Unmasking the inter-tissue communication networks regarding PGC-1α expression in morbid obesity, will give more insight into its significant role in obesity-induced diseases. PGC1α could potentially represent a future preventive and therapeutic target against obesity-induced disease, probably through enhancing mitochondrial biogenesis and metabolism.
We identified 30 eligible patients with endothelial function assessment pre- and post-ticagrelor cessation (86.7% men, 13.3% with diabetes and 33.3% current smokers; mean age: 63.6±11.5 years). The study's primary endpoint of RHI at Day 5 did not differ significantly compared with RHI at Day 0, 1.69 (1.45-2.23) vs 1.81 (1.59-2.13). ED rate did not differ significantly between Day 5 and Day 0, 40 vs 33.3%, p=0.8, respectively. No differences in RHI or ED rate were observed between Day 2 and Day 0, 1.64 (1.54-2.04) vs 1.8 1(1.59-2.13), p=0.3 and 53.3 vs 33.3%, p=0.2, respectively. In stable CAD patients there is no evidence of deterioration in endothelial function after discontinuing ticagrelor.
Background: Patients with acute severe aortic regurgitation (AR) due to infective endocarditis can progress rapidly from the hemodynamically stable patient to pulmonary edema and cardiogenic shock. We sought to identify patients at risk of decompensation where emergent surgery should be undertaken.
Methods:We identified 90 patients with acute severe AR from the echocardiography laboratory database. Baseline clinical, hemodynamic (heart rate (HR) and blood pressure (BP)), and echocardiographic data including mitral filling, premature mitral valve closure (PMVC), and diastolic mitral regurgitation (DMR) were identified. The primary endpoint was subsequent development of pulmonary edema or severe hemodynamic instability.Results: Patients who met the primary endpoint had a higher HR (98.5 bpm vs 80.5 bpm), lower diastolic BP (54 mm Hg vs 61.5 mm Hg), higher mitral E-wave velocity (113 cm/s vs 83 cm/s), higher E/e′ ratio (12.4 vs 8), higher proportion of DMR (27.8% vs 7.4%), and PMVC (25% vs 9.3%) than patients who did not meet the endpoint. The proportion of patients with the primary endpoint increased as HR increased ((≤81 bpm) 3/30 (10%), (81-94 bpm) 11/31 (35.5%), (≥94 bpm) 22/29 (75.9%), P < .0001) and as the diastolic BP reduced ((≤54 mm Hg) 19/31 (61.3%), (54-63 mm Hg) 12/31 (38.7%), (≥63 mm Hg) 5/28 (17.9%), P = .003). Independent predictors were a higher HR (OR 1.08 (95% CI 1.04-1.13) P = .0003) and DMR (OR 4.71 (95% CI 1.23-18.09), P = .02).
Conclusion:Decompensation in acute severe AR is common. Independent predictors of decompensation are increasing HR(≥94 bpm) and the presence of DMR. Those with these adverse markers should be considered for emergent surgery.
Background:
Estrogen receptor β (ERβ) plays an important role in human metabolism and some of its metabolic
actions are mediated by a positive “cross-talk” with Nuclear Factor of Activated T cells (NFAT) and the key metabolic
transcriptional coregulator Transcriptional Intermediary Factor 2 (TIF2).
Introduction:
Our study is an “in situ” morphological
evaluation of the communication between ERβ, NFAT and TIF2 in morbid obesity. Potential correlations with
clinicopathological parameters and with the presence of diabetes and non-alcoholic fatty liver disease (NAFLD) were also
explored. The aim of the present study was to determine the role of ERβ and NFAT in the underlying pathophysiology of obesity
and related comorbidities. We have investigated the expression of specific proteins using immunochemistry methodologies.
Methods:
Our population consists of 50 morbidly obese patients undergoing planned bariatric surgery, during which biopsies
were taken from visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), skeletal muscle (SM), extramyocellular
adipose tissue (EMAT) and liver and the differential protein expression was evaluated by immunohistochemistry.
Results:
We
demonstrated an extensive intra- and inter-tissue co-expression network, which confirms the tissue-specific and integral role of
each one of the investigated proteins in morbid obesity. Moreover, a beneficial role of ERβ and NFATc1 against NAFLD is
implicated, whereas the distinct roles of TIF2 still remain an enigma.
Conclusions:
We believe that our findings will shed light
on the complex underlying mechanisms and that the investigated biomarkers could represent future targets for the prevention
and therapy of obesity and its comorbidities.
Background:
Obesity is a global epidemic which is associated with several cardiometabolic
comorbidities and is characterized by chronic, low grade systemic inflammation. Numerous biomarkers
have been implicated in the pathophysiology of the disease, including transcription factors and
coregulators. Steroid Receptor Coactivator (SRC)-family represent the master regulators of metabolic
pathways and their dysregulation is strongly associated with numerous metabolic disorders.
Methods:
50 morbidly obese patients participated in the present study. Biopsies were collected from
visceral adipose tissue, subcutaneous adipose tissue, skeletal muscle, extra-myocellular adipose tissue
and liver. We evaluated the differential protein expression of NFATc1, SRC-2/TIF-2, SRC-3/AIB-1
and inflammatory biomarkers CD68 and CD3 by immunohistochemistry. The current study was designed
to determine any correlations between the transcription factor NFATc1 and the SRC coregulators,
as well as any associations with the inflammatory biomarkers.
Results:
We identified SRC-3 as a hepatic NFATc1 coactivator and we demonstrated its possible role
in energy homeostasis and lipid metabolism. Moreover, we revealed a complex and extensive intraand
inter-tissue network among the three main investigated proteins and the inflammatory biomarkers,
suggesting their potential participation in the obesity-induced inflammatory cascade.
Conclusions:
Steroid receptor coactivators are critical regulators of human metabolism with pleiotropic
and tissue-specific actions. We believe that our study will contribute to the better understanding of the
complex multi-tissue interactions that are disrupted in obesity and can therefore lead to numerous cardiometabolic
diseases. Further on, our present findings suggest that SRC-3/AIB-1 could constitute
possible future drug targets.
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