Harvey Gonick - Academia.edu (original) (raw)

Papers by Harvey Gonick

Kidney International, 1996

Clinical Orthopaedics and Related Research, 1976

Ethane-1-hydroxy-1, 1-diphosphonate (EHDP) was administered in a dose of 20 mg/kg/d to 21 patient... more Ethane-1-hydroxy-1, 1-diphosphonate (EHDP) was administered in a dose of 20 mg/kg/d to 21 patients with symptomatic Paget's disease. All patients were treated for 6 months and then followed for an additional 6 months. There was a striking decline in serum alkaline phosphatase and urinary hydroxy-proline excretion observed after 3 months of therapy which was not significantly improved in the succeeding 3 months. Concomitantly there was marked improvement in clinical symptoms and bone scans. Following cessation of therapy, continued biochemical and clinical evidence of remission persisted. Several patients on repeat treatment with EHDP appeared to respond promptly. Side effects were minimal except for a possibly related osteomalacia and increased incidence of pathologic fractures.

American Journal of Hypertension, 2000

Journal of Molecular Medicine-jmm, 1972

In 1957 Homer Smith first postulated the existence of a humoral “antinatriuretic system”. Subsequ... more In 1957 Homer Smith first postulated the existence of a humoral “antinatriuretic system”. Subsequently, the results of various investigators employing cross-circulation, bioassay or isolated biological membranes suggested the presence of a humoral natriuretic factor to be present in mammalian plasma and urine following expansion of the extracellular fluid compartment. Although micropuncture studies have pointed out the important influence of intrarenal physical factors on tubular sodium reabsorption, the natriuresis following extracellular volume expansion cannot exclusiveley be ascribed to changes in physical factors. Own experimental data support the existence of a low molecular weight substance isolated from plasma and urine by gel filtration which inhibits sodium transport by isolated frog skin and induces increased renal electrolyte excretion after i. v. injection in the rat. In vitro experiments suggest that such natriuretic factor might interfere with active tubular transport through inhibition of renal Na-K-ATPase. Estimated molecular weight and chemical and biological features suggest this hormone might be an oxytocin analogue. Its pathophysiological and clinical significance as a pathogenetic factor in various edematous states is discussed. Nachdem Homer Smith 1957 erstmals die Existenz eines humoralen „antinatriuretischen Systems“ gefordert hatte, ließen verschiedene Untersuchungen am gekreuzten Kreislauf, an isolierten biologischen Membranen sowie im Bioassay das Auftreten eines natriuretischen Faktors in Plasma und Urin von Säugern nach Expansion des Extracellularvolumens vermuten. Andererseits konnte an Hand von Mikropunktionsbefunden gezeigt werden, daß intrarenalen physikalischen Faktoren eine wesentliche Bedeutung für die verminderte tubuläre Natrium-Resorption nach extracellulärer Volumenexpansion zukommt. Eigene Untersuchungen lassen wiederum nach Gelfiltration von Plasma und Urin die Existenz eines niedermolekularen Faktors vermuten, der den Natrium-Transport der isolierten Froschhaut hemmt und im Bioassay zur gesteigerten Elektrolyt-Ausscheidung durch die Niere führt. Ein solcher humoraler Faktor könnte den tubulären Natrium-Transport über eine Hemmung der renalen Na-K-ATPase beeinflussen. Aufgrund des geschätzten Molekulargewichtes von etwa 1000 und den beobachteten chemischen und biologischen Eigenschaften wäre es denkbar, daß es sich bei einem solchen Hormon um ein Oxytocin-Analog handelt. Die mögliche pathophysiologische und klinische Bedeutung eines Natriuretischen Hormons in der Ödempathogenese verschiedener Erkrankungen wird diskutiert.

Mineral and Electrolyte Metabolism, 1999

The purpose of the present study was to investigate bone changes in the adult rat exposed to low ... more The purpose of the present study was to investigate bone changes in the adult rat exposed to low lead levels during intake of normal dietary calcium and to contrast these findings with data from our earlier studies performed with animals receiving low dietary calcium concurrent with lead exposure. The present study exposed adult rats to 100 ppm lead via drinking water for 12 weeks and assessed bone histology, 1,25-dihydroxyvitamin D, 25(OH)vitamin D and parathyroid hormone levels. No osteopenia was evident by quantitative bone histology, and circulating levels of 1,25-dihydroxyvitamin D, 25(OH) vitamin D and parathyroid hormone were normal. Bone ash findings documented incorporation of significant amounts of lead into bone mineral. These findings document absence of interference with vitamin D metabolism, absence of secondary hyperparathyroidism and absence of osteopenia following 12 weeks of low lead exposure in the adult rat maintained on normal calcium intake. Results stress the importance of adequate calcium intake in our elderly population who may be exposed to cumulative, low-level lead exposure.

Nephron, 1997

Two dialysis patients with markedly elevated plasma silicon (Si) levels (3,849 and 2,350 microgra... more Two dialysis patients with markedly elevated plasma silicon (Si) levels (3,849 and 2,350 micrograms/l, respectively) and a presumed Si-related syndrome are described in this report. One patient presented with transient hypercalcemia in the face of low PTH, vitamin D and plasma A1 levels. Both patients had painful, nodular skin eruptions and aberrant hair growth, characterized as perforating folliculitis on skin biopsy, compatible with known effects of organosilicon compounds in man and animals. Plasma Si was found to be moderately elevated in 30 dialysis patients studied at random (710 +/- 53 micrograms/l, dialysis, vs. 152 +/- 9 micrograms/l, normal control), but there was no significant difference between the arterial values before and after dialysis, implying that the source of Si was ingested foods and fluids rather than dialysate. In these patients, plasma Si was weakly correlated with serum calcium as well as with serum calcium corrected for serum albumen, indicating that Si, like aluminum, may affect calcium metabolism.

American Journal of Hypertension, 2001

Kidney International, 1997

Nephron, 1986

The potential role of trace metals in the pathogenesis of various disease states, especially of r... more The potential role of trace metals in the pathogenesis of various disease states, especially of renal and cardiovascular disease, has been recognized increasingly. Moreover, altered membrane transport was recently incriminated to play a role in renal tubular syndromes, such as the Fanconi syndrome, as well as in the pathogenesis of volume dependent hypertension. We therefore investigated the possible in vitro effects of various trace metals on Na-K-ATPase, the biochemical correlate of active cellular transmembrane sodium and sodium-dependent transport. To more closely mimic the in vivo situation, we deliberately chose as enzyme source renal tissue homogenate, which may contain protective agents. Under these experimental conditions, the metals studied inhibited the enzyme quantitatively in the following order: Hg greater than Pb greater than Cd greater than Ur greater than Cu greater than Zn greater than Mn greater than Ba greater than Ni greater than Sr. Enzyme kinetic studies showed that Hg, Pb, and Cd competitively, and Cu noncompetitively, inhibited the enzyme. In general, Mg-ATPase was significantly less sensitive to the trace metals. Accumulation of these metals may present serious health hazards by producing a general defect in cell membrane transport. From the other metals studied, i.e., Mn, Ba, Ni and Sr, some may have toxic effects via other mechanisms, whereas some may exert a protective role against toxicity of other agents including metal ions.