bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of 1-Year Ipriflavone Treatment on Lumbar Bone Mineral Density and Bone Metabolic Markers in PostmenopausalWomen with Low Bo ne Mass
Authors: Ohta Hiroaki , Komukai Shigeyuki , Makita Kazuya , Masuzawa Toshihide , Nozawa Shiro 
Published: April 2003

In vitro studies have shown that ipriflavone affects both bone formation and bone resorption, but the effect in early-stage postmenopausal women with low bone mass and a high turnover of bone metabolism is unknown. In this prospective study, we randomly assigned 60 patients with postmenopausal osteopenia or osteoporosis to receive either 600 mg/day of ipriflavone or 0.8 g/day calcium lactate, and compared the effects on bone mineral density (BMD) from the 2nd to 4th lumbar vertebrae (L2–4) and bone metabolic markers before and after one year of treatment. In the iprifravone-treated (IP) group, L2–4 BMD was similar before and after treatment (0.78 and 0.77 g/cm<sup>2</sup>, respectively), but in the calcium lactate-treated (CL) group, L2–4 BMD decreased significantly from 0.81 to 0.79 g/cm<sup>2</sup> after 1 year of treatment (p < 0.0001). Furthermore, the rate of the decrease in L2–4 BMD was significantly greater in the CL group than in the IP group (p < 0.01). The median deoxypyridinoline (Dpd) level was significantly lower after 1 year of treatment (5.8 mmol/mmol creatinine [Cr]) than the baseline value (10.2 mmol/mmol Cr) in the IP, but not in the CL group, suggesting that IP treatment suppresses bone resorption.
Ontogenetic Diurnal Variation of Adrenal Responsiveness to ACTH and Stress in Rats
Authors: Leal Ângela M.O. , Carvalho Jordana , Moreira Ayrton C. 
Published: April 2003

We performed studies in 8-, 16-, 24-, 30 and 35-day-old Wistar rats at 8.00 h (AM) and 20.00 h (PM) to investigate the relationship between the diurnal variations of basal plasma corticosterone (compound B, CB) and its responses to ACTH and ether stress during the postnatal period. Basal plasma CB levels increased at PM from 8 to 35 days of age and an AM-PM difference was observed at 16 days. Although an AM-PM difference in CB responsiveness to ACTH was detected only at 24 and 35 days, ACTH induced an increasingly higher CB response at PM than at AM from 8 to 35 days. A stress-induced CB response was observed starting at 8 days of age and presented an age-dependent increase; however, no AM-PM difference was observed at any age. The stress-induced CB levels were higher than ACTH-induced CB values at all ages tested except at PM in 8-day old rats. These data demonstrate that the basal CB levels and adrenal sensitivity to ACTH rise during the evening as a function of neonatal development.
Final Height, Armspan, Subischial Leg Length and Body Proportions in Juvenile Chronic Arthritis
Authors: Zak Marek , Müller Jørn , Karup Pedersen Freddy 
Published: April 2003

<i>Objective:</i> Assessment of growth disturbances in adults with a history of juvenile chronic arthritis (JCA). <i>Material and Methods:</i> Sixty-five subjects, 52 premenopausal females and 13 males with a mean age (range) of 32.2 years (22.3–49.4) participated. Mean age at disease onset was 5.7 years (0.8–15.8) and mean disease duration was 12.4 years (0.4–32). The follow-up time ranged from 18.7 to 46.9 years with a mean of 26.4 years. For each participant standard deviation scores (z-scores) for final height, delta-height (the difference between observed and expected height), armspan, subischial leg length and sitting height ratio, were calculated. <i>Results:</i> The study group as a whole did not exhibit linear growth impairment. The categorical distribution of heights differed significantly from a expected distribution in a healthy population (p < 0.001). A height z-score < –2 SD was present in 10.7% of the study group, of whom all had polyarticular course of JCA. Polyarticular and systemic course of JCA (versus pauciarticular) (p = 0.022), systemic steroid treatment (p = 0.006) and Steinbrocker functional class II–IV (vs. I) in 1979 (p = 0.043) were variables associated with reduced delta-height. In linear regression analyses, disease severity defining variables were statistically significant predictors of reduced final height and armspan. 27% of the study subjects had significantly reduced arm span (p < 0.001). Subischial leg length and body proportions (sitting height ratio) were normal. <i>Conclusion:</i> Our findings suggest that functionally impaired polyarticular and systemic JCA patients treated with systemic steroids may be at an increased risk of developing reduced final height and armspan. Disease control achieved by an aggressive therapeutic approach, if possible with a minimal use of systemic steroids, may reduce growth impairment in JCA.
Effect of Short-Term Testosterone Treatment on Leptin Concentrations in Boys with Pubertal Delay
Authors: Adan L. , Bussières L. , Trivin C. , Souberbielle J.C. , Brauner R. 
Published: April 2003

Testosterone administration increases growth hormone (GH) secretion and decreases the plasma leptin concentration in men. We evaluated the effect of increased GH secretion due to short-term testosterone treatment on leptin concentrations. Ten boys aged 14.8 ± 0.2 (mean ± SE) years with transient GH deficiency caused by pubertal delay were evaluated before and after (3 months) 4 intramuscular injections of 100 mg testosterone heptylate, given at 15-day intervals. The leptin concentration decreased from 5.4 ± 1.3 to 3.6 ± 1.1 μg/l (p < 0.001), despite a weight gain of 3.4 ± 0.5 kg. There were significant increases in body mass index (BMI), from –0.2 ± 0.5 to 0.2 ± 0.5 SD, p < 0.005, in GH peak after stimulation test, from 6.3 ± 0.5 to 21.7 ± 2.9 μg/l, p < 0.0003, in plasma testosterone, from 0.6 ± 0.1 to 6.5 ± 1.3 μg/l, p < 0.001, in insulin-like growth factor-I (IGF-I), from 152 ± 21 to 330 ± 30 μg/l, p < 0.0001, and in IGF-binding protein-3 (IGFBP-3), from 4.2 ± 0.5 to 5.4 ± 0.4 mg/l, p < 0.01. But there were no changes in blood glucose (4.7 ± 0.1 and 4.8 ± 0.1 mmol/l), or plasma fasting insulin (9.0 ± 1.2 and 8.1 ± 1.3 mIU/l). The leptin concentrations were positively correlated with the BMI before (p < 0.03) and after (p < 0.04) testosterone, but not with the GH peak after stimulation, or with plasma testosterone, IGF-I or IGFBP-3. The leptin and insulin concentrations after testosterone treatment were positively correlated (p < 0.04). Thus, short-term testosterone treatment of boys with pubertal delay decreases their leptin concentrations. The lack of correlation with GH secretion or with its changes, despite the dramatic increase in GH secretion, and the lack of change in insulin are additional features suggesting that testosterone increases the leptin concentration mainly by an effect on adipose tissue.
Nociceptin Stimulates Thyrotropin Secretion in Rats
Authors: Mitsuma Terunori , Hirooka Yoshifumi , Mori Yuichi , Kayama Masato , Adachi Koshin , Rhue Nebi , Ping Jing , Ikai Rumiko , Nakayashiki Atsuko , Nogimori Tsuyoshi 
Published: April 2003

Effects of nociceptin on thyrotropin (TSH) and thyrotropin-releasing hormone (TRH) secretion in rats were studied. Nociceptin (150 μg/kg) was injected intravenously and rats were serially decapitated after the injection. The effects of nociceptin on TRH release from the hypothalamus and TSH release from the anterior pituitary in vitro were also investigated. TRH and thyroid hormones were measured by individual radioimmunoassays. TSH was determined by enzyme immunoassay. TRH contents in the hypothalamus decreased significantly after nociceptin injection, whereas plasma TRH concentrations showed no changes. Plasma TSH concentrations increased significantly in a dose-related manner. The TRH release from the hypothalamus was enhanced significantly in a dose-related manner with the addition of nociceptin. The TSH release from the anterior pituitary in vitro was not affected by the addition of nociceptin. The plasma thyroxine and 3,3′,5-triiodothyronine levels did not change significantly after nociceptin administration. The inactivation of TRH by plasma or hypothalamus in vitro after nociceptin injection did not differ from that of controls. The findings suggest that nociceptin acts on the hypothalamus to stimulate TRH and TSH secretion.
Secretion of Noncomplexed ‘Big’ (10–18 kD) Forms of Insulin-Like Growth Factor-II by 12 Soft Tissue Sarcoma Cell Lines
Authors: Elmlinger Martin W. , Rauschnabel Uta , Koscielniak Ewa , Weber Karin , Ranke Michael B. 
Published: April 2003

The paraneoplastic production of pro-insulin-like growth factor-II (IGF-II) forms causes tumour hypoglycaemias and presumably also has an effect on tumour cell growth. We investigated the molecular weights of IGF-II forms and their ability to form complexes with IGF binding proteins (IGFBPs) in conditioned culture media (CM) from 12 paediatric soft tissue sarcoma (STS) cell lines and from two healthy fibroblast lines. Untreated CM were separated by size exclusion chromatography using biocompatible HPLC. Subsequently, IGF-II, IGFBP-2 and IGFBP-3 were determined in the HPLC fractions by specific RIAs. In the CM, IGF-II concentrations between 0.5 and 8.6 ng/10<sup>6</sup> cells were measured but no IGF-I was detectable. Parallel to this investigation, a high IGF-II mRNA level averaging 44.4 ± 29.7% was measured by semi-quantitative RT-PCR. The STS cell lines secreted a higher proportion of big-IGF-II forms reaching 10–18 kD (10–33% of the total IGF-II secreted) compared to the healthy fibroblasts (2.5–5%). At the same time, the proportion of IGF-II bound with IGFBP in complexes of 35– 70 kD and 150 kD was reduced by up to 85% in CM from tumour cells. The tumour cell lines apparently secrete a different spectrum of IGF-II forms than healthy fibroblasts. The reduced ability to form complexes with IGFBP and the higher molecular weight of the IGF-II forms produced by the tumour cells indicate that these forms could in fact be the known tumour-associated pro-IGF-II forms. Due to these characteristics, the big-IGF-II forms probably have an altered biological effect on the tumour cells when compared to IGF-II.
Leptin Levels in Menopause: Effect of Estrogen Replacement Therapy
Authors: Cento Rosa Maria , Proto Caterina , Spada Rosario Sebastiano , Napolitano Valerio , Ciampelli Mario , Cucinelli Francesco , Lanzone Antonio 
Published: April 2003

To evaluate the effect of menopause and estrogen replacement therapy on leptin levels, 17 white postmenopausal women were recruited for the study. After an overnight fasting, blood samples were collected for LH, FSH, estradiol, testosterone, androstenedione, DHEA sulfate, insulin and leptin assays. Body mass index (BMI) and the waist-to-hip ratio were also evaluated. Patients were reanalyzed after a 12-week administration of transdermal estrogen patches delivering 50 μg 17β-estradiol. The results were compared to those obtained from a group of 11 female volunteers in reproductive age, in whom basal blood was sampled during the early follicular phase of their cycle. Patients were divided into lean and obese according to their BMI. Obese postmenopausal women showed lower leptin levels when compared to premenopausal counterparts (25.1 ± 5.9 vs. 37 ± 11.3; p < 0.05), whereas no significant differences were found between the lean groups (14.5 ± 3.8 vs. 14.4 ± 4.9). Estrogen administration did not significantly change serum leptin concentrations in hypoestrogenized women (obese: 25.1 ± 5.9 vs. 28.6 ± 9.2; lean: 14.4 ± 4.9 vs. 17.6 ± 7.2). A positive linear correlation was found between leptin plasma levels and BMI only in obese patients (r = 0.58; p < 0.01) both before and after estrogen treatment. Menopause is characterized by a decreased expression of the obese gene, even if estrogens do not seem to represent a main causal factor.
Tamoxifen Inhibits Lipoprotein Activity: In vivo and in vitro Studies
Authors: Hozumi Yasuo , Kawano Mikihiko , Hakamata Yoji , Miyata Michio , Jordan V. Craig 
Published: April 2003

Tamoxifen, a nonsteroidal antiestrogenic antitumor agent, has weak estrogen-like effects on lipid metabolism, however, the mechanism remains unknown. We previously reported that tamoxifen decreases the activity of lipoprotein lipase (LPL), a key enzyme in triglyceride metabolism, in patients with breast cancer. This study evaluated the effect of tamoxifen on LPL activity in vitro and in vivo. In experiment 1, total cholesterol, triglyceride, adipose tissue weight, and LPL activity of post-heparin plasma were measured in ovariectomized female rats with and without tamoxifen treatment. In experiment 2, purified very-low-density lipoprotein (VLDL) and purified LPL were incubated with and without tamoxifen or estrogen, and the triglycerides in VLDL were measured using an enzymatic method. In experiment 1, total cholesterol and adipose tissue weight decreased significantly in tamoxifen-treated rats (p < 0.001 and p < 0.01, respectively). Triglyceride measurements were not significantly different between the two groups, however, the LPL activity was lower in tamoxifen-treated rats (p < 0.005). In experiment 2, triglycerides in VLDL were significantly higher after VLDL and LPL were incubated with tamoxifen and estrogen (p < 0.005). We concluded that tamoxifen inhibits the hydrolytic activity of LPL in vivo and in vitro. This mechanism may explain the elevated serum triglyceride levels in some patients treated with tamoxifen.
Estrogen Receptors and the Activity of Nitric Oxide Synthase in the Artery of Female Rats Receiving Hormone Replacement Therapy
Authors: Wu Saizhu , Ruan Yunjun , Zhu Xiaohu , Lai Wenyan 
Published: April 2003

<i>Objective:</i> To observe the expression of estrogen receptor and the activity of NOS in the arteries of female rats receiving estrogen replacement therapy. <i>Methods:</i> Seventy-two female rats were randomly divided into four groups: group A: sham-ovariectomy; group B: ovariectomy; group C: ovariectomy with estrogen replacement therapy (benzoate estradiol, 5 μg i.m. once in 2 days); group D: ovariectomy with estrogen and progesterone replacement therapy (benzoate estradiol, 5 μg i.m. once in 2 days and progesterone, 1 mg i.m. once in 2 days). The rats were killed after 2 months. The receptor-binding assay was adopted to measure the estrogen receptors in the arteries of the rats, and the activity of NOS in the arteries was assessed by the hemoglobin reductase method. <i>Results:</i> The ER number and NOS activity in the arteries of the ovariectomized group are less than those in sham-ovariectomy group (p < 0.05). The ER number and NOS activity in the arteries of groups C and D are larger and higher than those in the ovariectomized group (p < 0.05). No significant differences in the ER number and NOS activity were observed between groups C and D. <i>Conclusion:</i> The ER number and NOS activity in the rat artery significantly decrease after ovariectomy, while hormone replacement therapy can significantly increase the artery NOS activity and retain the ER number in the artery of the ovariectomized rats to normal level. The result may contribute to explaining the beneficial effect of estrogen in the prevention of coronary artery diseases in postmenopausal women.
Effects of Octreotide Infusion, Surgery and Estrogen on Suppression of Height Increase and 20K Growth Hormone Ratio in a Girl with Gigantism due to a Growth Hormone-Secreting Macroadenoma
Authors: Minagawa Masanori , Yasuda Toshiyuki , Someya Tomohiro , Kohno Yoichi , Saeki Naokatsu , Hashimoto Yoshihide 
Published: April 2003

We treated an extremely tall 13-year-old girl with a growth hormone (GH)-secreting macroadenoma and GH levels of 120–495 ng/ml with a combination of preoperative octreotide infusion, surgery and postoperative octreotide infusion plus estrogen, which resulted in reduced tumor size prior to surgery, reduced GH levels and completely suppressed growth after surgery. 20K GH is produced by alternative splicing of 22K GH mRNA and the ratio of 20K GH to 22K GH is within a small range in the normal population and high in a GH-secreting tumor. The 20K/22K GH ratio in this patient was persistently elevated during each phase of the treatment and may serve as a sensitive index of tumor-derived GH secretion.
Growth Hormone Normalises Height, Prediction of Final Height and Hand Length in Children with Prader-Willi Syndrome after 4 Years of Therapy
Authors: Eiholzer Urs , l’Allemand Dagmar 
Published: April 2003

<i>Background:</i> Based on the reported favourable effects of growth hormone (GH) treatment on growth and body composition in Prader-Labhart-Willi syndrome, we studied age dependency and the long-term effects on growth dynamics to elucidate the assumed hypothalamic GH deficiency. <i>Methods:</i> We examined 23 children treated with hGH (24 U/m<sup>2</sup>/week) during a median of 4 (range 1.5–5.5) years; group 1: 10 young underweight (age 0.3–4.1 years), group 2: 8 prepubertal overweight (age 3.7–9.5 years) and group 3: 5 pubertal overweight children (age 9.0–14.6 years). <i>Results:</i> After 4 years of therapy, height gain amounted to 1.8 SD; height (0.0 SD) and hand length (–0.2 SD) were normalised in the 2 prepubertal groups; in children above 6 years, height prediction approached parental target height. Weight for height rose in group 1 (to 0.64 SD) and decreased in group 2 (to 0.71 SD) to normal levels. Bone maturation of the pubertal children was too advanced to show a clear growth response to GH (height gain 0.42 SD). Even in this group, weight for height was reduced, but remained supernormal. <i>Conclusion:</i> Under exogenous GH, growth and body proportions are normalised in prepubertal children. With early institution of treatment, final height prediction reaches the parental target height range after 3 years. Such a growth-promoting effect of exogenous GH has so far only been described in children with GH deficiency.
Energy Expenditure, Energy Intake and Prevalence of Obesity after Therapy for Acute Lymphoblastic Leukemia during Childhood
Authors: Mayer Eleonore I. E. , Reuter Marianne , Dopfer Roland E. , Ranke Michael B. 
Published: April 2003

<i>Objectives:</i> To investigate the prevalence and potential risk factors of obesity after therapy for childhood acute lymphoblastic leukemia (ALL). <i>Study Design:</i> 39 ALL patients (age 10.7–20.5 years) who were in first remission for 3.4–14.6 years after standardized treatment with chemotherapy plus cranial irradiation (n = 25) or with chemotherapy alone (n = 14) were examined. After fasting overnight, the following parameters were investigated: body mass index (BMI) of patients and their parents; patients’ BMI before ALL therapy; serum free thyroxin, growth hormone-dependent factors, estradiol, testosterone, cortisol, leptin and c-peptide; fat-free mass (bioelectrical impedance); resting metabolic rate (RMR, indirect calorimetry); caloric intake (24-hour recall); and physical activity (questionnaire). RMR data were applied to the fat-free mass and compared with 83 controls. <i>Results:</i> The prevalence of obesity (criterion: BMI > 2 SDS) was significantly (p < 0.05) higher after ALL therapy (38%; irradiated patients 48%, non-irradiated patients 21%) than before therapy (3%). Compared to non-irradiated patients, irradiated patients had significantly lower RMRs (–1.07 ± 0.24 vs. –0.32 ± 0.21 SDS; p < 0.05), reduced physical activity levels (1.41 ± 0.03 vs. 1.52 ± 0.03; p < 0.05), and lower concentrations of insulin-like growth factor-binding protein-3 (–0.65 ± 0.17 vs. 0.25 ± 0.33 SDS; p < 0.05) and of free thyroxin (1.17 ± 0.06 vs. 1.38 ± 0.08 ng/dl; p < 0.05). Caloric intake was adequate. <i>Conclusions:</i> After ALL during childhood, patients face a higher risk of obesity. In the cranially irradiated patients, the likely causes are low physical activity, RMRs and hormonal insufficiency.
A Novel Arginine Vasopressin-Neurophysin II Mutation Causes Autosomal Dominant Neurohypophyseal Diabetes insipidus and Morphologic Pituitary Changes
Authors: Skordis Nicos , Patsalis Philippos C. , Hettinger Joe A. , Kontou Maria , Herakleous Eleni , Krishnamani M.R.S. , Phillips III J.A. 
Published: April 2003

To determine the genetic basis of autosomal dominant neurohypophyseal diabetes insipidus (ADNDI) in a Cypriot family, we ascertained and studied a large, four-generation kindred in which all participating family members had arginine vasopressin-neurophysin II (AVP-NP-II) gene analyses done. A G to A transition was found by DNA sequence analysis at position 1773 (G1773A) of the AVP-NPII gene which is predicted to encode a substitution of tyrosine for cysteine in codon 59 (CYS59TYR). The mutation was confirmed by restriction endonuclease analysis of PCR amplification products that contain the corresponding segment of the AVP-NPII gene. To clarify the morphologic status of the pituitaries of family members, 12 affected and 3 nonaffected members had magnetic resonance imaging (MRI) studies. The bright spot of the posterior pituitary lobe was completely absent in 75% and faintly identified in 25% of the affected members who were examined with MRI. We conclude that (1) a novel G1773A transition in exon 2 of the AVP-NPII gene causes ADNDI in the large Cypriot kindred studied, (2) this mutation is predicted to encode a CYS59TYR substitution in NPII, and (3) MRI studies of the posterior pituitary lobes of affected family members show either a decreased intensity or a complete absence of the bright spot in all cases studied.
The US5 Open Reading Frame of Herpes simplex Virus Type 1 Does Encode a Glycoprotein (gJ)
Authors: Ghiasi Homayon , Nesburn Anthony B. , Cai Steve , Wechsler Steven L. 
Published: April 2003

Based on sequence analysis, the protein encoded by the US5 open reading frame (ORF) of herpes simplex virus type 1 (HSV-1) was predicted to contain an N-glycosylation site and was given the designation of glycoprotein J (gJ). However, the US5 gene product has not been identified and the identity of gJ as a glycoprotein has not been confirmed. We have cloned and expressed the DNA encoding the complete sequence of the US5 ORF, using a baculovirus expression system. Western blotting, using polyclonal antibody raised against synthetic US5 peptides, revealed two major baculovirus-US5-expressed protein bands with apparent molecular weights of 16–17 and 10 kD. The recombinant US5 was found on the membrane of <i>Spodoptera frugiperda</i> cells and was susceptible to tunicamycin, endoglycosidase H, glycosidase F and partially resistant to endoglycosidase F. Vaccination of mice with baculovirus-expressed US5 did not induce a neutralizing antibody to HSV-1 or provide protection against lethal HSV-1 challenge. However, serum from these vaccinated mice was able to recognize US5 in purified HSV-1 virions by Western blot analyses and on the surface of HSV-1-infected cells by immunofluorescence. These findings establish that US5 does encode a glycoprotein and confirm the appropriateness of naming the US5 gene product gJ.