Search PubMed⌕ Search

Biomedical subjects

M Goldberg

Publications and source records attributed to M Goldberg.

At least 685 records · Page 38Linked to original sources
PubMed1977

[Ultrastructure of epiphyseal cartilage after extraction on thin sections of "Epon" of proteoglycans by calcium chloride].

Dissociative methods are commonly used to extract proteoglycans. With a 2 M CaCl2 solution these components can be also extracted from thin sections of fixed, "Epon" included material. Secretory granules of the chondrocytes, granular components of extracellular matrix as matrix vesicles lost their electron density. Glycoproteins of the cell coat as non collagenous glycoproteins disappear. The method seems to be valuable for extracting proteoglycans from thin sections prepared for electron microscope investigations.

Animals↗
PubMed1977

Acute effects of bovine growth hormone on renal calcium and phosphate excretion.

To evaluate the acute effects of bovine growth hormone upon renal hemodynamics and urinary electrolyte excretion, clearance studies were performed in intact and thyroparathyroidectomized dogs, receiving either vehicle alone or bovine growth hormone. Growth hormone had no effect when compared to controls upon glomerular filtration rate, renal plasma flow, or clearance of sodium, calcium, and phosphate either in the presence or absence of parathyroid hormone. It is concluded that acute changes in circulating growth hormone levels do not play an important role in calcium and phosphate homeostasis. The data suggest that previously described antiphosphaturic and hypercalciuric actions of growth hormone are not due to direct acute renal tubular effects but may be the result of indirect effects of chronic growth hormone administration.

Animals↗
PubMed1977

Renal tubular effects of chronic phosphate depletion.

The effects of chronic phosphate depletion on renal tubular function were evaluated by micropuncture and free water clearance studies in the dog. Proximal tubular punctures demonstrated that chronic hypophosphatemia led to a reduction in ratio of tubular fluid to plasma inulin in late superficial tubular from 1.59+/-0.08 in control animals to 1.29+/-0.06 in phosphate-depleted dogs, with proportional inhibition of calcium and sodium reabsorption. The chronic decrease in proximal tubular fluid reabsorption was confirmed by the analysis of sustained water diuresis in conscious, phosphate-depleted dogs, before and after repletion of body PO4 stores, and in control animals. Urine flow rate/100 ml glomerular filtration rate (V/GFR) was significantly higher in PO4 DEPLETION THAN CONTROL (15.8+/-1.1 VS. 10.7+/-0.82). In addition, acetazolamide infusion did not increase V/GFR in phosphate-depleted dogs (15.8+/-1.1 vs. 17.16+/-0.9), supporting the conclusion that inhibition of proximal tubular fluid reabsorption was responsible for the elevated urine flow rate. PO4 repletion over 5 days reduced V/GFR to 9.2+/-0.7 despite no change in urine osmolality and no change in GFR, further suggesting a specific reversible alteration in proximal tubular reabsorption in phosphate depletion. Although hypercalciuria was a constant finding in phosphate depletion (fractional excretion of calcium of 2.04+/-0.4% vs. 0.47+/-0.13% in controls), the enhanced distal delivery of calcium was not a crucial factor; acute phosphate infusion reduced urinary calcium excretion to control values without affecting the reduced proximal tubular reabsorption in either intact or thyroparathyroidectomized phosphate-depleted dogs the change in distal nephron calcium reabsorption was independent of parathyroid hormone (PTH) levels since infusion of PTH failed to alter urinary calcium excretion. We conclude that chronic phosphate depletion leads to a reversible, sustained inhibition in proximal tubular reabsorptive fuction as well as a specific decrease in distal nephron calcium reabsorption. This latter reabsorptive defect is sensitive to phosplate infusion but not corrected by PTH.

Acetazolamide↗
PubMed1977

Impaired renal tubular potassium secretion in systemic lupus erythematosus.

Two patients with long-standing systemic lupus erythematosus were found to have persistent hyperkalemia. The hyperkalemia could not be explained by renal insufficiency, oliguria, diminished distal sodium delivery, acidemia, or hemolysis. After sodium depletion, urinary aldosterone excretion and plasma aldosterone concentration rose appropriately. No increase in urinary potassium excretion or decrease in serum potassium concentration was noted after fludrocortisone acetate, furosemide, or acetazolamide plus sodium bicarbonate. We conclude that these patients have a primary defect in renal tubular potassium secretion that may be related to an immune complex interstitial nephritis.

Acetazolamide↗
PubMed1977

Erysipelas: facial lymphangitis.

Two cases of facial lymphangitis have been described, and the pathophysiology of erysipelas has been discussed. Now rarely observed by hospital residents, this potentially serious infection can create considerable diagnostic confusion in medical as well as dental services. Rapid response of erysipelas to penicillin therapy is the modern expectation.

Child, Preschool↗
PubMed1977

Giant kidneys in Waldenström's macroglobulinemia.

A patient with Waldenström's macroglubulinemia had the unique feature of having one kidney infiltrated with malignant cells to such an extent as to produce a large palpable abdominal mass. Other unusual aspects of this case include the destruction of renal tubules by the invading cells that resulted in interstitial fibrosis and was probably responsible for the appearance of whole IgM in the urine.

Aged↗
PubMed1977

Tubular effects of acute metabolic acidosis in the rat.

Micropuncture and clearance studies were performed to evaluate the effects of acute NH4Cl-induced metabolic acidosis. Studies were performed in four groups of rats: controls, urea-saline, saline, and NH4Cl. Acidosis (pH: 7.25 +/- 0.02[S.E.M.], HCO3- = 12.4 +/- 0.7 mEq/L) was associated with increased fractional sodium excretion, 9.13% +/- 0.52 and calcium excretion, 1.32% +/- 0.43, which was significantly greater than controls, 0.30% +/- 0.07 and 0.30% +/- 0.07; urea-saline, 0.54% +/- 0.1 and 0.54% +/- 0.13; saline, 0.71% +/- 0.17 and 0.47% +/- 0.09. In the proximal tubule, however, fractional reabsorption was less with saline, 41.5 +/- 1.7, than either urea-saline, 51.1 +/- 1.3, or the NH4Cl-infused group, 46.9 +/- 0.4. The data indicate that natriuresis of acute NH4Cl loading is associated with but cannot be accounted for by inhibition of proximal tubular reabsorption. The mechanism of inhibition of transport at sites beyond the proximal tubule is not clear but cannot be either volume expansion or increased solute load due to urea excretion.

Acidosis↗