Search PubMed⌕ Search

Biomedical subjects

J Kaufman

Publications and source records attributed to J Kaufman.

At least 217 records · Page 12Linked to original sources
PubMed1980

Bacteria mature preproinsulin to proinsulin.

By inserting the rat preproinsulin gene into the bacterial prepenicillinase gene, we formed a variety of hybrid bacterial-eukaryotic signal sequences attached to proinsulin. Among these were the four following constructions: rat proinsulin attached to the entire penicillinase signal sequence and rat preproinsulin fused to all of, to half of, or only to the first four amino acids of the bacterial signal sequence. In all four cases, more than 90% of the rat insulin antigen appeared in the periplasmic space. By immunoprecipitation and determination of the amino acid sequences of the radiolabeled products, we show that the bacteria correctly process both the bacterial and the eukaryotic signal sequences of these hybrid proteins. The cleavage of the eukaryotic signal by bacterial peptidase, in this case, generates proinsulin.

Amino Acid Sequence↗
PubMed1980

Pulmonary thromboembolism. 2. New trends in prophylaxis and therapy.

Although low-dose heparin therapy is the technique most commonly used for prophylaxis of pulmonary thromboembolism, its usefulness is being questioned. Platelet deaggregation prophylaxis with either aspirin or dipyridamole, or both, apparently is a reasonable alternative, but further studies are needed. For treatment of pulmonary thromboembolism, continuous conventional-dose heparin therapy is the approach of choice. It has the highest therapeutic/toxic ratio and is the most effective technique for prevention of clot propagation. The patient's fibrinolytic network must be intact, however, if clot degradation is to occur. Fibrinolytic therapy with urokinase or streptokinase should be restricted to use in patients with massive pulmonary embolism in whom hemodynamics are unstable. Caval interruption and pulmonary embolectomy have lower benefit/risk ratios than do the medical alternatives and are rarely used for pulmonary thromboembolism.

Aspirin↗
PubMed1978

Thermal oxidative degradation studies of phosphate esters.

Five phosphate esters - tri-p-tolyl phosphate, tributyl phosphate, tris(1,3-dichloro-2-propyl)phosphate, tris(2,3-dibromopropyl)phosphate, and tris(2-chloroethyl)phosphate- were subjected to thermal oxidative degradation in air at 370 degrees C. Degradation mechanisms were postulated and the toxic hazards assessed based on the volatiles produced. Tri-p-tolyl phosphate was found to undergo only minimal degradation; the other compounds were decomposed extensively. Butene was the main product formed on tributyl phosphate decomposition; hydrogen halides and halogenated C2- and C3- species were the main products formed by the halogenated phosphate ester. In the case of tris(1,3-dichloro-2-propyl)phosphate acrolein, not hydrogen chloride, presented the major toxic hazard.

Acrolein↗
PubMed1977

Combined therapy of advanced prostatic carcinoma with estramustine and prednimustine.

We treated 21 patients with stage D prostatic adenocarcinoma who had had unsuccessful hormonal therapy with a combination of 600 mg. per M.2 per day estramustine phosphate (Estracyt) and 15 mg. per M.2 per day prednimustine (Stereocyt, Leo 1031) in daily oral doses. Estramustine is a combination of estradiol and nitrogen mustard, and alone has shown objective responses in advanced prostatic cancer. Prednimustine is an ester of chlorambucil and prednisone. The preliminary results (after 2 to 9 months of therapy) show 5 patients (24 per cent) did not benefit from the drug and 7 patients (33 per cent) are stable. These preliminary results indicate the possible advantage of adding an alkylating agent (prednimustine) to estramustine in advanced prostatic carcinoma. Currently, a national randomized trial by the National Prostatic Cancer Project is evaluating this therapeutic innovation.

Aged↗
PubMed1977

Canine and human renal toxicity of inosine dialdehyde (NSC 118994).

A new antitumor agent, inosine dialdehyde, has shown minimal hematologic, but dose limiting, renal toxicity. The renal impairment is tubular necrosis due to reduction in renal blood by the drug. In addition, elevated serum calcium will return to normal within one week of drug administration. This effect is not secondary to urinary calcium excretion, but possibly an alteration of bone metabolism.

Acute Kidney Injury↗
PubMed1976

Distal Tubule [Na+] and juxtaglomerular apparatus Renin activity in uranyl nitrate induced acute renal failure in the rat. An evaluation of the role of tubuloglomerular feedback.

It has been previously demonstrated that single neophron filtration rate, whole kidney glomerular filtration rate and total renal blood flow decreased by 30-35% 6 h after uranyl nitrate induced acute renal failure in the rat. In order to evaluate a role of the renin-angiotensin system in the initiating phase (0-6 h) of this model of acute renal failure determinations of plasma renin activity, superficial (S) and deep (D) juxtaglomerular apparatus (JGA) renin activity and distal nephron [Na+] were obtained. Plasma renin activity increased from the control value of 1.5 +/- 0.3 (S.E.M.) to 2.9 +/- 0.4 ng/ml/h (P less than 0.005) at 6 h. Mean renin activity in S- and D-JGA's of control rats was 6.99 +/- 0.41 and 2.67 +/- 0.21 ng/JGA/h, respectively. After uranyl nitrate, renin activity in S-JGA's increased to 13.62 +/- 0.80 ng/JGA/h (P less than 0.001) at 2 h and remained elevated, 12.56 +/- 0.90 and 12.75 +/- 0.87 ng/JGA/h at 4 and 6 h. D-JGA renin activity increased (P less than 0.05) to 7.04 +/- 0.53, 6.23 +/- 0.31 and 3.44 +/- 0.33 ng/JGA/h at 2, 4 and 6 h after uranyl nitrate. Distal tubule [Na+], 27 samples in 6 rats, increased from a mean control value of 53.7 +/- 1.2 mEq/l to 116.9 +/- 2.5 mEq/l, 24 samples in 6 rats (P less than 0.001). Prompt increases in JGA renin activity were observed in the initiating phase of acute renal failure, suggesting a role for the renin-angiotensin system in the pathophysiology of this nephrotoxic model. The association of increased JGA renin activity and increased distal [Na+] is consistent with a role for the tubuloglomerular feedback mechanism in the initiating phase of uranyl nitrate induced acute renal failure in the rat.

Acute Kidney Injury↗
PubMed1976

Brain metastasis from prostatic carcinoma.

Between 1959 and 1971 there were 91 patients with clinically diagnosed prostatic carcinoma who were autopsied at Roswell Park Memorial Institute. In four of these 91 (4.4%) intracerebral metastasis were found at autopsy, but only in one of these four was the diagnosis arrived at pre-mortem. This report describes the diagnosis and management of intracerebral metastasis from prostate carcinoma. It appears, on the basis of our initial experience, that the clinical diagnosis of this entity deserves more frequent consideration.

Adenocarcinoma↗