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- Isgaard, Jörgen, 1959
(författare)
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Ghrelin and the cardiovascular system.
- 2013
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Ingår i: The Ghrelin System. Eds: Benso A.; Casanueva F.F.;Granata R.. - : Karger. - 1662-2979. - 9783805599085 ; 25, s. 83-90
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Bokkapitel (refereegranskat)abstract
- Although ghrelin was initially associated with regulation of appetite, the cardiovascular system has also been recognized as a potentially important target for its effects. Moreover, experimental and a limited number of clinical studies suggest a potential role for ghrelin in the treatment of congestive heart failure. So far, reported cardiovascular effects of growth hormone secretagogues and/or ghrelin include lowering of peripheral resistance, either direct at the vascular level and/or by modulating sympathetic nervous activity. Other observed effects indicate possible improvement of contractility and cardioprotective and anti-inflammatory effects both in vivo and in vitro. Taken together, these results offer an interesting perspective on the future where further studies aiming at evaluating a role of growth hormone secretagogues and ghrelin in the treatment of cardiovascular disease are warranted.
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- Ljunggren, Östen, et al.
(författare)
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Allele-Specific Gene Silencing in Osteogenesis Imperfecta
- 2011
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Ingår i: Cartilage and Bone Development and Its Disorders. - : S. Karger AG. - 9783805597920 ; 21, s. 85-90
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Konferensbidrag (refereegranskat)abstract
- OI is caused by mutations in the genes encoding for collagen type I COL1A1 and COL1A2, respectively. The patients suffer from bone fragility, and the severity can range from mild, with fractures in the youth, to lethal forms. Today, there is no effective treatment for the disorder. OI is caused by dominant negative mutations. A tempting approach to treat the disease would be to silence the allele carrying the mutation. This could in theory be done with siRNAs. Today, more than 800 various mutations are reported, and to create siRNA against a specific mutation is difficult. Instead, by developing siRNA against common polymorphic variations, it would be possible to silence the mutation by a standardized method regardless where the mutation is located on the allele. If the concept of allele-specific gene silencing by inhibitory RNA directed towards dominant negative mutations could be proven, this might be a novel approach to gene therapy in OI.
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- Menzies, John R W, et al.
(författare)
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Ghrelin, reward and motivation.
- 2013
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Ingår i: Endocrine development. - : S. Karger AG. - 1662-2979. ; 25, s. 101-11
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Forskningsöversikt (refereegranskat)abstract
- Almost all circulating gut peptides contribute to the control of food intake by signalling satiety. One important exception is ghrelin, the only orexigenic peptide hormone thus far described. Ghrelin secretion increases before meals and behavioural and electrophysiological evidence shows that ghrelin acts in the hypothalamus via homeostatic pathways to signal hunger and increase food intake and adiposity. These findings strongly suggest that ghrelin is a dynamically regulated peripheral hunger signal. However, ghrelin also interacts with the brain reward pathways to increase food intake, alter food preference and enhance food reward. Here we discuss ghrelin's role as an endocrine gut-brain reward signal in relation to homeostatic and hedonic feeding control.
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- Norjavaara, Ensio, 1954, et al.
(författare)
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Sex Steroid Replacement Therapy in Female Hypogonadism from Childhood to Young Adulthood.
- 2016
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Ingår i: Endocrine development. - : S. Karger AG. - 1662-2979 .- 1421-7082. ; 29, s. 198-213
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Tidskriftsartikel (refereegranskat)abstract
- The overall goal of pubertal sex hormone replacement therapy (HRT) in girls is not only about development of secondary sexual characteristics, but also to establish an adult endocrine and metabolic milieu, as well as adult cognitive function. Estradiol (E2) is the first choice for HRT compared to ethinyl estradiol (EE2). E2 is the most potent endogenous estrogen in the circulation, with established levels during spontaneous puberty. Transdermal E2, compared to oral administration, is the first choice to start pubertal HRT. Transdermal application avoids liver exposure to supraphysiologic estrogen concentrations and provides a more physiologic mechanism for hormone delivery. By cutting E2 matrix patches in doses of 0.05-0.07 µg/kg or administrate E2 gel in doses of 0.1 mg/day, serum concentrations of E2 seen in early spontaneous puberty can be obtained. Patches can be removed in the morning and thereby mimic the normal circadian rhythm. For those clinics with access to sensitive E2 determinations methods (extraction followed by radioimmunoassay or mass spectrometry) monitoring the attained E2 serum levels is recommended in order to optimally mimic the levels seen in early puberty as well as growth velocity, breast and uterus development. Mid- and late pubertal HRT is obtained by increased doses of E2, adding cyclic oral or transdermal progestin, as well as testosterone gel over the pubic area if indicated.
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