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Biomedical subjects

A Rogol

Publications and source records attributed to A Rogol.

At least 19 recordsLinked to original sources
PubMed2007

Management of the child born small for gestational age through to adulthood: a consensus statement of the International Societies of Pediatric Endocrinology and the Growth Hormone Research Society.

OBJECTIVE: Low birth weight remains a major cause of morbidity and mortality in early infancy and childhood. It is associated with an increased risk of health problems later in life, particularly coronary heart disease and stroke. A meeting was convened to identify the key health issues facing a child born small for gestational age (SGA) and to propose management strategies. PARTICIPANTS: There were 42 participants chosen for their expertise in obstetrics, peri- and neonatal medicine, pediatrics, pediatric and adult endocrinology, epidemiology, and pharmacology. EVIDENCE: Written materials were exchanged, reviewed, revised, and then made available to all. This formed the basis for discussions at the meeting. Where published data were not available or adequate, discussion was based on expert clinical opinions. CONSENSUS PROCESS: Each set of questions was considered by all and then discussed in plenary sessions with consensus and unresolved issues identified. The consensus statement was prepared in plenary sessions and then edited by the group chairs and shared with all participants. CONCLUSIONS: The diagnosis of SGA should be based on accurate anthropometry at birth including weight, length, and head circumference. We recommend early surveillance in a growth clinic for those without catch-up. Early neurodevelopment evaluation and interventions are warranted in at-risk children. Endocrine and metabolic disturbances in the SGA child are recognized but infrequent. For the 10% who lack catch-up, GH treatment can increase linear growth. Early intervention with GH for those with severe growth retardation (height sd score, <-2.5; age, 2-4 yr) should be considered at a dose of 35-70 microg/kg x d. Long-term surveillance of treated patients is essential. The associations at a population level between low birth weight, including SGA, and coronary heart disease and stroke in later life are recognized, but there is inadequate evidence to recommend routine health surveillance of all adults born SGA outside of normal clinical practice.

Adult↗
PubMed1998

Discordant phenotypes and 45,X/46,X,idic(Y).

Mosaicism introduces wide variability into the clinical expression of numerical and unbalanced structural chromosomal abnormalities. The phenotypic range of variability of 45,X/46,XY mosaicism extends from Turner syndrome to mixed gonadal dysgenesis to normal males. The specific phenotype is primarily dependent on the chromosomal constitution of the developing gonad. Similar phenotypic variability is observed with mosaicism for 45,X and a second cell line with an abnormal sex chromosome. This report describes a patient with Turner syndrome and a patient with mixed gonadal dysgenesis who have identical karyotypes, namely 45,X/46,X,idic(Y)(p11.2). While mosaicism alone might have accounted for the phenotypic differences, by PCR analysis the Turner syndrome patient was SRY and ZFY negative and the mixed gonadal dysgenesis patient was SRY and ZFY positive.

Adolescent↗
PubMed1997

Partial growth-hormone insensitivity: the role of growth-hormone receptor mutations in idiopathic short stature.

Mutations in the GHR locus may play a role in the cause of idiopathic short stature (ISS) by impairing growth-hormone (GH) receptor (GHR) function. At one extreme, mutations that nullify the function of the GH receptor are linked to complete GH insensitivity syndrome, or Laron syndrome, and we hypothesized that less-disruptive mutations could contribute to partial GH insensitivity syndrome. Low levels of GH binding protein may indicate mutations in the extracellular domain of the receptor, and by focusing on 14 children with ISS who had low GH binding protein and insulin-like growth factor I levels, we found three heterozygotes and one compound heterozygote for mutations in the extracellular domain of the receptor. We have since extended our study to a broader spectrum of patients, adding 76 patients with ISS who were treated with GH in a phase II study of the safety and efficacy of recombinant human GH in ISS and also adding 10 patients who were ascertained as having ISS by pediatric endocrinologists in private practice. The GHR gene has thus been analyzed in 100 patients with ISS, eight of whom were found to carry mutations: four in our original study and four with normal or elevated levels of GH binding protein. The latter group consists of three carriers of heterozygous extracellular domain mutations and one carrier of a heterozygous intracellular domain mutation. Family data suggest that the carriers of these mutations have a range of phenotypes, supporting our hypothesis that the expression of these heterozygous mutations as partial GH insensitivity syndrome depends on the genetic makeup of the person.

Body Height↗
PubMed1995

Role of steroidogenic acute regulatory protein in adrenal and gonadal steroidogenesis.

Congenital lipoid adrenal hyperplasia is an autosomal recessive disorder that is characterized by impaired synthesis of all adrenal and gonadal steroid hormones. In three unrelated individuals with this disorder, steroidogenic acute regulatory protein, which enhances the mitochondrial conversion of cholesterol into pregnenolone, was mutated and nonfunctional, providing genetic evidence that this protein is indispensable normal adrenal and gonadal steroidogenesis.

Adrenal Glands↗
PubMed1990

Percentages of maximal heart rate, heart rate reserve and VO2max for determining endurance training intensity in male runners.

The use of 60%-95% of maximal heart rate (HR), heart rate reserve (HRR) and VO2max as exercise training intensities was examined in male runners, and these intensities were related to VO2 observed at the lactate threshold (LT) and fixed blood lactate concentrations (FBLC) of 2.0, 2.5, and 4.0 mM. Thirty-one subjects (means age = 29.9 +/- 9.1 yrs; means ht = 177.3 +/- 8.2 cm; means wt = 69.2 +/- 9.9 kg) completed a level running treadmill protocol. The mean values at LT, FBLC of 2.0, 2.5, 4.0 mM and max for VO2 were 52.7, 56.4, 58.0, 61.2 and 63.5 ml/kg.min -1, respectively: for velocity they were 237.4, 252.2, 260.6, 274.4 and 286.5 m/min, respectively; and for HR were 165.7, 172.7, 176.5, 182.3 and 187.4 bts/min, respectively. The majority of subjects were not above LT (N = 20), until an intensity of 90% HR max was attained. At 95% HR max the majority of subjects were above 2.0 mM (N = 23) and 2.5 mM (N = 17) but below 4.0 mM (N = 26). For HRR, 85% HRR was necessary for the majority of subjects to be above LT (N = 20), 90% HRR resulted in the majority of subjects being above 2.0 mM (N = 19), while 95% HRR was required for the majority of subjects to be above 2.5 mM (N = 23). At 95% HRR 14 subjects were above 4.0 mM. For % VO2max, the intensities required for the majority of subjects to be above LT, FBLC of 2.0, and 2.5 mM were 90%, 95% and 95% VO2max, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Prediction of lactate threshold (LT) and fixed blood lactate concentrations (FBLC) from 3200-m running performance in women.

The present study evaluated the accuracy of predicting velocity and oxygen consumption (VO2) at the LT lactate threshold and FBLC fixed blood lactate concentrations from a 3200-m time trial in women. Forty-four women (mean age = 31.1 yrs, mean ht = 164.9 cm, mean wt = 65.0 kg) completed a treadmill protocol for the determination of LT and FBLC and a 3200-m time trial. Velocity and VO2 values at LT, FBLC of 2.0 2.5, and 4.0 mM, and peak were determined. Mean VO2 and velocity ranged from 27.8 +/- 10.8 ml/kg.min-1 at LT to 42.5 ml/kg.min-1 at peak and from 129.8 +/- 44.0 m.min-1 at LT to 187.0 +/- 52.4 m.min-1 at peak, respectively. Results indicated that a 3200-m time trial (mean time = 20.6 +/- 6.6 min) was a good predictor of VO2 and velocity at LT, FBLC, and peak. Correlation coefficients (using a quadratic model) for velocity ranged from R = 0.96 to R = 0.98 with SEE ranging from 9.0 to 13.1 m.min-1. Correlation coefficients for VO2 ranged from R = 0.94 to R = 0.96 with SEE ranging from 2.8 to 3.6 ml/kg.min. The validity of these regression equations was examined in 13 women who completed a 12-month running program (VO2 LT, VO2 at FBLC of 2.0, 2.5 and 4.0 mM, and VO2 peak increased by 34.7, 19.9, 16.9, 11.9, and 5.4%, respectively, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Primary cortisol resistance presenting as isosexual precocity.

Primary cortisol resistance (PCR) is a rare cause of hypercortisolism and usually does not produce clinical manifestations. This report describes primary cortisol resistance in a boy with isosexual precocity. A 6 7/12-yr-old boy had Tanner stage 3 pubic hair, accelerated linear growth, and advanced bone age (10 yr), but normal (for age) tests. There were no features of glucocorticoid excess. Serum androstenedione and dehydroepiandrosterone concentrations were 4.7 +/- 0.3 nmol/L (mean +/- SEM of four measurements; normal less than 1.2) and 13.5 nmol/L (single measurement; normal, 1.0-2.2), respectively. The serum testosterone concentration was 0.9 nmol/L (normal, less than 0.7), and FSH and LH were normal. Serum cortisol concentrations were 1590 +/- 110 nmol/L (normal, 190-630) and 580 +/- 60 nmol/L (normal, 50-410) at 0800 and 2000 h, respectively. Serum cortisol responded normally to insulin-induced hypoglycemia. Glucocorticoids and adrenal androgens were resistant to suppression by dexamethasone. The Kd of [3H]dexamethasone binding to the glucocorticoid receptors of mononuclear leukocytes was increased (6.4 +/- 0.8 nM; mean +/- SEM of four determinations; normal, 1.4-3.4; P less than 0.001), but the binding capacity was normal. This patient with isosexual precocity has PCR, as indicated by functionally abnormal glucocorticoid receptors and hypercortisolism without other clinical or biochemical manifestations of Cushing's syndrome. Excessive adrenal stimulation by ACTH caused increased secretion of both cortisol and adrenal androgens, and the latter caused the clinical manifestations. PCR should be considered in other male children with isosexual precocity or female children with heterosexual precocity.

Adrenal Glands↗
PubMed1989

Prediction of lactate threshold and fixed blood lactate concentrations from 3200-m time trial running performance in untrained females.

The present study examined the effectiveness of a 3200-m time trial run for predicting VO2 and running velocity at lactate threshold (LT), and fixed blood lactate concentrations (FBLC) of 2.0, 2.5, and 4.0 mM and peak in untrained women. Thirty-nine female subjects completed a VO2peak/LT test a 3200-m time trial run. Twenty-eight subjects were randomly assigned to a validation sample and the remaining subjects were used for cross-validation purposes. In the validation sample, VO2 measurements at LT, FBLC of 2.0, 2.5, 4.0 mM, and peak were 22.5, 29.2, 31.2, 36.5, and 38.5 ml/kg.min-1, respectively. Velocities at LT, FBLC of 2.0, 2.5, 4.0 mM, and peak were 107.1, 129.7, 136.6, 155.1, and 163.2 m/min, respectively. Regression analysis in the validation group revealed that the 3200-m time trial was an accurate predictor of velocities at LT, FBLC of 2.0, 2.5, 4.0 mM, and peak with correlations of r = 0.70, r = 0.84, r = 0.85, r = 0.87, and r = 0.95, respectively, and standard errors of estimate ranging from +/- 9.5 m/min (for velocity peak) to +/- 13.7 m/min (velocity LT). Vor VO2 prediction, correlations ranged from r = 0.61 (3200-m time vs VO2 LT) to r = 0.77 (3200-m time vs VO2 peak) with the standard errors of estimate ranging from +/- 4.18 (VO2 2.0 mM) to +/- 4.87 ml/kg.min-1 (VO2 4.0 mM).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Percentages of maximal heart rate, heart rate reserve, and VO2peak for determining endurance training intensity in sedentary women.

The use of 60%-95% of maximal heart rate (HR max), heart rate reserve (HRR), and VO2peak as exercise training intensities was examined in sedentary women, and these intensities were related to HR and VO2 observed at the lactate threshold (LT) and fixed blood lactate concentrations of 2.0, 2.5, and 4.0 mM. Thirty-three subjects (means age = 32.5 +/- 3.9 yrs; means ht = 164.2 +2- 5.0 cm; means wt = 67.6 +/- 13.9 kg) completed a VO2/LT treadmill test using a level running protocol. The values at LT, 2.0, 2.5, 4.0 mM, and peak for VO2 were 22.3, 29.0, 31.0, 36.2, and 39.1 ml/kg.min-1, respectively; for velocity were 107.0, 128.9, 135.8, 152.8, and 164.4 m/min, respectively; and for HR were 142.1, 162.9, 169.4, 183.2, and 189.7 bts/min, respectively. The minimum intensity necessary for the majority of subjects to be above LT (n = 17) was 75% HR max while 90% HR max was required for the majority of subjects to be above 2.0 mM (n = 23) and 2.5 mM (n = 19). At 95% HR max 12 subjects were above 4.0 mM. For the majority of subjects to be above LT (n = 18), 55% HRR was necessary; 75%, 85%, and 95% HRR was required for the majority of subjects to be above 2.0 mM (n = 18), 2.5 mM (n = 19), and 4.0 mM (n = 20), respectively. For percent VO2peak, the intensities required for the majority of subjects to be above LT, 2.0 mM, 2.5 mM, and 4.0 mM were 55%, 75%, 80%, and 95% VO2peak, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Phosphatidylinositol-glycan anchors of membrane proteins: potential precursors of insulin mediators.

BC3H1 myocytes release membrane-bound alkaline phosphatase to the incubation medium upon stimulation with insulin, following a time course that is consistent with the generation of dimyristoylglycerol and the appearance of a putative insulin mediator in the extracellular medium. The use of specific blocking agents shows, however, that alkaline phosphatase release and dimyristoylglycerol production are independent processes and that the blockade of either event inhibits the production of insulin mediator. These experiments suggest a new model of insulin action.

Alkaline Phosphatase↗
PubMed1987

Prediction of lactate threshold and fixed blood lactate concentrations from 3200-m running performance in male runners.

To determine the effectiveness of a 3200-m time trial for predicting VO2 and running velocity at lactate threshold (LT), fixed blood lactate concentrations of 2.0, 2.5, and 4.0 mM, and peak, 42 male runners (means age = 31.1 +/- 8.3 years; means ht = 176.8 +/- 6.6 cm; means wt = 70.4 +/- 10.0 kg) completed a VO2 peak/LT test and a 3200-m time trial. The continuous treadmill protocol started at 0% grade 150 m/min and increased 10 m/min every 3 min until exhaustion. Velocity at LT, 2.0, 2.5, and 4.0 mM was determined from individual velocity blood lactate relationships, and VO2 values were determined from individual plots ov VO2 vs velocity. VO2 peak and velocity peak were chosen as the highest values observed. Oxygen uptake at LT, 2.0, 2.5, 4.0 mM, and peak was 52.51, 56.61, 58.31, 61.70, and 64.21 ml/kg.min-1, respectively, while the velocities associated with LT, 2.0, 2.5, 4.0 mM, and peak were 235.5, 251.5, 259.8, 273.5, and 285.5 m/min, respectively. During the 3200-m time trial (means time = 11.28 +/- 0.96 min), 400-m split times and cumulative times were recorded. Twenty-nine subjects were randomly assigned to a validation sample and the remaining subjects were used for cross-validation purposes. Regression analysis revealed that a 3200-m time trial was a good predictor of both VO2 (ml/kg.min-1) and velocity (m/min) at LT, 2.0, 2.5, 4.0 mM, and peak.

Adult↗
PubMed1983

Apomorphine response and subtyping of schizophrenia.

(1) We conducted a double-blind study of acute effects of low-dose apomorphine (0.01 mg/kg) in 12 chronic schizophrenic patients. (2) Overall, there was no significant difference in therapeutic response to apomorphine versus placebo. (3) Of the individual subscales of the Brief Psychiatric Rating Scale, anxiety and depression syndromes showed significant improvement with apomorphine. (4) On dividing the schizophrenic patients into two groups on the basis of computed tomography (CT) scans, it was found that there was a significant difference in their responsiveness to apomorphine. (5) Patients with abnormal CT scans (primarily, large ventricles) tended to have improvement or no change with apomorphine, whereas those with normal CT scans tended to have worsening of symptoms. (6) Possible implications of our findings are discussed.

Adult↗
PubMed1982

Naloxone in chronic schizophrenic patients: neuroendocrine and behavioral effects.

Naloxone produced improvement in abnormal thought content in medicated chronic schizophrenic patients, but not in drug-free patients. In contrast, drowsiness and increases in plasma prolactin concentrations were seen only in drug-free schizophrenic patients. Although growth hormone concentrations increased in drug-free and medicated schizophrenic patients, the time course was different in the two groups. Neuroleptics appear to alter naloxone's clinical and neuroendocrine effects in chronic schizophrenic patients.

Adult↗
PubMed1981

Lymphocyte monoamine oxidase and plasma prolactin and growth hormone in tardive dyskinesia.

Twelve elderly women with tardive dyskinesia were matched with 12 patients without dyskinesia. Lymphocyte monoamine oxidase (MAO) activity and plasma prolactin and growth hormone concentrations were determined "blind" in these 12 pairs of patients. Chronic schizophrenic patients with tardive dyskinesia had significantly lower lymphocyte MAO activity as compared to controls. Organic brain syndrome patients with dyskinesia did not differ from controls in the lymphocyte MAO activity. These results with lymphocyte MAO parallel our earlier findings on platelet MAO. No significant differences were found between dyskinesia group and controls in the plasma prolactin and growth hormone concentrations. Possible implications of our findings are discussed.

Aged↗
PubMed1979

A correlation between platelet monoamine oxidase activity and plasma prolactin concentrations in man.

Increases in plasma prolactin concentrations produced by alpha-methyl-p-tyrosine, a catecholamine synthesis inhibitor, varied inversely with baseline platelet monoamine oxidase activity in 12 patients with chronic schizophrenia. In normal volunteers with low monoamine oxidase activity and in unmedicated patients with chronic schizophrenia, plasma prolactin concentrations varied directly with platelet monoamine oxidase activity. No such relationship was found in normal subjects with high platelet monoamine oxidase activity. These data suggest that platelet monoamine oxidase activity reflects monoaminergic activity in the tubero-infundibular system, which in turn affects plasma prolactin concentrations. This relationship may be important in patients with low platelet monoamine oxidase activity, such as some chronic schizophrenics.

Blood Platelets↗
PubMed1977

Possible effects of growth hormone on development of acute lymphoblastic leukaemia.

Growth hormone (G.H.) or a G.H.-dependent somatomedin may be involved in the process of acute lymphoblastic leukaemia (A.L.L.). Growth hormone has a trophic effect on lymphoid tissue and also specific receptors on lymphocytes, most probably T cells. Hypophycess. Resting concentrations of G.H. and somatomedin activity are raised in some children with A.L.L. and may be reduced after remission is achieved. It is suggested that control of G.H. and/or somatomedin concentrations may be necessary for adequate treatment of some cases of A.L.L. in children.

Adolescent↗