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Articles by S Sebastian
Total Records ( 2 ) for S Sebastian
  R. S Padilla , S Sebastian , Z Jiang , I Nindl and R. Larson
 

Objectives  To identify and compare the gene expression profiles of actinic keratosis (AK) and squamous cell carcinoma (SCC) and to further clarify critical genetic alterations in the evolution of SCC from normal sun-damaged human skin.

Design  Observational study.

Setting  University practice.

Patients  Skin biopsy specimens were obtained from 16 patients. The specimens included 14 normal non–sun-exposed skin samples, 14 normal sun-exposed skin samples, 5 AKs, and 15 cutaneous SCCs.

Main Outcome Measures  Gene expression profiles from normal non–sun-exposed skin, normal sun-exposed skin, AKs, and SCCs.

Results  Using a highly astringent shrunken centroid threshold of 6.52 and the prediction analysis of microarrays, we identified 89 unique genes that most likely contribute to the molecular evolution of SCC. Our model was cross-validated using data from a separate study and clearly distinguishes between skin tumors (AK and SCC) and normal skin independent of sun exposure. Genes that were upregulated in AK and SCC were downregulated in normal skin, and genes that were downregulated in AK and SCC were upregulated in normal skin.

Conclusions  The finding of similar differentially expressed genes in AK and SCC confirms that AK is a precursor lesion of SCC and indicates that they are closely related genetically. Clear elucidation of these relationships will be critical to improving therapeutic approaches.

  Z Zuberi , M Nobles , S Sebastian , A Dyson , S. Y Lim , R Breckenridge , L Birnbaumer and A. Tinker
  Background—

We explored the role that inhibitory heterotrimeric G-proteins play in ventricular arrhythmia.

Methods and Results—

Mice with global genetic deletion of Gi2 [Gi2 (–/–)] were studied and found, based on telemetry, to have a prolonged QT interval on surface ECG when awake. In vivo electrophysiology studies revealed that the Gi2 (–/–) mice have a reduced ventricular effective refractory period and a predisposition to ventricular tachycardia when challenged with programmed electrical stimulation. Neither control nor combined global deletion of Gi1 and Gi3 mice showed these abnormalities. There was no evidence for structural heart disease at this time point in the Gi2 (–/–) mice as assessed by cardiac histology and echocardiography. The absence of Gi2 thus leads to a primary electrical abnormality, and we explored the basis for this finding. With patch clamping, single isolated ventricular cells showed that Gi2 (–/–) mice had a prolonged ventricular action potential duration (APD) but steeper action potential shortening as the diastolic interval was reduced in restitution studies. Gene expression studies showed increased expression of L-type Ca2+ channel subunits, and patch clamping revealed an increase in these currents in Gi2 (–/–) mice. There were no changes in K+ currents.

Conclusions—

The absence of inhibitory G-protein signaling mediated through Gi2 is a substrate for ventricular arrhythmias.

 
 
 
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