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PubMed2001

Potocytosis. Robert Feulgen Lecture.

Potocytosis represents a mechanism by which small and large molecules as well as macromolecular complexes are sequestered and transported by caveolae. Caveolae are flask-shaped plasma membrane specializations characterized by a filamentous coat consisting of caveolins that decorates the inside surface of each caveola membrane. They have endocytotic functions that differ from the clathrin-coated pit pathway. Ligands bound to receptors that are internalized by caveolae can be delivered to four different locations in the cell bypassing the lysosome and at least four different caveolae membrane traffic patterns during potocytosis can be distinguished. Hence, cells have two endocytic machines and each is designed to accomplish different tasks. This review provides a brief summary of the discovery of caveolae and of potocytosis, and focuses on recent discoveries of the unique endocytic capabilities of caveolae in a variety of different cells.

Animals↗
PubMed2001

The secretory membrane system studied in real-time. Robert Feulgen Prize Lecture, 2001.

The discovery and development of green fluorescent protein (GFP) from the jellyfish, Aequorea victoria, has revolutionized studies on protein localization and dynamics by allowing direct observation of a protein's life history and pathway in living cells, previously only deduced from genetic, biochemical, or immunolabeling studies. Applied to the secretory membrane system, which regulates delivery of newly synthesized proteins and lipids to the cell surface, GFP-based studies are providing important new insights into the maintenance and biogenesis of organelles, as well as the origin, pathway, and fate of secretory transport intermediates.

Cell Membrane↗
PubMed2003

Nitrosative stress in early Type 1 diabetes. David H. P. Streeten Memorial Lecture.

Although hyperglycemia has been shown to cause peripheral nerve dysfunction in patients with diabetes, the biochemical mechanisms for this effect are poorly understood. The excessive production of reactive oxygen species and reactive nitrogen species has been proven to be detrimental in experimental diabetes, but there is little evidence that these metabolic events take place clinically and are physiologically important in man. To assess this we measured nitrite and nitrate (indices of nitric oxide production), nitrotyrosine (an index of peroxynitrite), 8-isoprostaglandin F-2 alpha, an isoprostane reflective of oxidative stress and lipid peroxidation, and uric acid, an index of antioxidant defense in patients with recently diagnosed Type 1 diabetes and aged-matched controls. The diabetic patients were followed for three years. We documented the overproduction of nitric oxide and increased lipid peroxidation in early diabetes and showed these changes had detectable adverse effects on peripheral nerve function especially sympathetic sudomotor nerves. We documented the suppression of uric acid and showed this was associated with multiple abnormalities in autonomic function. In addition, we present indirect evidence that overproduction of reactive oxygen species and reactive nitrogen species have adverse effects on beta cell function and blood pressure.

Adolescent↗
PubMed1999

The 1999 James Ewing Lecture: in pursuit of molecules of oncogenesis and neoplastic therapy.

Breast cancer is a progressive, phenotypic, genetic and epigenetic alteration, induced by various stimulants of which the principal steroid hormone, estrogen, initiates and promotes neoplastic transformation of normal ductal mammary epithelium to acquire distinct biochemical and molecular characteristics. The molecular events that characterize oncogenesis with dysregulated physiologic states represent an area of intense translational research. The progress of the last century suggests that the targeted responses initiated by this steroid hormone can be attenuated and modified with anti-estrogen therapies or through applied intervention with selective estrogen receptor modulation. New pharmacological, genetic, and biological agents will undoubtedly afford clinical investigators of the next millennium the opportunity to provide major impact on the disease progression of this neoplasm, through these targeted endocrine responses for estrogen.

Antineoplastic Agents↗
PubMedDate not supplied

Komrower lecture: Treatment of inborn errors of metabolism: a review.

Although the treatment of a small number of inborn errors is very good, for the majority the outcome is less satisfactory. This review examines current treatment critically and suggests how the information on which decisions about the management of patients with inborn errors might be improved.

Decision Support Techniques↗
PubMed2006

Private-sector research ethics: marketing or good conflicts management? The 2005 John J. Conley Lecture on Medical Ethics.

Pharmaceutical companies are major sponsors of biomedical research. Most scholars and policymakers focus their attention on government and academic oversight activities, however. In this article, I consider the role of pharmaceutical companies' internal ethics statements in guiding decisions about corporate research and development (R&D). I review materials from drug company websites and contributions from the business and medical ethics literature that address ethical responsibilities of businesses in general and pharmaceutical companies in particular. I discuss positive and negative uses of pharmaceutical companies' ethics materials and describe shortcomings in the companies' existing ethics programs. To guide employees and reassure outsiders, companies must add rigor, independence, and transparency to their R&D ethics programs.

Biomedical Research↗
PubMed1996

Pathophysiology of the burn wound and pharmacological treatment. The Rudi Hermans Lecture, 1995.

The body's reaction to thermal injury is much more than an initial, local inflammatory response. The burn wound is a continuous, severe threat against the rest of the body due to invasion of infectious agents, antigen challenge and repeated additional trauma caused by wound cleaning and excision. The inflammatory mediators which control blood supply and microvascular permeability in the wound have been extensively studied and are largely understood. Attempts to suppress the inflammatory reaction by different drugs, have, however, been less successful. Extensive thermal injury and sepsis also results in immunosuppression. The defects causing immunosuppression are still very much under consideration. An understanding of these defects is essential for the development of therapies. The increasing interest in the control of the inflammatory reactions by cytokines may, in the near future, be of great importance.

Animals↗
PubMed2006

LXII Edward Jackson lecture: open angle glaucoma after vitrectomy.

PURPOSE: To present data and an hypothesis for the late development of open angle glaucoma (OAG) after vitrectomy. DESIGN: A retrospective observational case series. METHODS: The records of 453 eyes that had undergone vitrectomy were reviewed for postoperative OAG. Eyes with confounding factors were excluded. Sixty-eight eyes of 65 patients that underwent routine vitrectomy were followed for a mean of 56.9 months (range, seven to 192 months). For the main outcome measures, patients were classified into three groups: patients with suspected glaucoma, patients in whom glaucoma developed after the operation, and patients with pre-existing glaucoma. RESULTS: In glaucoma suspects, the mean intraocular pressure was significantly higher in the operated eye compared with the fellow eye (P = .0001). In eyes with new onset glaucoma, 23 of 34 eyes (67.6%) had it in the vitrectomized eye only. In phakic eyes, the time interval between vitrectomy and the development of glaucoma (mean, 45.95 months) was significantly longer than eyes that were nonphakic at the time of vitrectomy (mean, 18.39 months; P = .0115). When the interval between cataract surgery in phakic eyes to the development of glaucoma was compared with the interval from vitrectomy to glaucoma diagnosis in the nonphakic group, the difference was not statistically significant. In eyes with glaucoma before the operation, the mean number of antiglaucoma medications that were required to control the intraocular pressure was significantly higher in the vitrectomized eye, compared with the fellow eye (2.9 medications +/- 1.2 vs 2.0 medications +/- 1.4; P = .0215; n = 14). CONCLUSION: There is an increased risk of OAG after vitrectomy. The presence of the lens may be protective. In established OAG before the operation, the number of antiglaucoma medications may increase after surgery. Oxidative stress is hypothesized to have a role in the pathogenesis.

Adolescent↗
PubMed2006

LXIII Edward Jackson Memorial Lecture: Eye care: dollars and sense.

PURPOSE: The development of health economic data for vision loss and eye disease is described. DESIGN: Data from population-based epidemiologic studies of eye disease, studies of the impact of vision loss on daily living, Australian national health-care costs, census, and demographic projections were combined to develop a model of the economic impact of vision loss in Australia. METHODS: Data were considered to assess the current magnitude and costs of vision loss and to make projections as to future costs. Further analysis investigated the costs and economic benefits of various interventions to address avoidable vision loss. RESULTS: The amount of vision loss increases three-fold and the number with vision loss will double in 20 years. Vision loss cost Australia a total of AU $9.85 billion in 2004. Vision loss ranks seventh in causes of loss of well-being. An intervention package to address avoidable vision loss would cost AU $190 million or AU $5,591/Quality Adjusted Life Year (QALY) and give lifetime savings of AU $911 million. CONCLUSIONS: Although specific for Australia, these data can help guide health care policy debate and the priority given to eye care in other developed economies. For each dollar spent on the prevention of vision loss and eye care, there is a 5 dollar return to the community.

Activities of Daily Living↗
PubMed2006

Young Scholars Award Lecture: Intratubular angiotensinogen in hypertension and kidney diseases.

Recent findings related to the renin-angiotensin system have provided a more elaborated understanding of the pathophysiology of hypertension and kidney diseases. These findings have led to unique concepts and issues regarding the intrarenal renin-angiotensin system. Angiotensinogen is the only known substrate for renin that is the rate-limiting enzyme of the renin-angiotensin system. Because the level of angiotensinogen in human beings is close to the Michaelis-Menten constant value for renin, changes in angiotensinogen levels can control the activity of the renin-angiotensin system, and its upregulation may lead to elevated angiotensin peptide levels and increases in blood pressure. Enhanced intrarenal angiotensinogen mRNA or protein levels or both have been observed in multiple models of hypertension including angiotensin II-dependent hypertensive rats, Dahl salt-sensitive hypertensive rats, and spontaneously hypertensive rats, as well as in kidney diseases including diabetic nephropathy, immunoglobulin A (IgA) nephropathy, and radiation nephropathy. Renal angiotensinogen is formed primarily in proximal tubular cells and is secreted into the tubular fluid. Urinary angiotensinogen excretion rates show a clear relationship to kidney angiotensin II contents and kidney angiotensinogen levels, suggesting that urinary angiotensinogen may serve as an index of the intrarenal renin-angiotensin system status. Establishment of concise and accurate methods to measure human angiotensinogen may allow clinical studies that would provide important information regarding the roles of intrarenal angiotensinogen in the development and progression of hypertension and kidney diseases.

Angiotensinogen↗