Browsing by Subject "Surgery"
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Item Absorption from the Urinary Tract(1922-03) Magoun, James Albert HughesItem The Blood Supply of the Thyroid Gland and its Surgical Significance(1922-04) Mastin, Edward VernonItem Blood Transfusion(1918-06) Pemberton, John deJarnetteItem Cancer of the Stomach(1919-05) McDowell, Ivan WodrowItem Item Chronic Arthritis: A Clinical and Bacteriological Study of Eighty Cases(1922-04) Brock, SamItem Cystic and Fibrocystic Disease of the Long Bones(1918-06) Meyerding, Henry WilliamItem The Determination of An Effective Smile(2016-04-14) Ruprecht, Mark, R.; Helwig, Nathaniel, E.Item Determinations of Gastric Acidity Following Gastro-Enterostomy(1920-05) White, Paul AmosItem Diseases of the Thyroid Gland(1922-04) Jackson, Arnold StevensItem The Effect Upon the Kidney of Various Surgical Procedures upon its Ureter, Blood Supply and Capsule(1920-05) Harrington, Stuart WilliamItem Elephantiasis: A Clinical Review and an Attempt at Experimental Reproduction(1921-05) Mahon, George DixonItem Epithelioma of the Penis (A Study of Fifty-Four Cases)(1921-05) Sanderson, Frederick RomanItem Experimental and Clinical Results of Nerve Anastomoses(1918-06) Adson, Alfred WashingtonItem Graft antigen-specific CD4+ T cells require CD154 expression to clonally expand and differentiate to the TH1 phenotype and initiate mTOR dependant intimal hyperplasia in cardiac allografts(2009-08) Huddleston, Stephen James MDA defined model system was used to address the role of minor histocompatibility antigen-specific CD4+ T cells in cardiac allograft vasculoopathy (CAV). The coronary arteries of vascularized heart grafts from Act-mOVA transgenic mice expressing the model antigen ovalbumin developed CAV in normal recipients and those lacking CD8+ T cells but not in those lacking CD4+ T cells. Furthermore, purified ovalbumin-specific CD4+ T cells from T cell antigen receptor (TCR) transgenic mice caused CAV in ovalbumin-expressing heart grafts in lymphocyte-deficient mice. This model system was used to study the role of CD154 expression, specific T helper subtype cytokine secretion, and the post CD4+ T cell-mediated injury phase of intimal hyperplasia. The graft antigenspecific CD4+ T cells only caused intimal hyperplasia when expressing CD154 and were found in the intima of the affected coronary arteries along with CD40+ cells. These results show that minor histocompatibility antigen-specific CD4+ T cells are required to cause cardiac allograft vasculopathy. They are capable of doing so without contributions from other lymphocytes, and may cause CAV by using CD154 to stimulate other nonlymphoid cells in the intima. The mechanism of CD154-dependant CD4+ T cell mediated CAV is not known. In order to determine the relevant cytokine profile involved in CD4+ T cell mediated CAV, ovalbumin-specific CD4+ T cells were differentiated in vitro into TH1, TH2, and TH17 cells, which produce the prototypic cytokines, IFN-, IL-4, and IL-17, respectively, and transferred into lymphocyte-deficient recipients of ovalbuminexpressing heart grafts. In vitro-generated TH1 and TH17, but not TH2 cells caused CAV. However, naïve ovalbumin-specific CD4+ T cells differentiated only into TH1 cells in vivo in recipients of ovalbumin-expressing heart grafts. Surprisingly, ovalbuminexpressing grafts transplanted into both STAT-4-deficient recipients with defective TH1 subset generation and IFN-y-deficient recipients developed CAV, although to a less severe degree than in wild-type recipients. Furthermore, IFN-y-deficient ovalbuminspecific CD4+ T cells caused CAV similar to normal ovalbumin-specific CD4+ T cells. Thus, minor antigen-specific CD4+ T cells differentiate to the TH1 subset in the presence of heart grafts expressing the relevant antigen, causing CAV in the absence of other lymphocytes. Although IFN-y is involved, it is not the only factor produced by these cells that causes CAV. Whether a single episode of CD4+ T cell mediated injury, as opposed to multiple rejection episodes or ongoing activation, are required for the development of CAV is not known. When CD4+ T cells were depleted after the peak of clonal expansion but before the onset of intimal hyperplasia, CAV still developed in Act-mOVA grafts, suggesting that graft antigen-specific CD4+ T cells are critical for the immune injury phase of CAV but are not required once the graft is injured. Furthermore, the intimal hyperplasia phase of CAV was found to be mTOR dependant. Although graft antigenspecific CD4+ T cells initiate CAV, they are not necessary for progression of CAV.Item The Histogenesis of Carcinoma in the Islets of the Pancreas(1919-05) Horgan, Edmund JosephItem Infections of the Kidney(1919-05) Tucker, William JosephItem Interview with Alfred Michael(University of Minnesota, 2012-04-25) Tobbell, Dominique A.; Michael, Alfred F.Dr. Alfred Michael begins his interview with a reflection on his childhood and education in Philadelphia and his interests in medicine and pediatrics. He describes his decision to move to the University of Minnesota in order to work with Dr. Robert A. Good. He then discusses all of the following in relation to his research: working with Robert Vernier; changes in technology and methodology related to testing the kidney; his graduate work in biochemistry; specialization in medical research; work on transplantation and dialysis with John Najarian and Carl Kjellstrand; kidney research at the University; the expansion of and coverage for dialysis; and his time in Copenhagen. Dr. Michael then describes Dr. John Anderson’s tenure as department chair and his own tenure as dean, during which he made efforts to create a major children’s hospital facility in combination with the University. He also reflects on the larger context of changes in healthcare structures in the period, particularly the emergence of HMOs and Minnesota’s role in the development of HMOs, and town/gown relations in the Twin Cities. Dr. Michael then discusses Robert Howard and David Brown’s tenures as dean of the Medical School and issues with private practice and finances at the University. Turning to administrative matters, Dr. Michael describes his work with Win Wallin; William Brody’s tenure as provost of the AHC; and the growth of the administrative power of the AHC. He then elaborates on the creation of University of Minnesota Clinical Associates and University of Minnesota Physicians; the sale of University Hospital to Fairview; divisions of responsibility and administration within the AHC; relations between different schools in the AHC; and the investigation of John Najarian in connection with Antilymphocyte Globulin (ALG). He concludes with reflections on the balance of research, teaching, and clinical work; his moves into administrative positions; his work on various boards; his work with the Legislature; and the Medical School’s standing.Item Interview with Davitt Felder(University of Minnesota, 2009-12-04) Tobbell, Dominique A.; Felder, DavittDavitt Felder discusses his background and provides an overview of his career. He describes why he went into medicine and surgery; his decision to enter private practice; and his decision to retire. He discusses at length the establishment of the Northern Association for Medical Education and the organization’s attempt to establish a medical school in St. Paul. He describes his work in vascular surgery and the establishment of the Midwestern Board for Medical and Allied Education. He discusses the relationship between Minneapolis and St. Paul private physicians and the University of Minnesota; the private practice issue at the University of Minnesota; and Robert Howard, Owen Wangensteen, Walter Lillehei, Michael E DeBakey; the relationship between the Surgery Department and other clinical departments; and his work with the Health Care Financing Administration.Item Interview with Ellis Benson(University of Minnesota, 2009-12-01) Tobbell, Dominique A.; Benson, EllisEllis Benson starts with his background, including growing up in China (his parents were missionaries), why he went into medicine and academic medicine, and his educational history. He discusses his residency in pathology at the UMN, his internal medicine residency at the VA Hospital, joining the Department of Laboratory Medicine, his work while he was in charge of the blood bank, his work as director of Clinical Laboratories, and his work as head of Pathology. He offers reflections on cardiac surgeons Richard Varco and Walter Lillehei and how they dealt with the Lab and the Blood Bank, as well as working with the Department of Surgery and surgeons more generally. He discusses the appointment of Robert Howard as dean of the College of Medical Sciences in 1959 and Howard’s deanship, the Vice President of the Health Sciences search and the appointment of Lyle French. He also discusses Franz Halberg, and David Brown. He discusses his work on protein chemistry and going to the Carlsberg Laboratory in Copenhagen, the UMN’s Clinical Laboratory providing community services to anyone in Minnesota, the Medical Technology program, why technologists tended to be women, and specialization in medicine. He describes the founding of the Academy of Clinical Laboratory Physicians and Scientists, the creation of the Department of Laboratory Medicine at the UMN in 1959, space issues in the late 1950s and early 1960s, the merger of Laboratory Medicine and Pathology, and the relationships between the clinical and basic science departments within the Medical School. He discusses the attempt to establish a second medical school in St. Paul, relations between the Medical School and other UMN health science schools in the 1960s and 1970s, faculty attitudes toward the 4 reorganization in 1970, the impact of the introduction of Medicaid and Medicare, the attempt to create a School of Allied Health Sciences in the late 1960s and early 1970s, relations between the Medical School and the Mayo Clinic, and relations with the University Hospitals.