Academic literature on the topic 'Growth hormone – Adverse effects'

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Journal articles on the topic "Growth hormone – Adverse effects"

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Lehmann, Sharon, and Frank B. Cerra. "Growth Hormone and Nutritional Support: Adverse Metabolic Effects." Nutrition in Clinical Practice 7, no. 1 (February 1992): 27–30. http://dx.doi.org/10.1177/011542659200700127.

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&NA;. "Lack of adverse effects on LV with growth hormone." Inpharma Weekly &NA;, no. 988 (May 1995): 19. http://dx.doi.org/10.2165/00128413-199509880-00041.

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Souza, Flavio Moutinho, and Paulo Ferrez Collett-Solberg. "Adverse effects of growth hormone replacement therapy in children." Arquivos Brasileiros de Endocrinologia & Metabologia 55, no. 8 (November 2011): 559–65. http://dx.doi.org/10.1590/s0004-27302011000800009.

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Human growth hormone (hGH) replacement therapy has been widely available for clinical purposes for more than fifty years. Starting in 1958, hGH was obtained from cadaveric pituitaries, but in 1985 the association between hGH therapy and Creutzfeldt-Jakob disease was reported. In the same year, the use of recombinant hGH (rhGH) was approved. Side effects of rhGH replacement therapy in children and adolescents include rash and pain at injection site, transient fever, prepubertal gynecomastia, arthralgia, edema, benign intracranial hypertension, insulin resistance, progression of scoliosis, and slipped capital femoral epiphysis. Since GH stimulates cell multiplication, development of neoplasms is a concern. We will review the side effects reported in all rhGH indications.
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Darendeliler, Feyza. "Growth and growth hormone: recent papers on efficacy and adverse effects of growth hormone and World Health Organisation growth standards." Journal of Pediatric Endocrinology and Metabolism 31, no. 1 (January 26, 2018): 1–3. http://dx.doi.org/10.1515/jpem-2017-0531.

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Wass, John A. H., and Raghava Reddy. "Growth hormone and memory." Journal of Endocrinology 207, no. 2 (August 9, 2010): 125–26. http://dx.doi.org/10.1677/joe-10-0126.

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Growth hormone (GH) replacement unequivocally benefits growth, body composition, cardiovascular risk factors and quality of life. Less is known about the effects of GH on learning and memory. The recent paper on ‘early onset – GH deficiency (GHD) results in spatial memory impairment in mid life – and is prevented by GH supplementation’ by Nieves-Martinez importantly adds to this literature. Other data suggest that GH beneficially affects cognitive function in rats. In man, treatment of GHD has been associated with improvements in measures of memory and attention. There are also differences in verbal memory of patients with childhood onset GHD. Further questions remain, and the beneficial effects or otherwise of treating GHD in different age groups remain to be better defined. Certainly for reasons of maturation of neural connections and their development to young adulthood contemporaneous with rises in GH and IGF1 make these important areas for further study in man. Lastly because of what we already know in terms of cognitive effects of GHD, it is important to replace GH when studying other potential causes of adverse effects on cognition, for example, with radiotherapy.
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&NA;, &NA;. "Growth Hormone In the Elderly: Trying to Balance Dose and Adverse Effects." AJN, American Journal of Nursing 94, no. 3 (March 1994): 53. http://dx.doi.org/10.1097/00000446-199403000-00032.

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Bessarione, D., F. Perfumo, M. Giusti, F. Ginevri, G. Mazzocchi, R. Gusmano, and G. Giordano. "Growth hormone response to growth hormone-releasing hormone in normal and uraemic children. Comparison with hypoglycaemia following insulin administration." Acta Endocrinologica 114, no. 1 (January 1987): 5–11. http://dx.doi.org/10.1530/acta.0.1140005.

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Abstract. The uraemic syndrome is characterized by several endocrinological disturbances. This study was undertaken in order to evaluate the GH response to growth hormone-releasing hormone (GRH) in children with chronic renal failure (CRF) and to compare the results with those observed after insulin hypoglycaemia. Twenty-two children with CRF, 10 undergoing continuous ambulatory peritoneal dialysis (CAPD) and 12 on conservative treatment (CT), age ranges 2–15 years, were studied and the data were compared with those from 14 children with normal renal function and normal hormonal behaviour, affected by short stature (NC), and those form 13 healthy adult volunteers (NA). The GRH test (1 μg/kg body weight, iv) was carried out in 8 CAPD, 8 CT, 9 NC and 10 NA subjects. The blood samples were taken every 30 min for 3 h in CAPD and CT and for 2 h in NC and NA starting at 09.00 h. The following hormones were measured: GH, LH, FSH, Prl, TSH and cortisol (F). The insulin test (0.1 U/kg body weight, iv) was carried out in 5 CAPD, 5 CT, 10 NC and 9 NA on blood samples taken every 30 min for 2 h, measuring GH and glycaemia. No adverse effects were observed after the infusion of GRH. GRH administration induced a prompt response in all subjects, but GH plasma levels were significantly higher in uraemic children than in adults (peak value of 43.5 ± 8.2, 45.0 ± 8.4, 27.8 ± 6.0; 13.5 ± 2.6 μg/ml in CAPD, CT, NC and NA, respectively). The secretory areas were significantly narrower in NC (P < 0.05) and NA (P < 0.01) than in CAPD, and in NA than in CT (P < 0.01). The GH response to insulin did not differ in the 4 groups. The secretory area in CAPD and CT was wider after GRH than after insulin. The GH peak value of CAPD and NC was significantly higher after GRH than following insulin. No significant variation in TSH, LH and FSH was observed after the infusion of the neuropeptide, whereas Prl and F showed a reduction. The behaviour of Prl and F in NA and NC was similar after placebo and GRH. Our data show: a) There is a greater response of GH to GRH in children than in adults; b) compared with the insulin test, GRH stimulation seems to be a reliable means of evaluating GH secretion both in normal and uraemic children owing to the absence of qualitatively different responses and to the freedom from the adverse effects or risks which follow insulin infusion; c) GRH administration does not induce any significant variation on other hypophyseal hormones and the reduction of Prl and F seems to follow the normal sleep-wake and circadian behaviour.
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Jørgensen, Jens O. L., Søren A. Pedersen, Leif Thuesen, Jørgen Jørgensen, Jens Møller, Jørn Müller, Niels E. Skakkebæk, and Jens S. Christiansen. "Long-term growth hormone treatment in growth hormone deficient adults." Acta Endocrinologica 125, no. 4 (October 1991): 449–53. http://dx.doi.org/10.1530/acta.0.1250449.

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Abstract. Growth hormone treatment in GH-deficient adults has proved beneficial in recent short-term trials, but long-term results have not yet been reported. Thirteen GH-deficient adults (4 females, 9 males; mean (sem) age 26.4 (1.7) years), who had completed 4 months of GH therapy in a double-blind placebo-controlled cross-over study were followed, for further 16.1 (0.8) months of uninterrupted GH therapy in an open design. A significant mean increase of 1.3 cm in linear height was recorded, whereas body mass index remained unchanged. Mean muscle volume of the thigh, estimated by computerised tomography, increased significantly compared with that of the initial placebo period (p=0.01), and a slight decrease was recorded in adipose tissue volume of the thigh (p=0.10) and subscapular skinfold thickness (p=0.10). Still, the muscle to fat ratio of the thigh was significantly lower compared with that of normal subjects (72.6/27.4 vs 77.9/22.1) (p<0.01). The mean isometric strength of the quadriceps muscles increased significantly during long-term GH therapy (p<0.01), but remained lower compared with that of normal subjects (1.66 (0.10) vs 2.13 (0.11) Nm/kg body weight). Exercise capacity performed on a bicycle ergometer increased significantly after long-term therapy (p<0.05), but still did not reach the values seen in normal subjects (22.5 (3.4) vs 37.4 (4.2) watt · min · kg−1· No adverse reactions were recorded during long-term therapy and hemoglobin A1c remained unchanged. These data suggest that long-term GH replacement therapy in GH-deficient adults has beneficial effects on several physiological features which are subnormal in these patients.
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Galbraith, Hugh. "Hormones in international meat production: biological, sociological and consumer issues." Nutrition Research Reviews 15, no. 2 (December 2002): 293–314. http://dx.doi.org/10.1079/nrr200246.

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AbstractBeef and its products are an important source of nutrition in many human societies. Methods of production vary and include the use of hormonal compounds (‘hormones’) to increase growth and lean tissue with reduced fat deposition in cattle. The hormonal compounds are naturally occurring in animals or are synthetically produced xenobiotics and have oestrogenic (oestradiol-17β and its esters; zeranol), androgenic (testosterone and esters; trenbolone acetate) or progestogenic (progesterone; melengestrol acetate) activity. The use of hormones as production aids is permitted in North American countries but is no longer allowed in the European Union (EU), which also prohibits the importation of beef and its products derived from hormone-treated cattle. These actions have resulted in a trade dispute between the two trading blocs. The major concern for EU authorities is the possibility of adverse effects on human consumers of residues of hormones and metabolites. Methods used to assess possible adverse effects are typical of those used by international agencies to assess acceptability of chemicals in human food. These include analysis of quantities present in the context of known biological activity and digestive, absorptive, post-absorptive and excretory processes. Particular considerations include the low quantities of hormonal compounds consumed in meat products and their relationships to endogenous production particularly in prepubertal children, enterohepatic inactivation, cellular receptor- and non-receptor-mediated effects and potential for interference with growth, development and physiological function in consumers. There is particular concern about the role of oestradiol-17β as a carcinogen in certain tissues. Now subject to a ‘permanent’ EU ban, current evidence suggests that certain catechol metabolites may induce free-radical damage of DNA in cell and laboratory animal test systems. Classical oestrogen-receptor mediation is considered to stimulate proliferation in cells maintaining receptivity. Mathematical models describing quantitative relationships between consumption of small amounts of oestrogens in meat in addition to greater concentrations from endogenous production, chemical stoichiometry at cellular level and human pathology have not been developed. Such an approach will be necessary to establish ‘molecular materiality’ of the additional hormone intake as a component of relative risk assessment. The other hormones, although generally less well researched, are similarly subject to a range of tests to determine potentially adverse effects. The resulting limited international consensus relates to the application of the ‘precautionary principle’ and non-acceptance by the European Commission of the recommendations of the Codex Alimentarius Commission, which determined that meat from cattle, hormone-treated according to good practice, was safe for human consumers. The present review considers the hormone issue in the context of current international social methodology and regulation, recent advances in knowledge of biological activity of hormones and current status of science-based evaluation of food safety and risk for human consumers.
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Ranke, Michael B. "Effects of Growth Hormone on the Metabolism of Lipids and Water and Their Potential in Causing Adverse Events during Growth Hormone Treatment." Hormone Research 39, no. 3-4 (1993): 104–6. http://dx.doi.org/10.1159/000182707.

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Dissertations / Theses on the topic "Growth hormone – Adverse effects"

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Ödmark, Inga-Stina. "Hormone replacement therapy : benefits and adverse effects." Doctoral thesis, Umeå universitet, Obstetrik och gynekologi, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-243.

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Background: Numerous studies have shown that estrogen replacement therapy (ERT) is an effective treatment for vasomotor symptoms, insomnia and vaginal dryness. Beneficial effects have also been shown on lipid patterns and on the incidence of osteoporotic fractures. As ERT increases the risk of endometrial adenocarcinoma, combinations with various progestogens have been developed in order to protect the endometrium. However, the addition of progestogens tends to reduce the beneficial effects of estrogens on mood, cognition and lipid metabolism. The added progestogen often causes side effects such as irritability and depression. There is evidence that the effect on wellbeing varies between women and with the type of progestogen used. Women who prefer to avoid withdrawal bleedings can be given continuous combined hormone replacement therapy (HRT). Unfortunately, irregular bleedings are common at the beginning of treatment and reduces compliance. Recently, several studies have reported an increased risk of breast cancer and venous thrombosis, and therefore long-term treatment with HRT for women without climacteric symptoms is no longer recommended. The ongoing debate has, for the time being, resulted in a recommendation that improving quality of life (QoL) by treatment of climacteric symptoms should be the only indication for prescribing HRT. Aims and methods: The aims of the study were to investigate bleeding patterns, changes in wellbeing at onset and during long-term treatment, and lipid and lipoprotein profiles with two different types of continuous combined HRT. In addition, women starting, and women switching from mainly sequential HRT were compared. The design was a randomised, double-blind, one year, prospective, multicentre study including 249 healthy postmenopausal women who were given continuous daily oral treatment with either combined 0.625mg conjugated estrogen (CE) and 5mg medroxyprogesterone acetate (MPA) or combined 2mg 17β - estradiol (E2) and 1mg norethisterone acetate (NETA). Bleedings, if any, were recorded daily throughout the study. The main outcome measures (changes in wellbeing and climacteric symptoms) consisted of daily ratings of 12 items on a validated symptom scale. Serum concentrations of lipids and lipoproteins were measured at baseline and after one year of treatment. Results and conclusions: The majority of drop-outs were confined to the first three months, and the main reasons were bleedings and/or decreased wellbeing. Drop-outs were three times more common in the E2/NETA group. During the first month, 67% of the women reported irregular bleedings. The number of bleeding days decreased on both treatments during the first four months. Treatment with CE/MPA resulted in less irregular bleedings and a shorter time to amenorrhoea compared to E2/NETA. As expected, "starters" experienced more sweats than "switchers" at the onset of treatment, but both groups improved significantly. Side effects such as breast tenderness, swelling, depression and irritability appeared during the first treatment week in both groups. The side effects of HRT appeared much more quickly than the benefits and were more frequent in women with a history of premenstrual syndrome (PMS). Breast tenderness was more common in the E2/NETA group throughout the whole study period. Apart from that, there were no differences between the two treatment regimens as regards effects on well-being at the end of the study. Lipoprotein(a) levels, an important risk factor for cardiovascular disease, decreased in both treatment groups. Triglyceride levels increased in women treated with CE/MPA, and levels of total cholesterol, high density lipoprotein and low density lipoprotein fell in the E2/NETA group. In conclusion, treatment with E2/NETA caused more bleeding problems than treatment with CE/MPA. CE/MPA was better tolerated than E2/NETA at the beginning of the study, but among the women remaining in the study there was no difference in QoL between the two treatment groups. HRT counselling should take into account that a history of PMS increases the likelihood of side effects and that these may precede any beneficial effects. Both treatments produced beneficial effects on lipid and lipoprotein levels, and neither of the regimens was superior in this respect.
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Ödmark, Inga-Stina. "Hormone replacement therapy : benefits and adverse effects /." Umeå : Univ, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-243.

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Melkersson, Kristina. "Influence of antipsychotic drugs on hormone levels /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4089-4/.

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Mahajan, Tripti. "Diagnosis of growth hormone deficiency and study of the effects of growth hormone treatment in growth hormone deficient adults." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247557.

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Björn, Inger. "Hormone replacement therapy and effects on mood." Doctoral thesis, Umeå universitet, Obstetrik och gynekologi, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-94115.

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Background: During the past 5 decades, hormone replacement therapy (HRT) has been used, and appreciated for its beneficial effects, by millions of women in their menopause. As treatment for climacteric symptoms, estrogen is outstanding, and effects on hot flushes, vaginal dryness, and insomnia have been widely documented. The increased risks of venous thrombosis and breast cancer, however, restrict the use of estrogen. Estrogen treatment in women with a remaining uterus includes a progestin, added to protect the endometrium from hyperplasia and malignancies. The long-standing clinical impression, that progestin addition negatively influences mood, has been discussed in previous studies. Mood deterioration is, however, not mortal, although mood is important to the wellbeing and daily functioning of women treated with hormones. Studies of the mental side effects of HRT add to our understanding of steroid effects in the brain. Aims and methods: In our studies, we aimed to establish to what extent negative side effects cause women to discontinue HRT, and find out which drug compounds lead to mood deterioration. The questions asked were whether the type and dose of progestin and the estrogen dose during the progestin addition influence the mood and physical symptoms during sequential HRT. Compliance with HRT and reasons for discontinuing the therapy were evaluated in a retrospective longitudinal follow-up study. Treatment effects were studied in three randomized, double-blind, cross-over trials. During continuous estrogen treatment, effects of sequential addition of a progestin were studied by comparing two different progestins, medroxyprogesterone acetate (MPA) andnorethisterone acetate (NETA), comparing different doses of the same progestin, MPA, and comparing two doses of estrogen during addition of the same dose of MPA. The main outcome measure was the daily rating on mood and physical symptoms kept by the participants throughout the studies. The clinical trials were carried out at three gynecological centers in northern Sweden. Results and conclusions: Besides fear of cancer and a wish to determine whether climacteric symptoms had meanwhile disappeared, negative side effects was the most common reason or discontinuing HRT. Tension in the breasts, weight gain, a depressed mood, abdominal bloating, and irritability were the most important side effects seen both in women who continued HRT and in women who had discontinued the therapy. In our clinical trials, we showed that addition of a progestin to estrogen treatment induces cyclic mood swings characterized by tension, irritability, and depression, as well as increased breast tension, bloatedness, and hot flushes. Women with a history of premenstrual syndrome (PMS) appeared to be more sensitive to the progestin addition and responded with lower mood scores compared with women without previous PMS. In our studies, MPA provoked depressed mood to a lesser extent than did NETA. Surprisingly, the higher dose of MPA (20 mg) enhanced the mood, compared with 10 mg, when added to estrogen treatment. In women continuously treated with 3 mg estradiol, mood and physical symptoms worsened during the progestin addition, as compared with treatment with 2 mg estradiol. The negative side effects seen during sequential HRT have much in common with symptoms seen in the premenstrual dysphoric disorder (PMDD), which is a psychoneuroendocrine disorder with psychiatric expression. Explanations for treatment effects on mood are likely to be found in drug interactions with neurotransmitter systems of the brain.

Diss. (sammanfattning) Umeå : Umeå universitet, 2003


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Pagano, Christopher. "Role of the truncated form of the human growth hormone receptor in regulating growth hormone effects." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114445.

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The binding of human Growth Hormone (GH) to its receptor (GHR) on target cells leads to activation of three major intracellular signaling pathways: JAK2/STAT5, PI3K/AKT and ERK/MAPK. However, in addition to the full length (FL) GHR, there exist two truncated (Tr) GHR isoforms, GHR1-279 and GHR1-277, that lack the majority of their intracellular domain as a result of alternative splicing of GHR mRNA. While both in vitro and in vivo studies suggest that the Tr GHR isoforms have a dominant negative effect on FL GHR by forming stable heterodimers, little is known about their normal physiological functions and their effects on the three major GH signaling pathways. We hypothesized that Tr GHR isoforms play a functionally significant role in human cells and tissues, fine-tuning the ability of GH to activate intracellular signaling and, thus, its biological effectiveness. In HEK293 cells, GH stimulation resulted in rapid and transient effects on pSTAT5b, pAKT and pERK1. Increasing the Tr/FL GHR ratios by transient transfection of a Tr GHR1-279 expression vector resulted in a significant dose-related inhibition of GH's ability to phosphorylate STAT5b, but with no significant inhibition of its ability to phosphorylate AKT and ERK1.These data suggest that Tr GHR can limit the target cell's STAT5b signaling in response to GH, while there is likely an alternative mechanism through which GH is able to activate AKT and ERK. This reveals a possible physiological role for Tr GHR in modulating GH's biological activity differentially in its target tissues.
La liaison de l'Hormone de Croissance humaine (GH) à son récepteur (GHR) sur les cellules cibles conduit à l'activation de trois voies de signalisation intracellulaires majeures: JAK2/STAT5, PI3K/AKT et ERK/MAPK. Cependant, en plus de la forme intégrale (FL) du GHR, il existe deux isoformes tronquées (Tr) du GHR, GHR1-279 et GHR1-277 qui ont perdu la majorité de leur domaine intracellulaire dû à l'épissage alternatif de l'ARNm du GHR. Alors que les études in vitro et in vivo suggèrent que les isoformes tronqués du GHR auraient un effet de dominant négatif sur le GHR FL en formant des hétérodimères stables, peu d'éléments sont connus au niveau de leurs fonctions physiologiques normales et de leurs effets sur les trois voies de signalisation majeure de GH. Nous avons émis l'hypothèse que les isoformes de GHR Tr auraient un rôle fonctionnel significatif dans les cellules et les tissus humains, en régulant de façon précise la capacité de GH à activer la signalisation intracellulaire et donc son efficacité biologique. Dans les cellules HEK293, la stimulation par GH a conduit à des effets rapides et transitoires sur pSTAT5b, pAKT and pERK1. L'augmentation des ratios Tr/FL du GHR par transfection transitoire du vecteur exprimant le GHR1-279 Tr a résulté en une inhibition significative et dépendante de la dose sur la capacité de GH à phosphoryler STAT5b, mais cependant sans inhibition significative sur sa capacité à phosphoryler AKT et ERK1. Ces données suggèrent que le GHR Tr peut limiter la signalisation par STAT5b dans la cellule cible en réponse à GH, tandis qu'il existerait probablement un mécanisme alternatif par lequel GH serait capable d'activer AKT et ERK. Cela révèle un possible rôle physiologique pour le GHR Tr dans la modulation de l'activité biologique de GH de façon différentielle dans ses tissus cibles.
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Smith, Jamie C. "The effects of growth hormone on vascular reactivity and oxidative stress in hypopituitary adults with growth hormone dificiency." Thesis, Cardiff University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402851.

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Almeida, Nisha. "Measures of maternal tobacco smoke exposure and foetal growth." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=112375.

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Objective. Most biomarker studies of maternal smoking have been based on a single blood or urinary cotinine value, which is inadequate in capturing maternal tobacco exposure over the entire pregnancy. This thesis used maternal hair biomarkers to investigate the association between maternal active and passive smoking, and birthweight for gestational age (BW for GA).
Methods. Subjects were 444 term controls drawn from 5,337 participants of a multi-centre nested case-control study of preterm birth in Montreal. Maternal hair, collected after delivery, was measured for average nicotine and cotinine concentration across the pregnancy, assuming hair growth of 1 cm/month. The BW for GA z-score used Canadian population-based standards. Multiple linear regression was used to assess effects on the z-score, after controlling for potential confounders.
Results. In regression models for maternal active smoking analysis, the addition of hair nicotine to models containing either self-report or hair cotinine or both self-report and cotinine explained significantly more variance in the BW for GA z-score (p=0.009, p=0.017, and p=0.033, respectively). In maternal passive smoking analysis, no significant effect of ETS on BW for GA was found using hair biomarkers.
Conclusion. These results indicate that hair biomarkers are sensitive tools capable of predicting reductions in birthweight for maternal active smoking. The stronger results obtained for nicotine are reflective of the fact that hair nicotine is a better measure of maternal smoking, but it could also suggest that nicotine plays an aetiologic role in affecting foetal growth.
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Lindgren, Ann Christin. "Prader-Willi syndrome : diagnosis and effects of growth hormone treatment /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-3135-6/.

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Westbrook, Reyhan Marcus. "The Effects of Altered Growth Hormone Signaling on Murine Metabolism." OpenSIUC, 2012. https://opensiuc.lib.siu.edu/dissertations/549.

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Growth hormone signaling influences longevity but the mechanism through which decreased GH action extends lifespan in mice is unknown. It is likely that the key to understanding this phenomenon, and the process of aging itself, is to understand the alterations in metabolism caused by decreased GH action. We investigated changes in energy metabolism in long-lived mice, in hope that these findings can suggest means of improving human health and longevity. These studies consisted of three projects. The influence of altered GH signaling on metabolism was tested by monitoring oxygen consumption, respiratory quotient, and heat production. Intriguingly, long-lived mice have increased oxygen consumption, and decreased respiratory quotient; while short lived mice had opposite effects. These data indicate that decreased GH signaling associates with increased metabolism per unit of body weight and may beneficially affect mitochondrial flexibility by increasing the capacity for fat oxidation; while GH excess generally produces opposite metabolic effects. We then hypothesized that the metabolic characteristics observed in young long-lived mice would persist into old age. Further, we investigated whether caloric restriction or every-other-day diet, two life extending feeding regimens, had any interaction with the metabolic phenotype observed in long-lived mice. The results support our hypothesis that the alterations in metabolism observed in young long-lived mice persist into old age. Neither dietary regimen significantly altered oxygen consumption in GHRKO mice, however, every-other-day diet reduced 24-hour oxygen consumption per gram body weight. These experiments showed that GHRKO mice had increased oxygen consumption regardless of age and life extending dietary interventions we placed them on. We hypothesized that increased oxygen consumption in long-lived mice is the result of increased thermogenesis. To test this hypothesis, we measured oxygen consumption in long-lived mice and controls at the standard lab temperature 23°C, and at 30°C, the murine thermoneutral temperature. When the oxygen consumption of long-lived mice was measured at 30°C, the differences between long-lived and normal mice measured at 23°C were abrogated. These data indicate that increased energy utilization for thermogenesis may contribute to extended longevity of these mutants. Collectively, our results provide important insights into the metabolic characteristics of long-lived mice.
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Books on the topic "Growth hormone – Adverse effects"

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Wambera, Katherine Martina. Potential memory enhancing effects of peripheral growth hormone administration. Ottawa: National Library of Canada, 1992.

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Lindgren, Ann Christin. Prader-Willi syndrome: Diagnosis and effects of growth hormone treatment. Stockholm: Repro Print AB, 1998.

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Hormone toxicity in the newborn. Berlin: Springer-Verlag, 1990.

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Toxic bodies: Hormone disruptors and the legacy of DES. New Haven [Conn.]: Yale University Press, 2010.

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The greatest experiment ever performed on women: Exploding the estrogen myth. New York: Seven Stories Press, 2009.

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Nerve growth factor and pain. New York: Nova Science Publishers, 2010.

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Julie, Taguchi, and Formby Bent, eds. Sex, lies, and menopause: The shocking truth about hormone replacement therapy. New York: Morrow, 2003.

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Mahmud, Iffat. Water, sanitation, hygiene, and nutrition in Bangladesh: Can building toilets affect children's growth? Washington, DC: International Bank for Reconstruction and Development/The World Bank, 2015.

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Meletis, Chris D. The male menopause controversy: Arguments, affects, and treatments of andropause. Westport, Conn: Praeger Publishers, 2009.

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The greatest experiment ever performed on women: Exploding the estrogen myth. New York: Hyperion, 2003.

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Book chapters on the topic "Growth hormone – Adverse effects"

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Isgaard, Jörgen. "GH Effects on Cardiac Function." In Growth Hormone, 253–60. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5163-8_16.

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Rosén, Thord. "Effects of GH on Body Composition." In Growth Hormone, 135–48. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5163-8_9.

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Johannsson, Gudmundur. "Effects of GH on Lipid Metabolism." In Growth Hormone, 149–62. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5163-8_10.

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Monson, John P. "Side Effects of Growth Hormone Treatment." In Growth Hormone, 291–305. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5163-8_19.

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Landin-Wilhelmsen, Kerstin. "Effects of Growth Hormone on Blood Coagulation and Fibrinolysis." In Growth Hormone, 173–88. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5163-8_12.

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Jørgensen, Jens Otto Lunde, Rolf Dall, Nina Vahl, Helene Nørrelund, and Jens Sandahl Christiansen. "Effects of Growth Hormone on Muscle Mass and Function." In Growth Hormone, 227–36. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5163-8_14.

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Ohlsson, Claes. "Effects of GH on Bone Metabolism and Bone Mass." In Growth Hormone, 237–52. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5163-8_15.

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Russell-Jones, D. L., and A. M. Umpleby. "The Effects of Growth Hormone on Glucose & Protein Metabolism." In Growth Hormone, 163–72. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5163-8_11.

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Johansson, Jan-Ove, and Bengt-Åke Bengtsson. "Psychological Well-Being in Growth Hormone Deficiency and Central Nervous Effects of Growth Hormone." In Growth Hormone, 261–79. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5163-8_17.

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Marcus, Robert, Leah Holloway, and Gail E. Butterfield. "Effects of Growth Hormone in Older People." In Growth Hormone II, 150–54. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4613-8372-7_11.

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Conference papers on the topic "Growth hormone – Adverse effects"

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Askew, Michael J., Gary B. Schneider, Kristina J. Grecco, Jason Hsu, Emily Mugler, and Donald A. Noe. "Effect of Pharmaceutical Bone Growth Stimulation With Novel Anabolic Peptides: Biomechanical and Bone Density Measurements in a Rat Model." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43044.

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Pharmaceutical bone growth stimulation holds promise for prevention and treatment bone disorders, and the enhancement of fracture healing. Bone growth hormones have begun to have limited clinical use, but can illicit adverse side effects. Recent studies have shown that short peptides (less than 15 amino acids) derived from the protein sequence of Vitamin D Binding Protein (DBP), can enhance bone formation (osteogenesis). These peptides may have potential as controllable bone growth stimulators without the adverse side effects and cost of bone growth hormones. Rats, injected every other day for two weeks with DBP-based peptide fragments ranging from 3 to 13 amino acids in length, were euthanized and the tibias and femurs were scanned by peripheral quantitative computerized tomography (pQCT) to determine bone density and cross-sectional geometric properties. The bones were then tested in three-point bending to determine strength and bending modulus. Injection of DBP-based peptides over only a 2-week period resulted in significant (p&lt;0.05) increases in bone density and material properties in the experimental rat bones in comparison to controls injected with saline. The short length of these effective peptides suggests their use not only in systemic injections but also as clinically convenient pills taken orally for pharmaceutically induced bone growth stimulation.
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Pradeep, Sunila, Jie Huang, Edna Mora, Alpa Nick, Minsoon Cho, Sherry Wu, Rajesha Rupaimoole, et al. "Abstract 1952: Adverse effects of erythropoietin stimulates tumor growth via EphB4." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1952.

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Fan, Yanping, Xiancong Zhang, Siyu Zhang, Guochao Sun, and Xun Wang. "Effects of hormone seed soaking and substrate cultivation on the growth of blueberry." In 2018 7th International Conference on Energy and Environmental Protection (ICEEP 2018). Paris, France: Atlantis Press, 2018. http://dx.doi.org/10.2991/iceep-18.2018.50.

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Buchholz, S., F. Koester, A. Schally, A. Krishan, A. Papadia, O. Ortmann, and S. Seitz. "Combination of a Novel Growth Hormone Releasing Hormone Antagonist JMR 132 and Tamoxifen Enhances the Inhibitory Effects on Growth of ZR 75 and T47D Estrogen Dependent Human Breast Cancer Cells In Vitro and In Vivo." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-5073.

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Arkhipova, T. N., E. V. Martynenko, L. Yu Kuzmina, and D. S. Veselov. "Comparison of the influence bacteria producing either auxin or cytokinin on growth and water relation of wheat plants under salinity." In 2nd International Scientific Conference "Plants and Microbes: the Future of Biotechnology". PLAMIC2020 Organizing committee, 2020. http://dx.doi.org/10.28983/plamic2020.027.

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Rhizobacteria reduced the negative effects of salinity on wheat plants. Similarities and differences in the effect of hormone-producing halotolerant bacteria on plant growth and water relations during salinity are discussed.
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Craven, Dalton M., Laura A. Smith, Michael F. Coleman, Elaine M. Glenny, and Stephen D. Hursting. "Abstract 2575: Intermittent calorie restriction reverses the adverse effects of obesity and advanced age on tumor growth in a mouse model of breast cancer." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2575.

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Uddin, Sardar M. Zia, and Yi-Xian Qin. "Anabolic Effects of Ultrasound as Countermeasures of Simulated Microgravity in In-Vitro and In-Vivo Functional Disuse Models." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53796.

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Microgravity (MG) during space flight has been known to cause adverse effect on bone quality. Data collected from studies done on spaceflights show loss of 1–1.6% bone mineral density (BMD) per space-flight-month[1]. Most BMD has been recorded in load-bearing bones [2]. Some studies has considered using drugs and different growth factors to maintain bone mass in microgravity conditions but it can be too expensive to maintain over longer periods of time besides the systematic effects of such treatments [3]. Considering the effects of microgravity are partially attributed to lack of mechanical force on bone tissue, which alters gene expression, reduction in transcription factors and growth factors. Furthermore, lack of gravity effects cell growth, proliferation, differentiation, cytoskeleton polymerization and cellular morphology [4, 5]. Thus to reverse these adverse effects on bone physiology, it is important to provide cells with mechanical stimulus which can provide essential mechanical signal for cells to counter the effects of microgravity. Ultrasound acoustic vibrations can be readily applied in, in vivo and human studies and has shown anabolic effects on osteopenic bone tissue [6]. Furthermore, ultrasound is a non-invasive and more target specific treatment relative to cyclic strain and vibration. The objective of this study is to see effects of low intensity pulsed ultrasound (LIPUS) on disused bone model and osteogenic activity of osteoblast cells cultures in simulated microgravity. This will help us understand that effects of ultrasound on microgravity and mechanotransduction pathway responsible for anabolic effect on bone cells.
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Jessen, Wilhelm, Martin Konopka, and Wolfgang Schro¨der. "Particle-Image Velocimetry Measurements of Film Cooling in an Adverse Pressure Gradient Flow." In ASME Turbo Expo 2010: Power for Land, Sea, and Air. ASMEDC, 2010. http://dx.doi.org/10.1115/gt2010-22411.

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The turbulent flow field of a film cooling flow is investigated using the particle-image velocimetry (PIV) technique. Cooling jets are injected from a multi-row hole configuration into a turbulent boundary layer flow of a flat plate in the presence of a zero and an adverse pressure gradient. The investigations focus on full-coverage film cooling. Therefore, the film cooling configuration consists of three staggered rows of holes with a lateral spacing of p/D = 3 and a streamwise row distance of l/D = 6. The inclined cooling holes feature a fan-shaped exit geometry with lateral and streamwise expansions. Jets of air and CO2 are injected separately at different blowing ratios into a boundary layer to examine the effects of the density ratio between coolant and mainstream on the mixing behavior and consequently, the cooling efficiency. For the zero pressure gradient case the measurement results indicate the different nature of the mixing process between the jets and the crossflow after the first, second, and third row. The mainstream velocity distributions evidence the growth of the boundary layer thickness at increasing row number. The interaction between the undisturbed boundary layer and first two rows leads to maximum values of turbulent kinetic energy. The presence of an adverse pressure gradient in the mainstream clearly intensifies the growth of the boundary layer thickness and increases the velocity fluctuations in the upper mixing zone. The measurements considering an increased density ratio show higher turbulence intensities in the shear zone between the jets and the main flow leading to a more pronounced mixing in this area. The results of the experimental measurements are used to validate numerical findings from a large-eddy simulation. This comparison shows a very good agreement for mean velocity distributions and velocity fluctuations.
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Ameryoun, Hamed, and Franck Schoefs. "Probabilistic Modeling of Roughness Effects Caused by Bio-Colonization on Hydrodynamic Coefficients: A Sensitivity Study for Jacket-Platforms in Gulf of Guinea." In ASME 2013 32nd International Conference on Ocean, Offshore and Arctic Engineering. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/omae2013-11101.

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Nowadays, challenge for requalification of existing offshore platforms through the reassessment process leads to consider the importance of updating new information (e.g. environmental data, new regulations, etc.). Regarding to this information and depending on offshore fields, data of marine growth colonization is shown to have a dominant effect. This is a real challenge in the Gulf of Guinea that this study focuses on. Marine growth is known to cause adverse effects on the performance of offshore structures. Its presence can change the roughness and the diameter of structural members and hence change the level of hydrodynamic coefficients. Moreover, modifying the added mass can change the natural period and hence dynamic responses of structures. Even platforms with the best protection schemes against marine organisms will after few weeks at least few months start to be covered by various types of marine growth. Generally, it was also recognized that the most important source of loading exerted on offshore structures comes from hydrodynamic actions which are influenced by hydrodynamic coefficient values. The colonization process is very complex and results are in a large diversity of marine growth type (animal, vegetal — hard, soft) and species. This study therefore proposes a stochastic modeling of marine growth and the roughness of hard species based on Response Surface Methodology. A geometrical description of nth order of Stokes model, formed by a random linear combination of deterministic vectors is employed. Finally, the complexity level of roughness modeling is analyzed and the results are discussed.
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Mazumdar, Darshana. "Association of organochlorine pesticides and risk of epithelial ovarian cancer: A case control study." In 16th Annual International Conference RGCON. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0039-1685303.

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Background: Organochlorine pesticides (OCPs) belongs to the class of hydrocarbons characterized by its cyclic structure. Due to their persistent nature OCP gets accumulated in the food chain and cause possible adverse health effects specifically various hormone mediated disorders. Ovarian cancer is also one of the hormone dependant cancer and begins with the transformation of cells that comprises the ovaries including surface epithelial, germ cells, etc. It has been suggested that endocrine disruption, exposure to xenobiotic and subsequent oxidative stress may antedate ovarian cancer and contribute to its pathogenesis. However, no report regarding any association of OCP level with etiology of epithelial ovarian cancer is so far available among North Indian population. Methods: A total of 120 subjects were included in this case control study, consisting of 60 histological proven cases of epithelial ovarian cancer and 60 controls subjects. Quantification of OCP levels was done by Perkin Elmer Gas Chromatograph (GC) equipped with 63Ni selective Electron Capture Detector. Results: Levels of b-HCH, endosulfan I, p’p’-DDT, p’p’-DDE and heptachlor were found significantly high in cases of epithelial ovarian cancer as compared to control. A significant association was also observed between higher levels of b-HCH and heptachlor and EOC with odds ratio of 2.76 and 2.97 respectively. Conclusion: Results indicate the plausible role of OCPs with the pathogenesis of epithelial ovarian cancer among North Indian population. Moreover, it is one of the first report suggesting significant level of heptachlor among north Indian women population with epithelial ovarian cancer.
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Reports on the topic "Growth hormone – Adverse effects"

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Cho, Sang-Joon, Jin-Sook Lee, Eric D. Mathias, Sender Lkhagvadorj, Lloyd L. Anderson, Ching Chang, and Gerard J. Hickey. Central and Peripheral Administration of Growth Hormone Secretagogue L-692-585, Somatostatin, Neuropeptide Y and Galanin in Pig: Dose-dependent Effects on Growth Hormone Secretion. Ames (Iowa): Iowa State University, January 2011. http://dx.doi.org/10.31274/ans_air-180814-840.

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