Poster Session Semi-Finalists, Fellows and Medical School Student Projects
(Visit GSEC Poster Session Semi-Finalists, Fellows and Medical School Student Project Posters)
Consequences of thiol oxidative stress on cytosolic proteostasis in yeast Join Meeting
Alec M. Santiago a,b, Kevin A. Morano a
a Department of Microbiology and Molecular Genetics, McGovern Medical School, UTHealth, Houston, TX 77030
b MD Anderson UTHealth Graduate School of Biomedical Sciences, UTHealth, Houston, TX 77030
Neurodegenerative disease affects millions of Americans every year, through diagnoses such as Alzheimer’s, Parkinson’s, and Huntington’s diseases. A core characteristic of these diseases is the presence of misfolded protein aggregates, often linked to decreased motor control and chronic injury to the brain. Although treatments exist, there are currently no cures for neurodegenerative pathologies. One factor linked as a precursor to the formation of these aggregates is damage sustained to proteins by oxidative stress, which can disrupt tertiary structure, causing misfolding. Cellular protein homeostasis (proteostasis) relies on the involvement of chaperone proteins, with the ubiquitous Hsp70 chaperone family playing a prominent role in prevention of aggregates and protection of misfolded protein precursors. Hsp70 activity has been shown to be affected by cysteine modification through oxidizing or thiol-modifying compounds. In the yeast cytosol, Hsp70 isoforms exist either as highly expressed, constitutive forms (Ssa1 and Ssa2) or as stress-inducible forms (Ssa3 and Ssa4). To investigate the biological consequences of cysteine modification on Ssa1, we attempted to generate a strain lacking all four SSA genes and expressing a mutant with aspartic acid substitution at C264 and C303 but were unable to do so, demonstrating that oxidation or modification of these residues may be unsustainable for cellular growth. Cells lacking SSA1 and SSA2 and expressing the same allele were viable but slow-growing, and this strain was utilized to probe the impacts of Ssa1 cysteine modification on Hsp70 biological roles including repression of Hsf1, protein biogenesis and folding, and chaperone-mediated degradation of misfolded proteins. Using an Hsf1-controlled expression reporter, the C264D/C303D SSA1 mutant was shown to constitutively activate Hsf1 and elevate expression of downstream stress-related genes. Luciferase activity assays revealed a reduced capacity to correctly fold the nascent reporter protein FFL-GFP, and to refold FFL-GFP after heat-induced misfolding. Ongoing cycloheximide chase experiments suggest significant deficiency in Ssa1-dependent degradation of chronically misfolded proteins. Taken together, these experiments demonstrate that modeling cysteine modification in the constitutive cytosolic chaperone Ssa1 results in a significant impact on several of its roles in proteostasis. Future experiments will examine the ability of modified Ssa1 to bind, hydrolyze, and release nucleotide in vitro to assess the potential biochemical causes of the in vivo deficiencies. Understanding how oxidation affects not only proteins, but also the protective systems that prevent and manage insults to proteostasis increases our ability to comprehend the complex disease state surrounding neurodegenerative disorders and more effectively treat them.
Angiogenic Gene Networks are Dysregulated in Postmortem Brain of Opioid Use Disorder Subjects: Evidence from Multi-Omics and Imaging Approaches Join Meeting
Emily Mendez1, Haichao Wei2, Ruifeng Hu3, Laura Stertz1, Gabriel R. Fries1,3, Xizi Xu2, Katherine Najera1, Christie Lincoln4, Joo-won Kim4, Karla Moriel1, Thomas Meyer1, Zhongming Zhao1,3, Junqian Xu4, Jiaqian Wu2, Consuelo Walss-Bass1
1Louis A. Faillace, MD, Department of Psychiatry and Behavioral Sciences, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA; 2Institute of Molecular Medicine for the Prevention of Human Diseases, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA; 3Center for Precision Health, School of Biomedical Informatics, University of Texas Health Science Center at Houston, Houston, TX, USA; 4Department of Radiology, Baylor College of Medicine, Houston, TX, USA
Opioid use disorder (OUD) is a public health crisis in the U.S. that causes over 50 thousand deaths annually due to overdose. Therefore, understanding the molecular effects of OUD is critical in this time of widespread opioid use. We used next-generation RNA sequencing and proteomics techniques to test the hypothesis that OUD causes differential regulation of gene networks in dorsolateral prefrontal cortex (Brodmann Area 9, or BA9) of human brain. We identified 394 differentially expressed (DE) coding and long noncoding (lnc) RNAs as well as 213 DE proteins in BA 9 of OUD subjects. The RNA and protein changes converged on pro-angiogenic gene networks and cytokine signaling pathways. Four genes (LGALS3, SLC2A1, PCLD1, VAMP1) were dysregulated in both RNA and protein. Dissecting these DE genes and networks, we found cell type specific effects with enrichment in astrocyte and endothelial correlated genes. Weighted-genome correlation network analysis (WGCNA) revealed cell type correlated networks including an astrocytic/endothelial network involved in angiogenic cytokine signaling as well as a neuronal network involved in synaptic vesicle formation. In addition, using an innovative ex vivo imaging approach, we identified increased vascularization in postmortem brains from subjects with OUD. This is the first study of its kind relating dysregulation of astrocytic and endothelial angiogenic gene networks in OUD with imaging evidence of hypervascularization in postmortem brain.
Integrative analysis of molecular networks and genomic information evaluates disease-gene relevance in Alzheimer’s Disorder Join Meeting
Yashwanth Lagisetty1,2, Thomas Bourquard2, Kwanghyuk Lee2, Carl Grant Mangleburg2, Edgar T. Walters1, Olivier Lichtarge2,3
1Department of Biology and Pharmacology, UTHealth McGovern Medical School, Houston, TX; 2Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX; 3Computational & Integrative Biomedical Research Center, Baylor College of Medicine, Houston, TX
Alzheimer disease (AD) is the leading cause of dementia worldwide and it is characterized by a plethora of debilitating neurological dysfunctions. Despite having an estimated genetic heritability of close to 80%, only a small fraction of this is explained by Genome Wide Association Studies (GWAS) loci. It is thought a large portion of this missing heritability may arise from gene-gene/protein-protein interactions. In this study, we develop an approach which exploits this hypothesis and assess the relevance of genes in disease pathology through a protein-protein interaction network (PPIN).
Our approach, GeneEMBED (gene embedding based detection of disease-relevant genes) first consolidates functional impact scores of all single nucleotide variant (SNV) in a given set of SNVs to calculate a gene level impact score per study participant. Edge weights of a PPIN are then calculated as a function of the impact scores of the constituent genes, producing personalized PPINs for each study participant which reflects their genomic information. To consolidate signal, personalized PPINs of study participants are averaged to generate one network representing cases and another representing controls. Finally, the GraphWave algorithm is used to calculate node embeddings for each gene in both case and control networks and quantitatively examine the difference in embeddings.
To demonstrate feasibility of our approach, we analyzed whole exome sequences for 2,729 AD individuals and 2,440 controls from the Alzheimer Disease Sequencing Project (ADSP)–Discovery phase, and separately 481 AD individuals and 488 controls from the ADSP-Extension phase. Using STRINGv10 as our PPIN we performed GeneEMBED on these cohorts and compared identified genes against those identified by commonly used methods, MAGMA and GWAS. For both cohorts, gene sets identified by GeneEMBED showed significant recovery of known AD genes (p~0.047-3.19e-6). They also demonstrated more interactive relatedness to known AD genes (AUC~0.74-0.83, z-score ~3.19-3.99) than genes identified by MAGMA and GWAS. Strikingly, in both cohorts genes identified by GeneEMBED were significantly enriched in genes that were differentially expressed in post-mortem brain tissue of AD individuals vs control (p~0.037, p~4.1e-7), while genes identified by MAGMA and GWAS were not. This suggests GeneEMBED can consistently identify genes relevant to disease pathology across ‘-omic’ modalities. We further found between the two gene sets identified by GeneEMBED 16 genes overlapped (p~1.92e-14), eight of which demonstrated abnormal neurological phenotypes in Mouse Genome Informatics database (~53%, p~0.021), and further five (LGALS3, CSF1R, REST, FRZB, PLEC) had significant differential expression in RNA data. Lastly, we tested GeneEMBED with other networks and found similarly robust recovery of known AD genes (p~0.036) and functional relatedness to known AD genes (AUC~0.76-0.69,z-score~2.67-7.30), suggesting GeneEMBED may be used with any kind of network.
Our results identify several novel genes previously unidentified by other methods that may serve as potential AD therapeutic targets. Unlike other methods, the disease relevance of genes identified by GeneEMBED is not limited to genetic association but also shows disease association in other data modalities. These findings highlight the notable capability of GeneEMBED to identify disease-relevant genes, suggesting its utility in other complex genetic diseases.
Cutaneous and Musculoskeletal Findings in Adolescents and Young Adults with Orthostatic Intolerance Join Meeting
Caroline T. Starling, BSA1, Eugenio Galindo, MD2, Ian J. Butler, MB.BS3, Mohammed T. Numan, MD3, Syed S. Hashmi, MD, MPH, PhD3, Adelaide A. Hebert, MD2,3
Affiliations: 1UTHealth McGovern Medical School, Houston, TX, USA, 2Department of Dermatology, UTHealth McGovern Medical School, Houston, TX, USA, 3Department of Pediatrics, UTHealth McGovern Medical School, Houston, TX, USA
Introduction: Orthostatic intolerance (OI) is common in children, adolescents, and young adults and may present with syncope or nonspecific signs such as lightheadedness, fatigue, or tachycardia. Cutaneous manifestations of orthostatic intolerance have been described in smaller groups of patients with postural orthostatic tachycardia syndrome ranging from 20-100 patients; joint hypermobility is often associated with OI as well. Due to the variability in symptoms experienced by patients with OI, many patients have delays in receiving a correct diagnosis up to 6 years. The purpose of this study is to estimate the prevalence of cutaneous and musculoskeletal symptoms in a large patient cohort with orthostatic intolerance and to increase providers’ awareness of these manifestations.
Methods: This study is a retrospective review of data derived from 576 questionnaires administered to patients at the UTHealth Dysautonomia Center between 2012 to 2017. Patient responses regarding symptoms they experience were classified into three categories: 1) “Never or almost never,” 2) “Occasionally,” and 3) “Frequently.” Data input and analysis were performed using Microsoft Excel and SAS. The study was approved by UTHealth Institutional Review Board (HSC-18-1034).
Results: Patients aged 10 years to 40 years of age were included in the analysis. Overall, cutaneous and musculoskeletal manifestations were highly prevalent in this population of patients with orthostatic intolerance, with 92% and 87% of patients reporting at least one cutaneous or musculoskeletal manifestation, respectively. Among the cutaneous symptoms, facial pallor was the most common, reported by 360 patients, occurring occasionally or frequently. For the musculoskeletal symptoms, weakness was most common, reported by 430 patients, occurring occasionally or frequently. Patients between 31-40 years of age experienced symptoms more frequently compared to younger patients. The prevalence of these symptoms was much higher in this cohort of patients with OI compared to the general population.
Conclusions and Discussion: Cutaneous and musculoskeletal manifestations of orthostatic intolerance, including pallor, heat/cold intolerance, and weakness were common and occurred frequently. This study helps further characterize the symptomatology experienced by patients with OI, which ultimately can help healthcare providers recognize the condition sooner and decrease the delay in diagnosis.
Laparoscopic hiatal hernia repair as same day surgery: Feasibility, short-term outcomes and costs Join Meeting
Rigoberto Gutierrez1, Colleen O’Neill1, Anshu Khanna1, Andre Miller2, Farzaneh Banki MD1,2
Department of Surgery at McGovern Medical School at the University of Texas Health Science Center at Houston (UTHealth), Houston, TX, United States1, Memorial Hermann Southeast Esophageal Disease Center, Houston, TX, United States2
Background: Laparoscopic hiatal hernia repair is commonly performed with 1 night hospitalization. The aim was to assess repairs as same-day-surgery (SDS).
Methods: Costs/short-term outcomes of SDS were compared to hospital-stay < 24-h: observation (OBS) and hospital-stay ≥ 24-h: inpatient (INP). Outcomes were assessed by postoperative 30-day ER visits/ readmissions.
Results: There were 262 procedures, excluding 50 re-operative repairs, 212 procedures were included: There were 66 SDS, 65 OBS and 81 INP. SDS vs. OBS: OBS were older, had higher ASA, less type I and more type III and IV hernias. Costs were significantly less in the SDS group with no difference in post-operative ER visits/post-discharge readmissions. SDS vs. INP: INP were older, had higher ASA, less type I and more type III and IV hernias. Costs were significantly less in the SDS group with no difference in post-operative ER visits/post-discharge readmissions.
Conclusion: Laparoscopic hiatal hernia repair can be performed as SDS in majority of elective repairs with good short-term outcomes and reduced cost.
TBK1 inhibition potentiates the efficacy of Axl-targeted therapy in inflammatory breast cancer Join Meeting
Lan Thi Hanh Phi,1,2,3 Naoto T. Ueno, 2,3,* and Xiaoping Wang2,3,*
1The University of Texas MD Anderson Cancer Center UT Health Graduate School of Biomedical Sciences, 2Morgan Welch Inflammatory Breast Cancer Research Program and Clinic, 3Department of Breast Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
* Corresponding authors
Background: Inflammatory breast cancer (IBC) is the most lethal and aggressive form of breast cancer. Currently, there are no FDA-approved targeted therapies for IBC. There is a critical need to establish novel targeted therapy for patients with IBC. Oncogenic receptor tyrosine kinase Axl is a crucial protein that contributes to the aggressiveness of IBC. It promotes IBC cell proliferation, motility, and tumor growth. We have shown that targeting the Axl pathway using TP-0903, an Axl tyrosine kinase inhibitor, inhibited the proliferation, migration, and mammosphere formation of IBC cells and significantly reduced tumor growth of SUM149 and BCX010 in vivo. TP-0903 treatment also reduced the polarization of M2 macrophages, a critical tumor microenvironment (TME) component driving the IBC clinical phenotype and promoting IBC metastasis. These results suggest that Axl is a potential therapeutic target in IBC. To further enhance the efficacy of Axl-targeted therapy for patients with IBC, our group conducted functional genomic, synthetic-lethal kinome pooled siRNA screening and identified TANK-binding kinase 1 (TBK1) as a target whose inhibition might enhance the efficacy of TP-0903 in IBC. TBK1 is a vital serine/threonine-protein kinase regulating innate and adaptive immune response, T cell migration, and anti-tumor immune responses. In the present work, we validated the synergistic effect of targeting Axl and TBK1 in IBC.
Methods: To test the synergistic effect of Axl and TBK1 inhibition in vitro, (1) siRNA-mediated knockdown as functional gene silencing; and (2) TBK1 or Axl inhibitors as a pharmacologic blockade will be used to inhibit the TBK1 or Axl pathway. CTB assay and clonogenic assay were conducted to examine cell proliferation and colony-forming ability, respectively.
Results: TBK1 knocking down in SUM149 cells using two independent TBK1-siRNA only showed a very slight synergistic effect on the suppression of cell proliferation by TP-0903. However, a combination of TP-0903 and TBK1-siRNA significantly decreased the number of colonies, suggesting that TP-0903 was more effective when TBK1 was silenced. Similar to the results obtained from TBK1 silencing, a combination of TBK1 inhibitors (BX795 and CYT387) and TP-0903 treatment significantly reduces cell growth compared to a single treatment. The results were then analyzed using the Compusyn and both BX597 and CYT387, in combination with TP-0903 treatment, which displayed a synergistic effect in SUM149 cells with a combination index (CI) score below 1 (0.4~0.7). Consistently, TBK1 inhibitors also significantly suppressed the colony-forming ability in combination with TP-0903 compared to a single treatment in SUM149 cells.
Conclusion: These data suggested that targeting TBK1 could enhance the sensitivity of IBC cells to TP-0903. This in vivo synergistic effect and the underlying molecular mechanism need to be further investigated. We will also investigate the effect of targeting TBK1 and Axl on IBC TME.
The functional role of GRK3-HDAC2 axis in prostate cancer progression Join Meeting
Samira Naderinezhad 1,2, Wenliang Li 1,2
1 MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences
2 Texas Therapeutics Institute, The Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center at Houston
Prostate cancer (PC) is the second most frequent cancer and the second leading cause of mortality in men in the United States, with only 31% of 5-year survival rate in the advanced stages. Progression to castration resistant prostate cancer (CRPC) is the major cause of prostate cancer death. Neuroendocrine prostate cancer (NEPC), an aggressive CRPC subtype, is responsible for 25% lethal CPRC with no cure. NEPC is characterized by lose of androgen receptor and gain of NE markers. The development of a therapeutic target for this aggressive disease is an urgent and unmet need. However, transformation of CRPC to NEPC is largely unclear. To fill the gap in knowledge, our project is mainly focusing on studying a novel regulatory pathway, i.e., GRK3-HDAC2 axis, which we believe is a missing critical link connecting NE transformation and angiogenesis in PC.
Using RNA-seq and gene set enrichment analysis, we found GRK3 regulates pathways involved in cancer progression, metastasis, and drug resistance. Interestingly, GRK3 suppresses angiogenesis repressor TSP1 and neuroendocrine transcriptional repressor REST (RE-1 silencing transcription factor). We found that HDAC2’s binding to the promoter of REST and TSP1 is significantly increased in NEPC cells, and increased by overexpressing GRK3 in PC cells, suggesting that GRK3 may represses REST and TSP1 through HDAC2. Of note, HDAC2’s interacting with GRK3 has increased in NEPC cells compare to androgen dependent PC cells. Using RNAi and cDNA approach together with novel GRK3-specific inhibitors we recently identified, we will further study the impact of the GRK3-HDAC2 axis on a panel of PC cell lines and PDX models to elucidate its impact on of PC progression to NEPC. Then we will test our hypothesis on NEPC genetically engineered mouse model.
The results of this study could expand our knowledge of PC progression to NEPC and provide druggable targets for patient with CRPC/NEPC.
Speech outcomes of conversion Furlow palatoplasty with and without buccal flap augmentation Join Meeting
Austin Lignieres, Brady Anderson, Oluwatofe Alimi, Alfredo Cepeda, MD, Phuong D. Nguyen, MD1, Matthew R. Greives, MD1
1Division of Plastic Surgery, Department of Surgery, McGovern Medical School at The University of Texas Health Science Center at Houston, Houston, TX, USA
Background/Aims: Velopharyngeal insufficiency (VPI) following primary palatoplasty can result in hypernasality of the voice and may require surgical revision of the palate to address palatal length or function. The conversion Furlow procedure not only improves muscle positioning, but also lengthens the soft palate using a double-opposing Z-plasty technique. Buccal flaps have been described to improve cleft palate repair and can provide additional well-vascularized local tissue to augment palate length. Although previous studies have shown some benefits to using the buccal flap approach with primary Furlow palatoplasty, the effectiveness of buccal flaps with conversion Furlow in secondary management of VPI is unknown.
Methods: A retrospective chart review of consecutive non-randomized patients undergoing revision palatoplasty for VPI after primary straight-line repair from 2014-2020 was performed. VPI was diagnosed in patients by a speech therapist and confirmed with nasoendoscopy. Two cohorts were identified: those who received the conversion Furlow palatoplasty alone (FA) versus those with conversion Furlow with buccal flap(s) (FB), which was initiated in 2018 at our institution. Speech assessments measured pre-operative and at least 3-month post-operative hypernasality and total parameter scores using Universal Parameters for Reporting (UPR). Secondary outcomes, including fistula rates, need for revision surgeries for recurrent VPI, infections, and length of stay, were also examined. Univariate analyses of the data were performed.
Results: Of the 77 patients who underwent revision Furlow palatoplasty for VPI, 21% (n=16) had a repair that incorporated at least one buccal flap. The median age at cleft palate revision surgery was 8.76 years, with patients in the FB group being younger (7.96 years vs 8.97, p=0.337). Four patients (7%) in the FA cohort developed a post-operative fistula of the soft palate (Pittsburgh 2-3), compared to zero patients in the FB cohort. Nine patients (15%) in the FA cohort required additional revision surgery for persistent hypernasality, compared to zero patients in the FB cohort. The average time between revision surgery and most recent assessment of speech for all patients was 1.8 years (range of 3 months–4.8 years). Both cohorts demonstrated a decrease post-operatively in hypernasality (0.82 for the FA group and 0.66 for the FB group) and total parameter scores (3.47 for the FA group and 0.25 for the FB group).
Conclusion/Summary: Our study demonstrates that while there are no significant differences in speech outcomes between these two reconstructive modalities, there are reduced fistula rates and revision surgery rates among patients in which buccal flaps were used. Longer term follow-up will be necessary to determine if these speech results continue to improve with time. This information may be useful for cleft surgeons in choosing appropriate procedures to correct VPI, though a larger cohort or randomized trial would be ideal to determine any true significance.
Yap and Taz are required in neural crest derived heart development Join Meeting
Shannon Erhardt1,2, Xiaolei Zhao1, Mingjie Zheng1, Jun Wang1,2
1Department of Pediatrics, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA
2MD Anderson Cancer Center and UTHealth Graduate School of Biomedical Sciences, The University of Texas, Houston, TX, USA
Congenital Heart Diseases (CHDs), the most common type of birth defect, affect one in every 100 new born babies. Cardiac neural crest cells (cNCCs) are a migratory cell population that make significant contributions to the formation of the heart and great vessel structures, such as the cardiac outflow tract (OFT), cardiac valves, and septum. Here we discovered the pivotal role of the Hippo-Yap pathway in cNCC derived cardiovascular formation. The Hippo-Yap pathway is a fundamental pathway for the regulation of organ size and development, yet its role in cNCCs is largely unknown. Patients with alterations of either Hippo signaling effector Yap or Taz, have common CHDs such as Ventricular Septum Defect (VSD) or Tetralogy of Fallot (TOF). To study the roles of the Hippo-Yap pathway in cNCCs, we generated the conditional knockout (CKO) of Yap and Taz using the neural crest specific Wnt1Cre-SOR driver. The complete deletion of Yap and Taz (Yap-/-; Taz-/- CKO) were lethal at embryonic day (E)10.5 and showed proliferation and apoptotic defects. Yap+/-; Taz-/- CKO mutants did not show obvious phenotypes nor proliferation defects at E10.5, but survived from E14.5 to postnatal week (P)8, with a variety of cardiovascular abnormalities such as abnormal aortic branching, valve defects, VSD, and Double Outlet Right Ventricle (DORV). The collective analysis of Reverse Phase Protein Array (RPPA), Cleavage Under Targets & Release Using Nuclease (CUT&RUN), Assay for Transposase-Accessible Chromatin sequencing (ATAC-seq), Transient Transcriptome sequencing (TT-seq) and RNA-sequencing (RNA-seq) studies have revealed Yap/Taz regulate genes important for different processes and functions of neural crest cells, such as Snail2, Sox9, Twist1, and Zeb1 in migration. We further found that Yap/Taz deficiency impaired migratory abilities of NCCs. Together, we discovered that Yap/Taz play a critical role in proper cNCC derived cardiovascular formation.
The role of telemedicine for forward triage during a pandemic Join Meeting
Elizabeth C. Popp1, Vikas S. Gupta, MD2, Elisa I. Garcia2, Sahar Qashqai, MPH3, Christy Ankrom, MHA4, Tzu-Ching Wu, MD4, and Matthew T. Harting, MD2
1McGovern Medical School at the University of Texas Health Science Center, Houston, TX; 2Department of Pediatric Surgery, McGovern Medical School at the University of Texas Health Science Center and Children’s Memorial Hermann Hospital, Houston, TX; 3UT Physicians, Healthcare Transformation Initiatives, Houston, TX; 4Department of Neurology, McGovern Medical School at the University of Texas Health Science Center and Memorial Hermann Hospital, Houston, TX
Background:
The coronavirus disease 2019 (COVID-19) pandemic has presented an enormous challenge to healthcare systems around the world. Hospitals, clinics, and emergency departments (ED) worldwide face rising numbers of COVID-19 positive patients while simultaneously handling a shortage of medical equipment and personnel. Optimizing access to healthcare while minimizing face-to-face patient encounters is critical to limiting exposures, conserving resources, and preserving health. Forward triage is the process of sorting patients prior to ED presentation and is a critical component of preventing unnecessary encounters and preserving medical resources. The COVID-19 pandemic has created a strong push for the expansion and development of telemedicine, but evidence supporting the use of virtual visits for forward triage of COVID-19 complaints remains limited.
Objective:
We aimed to evaluate the effectiveness of telemedicine as a method of forward triage during the COVID-19 pandemic and assess patient satisfaction with COVID-19 virtual encounters.
Methods:
We performed a retrospective study of all patients with COVID-related virtual visits (InTouch/Teladoc Health) at our center between March and May 2020. Demographic, satisfaction, and clinical information were gathered using a modified, validated telehealth satisfaction questionnaire disseminated via email or telephone using a standardized script. The outcomes of interest were the number of in-person clinical encounters avoided and patient satisfaction with the virtual system. Data were analyzed using Stata.
Results:
Of 580 eligible patients, 179 (31%) responded to the survey. Of the respondents, 65% were female, and the mean age was 34.6 ± 22.3 years old. Symptoms (73%) and possible exposure (22%) were the main reasons cited for pursuing a virtual visit. Cough (44%) and fever (36%) were the most common presenting symptoms. 99 (54%) patients were tested for COVID-19, and 15 (15%) tested positive. For each patient satisfaction question on the survey, a majority of patients rated the experience as “very good” or “excellent” (Figure), and patients were most satisfied with how well their privacy was respected. Of the respondents, 93% said they were likely to use telemedicine again in the future and 94% would encourage others to use telemedicine. Over 81% of patients indicated that, if telehealth was not an option, they would have sought an in-person encounter. Ultimately, only 27% of patients pursued a face-to-face encounter after participating in the virtual visit, representing a 67% reduction in the number of in-person visits for our cohort.
Conclusion:
These results suggest that telemedicine is an effective method for forward triage during the COVID-19 pandemic. Patients were less likely to pursue an in-patient visit after a virtual encounter, and they expressed high satisfaction with the telemedicine process. Although limited to a single center, these findings have the potential to reduce exposures while conserving resources and preserving health.
The Effect of Simulated Patient Death on Participants’ Self-Confidence Join Meeting
Clydell Adams III BS1, Devonne Harris BS1, Hilary Fairbrother MD1
1Department of Emergency Medicine, UTHealth McGovern Medical School, Houston, TX, USA.
Background: The psychosocial effects of high-fidelity simulation are often neglected in many studies. A handful of cases have looked at non-academic outcomes such as anxiety, stress, and emotional responses in the presence of simulated patient death. To the best of our knowledge, only one or two studies have specifically investigated if a student’s self-confidence is significantly altered by simulated patient mortality. This study was designed to establish if there exists a correlation between participant’s self-confidence and simulated patient death.
Objectives: The aim of this project is to determine if the self-confidence, sometimes referred to as self-efficacy, of participants in high fidelity simulation cases is affected by simulated patient death. It is also important for us to determine if the order of simulated patient outcomes (for example, completing a case with a stable patient prior to a case when the patient dies) may alter the participants’ self-confidence. Participant’s demographics and prior educational simulation experiences will also be assessed in the scope of perceived self-confidence.
Methods: This is a prospective observational study including clinical medical students participating in an emergency medicine or ambulatory elective at a large academic institution. Students were randomly divided into two groups and each group completed the same two simulation cases. Group A completed a case with simulated patient death (case 1) first followed by a case in which the patient does not die (case 2). Group B completed the cases in the reverse order. After each case, students completed an anonymous survey of their self-confidence based on a validated confidence scale.
Results: There were 46 participants in this study. The completion rate of paired surveys was 78%. The self-confidence scale (C-scale) ranged from 5 (low self-confidence) to 25 (high self-confidence). The mean C-scale for case 1 and case 2 were 13.2 and 14.9, respectively (p>0.05). The mean C-scale for group A (n=21) and group B (n=18) were 12.2 and 16.0, respectively (p<0.05). The mean C-scale for males and females were 12.5 and 13.9, respectively (p>0.05). The mean C-scale for those with ≤4 simulation experiences (n=10) and those with ≥5 simulation experiences (n=15) is 10.3 and 15.4, respectively (p>0.05).
Conclusions: There was no statistical difference between the C-scales reported in case 1 and 2 which suggests that simulated patient death does not directly impact a learner’s self-confidence. However, a relationship between the order of the cases and self-confidence appears to exist. Learners who first completed the case without death were overall more confident than their counterparts who first completed the case with death. Additionally, there was no statistical difference between the C-scales of males and females; however, a relationship between prior simulation experience and perceived self-confidence exists. Senior learners with 5 or more simulation experiences consistently had higher C-scores, when compared to the junior learners, regardless of which group they were in. Qualitatively, participant’s learning despite reported C-score was not hindered as free text responses, irrespective of cases, highlighted the best part of the simulation was the ending debrief.
Looking for closure – variations in gastroschisis pain management in a level 1 NICU Join Meeting
Rachel L. Bergeson, BS1, Nutan B. Hebballi, BDS, MPH1, Vikas S. Gupta, MD1, Elisa I. Garcia, BSN, RN, CCRP1, Mary T. Austin, MD1, Kuojen Tsao, MD1,3, Eric W. Reynolds, MD, MPH2,3, Linda T. Li, MD1,3
1 Department of Pediatric Surgery, McGovern Medical School at the University of Texas Health Science Center at Houston, Houston, Texas, United States
2 Division of Neonatology, McGovern Medical School at the University of Texas Health Science Center at Houston, Houston, Texas, United States
3 Children’s Memorial Hermann Hospital, Houston, Texas, United States
Introduction: In a prior study, we demonstrated significant variation in the use of opioids for pain management in patients with gastroschisis. To further understand this variation, we evaluated provider’s perceptions of pain and their pain management preferences when managing gastroschisis patients.
Methods: We conducted a cross-sectional survey of providers in the neonatal intensive care unit (NICU) including neonatology faculty, neonatology fellows, NICU nurse practitioners, NICU bedside nurses, and pediatric surgery faculty. The survey depicted four vignettes with different gastroschisis management strategies. Providers rated their impression of infant pain experience and made pain management recommendations at specific times during the treatment course. We used weighted Gwet AC2 kappa statistics (ĸ) to analyze the level of agreement between five groups of providers to assess their agreement on intensity of pain and medication recommendations.
Results: For pain intensity, the overall percentage agreement between the providers varied from 74% to 87.2% with weighted ĸ between 0.59 and 0.82, indicating moderate to almost perfect agreement. Likewise, the overall percentage agreement for medication recommendations among providers ranged from 81.5% to 87.2% with weighted ĸ between 0.71 and 0.80, indicating substantial agreement for all clinical vignettes. Overall, morphine was the most commonly recommended pain medication, followed by acetaminophen.
Conclusions: Providers agree on perceptions of pain experienced by gastroschisis patients and pharmacologic pain management strategy. The reported agreement is at odds with the variation identified in actual practice, and a standardized perioperative pain management protocol may be feasible and beneficial for this patient population.