935 resultados para TESTICULAR ATROPHY
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The aim of this tudy was to evaluate corporal and testicular development in wild boars (Sus scrofa scrofa) from birth to 12 months of age, evaluating body weight, biometric testicular parameters, and gonadosomatic index. Thirty-nine male wild boars from a commercial farm licensed by IBAMA were used in the study. The animals were weighed and assigned to 13 experimental groups. The testes were recovered through unilateral orchiectomy, weighed on an analytical balance and measured for length, width and thickness. Body weight and testicular measures increased with the age, up to 12 months, and were more accelerated in the first and ninth months. Initially the testicular growth pattern, between zero and nine months, followed the body growth, and the gonadosomatic index varied from 0.07 to 0.09%. Between 9 and 11 months, the testicular growth was superior to the body growth, and the gonadosomatic index varied from 0.09 to 0.16%. Finally, after 11 months of age, testicular and body growth had a similar behavior. In conclusion, body weight, testicular biometry, and gonadosomatic index development accelerated in the ninth month.
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Pós-graduação em Ciência e Tecnologia Animal - FEIS
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Dissertação de Mestrado em Ambiente, Saúde e Segurança.
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A displasia quística testicular é uma patologia benigna e rara, frequentemente associada a outras anomalias génito-urinárias, que se apresenta na infância sobretudo com aumento do volume escrotal, fazendo diagnóstico diferencial com situações neoplásicas e inflamatórias do testículo. Embora classicamente considerada indicação para orquidectomia, não parece haver qualquer potencial maligno, pelo que se pode argumentar uma abordagem conservadora. No entanto é importante confirmar o diagnóstico e manter vigilância para precaver a atrofia do parênquima testicular. Os autores apresentam o caso clínico de um doente com antecedentes de agenésia renal esquerda e megauretero obstructivo direito, submetido a orquidectomia no contexto de displasia quística testicular esquerda com atrofia importante do parênquima.
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AbstractDespite its infrequent occurrence, testicular schistosomiasis forming pseudo-tumors can be considered in the differential diagnosis of testicular tumors, especially in areas where the parasitic disease is endemic. In this report, we present a case of testicular schistosomiasis caused by Schistosoma mansoni and mimicking a testicular neoplasm. We describe the patterns of a testicular nodule on ultrasonography and magnetic resonance images in a 46-year-old man. The nodule was removed after a pre-operative diagnosis of a non-malignant lesion. Histology demonstrated granulomas with epithelioid macrophages and eosinophils around S. mansoni eggs within a fibrous tissue that formed a nodular structure.
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PURPOSE: Infertility is one of the less common presenting features associated with testicular tumors. We evaluated the histologic and biochemical findings, and pregnancy outcome in patients presenting with infertility who were found to have testicular tumors. METHODS: Seven patients with infertility were found to have testicular cancer over a 15-year period. All patients had a testicular ultrasound evaluation. The indications for the ultrasound were testicular pain in 2 patients, suspicious palpable mass in 4, and to rule out the presence of germ cell neoplasia in a patient with carcinoma in situ detected on a previous biopsy. Physical exam, histological findings, hormonal levels, tumor markers, and pregnancy outcome results were recorded from the patients medical charts. RESULTS: Two men had elevated serum follicle stimulant hormone and luteinizing hormone levels, 1 of them had an abnormally low serum testosterone level. Tumor markers were normal in all patients. In 4 patients the tumor was on the right side and in 3 on the left. The histological diagnoses were seminoma (n = 5), Leydig cell tumor (n = 1), and carcinoma in situ (n = 1). Of the 7 patients, 5 underwent adjuvant radiation therapy. Two patients had sperm cryopreserved. Follow up on fertility status was available in 6 cases. One patient has established a pregnancy and 5 did not achieve a pregnancy after treatment for their cancer. CONCLUSIONS: Most of the men who have testicular cancer and male infertility have a seminona. Therefore, men who present with infertility should be thoroughly investigated to rule out such serious, concomitant diseases along with their infertility.
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Estudos relacionados à obtenção e avaliação de sêmen de Tayassu tajacu são escassos, sendo necessárias pesquisas a respeito. Os objetivos do estudo foram avaliar a biometria testicular de caititus adultos cativos, testar a eficiência da eletroejaculação para obtenção de sêmen e avaliar suas características seminais ao longo do ano. Procedeu-se à eletroejaculação em oito animais adultos e as amostras de sêmen colhidas foram avaliadas quanto às características físicas e morfológicas. Os animais tinham testículo esquerdo com 3,8 ± 0,4 cm X 2,6 ± 0,3 cm e 2,3 ± 0,2 de consistência, e testículo direito com 3,8 ± 0,5 cm X 2,7 ± 0,3 cm e 2,3 ± 0,2 de consistência. A taxa de sucesso nas colheitas foi de 75,21%. O sêmen possuiu: volume 0,81 ± 0,86 mL, concentração 137,44 ± 153 x 106 sptz mL-1, pH 7,92 ± 0,73, motilidade 52,66 ± 28,79%, vigor 2,2 ± 0,8, integridade de membrana plasmática 55,84 ± 28,55%, defeitos maiores 22,87 ± 12,93%, defeitos menores 9,11 ± 5,88% e defeitos totais 31,52 ± 13,81%. Os animais apresentaram simetria testicular, a eletroejaculação se mostrou eficiente para a obtenção de ejaculados em caititus e as flutuações observadas na produção seminal não foram suficientes para caracterizá-los como animais de reprodução sazonal.
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En el presente trabajo se describen las características morfohistológicas del testículo de individuos adultos (n=5) de Ceratophrys ornata (Bell, 1843) provenientes de humedales del centro de Argentina. Los mismos se procesaron mediante técnicas histológicas de rutina, se cortaron a 8 µm y las láminas obtenidas se tiñeron con hematoxilina-eosina y tricrómico de Masson. Las gónadas son órganos pares, amarillentos, alargados y contorneados de 18,58 ± 0,23 mm de largo por 1,51 ± 0,13 mm de ancho. Histológicamente se observa una delgada túnica albugínea (6,29 ± 0,83 µm) rodeando a los testículos. En su interior se hallan lóculos seminíferos que miden 240,64 ± 38,52 µm de diámetro, en ellos se distinguen cistos con células espermatogénicas en distintas etapas de desarrollo. El tejido intersticial es escaso y en él se destacan las células de Leydig y vasos sanguíneos. Las espermatogonias I son las células más grandes de la serie germinal (20,03 ± 2,27 µm); poseen la cromatina granular y de aspecto multilobular, hallándose comúnmente una por cisto, estas originan a las espermatogonias II, más pequeñas (12,06 ± 1,14 µm). Los espermatocitos I presentan la cromatina levemente condensada y son un poco más chicos que sus precedentes (11,64 ± 0,36 µm). Los espermatocitos II miden 8,85 ± 0,54 µm. Las espermátidas I son esféricas, miden 5,95 ± 0,42 µm y se agrupan en cistos redondeados. Las espermátidas II, en cambio son alargadas y no se hallan dentro de cistos, pero siguen organizadas en paquetes asociadas a células de Sertoli. Los espermatozoides son células libres hacia el centro del lóculo, alargadas, flageladas y con una notable compactación nuclear. La morfohistología de los testículos analizados muestran características macroscópicas e histológicas similares a las observadas en otras especies de anfibios anuros neotropicales, presentando todas las células del linaje espermatogénico en un mismo lóculo, lo que indicaría que presentan ciclos espermatogénicos continuos.
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The authors summarize the results of former works, based on the technics of parabiosis. After parabiotic union of two infantile rats, normal + castrate, the normal fellow enters into precocious puberty in about 7 days (Kallas). In the case of pairs: castrated male + normal female, the implants of testicles, or injection of maceration or aqueous extracts of testis in the castrated fellow, prevents the induction of early puberty in the normal female. In the case: castrated female + normal female, no inhibiting effect is provoked by that treatment. There is therefore a testicular hormone that regulates the hypophysis. After castration, this gland manifests a hyper-function and shows histological alterations, the chief character of these being the appearing in the anterior lobe, of the so-called castration cells, probably originated from basophile cells. Implants or injections of testis material prevent those alterations. This is a useful test; the effect is controlled by estimating the castration cells in the microscopic field. The testicular hormone that regulates the anterior lobe is probably another one, quite different from that which regulates the accessory genitalia. On account of the facts and experiments, it may be assumed that this new hormone is elaborated by the germinal epithelium of the testicles.
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Abstract : The term "muscle disuse" is often used to refer collectively to reductions in neuromuscular activity as observed with sedentary lifestyles, reduced weight bearing, cancer, chronic obstructive pulmonary disease, chronic heart failure, spinal cord injury, sarcopenia or exposure to microgravity (spaceflight). Muscle disuse atrophy, caused by accelerated proteolysis, is predominantly due to the activation of the ATP-dependent ubiquitin (Ub) proteasome pathway. The current advances in understanding the molecular factors contributing to the Ub-dependent proteolysis process have been made mostly in rodent models of human disease and denervation with few investigations performed directly in humans. Recently, in mice, the genes Atrogin-1 and MuRF1 have been designated as primary candidates in the control of muscle atrophy. Additionally, the decreased activity of the Akt/GSK-3ß and Akt/mTOR pathways has been associated with a reduction in protein synthesis and contributing to skeletal muscle atrophy. Therefore, it is now commonly accepted that skeletal muscle atrophy is the result of a decreased protein synthesis concomitant with an increase in protein degradation (Glass 2003). Atrogin-1 and MuRF1 are genes expressed exclusively in muscle. In mice, their expression has been shown to be directly correlated with the severity of atrophy. KO-mice experiments showed a major protection against atrophy when either of these genes were deleted. Skeletal muscle hypertrophy is an important function in normal postnatal development and in the adaptive response to exercise. It has been shown, in vitro, that the activation of phosphatidylinositol 3-kinase (PI-3K), by insulin growth factor 1 (IGF-1), stimulates myotubes hypertrophy by activating the downstream pathways, Akt/GSK-3ß and Akt/mTOR. It has also been demonstrated in mice, in vivo, that activation of these signalling pathways causes muscle hypertrophy. Moreover, the latter were recently proposed to also reduce muscle atrophy by inhibiting the FKHR mediated transcription of several muscle atrophy genes; Atrogin-1 and MuRF1. Therefore, these targets present new avenues for developing further the understanding of the molecular mechanisms involved in both skeletal muscle atrophy and hypertrophy. The present study proposed to investigate the regulation of the Akt/GSK-3ß and Akt/mTOR signalling pathways, as well as the expression levels of the "atrogenes", Atrogin-1 and MuRF1, in four human models of skeletal muscle atrophy. In the first study, we measured the regulation of the Akt signalling pathway after 8 weeks of both hypertrophy stimulating resistance training and atrophy stimulation de-training. As expected following resistance training, muscle hypertrophy and an increase in the phosphorylation status of the different members of the Akt pathway was observed. This was paralleled by a concomitant decrease in FOXO1 nuclear protein content. Surprisingly, exercise training also induced an increase in the, expression of the atrophy genes and proteins involved in the ATP-dependant ubiquitin-proteasome system. On the opposite, following the de-training period a muscle atrophy, relative to the post-training muscle size, was measured. At the same time, the phosphorylation levels of Akt and GSK-3ß were reduced while the amount of FOXO1 in the nucleus increased. After the atrophy phase, there was also a reduction in Atrogin-1 and MuRF1 contents. In this study, we demonstrate for the first time in healthy human skeletal muscle, that the regulation of Akt and its downstream targets GSK-3ß, mTOR and FOXO1 are associated with both thé skeletal muscle hypertrophy and atrophy processes. Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by the loss of both upper and lower motor neurons, which leads to severe muscle weakness and atrophy. All measurements were performed in biopsies from 22 ALS patients and 16 healthy controls. ALS patients displayed an increase in Atrogin-1 mRNA and protein content which was associated with a decrease in Akt activity. However there was no difference in the mRNA and phospho-protein content of FOXO1, FOXO3a, p70S6K and GSK-3ß. The transcriptional regulation of human Atrogin-1 may be controlled by an Akt-mediated transcription factor other than FKHR or via an other signalling pathway. Chronic complete spinal cord injury (SCI) is associated with severe muscle atrophy which is linked to co-morbidity factors such as diabetes, obesity, lipid disorders and cardiovascular diseases. Molecular mechanisms associated with chronic complete SCI-related muscle atrophy are not well understood. The aim of the present study was to determine if there was an increase in catabolic signalling targets such as Atrogin-1, MuRF1, FOXO and myostatin, and decreases in anabolic signalling targets such as IGF, Akt, GSK-3ß, mTOR, 4E-BP1 and p-70S6K in chronic complete SCI patients. All measurements were performed in biopsies taken from 8 complete chronic SCI patients and 7 age matched healthy controls. In SCI patients when compared with controls, there was a significant reduction in mRNA levels of Atrogin1, MuRF1 and Myostatin. Protein levels for Atrogin-1, FOX01 and FOX03a were also reduced. IGF-1 and both phosphorylated GSK-3ß and 4E-BP1 were decreased; the latter two in an Akt and mTOR independent manner, respectively. Reductions in Atrogin-1, MuRF1, FOXO and myostatin suggest the existence of an internal mechanism aimed at reducing further loss of muscle proteins during chronic SCI. The downregulation of signalling proteins regulating anabolism such as IGF, GSK3ß and 4E-BP1 would reduce the ability to increase protein synthesis rates in this chronic state of muscle wasting. The molecular mechanisms controlling age-related skeletal muscle loss in humans are poorly understood. The present study aimed to investigate the regulation of several genes and proteins involved in the activation of key signalling pathways promoting muscle hypertrophy such as GH/STAT5/IGF, IGF/Akt/GSK-3ß/4E-BP1 and muscle atrophy such as TNFα/SOCS3 and Akt/FOXO/Atrogin-1 or MuRF1 in muscle biopsies from 13 young and 16 elderly men. In the older, as compared with the young subjects, TNFα and SOCS-3 were increased while growth hormone receptor protein (GHR) and IGF-1 mRNA were both decreased. Akt protein levels were increased however no change in phosphorylated Akt content was observed. GSK-3ß phosphorylation levels were increased while 4E-BP1 was not changed. Nuclear FKHR and FKHRL1 protein levels were decreased, with no changes in their atrophy target genes, Atrogin-1 and MuRF1. Myostatin mRNA and protein levels were significantly elevated. Human sarcopenia may be linked to a reduction in the activity or sensitivity of anabolic signalling proteins such as GHR, IGF and Akt. TNFα, SOCS-3 and myostatin are potential candidates influencing this anabolic perturbation. In conclusion our results support those obtained in rodent or ín vitro models, and demonstrate Akt plays a pivotal role in the control of muscle mass in humans. However, the Akt phosphorylation status was dependant upon the model of muscle atrophy as Akt phosphorylation was reduced in all atrophy models except for SCI. Additionally, the activity pattern of the downstream targets of Akt appears to be different upon the various human models. It seems that under particular conditions such as spinal cord injury or sarcopenia, .the regulation of GSK-3ß, 4eBP1 and p70S6K might be independent of Akt suggesting alternative signalling pathways in the control of these the anabolic response in human skeletal muscle. The regulation of Atrogin-1 and MuRF1 in some of our studies has been shown to be also independent of the well-described Akt/FOXO signalling pathway suggesting that other transcription factors may regulate human Atrogin-1 and MuRF1. These four different models of skeletal muscle atrophy and hypertrophy have brought a better understanding concerning the molecular mechanisms controlling skeletal muscle mass in humans.
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The respective roles of the medial temporal lobe (MTL) structures in memory are controversial. Some authors put forward a modular account according to which episodic memory and recollection-based processes are crucially dependent on the hippocampal formation whereas semantic acquisition and familiarity-based processes rely on the adjacent parahippocampal gyri. Others defend a unitary view. We report the case of VJ, a boy with developmental amnesia of most likely perinatal onset diagnosed at the age of 8. Magnetic resonance imaging (MRI), including quantitative volumetric measurements of the hippocampal formation and of the entorhinal, perirhinal, and temporopolar cortices, showed severe, bilateral atrophy of the hippocampal formation, fornix and mammillary bodies; by contrast, the perirhinal cortex was within normal range and the entorhinal and temporopolar cortex remained within two standard deviations (SDs) from controls' mean. We examined the development of his semantic knowledge from childhood to teenage as well as his recognition and cued recall memory abilities. On tasks tapping semantic memory, VJ increased his raw scores across years at the same rate as children from large standardisation samples, except for one task; he achieved average performance, consistent with his socio-educational background. He performed within normal range on 74% of recognition tests and achieved average to above average scores on 42% of them despite very severe impairment on 82% of episodic recall tasks. Both faces and landscapes-scenes gave rise to above average scores when tested with coloured stimuli. Cued recall, although impaired, was largely superior to free recall. This case supports a modular account of the MTL with episodic, but not semantic memory depending on the hippocampal formation. Furthermore, the overall pattern of findings is consistent with evidence from both brain-damaged and neuroimaging studies indicating that recollection requires intact hippocampal formation and familiarity relies, at least partly, on the adjacent temporal lobe cortex.
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Posterior cortical atrophy (PCA) is a group of neurodegenerative dementing disorders characterized by initial predominant visual complaints followed by progressive decline in cognitive functions. The visuospatial and visuoperceptual defects arise from the dysfunction of, respectively, the dorsal (occipito-parietal) and the ventral (occipito-temporal) streams. Clinical symptoms, results of neuropsychological examination, and findings of posterior cerebral atrophy and/or posterior hypoperfusion/hypometabolism contribute to the diagnosis. However, owing to the insidious onset of PCA and the non-specificity of initial symptoms, the diagnosis is often delayed. Specific etiologies include Alzheimer's disease, dementia with Lewy bodies, subcortical gliosis, corticobasal degeneration, and prion-associated diseases. Alzheimer's disease accounts for at least 80 % of PCA cases. Recent research has concentrated on better defining the clinical presentation of PCA, improving neuroimaging analysis, testing new neuroimaging techniques, and developing biological measurements. Selected recent papers on PCA are reviewed in this article.
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Primary testicular lymphoma is a rare form of non-Hodgkin's lymphoma. It occurs more frequently in older patients, and it is a potentially lethal disease. For early stages (I and II), the management consists of orchidectomy followed by chemotherapy combined with monoclonal antibodies directed against the CD20 antigen and scrotal radiotherapy (sanctuary site) with/or without iliac and/or paraaortic lymph node radiotherapy. For advanced stages (III and IV), chemo-immunotherapy is the treatment of choice while scrotal radiotherapy can be discussed. Both in early or advanced disease, intrathecal chemotherapy is necessary to prevent central nervous system relapse. New molecular approaches and/or more aggressive treatments are to be explored in this rare disease. To cite this journal: Oncologie 13 (2011).