There is growing and compelling evidence demonstrating the extra-skeletal role of vitamin D and the importance of maintaining adequate levels of this nutrient. Currently, there is very limited information available on the vitamin D status in children and adults in underserved groups, including Puerto Ricans. We assessed the vitamin D status of 4,090 Puerto Ricans living in six geographical regions in the island. Only 31.5% of the studied population had sufficient vitamin D levels (>30 ng/ml). The 18–39 year age group and the females showed inadequate (<30 ng/ml) levels of vitamin D (76.9% and 69.8%, respectively). Participants aged 60 or older showed the highest mean values of serum 25(OH)D (28.8 ng/ ml) and the highest percentage (37.1%) of suffi cient levels (>30 ng/ml). Future studies are certainly warranted to understand the prevalence of vitamin D deficiency and influencing factors (including obesity) in Puerto Ricans.
Background Coronary heart disease (CHD) is the number one cause of death in the US. The adipokine adiponectin has been studied intensively for presenting and inversed association with almost every stage of CHD. For instance, the evaluation of molecules capable of enhancing endogenous adiponectin expression is well justified. In this study, we investigated the effect of the vitamin D receptor activator (VDRA) paricalcitol and the angiotensin-converting enzyme inhibitor (ACEI) enalapril on adiponectin expression, lipid profiles, adenosine monophosphate activated protein kinase (AMPK) expression, monocyte chemo-attractant protein-1 (MCP-1), tumor necrosis factor-alpha (TNFα), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), antioxidant capcity, CuZn-superoxide dismutase (CuZn-SOD), Mn-SOD, NADPH p22phox subunits, inducible nitric oxidesynthase (iNOS), endothelial marker eNOS, and 81 atherosclerosis-related genes in ApoE-deficient mice. Method Seven-week-old ApoE-deficient mice were treated for 16 weeks as follows: Group 1, ApoE vehicle control (intraperitoneal [i.p.] 100 μl propylene glycol); Group 2, ApoE-paricalcitol (200 ng i.p., 3/week); Group 3, ApoE-Enalapril (30 mg/kg daily); Group 4, ApoE-paricalcitol + enalapril (described dosing); and Group 5, wild-type control (C57BLV). Results All treated groups presented significant changes in circulating and cardiac adiponectin, cardiac cholesterol levels, AMPK, MCP-1, TNF-α, COX-2, iNOS, eNOS, CuZn-SOD, Mn-SOD and p22phox. There were 15 genes that differed in their expression, 5 of which are involved in cardioprotection and antithrombotic mechanisms: Bcl2a1a, Col3a1, Spp1 (upregulated), Itga2, and Vwf (downregulated). Conclusion Together, our data presented a novel role for VDRA and ACEI in reducing factors associated with CHD that may lead to the discovery of new therapeutic venues.
Pulmonary Arterial Hypertension (PAH) is overrepresented in People Living with Human Immunodeficiency Virus (PLWH). HIV protein gp120 plays a key role in the pathogenesis of HIV-PAH. Genetic changes in HIV gp120 determine viral interactions with chemokine receptors; specifically, HIV-X4 viruses interact with CXCR4 while HIV-R5 interact with CCR5 co-receptors. Herein, we leveraged banked samples from patients enrolled in the NIH Lung HIV studies and used bioinformatic analyses to investigate whether signature sequences in HIV-gp120 that predict tropism also predict PAH. Further biological assays were conducted in pulmonary endothelial cells in vitro and in HIVtransgenic rats. We found that significantly more persons living with HIV-PAH harbor HIV-X4 variants. Multiple HIV models showed that recombinant gp120-X4 as well as infectious HIV-X4 remarkably increase arachidonate 5-lipoxygenase (ALOX5) expression. ALOX5 is essential for the production of leukotrienes; we confirmed that leukotriene levels are increased in bronchoalveolar lavage fluid of HIV-infected patients. This is the first report associating HIV-gp120 genotype to a pulmonary disease phenotype, as we uncovered X4 viruses as potential agents in the pathophysiology of HIV-PAH. Altogether, our results allude to the supplementation of antiretroviral therapy with ALOX5 antagonists to rescue patients with HIV-X4 variants from fatal PAH. Today, in the days of antiretroviral therapy (ART), infection with Human Immunodeficiency Virus (HIV) is a chronic disease with almost no HIV-associated opportunistic infections and a long life expectancy 1, 2. However,
People living with HIV and who receive antiretroviral therapy have a significantly improved lifespan, compared to the early days without therapy. Unfortunately, persisting viral replication in the lungs sustains chronic inflammation, which may cause pulmonary vascular dysfunction and ultimate life-threatening Pulmonary Hypertension (PH). The mechanisms involved in the progression of HIV and PH remain unclear. The study of HIV-PH is limited due to the lack of tractable animal models that recapitulate infection and pathobiological aspects of PH. On one hand, mice with humanized immune systems (hu-mice) are highly relevant to HIV research but their suitability for HIV-PH research deserves investigation. On another hand, the Hypoxia-Sugen is a well-established model for experimental PH that combines hypoxia with the VEGF antagonist SU5416. To test the suitability of hu-mice, we combined HIV with either SU5416 or hypoxia. Using right heart catheterization, we found that combining HIV+SU5416 exacerbated PH. HIV infection increases human pro-inflammatory cytokines in the lungs, compared to uninfected mice. Histopathological examinations showed pulmonary vascular inflammation with arterial muscularization in HIV-PH. We also found an increase in endothelial-monocyte activating polypeptide II (EMAP II) when combining HIV+SU5416. Therefore, combinations of HIV with SU5416 or hypoxia recapitulate PH in hu-mice, creating well-suited models for infectious mechanistic pulmonary vascular research in small animals.
House dust mites are microarthropods implicated in the cause of allergic diseases. Currently, there is no phylogenetic analysis of dust mites based on genomic or mitochondrial DNA (mtDNA) evidence. For the first time, we report evolutionary relationships based on partial mtDNA 12S rRNA sequences among the four dust mite families Pyroglyphidae (Dermatophagoides pteronyssinus), Glycyphagoidea (Glycyphagus privatus), Acaridae (Aleuroglyphus ovatus), and Echimyopodidae (Blomia tropicalis). Thirteen sequence variants were obtained and phylogenetic analysis showed two monophyletic clades composed of two species each. Contrary to current taxonomic classification, the Acaridae clustered in a monophyletic group with the Pyroglyphidae. Considering the current difficulties in identifying these medically important species for the purpose of eradication and treatment, it is significant that sequence data are capable of discriminating between species belonging to different families of dust mites.
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