Future studies are needed to determine the roles and timing of expression of anti-SP1 antibodies in Sjogren’s syndrome. (C) 2014 Elsevier Inc. All rights reserved.”
“Gokina NI, Bonev AD, Gokin AP, Goloman G. Role of impaired endothelial cell Ca2+ signaling in uteroplacental vascular dysfunction during diabetic rat pregnancy. Am J Physiol Heart Circ Physiol 304: H935-H945, 2013. First published February 1, 2013; doi:10.1152/ajpheart.00513.2012.-Diabetes mellitus in pregnancy is associated

with impaired endothelium-mediated dilatation of maternal arteries, although the underlying cellular mechanisms remain unknown. In this study, we hypothesized that diabetes during rat gestation attenuates agonist-induced uterine vasodilation through reduced endothelial cell (EC) Ca2+ elevations and impaired smooth muscle cell (SMC) hyperpolarization selleckchem and SMC intracellular Ca2+ concentration ([Ca2+](i)) responses. Diabetes

was induced by an injection of streptozotocin to second-day pregnant rats and confirmed by the development of maternal hyperglycemia. Control rats were injected with a citrate buffer. Fura-2-based measurements of SMC [Ca2+](i) or microelectrode recordings of SMC membrane potential were performed concurrently with dilator responses to ACh in uteroplacental arteries from control and diabetic pregnant rats. Basal levels of EC [Ca2+](i) and ACh-induced EC [Ca2+](i) elevations in pressurized vessels and small EC sheets were studied as well. selleck kinase inhibitor Diabetes reduced ACh-induced vasodilation due to a markedly impaired EDHF-mediated response. Diminished vasodilation to ACh was associated with attenuated SMC hyperpolarization and [Ca2+](i) responses. Basal levels of EC [Ca2+](i) and ACh-induced EC [Ca2+](i) elevations were significantly reduced by diabetes. In conclusion, these data demonstrate that reduced endothelium-mediated hyperpolarization contributes to attenuated uteroplacental vasodilation and SMC [Ca2+](i) responses to ACh in diabetic pregnancy. Impaired

endothelial Ca2+ signaling is in part responsible for endothelial dysfunction in the uterine resistance vasculature of diabetic rats. see more Pharmacological improvement of EC Ca2+ handling may provide an important strategy for the restoration of endothelial function and enhancement of maternal blood flow in human pregnancies complicated by diabetes.”
“Autosomal recessive proximal spinal muscular atrophy is caused by deletions in the survival of motor neuron (SMN1) gene, while autoimmune myasthenia gravis is an acquired disorder. An association between these two diseases has not been reported. Our patient with intermediate spinal muscular atrophy (SMA type II) did not need alimentary or respiratory aid until age 51 when he suddenly developed bulbar weakness and respiratory insufficiency. Seropositive myasthenia gravis was confirmed and the corresponding symptoms resolved on treatment. (c) 2011 Elsevier B.V. All rights reserved.