819 resultados para age-related


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Prostatic diseases have been a common problem in middle age and older intact male dogs. Among these, benign prostatic hyperplasia (BHP) is the most frequent, age-related and hormonal-dependent condition of human and canine prostate. Blood samples were collected from 37 male intact dogs, tree years old dogs or more to determine androgens, estrogen, prostatic acid phosphatase (PAP) and prostatic specific antigen (PSA) according to histopathological aspects. Low levels of estrogen and high levels of prostatic specific antigen (PSA) were founded in dogs with BHP, respectively. Seric and urinary PAP levels were high in dogs with hyperplasia.

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Aging is associated with decline in muscle mass and strength and reduced bone density. Age-related bone loss is a primary factor in osteoporosis and all individuals are potential candidates for osteoporosis because bone loss with aging occurs in men and women, but less studied in men. To examine the appropriateness of hindlimb elevation, by tail suspension as a model for diminished mechanical loading, and to determine the influence of age on bone responsiveness to skeletal unloading, we use dual X ray absorptiometry (DXA) and digital radiographic images to analyze the response of the femur from mature rats to biomechanical loads. Femurs from male Wistar rats (9-mo-old) were scanned using DXA and DIGORA and measures obtained in ephipyseal and diaphyseal regions of interest. The mechanical testing was divided into compression load to fracture the head and a three-point bending load to fracture the femur middiaphysis. In femoral epiphysis from hindlimb unload (HU), animals presented significant differences between mineral bone content and density assessed by DXA. Detailed regions of femoral epiphysis (head, throcanteric fossa, throcanter and metaphysis) presented significant lower values from radiographic density. Only compressive load necessary to fracture the femoral head neck was also significantly diminished in HU animals. Disuse induced, as in elderly patients, deterioration of the trabecular bone architecture with critical effect on bone fragility. Rats with 21 days of hindlimb unloading can simulate disuse, suggesting that certain sub-regions of their aging bones are more susceptible to fracture, while other, i.e. diaphyses, are not.

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West syndrome is a severe epilepsy, occurring in infancy, that comprises epileptic seizures known as spasms, in clusters, and a unique EEG pattern, hypsarrhythmia, with psychomotor regression. Maturation of the brain is a crucial component. The onset is within the first year of life, before 12 months of age. Patients are classified as cryptogenic (10 to 20%), when there are no known or diagnosed previous cerebral insults, and symptomatic (80 to 90%), when associated with pre-existing cerebral damages. The time interval from a brain insult to infantile spasms onset ranged from 6 weeks to 11 months. West syndrome has a time-limited natural evolutive course, usually disappearing by 3 or 4 years of age. In 62% of patients, there are transitions to another age-related epileptic encephalopathies, the Lennox-Gastaut Syndrome and severe epilepsy with multiple independent foci. Spontaneous remission and remission after viral infections may occur. Therapy with ACTH and corticosteroids are the most effective. Reports about intravenous immunoglobulins action deserve attention. There is also immune dysfunction, characterized mainly by anergy, impaired cell-mediated immunity, presence of immature thymocytes in peripheral blood, functional impairment of T lymphocytes induced by plasma inhibitory factors, and altered levels of immunoglobulins. Changes in B lymphocytes frequencies and increased levels of activated B cells have been reported. Sensitized lymphocytes to brain extract were also described. Infectious diseases are frequent and may, sometimes, cause fatal outcomes. Increase of pro-inflamatory cytokines in serum and cerebrospinal fluid of epileptic patients were reported. Association with specific HLA antigens was described by several authors (HLA-DR7, HLA-A7, HLA-DRw52, and HLA-DR5). Auto-antibodies to brain antigens, of several natures (N-methyl-d-aspartate glutamate receptor, gangliosides, brain tissue extract, synaptic membrane, and others), were described in epileptic patients and in epileptic syndromes. Experimental epilepsy studies with anti-brain antibodies demonstrated that epileptiform discharges can be obtained, producing hyperexcitability leading to epilepsy. We speculate that in genetically prone individuals, previous cerebral lesions may sensitize immune system and trigger an autoimmune disease. Antibody to brain antigens may be responsible for impairment of T cell function, due to plasma inhibitory effect and also cause epilepsy in immature brains. © 2008 Bentham Science Publishers Ltd.

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Includes bibliography

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Includes Bibliography

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BACKGROUND: Age-related loss in lower limb strength is related with impaired mobility. However, the association between decreased lower limb strength and gait biomechanical abnormalities is unclear. %In line with this, With respect to these statements, our study aimed to compare the maximum isokinetic voluntary strength (MIVS) of hip, knee and ankle of older women with and without history of falls. Also, we correlate the strength of each group with gait biomechanics. METHODS: The MIVS were assessed during concentric/concentric movements performed for hip, knee and ankle joints. Gait biomechanics (kinematic and electromyography) were assessed during 1-minute recorded during the volunteers walking on the treadmill at self-selected speed. Electromyographic signal was analyzed by the linear envelop after heel strike and before toe-off. The kinematic data were analyzed using the variables: step time, length and step width and ankle angle at heel strike, and hip angle at toe-off. RESULTS: In faller group, we found that a decreased hip abduction and adduction MIVS is associated with a higher tibialis anterior activation at initial stance (p =0.04 and r =-0.53 and p=0.04 and r=-0.52). CONCLUSION: Therefore, an impaired strength of hip could causes compensation in ankle stabilizer muscles activation at initial stance in older female fallers. © 2013 - IOS Press and the authors. All rights reserved.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Pós-graduação em Ciências da Motricidade - IBRC

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Pós-graduação em Alimentos e Nutrição - FCFAR

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Pós-graduação em Medicina Veterinária - FMVZ

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The accumulation of somatic mutations in mtDNA is correlated with aging. In this work, we sought to identify somatic mutations in the HVS-1 region (D-loop) of mtDNA that might be associated with aging. For this, we compared 31 grandmothers (mean age: 63 ± 2.3 years) and their 62 grandchildren (mean age: 15 ± 4.1 years), the offspring of their daughters. Direct DNA sequencing showed that mutations absent in the grandchildren were detected in a presumably homoplasmic state in three grandmothers and in a heteroplasmic state in an additional 13 grandmothers; no mutations were detected in the remaining 15 grandmothers. However, cloning followed by DNA sequencing in 12 grandmothers confirmed homoplasia in only one of the three mutations previously considered to be homoplasmic and did not confirm heteroplasmy in three out of nine grandmothers found to be heteroplasmic by direct sequencing. Thus, of 12 grandmothers in whom mtDNA was analyzed by cloning, eight were heteroplasmic for mutations not detected in their grandchildren. In this study, the use of genetically related subjects allowed us to demonstrate the occurrence of age-related (> 60 years old) mutations (homoplasia and heteroplasmy). It is possible that both of these situations (homoplasia and heteroplasmy) were a long-term consequence of mitochondrial oxidative phosphorylation that can lead to the accumulation of mtDNA mutations throughout life.