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Biomedical subjects

P Stern

Publications and source records attributed to P Stern.

At least 73 records · Page 4Linked to original sources
PubMed1978

Calcium and sodium excretion in rats in response to prolonged treatment with polythiazide.

The hypocalciuric response to prolonged polythiazide (PTZ) administration has been investigated in intact and thyroparathyroidectomized (TPTX) rats. After 3 control days, PTZ was given for 6 days (0.1 mg/100 g body weight . 24 h p.o.). In both groups, calcium excretion fell on day 1 of PTZ and remained depressed thereafter. In the intact rats, this decrease was associated with increased sodium excretion and urine output on treatment day 1. In the TPTX rats, hypocalciuria occurred without change in sodium excretion or body weight; urine output increased on the first 2 days. Thus PTZ can reduce calcium excretion in the absence of parathyroid hormone, changes in sodium excretion, and changes in body weight (an estimate of body fluid balance with constant food intake).

Animals↗
PubMed1977

Renal clearances of 14C-inulin and polyfructosan in the rat. Effect of increased ureteral pressure.

Polyfructosan has been used as a substitute for inulin in GFR determinations. However, the validity of this substitution in conditions where renal tubular permeability to other substances, such as mannitol, sucrose and other substances, such as mannitol, sucrose and iothalamate, is increased has not been tested. Experiments were performed on 8 rats to compare the clearances of polyfructosan (CPF) and 14C-inulin (CIN) during hydropenia, 3% BW saline expansion, elevation of one ureteral catheter by 30 cm, and following return of increased ureteral pressure to the control level. No significant difference between CPF and CIN could be detected except in the kidney subjected to increased ureteral pressure. However, the magnitude of this difference--which may relate to the different molecular weights of the two compounds--was so small that we conclude that the use of CPF, as an index of GFR, is no less reliable than CIN under the conditions tested.

Animals↗
PubMed1976

Effects of serine on morphine-dependent mice.

Single doses of serine (250 mg/kg i.p.) failed to elevate central glycine in mice (1 h after injection), or to compensate for losses caused by implantation of morphine base (70 mg/animal), and reduced the jumping response to nalorphine (100 mg/kg i.p.). In contrast, sustained treatment with 250-mg/kg doses of serine at 24-hour intervals produced increases in brain and medullar glycine (1 h after 4th injection: 46-50% in normal, 39-75% in morphine-dependent mice, and enhanced the jumping response (40% over controls).

Animals↗
PubMed1976

The deiodination of thyroxine in hyperthyroid rats as determined by renal clearance of iodide.

Other investigators have reported that whole body clearance of thyroxine (T4) is increased in hyperthyroid rats isotopically equilibrated with radioactive T4, using the 24 h post-injection serum T4 concentration in the clearance calculation. Data from this laboratory indicate that serum T4 concentration is lowest at this point yielding falsely high clearance values, particularly when high doses of T4 are injected. To investigate this problem further, two types of experiments were performed. First, rats were equilibrated with [125I]T4, 5 or 20 mug/day, and the urinary clearance of iodide derived from T4 (deiodinative clearance) was measured from 0-7 and 7-24 h after a T4 injection, using the T4 concentration in serum obtained at the midpoint of each urine collection period. Urine was then collected from the ureters for several 1 h periods during the 4th to 8th h following T4 injection, calculating clearances using the midpoint plasma T4 concentration. Second, normal rats were given a single dose of [125I]T4, 5 or 55 mug/rat, and deiodinative clearance was determined during the subsequent 0-7 and 7-24 h periods. The first experiment indicated that deiodinative clearance was significantly enhanced in rats equilibrated with the large dose of T4 under all conditions studied. In contrast, the clearance in normal rats given a single large dose of T4 was not significantly different from that of normal rats given a small dose of T4. These results support the view that T4 clearance is increased in hyperthyroidism, due in part to an increase in the deiodination of T4.

Animals↗
PubMed1975

Cytoplasmic glucocorticoid binding proteins in bone cells.

The binding of 3H-dexamethasone (3H-DM) was studied in the cytoplasmic fraction of bone cells isolated from fetal rat calvaria by enzymatic digestion. An high-affinity glucocorticoid binding protein resembling those described in other target tissues was demonstrated. Scatchard analysis revealed a single class of binding sites with an apparent dissociation constant for 3H-DM (0C) of 7 x 10-9M and a concentration of binding sites of 0.11 pmoles/mg cytosol protein. The number of cytoplasmic binding sites per cell was calculated at 6,000 which is probably an underestimate due to occupancy of some sites by endogenous steroids. The binding sites appeared protein in nature since incubation with pronase destroyed 100% of the binding. Nuclear transfer was demonstrated in a reconstituted system utilizing bone cytosol as donor and liver nuclei as the acceptor. Competitive binding analysis revealed corticosterone to be equivalent to DM in binding affinity; progesterone was 75% as potent as DM. Aldosterone and SC-26304 (a spirolactone analogue) had, respectively, 1

17-Hydroxycorticosteroids↗
PubMed1975

Antileukemic effect of L-aspartyl-hydrazine.

Beta-L-aspartyl-hydrazine can significantly prolong survival of the A mouse strain infected with a lymphatic leukemia sensitive to L-asparaginase. By combining the above substance with L-asparaginase even better results can be obtained.

Animals↗
PubMed1975

The effect of specific brain phospholipid on the rat's allergic encephalomyelitis.

A new preparation which contains specific brain phospholipids (Gricertine) acts as a histamine liberator in CNS and protects rats from allergic encephalomyelitis. It is supposed that the protective effect of Gricertine on the allergic encephalomyelitis is based on its histamine-liberator properties which can occur during the first days of therapy: this would explain the large decrease of the brain histamine after 3 weeks of treatment. Gricertine is also able to remove clinical symptoms of allergic encephalomyelitis in rats. It is presumed that Gricertine may also be acting independently of that mechanism, in the way that it replaces phospholipids that disappeared in the cases where demyelinisation had taken place.

Animals↗