RESUMO
INTRODUCTION: Augmentation cystoplasty (AC) is a surgical option to restore a good capacity bladder reservoir able to fill at low pressure. METHODS: The authors present the main principles for perioperative management for urologic nurses. RESULTS: AC is usually made with a piece of ileum patched to the bladder. Patient education programs are very important and are usually managed by urologic nurses. It begins in preoperative phase with the self-catheterization learning and continue in the postoperative phase with advises and prevention of the urinary mucus. CONCLUSION: AC are tricky surgeries but management and education of patients by urological nurses are key points to avoid chronic infection, stones or AC perforation.
Assuntos
Enfermagem em Nefrologia/métodos , Assistência Perioperatória/enfermagem , Bexiga Urinária/cirurgia , Coletores de Urina , Humanos , Procedimentos Cirúrgicos Urológicos/métodosRESUMO
AIM: To explore different effects of 12 beticolins, Cercospora beticola toxins, on ras-transformed adrenocortical cell growth inhibition and their functional mechanism. METHODS: Beticolin-induced inhibition was measured with survival cell number determined by an automated photocolorimetric method. The penetration of beticolin was examined by confocal microscopy. Ras protein determined by Lowry method were separated by 14 % SDS-PAGE and electroblotted to Immobilon-P transfer membrane and detected with pan-Ras (Ab-3) monoclonal antibody. The Ca2+ chelation by beticolin was investigated using a calcium ionophore. RESULTS: Cell growth inhibition was found dose- and time-dependently at submicromolar level for beticolin-1, -2, and -13 (IC50 = 250 nmol/L) and for beticolin-0, 6, and -11 (400 nmol/L < IC50 = 500 nmol/L). The inhibition by beticolin-1 was immediate, independent of cell culture step and not reversible for 3-day treatment. Beticolin-3 and -4 were slightly active (1 micromol/L < IC50 = 2 micromol/L) and beticolin-7, -9, -12, and -5 were inactive at micromolar level. The beticolin-induced cell growth inhibition was correlated with the hydrophobicity of these compounds. Beticolin-1 fluorescence in RTAC cells was detected by confocal microscopy whereas beticolin-3 and -12 were not even after a 24 h incubation period. Beticolin-1-induced cell growth inhibition was partially reverted by calcium ionophore suggesting a role of intracellular Ca2+ chelation by beticolin-1 on cell growth inhibition. Furthermore, beticolin-1 blocked up Ras p21 translocation to membrane and induced accumulation of Ras in the cytosol as an inactive form by different ways. CONCLUSION: Beticolins with high hydrophobicity inhibit tumorigenic cell proliferation by different ways.
Assuntos
Córtex Suprarrenal/metabolismo , Fungos/metabolismo , Interações Hidrofóbicas e Hidrofílicas , Micotoxinas/farmacologia , Córtex Suprarrenal/citologia , Animais , Animais Recém-Nascidos , Cálcio/metabolismo , Divisão Celular/efeitos dos fármacos , Linhagem Celular , Compostos Heterocíclicos de 4 ou mais Anéis , Proteínas Proto-Oncogênicas p21(ras)/genética , Ratos , Translocação GenéticaRESUMO
The dynamics of microtubular cytoskeleton were studied in tobacco (Nicotiana tabacum cv Xanthi) cells in response to two different plant defense elicitors: cryptogein, a protein secreted by Phytophthora cryptogea and oligogalacturonides (OGs), derived from the plant cell wall. In tobacco plants cryptogein triggers a hypersensitive-like response and induces systemic resistance against a broad spectrum of pathogens, whereas OGs induce defense responses, but fail to trigger cell death. The comparison of the microtubule (MT) dynamics in response to cryptogein and OGs in tobacco cells indicates that MTs appear unaffected in OG-treated cells, whereas cryptogein treatment caused a rapid and severe disruption of microtubular network. When hyperstabilized by the MT depolymerization inhibitor, taxol, the MT network was still disrupted by cryptogein treatment. On the other hand, the MT-depolymerizing agent oryzalin and cryptogein had different and complementary effects. In addition to MT destabilization, cryptogein induced the death of tobacco cells, whereas OG-treated cells did not die. We demonstrated that MT destabilization and cell death induced by cryptogein depend on calcium influx and that MT destabilization occurs independently of active oxygen species production. The molecular basis of cryptogein-induced MT disruption and its potential significance with respect to cell death are discussed.
Assuntos
Proteínas de Algas/farmacologia , Citoesqueleto/ultraestrutura , Microtúbulos/ultraestrutura , Nicotiana/ultraestrutura , Cálcio/fisiologia , Bloqueadores dos Canais de Cálcio/farmacologia , Células Cultivadas , Citoesqueleto/efeitos dos fármacos , Ácido Egtázico/farmacologia , Proteínas Fúngicas , Microtúbulos/efeitos dos fármacos , Nicotiana/efeitos dos fármacos , Nicotiana/fisiologiaAssuntos
Síndrome da Imunodeficiência Adquirida/complicações , Calcinose/diagnóstico , Nefropatias/diagnóstico , Adulto , Calcinose/patologia , Feminino , Humanos , Córtex Renal/patologia , Nefropatias/etiologia , Imageamento por Ressonância Magnética , Tomografia Computadorizada por Raios X , UltrassonografiaRESUMO
The proliferation of GM16 and 4CDT ras-transformed newborn rat adrenocortical (RTAC) cells and Y1 mouse adrenal tumor cells was inhibited by beticolins, the fungal toxins extracted from Cercospora beticola, at submicromolar concentrations in a dose-dependent manner. Inhibitory concentrations for half the maximum inhibition were 150, 75 and 25 nM for beticolin-1 and 230, 150 and 50 nM for beticolin-2 in GM16, 4CDT and Y1 cells respectively. Beticolins strongly inhibited the production of 11 beta-hydroxysteroids on the second and third days of treatment in a dose-dependent manner between 0.1 and 1 microM. Beticolins were shown by confocal microscopy to be localized in cytoplasmic organelles about 30-40 min after treatment. This finding favors a direct action of beticolins on mitochondrial steroid 11 beta-hydroxylase albeit another less direct mechanism involving a cytoplasmic signaling pathway cannot be excluded.
Assuntos
Córtex Suprarrenal/efeitos dos fármacos , Neoplasias das Glândulas Suprarrenais/patologia , Genes ras , Inibidores do Crescimento/farmacologia , Hidroxiesteroides/metabolismo , Micotoxinas/farmacologia , Proteínas de Neoplasias/antagonistas & inibidores , Esteroide 11-beta-Hidroxilase/antagonistas & inibidores , Córtex Suprarrenal/metabolismo , Neoplasias das Glândulas Suprarrenais/metabolismo , Animais , Animais Recém-Nascidos , Divisão Celular/efeitos dos fármacos , Transformação Celular Neoplásica/genética , Transformação Celular Neoplásica/metabolismo , Células Cultivadas , Relação Dose-Resposta a Droga , Compostos Heterocíclicos de 4 ou mais Anéis , Camundongos , Microscopia Confocal , Proteínas de Neoplasias/metabolismo , Ratos , Esteroide 11-beta-Hidroxilase/metabolismo , Relação Estrutura-Atividade , Transfecção , Células Tumorais CultivadasRESUMO
The authors report the first case of arrhythmogenic right ventricular dysplasia presenting with a sudden death due to primary ventricular fibrillation (ventricular fibrillation not preceded by ventricular tachycardia) recorded by the Holter method. The patient was a 56 year old man whose only complaint was near syncopal case is the fact that it is the first documented case of ventricular fibrillation revealing arrhythmogenic right ventricular dysplasia, the diagnosis of which was made at autopsy. In addition, the Holter recording showed the factors which triggered the arrhythmia: the "trigger" of 4 monomorphic ventricular extrasystoles during the minute preceding the ventricular fibrillation; the arrhythmogenic substrate giving rise to late ventricular potentials and, finally, the analysis of the R-R intervals suggesting a role of the sympathetic and parasympathetic nervous systems. Holter recordings could help identify subjects at high risk of severe ventricular arrhythmias.
Assuntos
Cardiomiopatias/complicações , Morte Súbita Cardíaca/etiologia , Eletrocardiografia Ambulatorial , Ventrículos do Coração/patologia , Fibrilação Ventricular/complicações , Tecido Adiposo/patologia , Arritmias Cardíacas/complicações , Arritmias Cardíacas/diagnóstico , Cardiomiopatias/patologia , Morte Súbita Cardíaca/patologia , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Risco , Fibrilação Ventricular/diagnóstico , Função Ventricular DireitaRESUMO
We report 6 cases of corticotroph macroadenomas which show heterogeneity of clinical and biological features (from Cushing's syndrome to silent adenoma) and heterogeneity of immunocytochemical staining. One patient reported on had skin hyperpigmentation and ACTH hypersecretion without clear abnormal adrenocortical function; we believe that this patient's plasma contained ACTH with very low bioactivity.
Assuntos
Adenoma/diagnóstico , Hormônio Adrenocorticotrópico/metabolismo , Neoplasias Hipofisárias/diagnóstico , Adenoma/metabolismo , Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Neoplasias Hipofisárias/metabolismoRESUMO
The intranuclear distribution of newly replicated DNA and of the proliferating cell nuclear antigen (PCNA) was mapped by confocal laser scanning microscopy after simultaneous immunofluorescent labelling of incorporated bromodeoxyuridine (BrdUrd) and PCNA. A mild hydrolysis with HCl followed by an enzymic digestion of DNA was used to produce single-stranded DNA required for BrdUrd immunorevelation, since this procedure preserves PCNA antigenicity. Optical sections obtained with a laser scanning microscope clearly showed a similar distribution of PCNA and BrdUrd within the nuclei, thus confirming previous observations on parallel labelled synchronized cultures. The intranuclear distribution of PCNA and BrdUrd varies concomitantly during the S phase of MCF-7 cells.