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  • Book
    Aristidis Veves, John M. Giurini, Frank W. LoGerfo, editors.
    Contents:
    Clinical features and diagnosis
    Principles of care in the diabetic surgical patient
    Epidemiology and health care cost of diabetic foot problems
    Diabetic polyneuropathy
    Clinical examination and risk classification of the diabetic foot
    Clinical features and diagnosis of peripheral arterial disease
    Imaging of infection in the diabetic foot
    Pathophysiology
    Physiology and pathophysiology of wound healing in diabetes
    Neuropeptides and diabetic wound-healing
    Induced regeneration of skin and peripheral nerves in the adult
    Microvascular changes in the diabetic foot
    Biomechanics of the diabetic foot: the road to foot ulceration
    Diabetic foot ulcers: effects of hypertoxia and stromal-derived factor-1[alpha] on endothelial progenitor cells
    Management of the diabetic foot
    Wound bed preparation of the diabetic foot ulcer
    Foot pressure abnormalities in the diabetic foot
    Proactive wound care
    Local care of diabetic foot ulcers: assessment, dressings, and topical treatments
    Surgical treatment of the ulcerated foot
    Microbiology and treatment of diabetic foot infections
    Lower extremity arterial reconstruction in patients with diabetes mellitus: principles of treatment
    Charcot arthropathy in the diabetic foot
    Soft tissue reconstruction options for the ulcerated or gangrenous diabetic foot
    Amputations and rehabilitation
    Organization and preventive care
    Organization of the diabetic foot care team
    Quality of health care
    Psychosocial and educational implications of diabetic foot complications
    Role of footwear in the prevention of diabetic foot problems.
    Digital Access Springer 2012
  • Article
    Bell EB, Shand FL, Gradwell S.
    Eur J Immunol. 1977 Jun;7(6):406-12.
    The ability of immunogens to maintain or extend a state of unresponsiveness was investigated in unbred rats using a human serum albumin (HSA) model of tolerance. Rats initially challenged with immunogen within two weeks of high or low dose tolerance induction by tolerogen (soluble HSA) remained hyporesponsive even a year and a half later and in some cases became less responsive following a subsequent challenge. An inhibitory effect of immunogen on escape from tolerance was formally demonstrated: in comparison with an unchallenged group, tolerant rats which received a second immunogen challenge 6 months after the first, synthesized less antibody; this antibody underwent a gradual decline in affinity after each challenge which suggested that higher avidity B cells were progressively lost. In addition, immunogen-maintained tolerant rats (a) had demonstrable helper T cell activity among their thoracic duct lymphocytes on adoptive transfer, (b) did not produce a significant increase in antibody synthesis after receiving peripheral T cells and (c) provided no evidence that suppressor cells were playing a role. The results suggested that the mechanisms of tolerance induction by tolerogen and tolerance maintenance by immunogen are fundamentally different.
    Digital Access Access Options