Prevalence and clinical correlation of left ventricular systolic dysfunction in african americans with ischemic stroke.

BACKGROUND: The goal of the present study was to determine the prevalence of left ventricular systolic dysfunction (LVSD) and associated clinical correlates in African Americans (AA) diagnosed with ischemic stroke (IS). METHODS: Retrospective chart analysis was done on all diagnosed AA IS patients between January 2010 and March 2012. Patients with atrial fibrillation were excluded. A total of 147 patients were included in the study. Transthoracic 2-dimensional echocardiography was used to assess left ventricular systolic function, and study groups were categorized as normal, mild, moderate, and severely abnormal, based on the ejection fraction (EF). Available imaging studies were analyzed for data collection. Logistic regression and Pearson chi-square tests were performed. RESULTS: Normal EF was present in 114 of 147 patients (78%). Mild abnormality was present in 9 of 147 (6%), moderate in 8 of 147 (5%), and severe in 16 of 147 (11%) patients. In patients with mildly reduced EF, smoking was the most common (RF). In patients with moderately and severely reduced EFs, hypertension was the most common RF. History of smoking was commonly found in systolic dysfunction group compared with normal group (P = .001). Logistic regression analysis revealed that smoking and advanced age were the significant predictors for LVSD. Large-vessel IS were more common in systolic dysfunction group than normal EF group (P = .017). CONCLUSIONS: Prevalence of LVSD in AA with IS was 22% in our study. Smoking was a significant modifiable RF associated with systolic dysfunction. A history of smoking and higher age could predict the occurrence of LVSD. There were more large-vessel IS in patients with LVSD.

Id proteins in cell growth and tumorigenesis.

Since the gene encoding Id1 was cloned in 1990, Id proteins have been implicated in regulating a variety of cellular processes, including cellular growth, senescence, differentiation, apoptosis, angiogenesis, and neoplastic transformation. The development of knockout and transgenic animal models for many members of the Id gene family has been particularly useful in sorting out the biologic relevance of these genes and their expression during normal development, malignant transformation, and tumor progression. Here we review the current understanding of Id gene function, the biologic consequences of Id gene expression, and the implications for Id gene regulation of cell growth and tumorigenesis.

A Rare Case of Immune Reconstitution Inflammatory Syndrome Development in an Immunocompromised Patient with Progressive Multifocal Leukoencephalopathy and Multicentric Castleman's Disease.

Immune reconstitution inflammatory syndrome (IRIS) development in HIV with preexistent progressive multifocal leukoencephalopathy (PML) has been extensively studied. PML-IRIS typically manifests clinically as new or worsening neurologic symptoms in conjunction with enlarging CNS lesions and occurs in approximately 10-20 percent of HIV-infected patients with PML who begin HAART. Likewise, Multicentric Castleman's Disease (MCD), a rare malignant lymphoproliferative disorder, has a strong and well-known association with HIV. Our case provides a rare instance of PML-IRIS in combination with MCD in an HIV-positive individual. The combination of all three diseases has never been reported in the literature. Both MCD and PML were present during initial determination of HIV infection in our patient and their disease courses were altered during the subsequent development of IRIS.

Id1 expression is transcriptionally regulated in radial growth phase melanomas.

Id genes have been demonstrated to be upregulated in a wide variety of human malignancies and their expression has been correlated with disease prognosis; however, little is known about the mechanisms of Id gene activation in tumors. We have previously shown that the helix-loop-helix transcription factor, Id1, is highly expressed in primary human melanomas during the radial growth phase and that Id1 is a transcriptional repressor of the familial melanoma gene CDKN2A. Here we use a series of melanoma cell lines that recapitulate the phenotypic characteristics of melanomas at varying stages of malignant progression to evaluate the expression levels of Id1 in this model system and determine the mechanism of Id1 dysregulation in these tumor cells. We find elevated protein levels of Id1 to be present consistently in radial growth phase tumor cells in accordance with our primary tumor data. Id1 transcript levels were also found to be elevated in these radial growth phase melanoma cells without any appreciable evidence of gene amplification and Id1 promoter activity was found to correlate with Id expression levels. We therefore conclude that Id1 expression is primarily regulated at the transcriptional level in radial growth phase melanomas and expect that therapies that target Id1 gene expression may be useful in the treatment of Id-associated malignancies.