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Filename: drivers/Session_files_driver.php
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File: /var/www/html/index.php
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Function: require_once
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Filename: Session/Session.php
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File: /var/www/html/index.php
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Function: require_once
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Message: Undefined array key "choices"
Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
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Function: require_once
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 249
Function: _error_handler
File: /var/www/html/index.php
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Function: require_once
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
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Filename: models/Detail_model.php
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Function: strpos
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Function: insertAPISummary
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Function: require_once
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Filename: helpers/my_audit_helper.php
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File: /var/www/html/application/helpers/my_audit_helper.php
Line: 8919
Function: str_replace
File: /var/www/html/application/controllers/Detail.php
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Function: formatAIDetailSummary
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Function: require_once
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Message: Trying to access array offset on value of type null
Filename: controllers/Detail.php
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Line: 256
Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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Function: _error_handler
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Function: _error_handler
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Filename: controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Message: Undefined array key "usage"
Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
Line: 260
Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
File: /var/www/html/index.php
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Filename: controllers/Detail.php
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Backtrace:
File: /var/www/html/application/controllers/Detail.php
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Function: _error_handler
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Function: require_once
Patients with nonalcoholic fatty liver disease/steatohepatitis (NAFLD/NASH) commonly develop atherosclerosis through a mechanism that is not well delineated. These diseases are associated with steatosis, inflammation, oxidative stress, and fibrosis. The role of insulin resistance in their pathogenesis remains controversial. Albumin () mice with the liver-specific null deletion of the carcinoembryonic antigen-related cell adhesion molecule 1 (; alias ) gene display hyperinsulinemia resulting from impaired insulin clearance followed by hepatic insulin resistance, elevated lipogenesis, and ultimately visceral obesity and systemic insulin resistance. We therefore tested whether this mutation causes NAFLD/NASH and atherosclerosis. To this end, mice were propagated on a low-density lipoprotein receptor () background and at 4 months of age were fed a high-cholesterol diet for 2 months. We then assessed the biochemical and histopathologic changes in liver and aortae. mice developed chronic hyperinsulinemia with proatherogenic hypercholesterolemia, a robust proinflammatory state associated with visceral obesity, elevated oxidative stress (reduced NO production), and an increase in plasma and tissue endothelin-1 levels. In parallel, they developed NASH (steatohepatitis, apoptosis, and fibrosis) and atherosclerotic plaque lesions. Mechanistically, hyperinsulinemia caused down-regulation of the insulin receptor followed by inactivation of the insulin receptor substrate 1-protein kinase B-endothelial NO synthase pathway in aortae, lowering the NO level. This also limited CEACAM1 phosphorylation and its sequestration of Shc-transforming protein (Shc), activating the Shc-mitogen-activated protein kinase-nuclear factor kappa B pathway and stimulating endothelin-1 production. Thus, in the presence of proatherogenic dyslipidemia, hyperinsulinemia and hepatic insulin resistance driven by liver-specific deletion of caused metabolic and vascular alterations reminiscent of NASH and atherosclerosis. Altered CEACAM1-dependent hepatic insulin clearance pathways constitute a molecular link between NASH and atherosclerosis.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7603529 | PMC |
http://dx.doi.org/10.1002/hep4.1590 | DOI Listing |
Cell Physiol Biochem
November 2024
Zoology Department, Faculty of Science, Al-Azhar University, Cairo 11884, Egypt.
Background/aims: Gestational Diabetes Mellitus (GDM), a prevalent complication in pregnancy, is characterized by the Diabetes Association as diabetes diagnosed in the second or third trimester, often remaining asymptomatic. This study investigates the intricate effects of Streptozotocin on pregnant rats, unraveling its impact on Gestational Type 2 Diabetes (GTD). The research delves into the potential therapeutic roles of mesenchymal stem cells (MSCs) and olive leaf extract (OLE) in mitigating the consequences of Streptozotocin-induced pancreatic impairment.
View Article and Find Full Text PDFEClinicalMedicine
January 2025
Department of Epidemiology, NHC Key Laboratory for Health Technology Assessment, Fudan University School of Public Health, 138 Yi Xue Yuan Road, Shanghai, 200032, China.
Background: Depression is a severe mental disorder commonly co-morbid with diabetes, but it remains to elucidate whether depression is associated with the risks of a wide range of vascular complications in people with type 2 diabetes mellitus (T2DM) and whether metabolic biomarkers may mediate this pathway.
Methods: We conducted this prospective analysis among the participants of the UK Biobank who were diagnosed with T2DM and free of vascular complications at baseline between March 13, 2006 and September 30, 2010. Major depressive disorder (MDD) was ascertained according to the hospital admission records and self-report of doctor-diagnosed conditions, while the presence of depressive symptoms was assessed using the Patient Health Questionnaire-2.
Biomed Rep
February 2025
Department of Gastroenterology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, P.R. China.
Non-alcoholic fatty liver disease (NAFLD) is common in patients with type 2 diabetes mellitus (T2DM). The present study evaluated the effect of dapagliflozin on the liver fat content in patients with T2DM and NAFLD. The changes in biochemical data and metabolic parameters were analyzed.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
December 2024
Trauma Orthopedics, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China.
As the population ages, the occurrence of osteoporosis is becoming more common. Diabetes mellitus is one of the factors in the development of osteoporosis. Compared with the general population, the incidence of osteoporosis is significantly higher in diabetic patients.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
December 2024
Changzhou Clinical College, Xuzhou Medical University, Changzhou, China.
Objective: This study investigated the associations between non-insulin-based insulin resistance indices (METS-IR, TyG, TG/HDL, and TyG-BMI) and the risk of diabetic nephropathy (DN) in US adults with diabetes mellitus (DM).
Methods: This study was based on the 1999-2018 National Health and Nutrition Examination Survey (NHANES) database and included 6,891 patients with DM for cross-sectional analysis. Multivariate adjusted models and restricted cubic spline (RCS) models were employed to assess the association between the insulin resistance index and the risk of DN.
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