The

level of angiotensin II receptor type 1 or type 2 mRNA transcription was measured by means of a semiquantitative reverse transcription-polymerase chain reaction technique. Expression of angiotensin II receptor type 1 or type 2 protein was detected by means of immunohistochemistry assay and Western blot analysis.

Results: The inner diameter of the left atrium was clearly enlarged in the atrial fibrillation group in comparison with that seen in the sinus rhythm group. The expression levels of both angiotensin II receptor type 1 mRNA and protein in the left atrial tissue were significantly increased in the patients with atrial fibrillation compared with those seen in patients with sinus rhythm (P < .05). Interestingly, the comparison of angiotensin II receptor type 2 expression levels in the left atrial tissue between these 2 groups is not statistically significant. In addition, the results of angiotensin II receptor type 1 or 2 expression in Elafibranor WZB117 chemical structure the right atrial tissue did not show any obvious change in the patients with atrial fibrillation versus those with sinus rhythm.

Conclusions: Expression of angiotensin II receptor type 1 but not type 2 is highly upregulated only in the

left atrial tissue of patients with rheumatic valvular disease with atrial fibrillation. This suggests that there is a possible pathophysiologic role of the renin-angiotensin system in patients with atrial fibrillation and that a series of effects mediated by the activation of angiotensin II receptor type 1 in the left atrial tissue might be one of the molecular mechanisms involved in the process of atrial remodeling in atrial fibrillation.

MK5108 (J Thorac Cardiovasc Surg 2010;140:298-304)”
“Developmental dyslexia is a language-based learning disability, and a number of candidate dyslexia susceptibility genes have been identified, including DYX1C1, KIAA0319, and DCDC2. Knockdown of function by embryonic transfection of small hairpin RNA (shRNA) of rat homologues of these genes dramatically disrupts neuronal migration to the cerebral cortex by both cell autonomous and non-cell autonomous effects. Here we sought to investigate the extent of non-cell autonomous effects following in utero disruption of the candidate dyslexia susceptibility gene homolog Dyx1c1 by assessing the effects of this disruption on GABAergic neurons. We transfected the ventricular zone of embryonic day (E) 15.5 rat pups with either Dyx1c1 shRNA, DYX1C1 expression construct, both Dyx1c1 shRNA and DYX1C1 expression construct, or a scrambled version of Dyx1c1 shRNA, and sacrificed them at postnatal day 21. The mothers of these rats were injected with BrdU at either E13.5, E15.5, or E17.5. Neurons transfected with Dyx1c1 shRNA were bi-modally distributed in the cerebral cortex with one population in heterotopic locations at the white matter border and another migrating beyond their expected location in the cerebral cortex.