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Delayed closure of epiphyseal cartilages induced by the aromatase inhibitor anastrozole : would it help short children grow up?
No full textEstrogens locally generated from androgen precursors due to the action of aromatase play a main role in epiphyseal cartilage fusion. Treatment with an aromatase inhibitor (anastrozole, 1 mg/day for 3 yr) in a boy previously operated on for a hamartoma causing precocious puberty and presenting with advanced bone maturation and nearly fused epiphyseal cartilages, slowed cartilage fusion consenting a higher final stature than expected (164.4 cm vs 158.4 cm). It is suggested that treatment with aromatase inhibitors, alone or in combination with rh-GH, may also be useful in children with constitutional short stature in order to delay epiphyseal closure and improve the final height
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
Variations on the Author
Full text link“Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship
Effects of 12-month GH treatment on bone metabolism and bone mineral density in adults with adult-onset GH deficiency
No full textSerum bone-GIa protein (BGP), bone alkaline phosphatase (B-AP), and C-terminal cross-linked telopeptide of type I collagen (ICTP) levels were evaluated in 18 adults with acquired GH deficiency (GHD, 14 males and 4 females, age range: 25-59 yr) before, at 3, 6, 9 and 12 months of rec-GH treatment (0.125 IU/kg/week for the first month, followed by 0.25 IU/kg/week for 11 months) and 6 months after the withdrawal of therapy. Total body bone mineral density (BMD, g/cm2) was measured with dual energy X-ray absorptiometry (Hologic QDR 1000/W) before, at 12 months of GH treatment and 6 months after its withdrawal. Before treatment, BGP (mean±SE: 5.1±0.4 ng/ml), B-AP (59.4±6.5 IU/I), ICTP (3.1±0.3 ng/ml) levels of patients were similar to in healthy controls (BGP: 5.4±0.1 ng/ml; B-AP: 58.2±2.0 IU/I; ICTP: 4.1±0.3 ng/ml). GH treatment caused a significant increase of BGP, B-AP, ICTP levels, the maximal stimulation of bone resorption, occurring after 3 months of GH treatment, while the maximal effect on bone formation being evident later (at 6th month). A slight decline in BGP, B-AP, T-AP and ICTP levels occurred at 9-12 months of therapy, although the values remained significantly higher than in basal conditions and with respect to healthy controls. Before treatment, mean total body BMD of patients (1.110±0.027 g/cm2, range: 0.944-1.350 g/cm2) was not significantly different (z-score: +0.47±0.31, NS) from that observed in healthy controls (1.065±0.008 g/cm2, range: 1.008-1.121 g/cm2). GH therapy was associated with a significant reduction of mean total body BMD values (6th month: -1.8±0.5%, p<0.01; 12th month: -2.1±1.0%, p<0.05 vs baseline), particularly evident in the first six months of treatment. Six months after the withdrawal of GH therapy, BGP (5.9±0.5 ng/ml), B-AP (57.3±7.0 IU/I) and ICTP (3.2±0.1 ng/ml) levels returned similar to those recorded before treatment, while total BMD increased (+1.5±0.7, p<0.05), remaining however slightly lower than in basal conditions (-0.6±1.2, NS). In conclusion, our study shows that: a) acquired GHD in adulthood is associated with both normal bone formation/resorption indexes and normal total body BMD; b) GH therapy causes a significant rise of bone formation/resorption markers (earlier and greater for bone resorption); c) one-year GH therapy is associated with a reduction of total body BMD values, particularly evident in the first 6 months of treatment; d) the effects of GH therapy on bone turnover are transient, being completely reverted six months after the withdrawal of GH therapy; e) the increase of total body BMD (up to baseline values) after GH withdrawal might be explained as consequence of persisting effects of previous GH stimulation on bone remodeling
Appropriate Similarity Measures for Author Cocitation Analysis
Full text linkWe provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis
Alterations of haemostatic and fibrinolytic markers in adult patients with growth hormone deficiency and with acromegaly
No full textAlterations of coagulation and fibrinolytic systems might contribute to the increased cardiovascular and cerebrovascular mortality observed in patients with both chronic growth hormone (GH) excess (acromegaly) and deficiency (GHD). However, contrasting results have been so far reported. To assess the importance of GH in modulating haemostatic system, several haemostatic variables in patients with GHD and acromegaly were measured. Twenty-four adult patients with GHD (8 childhood- and 16 adult-onset: age: 41+/-12 years, insulin like growth factor-I, IGF-I: 6.7+/-4 nmol/L), 10 non-diabetic acromegalic patients (age: 39 +/- 15 years; IGF-I: 109+/-37 nmol/L) and 64 healthy volunteers age and sex-matched with cases were studied. The plasma levels of tissue-type plasminogen activator antigen (t-PA), prothrombin fragment 1+2(F1+2) and thrombin-antithrombin complex (TAT) were measured by ELISA. Plasminogen activator inhibitor type 1 (PAI-1) was measured by an immunoactivity assay and fibrinogen by von Clauss method. GH levels were measured by IFMA and IGF-I by RIA. GHD patients had higher PAI-1 (12.7+/-16.7 vs 4.8 +/-5.3 U/ml, p<0.01), fibrinogen (363+/-104 vs 291+/-71 mg/dL, p<0.05) and TAT levels (6.8+/-9 vs 3.6+/-2.8ng/ml, p<0.05) than controls. Taking the 95th percentile of the normal distribution in the control group as the cut-off point for normal plasma levels of the haemostatic variables, high PAI levels were found in 25% of patients with GHD (P<0.01) while high fibrinogen and TAT levels were observed in 21% (P<0.05). The alterations were mostly present in patients with adult-onset GHD, with the exception of hyperfibrinogenaemia which was equally present in adult- and childhood-onset patients. Acromeyalic patients had higher mean fibrinogen levels than controls (398+/-111 vs 291+/-71 mg/dL, p<0.05), 40% having hyperfibrinogenaemia (P<0.01, vs controls). They also had t-PA levels lower than controls and GHD. No correlations between hormonal and haemostatic variables were found. Body mass index and waist to hip ratio correlated positively with PAI-1 levels in GHD patients only. In conclusion, this study shows that several abnormalities of coagulation variables (increased PAI-I, fibrinogen and TAT levels) are present in patients with GHD. while only hyperfibrinogenaemia is found in patients with acromegaly. These changes do not appear to be directly related to IGF-I levels or to the degree of GH deficiency/excess. However, these abnormalities may be an additional trigger for the development of coronary heart disease and thromboembolic complications mostly in patients with GHD
Long-term monitoring of rec-GH treatment by serial determination of serum aminoterminal propeptide of type III procollagen in children and adults with GH deficiency
No full textSerum aminoterminal propeptide of type III procollagen (PIIINP) levels, a reliable marker of collagen formation, were evaluated in children (C=7) and adults with childhood-onset (CO=10) and acquired (A=18) GH deficiency (GHD) before, during and after withdrawal of rec-GH therapy (C=0.6 IU/kg/week, CO=0.5 IU/kg/week, A=0.25 IU/kg/week). The duration of treatment was 12 months for C and A and 6 months for CO; investigations were carried out before and at 3, 6, 9 and 12 months (for C and A) and at 3 and 6 months (for CO) of GH treatment and 6 months after the withdrawal of therapy (for A and CO). Data obtained from patients were compared with those recorded in two age- and sex-matched control groups. Before treatment, serum PIIINP levels were significantly lower (p<0.001) in C with GHD (mean+/-SE: 2.9+/-0.4 ng/ml) than in controls (6.1+/-0.4 ng/ml), while no significant differences were recorded between adults with CO/A-GHD (3.7+/-0.5 ng/ml and 3.4+/-0.2 ng/ml) and controls (3.2+/-0.2 ng/ml). GH treatment caused a significant increase (p<0.0001) of PIIINP levels both in C (3(rd) month: 4.4+/-0.2 ng/ml, 6(th) month: 5.1+/-0.4 ng/ml, 12(th) month: 5.1+/-0.5 ng/ml), CO-GHD (3(rd) month: 12.7+/-1.2 ng/ml; 6(th) month: 10.2+/-0.6 ng/ml) and A-GHD (3(rd) month: 10.0+/-1.0 ng/ml; 6(th) month: 8.4+/-0.6 ng/ml; 12(th) month: 7.0+/-0.7 ng/ml), the increase being dose-dependent (more marked and sustained in adults with CO-GHD). The maximal stimulation of collagen synthesis occurred after 3 months of GH treatment in adults with GHD, while a more gradual and less relevant increase was observed in C with GHD. Six months after the withdrawal of GH therapy, serum PIIINP levels of adults with CO-GHD (3.6+/-0.3 ng/ml) were similar to those recorded before treatment, while in adults with A-GHD serum PIIINP levels (2.6+/-0.2 ng/ml) were significantly tower (p<0.01) than in basal condition. In conclusion, our study shows that: a) GHD is associated with a reduction of soft tissue formation in children, while it seems to exert no relevant effects in adults with GHD; b) GH therapy causes a rapid stimulation of collagen turnover, which shows a different pattern in children and adults; c) the OH-induced stimulation of collagen synthesis is rapidly removed after the withdrawal of GH treatment. For these reasons, the determination of peripheral markers of GH effects appears useful for the monitoring of Chi therapy and can contribute to assess the "tailored" substitutive dose for the individual patient
Lack of effect of hexarelin on TRH-induced TSH response in normal adult man
No full textThe mechanism of action of the synthetic growth hormone (GH)releasing peptide hexarelin is not yet fully understood. Although a direct effect on pituitary cells has been demonstrated, the peptide is also active at hypothalamic level, where specific binding sites have been found. The observation that hexarelin acts synergistically with GH-releasing hormone (GHRH) in releasing GH has suggested that it might suppress endogenous somatostatin secretion. As somatostatin is also inhibitory on TSH secretion, to verify the occurrence of modifications of the somatostatinergic tone induced by hexarelin, we studied its effects on TRH-induced TSH secretion. Seven normal subjects (4 women and 3 men aged 24-29 years) underwent the following tests on 3 different days: a) TRH (200 mu g/l iv)+placebo; b) hexarelin (1 mu g/Kg bw iv) +placebo c) combined TRH+hexarelin administration. Hexarelin induced significant and similar increases in serum GH levels when given in combination either with placebo or with TRH (1217+/-470 vs 986+/-208 mu g/min/l p:NS), while no modifications of GH levels were seen after TRH+placebo. Serum TSH levels were unmodified by hexarelin+placebo injection. The TSH increase elicited by hexarelin+ TRH was superimposable to that elicited by TRH+placebo (1124+/-530 and 1273+/-380 mU/min/l respectively). Circulating PRL levels slightly increased after hexarelin+placebo too (897 mu g/min/l), and the PRL response to hexarelin+TRH was slightly, although not significantly, greater than that observed after TRH+placebo (2680+/-1517 and 2243+/-1108 mu g/min/l, respectively). In conclusion, our data show that hexarelin does not alter basal and TRH-stimulated TSH secretion, thus suggesting that it does not inhibit somatostatin release. Furthermore a modest PRL-releasing effect of this peptide has been confirmed
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