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Biomedical subjects

H Henry

Publications and source records attributed to H Henry.

At least 37 records · Page 2Linked to original sources
PubMed1995

Glyoxysomal malate dehydrogenase and malate synthase from soybean cotyledons (Glycine max L.): enzyme association, antibody production and cDNA cloning.

In order to investigate a possible association between soybean malate synthase (MS; L-malate glyoxylate-lyase, CoA-acetylating, EC 4.1.3.2) and glyoxysomal malate dehydrogenase (gMDH; (S)-malate: NAD+ oxidoreductase, EC 1.1.1.37), two consecutive enzymes in the glyoxylate cycle, their elution profiles were analyzed on Superdex 200 HR fast protein liquid chromatography columns equilibrated in low- and high-ionic-strength buffers. Starting with soluble proteins extracted from the cotyledons of 5-d-old soybean seedlings and a 45% ammonium sulfate precipitation, MS and gMDH coeluted on Superdex 200 HR (low-ionic-strength buffer) as a complex with an approximate relative molecular mass (Mr) of 670,000. Dissociation was achieved in the presence of 50 mM KCl and 5 mM MgCl2, with the elution of MS as an octamer of M(r) 510,000 and of gMDH as a dimer of M(r) 73,000. Polyclonal antibodies raised to the native copurified enzymes recognized both denatured MS and gMDH on immunoblots, and their native forms after gel filtration. When these antibodies were used to screen a lambda ZAP II expression library containing cDNA from 3-d-old soybean cotyledons, they identified seven clones encoding gMDH, whereas ten clones encoding MS were identified using an antibody to SDS-PAGE-purified MS. Of these cDNA clones a 1.8 kb clone for MS and a 1.3-kb clone for gMDH were fully sequenced. While 88% identity was found between mature soybean gMDH and watermelon gMDH, the N-terminal transit peptides showed only 37% identity. Despite this low identity, the soybean gMDH transit peptide conserves the consensus R(X6)HL motif also found in plant and mammalian thiolases.

Amino Acid Sequence↗
PubMed1987

Comparison of butorphanol tartrate and meperidine in moderate to severe renal colic.

The analgesic efficacy and safety of parenteral butorphanol and meperidine were compared. The double-blind, randomized study involved 120 patients presenting with moderate to severe renal colic. Pain intensity and pain relief were evaluated by trained observers at fixed time intervals for four hours after study drug was administered. Eighty-three patients with documented upper urinary tract calculi were evaluated for efficacy. Butorphanol 4 mg was significantly more effective than butorphanol 2 mg and was equivalent to meperidine 80 mg. Overall efficacy assessments were "good" or "excellent" for 87 per cent, 72 per cent, and 85 per cent, respectively. There were no significant differences in side effects among treatment groups in the 83 evaluable and 27 inevaluable patients receiving study drugs. Butorphanol was effective and well-tolerated in this patient population, with important advantages over opiate analgesics.

Butorphanol↗
PubMed1984

The effects of familial relationships, age, body weight, and diet on blood pressure and the 24 hour urinary excretion of sodium, potassium, and creatinine in men, women, and children of randomly selected families.

Two hundred thirty-three randomly selected families provided a population for studying the effects of familial relationships, age, diet, body weight, and urinary electrolyte excretion on blood pressure. There was a strong familial component for urinary sodium, potassium, and creatinine excretion and for systolic blood pressure. In individuals, age, heart rate, and body weight were independently related to blood pressure. In women, urinary sodium and potassium levels were related to diastolic blood pressure. These individual relationships persisted when age was accounted for but were no longer significant after adjusting for both age and body weight, suggesting that heavier people eat more food, which in our culture means greater sodium intake. In fact, our randomly selected families were eating as much sodium (130 to 170 meq/day) and as little potassium (50 to 70 meq/day) as consumed by Americans several decades ago. Furthermore, this study again documented the rise in blood pressure with age, which may represent the effect of environmental influences on blood pressure over time. The familial aggregation of urinary sodium, potassium, and creatinine excretion, along with the well-established familial aggregation of body weight, emphasizes the importance of the entire family in the treatment and prevention of hypertension.

Adolescent↗
PubMed1983

Assessment of nutritional correlates of blood pressure.

Nutritional factors are thought to contribute to the development of hypertension in susceptible humans. This review categorizes the types of nutrition-related data currently available on the relation between diet and blood pressure and provides guidelines for interpreting and using these data. The nutrition data base and the net effect of specific nutrients on blood pressure are discussed, and examples from the Health and Nutrition Examination Survey are given to compare demographic characteristics of various nutrients with demographic characteristics of hypertension in our society. Criteria for evaluating the strength and relevance of a specific nutrient's influence on blood pressure are presented. A comprehensive, continued assessment of all studies of diet and blood pressure control should assure better understanding of the pathogenesis and treatment of human hypertension.

Adult↗
PubMed1980

Effects and interactions of 24R,25(OH)2D3 and 1,25(OH)2D3 on bone.

The effects of various combinations of therapy with 1 alpha,25-dihydroxycholecalciferol (1,25(OH)2D3) and 24R,25-dihydroxycholecalciferol (24R,25(OH)2D3) on structural and dynamic parameters of bone were evaluated in 40 chicks raised on a vitamin D-deficient diet from time of hatching and supplemented with the dihydroxylated metabolites. The results showed that: 1) the maintenance of volumetric density of bone is dependent on the presence of 1,25(OH)2D3, 2) lack of 1,25(OH)2D3 is associated with an increase in the number of osteocytes per unit volume of bone, most probably due to decreased amounts of bone formed by each osteoblast before becoming an osteocyte, 3) adequate quantities of either 24R,25(OH)2D3 or 1,25(OH)2D3 are needed to prevent accumulation of osteoid or the production of endosteal fibrosis, and 4) maintenance of normal tetracycline label width requires both hydroxylated compounds with one of them in sufficient amounts. The data of this study demonstrate that the integrity of certain parameters of bone structure could be maintained only with 1,25(OH)2D3, others with either dihydroxylated metabolites, and still others with a combination of both. These data underscore the biological activity of 24R,25(OH)2D3 by demonstrating its effectiveness on bone.

Animals↗
PubMed1978

Inhibition of parathyroid hormone secretion by 25-hydroxycholecalciferol and 24,25-dihydroxycholecalciferol in the dog.

We studied the effects of vitamin D metabolites on parathyroid hormone (PTH) secretion. Test materials were injected into the cranial thyroid artery of the dog, and immunoreactive PTH was measured frequently in serum samples from the inferior thyroid vein and the femoral vein. This model for the study of secretion had previously been validated with the use of known modulators on PTH secretion. In control experiments, injection of 100% ethanol, the vehicle in which cholecalciferol (D(3)) metabolites were suspended, resulted in no change in PTH secretion. Likewise, native vitamin D(3), in doses ranging from 250 to 1,250 ng had no effect on PTH secretion. 25-Hydroxycholecalciferol, 25-(OH)D(3), in doses of 125-240 ng, caused complete suppression of PTH secretion. When 24,25-dihydroxycholecalciferol, 24,25-(OH)(2)D(3), was injected in doses of 50-250 ng, suppression of PTH secretion was again complete; in doses of 5 ng, injection of this metabolite resulted in significant but incomplete suppression of secretion. In doses of 50-250 ng, 1,25-(OH)(2)D(3) strongly stimulated PTH secretion, but in a dose of 5 ng this metabolite had no effects. Injection of equal doses of 1,25-(OH)(2)D(3) and 24,25-(OH)(2)D(3) resulted in significant suppression of PTH secretion. Hypocalcemia-induced stimulation of PTH secretion was suppressed by 24,25-(OH)(2)D(3) while hypercalcemia-induced suppression of PTH secretion was stimulated by 1,25-(OH)(2)D(3). In all experiments showing suppression of PTH secretion, peripheral PTH decreased. Arguments are presented for considering the suppressive effects of D(3) metabolites as physiologic modulators. However, this stimulating effect of 1,25-(OH)(2)D(3) occurred only in pharmacologic doses and hence probably has no physiologic relevance.

Animals↗