Browsing by Subject "Gastroenterology"
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Item An ethical analysis of endoscopic therapy decision-making in patients with refractory substance use disorder and chronic pancreatitis(Elsevier, 2022) Al-Moussally, Feras; Fogel, Evan L.; Helft, Paul R.; Medicine, School of MedicineItem Artificial intelligence in gastrointestinal endoscopy: a comprehensive review(Hellenic Society of Gastroenterology, 2024) Ali, Hassam; Muzammil, Muhammad Ali; Dahiya, Dushyant Singh; Ali, Farishta; Yasin, Shafay; Hanif, Waqar; Gangwani, Manesh Kumar; Aziz, Muhammad; Khalaf, Muhammad; Basuli, Debargha; Al-Haddad, Mohammad; Medicine, School of MedicineIntegrating artificial intelligence (AI) into gastrointestinal (GI) endoscopy heralds a significant leap forward in managing GI disorders. AI-enabled applications, such as computer-aided detection and computer-aided diagnosis, have significantly advanced GI endoscopy, improving early detection, diagnosis and personalized treatment planning. AI algorithms have shown promise in the analysis of endoscopic data, critical in conditions with traditionally low diagnostic sensitivity, such as indeterminate biliary strictures and pancreatic cancer. Convolutional neural networks can markedly improve the diagnostic process when integrated with cholangioscopy or endoscopic ultrasound, especially in the detection of malignant biliary strictures and cholangiocarcinoma. AI's capacity to analyze complex image data and offer real-time feedback can streamline endoscopic procedures, reduce the need for invasive biopsies, and decrease associated adverse events. However, the clinical implementation of AI faces challenges, including data quality issues and the risk of overfitting, underscoring the need for further research and validation. As the technology matures, AI is poised to become an indispensable tool in the gastroenterologist's arsenal, necessitating the integration of robust, validated AI applications into routine clinical practice. Despite remarkable advances, challenges such as operator-dependent accuracy and the need for intricate examinations persist. This review delves into the transformative role of AI in enhancing endoscopic diagnostic accuracy, particularly highlighting its utility in the early detection and personalized treatment of GI diseases.Item Development of Endoscopy(Elsevier, 2018) DeWitt, John; Van Dam, Jacques; Medicine, School of MedicineItem Distinct histopathological phenotypes of severe alcoholic hepatitis suggest different mechanisms driving liver injury and failure(American Society for Clinical Investigation, 2022) Ma, Jing; Guillot, Adrien; Yang, Zhihong; Mackowiak, Bryan; Hwang, Seonghwan; Park, Ogyi; Peiffer, Brandon J.; Ahmadi, Ali Reza; Melo, Luma; Kusumanchi, Praveen; Huda, Nazmul; Saxena, Romil; He, Yong; Guan, Yukun; Feng, Dechun; Sancho-Bru, Pau; Zang, Mengwei; MacGregor Cameron, Andrew; Bataller, Ramon; Tacke, Frank; Sun, Zhaoli; Liangpunsakul, Suthat; Gao, Bin; Pathology and Laboratory Medicine, School of MedicineIntrahepatic neutrophil infiltration has been implicated in severe alcoholic hepatitis (SAH) pathogenesis; however, the mechanism underlying neutrophil-induced injury in SAH remains obscure. This translational study aims to describe the patterns of intrahepatic neutrophil infiltration and its involvement in SAH pathogenesis. Immunohistochemistry analyses of explanted livers identified two SAH phenotypes despite a similar clinical presentation, one with high intrahepatic neutrophils (Neuhi), but low levels of CD8+ T cells, and vice versa. RNA-Seq analyses demonstrated that neutrophil cytosolic factor 1 (NCF1), a key factor in controlling neutrophilic ROS production, was upregulated and correlated with hepatic inflammation and disease progression. To study specifically the mechanisms related to Neuhi in AH patients and liver injury, we used the mouse model of chronic-plus-binge ethanol feeding and found that myeloid-specific deletion of the Ncf1 gene abolished ethanol-induced hepatic inflammation and steatosis. RNA-Seq analysis and the data from experimental models revealed that neutrophilic NCF1-dependent ROS promoted alcoholic hepatitis (AH) by inhibiting AMP-activated protein kinase (a key regulator of lipid metabolism) and microRNA-223 (a key antiinflammatory and antifibrotic microRNA). In conclusion, two distinct histopathological phenotypes based on liver immune phenotyping are observed in SAH patients, suggesting a separate mechanism driving liver injury and/or failure in these patients.Item Down syndrome mouse models have an abnormal enteric nervous system(American Society for Clinical Investigation, 2019-04-18) Schill, Ellen M.; Wright, Christina M.; Jamil, Alisha; LaCombe, Jonathan M.; Roper, Randall J.; Heuckeroth, Robert O.; Biology, School of ScienceChildren with trisomy 21 (Down syndrome [DS]) have a 130-fold increased incidence of Hirschsprung Disease (HSCR), a developmental defect where the enteric nervous system (ENS) is missing from distal bowel (i.e., distal bowel is aganglionic). Treatment for HSCR is surgical resection of aganglionic bowel, but many children have bowel problems after surgery. Post-surgical problems like enterocolitis and soiling are especially common in children with DS. To determine how trisomy 21 affects ENS development, we evaluated the ENS in two DS mouse models, Ts65Dn and Tc1. These mice are trisomic for many chromosome 21 homologous genes, including Dscam and Dyrk1a, which are hypothesized to contribute to HSCR risk. Ts65Dn and Tc1 mice have normal ENS precursor migration at E12.5 and almost normal myenteric plexus structure as adults. However, Ts65Dn and Tc1 mice have markedly reduced submucosal plexus neuron density throughout the bowel. Surprisingly, the submucosal neuron defect in Ts65Dn mice is not due to excess Dscam or Dyrk1a, since normalizing copy number for these genes does not rescue the defect. These findings suggest the possibility that the high frequency of bowel problems in children with DS and HSCR may occur because of additional unrecognized problems with ENS structure.Item Drug-Induced Liver Injury Module for Medical Students(Association of American Medical Colleges, 2020-07-15) Dilly, Christen K.; Craven, Hannah J.; Molleston, Jean P.; Medicine, School of MedicineIntroduction No published curricula exist to introduce medical students to drug-induced liver injury (DILI). However, DILI is the most common cause of acute liver failure in the US, and drug-drug interactions are tested on the USMLE Step 1. Methods We developed an independent study module to introduce students to DILI. This module consisted of a narrated PowerPoint introduction, a journal article, and four example cases. Students completed the module independently. To evaluate the effectiveness of the activity, exam data and responses to the cases were reviewed, and end-of-course survey data were used. These responses were used to modify questions for clarity and to develop a feedback rubric. Results Mean scores on case-related questions in the module ranged from 44% to 73%. However, mean scores on test questions related to DILI ranged from 61% to 98%. It is possible that students learned from receiving feedback in the form of correct answers to the cases. On course evaluations, 52.4% of students agreed or strongly agreed that the online modules as a group (which included the DILI module) were an effective teaching method. Discussion This module introduces students to DILI and enables them to interact with valuable resources. We hope that modifications will improve the learning experience and effectiveness of the module. Going forward, we plan to collect validity evidence for the feedback rubric and develop an advanced version of the module for gastroenterology fellows.Item Genetic Testing and Counseling in Metabolic Liver Disease: An Interactive Lecture for Medical Students(Association of American Medical Colleges, 2020-10-19) McPheron, Molly A.; Craven, Hannah J.; Molleston, Jean P.; Dilly, Christen K.; Medical and Molecular Genetics, School of MedicineIntroduction Medical students have limited opportunities to learn about current genetic testing. This session provided exposure to different types of testing and the complex issues that physicians may encounter when counseling patients on proper testing and interpreting results. Methods We designed a 1-hour interactive lecture for second-year medical students. We presented an overview of the topic, then applied the concepts to specific disorders and cases. Students were asked to answer questions regarding cases using an audience response system, and we used their responses as the basis for our in-class discussion. This session has been held twice, with 25 students attending in 2018 and 31 students in 2019. The session was also recorded so that additional students not in attendance could watch, and was available to 151 students in 2018 and 333 students in 2019. Results Students answered questions via audience response system. There was a range of 47%–100% of students giving the correct answers in 2018, and 55%–93% in 2019. Exam questions covering genetic counseling issues were answered correctly by 66% and 77% of students in 2018, and 70% and 68% of students in 2019. Discussion This session provided an opportunity for medical students to be exposed to some of the complex ethical and psychosocial issues that may arise with genetic testing for liver disease and to consider how to navigate them. Using an audience response system during the lecture made the session more interactive and allowed the teacher to correct errors and teach based on the responses.Item Idiopathic omental infarction: managed conservatively(BMJ, 2019-03-08) McMillen, Brock; Hekman, Daniel Paul; Nguyen, Michelle Thuy Tien; Grewal, Dennis; Medicine, School of MedicineWe report a case of a 49-year-old woman who presented with acutely worsening episodic abdominal pain. Workup was negative but CT of the abdomen showed right upper quadrant omental fat stranding, suggestive of fat necrosis or infarct. Treatment for the patient was largely supportive with pain management and fluid resuscitation.Item Impact of COVID-19 on gastroenterology fellowship training: a multicenter analysis of endoscopy volumes(Thieme, 2021-09-16) Paleti, Swathi; Sobani, Zain A.; McCarty, Thomas R.; Gutta, Aditya; Gremida, Anas; Shah, Raj; Nutalapati, Venkat; Bazerbachi, Fateh; Jesudoss, Randhir; Amin, Shreya; Okwara, Chinemerem; Kathi, Pradeep Reddy; Ahmed, Ali; Gessel, Luke; Hung, Kenneth; Masoud, Amir; Yu, Jessica; Mony, Shruti; Akshintala, Venkata; Jamil, Laith; Nasereddin, Thayer; Kochhar, Gursimran; Vyas, Neil; Saligram, Shreyas; Garg, Rajat; Sandhu, Dalbir; Benrajab, Karim; Konjeti, Rajesh; Agnihotri, Abhishek; Trivedi, Hirsh; Grunwald, Matthew; Mayer, Ira; Mohanty, Arpan; Rustagi, Tarun; Medicine, School of MedicineAbstract Background and study aims The COVID-19 pandemic has had a profound impact on gastroenterology training programs. We aimed to objectively evaluate procedural training volume and impact of COVID-19 on gastroenterology fellowship programs in the United States. Methods This was a retrospective, multicenter study. Procedure volume data on upper and lower endoscopies performed by gastroenterology fellows was abstracted directly from the electronic medical record. The study period was stratified into 2 time periods: Study Period 1, SP1 (03/15/2020 to 06/30/2020) and Study Period 2, SP2 (07/01/2020 to 12/15/2020). Procedure volumes during SP1 and SP2 were compared to Historic Period 1 (HP1) (03/15/2019 to 06/30/2019) and Historic Period 2 (HP2) (07/01/2019 to 12/15/2019) as historical reference. Results Data from 23 gastroenterology fellowship programs (total procedures = 127,958) with a median of 284 fellows (range 273–289; representing 17.8 % of all trainees in the United States) were collected. Compared to HP1, fellows performed 53.6 % less procedures in SP1 (total volume: 28,808 vs 13,378; mean 105.52 ± 71.94 vs 47.61 ± 41.43 per fellow; P < 0.0001). This reduction was significant across all three training years and for both lower and upper endoscopies (P < 0.0001). However, the reduction in volume was more pronounced for lower endoscopy compared to upper endoscopy [59.03 % (95 % CI: 58.2–59.86) vs 48.75 % (95 % CI: 47.96–49.54); P < 0.0001]. The procedure volume in SP2 returned to near baseline of HP2 (total volume: 42,497 vs 43,275; mean 147.05 ± 96.36 vs 150.78 ± 99.67; P = 0.65). Conclusions Although there was a significant reduction in fellows’ endoscopy volume in the initial stages of the pandemic, adaptive mechanisms have resulted in a return of procedure volume to near baseline without ongoing impact on endoscopy training.Item Loss of miR-29a/b1 promotes inflammation and fibrosis in acute pancreatitis(American Society for Clinical Investigation, 2021-10-08) Dey, Shatovisha; Udari, Lata M.; RiveraHernandez, Primavera; Kwon, Jason J.; Willis, Brandon; Easler, Jeffrey J.; Fogel, Evan L.; Pandol, Stephen; Kota, Janaiah; Medical and Molecular Genetics, School of MedicineMicroRNA-29 (miR-29) is a critical regulator of fibroinflammatory processes in human diseases. In this study, we found a decrease in miR-29a in experimental and human chronic pancreatitis, leading us to investigate the regulatory role of the miR-29a/b1 cluster in acute pancreatitis (AP) utilizing a conditional miR-29a/b1–KO mouse model. miR-29a/b1-sufficient (WT) and -deficient (KO) mice were administered supramaximal caerulein to induce AP and characterized at different time points, utilizing an array of IHC and biochemical analyses for AP parameters. In caerulein-induced WT mice, miR-29a remained dramatically downregulated at injury. Despite high-inflammatory milieu, fibrosis, and parenchymal disarray in the WT mice during early AP, the pancreata fully restored during recovery. miR-29a/b1–KO mice showed significantly greater inflammation, lymphocyte infiltration, macrophage polarization, and ECM deposition, continuing until late recovery with persistent parenchymal disorganization. The increased pancreatic fibrosis was accompanied by enhanced TGFβ1 coupled with persistent αSMA+ PSC activation. Additionally, these mice exhibited higher circulating IL-6 and inflammation in lung parenchyma. Together, this collection of studies indicates that depletion of miR-29a/b1 cluster impacts the fibroinflammatory mechanisms of AP, resulting in (a) aggravated pathogenesis and (b) delayed recovery from the disease, suggesting a protective role of the molecule against AP.