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Cardiovascular diseases (CVDs) are the leading cause of death in the world. Endothelial progenitor cells (EPCs) are currently being explored in the context of CVD risk. EPCs are bone marrow derived progenitor cells involved in postnatal endothelial repair and neovascularization. A large body of evidence from clinical, animal, and in vitro studies have shown that EPC numbers in circulation and their functionality reflect endogenous vascular regenerative capacity. Traditionally vitamin D is known to be beneficial for bone health and calcium metabolism and in the last two decades, its role in influencing CVD and cancer risk has generated significant interest. Observational studies have shown that low vitamin D levels are associated with an adverse cardiovascular risk profile. Still, Mendelian randomization studies and randomized control trials (RCTs) have not shown significant effects of vitamin D on cardiovascular events. The criticism regarding the RCTs on vitamin D and CVD is that they were not designed to investigate cardiovascular outcomes in vitamin D-deficient individuals. Overall, the association between vitamin D and CVD remains inconclusive. Recent clinical and experimental studies have demonstrated the beneficial role of vitamin D in increasing the circulatory level of EPC as well as their functionality. In this review we present evidence supporting the beneficial role of vitamin D in CVD through its modulation of EPC homeostasis.
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The heterogeneous nuclear ribonucleoprotein D (hnRNPD) serves as a prognostic marker for oral squamous cell carcinoma (OSCC). We evaluated the diagnostic potential of hnRNPD to differentiate between OSCC and normal mucosa. Immunohistochemistry for hnRNPD and a routinely used diagnostic marker deltaNp63 (p40) was performed in 32 normal mucosae and 46 OSCC specimens. Subsequently, receiver-operating characteristic analysis was performed to evaluate the diagnostic potential of hnRNPD in comparison to that of p40. Immunostaining for p40 and hnRNPD was observed in 39 (84.78%) and 38 (82.60%) cases, respectively, in OSCC specimens. The poorly differentiated squamous cell carcinoma displayed 100% (eight cases) immunoreactivity for hnRNPD as compared to 87.5% (seven cases) for p40. Nuclear staining of p40 and hnRNPD was observed in all OSCC specimens. p40 staining was restricted to basal cells, whereas both basal and para-basal cells displayed hnRNPD staining in OSCC specimens. Areas under the curve for p40 and hnRNPD were 0.86 and 0.87, respectively. p40 and hnRNPD showed equal sensitivities (80.95%). However, hnRNPD displayed marginally higher (88.23%) specificity for tumor cells as compared to that of p40 (85.29%). Conclusion: In addition to being a well-established prognostic marker, hnRNPD can serve as a diagnostic marker for OSCC.
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BACKGROUND: Bariatric surgery can alleviate cardiovascular risk via effects on cardiovascular disease (CVD) risk factors such as diabetes mellitus, hypertension, and dyslipidemia. Our study aimed to assess the cholesterol efflux capacity (CEC) of HDL as a negative risk factor for CVD in individuals with obesity and identify the factors associated with improvement in CEC 3 months following bariatric surgery. METHODS: We recruited 40 control individuals (mean BMI of 22.2 kg/m2) and 56 obese individuals (mean BMI of 45.9 kg/m2). The biochemical parameters, inflammatory status and CEC of HDL was measured for the obese individuals before bariatric surgery and at 3 months after surgery. The CEC was measured using a cell-based cholesterol efflux system of BODIPY-cholesterol-labelled THP-1 macrophages. RESULTS: A significant reduction in BMI (- 17%, p < 0.001), resolution of insulin sensitivity (HOMA2-IR = - 23.4%, p = 0.002; Adipo IR = - 16%, p = 0.009) and inflammation [log resistin = - 6%, p = 0.07] were observed 3 months post-surgery. CEC significantly improved 3 months after surgery [Pre: 0.91 ± 0.13; Post: 1.02 ± 0.16; p = 0.001] despite a decrease in HDL-C levels. The change in CEC correlated with the change in apo A-I (r = 0.39, p = 0.02) and adiponectin levels (r = 0.35, p = 0.03). CONCLUSION: The results suggest that improvements in CEC, through improvement in adipose tissue health in terms of adipokine secretion and insulin sensitivity could be an important pathway in modulating obesity-related CVD risk.
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BACKGROUND: Studies on mitochondrial DNA copy number reveal an increase or decrease in copy number that appears to be cancer specific, but data on acute lymphoblastic leukemia have been inconsistent regarding the significance of changes in mitochondrial DNA copies. The purpose of this pilot study was to analyze mitochondrial DNA copy number and mitochondrial DNA integrity. PROCEDURE: Copy number and mitochondrial deletion ratios were estimated in the bone marrow of 51 patients and peripheral blood of 30 healthy controls using quantitative real-time PCR. The copy number values were correlated with prognostic markers in patients. RESULTS: Significantly increased mitochondrial DNA copy number (P-value < 0.0001) and increased mitochondrial deletion ratios (P-value = 0.0018) were observed in patients compared with controls. The copy numbers were significantly decreased in patients after chemotherapy (P-value = 0.0232). Patients with higher copy numbers exhibited significantly inferior survival than patients with lower copy numbers (for event-free survival, P-value = 0.04 and overall survival, P-value = 0.1175). CONCLUSIONS: Significant decreases in mitochondrial DNA copy number with therapy indicates that copy number could be evaluated as a potential marker for therapeutic efficacy and a higher mitochondrial DNA copy number could be a poor prognostic marker.