Jonathan Komisar¹, Shubhika Srivastava², Miwa Geiger², John Doucette³, Helen Ko², Jay Shenoy², Rajesh Shenoy²

Congenital Heart Disease, Vol.12, No.1, pp. 67-73, 2017

Abstract Background: Antenatal diagnosis of congenital heart defects (CHD) can impact outcomes in neonates with severe CHD. Obstetric screening guidelines and the indications for fetal echocardiography (FE) have evolved in an attempt to improve the early prenatal detection of CHD. Analyzing yield for specific indications will help clinicians better stratify at-risk pregnancies.
Methods: Retrospective cohort study of all FE performed between 2000 and 2010 at a single tertiary care academic medical center in New York City. A total of 9878 FE met inclusion criteria for our study. In cases of multiple gestations (MG), each fetus was counted as a separate study.
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Anat Ratnovsky^∗,†, Matthew Mellema^*, Steven S. An^∗,‡, Jeffrey J. Fredberg^*, Stephanie A. Shore^*

Molecular & Cellular Biomechanics, Vol.4, No.3, pp. 143-158, 2007, DOI:10.3970/mcb.2007.004.143

Abstract Obesity is a risk factor for asthma. The purpose of this study was to determine whether metformin, an agent used in the treatment of an obesity-related condition (type II diabetes), might have therapeutic potential for modifying the effects of obesity on airway smooth muscle (ASM) function. Metformin acts via activation of AMP-activated protein kinase (AMPK), a cellular sensor of energy status. In cultured murine ASM cells, metformin (0.2--2 mM) caused a dose-dependent inhibition of cell proliferation induced by PDGF (10^-8 M) and serotonin (10^-4 M). Another AMPK activator, 5-aminoimidazole-4-carboxamide-1-ß-D-riboruranoside (AICAR), also inhibited PDGF-induced proliferation. Furthermore, cells treated with metformin or… More >