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Dive into the research topics where J. H. Sunder is active.

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Featured researches published by J. H. Sunder.


Clinical Pharmacology & Therapeutics | 1970

Serum lipids during oral contraceptive exposure.

D.G. Corredor; L. V. Mendelsohn; G. Sabeh; J. H. Sunder; T. S. Danowski

The serum total cholesterol did not change significantly du ring 6 to 60 months of exposure to an oral contraceptive steroid combination (mestranol and norethynodrel). Alpha lipoprotein levels increased and remained slightly elevated. Serum total triglycerides increased during the sixth to eighteenth month of exposure only.


Metabolism-clinical and Experimental | 1969

Growth hormone in insulin-treated diabetes mellitus.

G. Sabeh; L.V. Mendelsohn; D.G. Corredor; J. H. Sunder; L.M. Friedman; C.R. Morgan; T. S. Danowski

Diabetes mellitus of juvenile or adult onset under treatment with insulin is characterized by higher serum growth hormone levels prior to and during disposal of an oral glucose load. The possible role of such growth hormone excesses in diabetic microangiopathy is discussed.


Metabolism-clinical and Experimental | 1969

Growth hormone and insulin levels in newly discovered glucose intolerance

G. Sabeh; D.G. Corredor; L.V. Mendelsohn; C.R. Morgan; J.C. Sieracki; J. H. Sunder; J.P. Wingert; T. S. Danowski

Abstract Newly discovered glucose intolerance in nonobese and in obese adult females is associated with fasting levels of immunoassayable growth hormone in serum lower than those found in nonobese female control subjects without glucose intolerance. When glucose intolerance without or with obesity is present, the peak levels of growth hormone and the sums of the growth hormone levels recorded after an oral glucose load are lower than those recorded in control subjects. When carbohydrate is ingested by women with newly-identified glucose intolerance, the average insulin increment during the induced hyperglycemia appears to be excessive. Actually, the insulin responses prove to be deficient in relation to the concomitant increments in blood sugar during the early as well as the late hours of the tolerance test. This deficiency is evident in nonobese and obese persons with glucose intolerance. The insulin responses cited above represent average findings in a series of patients. The individual groups include some persons with glucose intolerance whose insulin responses in relation to increments in the blood sugar equal or even exceed those recorded in healthy control subjects with a normal glucose tolerance.


Metabolism-clinical and Experimental | 1969

Enhanced postglucose hypophosphatemia during starvation therapy of obesity

D.G. Corredor; G. Sabeh; L.V. Mendelsohn; R.E. Wasserman; J. H. Sunder; T. S. Danowski

Abstract In obese persons without and with glucose intolerance, the hyperglycemic response to an oral glucose load was increased and prolonged by 10 to 14 days of total fasting. The insulin and growth hormone responses of these individuals to oral glucose were not altered by the fast, but the associated hypophosphatemia was markedly accentuated. The accentuated hypophosphatemic response to glucose observed during starvation raises the possibility that fasting is associated with shunting of the disposal of the carbohydrate load from liver to muscle. Fasting did not modify the blood sugar, serum inorganic phosphate, insulin or growth hormone responses to tolbutamide, arginine, or glucagon infusion.


Metabolism-clinical and Experimental | 1964

Hydrocortisone and/or desiccated thyroid in physiologic dosage: XI. Effects of tryroid hormone excesses on lipids and other blood and serum solutes☆

Campbell Moses; J. H. Sunder; John W. Vester; T. S. Danowski

Abstract The ingestion of a preparation of desiccated thyroid (Proloid) during a 12-week period in dosages increasing progressively at 2-week intervals from 3 to 25 grains per day was accompanied by a 20 to 30 per cent decrease in the serum total and the alpha and beta lipoprotein cholesterol. These decreases were first noted at the 10 grains per day level and, except for transient escape in the case of the beta lipoprotein cholesterol, persisted as the dosage was further increased. Cessation of the desiccated thyroid therapy was followed by rebound increases in these lipid fractions to values above the pretherapy levels. Alpha lipoprotein triglycerides decreased during thyroid therapy, while the total and beta lipoprotein triglycerides remained unchanged or increased sporadically. Serum levels of NEFA did not increase. Serum sodium definitely decreased during the ingestion of 20 or 25 grains of thyroid per day, reflecting perhaps a decrease in cellular osmolarity. Relative hyperkalemia appeared during the ingestion of desiccated thyroid in large amounts. Serum albumin decreased by about 0.5 Gm. per cent in the course of thyroid feeding; a concomitant rise in the globulin levels during the ingestion of 20 grains per day did not persist when the dosage was further increased. A transient rise was recorded in serum calcium, reminiscent of the hypercalcemia which may appear in spontaneous thyrotoxicosis; also, a nonsustained lowering of the serum inorganic phosphorus occurred at the 10 grain dosage level. Whole blood NPN and levels of uric acid and of creatinine in serum decreased during therapy with large dosages of desiccated thyroid per day; serum creatine increased. Levels of the fasting blood sugar and the serum carbon dioxide and chloride did not change during the ingestion of desiccated thyroid. Alkaline phosphatase and creatine phosphokinase activity decreased during thyroid feeding; the levels of acid phosphatase and of lactic and malic acid dehydrogenase were not altered.


Clinical Pharmacology & Therapeutics | 1965

Ethyl chlorophenoxyisobutyrate (CPIB) effects in juvenile‐onset diabetes mellitus

T. S. Danowski; R. E. Cohn; N.R. Limaye; J. F. Novak; R. W. Saul; J. H. Sunder; Campbell Moses

Ethyl‐α (p‐chlorophenoxy)isobutyrate (Atromid‐S or CPIB) was administered for three months to 18 patients with diabetes mellitus of juvenile onset. The intensity of the diabetes, ;udging by serial fasting blood sugar levels, glucose tolerance tests, 24 hour urine glucose excretion, and tests of fractional urine specimens for sugar and acetone did not change significantly. The drug did not produce a hypolipidemic effect but pretherapy values for serum lipoprotein cholesterol and triglycerides were almost always within the normal range. Several nonsustained increases in cephalin flocculation and one instance of prothrombin time prolongation were observed. Other hepatic function indices remained unchanged. A slight increase in serum total CO2, and a slight decrease in serum inorganic phosphorus were not statistically significant. Serum uric acid did decrease: the differences between pretherapy and therapy values were statistically significant. No other parameters of blood, serum, body fluids, hepatic, thyroid, adrenal, or pituitary function were discernibly affected.


Metabolism-clinical and Experimental | 1965

HYDROCORTISONE AND/OR DESICCATED THYROID IN PHYSIOLOGIC DOSAGE. XVII. MAJOR AND MINOR THYROIDAL INDICES DURING THERAPY WITH LARGE DOSAGES OF DESICCATED THYROID.

T. S. Danowski; N.R. Limaye; J. H. Sunder; R. E. Cohn; Campbell Moses

Abstract Excesses of thyroid hormones induced in healthy adults by the administration of desiccated thyroid in dosages increased from 3 to 25 grains or higher in the course of 3 months or longer shortened the S-D and V-P interval in kinemometer tracings and in the contraction and contraction and relaxation phases in the photomotograph records of the Achilles reflex, raised the serum PBI and triiodothyronine binding to blood cells, lowered the serum total and alpha and beta lipoprotein cholesterol but not the triglycerides, increased the serum inorganic phosphorus, and lowered the serum albumin. There is no evidence that during such induced excesses of thyroid hormones the V-P interval of the kinemometer tracing is more sensitive than the S-D interval as an indicator of Achilles reflex changes. Also, comparable changes were recorded in the contraction and the contraction plus one-half the relaxation times of the Achilles reflex as calculated from photomotograph records. As in previous studies, these dosages of desiccated thyroid were well tolerated by the subjects. Occasional nervousness, increased sweating, and decreased endurance were reported. Tachycardia and slight elevations of the systolic and decreases in the diastolic blood pressure appeared in all. Electrocardiographic changes were minimal. Body weight decreased by an average of 26.0 pounds during the 22 weeks of treatment.


Clinical Pharmacology & Therapeutics | 1970

Biochemieal, endocrine, and other indices during quinestrol therapy

T. S. Danowski; F. M. Kenny; H. R. Wilson; G. Sabeh; J. H. Sunder; D.G. Corredor

Quinestrol (ethinylestradiol‐3‐cyclopentyl ether), a synthetic estrogenic compound with prolonged duration of action, was administered for 6 months to women at a dosage of 0.025 mg. twice daily with a minimum 01 untoward clinical efJects. This dosage produced a number of efJects indicative of or compatible with estrogenic activity, including increased cornification of menopausal vaginal epithelium, a slight rise in serum protein‐bound iodine and creatine, and a decrease in beta lipoprotein cholesterol. Unexplained slight decreases in serum acid phosphatase activity and in cephalin flocculation were recorded, and blood lymphocytes increased transiently. Also during quinestrol therapy ACTH produced a greater increase in plasma ll‐hydroxycorticosteroids at the 30 minute point of the stimulation test, but the values in the 1, 2, and 3 hour plasma sampies were comparable in the control and intratherapy studies. Urinary ll‐desoxycortisol metabolites diminished, but the change was very slight. Glucose‐induced hypophosphatemia was accentuated in nondiabetic individuals, glucose tolerance appeared to improve in patients with diabetes, and in both groups the increases in serum insulin evoked by a glucose load were less during quinestrol therapy. Other indices remained unchanged, including blood and serum solutes, a variety of serum enzymes, hematologic and hepatic indices, plasma ll‐hydroxycorticosteroids, urinary 17‐ketosteroids and Porter‐Silber chromogens, plasma ll‐hydroxycorticosteroid responses to intravenous ACTH (the 30 minute exception has been cited) and to pyrogen, and urinary pressor activity, gonadotrop ins, and total estrogens. The efJects of ll‐beta hydroxylase blockade by metyrapone on urinary steroids were not altered by 6 months of quinestrol therapy.


Hormone Research in Paediatrics | 1973

Effects of a Progestin, Quingestanol, in Older Diabetic Women

T. S. Danowski; H.R. Wilson; Ramesh C. Khurana; Y. Jung; Alejandro R. Gonzalez; J. H. Sunder

Quingestanol acetate (17-α-ethynyl-19-nortestosterone acetate, 3-cyclopentylenol ether), a synthetic progestational steroid, was well tolerated at a dosage of 300 µg/day per os by 17 diabetic women wh


Clinical Pharmacology & Therapeutics | 1976

Thyroid hormone‐like effects without thyrotoxicosis during one year's therapy with NA‐DT3 for hypercholesterolemia

T. S. Danowski; T. Stephan; S. Nolan; U. Ahmad; J. P. Wingert; D. H. Bowman; J. H. Sunder; Edwin R. Fisher

A thyroid hormone analogue, sodium dextro‐triiodothyronine (NaDT3), at a dosage of 1 mg/day for 1 or 2 yr, decreased serum cholesterol levels about 30% in 26 hyperlipidemic adults. There were less sustained decreases in the serum phospholipids, and occasional lowering of the serum triglycerides, but no effects on body weight, blood pressure, or pulse rate. Changes recognized as variable concomitants of spontaneous or induced thyrotoxicosis, such as transient increases in fasting blood glucose, calcium, and globulin, persistent rises in alkaline phosphatase, and nonsustained decreases in hematocrit are consonant with the fact that Na‐DT3 exerts about one tenth of the thyroid hormone activity of LT3. These changes, however, appear to represent actions of iodinated amino acids apart from those effects that result in clinical thyrotoxicosis.

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T. S. Danowski

University of Pittsburgh

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Campbell Moses

University of Pittsburgh

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G. Sabeh

University of Pittsburgh

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D.G. Corredor

University of Pittsburgh

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John W. Vester

University of Pittsburgh

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N.R. Limaye

University of Pittsburgh

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R. E. Cohn

University of Pittsburgh

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Clem Russ

University of Pittsburgh

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