vagotomy, as well as by blocking CCK(1) receptors. These results demonstrate for the first time that reduction of food intake in adult rats by endogenous CCK released by a nonnutrient mechanism requires CCK(1) receptors, the vagus nerve, and activation of the DVC, but not the myenteric plexus.

Vagotomy and capsaicin treatment attenuate dorsal vagal complex (DVC) but not myenteric Fos-like immunoreactivity (Fos-LI) induced by cholecystokinin-8 (CCK-8). The goal of this experiment is to test the role of the sympathetic nervous system in the pathway by which CCK-8 increases myenteric Fos-LI. Adult male Sprague-Dawley rats were pretreated with guanethidine sulfate (40 mg/kg daily for 5 weeks) or vehicle intraperitoneally (IP), and injected with CCK-8 (40 microg/kg) or saline IP. Fos-LI was then quantified in the DVC and the myenteric neurons of the duodenum and jejunum using a diaminobenzidine reaction. Guanethidine pretreatment attenuated myenteric but not DVC Fos-LI induced by CCK-8. These findings demonstrate that sympathetic neurons play a role in mediating the myenteric Fos-LI response to CCK. They also suggest differential mediation of myenteric and DVC responses to CCK.

We utilized a diaminobenzidine reaction enhanced with nickel to compare dorsal vagal complex (DVC) and myenteric neuronal Fos-Like immunoreactivity (Fos-LI), in response to sulfated cholecystokinin-8 (CCK-8) (5, 10, 20, 40 microg/kg), among Sprague-Dawley (SD), Standard Long-Evans (SLE), Otsuka Long-Evans Tokushima Fatty (OLETF), and Long-Evans Tokushima Otsuka (LETO) rats. All rat strains but OLETF expressed Fos-LI in response to CCK-8. In addition, SD rats expressed more Fos-LI in the area postrema and myenteric neurons than SLE and LETO rats. To investigate the basis for these differences, we utilized cuprolinic blue staining, which stains neuronal cell bodies, to quantify the number of myenteric neurons, and a reverse transcriptase chain polymerase reaction to measure the gene expression of CCK(1) receptor in the gut. We found that SD rats have significantly more duodenal myenteric neurons than the other strains. In addition, this strain expressed significantly higher levels of the CCK(1) gene in both the duodenum and jejunum than the other strains. In conclusion, SD rats may express more myenteric Fos-LI in response to CCK due to increased numbers of myenteric neurons or more intestinal CCK(1) receptors than the other strains of rats.