Impacto de um programa de fortalecimento muscular dos membros inferiores no equilíbrio e na performance funcional de idosos institucionalizados: um estudo controlado e randomizado

Functional performance is maximized through muscle strengthening programs in the elderly. However, few interventions have been implemented in institutionalized elderly to assess the effects of muscle strengthening exercise programs in outcomes such as balance, functional performance and muscle strength. Objective: Assess the impact of a lower limb muscle strengthening program at the balance, functional performance and muscle strength of institutionalized elderly. Methods: Controlled, randomized clinical trial. Balance, functional performance and muscle strength were assessed using the Berg Balance Scale (BSE), Tandem Gait (MT), Short Physical Performance Battery (SPPB) and Sphygmomanometer Test (TE) respectively. The experimental group (GE, n = 11) participated in the group exercise program, three times a week, for eight weeks, while the control group (CG, n = 8) continued their usual routine.The intervals of 95% confidence for the differences between the experimental and control groups (experimental - control) and between the two moments of observation (post - pre). Intent to treat analysis was performed. Results: EG showed a significant gain in relation to CG for BSE (DM = 3.7 IC95% 1.0 to 6.5), MT DM = 3.5 IC95% 0.7 to 6.2), FMEJ (DM = 33.2 95% CI 4.9 to 61.5) and FMD (DM = 37.5 95% CI 9.6 to 65.3). Conclusion: The muscle strengthening program was able to improve balance, functional performance and muscle strength in institutionalized elderly.A performance funcional é maximizada através de programas de fortalecimento muscular em idosos. Contudo, poucas intervenções foram implementadas em idosos institucionalizados para avaliar os efeitos de programas de exercícios de fortalecimento muscular em desfechos como o equilíbrio, performance funcional e força muscular. Objetivo: Avaliar o impacto de um programa de fortalecimento muscular de membros inferiores no equilíbrio, performance funcional e força muscular de idosos institucionalizados. Métodos: Ensaio clínico controlado e randomizado. O equilíbrio, a performance funcional e a força muscular foram avaliados através da Escala de Equilíbrio de Berg (EEB), Marcha Tandem (MT), Short Physical Performance Battery (SPPB) e Teste do Esfigmomanômetro (TE), respectivamente. O grupo experimental (GE, n=11) participou do programa de exercícios em grupo, três vezes semanais, durante oito semanas, enquanto o grupo controle (GC, n=8) continuou sua rotina habitual. Foram calculados os intervalos de 95% de confiança para as diferenças entre os grupos experimental e controle (experimental – controle) e entre os dois momentos de observação (pós – pré). Foi realizada análise de intenção de tratar. Resultados: O GE apresentou um ganho significativo em relação ao GC para a EEB (DM=3,7 IC95% 1,0 a 6,5), MT DM=3,5 IC95% 0,7 a 6,2), FMEJ (DM=33,2 IC95% 4,9 a 61,5) e FMD (DM=37,5 IC95% 9,6 a 65,3). Conclusão: O programa de fortalecimento muscular foi capaz de melhorar o equilíbrio, a performance funcional e a força muscular em idosos institucionalizados

Vesicular acetylcholine transporter knock down-mice are more susceptible to inflammation, c-Fos expression and sickness behavior induced by lipopolysaccharide.

In addition to the well-known functions as a neurotransmitter, acetylcholine (ACh) can modulate of the immune system. Nonetheless, how endogenous ACh release inflammatory responses is still not clear. To address this question, we took advantage of an animal model with a decreased ACh release due a reduction (knockdown) in vesicular acetylcholine transporter (VAChT) expression (VAChT-KD(HOM)). These animals were challenged with lipopolysaccharide (LPS). Afterwards, we evaluated sickness behavior and quantified systemic and cerebral inflammation as well as neuronal activation in the dorsal vagal complex (DVC). VAChT-KD(HOM) mice that were injected with LPS (10mg/kg) showed increased mortality rate as compared to control mice. In line with this result, a low dose of LPS (0.1mg/kg) increased the levels of pro-inflammatory (TNF-α, IL-1β, and IL-6) and anti-inflammatory (IL-10) cytokines in the spleen and brain of VAChT-KD(HOM) mice in comparison with controls. Similarly, serum levels of TNF-α and IL-6 were increased in VAChT-KD(HOM) mice. This excessive cytokine production was completely prevented by administration of a nicotinic receptor agonist (0.4mg/kg) prior to the LPS injection. Three hours after the LPS injection, c-Fos expression increased in the DVC region of VAChT-KD(HOM) mice compared to controls. In addition, VAChT-KD(HOM) mice showed behavioral changes such as lowered locomotor and exploratory activity and reduced social interaction after the LPS challenge, when compared to control mice. Taken together, our results show that the decreased ability to release ACh exacerbates systemic and cerebral inflammation and promotes neural activation and behavioral changes induced by LPS. In conclusion, our findings support the notion that activity of cholinergic pathways, which can be modulated by VAChT expression, controls inflammatory and neural responses to LPS challenge

Plasmodium berghei NK65 induces cerebral leukocyte recruitment in vivo: An intravital microscopic study.

Submitted by Nuzia Santos ([email protected]) on 2014-11-10T12:51:05Z No. of bitstreams: 1 Plasmodium berghei NK65 induces cerebral leukocyte recruitment in vivo.pdf: 1598176 bytes, checksum: 25e9eb15e4c6831e3a3328dec6b0c4bb (MD5)Approved for entry into archive by Nuzia Santos ([email protected]) on 2014-11-10T13:15:46Z (GMT) No. of bitstreams: 1 Plasmodium berghei NK65 induces cerebral leukocyte recruitment in vivo.pdf: 1598176 bytes, checksum: 25e9eb15e4c6831e3a3328dec6b0c4bb (MD5)Made available in DSpace on 2014-11-10T13:15:46Z (GMT). No. of bitstreams: 1 Plasmodium berghei NK65 induces cerebral leukocyte recruitment in vivo.pdf: 1598176 bytes, checksum: 25e9eb15e4c6831e3a3328dec6b0c4bb (MD5) Previous issue date: 2011Universidade Federal de Minas Gerais Departamento de Parasitologia. Belo Horizonte, MG, Brazil/Universidade Federal de Minas Gerais. Departamento de Fisiologia e Biofísica. Núcleo de Neurociências. Belo Horizonte, MG, BrazilUniversidade Federal de Minas Gerais. Departamento de Fisiologia e Biofísica. Núcleo de Neurociências. Belo Horizonte, MG, BrazilUniversidade Federal de Ouro Preto. Núcleo de Pesquisas em Ciências Biológicas. Escola de Farmácia. Departamento de Análises Clínicas. Laboratório de Imunopatologia. Ouro Preto, MG, BrazilUniversidade Federal de Minas Gerais. Instituto de Ciências Biológicas. Departamento de Bioquímica e Imunologia. Laboratório de Imunofarmacologia. Belo Horizonte, MG, BrazilUniversidade Federal de Minas Gerais. Faculdade de Medicina. Departamento de Clínica Médica. Belo Horizonte, MG, BrazilFundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Biomarcadores de Diagnóstico e Monitoração. Belo Horizonte, MG, Brazil. Minas Gerais, BrazilFundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Biomarcadores de Diagnóstico e Monitoração. Belo Horizonte, MG, Brazil. Minas Gerais, BrazilFundação Oswaldo Cruz. Centro de Pesquisas René Rachou. Laboratório de Biomarcadores de Diagnóstico e Monitoração. Belo Horizonte, MG, Brazil. Minas Gerais, BrazilUniversidade Federal de Minas Gerais Departamento de Parasitologia. Belo Horizonte, MG, BrazilUniversidade Federal de Minas Gerais. Departamento de Fisiologia e Biofísica. Núcleo de Neurociências. Belo Horizonte, MG, BrazilMalaria is second only to tuberculosis as the leading cause of morbidity and mortality as a consequence of a single infectious agent. Much of the pathology of malaria arises from the inappropriate or excessive immune response mounted by the host in an attempt to eliminate the parasite. We here report the inflammatory changes observed in the cerebral microvasculature of C57BL/6 and BALB/c mice that had been inoculated with Plasmodium berghei NK65, a lethal strain of rodent malaria. Although no neurological signs were observed in experimentally infected mice, inflammation of the cerebral microvasculature was clearly evident. Histopathological analysis demonstrated that alterations in cerebral tissue were more intense in infected C57Bl/6 mice than in infected BALB/c animals. Intravital microscopic examination of the cerebral microvasculature revealed increased leukocyte rolling and adhesion in pial venules of infected mice compared with non-infected animals. The extravasation of Evans blue dye into the cerebral parenchyma was also elevated in infected mice in comparison with their non-infected counterparts. Additionally, protein levels of TNF-α, MIG/CXCL9, MCP-1/CCL2, MIP-1α/CCL3 and RANTES/CCL5 were up-regulated in brain samples derived from infected C57Bl/6 mice. Taken together, the data reported here illustrate the complex strain-dependent relationships between leukocyte recruitment, blood brain barrier permeability and chemokine production

The Role of Astrocytes in the Neurorepair Process

Astrocytes are highly specialized glial cells responsible for trophic and metabolic support of neurons. They are associated to ionic homeostasis, the regulation of cerebral blood flow and metabolism, the modulation of synaptic activity by capturing and recycle of neurotransmitters and maintenance of the blood-brain barrier. During injuries and infections, astrocytes act in cerebral defense through heterogeneous and progressive changes in their gene expression, morphology, proliferative capacity, and function, which is known as reactive astrocytes. Thus, reactive astrocytes release several signaling molecules that modulates and contributes to the defense against injuries and infection in the central nervous system. Therefore, deciphering the complex signaling pathways of reactive astrocytes after brain damage can contribute to the neuroinflammation control and reveal new molecular targets to stimulate neurorepair process. In this review, we present the current knowledge about the role of astrocytes in brain damage and repair, highlighting the cellular and molecular bases involved in synaptogenesis and neurogenesis. In addition, we present new approaches to modulate the astrocytic activity and potentiates the neurorepair process after brain damage.publishe

Plasmodium berghei NK65 induces cerebral leukocyte recruitment in vivo: An intravital microscopic study

Malaria is second only to tuberculosis as the leading cause of morbidity and mortality as a consequence of a single infectious agent. Much of the pathology of malaria arises from the inappropriate or excessive immune response mounted by the host in an attempt to eliminate the parasite. We here report the inflammatory changes observed in the cerebral microvasculature of C57BL/6 and BALB/c mice that had been inoculated with Plasmodium berghei NK65, a lethal strain of rodent malaria. Although no neurological signs were observed in experimentally infected mice, inflammation of the cerebral microvasculature was clearly evident. Histopathological analysis demonstrated that alterations in cerebral tissue were more intense in infected C57Bl/6 mice than in infected BALB/c animals. Intravital microscopic examination of the cerebral microvasculature revealed increased leukocyte rolling and adhesion in pial venules of infected mice compared with non-infected animals. The extravasation of Evans blue dye into the cerebral parenchyma was also elevated in infected mice in comparison with their non-infected counterparts. Additionally, protein levels of TNF-α, MIG/CXCL9, MCP-1/CCL2, MIP-1α/CCL3 and RANTES/CCL5 were up-regulated in brain samples derived from infected C57Bl/6 mice. Taken together, the data reported here illustrate the complex strain-dependent relationships between leukocyte recruitment, blood brain barrier permeability and chemokine production