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Your search keyword '"Kim, Mindy M."' showing total 13 results
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13 results on '"Kim, Mindy M."'

11. Primary mucoepidermoid carcinoma of the skin: a retrospective investigation in the Surveillance, Epidemiology, and End Results Database from 1975 to 2016.

Author

Maloney, Nolan J., Nguyen, Kevin A., Tegtmeyer, Kyle, Kim, Mindy M., Zhao, Jeffrey, Yang, Jason J., Cheng, Kyle, and Bach, Daniel Q.

Subjects
EPIDEMIOLOGY, CARCINOMA, INVESTIGATIONS, SKIN, SWEAT glands
Abstract

Dear Editor, Mucoepidermoid carcinoma is typically a low-grade malignancy of the salivary glands. In addition, it is possible that cases of secondary metastasis of mucoepidermoid carcinomas could mistakenly be coded as primary tumors, and the workup and histopathologic examination to exclude another primary site or differentiate this tumor from adenosquamous carcinoma may have varied between patients. Mucoepidermoid carcinoma of the skin: a distinct entity from adenosquamous carcinoma: a case study with a review of the literature. [Extracted from the article]

Published
2020
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12. Maintenance of normal blood pressure is dependent on IP3R1-mediated regulation of eNOS.

Author

Qi Yuan, Jingyi Yang, Santulli, Gaetano, Reiken, Steven R., Wronska, Anetta, Kim, Mindy M., Osborne, Brent W., Lacampagne, Alain, Yuxin Yin, and Marks, Andrew R.

Subjects
REGULATION of blood pressure, ENDOTHELIAL cells, NITRIC oxide regulation, ENDOPLASMIC reticulum, INTRACELLULAR calcium
Abstract

Endothelial cells (ECs) are critical mediators of blood pressure (BP) regulation, primarily via the generation and release of vasorelaxants, including nitric oxide (NO). NO is produced in ECs by endothelial NO synthase (eNOS),which is activated by both calcium(Ca2+)-dependent and independent pathways. Here, we report that intracellular Ca2+ release from the endoplasmic reticulum(ER) via inositol 1,4,5-trisphosphate receptor (IP3R) is required for Ca2+-dependent eNOS activation. EC-specific type 1 1,4,5-trisphosphate receptor knockout (IP3R1-/-) mice are hypertensive and display blunted vasodilation in response to acetylcholine (ACh). Moreover, eNOS activity is reduced in both isolated IP3R1-deficient murine ECs and human ECs following IP3R1 knockdown. IP3R1 is upstream of calcineurin, a Ca2+/calmodulinactivated serine/threonine protein phosphatase. We show here that the calcineurin/nuclear factor of activated T cells (NFAT) pathway is less active and eNOS levels are decreased in IP3R1-deficient ECs. Furthermore, the calcineurin inhibitor cyclosporin A, whose use has been associated with the development of hypertension, reduces eNOS activity and vasodilation following ACh stimulation. Our results demonstrate that IP3R1 plays a crucial role in the ECmediated vasorelaxation and the maintenance of normal BP. [ABSTRACT FROM AUTHOR]

Published
2016
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13. Maintenance of normal blood pressure is dependent on IP3R1-mediated regulation of eNOS

Author

Yuxin Yin, Gaetano Santulli, Brent W. Osborne, Steven Reiken, Anetta Wronska, Qi Yuan, Alain Lacampagne, Andrew R. Marks, Mindy M. Kim, Jingyi Yang, Columbia University Medical Center [New York], New York Presbyterian Hospital, Peking University [Beijing], Columbia University Irving Medical Center (CUIMC), Department of Physiology & Cellular Biophysics, Columbia University [New York], Physiologie & médecine expérimentale du Cœur et des Muscles [U 1046] (PhyMedExp), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Columbia University College of Physicians and Surgeons, MORNET, Dominique, Yuan, Qi, Yang, Jingyi, Santulli, Gaetano, Reiken, Steven R, Wronska, Anetta, Kim, Mindy M, Osborne, Brent W, Lacampagne, Alain, Yin, Yuxin, Marks, Andrew R., Peking University Health Science Center, Beijing, and Peking University Health Science Center

Subjects
0301 basic medicine, medicine.medical_specialty, Endothelium, endothelium, Nitric Oxide Synthase Type III, Molecular biology, Physiology, [SDV]Life Sciences [q-bio], Vasodilator Agents, IP3 receptor, Vasodilation, Blood Pressure, Mice, Transgenic, Medical sciences, Nitric oxide, 03 medical and health sciences, chemistry.chemical_compound, Enos, Cyclosporin a, Internal medicine, medicine, Animals, Humans, Inositol 1,4,5-Trisphosphate Receptors, Cells, Cultured, Blood pressure--Regulation, Mice, Knockout, Multidisciplinary, calcium, biology, Endothelial Cells, NFAT, Inositol trisphosphate receptor, Biological Sciences, biology.organism_classification, Acetylcholine, Calcineurin, [SDV] Life Sciences [q-bio], Mice, Inbred C57BL, 030104 developmental biology, medicine.anatomical_structure, Endocrinology, chemistry, Gene Expression Regulation, Calcium--Physiological effect, FOS: Biological sciences, Hypertension, eNOS
Abstract

International audience; Endothelial cells (ECs) are critical mediators of blood pressure (BP) regulation, primarily via the generation and release of vasorelaxants, including nitric oxide (NO). NO is produced in ECs by endothelial NO synthase (eNOS), which is activated by both calcium (Ca(2+))-dependent and independent pathways. Here, we report that intracellular Ca(2+) release from the endoplasmic reticulum (ER) via inositol 1,4,5-trisphosphate receptor (IP3R) is required for Ca(2+)-dependent eNOS activation. EC-specific type 1 1,4,5-trisphosphate receptor knockout (IP3R1(-/-)) mice are hypertensive and display blunted vasodilation in response to acetylcholine (ACh). Moreover, eNOS activity is reduced in both isolated IP3R1-deficient murine ECs and human ECs following IP3R1 knockdown. IP3R1 is upstream of calcineurin, a Ca(2+)/calmodulin-activated serine/threonine protein phosphatase. We show here that the calcineurin/nuclear factor of activated T cells (NFAT) pathway is less active and eNOS levels are decreased in IP3R1-deficient ECs. Furthermore, the calcineurin inhibitor cyclosporin A, whose use has been associated with the development of hypertension, reduces eNOS activity and vasodilation following ACh stimulation. Our results demonstrate that IP3R1 plays a crucial role in the EC-mediated vasorelaxation and the maintenance of normal BP.

Published
2016

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