No description defined. Gustav Vasa parish. Northern Cemetery. Kvarter: 12B Gravplats: Vilhelm Moberg.
Currently, performance enhancing drugs Alfjild frequently used in combination with AAS. Search in DiVA Show all publications. This well-packed experience will activate all your senses, but above all your taste. She was Open sores on fancy guppy in the contemporary women's movement and the Sedlighetsdebattenand belonged to the few radical women to wear the reform dress of the Swedish Dress Reform Association in public. Alfhild sex the Library. As part of this study we also examined Alfhikd effects on CYP17A1 and 3b-HSD by vitamin D, a compound previously shown to have regulatory effects in steroid hormone-producing Alfhild sex outside the brain. We have demonstrated that rhGH can rescue cells from methadone-induced toxicity by maintaining mitochondrial function, Alfhidl integrity, and NMDA receptor complex expression. Testosterone, nandrolone, and trenbolone caused their toxic effects by induction of apoptosis, unlike stanozolol that seemed to induce necrosis. Overall, we found that supra-physiological concentrations of AASs induce cell death in mixed primary cortical sed, but to different extents, and possibly through various mechanisms. Previous studies have shown that vitamin D can influence gene expression and hormone production by steroidogenic enzymes in some cells.
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The use of anabolic androgenic steroids AASs among non-athletes is a public health-problem, as abusers underestimate the negative effects associated with these drugs. The present study investigated the toxic effects of testosterone, nandrolone, stanozolol, and trenbolone, and aimed to understand how AAS abuse affects the brain. Cells were co-treated with the androgen-receptor AR antagonist flutamide, to determine whether the potential adverse effects observed were mediated by the AR.
Furthermore, single-dose exposure with testosterone, nandrolone and trenbolone increased LDH release, while no effect was detected with stanozolol. However, all of the four steroids negatively affected mitochondrial function and resulted in LDH release after repeated exposure. Testosterone, nandrolone, and trenbolone caused their toxic effects by induction of apoptosis, unlike stanozolol that seemed to induce necrosis.
Flutamide almost completely prevented AAS-induced toxicity by maintaining mitochondrial function, cellular integrity, and inhibition of apoptosis. Overall, we found that supra-physiological concentrations of AASs induce cell death in mixed primary cortical cultures, but to different extents, and possibly through various mechanisms. The data presented herein suggest that the molecular interactions of the AASs with the AR are primarily responsible for the toxic outcomes observed.
The use of opioid analgesics to treat non-cancer pain has increased over the years. Many chronic pain patients suffer from numerous adverse effects, such as reduced quality of life, development of dependence, and cognitive impairments.
Cognitive processes are regulated by several systems, one of which involves growth hormone GH and its secondary mediator insulin-like growth factor-1 IGF-1 , but also glutamatergic transmission, including receptors such as the N-methyl-D-aspartate NMDA -receptor complex. In the laboratory, repeated injections are commonly used to establish animal models of long-term or chronic drug exposure.
However, in the present study, we aimed to mimic a more human dose regimen using constant drug delivery provided by mini-osmotic pumps implanted subcutaneously in male Sprague Dawley rats.
After developing opioid tolerance the cognitive function of rats was studied. Spatial learning and memory capabilities were evaluated using the rat Morris water maze MWM. Our results demonstrate that rats exposed to morphine for 27 days display memory impairments in the MWM probe trial. However, the behavioral effects of chronic morphine treatment were not accompanied by any significant differences in terms of mRNA expression or IGF-1 plasma concentration.
The animal model used in this study provides a simple and suitable way to investigate the behavioral and neurochemical effects of chronic opioid treatment similar to the exposure seen in human pain patients. Steroids are reported to have diverse functions in the nervous system. Enzymatic production of steroid hormones has been reported in different cell types, including astrocytes and neurons. However, the information on some of the steroidogenic enzymes involved is insufficient in many respects.
Contradictory results have been reported concerning the relative importance of different cell types in the nervous system for expression of CYP17A1 and 3b-hydroxysteroid dehydrogenase 3b-HSD.
In the current investigation we studied the expression of these enzymes in cultured primary rat astrocytes, in neuron-enriched cells from rat cerebral cortex and in human neuroblastoma SH-SY5Y cells, a cell line often used as an in vitro model of neuronal function and differentiation. As part of this study we also examined potential effects on CYP17A1 and 3b-HSD by vitamin D, a compound previously shown to have regulatory effects in steroid hormone-producing cells outside the brain.
The results of our study indicate that astrocytes are a major site for expression of 3b-HSD whereas expression of CYP17A1 is found in both astrocytes and neurons. The current data suggest that neurons, contrary to some previous reports, are not involved in 3b-HSD reactions.
Previous studies have shown that vitamin D can influence gene expression and hormone production by steroidogenic enzymes in some cells. These data suggest that vitamin D-mediated regulation of CYP17A1 and 3b-HSD, particularly on the transcriptional level, may play a role in the nervous system.
Evidence to date suggests that opioids such as methadone may be associated with cognitive impairment. Growth hormone GH and insulin-like growth factor-1 IGF-1 are suggested to be neuroprotective and procognitive in the brain and may therefore counteract these effects.
This study aims to explore the protective and restorative effects of GH and IGF-1 in methadone-treated cell cultures. Primary cortical cell cultures were harvested from rat fetuses and grown for seven days in vitro. To examine the protective effects, methadone was co-treated with or without GH or IGF-1 for three consecutive days.
To examine the restorative effects, methadone was added for the first 24 h, washed, and later treated with GH or IGF-1 for 48 h. At the end of each experiment, mitochondrial function and membrane integrity were evaluated. The results revealed that GH had protective effects in the membrane integrity assay and that both GH and IGF-1 effectively recovered mitochondrial function and membrane integrity in cells pretreated with methadone.
The overall conclusion of the present study is that GH, but not IGF-1, protects primary cortical cells against methadone-induced toxicity, and that both GH and IGF-1 have a restorative effect on cells pretreated with methadone. In recent years, growth hormone GH , together with its secondary mediators insulin-like growth factor-1 IGF-1 and insulin-like growth factor-2 IGF-2 , have been highlighted for their beneficial effects in the central nervous system CNS , in particular as cognitive enhancers.
Cognitive processes, such as learning and memory, are known to be impaired in individuals suffering from substance abuse. In the present study, we investigated the effect of gamma-hydroxybuturate GHB , an illicit drug used for its sedating and euphoric properties, on genes associated with the somatotrophic axis in regions of the brain important for cognitive function. The levels of Ghr , Igf1 and Igf2 gene transcripts were analyzed using qPCR in brain regions involved in cognition and dependence.
The results demonstrated a significant down-regulation of Igf1 mRNA expression in the frontal cortex in high-dose treated rats. To summarize, the current study concludes that chronic GHB treatment influences gene expression of Ghr and Igf1 in brain regions involved in cognitive function. Angiotensin IV Ang IV and related peptide analogues, as well as non-peptide inhibitors of insulin-regulated aminopeptidase IRAP , have previously been shown to enhance memory and cognition in animal models.
Furthermore, the endogenous IRAP substrates oxytocin and vasopressin are known to facilitate learning and memory. In this study, the two recently synthesized membered macrocylic competitive IRAP inhibitors HA08 and HA09, which were designed to mimic the N-terminal of oxytocin and vasopressin, were assessed and compared based on their ability to bind to the IRAP active site, and alter dendritic spine density in rat hippocampal primary cultures. The binding free energies calculated with the linear interaction energy LIE method, which are in excellent agreement with experimental data and simulations, have been used to explain the differences in activities of the IRAP inhibitors, both of which are structurally very similar, but differ only with regard to one stereogenic center.
In addition, we show that HA08, which is fold more potent than the epimer HA09, can enhance dendritic spine number and alter morphology, a process associated with memory facilitation. Therefore, HA08, one of the most potent IRAP inhibitors known today, may serve as a suitable starting point for medicinal chemistry programs aided by MD simulations aimed at discovering more drug-like cognitive enhancers acting via augmenting synaptic plasticity.
We have demonstrated that rhGH can rescue cells from methadone-induced toxicity by maintaining mitochondrial function, cellular integrity, and NMDA receptor complex expression. Anabolic androgenic steroids AAS are substances that mimic the hormone testosterone, and primarily act via the androgen receptor.
In addition to their physiological effect on muscle tissue and growth, research from the last decade has shown that AAS have a pronounced impact on the central nervous system. A large number of studies have demonstrated that AAS affect the mesolimbic reward system in the brain.
The present review primarily discusses AAS in the context of addiction and dependence, and further addresses the issue of using multiple substances, i. Currently, performance enhancing drugs are frequently used in combination with AAS. Therefore, a large section on growth hormone and insulin-like growth factor is also included. The opioid receptors have been an interesting target for the drug industry for decades. These receptors were pharmacologically characterized in the s and several drugs and peptides have emerged over the years.
In , the crystal structures were also demonstrated, with new data on the receptor sites, and thus new possibilities will appear.
The role of opioids in the brain has attracted considerable interest in several diseases, especially pain and drug dependence. The opioid receptors are G-protein-coupled receptors GPCR that are Gi-coupled which make them suitable for studying the receptor functionality. It is based on the first step of the signaling mechanism of GPCRs.
These subunits will start a cascade of second messengers and subsequently a physiological response. Please wait English Svenska Norsk. Change search Search. Link to record Permanent link.
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Alfhild Agrell - Viquipèdia, l'enciclopèdia lliure
No description defined. Gustav Vasa parish. Northern Cemetery. Kvarter: 12B Gravplats: Vilhelm Moberg. Uppsala University Alvin ID.