RESUMO
Idiopathic normal pressure hydrocephalus (iNPH) is a condition characterized by gait disturbance, dementia and/or urinary incontinence and enlarged ventricular system due to disturbance of cerebrospinal fluid (CSF). This study aims to describe the long-term experience with patients with iNPH submitted to ventriculoperitoneal shunt (VPS) with the programmable valve STRATA® (Medtronic). We prospectively selected a cohort of patients with a diagnosis of iNPH from January 2010 to April 2013 in a Brazilian tertiary hospital. All patients underwent clinical evaluation, which consists of the Mini-Mental State Examination and Time Up and Go tests and the application of Japanese Scale for Idiopathic Normal Pressure Hydrocephalus in three stages: prior to the TT, 3 h after the TT and 72 h after the TT. Fifty patients were submitted to VPS and followed. There were 32 men and 18 women. Mean age was 77.1 with standard deviation of 10.9. Follow-up time ranged from 96 to 120 months, with mean of 106 months. After 1 year of follow-up, 42 (83%) patients presented with clinical improvement, decreasing to 62% of patients at mid-term follow-up and 38% of patients at late follow-up. Complications occurred in 18% of subjects, needing reoperation in 16%. Our results show relevant clinical impact of shunting in iNPH patients, decreasing over time. Complications should not be underestimated, reaching up to 18% and demanding reoperation in 16% of cases. Thus, although much has been improved with current shunt technology, it is still important to consider the drawbacks of treatment.
Assuntos
Hidrocefalia de Pressão Normal/diagnóstico por imagem , Hidrocefalia de Pressão Normal/cirurgia , Derivação Ventriculoperitoneal/tendências , Idoso , Idoso de 80 Anos ou mais , Brasil/epidemiologia , Feminino , Seguimentos , Humanos , Hidrocefalia de Pressão Normal/epidemiologia , Masculino , Estudos Prospectivos , Fatores de Tempo , Resultado do Tratamento , Derivação Ventriculoperitoneal/métodosRESUMO
Pituitary adenomas account for 10-15% of primary intracranial tumors. Growth hormone (GH)-secreting adenomas account for 13% of all pituitary adenomas and cause acromegaly. These tumors can be aggressive, invade surrounding structures and are highly recurrent. The objective of this study was to evaluate E-cadherin, Slug and neural cell adhesion molecule (NCAM) expression in GH-secreting pituitary adenomas and its relationship to tumor invasiveness. A cross-sectional study of patients who underwent hypophysectomy due to GH-secreting pituitary adenoma from April 2007 to December 2014 was carried out. The medical records were reviewed to collect clinical data. Immediately after surgery, tumor samples were frozen in liquid nitrogen and stored in a biofreezer at -80°C for assessment of E-cadherin 1 (CDH1), SLUG (SNAI2), and NCAM (NCAM1) by real-time PCR. The samples were fixed in formalin and embedded in paraffin for immunohistochemical analysis of E-cadherin and NCAM. Thirty-five patients with acromegaly were included in the study. Of these, 65.7% had invasive tumors. Immunohistochemically, E-cadherin was expressed in 96.7% of patients, and NCAM in 80% of patients. There was no statistically significant relationship between tumor grade or invasiveness and immunohistochemical expression of these markers. Regarding gene expression, 50% of cases expressed CDH1, none expressed SNAI2, and 53.3% expressed NCAM1. There was no statistically significant relationship between tumor grade or invasiveness and gene expression of CDH1, SNAI2, and NCAM1. The absence of Slug overexpression and of E-cadherin and NCAM suppression suggests that expression of these markers is not associated with tumor invasiveness in GH-secreting pituitary adenomas.
Assuntos
Humanos , Masculino , Feminino , Adolescente , Adulto , Pessoa de Meia-Idade , Idoso , Adulto Jovem , Acromegalia/patologia , Adenoma/patologia , Caderinas/análise , Moléculas de Adesão de Célula Nervosa/análise , Fatores de Transcrição da Família Snail/análise , Acromegalia/genética , Acromegalia/metabolismo , Imuno-Histoquímica , Biomarcadores Tumorais/análise , Adenoma/genética , Adenoma/química , Expressão Gênica , Estudos Transversais , Gradação de TumoresRESUMO
Pituitary adenomas account for 10-15% of primary intracranial tumors. Growth hormone (GH)-secreting adenomas account for 13% of all pituitary adenomas and cause acromegaly. These tumors can be aggressive, invade surrounding structures and are highly recurrent. The objective of this study was to evaluate E-cadherin, Slug and neural cell adhesion molecule (NCAM) expression in GH-secreting pituitary adenomas and its relationship to tumor invasiveness. A cross-sectional study of patients who underwent hypophysectomy due to GH-secreting pituitary adenoma from April 2007 to December 2014 was carried out. The medical records were reviewed to collect clinical data. Immediately after surgery, tumor samples were frozen in liquid nitrogen and stored in a biofreezer at -80°C for assessment of E-cadherin 1 (CDH1), SLUG (SNAI2), and NCAM (NCAM1) by real-time PCR. The samples were fixed in formalin and embedded in paraffin for immunohistochemical analysis of E-cadherin and NCAM. Thirty-five patients with acromegaly were included in the study. Of these, 65.7% had invasive tumors. Immunohistochemically, E-cadherin was expressed in 96.7% of patients, and NCAM in 80% of patients. There was no statistically significant relationship between tumor grade or invasiveness and immunohistochemical expression of these markers. Regarding gene expression, 50% of cases expressed CDH1, none expressed SNAI2, and 53.3% expressed NCAM1. There was no statistically significant relationship between tumor grade or invasiveness and gene expression of CDH1, SNAI2, and NCAM1. The absence of Slug overexpression and of E-cadherin and NCAM suppression suggests that expression of these markers is not associated with tumor invasiveness in GH-secreting pituitary adenomas.
Assuntos
Acromegalia/patologia , Adenoma/patologia , Caderinas/análise , Moléculas de Adesão de Célula Nervosa/análise , Neoplasias Hipofisárias/patologia , Fatores de Transcrição da Família Snail/análise , Acromegalia/genética , Acromegalia/metabolismo , Adenoma/química , Adenoma/genética , Adolescente , Adulto , Idoso , Biomarcadores Tumorais/análise , Antígeno CD56/análise , Estudos Transversais , Feminino , Expressão Gênica , Humanos , Imuno-Histoquímica , Masculino , Pessoa de Meia-Idade , Gradação de Tumores , Invasividade Neoplásica , Neoplasias Hipofisárias/química , Neoplasias Hipofisárias/genética , Reação em Cadeia da Polimerase em Tempo Real , Estatísticas não Paramétricas , Adulto JovemRESUMO
Stationary and time-dependent solutions of a nonlinear Kramers equation, as well as its associated nonlinear Fokker-Planck equations, are investigated within the context of Tsallis nonextensive statistical mechanics. Since no general analytical time-dependent solutions are found for such a nonlinear Kramers equation, an ansatz is considered and the corresponding asymptotic behavior is studied and compared with those known for the standard linear Kramers equation. The H-theorem is analyzed for this equation and its connection with Tsallis entropy is investigated. An application is discussed, namely the motion of Hydra cells in two-dimensional cellular aggregates, for which previous measurements have verified q-Gaussian distributions for velocity components and superdiffusion. The present analysis is in quantitative agreement with these experimental results.
RESUMO
We analyze a nonlinear fractional diffusion equation with absorption by employing fractional spatial derivatives and obtain some more exact classes of solutions. In particular, the diffusion equation employed here extends some known diffusion equations such as the porous medium equation and the thin film equation. We also discuss some implications by considering a diffusion coefficient D(x,t)=D(t)/x/(-theta) (theta in R) and a drift force F=-k(1)(t)x+k(alpha)x/x/(alpha-1). In both situations, we relate our solutions to those obtained within the maximum entropy principle by using the Tsallis entropy.