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Biomedical subjects

M Baum

Publications and source records attributed to M Baum.

At least 163 records · Page 9Linked to original sources
PubMed1997

Social class and weight as prognostic factors in early breast cancer.

Data from the Cancer Research Campaign trial for early breast cancer have been used to study the effect of social class and weight on prognosis after primary treatment either by a simple mastectomy plus post-operative radiotherapy or by a simple mastectomy followed by a watch policy. There were 2455 patients for whom both social class could be determined and weight was recorded. These patients presented in clinical stages I and II and were recruited between June 1970 and April 1975. The cut-off date for the analysis was 31 December 1991. When the survival curves of patients in manual classes were compared with those in non-manual classes, there was a tendency for the latter to do better, but the difference was not statistically significant (P = 0.12). By contrast, there was a highly significant difference (P = 0.002) in survival favouring patients weighing less than or equal to 60 kg compared with those weighing greater than 60 kg. The difference was confined to post-menopausal patients and was still highly significant when included in a multivariate analysis with social class, age, tumour size, clinical stage and tumour grade. The effect of weight was to increase the mortality due to breast cancer rather than other causes.

Body Weight↗
PubMed1997

Maturational changes in rabbit renal cortical phospholipase A2 activity.

Several studies have demonstrated that the neonatal kidney has a markedly attenuated response to parathyroid hormone (PTH); however, the cause for this blunted response is unknown. PTH stimulated cAMP production by 215 +/- 18% in neonatal proximal tubule suspensions compared to a 35 +/- 7% increase in adult proximal tubules. Thus, neonatal proximal tubules have functioning PTH receptors and a greater adenylate cyclase response than the adult segment. In adult proximal tubules, PTH stimulates phospholipase A2 (PLA2) activity and the inhibition of Na,K-ATPase activity by PTH is blocked by inhibitors of PLA2. We examined whether maturational changes in renal cortical activity could play a role in the attenuated response to PTH in the neonatal proximal tubule. Compared to adults, neonates had a lower renal cortical cytosolic PLA2 (cPLA2) activity, assessed as the release of 14C-arachidonic acid (AA) from labeled phosphatidyl choline (0.44 +/- 0.10 vs. 0.74 +/- 0.06% 14C-AA released/min/mg protein, P < 0.05) and microsomal PLA2 activity (0.32 +/- 0.03 vs. 1.20 +/- 0.13% 14C-AA released/min/mg protein, P < 0.001). The protein abundance of cPLA2 was not different between the neonatal and adult renal cortex as assessed by immunoblot assay. Thus, the difference in activities must be due to a difference in regulation of cPLA2. Annexin 1 (lipocortin 1) has been shown to inhibit PLA2 activity by binding to phospholipid substrate. Annexin 1 protein abundance was higher in neonatal than in adult renal cortex (P < 0.001). Thus, the lower activity of PLA2 in the neonatal tubules may be due in part to higher expression of annexin 1. PLA2 activation by PTH, -8-bromo-cAMP and PMA was assessed as 3H-AA release from prelabeled suspensions of neonatal and adult proximal tubules. PTH (10(-7) M), 8-bromo-cAMP (10(-4) M) and PMA (5 x 10(-8) M) significantly increased 3H-AA release from adult tubules (P < 0.05) but had no effect on neonatal tubules (P = NS). Thus, PTH, 8-bromo-cAMP and PMA stimulated PLA2 in adult but not neonatal proximal tubules. In conclusion, the maturational changes in renal cortical PLA2 activity may be a factor in the blunted response of neonatal proximal tubules to PTH.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1997

Serum creatinine is a poor marker of glomerular filtration rate in patients with spina bifida.

Serum creatinine is used to estimate the glomerular filtration rate (GFR). The serum creatinine, however, may not accurately reflect the GFR in spina bifida patients, who often have decreased overall muscle mass resulting from spinal cord abnormalities. The relationship between the serum creatinine and GFR (obtained by [(125)I]iothalamate clearance) was examined in a population of spina bifida patients. Age-matched patients without spina bifida were used as controls. Results demonstrate that, for serum creatinines above 0.5 mg/dL, serum creatinine is a very poor predictor of GFR. Two patients with serum creatinines of 2.2 mg/dL are near end-stage renal disease with GFRs of 12.5 and 13 mL/minute per 1.73m2 and two patients were initiated on dialysis at the conclusion of the study. It is concluded that obtaining a GFR from a clearance study and not serum creatinine is the only reliable method to assess renal function in spina bifida patients once the serum creatinine is greater than 0.5 mg/dL.

Adolescent↗
PubMed1997

Effect of luminal angiotensin II on rabbit proximal convoluted tubule bicarbonate absorption.

The present in vitro microperfusion study examined the effect of luminal angiotensin II on proximal convoluted tubule (PCT) volume absorption and bicarbonate transport. Neither 10(-11) M, 10(-10) M, nor 2 x 10(-8) M luminal angiotensin II significantly affected PCT transport. When tubules were first perfused with enalaprilat to inhibit endogenous angiotensin II production, addition of 10(-10) M luminal angiotensin II increased volume absorption (0.72 +/- 0.08 vs. 0.86 +/- 0.07 nl x mm(-1) xmin(-1), P < 0.01) and bicarbonate transport (52.3 +/- 3.7 vs. 67.9 +/- 4.2 pmol x mm(-1) min(-1), P < 0.01). Addition of 10(-6) M losartan, an AT1 inhibitor, to the luminal perfusate inhibited volume absorption (0.95 +/- 0.14 vs. 0.72 +/- 0.11 nl x mm(-1) x min(-1), P < 0.05) and bicarbonate transport (65.0 +/- 7.3 vs. 54.7 +/- 9.2 pmol x mm(-1) x min(-1), P < 0.05). Addition of 10(-4) M luminal PD-123319, an AT2 inhibitor, was without effect. In tubules perfused with 10(-4) M luminal enalaprilat and 10(-4) M luminal PD-123319, addition of 10(-10) M luminal angiotensin II in the experimental period resulted in a stimulation in volume absorption (0.61 +/- 0.08 vs. 0.81 +/- 0.10 nl x mm(-1) x min(-1), P < 0.01) and bicarbonate transport (49.9 +/- 6.3 vs. 77.4 +/- 14.3 pmol x mm(-1) x min(-1), P < 0.01). In tubules perfused with 10(-6) M losartan and 10(-4) M enalaprilat, addition of luminal 10(-10) M angiotensin II resulted in no change in transport. These data are consistent with endogenous angiotensin II affecting PCT bicarbonate transport in vitro via luminal AT1 receptors.

Absorption↗
PubMed1997

Effect of glucocorticoids on neonatal rabbit renal cortical sodium-inorganic phosphate messenger RNA and protein abundance.

Administration of glucocorticoids to neonates increases proximal tubule volume absorption by increasing glucose, bicarbonate, and amino acid transport. We have recently demonstrated that glucocorticoids may contribute to the maturational decrease in phosphate transport. This study examines the maturation of NaPi-6 [the regulated proximal tubule sodium-inorganic phosphate (Na-Pi) transporter] mRNA and protein abundance and the mechanism for the decrease in phosphate transport by glucocorticoids. Weaned young rabbits (5 wk) had a 2-fold greater brush border membrane NaPi-6 protein abundance than that measured in adults. Renal cortical NaPi-6 mRNA abundance was comparable in neonates (less than 10 d of age) and adults. Renal brush border membrane vesicles from dexamethasone-treated neonatal rabbits (10 micrograms/100 g of body weight for 4 d) had a lower rate of Na-Pi transport than vehicle-treated controls (46.8 +/- 6.5 versus 71.0 +/- 9.0 pmol 32P/10 s/mg of protein, p < 0.05). Abundance of NaPi-6 protein in brush border membrane vesicles was 3-fold lower in newborn rabbits treated with pharmacologic doses of dexamethasone than in vehicle-treated controls. NaPi-6 mRNA abundance was the same in both groups. NaPi-1, a brush border membrane phosphate transporter which is also an anion channel, mRNA, and protein abundance was not affected by glucocorticoids. These data demonstrate that there is a maturational decrease in NaPi-6 protein abundance and that glucocorticoids decrease neonatal phosphate transport, at least in part, by reducing the number of Na-Pi transporters.

Animals↗
PubMed1997

The effect of recombinant human growth hormone in children with X-linked hypophosphatemia.

BACKGROUND: X-linked hypophosphatemia (XLH) is characterized clinically by rickets and growth retardation. Conventional treatment of XLH with oral phosphate and vitamin D fails to normalize linear growth. Objective. To determine the benefit and the potential side effects of recombinant human growth hormone (rhGH) therapy in patients with XLH. DESIGN AND METHODS: A randomized, double-blind, crossover study was performed throughout a 24-month period in five children with XLH, each patient serving as his own control. The effect of 12 months of rhGH therapy on height, mineral metabolism, glucose and lipid metabolism, hemoglobin, thyroid and parathyroid function, serum 1,25-(OH)2 vitamin D, osteocalcin, growth hormone, urinary calcium, phosphate, nephrocalcinosis, renal function, and bone density was compared with the effects of 12 months of placebo administration on the same parameters. RESULTS: The average age (mean +/- SEM) of the patients at the start of the study was 5.6 +/- 1.4 years. Growth hormone therapy improved the height standard deviation score (z-score) from a baseline of -2.66 +/- 0.21 to -2.02 +/- 0.25 and to -1.46 +/- 0.28, after 3 and 12 months, respectively. At the start of the control period the height z-score was -2.27 +/- 0.30 compared with -2.22 +/- 0.16 after 12 months of placebo administration. The growth velocity standard deviation score was -1. 90 +/- 0.40 during the 12 months of placebo administration and +4.04 +/- 1.50 during the 12 months of rhGH therapy. An increase in serum phosphate from 0.88 +/- 0.07 mmol/L to 1.17 +/- 0.14 mmol/L and tubular maximum for phosphate reabsorption (TmP/GFR) from 2.12 +/- 0. 15 to 3.41 +/- 0.25 mg/dL, was observed after 3 months of rhGH therapy. However, both serum phosphate and TmP/GFR were unchanged from baseline after 6, 9, and 12 months of rhGH therapy. Neither serum phosphate nor TmP/GFR changed from baseline during the placebo administration. Insulin-like growth factor 1 (IGF-1) increased from 114 +/- 25 to 354 +/- 51 ng/mL after 12 months of rhGH therapy. Despite the increase in IGF-1 after rhGH therapy, the value did not exceed normal serum concentration. IGF-1 did not change from baseline after 12 months of placebo administration. Neither therapy with rhGH nor with placebo had an effect on glucose and lipid metabolism, hemoglobin, thyroid and parathyroid function, serum 1, 25-(OH)2 vitamin D, alkaline phosphatase, osteocalcin, urinary calcium excretion, the grade of nephrocalcinosis, glomerular filtration rate, or urinary albumin excretion. Twelve months of rhGH therapy increased bone mass and width but not density. Twelve months of placebo administration had no effect on bone mass, width, or density. CONCLUSION: Patients with XLH have an improvement in linear growth and a transient increase in serum phosphate attributable to a transient decrease in urinary phosphate excretion when treated with rhGH.

Child↗
PubMed1997

Cystic fibrosis presenting with hypokalemia and metabolic alkalosis in a previously healthy adolescent.

Cystic fibrosis (CF) is an exocrine disease affecting multiple organ systems. Patients with CF usually present with respiratory or gastrointestinal abnormalities. This study presents a case of a previously healthy 17-yr-old man who was diagnosed with CF after presenting with metabolic alkalosis and hypokalemia. The defect associated with CF is in the cystic fibrosis transmembrane regulator (CFTR), which acts primarily as a chloride channel. Partially functional CFTR may be associated with less severe pulmonary and gastrointestinal manifestations, as in the case presented. Dysfunctional CFTR in the sweat ducts of CF patients are responsible for excessive chloride and sodium losses, especially in warm weather. Hypokalemia seen with heat stress is secondary to sweat as well as renal potassium wasting. Metabolic alkalosis is maintained by the excessive sweat sodium chloride losses which leads to extracellular fluid (ECF) volume contraction and chloride depletion. Generation of alkalosis may be related to dysfunctional CFTR in the kidney, but is most likely secondary to hypokalemia with ECF volume contraction. Finally, one must consider CF when confronted with hypokalemia and alkalosis in a previously healthy patient.

Acidosis↗
PubMed1997

Regulation of proximal tubule transport by angiotensin II.

Angiotensin II maintains extracellular volume homeostasis, in part, by regulating proximal tubule transport. Physiological doses of angiotensin II stimulate volume and solute transport in the proximal tubule independent of changes in the glomerular filtration rate. Stimulation of bicarbonate transport primarily occurs via increasing activity of the sodium/hydrogen exchanger and the sodium/bicarbonate cotransporter. The effects of circulating angiotensin II are mediated by angiotensin II receptors on the basolateral membrane of the proximal tubule. Recently, the proximal tubule was found to synthesize and secrete angiotensin II into the lumen. The luminal membrane contains angiotensin II receptors and luminal angiotensin II levels are 100 to 200-fold higher than that found in plasma. Luminal angiotensin II receptor blockade or luminal inhibition of angiotensin II synthesis both significantly diminish proximal tubule transport, consistent with stimulation of proximal tubule transport by endogenously produced and luminally secreted angiotensin II. These data provide evidence for an autocrine/paracrine role for angiotensin II that functions independent of circulating angiotensin II.

Angiotensin II↗
PubMed1997

Subpectoral breast reconstruction using the biodimensional system.

Increasing awareness among the general public has fuelled a demand for post-mastectomy breast reconstruction. However, owing to the limited number of plastic surgical centres this need is unlikely to be fulfilled in the near future. We report our early experience with a modified technique using a new subpectoral implant--the Biodimensional System. Seventeen consecutive patients underwent reconstruction (16 immediately) after mastectomy. In the group of patients having immediate reconstruction, the surgery was undertaken by the breast surgeon performing the primary procedure. This study demonstrates that an acceptable result can be obtained in the majority of patients and that it is possible for a breast surgeon to undertake primary reconstruction on selected patients using the Biodimensional System. It is hoped that this may aid patients in their physical and mental rehabilitation.

Breast Implants↗
PubMed1996

Endogenous production of angiotensin II modulates rat proximal tubule transport.

There is evidence that angiotensin II is synthesized by the proximal tubule and secreted into the tubular lumen. This study examined the functional significance of endogenously produced angiotensin II on proximal tubule transport in male Sprague-Dawley rats. Addition of 10(-11), 10(-8), and 10(-6) M angiotensin II to the lumen of proximal convoluted tubules perfused in vivo had no effect on the rate of fluid reabsorption. The absence of an effect of exogenous luminal angiotensin II could be due to its endogenous production and luminal secretion. Luminal 10(-8) M Dup 753 (an angiotensin II receptor antagonist) resulted in a 35% decrease in proximal tubule fluid reabsorption when compared to control (Jv = 1.64 +/- 0.12 nl/mm.min vs. 2.55 +/- 0.32 nl/mm.min, P < 0.05). Similarly, luminal 10(-4) M enalaprilat, an angiotensin converting enzyme inhibitor, decreased fluid reabsorption by 40% (Jv = 1.53 +/- 0.23 nl/mm.min vs. 2.55 +/- 0.32 nl/mm.min, P < 0.05). When 10(-11) or 10(-8) M exogenous angiotensin II was added to enalaprilat (10(-4) M) in the luminal perfusate, fluid reabsorption returned to its baseline rate (Jv = 2.78 +/- 0.35 nl/mm.min). Thus, addition of exogenous angiotensin II stimulates proximal tubule transport when endogenous production is inhibited. These experiments show that endogenously produced angiotensin II modulates fluid transport in the proximal tubule independent of systemic angiotensin II.

Angiotensin II↗