Caribbean University is a nonprofit private university system in Puerto Rico composed of four campuses. It was founded on February 28, 1969, as the Caribbean Junior College in the municipality of Bayamon. In 1978, it was renamed to Caribbean University College after being accredited by the Council on Higher Education of Puerto Rico. In 1990, after starting to offer graduate studies, it was renamed to Caribbean University.The university is accredited by the Middle States Commission on Higher Education. Wikipedia.
Joseph T.D.,Caribbean University
Journal of Health Politics, Policy and Law | Year: 2016
The 2010 Patient Protection and Affordable Care Act (ACA) was passed to provide more affordable health coverage to Americans beginning in 2014. Modeled after the 2006 Massachusetts health care reform, the ACA includes an individual mandate, Medicaid expansion, and health exchanges through which middle-income individuals can purchase coverage from private insurance companies. However, while the ACA provisions exclude all undocumented and some documented immigrants, Massachusetts uses state and hospital funds to extend coverage to these groups. This article examines theACAreform using the Massachusetts reform as a comparative case study to outline how citizenship status influences individuals' coverage options under both policies. The article then briefly discusses other states that provide coverage to ACA-ineligible immigrants and the implications of uneven ACA implementation for immigrants and citizens nationwide. © 2016 by Duke University Press. Source
Voorbij A.M.W.Y.,University Utrecht |
van Steenbeek F.G.,University Utrecht |
Vos-Loohuis M.,University Utrecht |
Martens E.E.C.P.,University Utrecht |
And 4 more authors.
PLoS ONE | Year: 2011
Dwarfism in German shepherd dogs is due to combined pituitary hormone deficiency of unknown genetic cause. We localized the recessively inherited defect by a genome wide approach to a region on chromosome 9 with a lod score of 9.8. The region contains LHX3, which codes for a transcription factor essential for pituitary development. Dwarfs have a deletion of one of six 7 bp repeats in intron 5 of LHX3, reducing the intron size to 68 bp. One dwarf was compound heterozygous for the deletion and an insertion of an asparagine residue in the DNA-binding homeodomain of LHX3, suggesting involvement of the gene in the disorder. An exon trapping assay indicated that the shortened intron is not spliced efficiently, probably because it is too small. We applied bisulfite conversion of cytosine to uracil in RNA followed by RT-PCR to analyze the splicing products. The aberrantly spliced RNA molecules resulted from either skipping of exon 5 or retention of intron 5. The same splicing defects were observed in cDNA derived from the pituitary of dwarfs. A survey of similarly mutated introns suggests that there is a minimal distance requirement between the splice donor and branch site of 50 nucleotides. In conclusion, a contraction of a DNA repeat in intron 5 of canine LHX3 leads to deficient splicing and is associated with pituitary dwarfism. © 2011 Voorbij et al. Source
Rastogi D.,Yeshiva University |
Canfield S.M.,Yeshiva University |
Canfield S.M.,Columbia University |
Andrade A.,Yeshiva University |
And 5 more authors.
Chest | Year: 2012
Background: Obesity-associated asthma has been proposed to be a distinct entity, differing in immune pathogenesis from atopic asthma. Both obesity-mediated inflammation and increase in adiposity are potential mechanistic factors that are poorly defined among children. We hypothesized that pediatric obesity-associated asthma would be characterized by T helper (Th) 1, rather than the Th2 polarization associated with atopic asthma. Moreover, we speculated that Th1 biomarkers and anthropometric measures would correlate with pulmonary function tests (PFTs) in obese asthmatic children. Methods: We recruited 120 children, with 30 in each of the four study groups: obese asthmatic children, nonobese asthmatic children, obese nonasthmatic children, and nonobese nonasthmatic children. All children underwent pulmonary function testing. Blood was collected for measurement of serum cytokines. T-cell responses to mitogen, phorbol 12-myristate 13-acetate (PMA), or antigens tetanus toxoid or Dermatophagoides farinae were obtained by flow cytometric analysis of intracellular cytokine staining for interferon-γ (IFN-γ) (Th1) or IL-4 (Th2) within the CD4 population. Results: Obese asthmatic children had significantly higher Th1 responses to PMA (P < .01) and tetanus toxoid (P < .05) and lower Th2 responses to PMA (P < .05) and D farinae (P < .01) compared with nonobese asthmatic children. Th-cell patterns did not differ between obese asthmatic children and obese nonasthmatic children. Obese asthmatic children had lower FEV 1/FVC (P < .01) and residual volume/total lung capacity ratios (P < .005) compared with the other study groups, which negatively correlated with serum interferon-inducible protein 10 and IFN-γ levels, respectively. PFTs, however, did not correlate with BMI z score or waist to hip ratio. Conclusions: We found that pediatric obesity-associated asthma differed from atopic asthma and was characterized by Th1 polarization. The altered immune environment inversely correlated with PFTs in obese asthmatic children. © 2012 American College of Chest Physicians. Source
Macpherson C.C.,Caribbean University
Bioethics | Year: 2013
Climate change harms health and damages and diminishes environmental resources. Gradually it will cause health systems to reduce services, standards of care, and opportunities to express patient autonomy. Prominent public health organizations are responding with preparedness, mitigation, and educational programs. The design and effectiveness of these programs, and of similar programs in other sectors, would be enhanced by greater understanding of the values and tradeoffs associated with activities and public policies that drive climate change. Bioethics could generate such understanding by exposing the harms and benefits in different cultural, socioeconomic, and geographic contexts, and through interdisciplinary risk assessments. Climate change is a bioethics problem because it harms everyone and involves health, values, and responsibilities. This article initiates dialog about the responsibility of bioethics to promote transparency and understanding of the social values and conflicts associated with climate change, and the actions and public policies that allow climate change to worsen. © 2013 John Wiley & Sons Ltd. Source
Kung L.-H.,Loyola University Chicago |
Glasgow J.,Loyola University Chicago |
Ruszaj A.,Loyola University Chicago |
Ruszaj A.,University of Michigan |
And 3 more authors.
American Journal of Physiology - Regulatory Integrative and Comparative Physiology | Year: 2010
Serotonin is thought to contribute to the syncopal-like response that develops during severe blood loss by inhibiting presympathetic neurons of the rostroventrolateral medulla (RVLM). Here, we tested whether serotonin cells activated during hypotensive hemorrhage, i.e., express the protein product of the immediate early gene c-Fos, are critical for the normal sympathetic response to blood loss in unanesthetized rats. Serotonin-immunoreactive cells of the raphe obscurus and raphe magnus, parapyramidal cells of the B3 region, subependymal cells of the ventral parapyramidal region, and cells of the ventrolateral periaqueductal gray region were activated by hypotensive hemorrhage, but not by hypotension alone. In contrast to findings in anesthetized animals, lesion of hindbrain serotonergic cells sufficient to produce >80% loss of serotonin nerve terminal immunoreactivity in the RVLM accelerated the sympatholytic response to blood loss, attenuated recovery of sympathetic activity after termination of hemorrhage, and exaggerated metabolic acidosis. Hindbrain serotonin lesion also attenuated ventilatory and sympathetic responses to stimulation of central chemoreceptors but increased spontaneous arterial baroreflex sensitivity and decreased blood pressure variability. A more global neurotoxic lesion that also eliminated tryptophan hydroxylase- immunoreactive cells of the ventrolateral periaqueductal gray region had no further effect on the sympatholytic response to blood loss. Together, the data indicate that serotonin cells of the caudal hindbrain contribute to compensatory responses following blood loss that help maintain oxygenation of peripheral tissue in the unanesthetized rat. This effect may be related to facilitation of chemoreflex responses to acidosis. Copyright © 2010 the American Physiological Society. Source