Jeffrey L. Anderson, MD, FACC, FAHA, Chair 

Jonathan L. Halperin, MD, FACC, FAHA, Chair-Elect 

Nancy M. Albert, PhD, RN, FAHA

Biykem Bozkurt, MD, PhD, FACC, FAHA

Ralph G. Brindis, MD, MPH, MACC

Mark A. Creager, MD, FACC, FAHA[#][1]

Lesley H. Curtis, PhD, FAHA

David DeMets, PhD[#][1]

Robert A

/pdf/2014-aha-acc-hrs-guideline-for-the-management-of-patients-1v8ficsqox.pdf

2014 AHA/ACC/HRS Guideline for the Management of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society

Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis.

Prediction of cardiovascular events and all-cause mortality with arterial stiffness: a systematic review and meta-analysis.

https://www.ecnp.eu/~/media/Files/ecnp/communication/reports/ECNP%20EBC%20Report.pdf

The size and burden of mental disorders and other disorders of the brain in Europe 2010

NAFLD is one of the most important causes of liver disease worldwide and will probably emerge as the leading cause of end-stage liver disease in the coming decades, with the disease affecting both adults and children. The epidemiology and demographic characteristics of NAFLD vary worldwide, usually parallel to the prevalence of obesity, but a substantial proportion of patients are lean. The large number of patients with NAFLD with potential for progressive liver disease creates challenges for screening, as the diagnosis of NASH necessitates invasive liver biopsy. Furthermore, individuals with NAFLD have a high frequency of metabolic comorbidities and could place a growing strain on health-care systems from their need for management. While awaiting the development effective therapies, this disease warrants the attention of primary care physicians, specialists and health policy makers.

/pdf/global-burden-of-nafld-and-nash-trends-predictions-risk-2rbbbzfuoo.pdf

Global burden of NAFLD and NASH: trends, predictions, risk factors and prevention

The Rotterdam study

Effects of high glucose and advanced glycation end products on the expressions of sclerostin and RANKL as well as apoptosis in osteocyte-like MLO-Y4-A2 cells.

Role of Osteoglycin in the Linkage between Muscle and Bone

Diabetes mellitus is known to be associated with osteoporotic fractures through a decrease in osteoblastic bone formation rather than an increase in osteoclastic bone resorption. However, its precise mechanism is unknown, and we examined whether or not high glucose or advanced glycation end products (AGEs), which play key roles in the pathogenesis and complications of diabetes, would affect the osteoblastic differentiation, growth, and apoptosis of mouse stromal ST2 cells. Ten to 200 μg/mL AGE2 or AGE3 alone dose-dependently inhibited the mineralization. AGE2 or AGE3 alone (200 μg/mL) significantly inhibited alkaline phosphatase (ALP) activities as well as the mineralization of the cells (p < 0.01). In contrast, 22 mM glucose alone or in combination with 200 μg/mL AGE2 or AGE3 did not affect these cellular phenotypes. Real-time PCR showed that AGE2 or AGE3 alone (200 μg/mL) significantly decreased mRNA expressions of osteocalcin as well as osterix on day 14 (p < 0.01). Western blot analysis showed that AGE2 or AGE3 alone (200 μg/mL) also decreased the levels of Runx2 and osterix protein expressions on days 7 and 14. AGE2 or AGE3 significantly suppressed cell growth and increased apoptotic cell death in time- and dose-dependent manners (p < 0.01). Moreover, AGE3 alone (200 μg/mL) significantly increased mRNA expression of the receptor for AGEs (RAGE) on days 2 and 3 (p < 0.01). These results suggest that AGE2 and AGE3, but not high glucose, may inhibit the osteoblastic differentiation of stromal cells by decreasing osterix expression and partly by increasing RAGE expression, as well as inhibiting cell growth and increasing cell apoptosis.

Advanced Glycation End Products (AGEs), but not High Glucose, Inhibit the Osteoblastic Differentiation of Mouse Stromal ST2 Cells Through the Suppression of Osterix Expression, and Inhibit Cell Growth and Increasing Cell Apoptosis

Ken-ichiro Tanaka

Papers

The Rotterdam study

Effects of high glucose and advanced glycation end products on the expressions of sclerostin and RANKL as well as apoptosis in osteocyte-like MLO-Y4-A2 cells.

Role of Osteoglycin in the Linkage between Muscle and Bone

Advanced Glycation End Products (AGEs), but not High Glucose, Inhibit the Osteoblastic Differentiation of Mouse Stromal ST2 Cells Through the Suppression of Osterix Expression, and Inhibit Cell Growth and Increasing Cell Apoptosis

Active vitamin D possesses beneficial effects on the interaction between muscle and bone.