Browsing by Author "Li, Shuang"

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    Anti-Ferroptotic Treatment Deteriorates Myocardial Infarction by Inhibiting Angiogenesis and Altering Immune Response
    (MDPI, 2024-06-26) Stairley, Rebecca A.; Trouten, Allison M.; Li, Shuang; Roddy, Patrick L.; DeLeon-Pennell, Kristine Y.; Lee, Kyu-Ho; Sucov, Henry M.; Liu, Chun; Tao, Ge; Pediatrics, School of Medicine
    Mammalian cardiomyocytes have limited regenerative ability. Cardiac disease, such as congenital heart disease and myocardial infarction, causes an initial loss of cardiomyocytes through regulated cell death (RCD). Understanding the mechanisms that govern RCD in the injured myocardium is crucial for developing therapeutics to promote heart regeneration. We previously reported that ferroptosis, a non-apoptotic and iron-dependent form of RCD, is the main contributor to cardiomyocyte death in the injured heart. To investigate the mechanisms underlying the preference for ferroptosis in cardiomyocytes, we examined the effects of anti-ferroptotic reagents in infarcted mouse hearts. The results revealed that the anti-ferroptotic reagent did not improve neonatal heart regeneration, and further compromised the cardiac function of juvenile hearts. On the other hand, ferroptotic cardiomyocytes played a supportive role during wound healing by releasing pro-angiogenic factors. The inhibition of ferroptosis in the regenerating mouse heart altered the immune and angiogenic responses. Our study provides insights into the preference for ferroptosis over other types of RCD in stressed cardiomyocytes, and guidance for designing anti-cell-death therapies for treating heart disease.
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    Characterizing mechanism-based pain phenotypes in patients with chronic pancreatitis: a cross-sectional analysis of the PROspective Evaluation of Chronic Pancreatitis for EpidEmiologic and Translational StuDies
    (Wolters Kluwer, 2023) Saloman, Jami L.; Conwell, Darwin L.; Fogel, Evan; Vege, Santhi Swaroop; Li, Liang; Li, Shuang; Andersen, Dana K.; Fisher, William E.; Forsmark, Christopher E.; Hart, Phil A.; Pandol, Stephen J.; Park, Walter G.; Evans Phillips, Anna; Topazian, Mark; Van Den Eeden, Stephen K.; Serrano, Jose; Yadav, Dhiraj; Consortium for the Study of Chronic Pancreatitis, Diabetes and Pancreatic Cancer; Medicine, School of Medicine
    Pain is common in chronic pancreatitis (CP) and profoundly reduces quality of life (QoL). Multiple underlying mechanisms contribute to a heterogenous pain experience and reduce efficacy of pain management. This study was designed to characterize the distribution of mechanism-based pain phenotypes in painful CP. The data analyzed were collected as part of the PROspective Evaluation of Chronic Pancreatitis for EpidEmiologic and Translational StuDies, an NCI/NIDDK-funded longitudinal study of the natural history of CP. The PROspective Evaluation of Chronic pancreatitis for EpidEmiologic and translational stuDies includes patient-reported outcome (PRO) measures of pain, medication use, global health, and QoL. Of subjects (N = 681) with CP, 80% experienced abdominal pain within the year before enrollment. Subjects who experienced pain in the week before enrollment (N = 391) completed PROMIS Neuropathic and Nociceptive Pain Quality instruments which were then used to classify them by pain type: 40% had nociceptive, 5% had neuropathic-like, and 32% had both types of pain. The prevalence of having both types of pain was higher among women and subjects with diabetes mellitus, whereas nociceptive-only pain was more prevalent among men and those with pancreatic duct stricture. Other factors, including pain medication use and healthcare utilization, did not differ between groups based on pain type. Subjects in the Both group had significantly worse health and QoL scores relative to those with nociceptive-only pain, suggesting that using psychosocial pain surveys may be useful for understanding pain subtypes in patients with CP. Additional research is needed to identify biochemical and biophysical signatures that may associate with and predict responses to mechanism-specific interventions.
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    Joint Adversarial Domain Adaptation
    (ACM, 2019-10) Li, Shuang; Liu, Chi Harold; Xie, Binhui; Su, Limin; Ding, Zhengming; Huang, Gao; Computer Information and Graphics Technology, School of Engineering and Technology
    Domain adaptation aims to transfer the enriched label knowledge from large amounts of source data to unlabeled target data. It has raised significant interest in multimedia analysis. Existing researches mainly focus on learning domain-wise transferable representations via statistical moment matching or adversarial adaptation techniques, while ignoring the class-wise mismatch across domains, resulting in inaccurate distribution alignment. To address this issue, we propose a Joint Adversarial Domain Adaptation (JADA) approach to simultaneously align domain-wise and class-wise distributions across source and target in a unified adversarial learning process. Specifically, JADA attempts to solve two complementary minimax problems jointly. The feature generator aims to not only fool the well-trained domain discriminator to learn domain-invariant features, but also minimize the disagreement between two distinct task-specific classifiers' predictions to synthesize target features near the support of source class-wisely. As a result, the learned transferable features will be equipped with more discriminative structures, and effectively avoid mode collapse. Additionally, JADA enables an efficient end-to-end training manner via a simple back-propagation scheme. Extensive experiments on several real-world cross-domain benchmarks, including VisDA-2017, ImageCLEF, Office-31 and digits, verify that JADA can gain remarkable improvements over other state-of-the-art deep domain adaptation approaches.
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    Serum Biomarkers of Nociceptive and Neuropathic Pain in Chronic Pancreatitis
    (Elsevier, 2023) Saloman, Jami L.; Li, Yan; Stello, Kimberly; Li, Wenhao; Li, Shuang; Evans Phillips, Anna; Hall, Kristen; Fogel, Evan L.; Vege, Santhi Swaroop; Li, Liang; Andersen, Dana K.; Fisher, William E.; Forsmark, Christopher E.; Hart, Phil A.; Pandol, Stephen J.; Park, Walter G.; Topazian, Mark D.; Van Den Eeden, Stephen K.; Serrano, Jose; Conwell, Darwin L.; Yadav, Dhiraj; Consortium for the Study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer (CPDPC); Medicine, School of Medicine
    Debilitating abdominal pain is a common symptom affecting most patients with chronic pancreatitis (CP). There are multiple underlying mechanisms that contribute to CP-related pain, which makes successful treatment difficult. The identification of biomarkers for subtypes of pain could provide viable targets for nonopioid interventions and the development of mechanistic approaches to pain management in CP. Nineteen inflammation- and nociception-associated proteins were measured in serum collected from 358 subjects with definite CP enrolled in PROspective Evaluation of Chronic Pancreatitis for EpidEmiologic and Translational StuDies, a prospective observational study of pancreatitis in US adult subjects. First, serum levels of putative biomarkers were compared between CP subjects with and without pain. Only platelet-derived growth factor B (PDGF-B) stood out, with levels significantly higher in the CP pain group as compared to subjects with no pain. Subjects with pain were then stratified into 4 pain subtypes (Neuropathic, Nociceptive, Mixed, and Unclassified). A comparison of putative biomarker concentration among 5 groups (no pain and 4 pain subtypes) identified unique proteins that were correlated with pain subtypes. Serum transforming growth factor beta 1 (TGFβ1) level was significantly higher in the Nociceptive pain group compared to the No pain group, suggesting that TGFβ1 may be a biomarker for nociceptive pain. The Neuropathic pain only group was too small to detect statistical differences. However, glycoprotein 130 (GP130), a coreceptor for interleukin 6, was significantly higher in the Mixed pain group compared to the groups lacking a neuropathic pain component. These data suggest that GP130 may be a biomarker for neuropathic pain in CP. PERSPECTIVE: Serum TGFβ1 and GP130 may be biomarkers for nociceptive and neuropathic CP pain, respectively. Preclinical data suggest inhibiting TGFβ1 or GP130 reduces CP pain in rodent models, indicating that additional translational and clinical studies may be warranted to develop a precision medicine approach to the management of pain in CP.
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    T1 signal intensity ratio of the pancreas as an imaging biomarker for the staging of chronic pancreatitis
    (Springer, 2022-07-20) Tirkes, Temel; Dasyam, Anil K.; Sham, Zarine K.; Fogel, Evan L.; Vege, Santhi Swaroop; Li, Liang; Li, Shuang; Chang, Stephanie T.; Farinas, Carlos A.; Grajo, Joseph R.; Mawad, Kareem; Takahashi, Naoki; Venkatesh, Sudhakar K.; Wachsman, Ashley; Fisher, William E.; Forsmark , Christopher E.; Hart, Phil A.; Pandol, Stephen J.; Park, Walter G.; Van Den Eeden, Stephen K.; Yang , Yunlong; Topazian, Mark; Andersen, Dana K.; Serrano, Jose; Conwell, Darwin L.; Yadav, Dhiraj; The Consortium for the Study of Chronic Pancreatitis, Diabetes, Pancreatic Cancer (CPDPC); Radiology and Imaging Sciences, School of Medicine
    Purpose Our purpose was to validate the T1 SIR (T1 score) as an imaging biomarker for the staging of CP in a large, multi-institutional, prospective study. Methods The prospective study population included 820 participants enrolled in the PROCEED study from nine clinical centers between June 2017 and December 2021. A radiologist at each institution used a standardized method to measure the T1 signal intensity of the pancreas and the reference organs (spleen, paraspinal muscle, liver), which was used to derive respective T1 scores. Participants were stratified according to the seven mechanistic stages of chronic pancreatitis (MSCP 0–6) based on their clinical history, MRCP, and CT findings. Results The mean pancreas-to-spleen T1 score was 1.30 in participants with chronic abdominal pain, 1.22 in those with acute or recurrent acute pancreatitis, and 1.03 in definite CP. After adjusting for covariates, we observed a linear, progressive decline in the pancreas-to-spleen T1 score with increasing MSCP from 0 to 6. The mean pancreas-to-spleen T1 scores were 1.34 (MSCP 0), 1.27 (MSCP 1), 1.21 (MSCP 2), 1.16 (MSCP 3), 1.18 (MSCP 4), 1.12 (MSCP 5), and 1.05 (MSCP 6) (p < 0.0001). The pancreas-to-liver and pancreas-to-muscle T1 scores showed less linear trends and wider confidence intervals. Conclusion The T1 score calculated by SIR of the pancreas-to-spleen shows a negative linear correlation with the progression of chronic pancreatitis. It holds promise as a practical imaging biomarker in evaluating disease severity in clinical research and practice.
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    Targeting miR-25 to alleviate DMD-related muscle dysfunction
    (Elsevier, 2024-06-17) Li, Shuang; Han, Renzhi; Pediatrics, School of Medicine