4 resultados para SIGN AND SYMPTOMS

em Digital Commons at Florida International University


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Background Low diet quality and depression symptoms are independently associated with poor glycemic control in subjects with type 2 diabetes (T2D); however, the relationship between them is unclear. The aim of this study was to determine the association between diet quality and symptoms of depression among Cuban-Americans with and without T2D living in South Florida. Methods Subjects (n = 356) were recruited from randomly selected mailing list. Diet quality was determined using the Healthy Eating Index-2005 (HEI-05) score. Symptoms of depression were assessed using the Beck Depression Inventory (BDI). Both linear and logistic regression analyses were run to determine whether or not these two variables were related. Symptoms of depression was the dependent variable and independent variables included HEI-05, gender, age, marital status, BMI, education level, A1C, employment status, depression medication, duration of diabetes, and diabetes status. Analysis of covariance was used to test for interactions among variables. Results An interaction between diabetes status, gender and HEI-05 was found (P = 0.011). Among males with a HEI-05 score ≤ 55.6, those with T2D had a higher mean BDI score than those without T2D (11.6 vs. 6.6 respectively, P = 0.028). Among males and females with a HEI-05 score ≤ 55.6, females without T2D had a higher mean BDI score compared to males without T2D (11.0 vs. 6.6 respectively, P = 0.012) Conclusions Differences in symptoms of depression according to diabetes status and gender are found in Cuban-Americans with low diet quality.

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One of the pathological hallmarks of Alzheimer's disease (AD) brain is extracellular β-amyloid (Aβ) plaques containing 39-42 amino acid Aβ peptides. The deposition of Aβ around blood vessels, known as Cerebral amyloid angiopathy (CAA), is also a common feature in AD brain. Vascular density and cerebral blood flow are reduced in AD brains, and vascular risk factors such as hypertension and diabetes are also risk factors for AD. We have shown previously that Aβ peptides can potently inhibit angiogenesis both in-vitro and in-vivo, but the mechanism of action for this effect is not known. Therefore, my first hypothesis was that particular amino acid sequence(s) within the Aβ peptide are required for inhibition of angiogenesis. From this aim, I found a peptide sequence which was critical for anti-angiogenic activity (HHQKLVFF). This sequence contains a heparan sulfate proteoglycan growth factor binding domain implying that Aβ can interfere with growth factor signaling. Leading on from this, my second hypothesis was that Aβ can inhibit angiogenesis by binding to growth factor receptors. I found that Aβ can bind to Vascular Endothelial Growth Factor Receptor-2 (VEGFR-2), and showed that this is one mechanism by which Aβ can inhibit angiogenesis. Since the vasculature is disrupted in AD brains, I investigated whether a strategy to increase brain vascularization would be beneficial against AD pathology. Therefore, my third hypothesis was that voluntary exercise (which is known to increase brain vascularization in rodents) can ameliorate Aβ pathology, increase brain vascularization, and improve behavioral deficits in a transgenic mouse model of AD. I found that exercise has no effect on Aβ pathology, brain vascularization or behavioral deficits. Therefore, in the transgenic mouse model that I used, exercise is an ineffective therapeutic strategy against AD pathology and symptoms.

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Cocaine and other drugs of abuse increase HIV-induced immunopathogenesis; and neurobiological mechanisms of cocaine addiction implicate a key role for microRNAs (miRNAs), single-stranded non-coding RNAs that regulate gene expression and defend against viruses. In fact, HIV defends against miRNAs by actively suppressing the expression of polycistronic miRNA cluster miRNA-17/92, which encodes miRNAs including miR-20a. IFN-g production by natural killer cells is regulated by miR-155 and this miRNA is also critical to dendritic cell (DC) maturation. However, the impact of cocaine on miR-155 expression and subsequent HIV replication is unknown. We examined the impact of cocaine on two miRNAs, miR-20a and miR-155, which are integral to HIV replication, and immune activation. Using miRNA isolation and analysis, RNA interference, quantitative real time PCR, and reporter assays we explored the effects of cocaine on miR-155 and miR-20 in the context of HIV infection. Here we demonstrate using monocyte-derived dendritic cells (MDCCs) that cocaine significantly inhibited miR-155 and miR-20a expression in a dose dependent manner. Cocaine and HIV synergized to lower miR-155 and miR-20a in MDDCs by 90%. Cocaine treatment elevated LTR-mediated transcription and PU.1 levels in MDCCs. But in context of HIV infection, PU.1 was reduced in MDDCs regardless of cocaine presence. Cocaine increased DC-SIGN and and decreased CD83 expression in MDDC, respectively. Overall, we show that cocaine inhibited miR-155 and prevented maturation of MDDCs; potentially, resulting in increased susceptibility to HIV-1. Our findings could lead to the development of novel miRNA-based therapeutic strategies targeting HIV infected cocaine abusers.

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Charles Perry standing by FIU sign and flag. Charles Edward Perry (Chuck), 1937-1999, was the founding president of Florida International University in Miami, Florida. He grew up in Logan County, West Virginia and received his bachelor's and masters's degrees from Bowling Green State University. He married Betty Laird in 1960. In 1969, at the age of 32, Perry was the youngest president of any university in the nation. The name of the university reflects Perry’s desire for a title that would not limit the scope of the institution and would support his vision of having close ties to Latin America. Perry and a founding corps opened FIU to 5,667 students in 1972 with only one large building housing six different schools. Perry left the office of President of FIU in 1976 when the student body had grown to 10,000 students and the university had six buildings, offered 134 different degrees and was fully accredited. Charles Perry died on August 30, 1999 at his home in Rockwall, Texas. He is buried on the FIU campus in front of the Graham Center entrance.