Hoarseness due to paralysis of vocal cord, as in Cardio-vocal syndrome, is caused by mechanical affection of left recurrent laryngeal nerve from enlarged cardiovascular structures. Mitral valve prolapse is rarely found to cause this syndrome. Case report presenting a 47 years old male visited the outpatient department with a clinical history of dyspnea and hoarseness since a year ago. Physical examination revealed late systolic murmur in apex and low-grade diastolic murmur in right second intercostal space. Echocardiography confirmed severe mitral regurgitation due to flail anterior mitral valve leaflet with severe left atrium dilatation (9.0 cm) and moderate aortic regurgitation due to mal-coaptation of aortic valves. Laryngoscopy revealed an immobile left vocal cord. He underwent successful double valve replacement after three months follow up the patient showed improvement of hoarseness. The incidence of Cardio-vocal syndrome in mitral valve disease varies from 0.6% to 5%. In cases diagnosed with thoracic disease, paralysis of the left vocal cord was reported 1.75 times more frequent than the right side. The aim of this case report is we have to aware that Cardio-vocal syndrome is a rare cause of vocal cord paralysis and should be considered as a differential diagnosis of hoarseness, particularly if the patient has a cardiac history. Comprehensive evaluation and prompt treatment may allow reversal of the damage to left recurrent laryngeal nerve. Permanent nerve damage can occur due to late diagnosis. Keywords             : Cardio-vocal syndrome, Mitral regurgitation, Aortic RegurgitationCorrespondence   : adityobasworo@gmail.com

IntroductionIt is possible to induce pluripotent stem cells from somatic cells, offering an infinite cell resource with the potential for disease research and use in regenerative medicine. Due to ease of accessibility, minimum invasive treatment, and can be kept frozen, peripheral blood mononuclear cells (PBMC) were an attractive source cell. VC6TFZ, a small molecule compound, has been successfully reprogrammed from mouse fibroblast induced pluripotent stem cells (iPSCs). However, it has not been confirmed in humans.ObjectiveThe aim of this research is to determine whether the small molecule compound VC6TFZ can induced pluripotency of PBMC to generate iPSCs detected with expression of SSEA4 and TRA1-60.MethodsUsing the centrifugation gradient density process, mononuclear cells were separated from peripheral venous blood. Mononuclear cells were cultured for 6 days in the expansion medium. The cells were divided into four groups; group 1 (P1), which was not exposed to small molecules (control group) and groups 2-4 (P2-P4), the experimental groups, subjected to various dosages of the small molecule compound VC6TFZ (VPA, CHIR, Tranylcypromine, FSK, Dznep, and TTNPB). The induction of pluripotency using small molecule compound VC6TFZ was completed within 14 days, then for 7 days the medium shifted to 2i medium. iPSCs identification in based on colony morphology and pluripotent gene expression, SSEA4 and TRA1-60 marker, using immunocytochemistry.ResultsColonies appeared on reprogramming process in day 7th. These colonies had round, large, and cobble stone morphology like ESC. Gene expression of SSEA4 and TRA 1-60 increased statisticaly significant than control group (SSEA4 were P2 p=0.007; P3 p=0.001; P4 p=0.009 and TRA 1-60 were P2 p=0.002; P3 p=0.001; P4 p=0.001).ConclusionSmall molecule compound VC6TFZ could induced pluripotency of human PBMC to generate iPSCs. Pluripotxency marker gene expression, SSEA 4 and TRA 1-60, in the experimental group was statistically significantly higher than in the control group.