Jennifer Leigh Rodgers Ph.D., Siva Kumar Panguluri Ph.D.
Supplemental 100% oxygen with mechanical ventilation is a standard of care in intensive care units (ICUs). However, this treatment has also been associated with poor outcomes in patients, and increased mortality rates. Our lab utilizes a mouse model in order to study the pathophsyiology of cardiac remodeling in mice due to hyperoxia treatment. This study delineates molecular insights of cardiac remodeling in our clinically relevant mouse model.
This is a retrospective chart review assessing cardiovascular abnormalities in patients with type II diabetes with and without obstructive coronary artery disease.
Donna Mae Pate, B.S., Dr. John Greene, Clarissa Maravilla, Shelby Power, Nichole Guidish
Patients with breast cancer may be at an increased risk for infection due to their immunosuppression. Anywhere from 2-24% of breast cancer patients suffer from infections caused by microorganisms, usually diagnosed following expander related reconstructive surgery. Tissue expander surgeries may develop complications that can often result in extending antibiotic treatment, increasing the rate of drug related complications, and removal of the implant. Deep wounds in immunocompromised patients are primarily caused by gram-negative bacteria. Evaluating the most common bacterial infections due to gram negative etiology, and identifying their susceptibilities may allow clinicians to prevent infections in cancer patients who have received breast reconstructive surgery.
Frank Zamudio, B.A., Shayna Smeltzer, M.S., Nicholas Stewart, Zainuddin Quadri, Ph.D.
Maj-Linda Selenica, Ph.D. This study explores the role of TDP43 in corticospinal neurons of the mouse cortex and during systemic inflammation. Our data support TDP43's neurotoxic effects while also revealing diverse microglial activation and peripheral cell infiltration. Surprisingly, systemic inflammation had an effect on TDP43 AAV mice, but not wild-type mice, also suggesting blood-brain barrier damage. We hypothesize that TDP43 signaling affects the neurovascular unit, leading to BBB permeability, peripheral cell infiltration, and changes in synaptic plasticity. We also expect to further explore the role of systemic inflammation in these processes.
Zainuddin Quadri, PhD, Sheba Sazi, Benjamin Cooper, Frank Zamudio
Maj-Linda B. Selenica, PhD Impairment of synaptic transmission is common in old age including Alzheimer disease. Tau protein helps to stablizes neurons disintegrates and truncated into shorter form known as C3-Tau. We found in our animal model that mice injected with C3-tau have impairment in long term potential and downregulation of few genes related to LTP. Neuritrohin-5 helps to maintane mature and release synaptic vesicle is one of the gene we found to be downregulate in our C3-tau injected mice.
Vetriselvan Manavalan, Andrew Rosenblum, Mayank Kesarwani, Benjamin Olson, Taylor Weber-Utpadel, Chao Ma, Daniel Lee, and Umesh Jinwal
Aggregation of hyperphosphorylated tau (pTau) is one of the major pathological signs of Alzheimer’s disease (AD) and many other neurodegenerative diseases. Tau related diseases are also termed as taopathies. Currently, a few pharmacological interventions are available for these diseases. Here, we are reporting a novel pTau reducing FDA approved drug molecule Hexachlorophene. We used multiple cellular AD models, Human neuroblastoma M17 cell line, HeLaC3 tau overexpressing cell line, HEK280 mutant tau expressing cell line, and mouse N2a Neuro2a tau-GFP expressing cell line to characterize and confirm the effects of Hexachlorophene on pTau. Western blot, Thioflavin-S staining, and Immunofluorescence techniques were used to analyze Hexachlorophene’s effect on tau. 24 hours’ treatment of Hexachlorophene showed reduction in pTau in a dose dependent manner in M17, HeLaC3, HEK280, and N2a AD cellular models. Furthermore, Thioflavin-S staining and Immunofluorescence show reduction in tau upon Hexachlorophene treatment. Overall, our results using cellular models clearly indicate Hexachlorophene as a promising drug for AD and tauopathies treatment.
Andrii Kovalenko BS, Chao Ma MS, Leslie A. Sandusky-Beltran PhD, John Calahatian, Huimin Liang MS, Mani Kallupurackal, Jerry Hunt BS, Kevin Nash PhD, Margaret Fahnestock PhD, Dave Morgan PhD, Paula Bickford PhD, Daniel Lee PhD.
By the middle of the 21st century, 8 billion Americans will be affected by Alzheimer's disease (AD). AD is the most prevalent among the neurodegenerative diseases, collectively called tauopathies. In tauopathies, hyperphosphorylation and aggregation of microtubule-stabilizing protein tau (MAPT) was shown to promote neuronal loss and brain atrophy. Although the research on tau has been conducted for more than a hundred years, the cause and the mechanism of tau pathology was not discovered. Available medical treatments are not capable of reversing the pathology and clearing the neurofibrillary tangles formed by aggregated tau. Barely slowing the progression of the disease and helping patients to cope with the disease and accepting the universally fatal outcome is the best we can do up to date.mTOR pathway is a master regulator of cellular metabolic state. Its inhibition leads to an increase in autophagy (catabolic state) and increased longevity associated with it, as shown in animal models. Thus it's thought to be one of the key modulators of aging and diseases like Alzheimer's for which age is a primary predictor. The great power of the mTOR pathway means that it has to be very tightly regulated. Nutrient availability is its potent regulator. Our research focuses on the availability of arginine, and it's role in the regulation of the mTOR pathway through interaction with CASTOR, a cytosolic nutrient sensor that controls the activation of the mTORC1 complex.
Leslie A. Sandusky-Beltran PhD, Andrii Kovalenko BS, Mallory D. Watler BS, Leenil Noel BS, Jerry B. Hunt, Jr. BS, Devon S. Placides PharmD, Sarah N. Fontaine PhD, Margaret Fahnestock PhD, Maj-Linda B. Selenica PhD, Kevin R. Nash PhD, Marcia N. Gordon PhD, Dave G. Morgan PhD, Daniel C. Lee PhD
Tau stabilizes microtubules; however, in Alzheimer’s disease (AD) and tauopathies, tau becomes hyperphosphorylated, aggregates, and results in neuronal death. Our group recently uncovered a unique interaction between polyamines and tau fate. Polyamines exert an array of physiological effects that support neuronal function and cognitive processing. Specific stimuli can elicit a polyamine stress response (PSR), resulting in altered central polyamine homeostasis. Evidence suggests that elevations in polyamines following a short-term stressor are beneficial; however, persistent stress and subsequent PSR activation may lead to maladaptive polyamine dysregulation, which occurs in numerous disease states, and may contribute to neuropathology and cognitive impairment in AD.
Zainuddin Quadri, Ph.D.,Sheba Saji, M.S., Benjamin Cooper, B.S., Frank Zamudio, B.S.,Maj-Linda B. Selenica, Ph.D
Impairment of synpatic transmission is common in neurodegenerative diseases, including Alzheimer's disease. Tau proteins allow for the stabilization of neurons, and to disintegrate and truncate into shorter forms, referred to as C3-Tau. The animal models in our lab shows that the mice injected with C3-Tau are impaired, and a few genes related to LTP are downregulated. Neurotrophin-5 helps to maintain maturity and releases synpatic vesicles, and is one of the genes that we have identified that would be downregulated in the C3-Tau injected mice.
Currently, limited data exists to describe how pharmacogenomic concepts can be introduced into secondary education.The purpose of this study is to determine if our teaching methods are effective in educating high school students about pharmacogenomics. Additionally, we aimed to produce data that could help schools determine when pharmacogenoic concepts could be implemented into secondary education.
Kristina Dogoda B.S, Amanda Elchynski B.S, Courtney Cantrell B.S
Basic health and nutritional information as well as motivational tips were sent to participants on either a weekly basis over a period of three months or all at once to determine whether there was a correlation between type of motivation and weight loss. Participants were given a survey at the beginning and end of the study that assessed basic demographic information, current weight, medications, and health conditions. The survey also included several assessment questions in order to determine baseline knowledge and if there was a gain in knowledge at the conclusion of the study.
Kyle M. Guerrero, BS, Kristal Urena, BS, Angela S. Garcia, PharmD, MPH, CPh, Radha V. Patel, PharmD, MPH, BCACP, CPh, Daniel Forrister, PharmD, MPH
Our project was to identify a geographic area demonstrating need for asthma interventions. By identifying different factors such as air quality, prevalence, asthma related hospitalizations and emergency department visits, we created a tool to identify and prioritize areas that could benefit from interventions like patient education and certification as an Asthma-Friendly School.
Sharon Baby, B.S., Mindy Huynh, B.S., Kevin B. Sneed, Pharm.D., William N. Kelly, Pharm.D
This proof-of-use, one-year, pilot study will evaluate the impact of enhanced pharmacist care and home telemonitoring on health care utilization and Medicare quality measures. This is a randomized cluster controlled trial (RCT) with three clusters (30 patients/cluster). Patients in the study group cluster will receive enhanced pharmacy care and home telemonitoring services managed by a clinical pharmacist for eight months. The clinical pharmacist will use an enhanced collaborative practice agreement and a clinical monitoring dashboard driven by a virtual integrated patient record. One control group will receive usual clinical pharmacist care and no home telemonitoring, while the other control group will receive neither of these interventions (a virtual control group). Each patient will be studied for eight months. The follow up period for the outcomes of interest will be two months.
This project assesses the efficacy of the neuronal peptide, humanin, in treating the inflammatory pathology that is characteristic of age-related macular degeneration. We have prepared and characterized humanin-loaded chitosan nanoparticles, and have tested their treatment efficacy in vitro using an animal retinal pigment epithelial (ARPE-19) cell line.
