Gender-Related Differences in the Prevalence of Cardiovascular Disease Risk Factors and their Correlates in Urban Tanzania.

\ud Urban areas in Africa suffer a serious problem with dual burden of infectious diseases and emerging chronic diseases such as cardiovascular diseases (CVD) and diabetes which pose a serious threat to population health and health care resources. However in East Africa, there is limited literature in this research area. The objective of this study was to examine the prevalence of cardiovascular disease risk factors and their correlates among adults in Temeke, Dar es Salaam, Tanzania. Results of this study will help inform future research and potential preventive and therapeutic interventions against such chronic diseases. The study design was a cross sectional epidemiological study. A total of 209 participants aged between 44 and 66 years were included in the study. A structured questionnaire was used to evaluate socioeconomic and lifestyle characteristics. Blood samples were collected and analyzed to measure lipid profile and fasting glucose levels. Cardiovascular risk factors were defined using World Health Organization criteria. The age-adjusted prevalence of obesity (BMI > or = 30) was 13% and 35%, among men and women (p = 0.0003), respectively. The prevalence of abdominal obesity was 11% and 58% (p < 0.0001), and high WHR (men: >0.9, women: >0.85) was 51% and 73% (p = 0.002) for men and women respectively. Women had 4.3 times greater odds of obesity (95% CI: 1.9-10.1), 14.2-fold increased odds for abdominal adiposity (95% CI: 5.8-34.6), and 2.8 times greater odds of high waist-hip-ratio (95% CI: 1.4-5.7), compared to men. Women had more than three-fold greater odds of having metabolic syndrome (p = 0.001) compared to male counterparts, including abdominal obesity, low HDL-cholesterol, and high fasting blood glucose components. In contrast, female participants had 50% lower odds of having hypertension, compared to men (95%CI: 0.3-1.0). Among men, BMI and waist circumference were significantly correlated with blood pressure, triglycerides, total, LDL-, and HDL-cholesterol (BMI only), and fasting glucose; in contrast, only blood pressure was positively associated with BMI and waist circumference in women. The prevalence of CVD risk factors was high in this population, particularly among women. Health promotion, primary prevention, and health screening strategies are needed to reduce the burden of cardiovascular disease in Tanzania.\u

Accounting for photodegradation dramatically improves prediction of carbon losses in dryland systems

Traditional models of decomposition fail to capture litter mass loss patterns in dryland systems. This shortcoming has stimulated research into alternative drivers of decomposition, including photodegradation. Here, we use aboveground litter decomposition data for dryland (arid) sites from the Long-term Intersite Decomposition Experiment Team data set to test hypotheses (models) about the mechanisms and impacts of photodegradation. Incorporating photodegradation into a traditional biotic decomposition model substantially improved model predictions for mass loss at these dryland sites, especially after four years. The best model accounted for the effects of solar radiation via photodegradation loss from the intermediate cellulosic and lignin pools and direct inhibition of microbial decomposition. Despite the concurrent impacts of photodegradation and inhibition on mass loss, the best photodegradation model increased mass loss by an average of 12% per year compared to the biotic-only decomposition model. The best model also allowed soil infiltration into litterbags to reduce photodegradation and inhibition of microbial decomposition by shading litter from solar radiation. Our modeling results did not entirely support the popular hypothesis that initial lignin content increases the effects of photodegradation on litter mass loss; surprisingly, higher initial lignin content decreased the rate of cellulosic photodegradation. Importantly, our results suggest that mass loss rates due to photodegradation may be comparable to biotic decomposition rates: Mass loss due to photodegradation alone resulted in litter mass losses of 6–15% per year, while mass loss due to biotic decomposition ranged from 20% per year during early-stage decomposition to 3% per year during late-stage decomposition. Overall, failing to account for the impacts of solar radiation on litter mass loss under-predicted long-term litter mass loss by approximately 26%. Thus, not including photodegradation in dryland decomposition models likely results in large underestimations of carbon loss from dryland systems

CLCA2 epigenetic regulation by CTBP1, HDACs, ZEB1, EP300 and miR-196b-5p impacts prostate cancer cell adhesion and EMT in metabolic syndrome disease

Prostate cancer (PCa) is the most common cancer among men. Metabolic syndrome (MeS) is associated with increased PCa aggressiveness and recurrence. Previously, we proposed C-terminal binding protein 1 (CTBP1), a transcriptional co-repressor, as a molecular link between these two conditions. Notably, CTBP1 depletion decreased PCa growth in MeS mice. The aim of this study was to investigate the molecular mechanisms that explain the link between MeS and PCa mediated by CTBP1. We found that CTBP1 repressed chloride channel accessory 2 (CLCA2) expression in prostate xenografts developed in MeS animals. CTBP1 bound to CLCA2 promoter and repressed its transcription and promoter activity in PCa cell lines. Furthermore, we found that CTBP1 formed a repressor complex with ZEB1, EP300 and HDACs that modulates the CLCA2 promoter activity. CLCA2 promoted PCa cell adhesion inhibiting epithelial–mesenchymal transition (EMT) and activating CTNNB1 together with epithelial marker (CDH1) induction, and mesenchymal markers (SNAI2 and TWIST1) repression. Moreover, CLCA2 depletion in PCa cells injected subcutaneously in MeS mice increased the circulating tumor cells foci compared to control. A microRNA (miRNA) expression microarray from PCa xenografts developed in MeS mice, showed 21 miRNAs modulated by CTBP1 involved in angiogenesis, extracellular matrix organization, focal adhesion and adherents junctions, among others. We found that miR-196b-5p directly targets CLCA2 by cloning CLCA2 3′UTR and performing reporter assays. Altogether, we identified a new molecular mechanism to explain PCa and MeS link based on CLCA2 repression by CTBP1 and miR-196b-5p molecules that might act as key factors in the progression onset of this disease.Fil: Porretti, Juliana Carla. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Dalton, Guillermo Nicolás. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Massillo, Cintia Lorena. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Scalise, Georgina Daniela. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Farré, Paula Lucía. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Elble, Randolph. Southern Illinois University; Estados UnidosFil: Gerez, Esther Noemi. Universidad de Buenos Aires. Facultad de Medicina. Hospital de Clínicas General San Martín; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Centro de Invest. Sobre Porfirinas y Porfirias. Grupo Vinculado Al Cipyp - Ffyb; ArgentinaFil: Accialini, Paula Lucia. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: Cabanillas, Ana Maria de Los A.. Universidad Nacional de Córdoba; ArgentinaFil: Gardner, Kevin. Columbia University; Estados UnidosFil: de Luca, Paola. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; ArgentinaFil: de Siervi, Adriana. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Biología y Medicina Experimental. Fundación de Instituto de Biología y Medicina Experimental. Instituto de Biología y Medicina Experimental; Argentin

Metabolic Syndrome and Cognitive Decline in Elderly Latinos: Findings from the Sacramento Area Latino Study of Aging Study

To investigate the effect of metabolic syndrome on cognitive function in an elderly Latino population and to determine whether inflammation modifies this association. DESIGN : A longitudinal cohort study. SETTING : Sacramento area and the surrounding California counties from 1998 to 1999. PARTICIPANTS : One thousand six hundred twenty-four Latinos aged 60 and older who participated in the Sacramento Area Latino Study of Aging. MEASUREMENTS : Baseline metabolic syndrome was calculated using the Third Adult Treatment Panel of the National Cholesterol Education Program. Cognitive function was measured using the Modified Mini-Mental State Examination (3MS) and the Delayed Word-List Recall (DelRec), a verbal memory test. The effect of metabolic syndrome on cognitive change scores was examined using random effects models; in addition, the effect of the individual components of the syndrome on cognitive change was examined. RESULTS : Of the 1,624 participants, 718 (44%) had metabolic syndrome at baseline. Those with metabolic syndrome had worse 3-year change scores on 3MS ( P =.04) and DelRec ( P =.03). Multivariate adjustment attenuated the results for DelRec but not for 3MS. This association was especially pronounced in participants with a high serum level of inflammation, resulting in an average 3MS score 0.64 points lower per year ( P =.03) for those with metabolic syndrome. Individual components of metabolic syndrome were not associated with cognitive decline except for elevated glucose on the DelRec ( P =.02) and high blood pressure on 3MS ( P =.05). CONCLUSION : Metabolic syndrome and inflammation may both contribute to cognitive decline in older people of diverse backgrounds. The results also suggest that, in elderly Latinos, the composite measure of metabolic syndrome is a greater risk for cognitive decline than its individual components.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65598/1/j.1532-5415.2007.01139.x.pd

Plasma homocysteine and the risk of venous thromboembolism: insights from the FIELD study

Background The lipid-lowering effect of fenofibrate is accompanied by a rise in plasma homocysteine, a potential risk factor for venous thromboembolism (VTE). This study investigated the relationship between homocysteine and the risk of VTE in patients treated with fenofibrate. Methods and results The relationship between homocysteine and deep-vein thrombosis or pulmonary embolism was investigated in 9522 participants of the 5-year Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) trial. All subjects received fenofibrate during a 6-week active run-in phase before randomization. A Cox proportional-hazards model was used to assess the effect of homocysteine on risk of venous thromboembolic events. During active-drug run-in, homocysteine rose on average by 6.5 μmol/L, accompanied by a substantial rise in plasma creatinine (+12%). Fenofibrate-induced changes in homocysteine and creatinine were fully reversible in the placebo group but persisted in the treatment group until reversing at the end of therapy. During follow-up, 1.8% had at least one episode of deep-vein thrombosis or pulmonary embolism: 103 on fenofibrate and 68 on placebo (log-rank P=0.006). In multivariate analysis, every 5 µmol/L higher baseline homocysteine was associated with 19% higher risk of VTE. Fenofibrate treatment was associated with 52% higher risk, but the change in homocysteine with fenofibrate was not significantly associated with VTE after adjustment for baseline homocysteine. Conclusions Hyperhomocysteinemia is prospectively associated with VTE. Fenofibrate may predispose individuals with high pretreatment homocysteine towards VTE. The fenofibrate-induced increase in homocysteine did not, however, explain the risk associated with fenofibrate therapy

The Influence of the Brain‐Derived Neurotropic Factor Val66Met ‐Genotype and HMG‐CoA Reductase Inhibitors on Insulin Resistance in the Schizophrenia and Bipolar Populations

Introduction: The brain‐derived neurotrophic factor (BDNF) Val66Met variant and HMG‐COA reductase inhibitors (statins) have been implicated in insulin resistance with a possible increased risk of diabetes. We sought to determine the effect of the BDNF Met variant and statin medication use on insulin resistance in schizophrenia and bipolar disorder using the homeostasis model assessment of insulin resistance (HOMA‐IR). Methods: A cross‐sectional design was used and patients with diabetes or on any medications affecting glucose regulation were ‐excluded. Associations between insulin resistance and genotype were then analyzed by ANOVA and regression analysis. Subjects were grouped by BDNF genotype as well as presence of statin. Results: Two hundred fifty‐two subjects with a mean age of 44 years were included. The group was 53% male and 41% had a diagnosis of bipolar disorder; 78% and 19% were receiving atypical antipsychotics (AAPs) and statin medications, respectively. Analysis showed schizophrenia subjects with the BDNF met allele as well as schizophrenia subjects with both the BDNF met allele and were receiving a statin had significantly higher HOMA‐IR values compared to the other groups ( p = 0.046 and p = 0.016, respectively). Conclusions: Our results suggest that in the metabolically high‐risk population of schizophrenia the BDNF met allele alone and in combination with statin medications is associated with higher insulin resistance values. This was not seen in the bipolar population. Further validation of these associations remains necessary. Clin Trans Sci 2012; Volume 5: 486–490Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/95082/1/cts.12001.pd

Evaluation of Metabolic Syndrome in Patients with Chronic Low Back Pain: Using the Fourth Korea National Health and Nutrition Examination Survey Data

The aim of this study was to investigate the frequency of the metabolic syndrome in patients with chronic lower back pain in Korea and to evaluate the differences in clinical characteristics in chronic lower back pain patients with and without metabolic syndrome. This was a cross-sectional study using data from the fourth Korea National Health and Nutrition Examination Survey (KNHANES IV) 2008. The sample consisted of 1085 participants with chronic lower back pain. The diagnosis of metabolic syndrome was made according to the criteria of the National Cholesterol Education Program Adult Treatment Panel III (NCEP-ATP III) and the Korean Society for the Study of Obesity. The prevalence of metabolic syndrome among chronic lower back pain patients was 36.2% (30.2% male, 38.6% female). According to our results, female sex, advanced age, and high BMI were risk factors for metabolic syndrome. These results from a representative sample show that metabolic syndrome is common in chronic lower back pain patients in Korea. Clinicians managing chronic lower back pain should consider the risk factors for metabolic syndrome

Dyslipidemia and changes in lipid profiles associated with rheumatoid arthritis and initiation of anti–tumor necrosis factor therapy

Objective To investigate the frequency of lipid testing in clinical practice and to explore the relationship between rheumatoid arthritis (RA), dyslipidemia, and other cardiovascular (CV) risk factors with RA treatment. Methods Patients in this retrospective database study were ages ≥18 years and had ≥2 physician diagnoses for RA or osteoarthritis (OA; comparator group) between March 2004 and March 2008. Outcomes of interest included the percentage of RA and OA patients receiving lipid tests, lipid profiles (total cholesterol, low‐density lipoprotein [LDL] cholesterol, and high‐density lipoprotein [HDL] cholesterol) of RA versus OA patients, and lipid profiles of RA patients before and after initiation with a tumor necrosis factor (TNF) inhibitor. We used multivariable regression to control potential confounders between the cohorts. Results Over a median ≥2‐year followup, fewer RA patients than OA patients had ≥1 lipid test (62.0% [95% confidence interval (95% CI) 61.5–62.5] versus 69.8% [95% CI 69.5–70.1]). Mean total cholesterol and LDL cholesterol were each 4 mg/dl lower in the RA cohort ( P < 0.0001); HDL cholesterol was similar between the cohorts. Across the RA cohort, 25.2% of patients had suboptimal LDL cholesterol levels (≥130 mg/dl). Among RA patients not receiving lipid‐lowering therapy who initiated TNF inhibitor therapy (n = 96), mean total cholesterol and LDL cholesterol increased by 5.4 and 4.0 mg/dl, respectively. Conclusion Patients with RA were less likely to be tested for hyperlipidemia and had more favorable lipid profiles than patients with OA. TNF inhibitor therapy modestly increased all lipid parameters. Additional studies are needed to determine the effect of traditional CV risk factors and inflammation and the impact of biologic agents on CV outcomes in RA patients.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/93521/1/21693_ftp.pd