Impact of COVID-19 on the US and Texas Economy: A General Equilibrium Approach

This paper examines the impact of COVID-19 on the US and Texas economy using a computable general equilibrium model, REMI PI+. We consider three scenarios based on economic forecasts from various sources, including the University of Michigan’s RSQE (Research Seminar in Quantitative Economics), IMF, and the Wi orld Bank. We report a GDP loss of $106 million (a 6$996 billion (a 5% decline) with 11.5 million jobs lost (5.5%) in the same year. By 2026, the aggregate total GDP loss in Texas ranges from $378 to$629 million. The estimated unemployment rate in Texas in 2021 ranges from 5% to 7.7%, depending on modeling assumptions. The granularity of the CGE results allow examination of the most and least impacted industries. Health Care and Social Assistance, Construction, and Accommodation and Food Services incur the most job loss while State and Local Government and Farm will likely see an increase in jobs for 2020. These insights separate our work from most current impact studies

Antioxidant responses and lipid peroxidation in gills and erythrocytes of fish (Rhabdosarga sarba) upon exposure to Chattonella marina and hydrogen peroxide : implications on the cause of fish kills

Author Posting. © Elsevier B.V., 2006. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Journal of Experimental Marine Biology and Ecology 336 (2006): 230-241, doi:10.1016/j.jembe.2006.05.013.Chattonella marina, a red tide or harmful algal bloom species, has caused mass fish kills and serious economic loss worldwide, and yet its toxic actions remain highly controversial. Previous studies have shown that this species is able to produce reactive oxygen species (ROS), and therefore postulated that ROS are the causative agents of fish kills. The present study investigates antioxidant responses and lipid peroxidation in gills and erythrocytes of fish (Rhabdosarga sarba) upon exposure to C. marina, compared with responses exposed to equivalent and higher levels of ROS exposure. Even though C. marina can produce a high level of ROS, gills and erythrocytes of sea bream exposed to C. marina for 1 to 6 h showed neither significant induction of antioxidant enzymes nor lipid peroxidation. Antioxidant responses and oxidative damage did not occur as fish mortality began to occur, yet could be induced upon exposure to artificially supplied ROS levels an order of magnitude higher. The result of this study implies that ROS produced by C. marina is not the principal cause of fish kills.This study was supported by a CERG grant (CityU 1109/03M / No. 9040864) of the University Grants Committee, Hong Kong SAR government. Support for Don Anderson was also provided by the U.S. National Science Foundation through grant no. OCE-0136861

European mtDNA Variants Are Associated With Differential Responses to Cisplatin, an Anticancer Drug: Implications for Drug Resistance and Side Effects.

Background: Cisplatin, a powerful antitumor agent, causes formation of DNA adducts, and activation of apoptotic pathways. Presently, cisplatin resistance develops in up to 70% of patients but the underlying molecular mechanism(s) are unclear and there are no markers to determine which patients will become resistant. Mitochondria play a significant role not only in energy metabolism but also retrograde signaling (mitochondria to nucleus) that modulates inflammation, complement, and apoptosis pathways. Maternally inherited mitochondrial (mt) DNA can be classified into haplogroups representing different ethnic populations that have diverse susceptibilities to diseases and medications. Methods: Transmitochondrial cybrids, where all cell lines possess identical nuclear genomes but either the H (Southern European) or J (Northern European) mtDNA haplogroups, were treated with cisplatin and analyzed for differential responses related to viability, oxidative stress, and expression levels of genes associated with cancer, cisplatin-induced nephrotoxicity and resistance, apoptosis and signaling pathways. Results: The cisplatin-treated-J cybrids showed greater loss of cell viability along with lower levels of reactive oxygen species and mitochondrial membrane potential compared to cisplatin-treated-H cybrids. After cisplatin treatment, J cybrids showed increased gene expression of BAX, CASP3, and CYP51A, but lower levels of SFRP1 compared to untreated-J cybrids. The cisplatin-treated-H cybrids had elevated expression of CDKN1A/P21, which has a role in cisplatin toxicity, compared to untreated-H cybrids. The cisplatin-treated H had higher transcription levels of ABCC1, DHRS2/HEP27, and EFEMP1 compared to cisplatin-treated-J cybrids. Conclusions: Cybrid cell lines that contain identical nuclei but either H mtDNA mitochondria or J mtDNA mitochondria respond differently to cisplatin treatments suggesting involvement of the retrograde signaling (from mitochondria to nucleus) in the drug-induced cell death. Varying toxicities and transcription levels of the H vs. J cybrids after cisplatin treatment support the hypothesis that mtDNA variants play a role in the expression of genes affecting resistance and side effects of cisplatin

Economic Damages of Wild Pigs in Non-Traditional Areas: From the Fairway to the After Life

Invasive wild pigs are widely known to cause damage to agricultural properties and commodities, but less has been reported about damages to other types of property. A survey was distributed to golf courses and cemeteries across Texas to explore the extent of damage these properties experience. While both property types reported significant damages, golf courses were found to experience more damage than cemeteries. Using average reported costs and predicted county-level damage, total costs for all golf courses and cemeteries across the state were estimated to exceed $1.6 million USD per year

Commute Times, Food Retail Gaps, and Body Mass Index in North Carolina Counties

Introduction: The prevalence of obesity is higher in rural than in urban areas of the United States, for reasons that are not well understood. We examined correlations between percentage of rural residents, commute times, food retail gap per capita, and body mass index (BMI) among North Carolina residents. Methods: We used 2000 census data to determine each county\u27s percentage of rural residents and 1990 and 2000 census data to obtain mean county-level commute times. We obtained county-level food retail gap per capita, defined as the difference between county-level food demand and county-level food sales in 2008, from the North Carolina Department of Commerce, and BMI data from the 2007 North Carolina Behavioral Risk Factor Surveillance System. To examine county-level associations between BMI and percentage of rural residents, commute times, and food retail gap per capita, we used Pearson correlation coefficients. To examine cross-sectional associations between individual-level BMI (n=9,375) and county-level commute times and food retail gap per capita, we used multilevel regression models. Results: The percentage of rural residents was positively correlated with commute times, food retail gaps, and county-level BMI. Individual-level BMI was positively associated with county-level commute times and food retail gaps. Conclusions: Longer commute times and greater retail gaps may contribute to the rural obesity disparity. Future research should examine these relationships longitudinally and should test community-level obesity prevention

Pharmacogenetics and Practice: Tailoring Prescribing for Safety and Effectiveness

The promise of pharmacogenomics testing, to find the right medication at the right dose for the right patient at the right time, sits at the heart of precision medicine. Identifying genetic variants that contribute to inter-patient variability in drug disposition and effect allows clinicians to select a more appropriate medication for a patient’s condition by limiting adverse drug events and maximizing beneficial effects. However, as pharmacogenomics is increasingly integrated into prevention-based healthcare, a major obstacle to effective implementation of pharmacogenomics testing is the lack of adequate knowledge of healthcare providers on interpretation of these test results

Zwitterionic PEG-PC hydrogels modulate the foreign body response in a modulus-dependent manner

Reducing the foreign body response (FBR) to implanted biomaterials will enhance their performance in tissue engineering. Poly(ethylene glycol) (PEG) hydrogels are increasingly popular for this application due to their low cost, ease of use, and the ability to tune their compliance via molecular weight and crosslinking densities. PEG hydrogels can elicit chronic inflammation in vivo, but recent evidence has suggested that extremely hydrophilic, zwitterionic materials and particles can evade the immune system. To combine the advantages of PEG-based hydrogels with the hydrophilicity of zwitterions, we synthesized hydrogels with co-monomers PEG and the zwitterion phosphorylcholine (PC). Recent evidence suggests that stiff hydrogels elicit increased immune cell adhesion to hydrogels, which we attempted to reduce by increasing hydrogel hydrophilicity. Surprisingly, hydrogels with the highest amount of zwitterionic co-monomer elicited the highest FBR we observed. Lowering the hydrogel modulus (165 kPa to 3 kPa), or PC content (20 wt% to 0 wt%), mitigated this effect. A high density of macrophages was found at the surface of implants associated with a high FBR, and mass spectrometry analysis of the proteins adsorbed to these gels implicated extracellular matrix, immune response, and cell adhesion protein categories as drivers of macrophage recruitment to these hydrogels. Overall, we show that modulus regulates macrophage adhesion to zwitterionic-PEG hydrogels, and demonstrate that chemical modifications to hydrogels should be studied in parallel with their physical properties to optimize implant design

Role of p85α in neutrophil extra- and intracellular reactive oxygen species generation

Drug resistance is a growing problem that necessitates new strategies to combat pathogens. Neutrophil phagocytosis and production of intracellular ROS, in particular, has been shown to cooperate with antibiotics in the killing of microbes. This study tested the hypothesis that p85α, the regulatory subunit of PI3K, regulates production of intracellular ROS. Genetic knockout of p85α in mice caused decreased expression of catalytic subunits p110α, p110β, and p110δ, but did not change expression levels of the NADPH oxidase complex subunits p67phox, p47phox, and p40phox. When p85α, p55α, and p50α (all encoded by Pik3r1) were deleted, there was an increase in intracellular ROS with no change in phagocytosis in response to both Fcγ receptor and complement receptor stimulation. Furthermore, the increased intracellular ROS correlated with significantly improved neutrophil killing of both methicillin-susceptible and methicillin-resistant S. aureus. Our findings suggest inhibition of p85α as novel approach to improving the clearance of resistant pathogens

Reduced mouse allergen is associated with epigenetic changes in regulatory genes, but not mouse sensitization, in asthmatic children

Chronic exposure to mouse allergen may contribute greatly to the inner-city asthma burden. We hypothesized that reducing mouse allergen exposure may modulate the immunopathology underlying symptomatic pediatric allergic asthma, and that this occurs through epigenetic regulation. To test this hypothesis, we studied a cohort of mouse sensitized, persistent asthmatic inner-city children undergoing mouse allergen-targeted integrated pest management (IPM) vs education in a randomized controlled intervention trial. We found that decreasing mouse allergen exposure, but not cockroach, was associated with reduced FOXP3 buccal DNA promoter methylation, but this was unrelated to mouse specific IgE production. This finding suggests that the environmental epigenetic regulation of an immunomodulatory gene may occur following changing allergen exposures in some highly exposed cohorts. Given the clinical and public health importance of inner-city pediatric asthma and the potential impact of environmental interventions, further studies will be needed to corroborate changes in epigenetic regulation following changing exposures over time, and determine their impact on asthma morbidity in susceptible children