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Experimentally Reevaluating Respiratory Contributions to Total Body Heat Loss in Human Thermoregulation: A Pilot Study
No full textThere are generally two anatomical systems in which heat is exchanged between the human body and the surrounding environment: the integument (skin) and the respiratory system. The skin is commonly reported to account for about 90% of total body heat loss to the environment, with respiration contributing the remaining 10%. Yet, variation in ambient air conditions (e.g., temperature, relative humidity) can alter the exact ratio of skin vs. respiratory heat loss. Accordingly, this pilot study sought to experimentally quantify the percentage of heat loss due to respiration under different temperature exposures. Five human volunteers (2 females, 3 males) were exposed to four climatic conditions: room temperature (22°C, 50% relative humidity (RH)), cold-dry (5°C, 80% RH), hot-dry (44°C, 15% RH), and hot-humid (37°C, 85% RH). Each exposure lasted for 45 minutes, with 30 minutes dedicated to collecting metabolic data and 15 minutes for respiratory data. The percentage of respiratory heat losses under the four conditions were assessed using established heat balance equations. Repeated-measures ANOVA revealed statistically significant differences in the percentage of respiratory heat loss between the conditions (p<0.001). Subsequent Tukey-Kramer post-hoc analysis test showed that the percentage of respiratory heat loss was significantly lower in the hot-humid condition compared to room temperature (p=0.001), cold-dry (p=0.007), and hot-dry (p<0.001) conditions. Importantly, these findings suggest that in hot-humid conditions the respiratory system likely still acts as a mechanism for shedding heat, somewhat offsetting a reduced capacity for heat loss through the skin, and thus potentially helping to minimize total heat gain from the environment. Moreover, these results provide evidence of differences in skin vs. respiratory contributions to total heat losses in different climatic conditions, thus underscoring the urgency to reassess conventional models in light of varying environmental conditions
Growing through Connection: The Impact of Peer to Peer Guidance in the Residency Application Process
No full textPurpose: The inherent complexity and nuances involved in the residency application process make it difficult for an academic institution to be able to provide one size fits all advice to their student population. The academic, research, and extracurricular commitments expected by different specialties can lead to varying requirements of students. A need was voiced by the student population for a program to specifically aid in connecting students with resources and mentorship based on similar specialty interests. This mentorship program was developed by the Medical Student Government Association in order to emphasize the value of knowledge and insight that can only be gained from peer to peer connection. Methods: This pilot program was focused on third and fourth year medical students from the Texas College of Osteopathic Medicine (TCOM). The initial interest form was developed for third year medical students to provide input on the top three specialties they were most interested in receiving guidance on in addition to extenuating circumstances that may affect their residency application process. A second form was generated for the fourth year medical students to provide what specialties they felt confident providing mentorship on and how many students they felt they could adequately advise. Third and fourth year students were paired based on their response. Third year students were provided a pre-program survey and a post-program survey utilizing a Likert scale and free response to gain student feedback. Results: Finalized results will be presented at RAD Day 2025 Conclusion: This program emphasized the value of peer to peer mentorship and connection involved in the residency application process. Through our results and student testimonies, we have observed the impact on both personal and professional development through mentorship. We have proved the value to be gained through lived experiences instead of solely standardized resources. Future development of this program will explore artificial intelligence integration and more detailed questionnaires to help ensure compatibility between mentors and mentees
Bridging the Gap: The Role of Advanced Imaging in Diagnosing Late-Stage Disease Among Underserved Emergency Department Populations
No full textNon-small cell lung cancer (NSCLC) represents a significant healthcare challenge, accounting for approximately 85% of all lung cancer cases. As a prevalent and often aggressive malignancy, timely diagnosis and appropriate management are critical for optimizing patient outcomes. While NSCLC is commonly detected in routine healthcare settings, a substantial proportion of cases initially present in emergency departments (EDs) due to acute respiratory symptoms or complications. The ED serves as an essential entry point for these patients, where prompt and accurate diagnosis is paramount for initiating appropriate treatment strategies. Treatment options depend highly on the timeliness of diagnosis and staging of NSCLC, suggesting increased awareness should be encouraged in emergency departments for patients with relevant medical histories and symptoms suggesting potential lung neoplasms. This case in particular examines a 54-year-old male with a 35 pack year smoking history who entered an emergency department with acute onset pleuritic chest pain with dry cough. History showed that the patient did not have a primary care physician, nor did he follow up frequently with his cardiologist. An immediate 12-lead electrocardiogram showed normal rate and rhythm, with myocardial infarction ruled out by troponin values within normal limits. A single frontal view chest X-ray was performed and came up negative for focal pulmonary consolidation, evidence of pneumothorax or pleural effusion, and cardio mediastinal silhouette appearing to be within normal limits. The patient was placed in a room, and albuterol breathing treatments were performed by a respiratory therapist, with moderate relief of symptoms to the patient. Nasopharyngeal swab results were negative for Influenza and COVID-19. Following blood draw, comprehensive metabolic panel results came back with elevated globulin, alkaline phosphatase, and a low A/G ratio. Complete blood count results were within normal limits for all values except low absolute neutrophil count (ANC), atypical lymphocytes, and polychromasia. The Quantitative D-Dimer test came back abnormally high. Following a visit from the emergency physician, the patient was discharged with antibiotics and a suspected bronchitis and/or lower respiratory tract infection. Follow up with the patients Cardiologist led to identification of a 2.2 cm opacity in the patient’s left upper lung lobe with necrotic left hilar/mediastinal adenopathy, suggestive of metastatic primary lung cancer. Subsequent bronchoscopy, PET-CT and Brain MRI led to a definitive diagnosis of Stage IIIa NSCLC and the patient underwent three rounds of immunotherapy and chemotherapy. Follow up PET-CT showed successful treatment of the cancer and the patient is currently in remission. The purpose of this case study is to improve awareness of the demand for modified triage algorithms to assess underlying disease in specific patient populations. Although overutilization of imaging modalities in the ED is a focus when assessing American healthcare spending, it is crucial to identify the ED as an entry point for underserved and undertreated populations who present late in their respective disease course. Current screening guidelines should be applied and utilized holistically for patients presenting with suggestive symptoms, appropriate medical history, and lack of primary care guidance and/or previous screening for lung cancer
Trajectories of Falls and Associated Factors Among Adults 65 and Older: Insights from the Health and Retirement Study
No full textPoster Highlight: College of Public Health, RAD 2025 Award Winning Posters & Oral PresentationsBackground: Falls are a major cause of injury among US adults aged 65 and older, with 14 million (1 in 4), reporting a fall annually. Falls resulted in 80 billion for non-fatal injuries in 2020. One major risk factor for falls is having a history of falls. Understanding risk factors for low fall-risk individuals can guide targeted interventions for this group. This longitudinal cohort study aimed to i) identify distinct trajectories for fall incidence among adults aged 65+ with no prior history of recent falls, and ii) investigate the associations between potential risk factors and fall trajectories. Methods: Data were analyzed from the Health and Retirement Study (HRS) (2006-2018), restricted to non-institutionalized participants aged 65+ with no reported falls two years prior the 2006 baseline. The primary outcome was incidence of first fall during follow-up. Potential risk factors include sociodemographic variables (age, race/ethnicity, sex, and educational attainment), clinical characteristics (self-reported history of cognitive impairment, visual function, body mass index (BMI), and depression), and physical function (difficulty with activities of daily living (ADL)). Group-based trajectory modeling identified distinct fall trajectories and multinomial logistic regression estimated the Odds Ratio (OR) and 95% Confidence Intervals (CI) for associations between risk factors and trajectory groups. Results: Among our sample (n = 5980), three distinct groups were identified over 12 years of follow-up: 55.5% of participants remained in the low-risk fall trajectory group, 25.2% had increasing risk over time, and 19.3% were at and remained in the high-risk trajectory group. Factors associated with remaining in the high-risk fall trajectory group include: being female (OR = 1.15, CI [1.02-1.32]), having ≥ 2 comorbidities (OR = 1.61, CI [1.39-1.87]), being obese (OR = 1.30, CI [1.08-1.58]), having fair or poor vision (OR = 1.23, CI[1.02-1.50]), having difficulty with any ADLs (OR = 1.54, CI[1.24-1.85]), and having high depressive symptoms (OR = 1.44, CI [1.20-1.73]). However, non-Hispanic Black or non-Hispanic Other racial groups were less likely to be in the high-risk fall trajectory group (OR = 0.45, CI [0.36-0.57] and OR = 0.47, CI [0.30-0.73], respectively). Factors associated with being in the increasing risk for falls trajectory group: Being female (OR = 1.16, CI [1.01-1.34]), as did being overweight (OR = 1.18, CI [1.08-1.39]) or obese (OR = 1.33, CI [1.10-1.60]), and having high depressive symptoms (OR = 1.23, CI [1.01-1.49]). Moreover, non-Hispanic Black individuals were less likely to be in the increasing risk for falls trajectory group (OR = 0.68, CI [0.55-0.85]). Discussion: Among older adults without recent fall history, we identified distinct fall trajectories and factors associated with these trajectories. Factors associated with being in high-risk or increasing risk fall trajectory groups include race/ethnicity, gender, comorbidities, being overweight or obese, having poor vision, difficulty with ADLs, or depressive symptoms. Results highlight the need for targeted fall prevention strategies in women and racial minorities and modifiable factors such as improving vision, and better management of weight, comorbidities, or depressive symptoms
Analysis of AT[N] Neuroimaging Outcomes and Mitochondrial Haplogroups in Alzheimer's Disease
No full textPoster Highlight: Texas College of Osteopathic Medicine - Research, RAD 2025 Award Winning Posters & Oral PresentationsPurpose: Alzheimer’s disease (AD) is the most common cause of dementia worldwide, and growing evidence suggests significant disparities in genetic risk factors across different racial/ethnic groups. Previous studies also show that mitochondrial dysfunction is implicated in AD pathology and is associated with increased beta-amyloid plaque production, a hallmark finding of AD. Preliminary research findings link AD risk to certain mitochondrial haplogroups, which are similar combinations of mitochondrial DNA single nucleotide polymorphisms (SNPs) that represent common maternal ancestry. While this association has been studied using non-neuroimaging biomarkers, the relationship between mitochondrial haplogroups and amyloid, tau, and neurodegeneration (AT[N]) neuroimaging outcomes in AD remains unexplored, particularly in a diverse, representative cohort. This study examines associations between mitochondrial genetics and imaging biomarkers, including Amyloid PET, Tau PET, cortical thickness, and white matter hyperintensity in a diverse population of Mexican Americans, African Americans, and non-Hispanic Whites. Methods: Genetic data and neuroimaging data were collected from the Health and Aging Brain Study – Health Disparities (HABS-HD). Mitochondrial DNA was isolated from buffy coat samples and genotyped into mitochondrial SNPs, which were analyzed using Haplogrep3 to generate mitochondrial haplogroups for each participant in each of the three ethnic groups. Covariates included age, sex, education, APOEe4 status, and the first two eigenvectors (EV1 & EV2) of the genetic similarity matrix assessed using principal component analysis. Linear regression models were generated to analyze the relationship between major mitochondrial haplogroups and neuroimaging biomarkers. Results: Our preliminary analyses indicated significant positive and negative associations between specific mitochondrial haplogroups and Amyloid PET accumulation in the Mexican American group. These associations were consistent across various brain regions of interest. Conclusions: These results highlight the value of further investigation into the relationship between mitochondrial genetics and AD risk and progression, especially using AT[N] neuroimaging biomarkers. As additional data from the HABS-HD cohort becomes available, our analysis will expand to include additional neuroimaging and genetic data (including mito-nuclear genetic interactions) from each of the three racial/ethnic groups in our study
A Surprise at Every May-Thurner: A Case Report on Endovascular Stenting in the Setting of a Long Standing Palma Bypass
No full textBackground: May-Thurner syndrome (MTS), or iliac vein compression between the contralateral iliac artery and lumbar vertebrae, is an anatomic variant common in the general population. While most cases are asymptomatic, patients with concomitant hypercoagulable risk factors are more likely to present with deep vein thromboses secondary to MTS. MTS compression obliterates iliac vein morphology, making mechanical thrombectomy alone an insufficient treatment for MTS-related venous obstruction. Percutaneous stenting has replaced the initial vascular surgery interventions that bypassed the affected iliac vein to redirect venous outflow. This case details endovascular iliac vein stenting in a patient with recurrent DVT in the setting of MTS and a long-standing Palma vein graft. Case Information: A 61-year-old male with history of homozygous Factor V Leiden and recurrent deep vein thrombosis (DVT), on Eliquis anticoagulation and testosterone therapy, presented to the emergency department with left lower extremity swelling and pain following a long flight. The patient’s procedural history consisted of a Palma vein graft in his early 20s, permanent inferior vena cava (IVC) filter placement 15 years ago, a left lower extremity fasciotomy, and recent superficial left lower extremity venous ablation. Lower extremity venous duplex ultrasound demonstrated an occlusive DVT in the left common femoral vein, Saphenofemoral junction, and proximal greater saphenous vein. An additional nonocclusive DVT in the left femoral vein was also identified. A computed tomography (CT) abdomen and pelvis study with contrast revealed a stable IVC filter and completely obstructed left external iliac vein. A thrombectomy was scheduled to restore baseline flow. Following ultrasound-guided access into the popliteal vein, fluoroscopic venogram demonstrated patency at the Palma bypass. The left popliteal, special femoral, and profunda femoral veins showed chronic thrombosis with extensive venous collaterals surrounding the obstruction. There was a thrombus in the left common femoral vein, and the left common and external iliac veins were completely occluded. The 0.035” guidewire and diagnostic catheter were advanced past the obstructed left external and common iliac veins into the IVC. The total occlusion in the iliac vasculature then underwent balloon angioplasty with a 4 mm balloon followed by endovascular stenting and post-stent angioplasty with 10 mm and 7 mm balloons. A trail of three 10 mm stents and one 7 mm stent reintroduced central flow to the left lower extremity venous system at the level of the left common femoral vein. The veins inferior to the left iliac stents underwent portal prolonged angioplasty with 7 mm balloon. Thrombectomy utilizing a 7 French catheter and Penumbra system successfully resolved a small thrombus at the left common femoral vein. Procedural venograms demonstrated improved flow from the left lower extremity to the IVC. Conclusion: This patient’s presentation makes a compelling case for additional upstream assessment of DVT through an anatomic lens. While most people with May-Thurner variant anatomy live complication-free, symptomatic patients spend their whole lives with treatments that scratch the surface on the cause of their thromboses. CT assessment of MTS-associated iliac fibrosis in patients with refractory DVT could steer eligible patients towards curative endovascular interventions
Parvovirus B19 Infection Resulting in Fetal Hydrops
Get PDFParvovirus B19 is a virus that commonly infects young children and causes the pathognomonic "slapped cheek" rash along with systemic symptoms such as fever, joint pain, and sore throat. However, infection with parvovirus B19 during pregnancy can result in vertical transmission to the fetus with associated adverse outcomes such as anemia, hydrops fetalis, and, ultimately, fetal loss. This case report illustrates a unique incidence of fetal parvovirus B19 that resulted in severe anemia and hydrops in a fetus with genetically mediated skeletal dysplasia. Due to this comorbidity, this fetus did not undergo therapeutic ultrasound-directed intrauterine transfusion. It is important for clinicians to educate their patients on vertically transmissible viruses and to consider the risks and benefits of guideline-directed treatment options based on unique patient scenarios.University of North Texas Health Science Center at Fort Worth Physician Assistant Progra
Retina-Targeted 17beta-Estradiol by the DHED Prodrug Rescues Visual Function and Actuates Neuroprotective Protein Networks After Optic Nerve Crush in a Rat Model of Surgical Menopause
Get PDFThe association between 17beta-estradiol (E2) deprivation, seen in menopause, and a risk for developing glaucoma has been shown. Thus, exogenous supplementation of E2 may protect against retinal ganglion cell (RGC) degradation and vision loss. Here, we investigated the utility of topical 10beta,17beta-dihydroxyestra-1,4-dien-3-one (DHED), a prodrug of E2 that selectively produces the neuroprotective hormone in the retina, on visual function after optic nerve crush (ONC) and ovariectomy (OVX). We used female Brown Norway rats that underwent either Sham or OVX surgeries. After ONC, OVX animals received DHED or vehicle eye drops for 12 weeks. Visual function, via the optomotor reflex, and retinal thickness, via optical coherence tomography, were followed longitudinally. Afterward, we performed mass spectrometry-based label-free retina proteomics to survey retinal protein interaction networks in our selected animal model and to identify E2-responsive proteins after OVX on neurodegeneration. We found that ONC with OVX caused a significant decline in visual functions that were ameliorated by DHED treatments. Discovery-driven retina proteomics identified numerous proteins associated with neurodegenerative processes due to ONC that were remediated by DHED eye drops. Altogether, our three-pronged phenotypic preclinical evaluation of the topical DHED in the OVX + ONC model of glaucoma reveals the therapeutic potential of the prodrug to prevent visual deficits after glaucomatous retinal injury.This work was supported by the National Eye Institute National Institutes of Health (NIH), Bethesda, MD, USA, grant numbers EY027005 (K.P.-T.), EY030871 and EY035468 (A.J.F.), the Robert A. Welch Foundation (endowment BK-0031 to L.P.) and the Department of Veterans Affairs Rehab R&D Service Career Development Awards to A.J.F. (CDA2; RX002342). A.K. was also supported by the Neurobiology of Aging and Alzheimer's Disease Training Grant (NIH T32 AG020494). G.S.-R. was also supported by the "La Caixa" Foundation fellowship (ID 100010434 and fellowship code LCF/BQ/EU21/11890105). This work was also supported, in part, by a Challenge Grant from Research to Prevent Blindness to the Department of Ophthalmology at Emory University and NIH P30EY06360 (to the Atlanta Vision Research Community)
Alzheimer's disease genetic risk: Top African American risk allele frequencies and genetic architecture among Mexican-, African-, and non-Hispanic White Americans
Get PDFINTRODUCTION: Alzheimer's disease (AD) continues to be the sixth leading cause of death in the United States. Significant efforts are spent researching etiology and potential management strategies. Although minorities face a higher disease burden and are anticipated to make up 43% of the US population by 2060, most literature on inherited AD risk has been derived from studying European ancestry. Here we evaluate frequencies of top AD risk alleles for late-onset AD (LOAD) in African- (AA), Mexican- (MA) and non-Hispanic White (NHW)-American participants enrolled in the Health & Aging Brain Study-Health Disparities (HABS-HD) cohort to determine ethnicity-specific differential genetic architecture. METHODS: Using DNA extracted from this community-based diverse cohort (N = 3207), we calculated the genotype frequencies in each population to determine whether a significant difference is detected among the three populations. DNA genotyping was performed per manufacturer's protocols. Imputation was used for single nucleotide polymorphisms (SNPs) that were not directly genotyped. Statistical analysis was performed using R Studio. RESULTS: Genotype frequencies for 12 out of 15 SNPs (2 apolipoprotein E [APOE] variants, SIPA1L2, PIK3C2G, GPC6, RBFOX1, ABCA7, VRK3, ALCAM, EDEM1, NSG/MSX2, and WDR70) differed significantly between groups. DISCUSSION: This analysis expands on our previous study supporting the notion that genetic risk for AD is heterogeneous across racial and ethnic populations. Our results continue to demonstrate the valuable nature of diversity in genetic risk investigations and suggest the importance of including diverse and underrepresented racial and ethnic populations in medical research. Perhaps the most interesting finding is observed in the SNPs not found to be significantly different between groups, indicating there may be shared pleiotropic gene architecture across ethnicities. HIGHLIGHTS: Alzheimer's disease (AD) burden is rapidly increasing in the United States; minorities are disproportionally affected.We investigate genetic health disparities in our community-based diverse cohort.Twelve of 15 evaluated single nucleotide polymorphisms significantly differ among ethnicities in the Health & Aging Brain Study-Health Disparities.National Institute on Aging; National Institutesof Health, Grant/Award Numbers:R01AG054073, R01AG058533,R01AG070862, T32AG020494,U19AG024904, U19AG078109; CancerPrevention and Research Institute of Texas,Grant/Award Number: #RP1730
Impaired axonal transport contributes to neurodegeneration in a Cre-inducible mouse model of myocilin-associated glaucoma
Get PDFElevation of intraocular pressure (IOP) due to trabecular meshwork (TM) dysfunction, leading to neurodegeneration, is the pathological hallmark of primary open-angle glaucoma (POAG). Impaired axonal transport is an early and critical feature of glaucomatous neurodegeneration. However, a robust mouse model that accurately replicates these human POAG features has been lacking. We report the development and characterization of a new Cre-inducible mouse model expressing a DsRed-tagged Y437H mutant of human myocilin (Tg.CreMYOCY437H). A single intravitreal injection of HAd5-Cre induced selective MYOC expression in the TM, causing TM dysfunction, reducing the outflow facility, and progressively elevating IOP in Tg.CreMYOCY437H mice. Sustained IOP elevation resulted in significant loss of retinal ganglion cells (RGCs) and progressive axonal degeneration in Cre-induced Tg.CreMYOCY437H mice. Notably, impaired anterograde axonal transport was observed at the optic nerve head before RGC degeneration, independent of age, indicating that impaired axonal transport contributes to RGC degeneration in Tg.CreMYOCY437H mice. In contrast, axonal transport remained intact in ocular hypertensive mice injected with microbeads, despite significant RGC loss. Our findings indicate that Cre-inducible Tg.CreMYOCY437H mice replicate all glaucoma phenotypes, providing an ideal model for studying early events of TM dysfunction and neuronal loss in POAG.These studies were supported by the NIH (EY034333, EY028616, and EY026177). The authors acknowledge support from NIH grant EY034238 and an unrestricted grant from Research to Prevent Blindness to the Gavin Herbert Eye Institute at the University of California, Irvine