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INFLUENCE OF ESTROGEN ON MUSCLE PLASTICITY  [PDF]
Peter M. Tiidus
Brazilian Journal of Biomotricity , 2011,
Abstract: TIIDUS, P. M. Influence of estrogen on muscle plasticity. Brazilian Journal of Biomotricity. v. 4, n. 3, p. 143-155, 2011. Estrogen and hormone replacement therapy (HRT) have been demonstrated to have significant benefits to metabolic health and skeletal muscle function in animal models. More recently these benefits have also been reproduced in post-menopausal human females. Estrogen and HRT will diminish exercise induced muscle damage and inflammation via stabilizing effects on muscle membranes and calcium channels. Estrogen and HRT will also enhance muscle repair and augment muscle size via effects on satellite cell activation and proliferation. In addition estrogen and HRT will augment muscle strength through direct action on myosin which will enhance myosin strong binding during muscular contraction. These benefits could be important in the longer term maintenance of health, muscle functioning and independent living in older post-menopausal females. The use of HRT should be considered in some of these individuals in the context of the overall health advantages versus drawbacks this population.
Rehabilitation with Poststroke Motor Recovery: A Review with a Focus on Neural Plasticity  [PDF]
Naoyuki Takeuchi,Shin-Ichi Izumi
Stroke Research and Treatment , 2013, DOI: 10.1155/2013/128641
Abstract: Motor recovery after stroke is related to neural plasticity, which involves developing new neuronal interconnections, acquiring new functions, and compensating for impairment. However, neural plasticity is impaired in the stroke-affected hemisphere. Therefore, it is important that motor recovery therapies facilitate neural plasticity to compensate for functional loss. Stroke rehabilitation programs should include meaningful, repetitive, intensive, and task-specific movement training in an enriched environment to promote neural plasticity and motor recovery. Various novel stroke rehabilitation techniques for motor recovery have been developed based on basic science and clinical studies of neural plasticity. However, the effectiveness of rehabilitative interventions among patients with stroke varies widely because the mechanisms underlying motor recovery are heterogeneous. Neurophysiological and neuroimaging studies have been developed to evaluate the heterogeneity of mechanisms underlying motor recovery for effective rehabilitation interventions after stroke. Here, we review novel stroke rehabilitation techniques associated with neural plasticity and discuss individualized strategies to identify appropriate therapeutic goals, prevent maladaptive plasticity, and maximize functional gain in patients with stroke. 1. Introduction Despite advances in acute management, stroke remains a major cause of disability worldwide [1–6]. A number of neurological functions are impaired by stroke, the most common of which is motor disability contralateral to the stroke lesion side [7]. Therefore, many rehabilitation techniques based on motor learning paradigms have been developed to facilitate the recovery of impaired movement in patients with stroke [3, 8–11]. Neural plasticity can change central nervous system structure and/or function [12–15]. Recently, advances in technologies enabling noninvasive exploration of the human brain have increased our understanding of neural plasticity and its relationship to stroke recovery [9, 12, 16, 17]. Various novel stroke rehabilitative methods for motor recovery have been developed based on basic science and clinical studies characterizing brain remodeling due to neural plasticity [9, 11, 18]. The effectiveness of these approaches has been verified by systematic reviews and meta-analysis studies [8, 19–22]. However, responses to rehabilitative interventions show large inter-individual variation because the mechanisms underlying motor recovery are heterogeneous across patients [3, 8, 11, 23]. Furthermore, these mechanisms involve
Prolonged systemic inflammation persistently modifies synaptic plasticity in the hippocampus: modulation by the stress hormones  [PDF]
Nicola Maggio,Ilan Blatt,Joab Chapman
Frontiers in Molecular Neuroscience , 2013, DOI: 10.3389/fnmol.2013.00046
Abstract: Transient systemic inflammation has been shown to cause altered behavior both in humans and in laboratory animals through activation of microglia and heightened level of cytokines detected in the brain and in the body. Furthermore, both activated microglia and the increased cytokines level have been associated with the sudden clinical deterioration in demented people or in aged patients upon systemic inflammation. Whilst it is increasingly becoming clear the role of transient systemic inflammation in promoting dementia in aged individuals, it is still a matter of debate whether prolonged systemic inflammation might persistently modify the brain. In this study, we examined the influence of a systemic long term inflammatory event on synaptic plasticity. We report that while a short exposure to LPS produces transient deficit in long term potentiation (LTP) expression, systemic prolonged inflammation impairs LTP in slices of animals previously primed by a Complete Freund’s adjuvant injection. Interestingly, steroids are able to modulate this effect: whereas glucocorticosteroid (GR) activation further reduces LTP, mineralocorticosteroid receptors (MR) activation promotes the full recovery of LTP. We believe that this research advances the current understandings on the role of the immune system in the onset and progression of cognitive deficits following long lasting systemic inflammation, and proposes possible insights on future strategies in order to prevent early dementia in these predisposed individuals.
Impact of acute inflammation on spinal motoneuron synaptic plasticity following ventral root avulsion
Roberta Barbizan, Alexandre LR Oliveira
Journal of Neuroinflammation , 2010, DOI: 10.1186/1742-2094-7-29
Abstract: Lewis rats were subjected to unilateral avulsion of lumbar ventral roots (VRA) and divided into three groups: VRA control, VRA at peak of EAE, and VRA during EAE remission. The animals were sacrificed and their lumbar spinal cords processed for immunohistochemistry, transmission electron microscopy, and motoneuron counting.The results indicate a reduction in astroglial reaction, a maintenance of microglial reactivity, and increases in synaptic covering of, and survival of, motoneurons in the VRA+EAE group as compared to VRA alone.The present findings indicate that CNS inflammation may directly influence synaptic plasticity as well as the stability of neuronal networks, positively influencing the survival of lesioned neurons.Traumatic lesions to the spinal cord, which involve neuronal death, convey devastating and permanent loss of function. Alterations also develop in response to the consequent local hemorrhage and ischemia [1]. Among these alterations, upregulation of receptors for neurotrophic factors such as the low affinity neurotrophin receptor p75NTR [2], the high affinity trkB receptor for BDNF [3], and the GFRa-1 receptor for glial derived neurotrophic factor (GDNF) [4], are well established examples. Additionally, upregulation of proteins such as growth associated protein-43 (GAP-43) [5,6] and calcitonin gene-related peptide (CGRP), and down-regulation of receptors and enzymes involved in neurotransmission, including choline acetyltransferase (ChAT) and NMDA receptors [6], may be cited as important responses to injury that are related to a regenerative strategy [5-8] in the cell body.In adults, such a physiological shift is more related to cell repair than to survival [8]. However, lesions close to the surface of the spinal cord may result in extensive degeneration of adult motoneurons, as is the case after avulsion of ventral roots (VRA), an experimental model used to investigate adult neuronal degeneration [6,9,10]. Koliatsos et al. [9] have demonstrated
Inflammation Subverts Hippocampal Synaptic Plasticity in Experimental Multiple Sclerosis  [PDF]
Robert Nisticò, Dalila Mango, Georgia Mandolesi, Sonia Piccinin, Nicola Berretta, Marco Pignatelli, Marco Feligioni, Alessandra Musella, Antonietta Gentile, Francesco Mori, Giorgio Bernardi, Ferdinando Nicoletti, Nicola B. Mercuri, Diego Centonze
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0054666
Abstract: Abnormal use-dependent synaptic plasticity is universally accepted as the main physiological correlate of memory deficits in neurodegenerative disorders. It is unclear whether synaptic plasticity deficits take place during neuroinflammatory diseases, such as multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis (EAE). In EAE mice, we found significant alterations of synaptic plasticity rules in the hippocampus. When compared to control mice, in fact, hippocampal long-term potentiation (LTP) induction was favored over long-term depression (LTD) in EAE, as shown by a significant rightward shift in the frequency–synaptic response function. Notably, LTP induction was also enhanced in hippocampal slices from control mice following interleukin-1β (IL-1β) perfusion, and both EAE and IL-1β inhibited GABAergic spontaneous inhibitory postsynaptic currents (sIPSC) without affecting glutamatergic transmission and AMPA/NMDA ratio. EAE was also associated with selective loss of GABAergic interneurons and with reduced gamma-frequency oscillations in the CA1 region of the hippocampus. Finally, we provided evidence that microglial activation in the EAE hippocampus was associated with IL-1β expression, and hippocampal slices from control mice incubated with activated microglia displayed alterations of GABAergic transmission similar to those seen in EAE brains, through a mechanism dependent on enhanced IL-1β signaling. These data may yield novel insights into the basis of cognitive deficits in EAE and possibly of MS.
The influence of diabetes enhanced inflammation on cell apoptosis and periodontitis  [PDF]
Tie-Lou Chen, Er-Li Xu, Heng Xu, Shi-Feng Wang, Hai-Jun Zhao, Yu-Ming Liu, Hui-Jie Lu
Advances in Bioscience and Biotechnology (ABB) , 2012, DOI: 10.4236/abb.2012.326092
Abstract: Aim: Diabetes mellitus is a metabolic disorder leading to hyperglycemia and exhibiting altered fat and protein metabolism. Diabetes altered cellular microenvironment caused myriad untoward effects. Periodontitis is chronic inflammatory disease. Diabetes and periodontitis had higher prevalence in populations. The objective studied the relationship between diabetes and periodontitis associated with cell apoptosis and the influence of diabetes enhanced inflammation on apoptosis and periodontitis. Methods: This paper studied and analyzed the papers which published in the worldwide associated with the influence of diabetes enhanced inflammation on cell apoptosis and periodontitis, and reviewed the probably mechanism associated with apoptosis. Results: Diabetes induced hyperglycemia enhanced inflammation related to cell apoptosis. Periodontitis had a higher morbidity on diabetes patients. Periodontal intervention may be benefit to controlling the diabetes. The bidirectional efficiency happened between diabetes and periodontitis. Anti-apoptotic and anti-inflammation option can improve the therapeutic effects on diabetes and periodontitis. The finding included following several aspects. 1) Advanced glycation end products enhanced inflammatory response; 2) Hyperglycemia induced cell apoptosis; 3) inflammatory cytokines caused cell apoptosis; 4) Mutuality between cell apoptosis and periodontitis; 5) Diabetes induce periodontitis and bone loss; 6) Periodontitis induced insulin resistance. 7) TNFα induce prostaglandins elicited cell apoptosis; 8) periodontal therapies had effects on diabetes. Conclusion: Diabetes can enhance inflamemation leading to apoptosis and periodontitis. Effective periodontal therapy and control glucose may produce better effects on diabetes or periodontitis. Further research required to investigate the bidirectional mechanism between diabetes and periodontitis.
Poststroke Fatigue: Who Is at Risk for an Increase in Fatigue?  [PDF]
Hanna Maria van Eijsden,Ingrid Gerrie Lambert van de Port,Johanna Maria August Visser-Meily,Gert Kwakkel
Stroke Research and Treatment , 2012, DOI: 10.1155/2012/863978
Abstract: Background. Several studies have examined determinants related to post-stroke fatigue. However, it is unclear which determinants can predict an increase in poststroke fatigue over time. Aim. This prospective cohort study aimed to identify determinants which predict an increase in post-stroke fatigue. Methods. A total of 250 patients with stroke were examined at inpatient rehabilitation discharge (T0) and 24 weeks later (T1). Fatigue was measured using the Fatigue Severity Scale (FSS). An increase in post-stroke fatigue was defined as an increase in the FSS score beyond the 95% limits of the standard error of measurement of the FSS (i.e., 1.41 points) between T0 and T1. Candidate determinants included personal factors, stroke characteristics, physical, cognitive, and emotional functions, and activities and participation and were assessed at T0. Factors predicting an increase in fatigue were identified using forward multivariate logistic regression analysis. Results. The only independent predictor of an increase in post-stroke fatigue was FSS (OR 0.50; 0.38–0.64, ). The model including FSS at baseline correctly predicted 7.9% of the patients who showed increased fatigue at T1. Conclusion. The prognostic model to predict an increase in fatigue after stroke has limited predictive value, but baseline fatigue is the most important independent predictor. Overall, fatigue levels remained stable over time. 1. Introduction A common symptom after stroke is fatigue, with reported frequencies ranging from 38% to 77% [1], indicating that poststroke fatigue is a major problem after stroke. Forty percent of the patients considered fatigue to be one of the worst sequelae of stroke [2]. Patients feel unprepared for the fatigue phenomenon and struggle to adapt to it in daily life [3]. Fatigue has a debilitating influence on activities of daily living [3, 4] and is independently associated with health-related quality of life [4] and the resumption of paid work [5]. Several studies have examined determinants related to poststroke fatigue, but for many determinants there is inconclusive or insufficient evidence [1]. A recent prospective study demonstrated that baseline fatigue was the main predictor of the development of poststroke fatigue over time [6]. Conflicting evidence was found for personal factors such as gender [2, 7–12], age [2, 6–12], and marital status [7, 8]. A few studies found significant results for stroke characteristics, for example, previous stroke [7] and infratentorial infarctions [6, 11]. A strong relationship between depression and poststroke fatigue
Role of miRNAs in CD4 T cell plasticity during inflammation and tolerance  [PDF]
Apoorva Sethi,Neeraja Kulkarni,Sandip Sonar,Girdhari Lal
Frontiers in Genetics , 2013, DOI: 10.3389/fgene.2013.00008
Abstract: Gene expression is tightly regulated in a tuneable, cell-specific and time-dependent manner. Recent advancement in epigenetics and non-coding RNA (ncRNA) revolutionized the concept of gene regulation. In order to regulate the transcription, ncRNA can promptly response to the extracellular signals as compared to transcription factors present in the cells. microRNAs (miRNAs) are ncRNA (~22 bp) encoded in the genome, and present as intergenic or oriented antisense to neighboring genes. The strategic location of miRNA in coding genes helps in the coupled regulation of its expression with host genes. miRNA together with complex machinery called RNA-induced silencing complex (RISC) interacts with target mRNA and degrade the mRNA or inhibits the translation. CD4 T cells play an important role in the generation and maintenance of inflammation and tolerance. Cytokines and chemokines present in the inflamed microenvironment controls the differentiation and function of various subsets of CD4 T cells [Th1, Th2, Th17, and regulatory CD4 T cells (Tregs)]. Recent studies suggest that miRNAs play an important role in the development and function of all subsets of CD4 T cells. In current review, we focused on how various miRNAs are regulated by cell's extrinsic and intrinsic signaling, and how miRNAs affect the transdifferentiation of subsets of CD4 T cell and controls their plasticity during inflammation and tolerance.
Influence of Inflammation to Lymphangiogenesis in Human Dental Pulp
Dragica Da?i? Simonovi?,Ljubinka Veli?kovi? Jankovi?,Stefan Da?i?,Ana Risti? Petrovi?
Acta Facultatis Medicae Naissensis , 2013, DOI: 10.2478/v10283-012-0031-5
Abstract: During inflammation, lymphangiogenesis takes place to enhance the transport of filtered fluid, proteins, and immune cells. Dental pulp tissue is frequently exposed to inflammatory insults, but the lymphatic system of the pulp and its responses to injury have not been investigated in detail using specific lymphatic markers. The aim of this study was to evaluate and to compare the lymphatic system in health dental pulp and pulp with inflammation, and to establish whether lymphangiogenesis takes place during dental pulp inflammation.Ten pulps with irreversibile pulpitis and eleven samples of healthy dental pulps were included in this study. All pulp samples were analyzed microscopically using the standard hematoxylin-eosin (HE) staining to detect the presence of inflammation. Immunohistochemical staining was performed using monoclonal anti-CD31 antibody (DAKO) at dilution 1:20. Microvessels identified by CD31, in which lumen the red blood cells were not detected, were considered as lymph vessels. Active areas of lymphangiogenesis (“hot spots”) were selected using low magnification. Images from five high power fields in the hot spot areas were recorded for each sample. Lymph vessels were counted using ImageJ program. The total number of lymph vessels so obtained was then divided by the number of the counted hot spots, and the result was used to denote the lymph vessel density.The mean number of lymphatic vessels, detected by CD31, in the group without inflammation was significantly lower than in the group with inflammation (3.75 versus 13.58, t=7.093, p<0.001).The present study established an increased number of lymphatic vessels in the inflamed human dental pulp suggesting that inflammation contributes to lymphangiogenesis.
Late Onset Poststroke Seizures  [cached]
Ba?ak Karakurum G?KSEL,Mehmet KARATA?,Meliha TAN,,Tülin YILDIRIM
Journal of Neurological Sciences , 2005,
Abstract: The most common cause of seizures is cerebrovascular disease in elderly population. Late onset seizures are not investigated as well as early onset seizures in patients with stroke. There is no common consensus about clinical, electrophysiological and radiological features of these seizures. In this study, 55 patients with late onset seizure who had stroke history were investigated. The 49 % of patients were women, the mean ages of patients were 63.9±9.2 years. The mean of duration between stroke and the first seizure was 30.4±36.8 months and the mean of following time was 14±13 months. The 89% of patients ischemic stroke and 11% of patients had hemorrhagic stroke. The lesion localizations were cortical in 17 (30.9%) patients, subcortical in 8 (14.5%) and cortico-subcortical in 29 (52.7%). As a result 84 % patients’ lesions were cortical localization. There were partial seizure in 39 (%70.9) patients, generalized tonic-clonic seizure in 16 (29.1%) patients. 43 (78%) patients had no seizure during antiepileptic therapy. 7 (12.7%) patients had seizure after beginning antiepileptic drug due to stopping drug, low blood level of drug and ineffectiveness of drug. 5 (9%) patients had not been given drug because of first seizure and no seizure during follow-up. In conclusion, the late onset poststroke seizures seem frequently in ischemic stroke, the reccurence rate was high and partial type seizures were more common than generalized and cortical localization was seen frequently. On the other hand, this condition has good prognosis.
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