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  • Book
    Giuseppe Mancia, Guido Grassi, Gianfranco Parati, Alberto Zanchetti.
    Summary: This book addresses all aspects of white coat hypertension? the phenomenon of raised blood pressure in a medical setting yet not elsewhere? from its history to its pathophysiology, diagnosis and treatment. White coat hypertension is a common condition, accounting for 30?40% of the overall hypertensive population. While many studies have addressed this condition, controversy still exists over whether it causes an increased risk to sufferers and should be treated. In the volume neurogenic and non-neurogenic mechanisms are discussed and the significance of various predictive factors, evaluated. The association of white coat hypertension with dysmetabolic risk factors, new-onset diabetes and other conditions is carefully reviewed. Further chapters consider the occurrence of asymptomatic organ damage and cardiovascular outcomes in affected patients, and helpful guidance is also provided on the controversial issue of when to treat and when not to treat. White Coat Hypertension is based largely on work done during the past 30 years by renowned researchers working in Milan, who have made key contributions in improving knowledge of the condition and whose work is well known across the world.

    Contents:
    1 Historical Notes
    2 Definition, Terminology and Prevalence
    3 Diagnostic Approach to white coat effect and white coat hypertension
    4 Neurogenic and Non-neurogenic Mechanisms
    5 Predictive Factors
    6 White coat hypertension and cardiovascular morbidity and mortality
    7 White coat hypertension and Target Organ Damage
    8 White Coat Hypertension, metabolic risk factors, and cardiovascular risk profile
    9 To Treat or Not To Treat?.
    Digital Access Springer 2015
  • Article
    Sagawa A, Abdou NI.
    J Clin Invest. 1979 Mar;63(3):536-9.
    Circulating antibodies that could be responsible for the suppressor thymus-derived (T)-cell dysfunction in active systemic lupus erythematosus (SLE) were investigated. Sera from 14 active and inactive SLE patients were compared with a pool of 22 normal sera. All sera were adsorbed with a pool of normal platelets to exclude antihistocompatibility leukocyte antigen antibodies; with AB erythrocytes to exclude isohemagglutinins; and with a pool of normal bone marrow-derived (B) lymphocytes, monocytes, and neutrophils to deplete anti-B-cell antibodies, Fc-receptor antibodies, and antibodies directed against neutrophils or monocytes. Sera from active SLE patients were capable of inhibiting the activation of normal, blood lymphocytes by concanavalin A to become suppressor cells. The latter were assayed by coculturing the concanavalin A-activated cells with autologous lymphocytes, which were then activated with either phytohemagglutinin for proliferative response or with pokeweed mitogen for B-cell immunoglobulin (Ig) synthesis and secretion. Specific incorporation of cultures with phytohemagglutinin showed a value of 67+/-13 (mean+/-SD) for suppressor cells treated with adsorbed, active SLE sera. This value was significantly different (P < 0.001) from that of cells treated with the inactive SLE sera or with the pool of normal sera. Similar findings were seen with respect to the B-cell target parameters. Cytoplasmic Ig and IgG in supernates of cultures with pokeweed mitogen showed values of 17+/-5% and 717+/-134 ng/culture, respectively, for suppressor cells treated with the adsorbed, active SLE sera. This was significantly different from those treated with the inactive SLE sera or with the pool of normal sera. The antisuppressor-cell factor was shown to be IgG, complement independent, not cytotoxic, active at 37 degrees C and at room temperature, but not at 4 degrees C, and adsorbable with T cells. Suppressor T-cell antibody in sera of active SLE patients could be responsible for the observed suppressor T-cell dysfunction seen in active SLE. The mechanisms responsible for the induction of the antisuppressor-cell antibody are unknown.
    Digital Access Access Options