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62 results on '"J. Alexander Palesty"'

51. Deletion of Newly Described Molecule, Pellino1, Aggravates Blood Perfusion and Neovascularization and Exerts Increased Tissue Fibrosis in a Murine Model of Hind-Limb Ischemia

Author

Vaithinathan Selvaraju, Inam A. Shaikh, Muhammad Tipu Rishi, Nilanjana Maulik, David W. McFadden, and J. Alexander Palesty

Subjects
Neovascularization, Pathology, medicine.medical_specialty, business.industry, Murine model, Tissue fibrosis, Medicine, Surgery, medicine.symptom, business, Perfusion, Hind limb ischemia
Published
2015
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52. The goldilocks paradigm of starvation and refeeding

Author

Stanley J. Dudrick and J. Alexander Palesty

Subjects
Starvation, Blood Glucose, 0303 health sciences, Nutrition and Dietetics, 030309 nutrition & dietetics, business.industry, Nutritional Support, Contraindications, Fatty Acids, Malnutrition, Medicine (miscellaneous), Proteins, Computational biology, 03 medical and health sciences, 0302 clinical medicine, Goldilocks principle, Medicine, Humans, 030211 gastroenterology & hepatology, medicine.symptom, business, Energy Metabolism
Published
2006

53. Side effects of therapy: case 3. Gastric cancer after radiotherapy of pediatric Hodgkin's disease

Author

J. Alexander Palesty, Wei Wang, Milind Javle, and Gary Y. Yang

Subjects
Oncology, Cancer Research, medicine.medical_specialty, Pediatric Hodgkin's disease, Radiotherapy, business.industry, Stomach, medicine.medical_treatment, Cancer, Neoplasms, Second Primary, medicine.disease, Hodgkin Disease, Lymphoma, Radiation therapy, medicine.anatomical_structure, Stomach Neoplasms, Internal medicine, medicine, Humans, Female, business, Child
Published
2004

54. Lymphoplasmacytic sclerosing pancreatitis: inflammatory mimic of pancreatic carcinoma

Author

Sharon M, Weber, Olcay, Cubukcu-Dimopulo, J Alexander, Palesty, Arief, Suriawinata, David, Klimstra, Murray F, Brennan, and Kevin, Conlon

Subjects
Adult, Male, medicine.medical_specialty, Pancreatic disease, Adolescent, Plasma Cells, Adenocarcinoma, Malignancy, Gastroenterology, Autoimmune Diseases, Diagnosis, Differential, Recurrent pancreatitis, Internal medicine, Carcinoma, Medicine, Humans, Lymphocytes, Pancreas, Autoimmune pancreatitis, Aged, Aged, 80 and over, Sclerosis, business.industry, Jaundice, Middle Aged, medicine.disease, Pancreatic Neoplasms, medicine.anatomical_structure, Pancreatitis, Surgery, Female, medicine.symptom, business
Abstract

Lymphoplasmacytic sclerosing pancreatitis (LP) is a rare cause of benign mass lesions of the pancreas that can resemble adenocarcinoma. This study evaluates and classifies a series of patients with LP. Patients with benign pancreatic disease were identified from a prospective pancreatic database, and these cases were reviewed to identify patients with LP. Patients were subdivided into two groups: (1) classic LP, which included those patients who had all four of the characteristic histologic features of LP, including lymphoplasmacytic infiltration of the pancreas, interstitial fibrosis, periductal inflammation, and peri-phlebitis; and (2) intermediate LP, which included patients with at least two of these histologic findings. Patient demographics, pathologic and clinical features, and outcome were analyzed. From 1985 to 2001, a total of 1287 pancreatic resections were performed at our institution, of which 159 were for benign disease. Of these, 31 had pathologic features consistent with LP, and all of these patients had a presumed preoperative diagnosis of pancreatic carcinoma. Most of these patients presented with jaundice (n = 21) or abdominal pain (n = 7). In 29 of 31 patients, curative resection was possible. Of these, 28% (8/29) developed recurrence after resection: seven with jaundice and one with recurrent pancreatitis (median time to recurrence, 11 months; median follow up, 38 months). All patients with recurrent jaundice appeared to have biliary strictures at the time of direct cholangiography and no patient had malignancy. A review of the pathology reports identified 19 patients with classic LP and 12 patients with intermediate LP, and there was no difference between these two groups. LP is a rare cause of pancreatitis that is difficult to differentiate from carcinoma preoperatively. Patients with classic and intermediate LP appear to demonstrate a similar clinical behavior. Nearly one third of patients have a progressive course after resection, with 25% developing recurrent jaundice; thus close follow-up is mandatory for all patients.

Published
2003

58. Thioredoxin-1 (Trx-1) engineered mesenchymal stem cell therapy increased proangiogenic factors, reduced fibrosis and improved heart function in the infarcted rat myocardium

Author

Vaithinathan Selvaraju, David W. McFadden, Mahesh Thirunavukkarasu, Juan A. Sanchez, Nilanjana Maulik, J. Alexander Palesty, and Sumanth C Suresh

Subjects
medicine.medical_specialty, business.industry, Mesenchymal stem cell, Thioredoxin-1, medicine.disease, Fibrosis, Internal medicine, Cancer research, Cardiology, medicine, Surgery, Rat myocardium, business, Function (biology)
Published
2013
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59. Overexpression of glutaredoxin-1 stimulates revascularization and improves blood perfusion in a murine hind-limb ischemia model

Author

Salim S. Abunnaja, Vaithinathan Selvara, J. Alexander Palesty, Mahesh Thirunavukka, Nilanjana Maulik, and David W. McFadden

Subjects
medicine.medical_specialty, business.industry, Internal medicine, Glutaredoxin, medicine.medical_treatment, medicine, Cardiology, Surgery, business, Revascularization, Perfusion, Hind limb ischemia
Published
2013
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62. Thioredoxin-1 augments wound healing and promote angiogenesis in a murine ischemic full-thickness wound model.

Author

Saad I, Fournier CT, Wilson RL, Lakshmanan R, Selvaraju V, Thirunavukkarasu M, Alexander Palesty J, McFadden DW, and Maulik N

Subjects
Adenoviridae genetics, Animals, Cells, Cultured, Disease Models, Animal, Genetic Vectors administration & dosage, Genetic Vectors genetics, Human Umbilical Vein Endothelial Cells, Humans, Ischemia etiology, Male, Mice, Oxidative Stress genetics, Skin injuries, Treatment Outcome, Genetic Therapy methods, Ischemia therapy, Neovascularization, Physiologic genetics, Thioredoxins genetics, Wound Healing genetics
Abstract

Background: Nonhealing wounds are a continuing health problem in the United States. Overproduction of reactive oxygen species is a major causative factor behind delayed wound healing. Previously we reported that thioredoxin-1 treatment could alleviate oxidative stress under ischemic conditions, such as myocardial infarction and hindlimb ischemia. In this study, we explored the potential for thioredoxin-1 gene therapy to effectively aid wound healing through improved angiogenesis in a murine ischemic wound model., Methods: Full-thickness, cutaneous, ischemic wounds were created in the dorsum skin flap of 8- to 12-week-old CD1 mice. Nonischemic wounds created lateral to the ischemic skin flap served as internal controls. Mice with both ischemic wounds and nonischemic wounds were treated with Adeno-LacZ (1 × 10 9 pfu) or Adeno-thioredoxin-1 (1 × 10 9 pfu), injected intradermally around the wound. Digital imaging was performed on days 0, 3, 6, and 9 to assess the rate of wound closure. Tissue samples collected at predetermined time intervals were processed for immunohistochemical analysis., Results: No significant differences in wound closure were identified among the nonischemic wounds control, nonischemic wounds-LacZ, and nonischemic wounds-thioredoxin-1 groups. Hence, only mice with ischemic wounds were further analyzed. The ischemic wounds-thioredoxin-1 group had significant improvement in wound closure on days 6 and 9 after surgery compared with the ischemic wounds control and ischemic wounds-LacZ groups. Immunohistochemical analysis indicated increased thioredoxin-1, vascular endothelial cell growth factor, and β-catenin levels in the ischemic wounds-thioredoxin-1 group compared with the ischemic wounds control and ischemic wounds-LacZ groups, as well as increased capillary density and cell proliferation, as represented by Ki-67 staining., Conclusion: Taken together, thioredoxin-1 gene therapy promotes vascular endothelial cell growth factor signaling and re-epithelialization and activates wound closure in mice with ischemic wounds., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Published
2018
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