bluuebunny/crossref_metadata_2025_split huggingface dataset:
Octreotide treatment increases exercise capacity in patients with acromegaly
Authors: Padayatty Sebastian J , Perrins Edward J , Belchetz Paul E 
Published: December 2008

Padayatty SJ, Perrins EJ, Belchetz PE. Octreotide treatment increases exercise capacity in patients with acromegaly. Eur J Endocrinol 1996:134:554–9. ISSN 0804–4643
This prospective study was conducted to determine the effect of Octreotide treatment on cardiovascular function in patients with active acromegaly. Ten acromegalic patients who failed to suppress growth hormone (GH) to < 5 mU/l during a 2 h oral glucose tolerance test were treated with 100 μg of Octreotide subcutaneously three times daily for 2 months, followed by 200 μg three times daily if the mean GH level was > 5 mU/l, for a total of 1 year. All patients had GH and insulin-like growth factor I (IGF-I) estimation, ejection fraction determined by Echocardiogram and multigated image acquisition scan, electrocardiogram (ECG), exercise ECG, 24-h ECG and chest x-ray. At 6 and 12 months, both GH and IGF-I were reduced but ECG, heart size and ejection fraction were unchanged. The patients improved symptomatically and had significant reduction in resting heart rate and increase in weight. Exercise time (mean±sd) increased from 637 ± 137s at baseline to 787 ± 101s at 1 year (p < 0.01) and work done increased from 9 ± 3.3 to 11.9 ± 2.7 metabolic equivalents (p< 0.001). We conclude that the decrease in GH and IGF-I following Octreotide treatment of acromegaly is accompanied by decreased heart rate and increased exercise capacity despite an unchanged ejection fraction.
Sebastian J Padayatty, Division of Endocrinology, Baylor College of Medicine, One Baylor Plaza, Room 537E, Houston TX 77030, USA
Autoimmune hypothyroidism and hyperthyroidism in patients with Turner's syndrome
Authors: Chiovato Luca , Larizza Daniela , Bendinelli Giovanna , Tonacchera Massimo , Marinò Michele , Mammoli Claudia , Lorini Renata , Severi Francesca , Pinchera Aldo 
Published: December 2008

Chiovato L, Larizza D, Bendinelli G, Tonacchera M, Marinò M, Mammoli C, Lorini R, Severi F, Pinchera A. Autoimmune hypothyroidism and hyperthyroidism in patients with Turner's syndrome. Eur J Endocrinol 1996;134:568–75. ISSN 0804–4643
A high prevalence of autoimmune thyroid disease (AITD) has been described in Turner's syndrome (TS) but the extent of this association is controversial for the prevalence of thyroid autoantibody and the clinical impact of thyroid dysfunction. In this study we searched for thyroid disease and thyroid autoantibodies in patients with TS. Seventy-five unselected TS patients (age range 3–30 years) were studied. Sera were tested for thyroid hormones, thyrotropin (TSH), thyroglobulin (TG-ab) and thyroperoxidase (TPO-ab) antibodies. The TSH-receptor antibodies with thyroid-stimulating (TS-ab) or TSH-blocking activity (TSHB-ab) were measured in the IgG fraction using a bioassay. Ten out of 75 (13.3%) TS patients had AITD: eight had autoimmune thyroiditis (AT) (six with subclinical and two with overt hypothyroidism and one with euthyroidism) and one had Graves' disease. The prevalence of AITD increased significantly (p < 0.05) from the first (15%) to the third (30%) decade of life. The prevalence of TPO-ab and/or TG-ab (20%) was higher (p < 0.05) in TS than in age-matched female controls and increased from the first (15%) to the third (30%) decade of life. Clinical AITD was diagnosed in 46% of TS patients with TPO-ab and/or TG-ab. Thyroid-stimulating antibody was detected in the hyperthyroid patient, and TSHB-ab was found in one of eight patients with hypothyroid AT. It was concluded that: TS patients are at higher than average risk of developing AITD not only in adolescence and adult age but also in childhood; hypothyroidism, mainly subclinical, is the most frequent thyroid dysfunction; elevated TPO-ab and/or TG-ab alone do not imply thyroid dysfunction; TS-ab or TSHB-ab are always associated with thyroid dysfunction although most cases of autoimmune hypothyroidism are not due to the latter antibody.
Luca Chiovato, Istituto di Endocrinologia, Università di Pisa, Viale del Tirreno, 64, 56018 Tirrenia, Pisa, Italy
Evidence for a role for insulin-like growth factor binding proteins in glucocorticoid inhibition of normal human osteoblast-like cell proliferation
Authors: Chevalley Thierry , Strong Donna D , Mohan Subburaman , Baylink David J , Linkhart Thomas A 
Published: December 2008

Chevalley T, Strong DD, Mohan S, Baylink DJ, Linkhart TA. Evidence for a role for insulin-like growth factor binding proteins in glucocorticoid inhibition of normal human osteoblast-like cell proliferation. Eur J Endocrinol 1996;134:591–601. ISSN 0804–4643
Glucocorticoids (GCs) inhibit bone formation in vivo and inhibit osteoblast proliferation and collagen synthesis in vitro. These effects may be mediated by alterations in the insulin-like growth factor (IGF) system. In the present study of normal human osteoblast-like (HOB) cells, we tested the hypothesis that dexamethasone (Dex) inhibits IGF anabolic activity in bone by altering expression of IGF binding proteins (IGFBPs), particularly by decreasing expression of IGFBP-5 and IGFBP-3 (which enhance IGF activity) and increasing expression of IGFBP-4 (which inhibits IGF actions). Dexamethasone treatment caused a dose-dependent inhibition of HOB cell proliferation (69 ± 4% of control at 10−8 mol/l Dex) in seven separate experiments. Dexamethasone decreased IGFBP-5 mRNA levels to 20–30% of control (10−8 and 10−7 mol/l for 24 h). In six of six HOB preparations, 10−8 mol/l Dex decreased IGFBP-5 mRNA levels (35 ± 7% of control) and this effect was time dependent. Dexamethasone also decreased IGFBP-3 mRNA levels (74 ± 9% of control in three HOB preparations). Dexamethasone decreased secretion of 29–31-kD IGFBP-5 and 38–42-kD IGFBP-3 proteins, determined by Western ligand blot and IGFBP-5 immunoblot, and induced a dose-dependent decrease in IGFBP-3 and IGFBP-5 secretion determined by specific radioimmunoassays. The effects of Dex on IGFBP-4 mRNA and on secretion of 25-kD IGFBP-4 levels were inconsistent between different cell preparations. Results suggest that GC inhibition of IGFBP-5 and IGFBP-3 production could decrease IGF activities and contribute to GC inhibition of bone formation.
Thomas A. Linkhart, Mineral Metabolism (151), Pettis VA Hospital, 11201 Benton Street, Loma Linda, CA 92357, USA
Stressful life events in the pathogenesis of Graves' disease
Authors: Radosavljević Vladan R , Janković Slavenka M , Marinković Jelena M 
Published: December 2008

Radosavljević VR, Janković SM, Marinković JM. Stressful life events in the pathogenesis of Graves' disease. Eur J Endocrinol 1996;134:699–701. ISSN 0804–4643
A case-control study was conducted in order to assess possible relationships between life events and Graves' disease. The study included 100 newly diagnosed patients with Graves' disease and 100 controls matched with respect to sex, age (±2 years) and type of residence (rural, urban). Paykel's Interview for Recent Life Events (a semistructured research interview covering 61 life events) was administered to each subject. In comparison with controls, the patients claimed to have had significantly more life events in the 12 months preceding the diagnosis (p = 0.0001). The following eight life events were significantly more prevalent among patients than controls: change in time spent on work (much overtime work, second job, much less work than usual) (McNemar = 12.04; RR= 7.00;95%CI= 2.35–20.80;p= 0.0001), unemployment for at least 1 month (McNemar = 4.00; RR = 8.00; 95%CI = 1.04–61.39; p = 0.039), arguments with one's superior at work or a coworker (McNemar = 4.50; RR = 3.50; 95%CI = 1.10–11.08; p = 0.031), change in the work conditions (new company division, new chief, large reorganization) (McNemar = 4.26; RR = 4.00; 95%CI = 1.07–14.92; p = 0.035), increased arguments with spouse (McNemar = 6.75; RR = 11.00; 95%CI = 1.82–66.44; p = 0.006), increased arguments with fiancé/fiancée or a steady date (McNemar = 4.00; RR = 8.00; 95%CI = 1.04–61.39; p = 0.039), hospitalization of a family member for serious illness (McNemar = 3.76; RR = 3.25; 95%CI = 1.01–10.68; p = 0.049) and moderate financial difficulties (McNemar = 8.50; RR = 3.25; 95%CI = 1.47–7.16; p = 0.003). Our findings indicate that life events may be a risk factor for Graves' disease.
Slavenka Janković, Institute of Epidemiology, Višegradska 26, PO Box 456, 11000 Belgrade, Yugoslavia
Bone mass, bone turnover and body composition in former hypothyroid patients receiving replacement therapy
Authors: Langdahl Bente L , Loft Anne Gitte R , Eriksen Erik F , Mosekilde Leif , Charles Peder 
Published: December 2008

Langdahl BL, Loft AGR, Eriksen EF, Mosekilde L, Charles P. Bone mass, bone turnover and body composition in former hypothyroid patients receiving replacement therapy. Eur J Endocrinol 1996;134:702–9. ISSN 0804–4643
The aim of the present cross-sectional study was to disclose whether long-term thyroxine replacement therapy (TRT) in primary hypothyroidism causes osteopenia. We compared 36 adult biochemically and clinically euthyroid patients who had received TRT for more than 5 years (mean 13 years) for primary hypothyroidism with 80 sex- and age-matched normal controls. Height, body weight and lean body mass were similar, but the patients had 21% higher fat body mass (p < 0.01) than their controls. Furthermore, compared to controls the patients had 29% higher serum thyroxine (T4) and 31% higher serum free T4 index (FT4I) levels (p < 0.001), whereas serum triiodothyronine (T3) and FT3I levels were both reduced by 7% (p < 0.05). In the patients, serum TSH was reduced significantly (p < 0.001). No significant differences were observed between patients and normals in regional or total bone mineral content or bone mineral density levels, apart from 20% higher lumbar bone mineral content among the premenopausal patients (p < 0.05). Surprisingly, the mean serum calcium level was slightly elevated (2.38 ± 0.08 vs 2.33 ± 0.07 nmol/l, p < 0.001), serum phosphate decreased (1.13 ± 0.19 vs 1.23 ± 0.16 mmol/l, p < 0.01) and 24-h renal calcium excretion was reduced by 19% (p < 0.05). No changes were observed in serum magnesium, intact parathyroid hormone or calcitriol. The biochemical markers of bone resorption (serum carboxyterminal telopeptide of type I collagen, renal excretion of hydroxyproline, pyridinoline and deoxypyridinoline) and formation (serum levels of carboxyterminal propeptide of type I procollagen, osteocalcin and total and bone alkaline phosphatase) were similar in the two groups. We conclude that long-term thyroxine replacement therapy in primary hypothyroidism does not exert a negative effect on bone mass or alter bone turnover.
Bente L Langdahl, University Department of Endocrinology and Metabolism, Aarhus Amtssygehus, Tage Hansensgade 2, DK-8000, Aarhus C, Denmark
Thermal regulatory dysfunction of growth hormone in classical heat stroke?
Authors: Alzeer Abdulaziz , Arifi Abdullah Al , El-Hazmi Mohsen , Warsy Arjumand S , Nylen Eric S 
Published: December 2008

Alzeer A, Al Arifi A, El-Hazmi M, Warsy AS, Nylen ES. Thermal regulatory dysfunction of growth hormone in classical heat stroke? Eur J Endocrinol 1996;134:727–30. ISSN 0804–4643
Growth hormone (GH) secretion associated with classical (non-exertional) heat stroke (HS) was evaluated in 26 HS victims and 10 control (non heat-exhausted) subjects during the annual Hajj in Makkah, Saudi Arabia. On admission to the HS treatment unit, the GH level was 1.54 ± 0.14 ng/ml (approximately 3.5-fold higher in the HS victims compared to controls; p = 0.005). The GH levels subsequently declined by 78% by 24 h. The categorized GH response was significantly associated with survival for those subjects with a GH level of < 5.53 ng/ml by 6 h (chi-squared test; p = 0.06). In those patients who died (N = 6), there was a continued increase in GH levels from the time of admission, which peaked at 6 h. In those patients who survived, the GH levels peaked at the time of admission and declined rapidly thereafter. There was a direct correlation of age and GH level upon admission (p = 0.02), as well as to peak GH (p = 0.041). However, there was no relationship of GH level to either body core temperature or the cooling time. In summary, HS induced significant GH secretion. The degree of GH response was not related to the body core temperature and was more pronounced in older individuals and in those that died. Although patients with GH deficiency and HS are characterized by anhidrosis/hypohidrosis, there does not appear to be dysfunction of GH response to heat stress-associated HS. In contrast, a vigorous GH response at 6 h suggested a worse outcome.
ES Nylen, Rm GE 246, VAMC, 50 Irving St, NW Washington, DC 20422, USA
Metabolic and clinical events preceding diabetes mellitus onset in cystic fibrosis
Authors: Cucinotta Domenico , Arrigo Teresa , De Luca Filippo , Di Benedetto Antonino , Lombardo Fortunato , Scoglio Riccardo , Sferlazzas Concetta , Magazzú Giuseppe 
Published: December 2008

Cucinotta D, Arrigo T, De Luca F, Di Benedetto A, Lombardo F, Scoglio R, Sferlazzas C, Magazzú G. Metabolic and clinical events preceding diabetes mellitus onset in cystic fibrosis. Eur J Endocrinol 1996;134:731–6. ISSN 0804–4643
Serial assessments of glucose tolerance, of glucose and insulin areas during an oral glucose tolerance test (OGTT) and of clinical parameters as well were evaluated retrospectively in seven diabetic cystic fibrosis patients (study group) during the 4–6.3 years that preceded diabetes mellitus diagnosis. The same metabolic and clinical parameters were also evaluated in seven age-matched patients who did not develop diabetes during a similar observation period (control group). In the study group, glucose tolerance was impaired in all patients but one since the first OGTT and glucose areas progressively increased over time, whereas in the control group glucose tolerance remained stable during the whole observation period. A significant and progressive blunting of insulin secretion occurred over time in both groups. Insulin secretion, however, was reduced but not exhausted at diabetes diagnosis. Neither modification of glycosylated haemoglobin levels over time nor serum islet cell antibodies at diabetes onset were observed in the study group. The overall clinical course of the disease was not different in either group and remained stable during the observation period. These results indicate that in cystic fibrosis diabetes mellitus onset is preceded by a long-standing deterioration of glucose tolerance, whilst insulin secretion progressively declines over time, irrespectively of glucose tolerance status. The prediabetic worsening of glucose tolerance is not necessarily linked to a worsening of overall clinical status.
Filippo De Luca, Istituto di Clinica Pediatrica, Policlinico Universitario, 98100 Messina, Italy
Role of protein kinase C in the regulation of ATP-triggered intracellular Ca2+ oscillations in chicken granulosa cells
Authors: Morley Paul , Chakravarthy Balu R , Mealing Geoffrey AR , Tsang Benjamin K , Whitfield James F 
Published: December 2008

Morley P. Chakravarthy BR, Mealing GAR, Tsang BK, Whitfield JF. Role of protein kinase C in the regulation of ATP-triggered intracellular Ca2+ oscillations in chicken granulosa cells. Eur J Endocrinol 1996;134:743–50. ISSN 0804–4643
These studies were designed to investigate the role of protein kinase C (PKC) in the regulation of ATP-triggered intracellular Ca2+ ([Ca2+]i) oscillations in chicken granulosa cells. Granulosa cells were obtained from the two largest preovulatory follicles (F1 and F2) of hens and [Ca2+]i was measured in cells loaded with the Ca2+-responsive fluorescent dye fura-2. Adenosine triphosphate (100 μmol/l) triggered an immediate, large [Ca2+]i spike that was followed by oscillations that returned to the resting level between spikes. The ATP (100 μmol/l) also stimulated a 1.70 ± 0.1-fold increase in membrane-associated PKC activity over control levels. The frequency of the ATP-triggered [Ca2+]i oscillations was reduced in a concentration-dependent (1–10 nmol/l) manner by treating the cells for 2 min with a PKC activator, 12-O-tetradecanoyl phorbol-13-acetate (TPA). A higher TPA concentration (100 nmol/l) completely prevented ATP from triggering the initial [Ca2+]i spike and oscillations. Adding TPA during the ATP-triggered [Ca2+]i oscillations immediately stopped the oscillatory activity. Interestingly, PKC inhibitors failed to amplify the ATP-triggered [Ca2+]i oscillations. Instead, adding the PKC inhibitors staurosporine (20 nmol/l), calphostin C (200 nmol/l) or 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H7; 100 μmol/l), either before or during the ATP (100μmol/l)-triggered [Ca2+]i response, also completely blocked the [Ca2+]i oscillations. Therefore, ATP-triggered [Ca2+]i oscillations in chicken granulosa cells appear to be regulated by a negative feedback loop requiring PKC, because the [Ca2+]i oscillations were prevented by either full activation or inhibition of PKC activity.
Paul Morley, Institute for Biological Sciences, National Research Council of Canada, Building M54, Montreal Road, Ottawa, Ontario, K1A OR6, Canada
Developmental aspects of prolactin receptor gene expression in fetal and neonatal mice
Authors: Brown-Borg Holly M , Zhang Fu-Ping , Huhtaniemi Ilpo , Bartke Andrzej 
Published: December 2008

Brown-Borg HM, Zhang F-P, Huhtaniemi I, Bartke A. Developmental aspects of prolactin receptor gene expression in fetal and neonatal mice. Eur J Endocrinol 1996;134:751–7. ISSN 0804–4643
The prolactin receptor (PRL-R), a member of the hematopoietin cytokine receptor superfamily, is widely distributed among mammalian tissues. To understand better the potential sites of action and onset of potential PRL responsiveness, the developmental distribution pattern of PRL-R mRNA expression in fetal and neonatal mice was examined. Fetal mouse tissues were collected at distinct stages from timed pregnancies. Following extraction of total RNA, onset of gene expression was evaluated via reverse transcription-polymerase chain reaction (RT-PCR) and Southern hybridization was employed for verification. Expression of PRL-R mRNA was first observed on day 14 in the liver and cranium and on day 15 in the kidney, lung and thymus gland. Pituitary and adrenal glands were positive for PRL-R at day 18 of gestation through to day 1 of postnatal life. Neither whole fetuses prior to day 14 (days 10–13) of gestation nor skin and bladder tissues from 2-day-old mice generated detectable RT-PCR signals for PRL-R. The presence of PRL-R mRNA in fetal thymus and spleen tissues suggests a possible role for PRL in the development of the immune system. Prolactin may act directly on the pituitary to influence its own secretion and/or that of other pituitary-derived factors, as evidenced by the presence of PRL-R mRNA in the pituitary glands of fetal and 1-day-old mice. These data are the first to show the presence of PRL-R gene expression in various organ systems in fetal mice and suggest that PRL is among several factors necessary to coordinate developmental activities.
Holly M Brown-Borg, Department of Physiology, University of North Dakota School of Medicine, Grand Forks, ND 58202-9037, USA
c-myc Expression is associated with increased proliferation activity in thyroid follicular cells of Graves' disease as stimulated by autoantibodies
Authors: Kashima Kenji , Yokoyama Shigeo , Daa Tsutomu , Takahashi Kenji , Nakayama Iwao , Noguchi Shiro 
Published: December 2008

Kashima K, Yokoyama S, Daa T, Takahashi K, Nakayama I, Noguchi S. c-myc Expression is associated with increased proliferation activity in thyroid follicular cells of Graves' disease as stimulated by autoantibodies. Eur J Endocrinol 1996:135:69–76. ISSN 0804–4643
Expression on thyroid follicular cells of HLA-DR, c-myc protein and proliferating cell nuclear antigen (PCNA) was examined immunohistochemically in 28 cases of Graves' disease (GD) and in 29 cases of Hashimoto's thyroiditis (HT). Immunoreactivity for PCNA in GD was seen not only in follicular cells adjacent to a lymphocytic infiltration, where the follicular cells were positive for HLA-DR, but also in hyperplastic follicular cells without the infiltration. The distribution of expressed c-myc protein was similar to that of PCNA in GD but not in HT. Semiquantitatively graded degrees of lymphocytic infiltration and expression of HLA-DR, c-myc and PCNA in GD showed a high correlation with one another. However, the degrees of c-myc expression in HT showed no significant correlation with any other degrees. Intraperitoneal injection of bovine TSH or of immunoglobulins derived from a patient with GD in rabbits induced hyperplastic change of thyroid follicular cells, as reflected in PCNA and c-myc immunoreactivity, as well as strong peroxidase and acid phosphatase activity. Immunization with synthesized peptide of thyrotropin receptor also exhibited the same results in the rabbit thyroids. Our results indicate that c-myc expression on follicular cells of GD may reflect a stimulation by autoantibodies mediated through the thyrotropin receptor.
Kenji Kashima, Department of Pathology, Oita Medical University, 1-1 Oita-gun, Oita 879-55, Japan