Tampa, Florida, United States
Tampa, Florida, United States

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With an upcoming publication in the Worldwide Leaders in Healthcare, Crystal Blair, MSN, ARNP, AGPCNP-BC, AGNP-C, PMHNP-BC, joins the prestigious ranks of the International Nurses Association. Crystal Blair is a Nurse Practitioner with three years of experience in her field and an extensive expertise in all facets of nursing, especially Adult-Gerontology Primary Care and Psychiatric Mental Health. Crystal is currently serving patients at James A. Haley Veterans Hospital in Tampa/St. Petersburg, Florida. Crystal graduated with her Nursing Degree, Bachelor of Science Degree in Nursing, and Master of Science Degree in Nursing all from the University of Florida. She holds an additional Postmaster’s Degree Certificate as a Psychiatric Mental Health Nurse Practitioner from Florida International University. An advocate for continuing education, Crystal is currently pursuing her Doctor of Nursing Practice Degree from the University of Florida. Crystal attributes her great success to her passion for quality patient care and her drive to make a difference. When she is not assisting patients, Crystal enjoys traveling. Learn more about Crystal here: http://inanurse.org/network/index.php?do=/4134490/info/ and read her upcoming publication in the Worldwide Leaders in Healthcare.


Desai S.,Haley Veterans Hospital | Desai S.,University of South Florida | Pillai P.,Haley Veterans Hospital | Pillai P.,University of South Florida | And 4 more authors.
Biochimica et Biophysica Acta - Molecular Cell Research | Year: 2011

The focus of this research was to investigate the role of protein kinase C-iota (PKC-ι) in regulation of Bad, a pro-apoptotic BH3-only molecule of the Bcl-2 family in glioblastoma. Robust expression of PKC-ι is a hallmark of human glioma and benign and malignant meningiomas. The results were obtained from the two human glial tumor derived cell lines, T98G and U87MG. In these cells, PKC-ι co-localized and directly associated with Bad, as shown by immunofluorescence, immunoprecipitation, and Western blotting. Furthermore, in-vitro kinase activity assay showed that PKC-ι directly phosphorylated Bad at phospho specific residues, Ser-112, Ser-136 and Ser-155 which in turn induced inactivation of Bad and disruption of Bad/Bcl-XL dimer. Knockdown of PKC-ι by siRNA exhibited a corresponding reduction in Bad phosphorylation suggesting that PKC-ι may be a Bad kinase. PKC-ι knockdown also induced apoptosis in both the cell lines. Since, PKC-ι is an essential downstream mediator of the PI (3)-kinase, we hypothesize that glioma cell survival is mediated via a PI (3)-kinase/PDK1/PKC-ι/Bad pathway. Treatment with PI (3)-kinase inhibitors Wortmannin and LY294002, as well as PDK1 siRNA, inhibited PKC-ι activity and subsequent phosphorylation of Bad suggesting that PKC-ι regulates the activity of Bad in a PI (3)-kinase dependent manner. Thus, our data suggest that glioma cell survival occurs through a novel PI (3)-kinase/PDK1/PKC-ι/BAD mediated pathway. © 2011.

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