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European Pancreas Center, Department of General, Visceral and Transplantation Surgery, Heidelberg University Hospital, Heidelberg, Germany
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. Journal of Lipid Research 2016 57 25 – 35 . ( https://doi.org/10.1194/jlr.R060020 ) 8 Barbayianni E Kaffe E Aidinis V Kokotos G . Autotaxin, a secreted lysophospholipase D, as a promising therapeutic target in chronic inflammation and cancer
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necessary for survival, excess aldosterone is associated with inflammation, fibrosis, vascular damage, and end-organ failure and induces vascular dysfunction and remodeling ( 2 ). The incidence of cardiovascular morbidity is higher among patients with PA
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characterized by neck pain, goiter, and systemic inflammation. Some scholars have proposed diagnostic criteria for SAT ( 2 , 3 ). This disease is usually diagnosed according to systemic symptoms, such as acute fever, thyroid pain, and the phenomenon of
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Nuclear Medicine Unit, Department of Medicine – DIMED, University-Hospital of Padova, Padova, Italy
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individuated in the CT after the discovery of pulmonary uptake in the 68 Ga-SSTR-PET/CT. Images of patient 15: (C) false-positive slight uptake (chest wall inflammation) after the first surgery for EAS (more than 12 months before). Images of patient 8: (E) the
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, alcohol abuse or nonalcoholic steatohepatitis. Regardless of the carcinogenic insult, it usually develops in patients with cirrhosis due to chronic inflammation and advanced fibrosis ( 2 ). Growth hormone (GH) is a major regulator of body growth and
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systemic inflammation. NAFLD is associated with a series of complex events. The ‘double-hit’ theory used to be a widely accepted explanation for the etiology of NAFLD ( 27 ). However, mounting evidence has suggested that the pathophysiology of NAFLD is
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develop type 2 diabetes mellitus 10 years after GDM ( 2 , 3 , 4 , 5 ). Women with GDM typically have different levels of insulin resistance and possible chronic low-grade inflammation, which trigger vascular injury and dysfunction and subsequent
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TNF-α and IL-6 release in 3T3-L1 adipocytes Chronic low-grade inflammation plays a major role in the development of insulin resistance. Our previous study found that TNF-α induced insulin resistance in HepG2 cells through activating the IRS-1/AKT
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Internal Medicine, S. Maria delle Croci Hospital, AUSL Romagna, Ravenna, Italy
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Istituto Auxologico Italiano, IRCCS, Obesity Unit - Laboratory of Nutrition and Obesity Research, Department of Endocrine and Metabolic Diseases, Milan, Italy
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phenotype which may be associated with reduced linear growth and even growth arrest ( 43 ). Greater inflammation would cause greater insulin resistance ( 44 ), further exacerbated by the use of steroid drugs. Against this hypothesis, we did not find a
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conditions ( 10 , 28 ). IR can lead to oxidative stress and inflammation, which further contributes to the development of both microangiopathy and macroangiopathy – conditions that impair blood vessel function and can contribute to the progression of LVH