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S Anderson

Publications and source records attributed to S Anderson.

At least 415 records · Page 23Linked to original sources
PubMed1989

Prediction of persistent immunodeficiency in the DiGeorge anomaly.

To assess the natural history of the immune defect in DiGeorge anomaly, we reviewed serial immunologic studies in 18 patients. The diagnosis was made with criteria based on the concept of the DiGeorge anomaly as a field defect. Initial or early follow-up laboratory examination suggested moderate to normal T cell function in 14 patients. None of these patients have lost T cell capability; they have never had infections characteristic of T cell deficiency. Four patients had clinical and laboratory evidence of profound immunodeficiency. A decreased number of CD4+ cells (less than 400/microliters) and a decrease in phytohemagglutinin responsiveness (stimulation index less than 10) may be useful in discriminating patients with immunodeficiency; absolute lymphocyte count and immunoglobulin values were not informative. At the time of surgery, the thymus was not found in 11 of 14 patients; however, only two of these patients had immunodeficiency. Patients with a persistently low number of CD4+ cells and decreased phytohemagglutinin response are candidates for immunologic reconstitution.

Aging↗
PubMed1989

Short and long term effects of antihypertensive therapy in the diabetic rat.

To compare the impact of differing antihypertensive regimens on the development of renal injury, studies were performed in three groups of moderately hyperglycemic diabetic rats, and one group of non-diabetic control (C) rats. One diabetic group (DM) received no therapy except insulin. The remaining diabetic groups received insulin and either the angiotensin I converting enzyme inhibitor captopril (CAP), or triple therapy (TRX) with reserpine, hydralazine and hydrochlorothiazide. CAP and TRX modestly and comparably lowered blood pressure. At 6 to 10 weeks, DM rats exhibited elevation of the single nephron glomerular filtration rate (SNGFR), due to elevations of the glomerular capillary plasma flow rate (QA) and the glomerular capillary hydraulic pressure (PGC). In both DM/CAP and DM/TRX rats, blood pressure reduction was associated with selective normalization of PGC, without change in SNGFR or QA. In long-term (70 weeks) studies, DM rats exhibited progressive albuminuria and marked glomerular sclerosis. CAP limited albuminuria and injury to values even lower than those in C rats, whereas TRX served only to delay, but not to prevent, the increase in albuminuria. TRX reduced glomerular sclerosis, but was less effective than CAP. At 70 weeks, CAP and TRX still reduced systemic blood pressure; PGC remained at normal levels with CAP but was no longer controlled with TRX. These results confirm the clinical observation that antihypertensive therapy slows diabetic glomerulopathy, but also suggest that CAP affords superior long-term protection as compared to the other antihypertensive drug regimen studied.

Animals↗
PubMed1989

Antihypertensive therapy and the progression of renal disease.

Systemic hypertension accelerates the progression of glomerular injury. Studies in experimental animals indicate that the beneficial effects of antihypertensive agents may relate to their intrarenal haemodynamic consequences, and specifically to their effects on the arteriolar resistances. Relative afferent arteriolar vasodilation allows transmission of systemic pressure into the glomerular capillary network; the resultant glomerular capillary hypertension is associated with progressive structural injury. Antihypertensive agents, such as angiotensin converting enzyme (ACE) inhibitors, relax the efferent arteriole, alleviate glomerular hypertension and protect the kidney from progressive injury. These agents are effective in numerous animal models, and preliminary clinical observations suggest that they may also be effective in humans. In contrast, vasodilator/diuretic regimens are effective in some animal models, but fail to reduce glomerular pressure or injury in others. Less is known about the potential renal protective effects of calcium channel blockers, with reported observations offering conflicting findings. Further experimental and clinical studies are needed to define the optimal antihypertensive therapy for patients at risk of glomerular injury.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

A mutant of Arabidopsis deficient in the chloroplast 16:1/18:1 desaturase.

Leaf tissue of a mutant of Arabidopsis thaliana contains reduced levels of both 18-carbon and 16-carbon polyunsaturated fatty acids and increased levels of the 18:1 and cis-16:1 precursors due to a single nuclear mutation at a locus designated fadC. Analysis of the fatty acid compositions of individual lipids and the kinetics of lipid labeling with [(14)C]acetate in vivo indicate that the mutant lacks activity of the chloroplast glycerolipid omega-6 desaturase. As a result, lipids synthesized by the prokaryotic pathway are not desaturated further than 18:1 and 16:1. Lipids derived from the eukaryotic pathway are desaturated-presumably by the endoplasmic reticulum 18:1 phosphatidylcholine desaturase. However, an increase in the level of 18:1 on all the phospholipids derived from the eukaryotic pathway in leaves of the mutant suggests that the mutation does exert an effect on the composition of extrachloroplast membranes. Synthesis of monogalactosyldiacylglycerol (MGD) by the prokaryotic pathway is reduced 30 to 35% in the mutant and there is a corresponding increase in MGD synthesis by the eukaryotic pathway. This shift in metabolism which results in a more unsaturated MGD pool, may reflect the existence of a regulatory mechanism which apportions lipid synthesis between the two pathways in response to alterations in the physical properties of the chloroplast membranes.

Journal Article↗
PubMed1989

Infection efficiency of T lymphocytes with amphotropic retroviral vectors is cell cycle dependent.

The role of the host cell cycle in determining the efficiency of infection with amphotropically packaged retroviral vectors was investigated in T lymphocytes and in fibroblasts. For T lymphocytes, the efficiency of infection with a retroviral vector was dependent on the cell cycle distribution of cells in culture at the time of exposure to the vector. When cultures enriched in the G0-G1 phase of the cell cycle (by serum starvation, aphidicolin treatment, or centrifugal elutriation) were exposed to retroviral vectors, the infection efficiency was severalfold lower than that in similar cultures enriched in the S, G2, and M phases. For fibroblasts, the efficiency of infection was not cell cycle dependent. These findings are relevant for studies with retrovirus-mediated gene transfer into hematopoietic tissues.

Animals↗
PubMed1989

Endothelin: a potent renal and systemic vasoconstrictor peptide.

Endothelin is an endothelial cell-derived peptide recently shown to possess potent vasoconstrictor properties. Bolus intravenous injections of endothelin (5-450 pmol) into anesthetized Munich-Wistar rats induced a marked pressor effect, the magnitude and duration of which were dose dependent. Maximal systemic and renal responses occurred within 20 min and persisted for greater than 90 min in the higher dose range. In response to bolus dosages of 25 pmol or greater, renal plasma flow fell proportionately more than glomerular filtration rate, resulting in an increase in filtration fraction. In micropuncture studies of rats given continuous intravenous infusions of endothelin (0.63 pmol/min), the peptide caused a proportionately greater elevation of efferent than afferent arteriolar resistance, with a marked elevation of glomerular capillary hydraulic pressure and a lower glomerular capillary ultrafiltration coefficient. Endothelin was modestly natriuretic when systemic pressure rose and renal function was not severely impaired. This potent renal and systemic vasoconstrictor may play an important role in glomerular injury and in the pathophysiology of a variety of clinical microvasculopathies.

Animals↗
PubMed1989

Myelodysplastic syndrome: prospective evaluation of fifty-one patients using the Dutcher scoring system.

Fifty-one patients with primary myelodysplastic syndrome were prospectively evaluated using a scoring system based on the presentation blood and bone marrow findings. Twenty-four patients (47%) evolved to acute nonlymphocytic leukemia. Stepwise regression model showed that the scoring system was the only significant variable for predicting transformation to acute leukemia (p = 0.0007, sensitivity 70.8%, specificity 77.8%). Seventy-six percent of patients with a score of 14 or greater developed acute leukemia compared to 19% with a score of 13 or less. Median survival of the entire group was 10 months. The most important prognostic factor for predicting survival was the scoring system (p = 0.0001). Survival correlated inversely with the score. This scoring system may be useful in the management of patients with myelodysplasia.

Acute Disease↗
PubMed1989

Enkephalinase inhibition increases plasma atrial natriuretic peptide levels, glomerular filtration rate, and urinary sodium excretion in rats with reduced renal mass.

To investigate the in vivo effects of inhibition of endopeptidase 24.11, an enkephalinase enzyme shown to be involved in atrial natriuretic peptide (ANP) breakdown in vitro, we infused phosphoramidon, a specific inhibitor of endopeptidase 24.11, into rats with reduced renal mass (and chronic extracellular volume expansion) and into normal rats. Relative to baseline values in rats with remnant kidneys, phosphoramidon led to elevations of plasma ANP levels and concomitant increases in urinary sodium excretion, fractional excretion of sodium, glomerular filtration rate, filtration fraction, and urinary cyclic GMP excretion. Similar changes in renal function and urinary cyclic GMP excretion were obtained with thiorphan, another endopeptidase 24.11 inhibitor. These enhanced ANP levels and renal actions were not observed with phosphoramidon in normal rats. These results show that plasma ANP levels can be modulated in rats with reduced renal mass by inhibition of endopeptidase 24.11.

Animals↗
PubMed1989

Hyperlipidemia and glomerular sclerosis: an alternative viewpoint.

Clinical and experimental observations suggest an association between hypercholesterolemia and progressive glomerular injury. In the main, most investigators have assumed that hypercholesterolemia induces an atherosclerotic process in the renal microvasculature analogous to that well recognized in larger vessels. The evidence for this line of reasoning is well described in other papers in this symposium. It is our belief that hypercholesterolemia may also lead to glomerular injury by hemodynamic mechanisms. In support of this latter view, diet-induced hypercholesterolemia often raises blood pressure in experimental animals and markedly impairs endothelial cell-dependent vascular relaxation in vitro. A high cholesterol diet also increases renal vascular resistance and contributes to glomerular capillary hypertension, a hemodynamic maladaptation known to cause glomerular sclerosis. In addition, hypercholesterolemia results in hyperviscosity, a rheologic abnormality leading to increased efferent arteriolar resistance and glomerular hypertension. The similar glomerular hemodynamic responses to two hyperviscosity states, elevated hematocrit and hypercholesterolemia, implicate efferent arteriolar hyperviscosity as a potential mechanism of injury common to hyperviscosity states. It therefore seems likely that as in atherosclerosis, multiple risk factors act synergistically to initiate glomerular structural injury. Specifically, we suggest that hypercholesterolemia and glomerular hypertension act synergistically to initiate structural injury. Although modification of either risk factor may limit injury, it seems likely that therapy targeted to each of multiple risk factors may afford superior protection.

Animals↗
PubMed1989

Pharmacotherapeutic treatment of panic disorder in patients presenting with chest pain.

While psychiatric populations with panic disorder have been shown to be responsive to several classes of psychoactive medications, there is little evidence that medical patients with panic disorder respond to similar interventions. In this non-blind, eight-week trial of alprazolam in patients presenting with chest pain and found to have panic disorder, 15 of 20 met the single criterion for improvement: a 50 percent or greater reduction in panic frequency. Several other measures were also significantly positive for those who completed the study. Furthermore, these patients reported a marginally significant drop in episodes of chest pain or discomfort. A double-blind, placebo-controlled trial is now required to test the validity of these findings.

Adult↗
PubMed1989

Cardiac transplantation: University of South Florida--Tampa General Hospital experience.

Cardiac transplantation has evolved from an experimental procedure to an accepted mode of therapy that prolongs life in patients with severe heart failure. The University of South Florida-Tampa General Hospital began performing cardiac transplantation for the treatment of end-stage cardiac disease in June 1985. Since then 42 heart transplantations have been performed and 30 patients are alive and well. The one-year actuarial survival is 78.73% and the two-year actuarial survival is 72.15%. Multiple complications have been encountered most notably rejection and infection. The recent approval of the USF/TGH program as a Medicare funded cardiac transplantation center is expected to greatly expand the number of potential recipients and will provide the residents of Florida, and the Southeastern United States, with an additional health care resource.

Adult↗
PubMed1988

Toxic shock syndrome toxin 1 as an inducer of human tumor necrosis factors and gamma interferon.

We present evidence that toxic shock syndrome toxin 1 (TSST-1) induces the production of high levels of TNF by human blood monocytes. Enriched lymphocyte preparations incubated with the staphylococcal toxin produced significant levels of TNF-like activity that is not neutralized by anti-rHuTNF antibodies and is likely to be lymphotoxin (LT or TNF-beta). We demonstrate also that TSST-1 is a potent inducer of IFN-gamma. When lymphocyte preparations were costimulated with PMA, the TSST-1 effect was strongly potentiated and the levels of cytotoxic factors, IFN-gamma, and IL-2 present in supernatant fluids were comparable to those observed after treatment with PMA and PHA. Thus, TSST-1, which is also known as an inducer of IL-1 and IL-2, stimulates the production of endogenous mediators that could play a role in the physiopathological processes of toxic shock syndrome (TSS). The described results suggest that the discrepancies in the clinical features between TSS and endotoxin shock may be related to qualitative differences in cytokine production.

Antibodies↗