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Articles by S Witt
Total Records ( 2 ) for S Witt
  R. H Perlis , J. W Smoller , J Mysore , M Sun , T Gillis , S Purcell , M Rietschel , M. M Nothen , S Witt , W Maier , D. V Iosifescu , P Sullivan , A. J Rush , M Fava , H Breiter , M Macdonald and J. Gusella
  Objective

Presymptomatic individuals with the Huntingtin (HTT) CAG expansion mutation that causes Huntington's disease may have higher levels of depressive symptoms than healthy comparison populations. However, the prevalence of HTT CAG repeat expansions among individuals diagnosed with major depressive disorder has not been established.

Method

This was a case-control genetic association study of HTT CAG allele size in two discovery cohorts of individuals with major depressive disorder and comparison subjects without major depression as well as a replication cohort of individuals with major depression and comparison subjects without major depression.

Results

CAG repeat lengths of 36 or greater were observed in six of 3,054 chromosomes from individuals with major depression, compared with none of 4,155 chromosomes from comparison subjects. In a third cohort, one expanded allele was observed among 1,202 chromosomes in the major depression group, compared with none of 2,678 chromosomes in comparison subjects. No clear pattern of clinical features was shared among individuals with the expanded repeats.

Conclusions

In clinical populations of individuals diagnosed with major depression, approximately 3 in 1,000 carried expanded HTT CAG alleles.

  R. B Hinton , J Adelman Brown , S Witt , V. K Krishnamurthy , H Osinska , B Sakthivel , J. F James , D. Y Li , D. A Narmoneva , R. P Mecham and D. W. Benson
  Rationale:

Elastin is a ubiquitous extracellular matrix protein that is highly organized in heart valves and arteries. Because elastic fiber abnormalities are a central feature of degenerative valve disease, we hypothesized that elastin-insufficient mice would manifest viable heart valve disease.

Objective:

To analyze valve structure and function in elastin-insufficient mice (Eln+/–) at neonatal, juvenile, adult, and aged adult stages.

Methods and Results:

At birth, histochemical analysis demonstrated normal extracellular matrix organization in contrast to the aorta. However, at juvenile and adult stages, thin elongated valves with extracellular matrix disorganization, including elastin fragment infiltration of the annulus, were observed. The valve phenotype worsened by the aged adult stage with overgrowth and proteoglycan replacement of the valve annulus. The progressive nature of elastin insufficiency was also shown by aortic mechanical testing that demonstrated incrementally abnormal tensile stiffness from juvenile to adult stages. Eln+/– mice demonstrated increased valve interstitial cell proliferation at the neonatal stage and varied valve interstitial cell activation at early and late stages. Gene expression profile analysis identified decreased transforming growth factor-β–mediated fibrogenesis signaling in Eln+/– valve tissue. Juvenile Eln+/– mice demonstrated normal valve function, but progressive valve disease (predominantly aortic regurgitation) was identified in 17% of adult and 70% of aged adult Eln+/– mice by echocardiography.

Conclusions:

These results identify the Eln+/– mouse as a model of latent aortic valve disease and establish a role for elastin dysregulation in valve pathogenesis.

 
 
 
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