The Florida College System, previously known as the Florida Community College System, comprises twenty-eight public community colleges and state colleges in the U.S. state of Florida. In 2011-12, enrollment consisted of more than 875,000 students. Together with the State University System of Florida, which includes Florida's twelve public four-year universities, it is part of Florida's system of public higher education.While governed by local boards of trustees, the colleges are coordinated under the jurisdiction of Florida's State Board of Education. Administratively, the Chancellor of the Florida College System is the chief executive officer of the system, reporting to the Commissioner of Education who serves as the chief executive officer of Florida's public education system. In 2009, the Florida Legislature changed the name from the "Florida Community College System" to the "Florida College System," reflecting the fact that some of its member institutions now offer four-year bachelor's degrees. As of 2014, only three members of the Florida College System retain the "community college" epithet. Wikipedia.
Conrad K.P.,Florida College
Seminars in Nephrology | Year: 2011
Relaxin is an approximately 6-kilodalton peptide hormone secreted by the corpus luteum, and circulates in the maternal blood during pregnancy. Relaxin administration to awake, chronically instrumented, nonpregnant rats mimics the vasodilatory phenomena of pregnancy. Furthermore, immunoneutralization of relaxin or its elimination from the circulation during midterm pregnancy in awake rats prevents maternal systemic and renal vasodilation, and the increase in global arterial compliance. Human investigation, albeit limited through 2010, also reveals vasodilatory effects of relaxin in the nonpregnant condition and observations consistent with a role for relaxin in gestational renal hyperfiltration. Evidence suggests that the vasodilatory responses of relaxin are mediated by its major receptor, the relaxin/insulin-like family peptide 1 receptor, RFXP1. The molecular mechanisms of relaxin vasodilation depend on the duration of hormone exposure (ie, there are rapid and sustained vasodilatory responses). Newly emerging data support the role of Gα i/o protein coupling to phosphatidylinositol-3 kinase/Akt (protein kinase B)-dependent phosphorylation and activation of endothelial nitric oxide synthase in the rapid vasodilatory responses of relaxin. Sustained vasodilatory responses critically depend on vascular endothelial and placental growth factors, and increases in arterial gelatinase(s) activity. Gelatinases hydrolyze big endothelin (ET) at a gly-leu bond to form ET 1-32, which activates the endothelial ET B/nitric oxide vasodilatory pathway. Although the relevance of relaxin biology to preeclampsia is largely speculative at this time, there are potential tantalizing links that are discussed in the context of our current understanding of the etiology and pathophysiology of the disease. © 2011 Elsevier Inc.
Williams C.A.,Florida College
American Journal of Medical Genetics, Part C: Seminars in Medical Genetics | Year: 2010
The Angelman syndrome is clinically delineated by the combination of seizures, absent speech, hypermotoric and ataxic movements and certain remarkable behaviors. Those with the syndrome have a predisposition toward apparent happiness and paroxysms of laughter, and this finding helps distinguish Angelman syndrome from other ones involving severe developmental handicap. In this review the core neurological features of the syndrome are discussed with a focus on those behaviors that make Angelman syndrome a prototypical genetic disorder expressing a behavioral phenotype. © 2010 Wiley-Liss, Inc.
Siemann D.W.,Florida College
Cancer Treatment Reviews | Year: 2011
The vasculature of solid tumors is fundamentally different from that of normal vasculature and offers a unique target for anti-cancer therapy. Direct vascular-targeting with Tumor-Vascular Disrupting Agents (Tumor-VDAs) is distinctly different from anti-angiogenic strategies, and offers a complementary approach to standard therapies. Tumor-VDAs therefore have significant potential when combined with chemotherapy, radiotherapy, and angiogenesis-inhibiting agents. Preclinical studies with the different Tumor-VDA classes have demonstrated key tumor-selective anti-vascular and anti-tumor effects. © 2010 Elsevier Ltd.
Streit W.J.,Florida College |
Xue Q.-S.,Florida College
Current Opinion in Immunology | Year: 2014
Microglial cells comprising the brain's immune system are essential for ensuring neuroprotection in the normal and pathological CNS. On the basis of histopathological observations in human brain, we believe that the ability of microglia to provide neuroprotection deteriorates as our brains get older and that such CNS immune senescence is a major factor contributing to the development of aging-related neurodegenerative diseases, notably Alzheimer's disease. The idea is consistent with the fact that immune senescence occurs naturally in the periphery, rendering the elderly people more susceptible to infections and cancers. There is an analogous situation in the brain, except that here the main impact comes down to diminished neuroprotection and resultant neurodegeneration. © 2014 Elsevier Ltd.
Kankotia S.,Florida College |
Stacpoole P.W.,Florida College
Biochimica et Biophysica Acta - Reviews on Cancer | Year: 2014
We reviewed the anti-cancer effects of DCA, an orphan drug long used as an investigational treatment for various acquired and congenital disorders of mitochondrial intermediary metabolism. Inhibition by DCA of mitochondrial pyruvate dehydrogenase kinases and subsequent reactivation of the pyruvate dehydrogenase complex and oxidative phosphorylation is the common mechanism accounting for the drug's anti-neoplastic effects. At least two fundamental changes in tumor metabolism are induced by DCA that antagonize tumor growth, metastases and survival: the first is the redirection of glucose metabolism from glycolysis to oxidation (reversal of the Warburg effect), leading to inhibition of proliferation and induction of caspase-mediated apoptosis. These effects have been replicated in both human cancer cell lines and in tumor implants of diverse germ line origin. The second fundamental change is the oxidative removal of lactate, via pyruvate, and the co-incident buffering of hydrogen ions by dehydrogenases located in the mitochondrial matrix. Preclinical studies demonstrate that DCA has additive or synergistic effects when used in combination with standard agents designed to modify tumor oxidative stress, vascular remodeling, DNA integrity or immunity. These findings and limited clinical results suggest that potentially fruitful areas for additional clinical trials include 1) adult and pediatric high grade astrocytomas; 2) BRAF-mutant cancers, such as melanoma, perhaps combined with other pro-oxidants; 3) tumors in which resistance to standard platinum-class drugs alone may be overcome with combination therapy; and 4) tumors of endodermal origin, in which extensive experimental research has demonstrated significant anti-proliferative, pro-apoptotic effects of DCA, leading to improved host survival. © 2014 Elsevier B.V.