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S Hurwitz

Publications and source records attributed to S Hurwitz.

At least 109 records · Page 6Linked to original sources
PubMed1989

Atrial natriuretic peptide and sodium nitroprusside stimulate cyclic GMP accumulation by avian skin fibroblasts and epiphyseal growth-plate chondroprogenitor cells.

Chondroprogenitor cells derived from avian tibia epiphyseal growth plate, and skin fibroblasts were cultured in vitro. In the fibroblasts, human (1-28) and rat (5-28) atrial natriuretic peptide (ANP) stimulated cyclic GMP (cGMP) production in a dose-dependent manner without affecting cAMP. Sodium nitroprusside also stimulated cGMP accumulation by chondroprogenitor cells and fibroblasts, but the maximum cGMP accumulation elicited by sodium nitroprusside was much lower than that obtained with ANP. The effects of ANP and sodium nitroprusside on chondroprogenitor cells and skin fibroblasts were additive. Human ANP increased cGMP production by the particulate fraction prepared either from chondroprogenitor cells or fibroblasts. Sodium nitroprusside, at concentrations of up to 1 mmol/l, did not affect cGMP production by the particulate fraction prepared from either cell type. The present study provides additional evidence that avian growth-plate chondroprogenitor cells and skin fibroblasts are targets for ANP. ANP and nitroprusside activate different guanylate cyclase isoenzymes--the particulate and soluble forms of the enzyme respectively. The data suggest that most of the guanylate cyclase activity in these cells is localized in the particulate fraction.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Severe feed restriction in pullets during the early growing period: performance and relationships among age, body weight, and egg weight at the onset of production.

The performance of egg type (Leghorn x Rhode Island Red) chickens that were feed restricted during the prelaying period was studied in two trials, each conducted with 300 hens. In Trial 1, treatments included 1) an ad libitum-fed control; 2) restriction for close to zero growth between 7 and 28 days of age; 3) the same restriction as (2) but continued by restriction of 50% growth up to 70 days; 4) restriction between 7 and 70 days for 50% growth; and 5) restriction for 50% growth between 7 and 98 days. In Trial 2, birds were restricted severely (close to zero growth) from 7 to 28 days of age, followed by restriction of 50% growth up to 28, 56, 84, and 112 days of age, respectively. In all cases, feed restriction resulted in a delay in the onset of egg production, leading to some increases in egg weight. Egg production rate and cumulative production were not affected, in most cases, by early feed restriction. The BW at the onset and after 20 mo of production was reduced when feed restriction was continued beyond the age of 84 days. Overall feed conversion (grams feed per egg) and feed efficiency (grams feed per gram egg mass) were not affected significantly by feed restriction, although feed efficiency (grams gain per gram feed) was improved during the prelaying period. Within each treatment, BW was positively correlated with age at onset of egg production. Egg weight was a function of both age and BW at the onset of production. The significant correlation between egg weight and BW was maintained even after a year of production.

Age Factors↗
PubMed1989

Effect of dietary protein, energy, and feed pelleting on the response of chicks to early feed restriction.

In three trials, male broiler chicks were subjected to a 6-day feed restriction regimen designed to retard growth severely. In one trial, the amino acid requirements during refeeding were evaluated by testing the adequacy of diets based on model calculations. In two additional trials, the response of feed-restricted birds to increased dietary energy density and to feed pelleting was compared with that of birds fed ad libitum. Results of the first trial showed that weight gain and feed efficiency during the first 2 wk of refeeding were reduced when the diet contained less than the model-calculated protein level for this period. No improvement in performance could be obtained when dietary protein was increased by 1% above model-calculated requirements. An increase in dietary nutrient density resulted in an enhanced growth rate. Feed efficiency was improved by an increase in nutrient density and by early feed restriction with no significant feed restriction x diet density interactions. Pellet-feeding resulted in improved growth without affecting feed efficiency, whereas feed restriction resulted in improved feed efficiency only. Interaction between pelleting and feed restriction was not significant for any of the variables. In all three trials, abdominal fat was reduced by feed restriction without any interaction with energy, protein, or dietary form. The results suggest that the requirements for some amino acid increase after feed restriction and that feed consumption does not limit the accelerated growth response at that time.

Animal Feed↗
PubMed1989

Posterior acetabular fracture-dislocations: fragment size, joint capsule, and stability.

In acetabular fractures, the size of a significant posterior wall fragment remains undefined as it affects joint stability. The purpose of this study was to quantitatively evaluate fragment size and hip stability in cadaveric specimens after serial osteotomies. Also, the role of the posterior capsule, in the various osteotomies, was evaluated for changes in hip stability. We found that fragments involving 25% or less of the acetabulum are insignificant, i.e., do not affect joint stability, while fragments involving 50% or more are significant. The significance of transitional fragments (25-50% of the acetabulum) is determined by the posterior capsule.

Acetabulum↗
PubMed1988

Nucleotide sequence of cloned cDNAs encoding chicken preproparathyroid hormone.

In order to characterize an avian parathyroid hormone gene, a lambda gt10 cDNA library constructed from chicken parathyroid gland mRNA was screened with a human preproparathyroid hormone (preproPTH) cDNA probe. Nucleotide sequence analysis of three independent clones confirmed that they encoded chicken preproPTH. This analysis, complemented by primer extension and Northern blot analysis of mRNA, demonstrated a 5'-untranslated region for chicken preproPTH of 127 nucleotides, a coding region of 357 nucleotides, and a 3'-untranslated region of approximately 2500 nucleotides. The coding sequence predicts a mature chicken PTH of 88 amino acids in contrast to the 84 amino acids of the mammalian hormones. Comparison of the avian and the mammalian hormones shows striking homology in the region of amino acids 1-32. The middle and carboxyl-terminal portions of chicken PTH, however, differ considerably from the mammalian hormones and include deletions of sequences conserved in mammalian PTH and insertions of novel peptide sequences. Comparison of the avian and mammalian structures suggests potential alterations of the mammalian sequences that may lead to altered bioactivity and/or hormone metabolism.

Amino Acid Sequence↗
PubMed1988

Patient and physician delay in melanoma diagnosis.

The sequence of events leading ultimately to the diagnosis and treatment of malignant melanoma was investigated. We conducted interviews with 275 patients and the physicians whom they had consulted regarding their suspicious lesions before their eventual referral to a melanoma center. An average of 1 year elapsed from the time that patients first noticed a new or changed lesion and the date of diagnosis. Major components of delay were attributable to both patients and physicians. An average of 6 months elapsed between patients' recognition of a new or changed lesion and their realization that the lesion was suspicious. For 21% of cases, at least 2 months elapsed between physicians' observation of lesions and a definitive diagnosis of malignant melanoma, and 13% were diagnosed a minimum of 4 months following a visit to the physician. Patients routinely cannot distinguish between melanomas and moles. Physicians do not always diagnose melanoma accurately or act promptly in response to suspicious lesions. We have yet to take adequate advantage of the unique opportunity for early detection and cure in this readily visible, rapidly increasing malignancy.

Adult↗
PubMed1988

Egg shell quality and cholecalciferol metabolism in aged laying hens.

Calcium-binding protein D28K (calbindin) synthesis, vitamin D metabolism and shell quality were investigated in young and aged laying hens fed diets containing either cholecalciferol (CC) or its 1-hydroxylated derivatives. Duodenal calbindin concentration was similar in the young and in the aged laying hens. Exogenous 1-hydroxylated CC derivatives increased duodenal calbindin concentration, regardless of age. Shell weight and shell density (mg/cm2) were significantly lower (P less than 0.01) in the aged than in the young hens. Egg shell weight and density tended to decrease along the clutch. The rate of decline was higher in aged than in young hens. Feeding aged hens a diet containing 5 micrograms 1,25-dihydroxycholecalciferol [1,25(OH)2CC] or 1 alpha-hydroxycholecalciferol per kilogram improved shell quality, slowed down the progressive reduction in shell quality during the clutch and increased culling and mortality. The results indicate a) that the capacity for expression of 1,25(OH)2D3 in the intestine is not altered by age and b) that prolonged feeding of 1-hydroxylated derivatives of vitamin D3 improves shell quality in aged laying hens and increases culling and mortality.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1988

The dysplastic nevus: recognition and management.

The recognition of atypical or dysplastic nevomelanocytic nevi potentially provides clinicians with another means of identifying individuals at increased risk for cutaneous malignant melanoma. However, a great deal of controversy still surrounds these lesions, their significance, and the clinical and histologic criteria needed for their diagnosis at present. In general, dysplastic nevi tend to be asymmetrical and larger (greater than 5 mm) than ordinary acquired nevi, have a macular component, irregular and ill-defined borders, and haphazard (variegate) coloration. A clinical diagnosis of dysplastic nevi must be confirmed by histopathology, since not all clinically atypical nevi are dysplastic. While precise histopathologic criteria for dysplastic nevi are lacking, most authorities agree that an abnormal nevomelanocytic proliferative pattern as manifested by increased numbers of basilar melanocytes and/or abnormal junctional nevomelanocytic nesting in the setting of lentiginous epidermal hyperplasia, variable degrees of nevomelanocytic nuclear atypia, and a lymphocytic host response are consistent with a histologic diagnosis of dysplastic nevi. Current data for individuals with dysplastic nevi and a family history of cutaneous malignant melanoma (at least two family members with cutaneous malignant melanoma) indicate a relative risk for cutaneous malignant melanoma about 148 times that of the general population. In comparison, cutaneous malignant melanoma risk seems lower for individuals with familial dysplastic nevi (but without familial cutaneous malignant melanoma) and "sporadic" dysplastic nevi. With respect to progression to melanoma, probably the vast majority of dysplastic nevi remain stable or possibly regress. Management of individuals with histologically confirmed dysplastic nevi involves periodic skin examinations. Regional overview and life-size photography are helpful in following these patients. Patients should also be instructed in the examination of their own skin. While a definite relationship between sun exposure and dysplastic nevi remains unproved, the use of sunscreens and avoidance of unnecessary sun exposure are advised. Examination of family members for atypical melanocytic lesions is also recommended.

Diagnosis, Differential↗
PubMed1988

The effect of parathyroid hormone and atrial natriuretic peptide on cyclic nucleotides production and proliferation of avian epiphyseal growth plate chondroprogenitor cells.

Cells derived from avian tibia epiphyseal growth plate were cultured in vitro. The cells which exhibited a polygonal phenotype and are termed chondroprogenitor cells, developed in culture as a monolayer with a doubling time of 40-48 h in 5% fetal calf serum. Production of cAMP by the chondroprogenitor cells was stimulated by human and bovine native (1-84) PTH. The effect of PTH on cAMP production could be blocked by the (3-34) PTH analog, suggesting interaction with specific receptors. cAMP production by avian chondroprogenitor cells was also stimulated by cholera toxin, forskolin, and prostaglandin E2 but not by ACTH or prostaglandin F2 alpha. PTH, cholera toxin, and forskolin also stimulated proliferation of the chondroprogenitor cells. In contrast, neither cAMP production nor proliferation of avian skin fibroblasts was affected by PTH. Human (1-28) and rat (5-28) atrial natriuretic peptide stimulated cGMP production by avian chondroprogenitor cells and also by skin fibroblasts. Atrial natriuretic peptide inhibited the basal and PTH-stimulated [3H]thymidine incorporation into DNA of chondroprogenitor cells, but did not affect avian skin fibroblast proliferation. These results suggest that the proliferation of avian epiphyseal growth plate chondroprogenitor cells is modulated by opposing mechanisms induced by PTH and ANP, probably mediated by cAMP and cGMP, respectively.

1-Methyl-3-isobutylxanthine↗
PubMed1988

Stimulation of chick adrenal steroidogenesis by avian parathyroid hormone.

Dispersed chick adrenocortical cells were incubated with avian parathyroid hormone (aPTH) or ACTH. Accumulation of cyclic AMP (cAMP), activity of cAMP-dependent protein kinase and the secretion of corticosterone and aldosterone, in response to these hormones, were measured. Accumulation of cAMP and activity of cAMP-dependent protein kinase were stimulated by both aPTH and ACTH as well as by cholera toxin. Cyclic AMP production followed a similar time-course when stimulated by either peptide hormone. Stimulation of steroid hormone secretion was detectable after 20 min of incubation with ACTH, but only after 40 min with aPTH. The maximal steroid hormone secretion by adrenocortical cells was similar when induced by either peptide hormone. The aPTH concentrations needed for half-maximal response of corticosterone and aldosterone secretion were higher than those for ACTH (2.5- and 2-fold respectively), but still within the physiological range. The 11 beta-hydroxylase inhibitor metyrapone inhibited the secretion of both corticosterone and aldosterone when induced by either aPTH or ACTH. The results suggest that aPTH is almost as potent as ACTH in stimulating the secretion of corticosterone and aldosterone from chick adrenocortical cells and utilizes a cAMP-dependent pathway similar to that of ACTH.

Adrenal Cortex↗
PubMed1988

Regulation of aldosterone secretion by avian adrenocortical cells.

Dispersed chick adrenocortical cells were incubated with mammalian and avian angiotensin-II, Ca2+, K+, verapamil, nifedipine, Ca2+ ionophore (A23187), protein kinase-C activator (phorbol 12-myristate 13-acetate; TPA), atrial natriuretic peptide (ANP), sodium nitroprusside (SNP) and ACTH. Secretion of aldosterone and corticosterone, and accumulation of cyclic nucleotides were assessed. Secretion of aldosterone was not affected by angiotensin-II, Ca2+ channel blockers, Ca2+ ionophore or TPA. ANP stimulated production of cyclic GMP (cGMP), and inhibited aldosterone secretion with a similar dose-response relationship. SNP also stimulated cGMP production and inhibited the ACTH-stimulated aldosterone secretion. The results indicate that ANP is an inhibitor of aldosterone secretion in birds and suggest that this inhibition is mediated by cGMP. In contrast to mammalian glomerulosa cells, angiotensin-II and the calcium-inositol phosphate-protein kinase C pathway appear not to be involved in the regulation of aldosterone secretion by avian adrenal cells.

Adrenal Cortex↗
PubMed1988

Early feed restriction in chicks: effect of age, duration, and sex.

Several regimens of feed restriction, calculated to support the maintenance of body weight without any allowance for growth, were applied beginning at the ages of 3 to 11 days for periods of 3 to 7 days using male and female broilers. In males, the 7-day feed restriction treatment resulted in improved feed efficiency on an age basis, or on a body weight basis after body weight had reached .7 to 1 kg. Feed restriction also resulted in a reduction in the amount of abdominal fat at the age of 54 to 59 days without any concomitant reduction in body weight. Within the range tested, 3 to 11 days of age, the initiation of the 7-day restriction treatment did not affect response. Similar responses were obtained in females, but with little benefit in feed efficiency when compared with ad libitum-fed birds on a body-weight basis. Also in females, reduction in 56-day body weight and loss of benefits derived from improved feed efficiency and reduced carcass fat could be avoided if the period of restriction was kept at 3 to 5 days.

Age Factors↗
PubMed1988

Response of growing turkeys to dietary fat.

Growth, feed efficiency, and carcass fat were evaluated in turkeys fed diets in which added fat varied, holding energy or the calories:protein ratio constant. In the 1 to 3-wk-old turkey, growth and feed efficiency increased with dietary energy, but did not change significantly when fat was added isocalorically. The 12 to 14-wk-old turkey responded with improved growth and feed efficiency when dietary fat was added either isocalorically or with increasing energy density. However, the response to the isocaloric fat addition was smaller in magnitude than the response when fat was added without calorie adjustment. No difference could be detected in 12 to 15-wk-old turkeys in the performance response to tallow and soybean oil. Carcass fat deposition generally increased with dietary fat supplementation, regardless of the caloric change. The results suggest that in the midterm of development of the growing turkey, dietary fat per se affects growth, feed efficiency, and carcass fat. Growth and feed efficiency responses to nutrient density occur in both young and older birds.

Adipose Tissue↗
PubMed1988

Calorie-nitrogen interactions in the parenterally fed primate.

To test the hypothesis that nonprotein calorie intake and nitrogen intake are equally important in establishing positive nitrogen balance, weight gain, and serum protein response in the depleted primate treated with total parenteral nutrition (TPN), 10 adult male chair-adapted primates (Macaque fascicularis) were studied. After 10 days of nutritional depletion (nothing by mouth; 5% dextrose with electrolytes administered intravenously) animals were randomized to receive one of four TPN diets for 10 days. The depletion/repletion cycle was repeated, after 1 month of caged free feeding, until all animals had received the four TPN diets. Two levels of nonprotein caloric intake (155% and 100% of primate resting energy expenditure) and two levels of nitrogen intake (200% and 100% of primate nitrogen requirement) were used to make the four different diets. Nitrogen balance (p = 0.01) and serum total iron-binding capacity response (p = 0.02) were significantly influenced by the level of nitrogen intake but not by nonprotein calorie intake, which significantly influenced only weight gain (p = 0.03). Fluid balance was not significantly different for any diet. Fat and protein stores may be selectively repleted in this model by adjusting the nonprotein calorie and nitrogen content of TPN.

Animals↗
PubMed1988

Pigmented nevi.

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Dysplastic Nevus Syndrome↗
PubMed1988

Integration of full-dose adjuvant chemotherapy with definitive radiotherapy for primary breast cancer: four-year update.

Controversy exists over the effect of definitive radiotherapy on the ability to administer full doses of adjuvant chemotherapy in primary breast cancer. Ninety-six consecutive women with clinical stage I and II breast cancer were treated with radiotherapy plus chemotherapy. Three combinations of drugs were used: cyclophosphamide and 5-fluorouracil (CF); cyclophosphamide, methotrexate, and 5-fluorouracil (CMF); or cyclophosphamide, methotrexate, 5-fluorouracil, and prednisone (CMFP). Chemotherapy consisted of two cycles of CF (cyclophosphamide at a dosage of 100 mg/m2 orally on days 1-14+5-fluorouracil at 600 mg/m2 iv on days 1 and 8) during concurrent radiotherapy, followed by six cycles of CMFP (same CF dosages+methotrexate at 40 mg/m2 iv on days 1 and 8+prednisone at 40 mg/m2 orally on days 1-14). The study included 63 premenopausal and 33 postmenopausal patients; 72 had 1-3 positive nodes, had greater than or equal to 4 positive nodes, and 9 had negative nodes and negative estrogen receptors. The mean CF doses delivered during concurrent radiotherapy were 95% of the optimal doses, and the mean CMF doses administered during the six cycles after radiotherapy were 89%. The CMF was delivered at level I (greater than or equal to 85% of optimal doses) to 73% of the patients. With a median follow-up of 36 months, 16 relapses have been observed. Two of these patients had treatment failure only in the breast or axilla and are disease free after mastectomy. Of the 72 patients with 1-3 positive nodes, 10 relapsed in distant sites, while 4 of 15 patients with greater than or equal to 4 positive nodes have had distant failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Antineoplastic Combined Chemotherapy Protocols↗