Carotenoids are strongly absorbing pigments that can self- assemble to form aggregates. These aggregates provide an opportunity to study exciton-coupling, which is the delocalization of an excitation over multiple molecules. Two zeaxanthin aggregates, previously denoted in our group as "J1" and "J2", exhibit red-shifted absorption relative to the monomer, and a third, "H", displays a strongly blue -shifted absorption. Raman scattering cross-sections as a function of excitation wavelength are reported for these three zeaxanthin aggregates and the monomer. The aggregates were modeled as dimers to probe the strength of exciton-coupling, intermolecular geometry, and vibrational displacements. The simulations of J1 and J2 suggest that these two aggregates consist of weakly-coupled, card- stacked carotenoids. J2 was found to have a smaller distance and larger rotation angle between the two chromophores, relative to J1. The H-aggregate was fit to a strongly coupled card-stacked orientation. The possibility of exciton-coupling in carotenoid-containing feathers was investigated with in situ resonance Raman spectroscopy, coupled with measurements of diffuse reflectance and transmittance. Rhodoxanthin is the major carotenoid pigment in five different feathers, but there is a large variation in color. Red-shifts in the absorption profiles of these feathers correlated with a decrease in the frequency of the ethylenic mode and an increase in intensity of hydrogen-out-of-plane modes. Isomeric effects were found to be insignificant in terms of the color of the feathers. These studies of zeaxanthin and rhodoxanthin allow for a better understanding of exciton-coupling and illustrate how environment and structure affect the photophysics of carotenoids

The ability of humans to sense chemical signals in ingested substances is implicit in the ability to detect the five basic tastes; sweet, sour, bitter, salty, and umami. Of these, sweet, bitter, and umami tastes are detected by lingual G-protein-coupled receptors (GPCRs). Recently, these receptors were also localized to the gut mucosa. In this review, we will emphasize recent advances in the understanding of the mechanisms and consequences of foregut luminal chemosensing, with special emphasis on cell surface GPCRs such as the sweet and proteinaceous taste receptors (TASRs), short- and long-chain fatty acid (FA) receptors, and bile acid receptors. The majority of these luminal chemosensors are expressed on enteroendocrine cells (EECs), which are specialized endocrine cells in the intestine and pancreas that release gut hormones with ligand activation. These gut hormones are responsible for a wide variety of physiologic and homeostatic mechanisms, including glycemic control, appetite stimulation and suppression, regulation of gastric emptying, and trophic effects on the intestinal epithelium. Released from the EECs, the gut peptides have paracrine, autocrine, and endocrine effects. Additionally, EECs have unique direct connections to the enteric nervous system enabling precise transmission of sensory data to and communication with the central nervous system. We will also describe how gut sensors are implicated in gut hormone release, followed by examples of how altered gut chemosensing has been implicated in pathological conditions such as metabolic diseases including diabetes and obesity, functional dyspepsia, helminthic infections, colitis, gastric bypass surgery, and gastric inflammation and cancer.

Human immunodeficiency virus (HIV) infection is associated with subclinical cardiomyopathy, diastolic dysfunction, and increased risk of cardiovascular death. However, the relationship between left atrial (LA) mechanics and left ventricular (LV) diastolic function has not been evaluated in people living with HIV (PLWH) relative to HIV-uninfected (HIV-) controls. This is a multicenter, cross-sectional cohort analysis using the HIV Cardiovascular Disease substudy of the Veterans Aging Cohort Study database, which aimed to examine a cohort of PLWH and HIV- veterans without known cardiovascular disease. A total of 277 subjects (180 PLWH, 97 HIV-) with echocardiograms were identified. LV and LA phasic strain were derived and diastolic function was evaluated. Relationship between LA strain, LV strain, and the degree of diastolic dysfunction were assessed using analysis of variance and ordinal logistic regression with propensity weighting. In the PLWH cohort, 91.7% were on antiretroviral therapy and 86.1% had HIV viral loads <500 copies/ml. The mean (± SD) duration of infection was 9.7 ± 4.9 years. Relative to HIV- veterans, PLWH did not differ in LA mechanics and proportion of diastolic dysfunction (p = 0.31). Using logistic regression with propensity weighting, we found no association between HIV status and degree of diastolic dysfunction. In both cohorts, LA reservoir strain and LA conduit strain were inversely and independently associated with the degree of diastolic dysfunction. Compared with HIV- veterans, PLWH who are primarily virally suppressed and antiretroviral-treated did not differ in LA strain or LV diastolic dysfunction. If confirmed in other cohorts, HIV viral suppression may curtail adverse alterations in cardiac structure and function.