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  1. Book ; Online: Xenobiotics and the Gut Microbiome in Health and Disease

    Pandol, Stephen J. / Li, Zhaoping

    2019  

    Keywords Science: general issues ; Physiology ; Xenobiotics ; Xenobiotic compounds ; gut microbiome
    Size 1 electronic resource (191 pages)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021231156
    ISBN 9782889630820 ; 288963082X
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: Management of chronic pancreatitis.

    Hines, O Joe / Pandol, Stephen J

    BMJ (Clinical research ed.)

    2024  Volume 384, Page(s) e070920

    Abstract: Chronic pancreatitis results from repeated episodes of pancreatic inflammation and associated fibrosis leading to the loss of functional exocrine and endocrine pancreatic function. The disease is manifested by abdominal pain, deterioration in quality of ... ...

    Abstract Chronic pancreatitis results from repeated episodes of pancreatic inflammation and associated fibrosis leading to the loss of functional exocrine and endocrine pancreatic function. The disease is manifested by abdominal pain, deterioration in quality of life, food maldigestion and malabsorption, diabetes, and an increased risk for pancreatic adenocarcinoma. This review summarizes the latest evidence on the diagnosis and management of chronic pancreatitis and its manifestations. In particular, this review discusses advances in understanding of the role of genetic disorders in the mechanisms of the disease and surgical options for patients refractory to medical therapy. Furthermore, clinical trials are under way to develop medical therapeutics.
    MeSH term(s) Humans ; Adenocarcinoma ; Quality of Life ; Pancreatic Neoplasms/diagnosis ; Pancreatic Neoplasms/therapy ; Pancreatitis, Chronic/diagnosis ; Pancreatitis, Chronic/etiology ; Pancreatitis, Chronic/therapy
    Language English
    Publishing date 2024-02-26
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1362901-3
    ISSN 1756-1833 ; 0959-8154 ; 0959-8146 ; 0959-8138 ; 0959-535X ; 1759-2151
    ISSN (online) 1756-1833
    ISSN 0959-8154 ; 0959-8146 ; 0959-8138 ; 0959-535X ; 1759-2151
    DOI 10.1136/bmj-2023-070920
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Serum Phosphate Levels and Alcohol-Induced Pancreatitis.

    Pandol, Stephen J

    Gastroenterology

    2021  Volume 162, Issue 3, Page(s) 995–996

    MeSH term(s) Humans ; Pancreatitis, Alcoholic ; Phosphates/adverse effects
    Chemical Substances Phosphates
    Language English
    Publishing date 2021-11-17
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2021.11.018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Calcium, mitochondria and the initiation of acute pancreatitis.

    Pandol, Stephen J / Gottlieb, Roberta A

    Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.

    2022  Volume 22, Issue 7, Page(s) 838–845

    Abstract: Acute pancreatitis is characterized by necrosis of its parenchymal cells and influx and activation of inflammatory cells that further promote injury and necrosis. This review is intended to discuss the central role of disorders of calcium metabolism and ... ...

    Abstract Acute pancreatitis is characterized by necrosis of its parenchymal cells and influx and activation of inflammatory cells that further promote injury and necrosis. This review is intended to discuss the central role of disorders of calcium metabolism and mitochondrial dysfunction in the mechanism of pancreatitis development. The disorders are placed in context of calcium and mitochondria in physiologic function of the pancreas. Moreover, we discuss potential therapeutics for preventing pathologic calcium signals that injure mitochondria and interventions that promote the removal of injured mitochondria and regenerate new and heathy populations of mitochondria.
    MeSH term(s) Humans ; Pancreatitis/pathology ; Calcium/metabolism ; Acute Disease ; Autophagy ; Mitochondria/metabolism ; Necrosis/pathology
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2022-08-03
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2056680-3
    ISSN 1424-3911 ; 1424-3903
    ISSN (online) 1424-3911
    ISSN 1424-3903
    DOI 10.1016/j.pan.2022.07.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Young-Onset Carcinogenesis - The Potential Impact of Perinatal and Early Life Metabolic Influences on the Epigenome.

    Barreto, Savio George / Pandol, Stephen J

    Frontiers in oncology

    2021  Volume 11, Page(s) 653289

    Abstract: The last decade has witnessed a significant rise in cancers in young adults. This spectrum of solid organ cancers occurring in individuals under the age of 40 years (some reports extending the age-group to <50 years) in whom aetiology of cancer cannot be ...

    Abstract The last decade has witnessed a significant rise in cancers in young adults. This spectrum of solid organ cancers occurring in individuals under the age of 40 years (some reports extending the age-group to <50 years) in whom aetiology of cancer cannot be traced back to pre-existing familial cancer syndromes, is referred to as termed young-, or early- onset cancers. The underlying causes for young-onset carcinogenesis have remained speculative. We recently proposed a hypothesis to explain the causation of this entity. We propose that the risk for young-onset cancer begins in the perinatal period as a result of the exposure of the foetus to stressors, including maternal malnutrition, smoking or alcohol, with the consequent epigenomic events triggered to help the foetus cope/adapt. Exposure to the same stressors, early in the life of that individual, facilitates a re-activation of these 'responses designed to be protective' but ultimately resulting in a loss of regulation at a metabolic and/or genetic level culminating in the evolution of the neoplastic process. In this manuscript, we will provide a rationale for this hypothesis and present evidence to further support it by clarifying the pathways involved, including elucidating a role for Acetyl-CoA and its effect on the epigenome. We present strategies and experimental models that can be used to test the hypothesis. We believe that a concerted effort by experts in different, but complementary fields, such as epidemiology, genetics, and epigenetics united towards the common goal of deciphering the underlying cause for young-onset cancers is the urgent need. Such efforts might serve to prove, or disprove, the presented hypothesis. However, the more important aim is to develop strategies to reverse the disturbing trend of the rise in young-onset cancers.
    Language English
    Publishing date 2021-04-29
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2021.653289
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Consortium for the study of chronic pancreatitis, diabetes, and pancreatic cancer: achievements and future directions.

    Pandol, Stephen J / Forsmark, Chris E

    Current opinion in gastroenterology

    2021  Volume 37, Issue 5, Page(s) 486–490

    Abstract: Purpose of review: To answer several important clinical questions, the Consortium for the study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer (CPDPC) research consortium has established several ongoing clinical cohort studies focused on ... ...

    Abstract Purpose of review: To answer several important clinical questions, the Consortium for the study of Chronic Pancreatitis, Diabetes, and Pancreatic Cancer (CPDPC) research consortium has established several ongoing clinical cohort studies focused on pancreatitis in adults and children, pancreatic cancer, and diabetes associated with pancreatic disease. These will provide a unique resource for clinical and basic science research into these hard-to-treat diseases.
    Recent findings: The cause, natural history, and prognosis of acute relapsing and chronic pancreatitis in adults and children are being delineated. The mechanisms of diabetes associated with chronic pancreatitis, acute pancreatitis, and pancreatic cancer are being defined. The ability to predict the presence of early-stage pancreatic cancer, thought the presence of new-onset diabetes, is being explored as a strategy to improve survival. The CPDPC is now also turning to developing clinically useful biomarkers, and initiating clinical trials in these difficult to treat pancreatic diseases.
    Summary: These large prospective patient cohorts, established and followed up by the CPDPC, provide a unique resource to improve the care of patients of all ages with pancreatitis, and to allow earlier diagnosis of pancreatic cancer.
    MeSH term(s) Acute Disease ; Diabetes Mellitus/diagnosis ; Diabetes Mellitus/therapy ; Early Detection of Cancer ; Humans ; Pancreatic Neoplasms/diagnosis ; Pancreatic Neoplasms/therapy ; Pancreatitis, Chronic/diagnosis ; Pancreatitis, Chronic/etiology ; Pancreatitis, Chronic/therapy ; Prospective Studies
    Language English
    Publishing date 2021-06-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 632571-3
    ISSN 1531-7056 ; 0267-1379
    ISSN (online) 1531-7056
    ISSN 0267-1379
    DOI 10.1097/MOG.0000000000000765
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Diagnostic and Prognostic Biomarkers of Chronic Pancreatitis: A Conceptual Framework Based on the PRoBE Design.

    Yadav, Dhiraj / Conwell, Darwin L / Pandol, Stephen J / Steen, Hanno / Feng, Ziding / Li, Liang

    Gastroenterology

    2024  

    Language English
    Publishing date 2024-02-28
    Publishing country United States
    Document type Journal Article
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2024.02.030
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: The burden of young-onset pancreatic cancer and its risk factors from 1990 to 2019: A systematic analysis of the global burden of disease study 2019.

    Dahia, Simranjeet Singh / Konduru, Laalithya / Pandol, Stephen J / Barreto, Savio George

    Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.

    2023  Volume 24, Issue 1, Page(s) 119–129

    Abstract: Objective: To investigate worldwide incidence, deaths, disability-adjusted life years (DALYs) and risk factors for young-onset pancreatic cancer (YOPC) using the Global Burden of Disease Study 2019-20 data.: Methods: We queried the Global Health Data ...

    Abstract Objective: To investigate worldwide incidence, deaths, disability-adjusted life years (DALYs) and risk factors for young-onset pancreatic cancer (YOPC) using the Global Burden of Disease Study 2019-20 data.
    Methods: We queried the Global Health Data Exchange tool for "pancreatic cancer" and "incidence", "deaths" as the "measure", and "DALYs" as the "cause" for the age group of 15-49 years to determine global, regional, and national trends in the incidence, deaths, and DALYs of YOPC. Sociodemographic index (SDI) was used to evaluate the associations between socioeconomic development and YOPC. Risk factors including smoking, tobacco use, hi2gh body mass index (BMI), and high fasting plasma glucose (FPG) were evaluated, and their attributable burden was estimated.
    Results: Global incidence, death, and DALY rates of YOPC significantly increased from 1990 to 2019 ((0.30 (p = 0.001), 0.25 (p = 0.001), and 11.18 (p = 0.002), respectively). Regions with the highest and lowest incidence, death, and DALY rates of YOPC were Eastern Europe and Central Sub-Saharan Africa, respectively. Incidence, death, and DALY rates increased with increasing age and SDI. Leading risk factors for YOPC in 2019 were smoking and tobacco use. DALYs attributable to smoking and tobacco use decreased from 1990 to 2019, especially in females, while those attributable to high BMI and FPG increased during the same period.
    Conclusions: The global incidence, death and DALY rates of YOPC have significantly increased over 3 decades. Certain regions and nations are witnessing a higher increase in this trend. There is an urgent need for global efforts targeting preventable causes of YOPC.
    MeSH term(s) Female ; Humans ; Adolescent ; Young Adult ; Adult ; Middle Aged ; Global Burden of Disease ; Quality-Adjusted Life Years ; Risk Factors ; Smoking/adverse effects ; Smoking/epidemiology ; Pancreatic Neoplasms/epidemiology ; Pancreatic Neoplasms/etiology ; Global Health
    Language English
    Publishing date 2023-12-22
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2056680-3
    ISSN 1424-3911 ; 1424-3903
    ISSN (online) 1424-3911
    ISSN 1424-3903
    DOI 10.1016/j.pan.2023.12.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Glycogen Synthase Kinase 3β: A True Foe in Pancreatic Cancer.

    Elmadbouh, Omer H M / Pandol, Stephen J / Edderkaoui, Mouad

    International journal of molecular sciences

    2022  Volume 23, Issue 22

    Abstract: Glycogen synthase kinase 3 beta (GSK-3β) is a serine/threonine protein kinase involved in multiple normal and pathological cell functions, including cell signalling and metabolism. GSK-3β is highly expressed in the onset and progression of multiple ... ...

    Abstract Glycogen synthase kinase 3 beta (GSK-3β) is a serine/threonine protein kinase involved in multiple normal and pathological cell functions, including cell signalling and metabolism. GSK-3β is highly expressed in the onset and progression of multiple cancers with strong involvement in the regulation of proliferation, apoptosis, and chemoresistance. Multiple studies showed pro- and anti-cancer roles of GSK-3β creating confusion about the benefit of targeting GSK-3β for treating cancer. In this mini-review, we focus on the role of GSK-3β in pancreatic cancer. We demonstrate that the proposed anti-cancer roles of GSK-3β are not relevant to pancreatic cancer, and we argue why GSK-3β is, indeed, a very promising therapeutic target in pancreatic cancer.
    MeSH term(s) Humans ; Apoptosis/physiology ; Glycogen Synthase Kinase 3 beta/genetics ; Glycogen Synthase Kinase 3 beta/metabolism ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Pancreatic Neoplasms/metabolism ; Signal Transduction ; Pancreatic Neoplasms
    Chemical Substances Glycogen Synthase Kinase 3 beta (EC 2.7.11.1)
    Language English
    Publishing date 2022-11-16
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms232214133
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Editorial: Innovations in Imaging for Early Diagnosis and Monitoring for Patients With Gastrointestinal Cancer.

    Pandol, Stephen J / Tirkes, Temel / Li, Debiao

    Frontiers in oncology

    2022  Volume 12, Page(s) 913387

    Language English
    Publishing date 2022-05-27
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2022.913387
    Database MEDical Literature Analysis and Retrieval System OnLINE

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