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Texas Prenatal Syphilis Screening Policy: Examining Communication within Medical Practices
No full textTexas Prenatal Syphilis Screening Policy: Examining Communication within Medical Practices Authors: Holly DeWitt, Ann T. Chirayil, Idara Akpan, Stacey B. Griner, PhD, MPH Purpose: Congenital Syphilis (CS) is rising in Texas surging 1,000-fold from 2016 to 2022. Congenital syphilis is preventable by diagnosing and treating the mother prior to childbirth or the newborn at birth. To address this problem, the Texas Department of Health and Human Services began requiring additional syphilis testing at delivery in 2019, a change from the previous recommendation of screening twice during pregnancy. However, there were gaps in translation of this policy into practice, potentially related to variable internal networks and communications. Therefore, this study examines the internal networks within clinical settings, including the dissemination of state policy updates to healthcare providers. Methods: We conducted in-depth interviews with prenatal providers (certified nurse midwives [CNMs], physician assistants [Pas], nurse practitioners [NPs], and physicians [DO/MD]; n=18) guided by the Consolidated Framework for Implementation Research (CFIR). The Consolidated Framework for Implementation Research is a metatheory which can guide the identification of contextual barriers to implementation. Interviews with the healthcare providers were conducted via Zoom, audio-recorded, and transcribed. Thematic analysis was conducted in MAXQDA utilizing a priori CFIR constructs and emergent codes. Results: A majority of providers learned about policy changes via clinic staff meetings, communications from hospital administration or clinical managers, and bulletins from their professional organizations, such as the American College of Obstetricians and Gynecologists. Additional sources of information were word of mouth through colleagues and emails from the Centers for Disease Control and Prevention. Conclusion: By identifying the different communication sources used by healthcare providers, more consistent, timely, and effective dissemination of policy changes can be developed. As health policies are created or modified to address public health needs, it is critical to explore implementation strategies that enhance the translation of these policies into clinical practice. This is particularly true for congenital syphilis, which has rapidly increased over the past few years
miRNA mediated mitochondrial function and gene regulation associated with Alzheimer's disease
Full text linkMicroRNAs (miRNAs) are small non-coding RNA molecules that are known to regulate gene expression in their target locations thereby contributing to epigenetic mechanisms associated with disease pathologies. Dysregulation of miRNA activity has been implicated in the pathology of Alzheimer's disease (AD), offering insights into potential biomarkers for early diagnosis and therapeutic targets. Mitochondrial dysfunction and its associated effects (such as oxidative stress) can be seen in early-onset AD. This review critically examines recent findings on mitochondrial-associated miRNAs-including miR-34a, miR-140, miR-455-3p, and miR-1273g-3p-highlighting their roles in mitochondrial bioenergetics, oxidative stress, and synaptic function. We discuss the therapeutic potential of targeting specific miRNAs to restore mitochondrial health and explore their utility as early biomarkers for AD diagnosis. A better understanding of miRNA-mediated mitochondrial regulation may open new avenues for early intervention in AD.The author(s) declare that financial support was received for the research and/or publication of this article. The author acknowledges the financial support from Texas Alzheimer's Research and Care Consortium under the direction of the Texas Council on AD and Related Disorders as well as the Neurobiology of Aging and Alzheimer's Disease Training Grant (NIH-T32 AG 020494) for the stipend during the preparation of this mini review article
Delayed Onset of Oculogyric Crisis following Risperidone Overdose
No full textBackground: Oculogyric crisis (OGC) is a rare dystonic reaction characterized by sustained bilateral and often upward deviation of the eyes, typically associated with dopamine-blocking antipsychotics. While OGC commonly occurs within hours of drug administration, or after an increase in dose, delayed-onset presentations following a single overdose remain unusual. Risperidone, a second-generation antipsychotic, has been implicated in dystonic reactions, though the timing of symptom onset varies. Case Presentation: We present the case of a 23-year-old female with a complex psychiatric history who developed an OGC approximately 24 hours after an intentionally taking 6mg of risperidone in an attempt to overdose. The patient exhibited bilateral fixed upward gaze without altered mental status or other neurological deficits. Our original differential list included OGC, dystonic reaction, stroke, drug toxicity, mysathenia graves electrolyte disturbance neuroleptic malignant syndrome, and extrapyramidal reaction. However, the physical exam showed the patient had intact mentation and no other significant findings besides bilateral ocular muscle involvement. Laboratory evaluation ruled out metabolic, and toxic causes, and an ECG was obtained which showed normal sinus rhythm. Given the history and lack of other findings, delayed onset risperidone-induced OGC was diagnosed. Symptoms resolved promptly with intravenous benztropine, and the patient was transferred to a psychiatric facility for further management without recurrence of symptoms. Conclusions: This case highlights an atypical delayed-onset OGC following a single ingestion of risperidone. Clinicians should recognize that drug-induced dystonias can present beyond the expected timeframe, necessitating a high index of suspicion for accurate diagnosis and prompt treatment to prevent prolonged distress and complications
Utilizing SharePoint as a Central Repository for Clinical Trial Criteria
Full text linkThe study explores the use of SharePoint as a centralized repository for clinical trial eligibility criteria in the Genitourinary (GU) Oncology department at UT Southwestern Medical Center, Dallas, TX, addressing challenges related to inefficient access and fragmented data sources. Surveys conducted via REDCap assessed physicians' experiences before and after SharePoint implementation, with results showing increased satisfaction due to easier access to trial criteria and improved workflows. The findings indicate that despite initial resistance, a centralized system can effectively reduce inefficiencies in clinical research data management and enhance patient care by minimizing enrollment delays
Treatment of a Patellar Osteochondral Defect with Intraosseous Platelet Rich Plasma Performed under Local Anesthesia: A Case Report
No full textBackground: Osteochondral defects are localized damage to joint cartilage, often caused by mechanical trauma, that may also affect the underlying bone. Due to the lack of blood supply to cartilage, repair by the body is usually inadequate hence the need for extraneous intervention. Currently, treatment for symptomatic osteochondral defects of the knee is directed towards surgical intervention. Platelet-rich plasma (PRP), rich in growth factors, shows promise for low-grade defects but remains underexplored for high-grade cases as a non-surgical alternative. Case Presentation: A 17-year-old male high-level basketball player presented with 6 months of left knee pain following a progressive worsening of an acute planting injury. His pain was sharp and localized around the joint line. It was worsened by running and jumping and relieved with rest. He was initially seen by two separate orthopedic surgeons and was diagnosed with a patellofemoral osteochondral defect. Both recommended surgical intervention. He subsequently underwent a trial of physical therapy with minimal improvement. Seeking nonoperative management, he presented to a nonoperative sports medicine specialist. Initial MRI and ultrasound imaging of the left knee demonstrated a grade 4 osteochondral lesion along the superior aspect of the lateral trochlear groove as well as the superomedial patella. Notable physical exam findings were tenderness over the mid-medial joint line and a vastus intermedius trigger point noted on osteopathic structural exam. He had no instability on provocative testing. Through history, physical exam, and imaging review, a diagnosis of a grade 4 osteochondral defect was made. For treatment, ultrasound guided intraosseous and intraarticular PRP injection to the superomedial patella was performed. The procedure was performed with the patient fully conscious using local periosteal anesthesia along with geniculate nerve blocks and lasted approximately one and a half hours from patient arrival to discharge. The patient began physical therapy two weeks post-procedure and was back to full sport activity within one month. Six-weeks following the procedure, the patient reported no swelling or pain following rigorous sport activity, the only significant reported deficit being a minimal loss of strength in that leg. He was released back to full activity at this time. He reported continued improvement on follow up at the 12 and 16 week marks. Conclusion: This case presentation discusses a novel treatment of a grade 4 superomedial patellofemoral osteochondral defect, and chondral wear in the femoral intercondylar notch with intraosseous and intraarticular platelet-rich plasma (PRP) injection. While PRP has yet to be investigated as a potential treatment option for osteochondral injuries of this severity, this case demonstrates how in-office intraosseous PRP may be an effective alternative to invasive surgical management, providing shorter recovery times, and offering a more cost-effective option for patients. Further investigation could support intraosseous PRP as an equally effective alternative to surgery in similar high-grade osteochondral lesions
Hemosoccus Pancreaticus: An Unexpected Complication from Glucagon-Like Peptide Agonism
No full textThe discovery of glucagon-like peptide 1 (GLP-1) agonist medications has changed the way diabetes and morbid obesity is managed. Promising results from studies have propelled these medications to becoming the standard of care for patients. These studies have investigated safety and potential adverse effects. One of the concerning potential side effects includes a risk of pancreatitis. Incidence of pancreatitis associated with GLP-1 medications has been reported to be less than 4%. We present an exceedingly rare case of severe pancreatitis leading to hemosuccus pancreaticus in a patient recently started on lixisentatide medication. Background: GLP-1 agonists are best known for increasing glucose dependent insulin release, a mechanism of endogenous insulin release which had previously been unachieved. They work by stimulating the pancreatic beta cells to produce insulin in response to glucose. They also promote satiety by stimulating GLP-1 receptors and slowing gastric emptying causing decreased appetite. The ELIXA trial was a study that assessed the cardiovascular safety of lixisenatide, a GLP-1 receptor agonist, in 6,068 patients with type 2 diabetes and a recent acute coronary syndrome. The trial found that lixisenatide was equivalent to placebo for major adverse cardiovascular events (MACE) and did not significantly increase the risk of acute pancreatitis or pancreatic cancer. However, concerns remain regarding potential pancreatic complications associated with GLP-1 receptor agonists. A cross-sectional study conducted in February 2024 by Aldhaleei et al. demonstrated that the risk for pancreatitis in patients on GLP-1 agonists was around the 4% mark. While that number may seem low, with more people starting these medications, the incidence is not minimal. Case Presentation: 74-year-old male with a notable history of chronic lymphocytic leukemia, type 2 diabetes, and known multivessel coronary artery disease presented with severe abdominal pain concerning for pancreatitis. Initially, the most common etiologies of pancreatitis were ruled out. Notably, the patient had recently been started on dual-combination injectable glargine with lixisentatide for management of his diabetes. He was not on any anticoagulation or anti-platelet therapy. Approximately a week later, patient presented for initial surgical evaluation of coronary artery bypass grafting (CABG). Preoperative lab studies revealed an exceedingly low hemoglobin, for which he was referred for endoscopic evaluation to rule out obscure gastrointestinal bleeding. A computed tomography angiography imaging study was performed, which demonstrated ampullary hemorrhage but no obvious evidence of pseudoaneurysm(s). Esophagogastroduodenoscopy was then performed, which revealed an adherent clot at the ampulla with continued periampullary oozing Discussion: This case illustrates the potential complications of GLP-1 agonist therapy, particularly in high-risk patients, highlighting the necessity for healthcare providers to be vigilant about monitoring for possible adverse effects associated with these increasingly prescribed medications. While the rate of development may be low, with more people starting these medications, it is important to know that this risk is a potential in anyone, not just patients with pancreatic risk factors. While hemobilia and hemosuccus pancreaticus are even rarer forms of biliary damage caused by GLP-1 agonsits, it is important to realize that the possibility is there
Pulsatile Perfusion Therapy at 0.1 Hz does not affect cardiac function during simulated hemorrhage in humans
No full textBackground: Pulsatile Perfusion Therapy (PPT) is a technique we developed to induce 0.1-Hz hemodynamic oscillations, as a potential treatment for conditions of tissue hypoperfusion. We have shown that PPT via oscillatory lower body negative pressure (LBNP) and bilateral inflatable thigh cuffs (newer method) is associated with protection of stroke volume, attenuated increase in heart rate, and protection of muscle and systemic tissue oxygenation during simulated hemorrhage in humans However, the effects of this new PPT method on cardiac function during simulated hemorrhage remains unknown. We hypothesize that PPT via thigh cuffs will improve cardiac function during simulated hemorrhage induced by LBNP in young and healthy humans. Methods: To simulate hemorrhage, 13 young and healthy human participants (5F, 8M) underwent two LBNP protocols to a chamber pressure of -60 mmHg for up to 10 min each. The two randomized protocols were: (1) PPT: during LBNP, bilateral thigh cuffs were inflated and deflated intermittently every 5-s (10-s cycles, i.e. 0.1-Hz) and (2) control: during LBNP, thigh cuffs were inactive. Beat-to-beat arterial pressure was measured via finger photoplethysmography, and stroke volume (SV) was estimated from this arterial pressure waveform. Heart rate (HR) was monitored using electrocardiography, and rate pressure product (RPP), an index of myocardial oxygen consumption, was calculated as product of HR and systolic arterial pressure. As venous return is known to progressively decrease with the duration of LBNP, “LBNP time” was used as a surrogate for venous return, and cardiac contractility was estimated as the slope of the relationship between SV and LBNP time. Paired t-tests were used to compare changes in SV, HR, RPP, and cardiac contractility (slopes) between PPT and control conditions after the first 5 min of LBNP (“Early LBNP”) and at the end of the LBNP protocol (“End LBNP”). Results: There were no differences in estimated cardiac contractility, or SV, HR, or RPP responses between conditions during either the early or end LBNP time points: Early LBNP: Cardiac contractility: Control slope, -0.11±0.04 ml/s vs. PPT slope, -0.10±0.04 ml/s; p=0.33. ∆SV: Control, -32.0±12.0 ml vs. PPT, -30.4±12.4 ml; p=0.33. ∆HR: Control, 25.0±10.3 beats/min vs. PPT, 22.0±17.3 beats/min; p=0.50. ∆RPP: Control, 1517±1087 mmHg*bpm vs. PPT: 1225±1528 mmHg*bpm; p=0.50. End LBNP: Cardiac contractility: Control slope, -0.07±0.03 ml/s vs. PPT slope, -0.06±0.03 ml/s; p=0.16. ∆SV: Control, -32.7±12.3 ml vs. PPT: -31.1±13.9 ml; p=0.48. ∆HR: Control, 28.1±13.0 beats/min vs. PPT, 23.4±16.9 beats/min; p=0.25. ∆RPP: Control, 1182±1470 mmHg*bpm vs. PPT, 924±1420 mmHg*bpm; p=0.58 Conclusion: Contrary to our hypothesis, cardiac function was not affected by PPT during simulated hemorrhage, either during early or end time points of the protocol. These findings are limited by the indirect assessment of cardiac contractility, stroke volume, and myocardial workload and oxygen demand. Future studies with gold standard and more direct methods of assessment, such as echocardiography, are needed to further investigate the effect of PPT on cardiac function in humans
Outcomes of Patients with Esophageal and Gastric carcinomas at a Safety-Net Healthcare System
No full textBackground: Outcomes for esophageal squamous (ES), esophageal (EA) and gastric adenocarcinomas (G) are poor except for those patients whose cancers are diagnosed at a very early stage. Prior studies in the real-world setting have demonstrated that only 76% of patients with advanced upper gastrointestinal (GI) adenocarcinomas received first line systemic therapy. Unique socioeconomic factors may result in worse outcomes in the safety-net setting given that these patients (pts) often seek care later in the disease course, complicating candidacy for therapy due to poor nutritional status or performance status. Methods: Pts diagnosed with ES, EA, G at John Peter Smith Health Network (JPS) in Fort Worth, Texas from January 1, 2018, to December 31, 2022, were identified in the tumor registry database. Gastroesophageal junction adenocarcinomas were grouped under EA or G based on clinical notes. Epic EHR was queried for pathology variables and to verify survival. Kaplan Meier curve was used to assess the difference in survival time across cancer stages from an index date of diagnosis with censoring at date of last contact. The log rank test was then performed to assess the survival distributions across exposures of interest. This study was approved by the North Texas IRB. Results: A total of 171 pts were included: 15 pts were under 40 and the median age was 57 years. 40% were Hispanic, 33% were non-Hispanic (NH) White, and 20% were NH Black. The majority were male (71%) and uninsured (65%). G was the most common primary site (n = 92, 54%), followed by EA (n = 58, 34%) and ES (n = 21, 12%). The majority of patients (n = 125, 73%) were stage 4B. Of these pts, 69 (55%) did not receive any treatment (50 pts went on hospice), 6 received only palliative radiation, the remainder received systemic therapy. One-year survival probability by stage is shown in Table. The overall log-rank test showed a statistical difference between the survival curves (p < .0001). Stage 4B was stratified by receipt of treatment. Of note, in patients with 4B the median overall survival for patients with treatment was 7.6 months (95% CI: (6.1-10), compared to 2.0 months (95% CI: (1.4-3.0) without treatment. Conclusions: In an urban safety-net population of JPS, several concerning trends in upper GI cancers were noteworthy. First, the majority of patients with advanced upper GI cancers did not receive systemic therapy, likely due to advanced stage and symptoms at diagnosis. Second, a concerning proportion of patients were young and Hispanic, highlighting an under-studied population of patients. Finally, outcomes appear worse stage-for-stage than in the previously published literature. Interventions to improve outcomes for these patients must consider their unique socioeconomic needs
APOE epistasis as population specific risk factors for Alzheimer’s Disease outcomes
No full textBackground: Alzheimer’s disease (AD) and AD related dementias (ADRD) have no single identifiable cause but it is understood that many risk factors may interplay to create AD sub-phenotypes. The strongest genetic risk factor for development of AD/ADRD is the presence of the ε4 allele in the apolipoprotein E (APOE) gene, however the allele frequency of ε4 and its impact on cognitive decline can vary significantly across racial/ethnic groups. Vascular disorders (e.g. hypertension or cardiovascular disease) are also strong risk factors for AD/ADRD. A multiethnic cohort study found that controlling for vascular disorders mediated the AD health disparity observed across racial/ethnic groups, suggesting vascular health has a significant influence on cognitive functions and neurodegeneration across these populations. Genetic variants in angiotensin-converting enzyme 2 (ACE2), ACE1, and angiotensinogen (AGT) are risk factors for vascular disorders due to the prominent role they play in the renin-angiotensin-aldosterone system’s (RAAS) regulation of vasculature tone and function. Recent studies suggest a potential interaction between ACE2 & APOE proteins, making ACE2 and other RAAS-mediating genes plausible candidates for epistatic studies connecting vascular disorders and AD/ADRD risks. This study aims to elucidate single nucleotide polymorphisms (SNPs) in genes of the RAAS pathway to identify candidate genes for epistasis studies with APOE. We hypothesize that RAAS genetic loci have population-specific SNPs associated with vascular disease and AD/ADRD, and that these contribute to group differences in AD risk and accelerated neurological dysfunction when found in epistasis with APOE. Methods: We conducted genomic association analysis of individuals enrolled in the Healthy Aging Brain Study-Health Disparities (HABS-HD) to identify RAAS gene variants implicated in vascular disorders within Mexican Americans, Black, and non-Hispanic White populations. Epistasis testing, allele frequency, and genotype distribution analysis was conducted to determine if gene-gene interactions differentially impact comorbidity-based risk for AD/ADRD in high-risk racial/ethnic populations. Results: We identified SNPs in ACE1 and AGT loci as candidates for translational studies on epistasis as a mechanism for differential AD outcomes. For each population, there were unique SNPs associated with different sets of phenotypes associated with AD co-morbidities or cognitive function. Conclusion: This extends an understanding of the interplay between genetic risk factors that differentially contribute to AD outcomes, specifically a co-occurrence of RAAS gene SNPs with APOE. Overall, this research provides promise in elucidating disease comorbidity and gene-gene interactions as a potential consideration for predicting AD risk and supports future mechanistic studies on cellular phenotypes associated with epistatic effects
Survivin as a potential therapeutic target for adjunctive cancer treatment: A literature review
No full textPurpose: Cancer represents a group of diseases characterized by uncontrolled cellular division and the potential to spread throughout the body. Many current cancer treatments lack specificity, targeting all rapidly dividing cells and leading to significant side effects. Survivin, an anti-apoptotic protein, is highly expressed in cancer cells with very low expression in normal adult tissues. It plays a dual role in inhibiting apoptosis and regulating the cell cycle, making it a promising therapeutic target. Additionally, high survivin levels are also associated with resistance to therapy. This literature review is focused on the mechanism of survivin in cancer cells and identifying small-molecules, drugs, and natural compounds that alter its expression levels. By decreasing levels of survivin these compounds offer promising options for combination treatments with standard chemotherapy agents or radiation, resulting in better outcomes with fewer side effects. Method: This literature review utilized various research databases including PubMed, ScienceDirect, Scopus, and Google Scholar to gather information on the role of survivin in cancer and its potential as a drug target. All articles are dated within the past 10 years. This study involved a review of survivin’s role in cancer biology and its impact on apoptosis and cell cycle. A major focus of the review was to summarize drugs and small-molecule compounds known to alter the expression of survivin. Result: Survivin inhibits apoptosis via caspase dependent and independent pathways and regulates the cell cycle by interacting with the mitotic spindle. While not comprehensive, we present a total of 21 compounds (11 pharmaceuticals and 10 naturally occurring compounds) that are able to reduce survivin expression or activity along with the mechanisms by which they achieve this. Conclusion: Survivin plays an important role in cancer progression through its regulation of the cell cycle and apoptosis inhibition, making it a valuable drug target. Various pharmaceutical and naturally occurring agents that decrease levels of survivin when used alongside chemotherapy regimens demonstrated increased anticancer activity and may improve treatment outcomes. This review highlights the need for further research to evaluate the efficacy of targeting survivin in combination with standard therapies, validating its potential for routine use in cancer treatments