Mind Over Body: A Comparison of Psychobiological Versus Physiological Focused Distance Runners

Previous research has shown that psychology can have significant effects on endurance performance. According to exercise physiologist Samuele Marcora all performance gains in endurance racing are due to a reduction of perceived effort at a given pace (Sherman, 2021). The proposed study will compare athletes focusing on reducing perceived effort at a given pace over a four month training period with athletes focused on improving physical fitness over the same period. The fitness group will complete workouts designed to maximize physiological indicators while the perceived effort groups will complete workouts designed to reduce perceived effort while running at a given pace. Participants will partake in a five-kilometer race before and after the four month training period. Expected results will include a greater increase in performance over the second race for the perceived effort group as well as less injuries in the perceived effort group

MODELING ALTERNATIVE POLICIES FOR GHG MITIGATION FROM FORESTRY AND AGRICULTURE

A key consideration for development of energy and climate policy affecting the forestry and agricultural sectors is that the selection of specific mechanisms implemented to achieve bioenergy production and/or greenhouse gas (GHG) mitigation targets may have substantial effects on landowner incentives to adopt alternative practices. For instance, the prices of allowances and offsets are expected to diverge under some policies being considered where there is a binding cap on the quantity of offsets from the agricultural and forest sectors. In addition, provisions that limit or exclude specific practices from receiving carbon payments will affect the quantity and cost of GHG mitigation opportunities available. In this study, the recently updated Forest and Agriculture Sector Optimization Model with GHGs (FASOMGHG) was used to estimate GHG mitigation potential for private land in the contiguous U.S. under a variety of GHG price policies. Model scenarios suggest that U.S. forestry and agriculture could provide mitigation of 200 – 1000 megatons carbon dioxide equivalent per year (Mt CO2e/year) at carbon prices of $15 to$50/tCO2e. Binding limits on offsets have increasingly large effects on both the total magnitude and distribution of GHG mitigation across options over time. In addition, discounting or excluding payments for forest sinks can reduce annualized land-based mitigation potential 37-90 percent relative to the full eligibility scenario whereas discounting or excluding agricultural practices reduces mitigation potential by less than 10 percent.Climate policy, energy policy, FASOMGHG, GHG mitigation, Agricultural and Food Policy, Environmental Economics and Policy, Resource /Energy Economics and Policy, C61, Q42, Q54,

Mechanisms Underlying the Essential Role of Mitochondria in Chronological Aging of the Yeast Saccharomyces cerevisiae

This thesis describes studies that have resulted in uncovering molecular and cellular mechanisms underlying the essential role of mitochondria in chronological aging of the baker’s yeast, Saccharomyces cerevisiae. The Titorenko laboratory has recently identified lithocholic acid (LCA), a bile acid and a natural compound that operates synergistically with caloric restriction (CR) to cause a substantial increase in yeast chronological lifespan under longevity-extending CR conditions. As a first step towards establishing a mechanism by which LCA extends longevity of chronologically aging yeast limited in calorie supply, I investigated the distribution of LCA within yeast cells. I found that exogenously added LCA enters yeast cells, is sorted only to mitochondria, resides mainly in the inner mitochondrial membrane and also associates with the outer membrane of mitochondria. I demonstrated that LCA-elicited changes in the membrane lipidome of mitochondria trigger age-related alterations in mitochondrial respiration, membrane potential, reactive oxygen species (ROS) quantity, oxidative macromolecular damage, respiratory complexes composition and ATP concentration. My findings provided evidence that the longevity-extending potential of LCA is due in part to its ability to alter the age-related dynamics of mitochondrially produced ROS in both chronologically ʺyoungʺ and ʺoldʺ cells, thus reducing the damaging effect of these ROS in ʺyoungʺ cells and amplifying their ʺhormeticʺ effect in ʺoldʺ cells. I demonstrated that LCA alters the age-related dynamics of changes in the levels of many mitochondrial proteins, as well as numerous proteins in cellular locations outside of mitochondria. My findings imply that LCA-driven changes in the mitochondrial lipidome alter the mitochondrial proteome and functionality, thereby enabling mitochondria to operate as signaling organelles that orchestrate the establishment of an anti-aging transcriptional program for many longevity-defining nuclear genes. Based on these findings, I proposed a model for how such LCA-driven changes early and late in the life of chronologically aging yeast cause a stepwise development of an anti-aging cellular pattern and its maintenance throughout lifespan. Moreover, I provided evidence that mitophagy, a selective autophagic degradation of aged and dysfunctional mitochondria, is a longevity assurance process that in chronologically aging yeast underlies the synergistic beneficial effects of CR and LCA on lifespan

Lithocholic bile acid selectively kills neuroblastoma cells, while sparing normal neuronal cells

Aging is one of the major risk factors of cancer. The onset of cancer can be postponed by pharmacological and dietary anti-aging interventions. We recently found in yeast cellular models of aging that lithocholic acid (LCA) extends longevity. Here we show that, at concentrations that are not cytotoxic to primary cultures of human neurons, LCA kills the neuroblastoma (NB) cell lines BE(2)-m17, SK-n-SH, SK-n-MCIXC and Lan-1. In BE(2)-m17, SK-n-SH and SK-n-MCIXC cells, the LCA anti-tumor effect is due to apoptotic cell death. In contrast, the LCA-triggered death of Lan-1 cells is not caused by apoptosis. While low concentrations of LCA sensitize BE(2)-m17 and SK-n-MCIXC cells to hydrogen peroxide-induced apoptotic cell death controlled by mitochondria, these LCA concentrations make primary cultures of human neurons resistant to such a form of cell death. LCA kills BE(2)-m17 and SK-n-MCIXC cell lines by triggering not only the intrinsic (mitochondrial) apoptotic cell death pathway driven by mitochondrial outer membrane permeabilization and initiator caspase-9 activation, but also the extrinsic (death receptor) pathway of apoptosis involving activation of the initiator caspase-8. Based on these data, we propose a mechanism underlying a potent and selective anti-tumor effect of LCA in cultured human NB cells. Moreover, our finding that LCA kills cultured human breast cancer and rat glioma cells implies that it has a broad anti-tumor effect on cancer cells derived from different tissues and organisms

Neuroprotective effects and mechanism of cognitive-enhancing choline analogs JWB 1-84-1 and JAY 2-22-33 in neuronal culture and Caenorhabditis elegans

<p>Abstract</p> <p>Background</p> <p>Our previous work indicated that novel analogs of choline have cytoprotective effects <it>in vitro </it>that might be useful in neurodegenerative conditions such as Alzheimer's disease (AD). Furthermore, two lead compounds (JWB1-84-1 and JAY2-22-33) from a library of more than 50 improved cognitive performances in a transgenic mouse model of AD. The purpose of these experiments was to more specifically investigate the neuroprotective capabilities of these lead compounds both <it>in vitro </it>and <it>in vivo</it>.</p> <p>Results</p> <p>We used N2a cells which express a Swedish mutation in the amyloid precursor protein and presenilin 1 genes to investigate the effect of JWB1-84-1 and JAY2-22-33 on β-amyloid (Aβ) levels and found that both compounds significantly reduced Aβ levels. JWB1-84-1 and JAY2-22-33 also protected rat primary cortical neurons from Aβ toxicity. Subsequently, we utilized the nematode <it>Caenorhabditis elegans </it>(<it>C. elegans</it>) as an <it>in vivo </it>model organism to identify potential molecular targets of these compounds. In the <it>C. elegans </it>model of Aβ toxicity, human Aβ is expressed intracellularly in the body wall muscle. The expression and subsequent aggregation of Aβ in the muscle leads to progressive paralysis.</p> <p>Conclusion</p> <p>We found that JAY2-22-33 (but not JWB1-84-1) significantly reduced Aβ toxicity by delaying paralysis and this protective effect required both the insulin signaling pathway and nicotinic acetylcholine receptors (nAChRs).</p

Targeted full energy and protein delivery in critically ill patients : A pilot randomized controlled trial (FEED Trial)

Background International guidelines recommend greater protein delivery to critically ill patients than they currently receive. This pilot randomized clinical trial aimed to determine whether a volume-target enteral protocol with supplemental protein delivered greater amounts of protein and energy to critically ill patients compared with standard care. Methods Sixty participants received either the intervention (volume-based protocol, with protein supplementation) or standard nutrition care (hourly-rate-based protocol, without protein supplementation) in the intensive care unit (ICU). Coprimary outcomes were average daily protein and energy delivery. Secondary outcomes included change in quadriceps muscle layer thickness (QMLT, ultrasound) and malnutrition (subjective global assessment) at ICU discharge. Results Mean (SD) protein and energy delivery per day from nutrition therapy for the intervention were 1.2 (0.30) g/kg and 21 (5.2) kcal/kg compared with 0.75 (0.11) g/kg and 18 (2.7) kcal/kg for standard care. The mean difference between groups in protein and energy delivery per day was 0.45 g/kg (95% CI, 0.33–0.56; P < .001) and 2.8 kcal/kg (95% CI, 0.67–4.9, P = .01). Muscle loss (QMLT) at discharge was attenuated by 0.22 cm (95% CI, 0.06–0.38, P = .01) in patients receiving the intervention compared with standard care. The number of malnourished patients was fewer in the intervention [2 (7%) vs 8 (28%); P = .04]. Mortality and duration of admission were similar between groups. Conclusions A high-protein volume-based protocol with protein supplementation delivered greater amounts of protein and energy. This intervention was associated with attenuation of QMLT loss and reduced prevalence of malnutrition at ICU discharge

Magnetic Exciton-Polariton with Strongly Coupled Atomic and Photonic Anisotropies

Anisotropy plays a key role in science and engineering. However, the interplay between the material and engineered photonic anisotropies has hardly been explored due to the vastly different length scales. Here we demonstrate a matter-light hybrid system, exciton-polaritons in a 2D antiferromagnet, CrSBr, coupled with an anisotropic photonic crystal (PC) cavity, where the spin, atomic lattice, and photonic lattices anisotropies are strongly correlated, giving rise to unusual properties of the hybrid system and new possibilities of tuning. We show exceptionally strong coupling between engineered anisotropic optical modes and anisotropic excitons in CrSBr, which is stable against excitation densities a few orders of magnitude higher than polaritons in isotropic materials. Moreover, the polaritons feature a highly anisotropic polarization tunable by tens of degrees by controlling the matter-light coupling via, for instance, spatial alignment between the material and photonic lattices, magnetic field, temperature, cavity detuning and cavity quality-factors. The demonstrated system provides a prototype where atomic- and photonic-scale orders strongly couple, opening opportunities of photonic engineering of quantum materials and novel photonic devices, such as compact, on-chip polarized light source and polariton laser

A feasibility study into the production of a mussel matrix reference material for the cyanobacterial toxins microcystins and nodularins.

Microcystins and nodularins, produced naturally by certain species of cyanobacteria, have been found to accumulate in aquatic foodstuffs such as fish and shellfish, resulting in a risk to the health of the seafood consumer. Monitoring of toxins in such organisms for risk management purposes requires the availability of certified matrix reference materials to aid method development, validation and routine quality assurance. This study consequently targeted the preparation of a mussel tissue reference material incurred with a range of microcystin analogues and nodularins. Nine targeted analogues were incorporated into the material as confirmed through liquid chromatography with tandem mass spectrometry (LC-MS/MS), with an additional 15 analogues detected using LC coupled to non-targeted high resolution mass spectrometry (LC-HRMS). Toxins in the reference material and additional source tissues were quantified using LC-MS/MS, two different enzyme-linked immunosorbent assay (ELISA) methods and with an oxidative-cleavage method quantifying 3-methoxy-2-methyl-4-phenylbutyric acid (MMPB). Correlations between the concentrations quantified using the different methods were variable, likely relating to differences in assay cross-reactivities and differences in the abilities of each method to detect bound toxins. A consensus concentration of total soluble toxins determined from the four independent test methods was 2425 ± 575 µg/kg wet weight. A mean 43 ± 9% of bound toxins were present in addition to the freely extractable soluble form (57 ± 9%). The reference material produced was homogenous and stable when stored in the freezer for six months without any post-production stabilization applied. Consequently, a cyanotoxin shellfish reference material has been produced which demonstrates the feasibility of developing certified seafood matrix reference materials for a large range of cyanotoxins and could provide a valuable future resource for cyanotoxin risk monitoring, management and mitigation