Mcp1 is upregulated after knockout of and promotes macrophage accumulation and cyst growth both proliferation-independent and proliferation-dependent mechanisms in this orthologous mouse model of ADPKD.
The drivers and the specification of CD4
+
T cell differentiation in the tumor microenvironment and their contributions to tumor immunity or tolerance are incompletely understood. Using models of pancreatic ductal adenocarcinoma (PDA), we show that a distinct subset of tumor-infiltrating dendritic cells (DC) promotes PDA growth by directing a unique T
H
-program. Specifically, CD11b
+
CD103
−
DC predominate in PDA, express high IL-23 and TGF-β, and induce FoxP3
neg
tumor-promoting IL-10
+
IL-17
+
IFNγ
+
regulatory CD4
+
T cells. The balance between this distinctive T
H
program and canonical FoxP3
+
T
REGS
is unaffected by pattern recognition receptor ligation and is modulated by DC expression of retinoic acid. This T
H
-signature is mimicked in human PDA where it is associated with immune-tolerance and diminished patient survival. Our data suggest that CD11b
+
CD103
−
DC promote CD4
+
T cell tolerance in PDA which may underscore its resistance to immunotherapy.
The use of evidences demonstrates that the appropriate use of lubricants for intermittent urinary catheterisation is fundamental for patient safety and the performance of the best practices.
PURPOSE:Fetal hydronephrosis is a frequent finding due to advances in prenatal ultrasonography. The definition of fetal and neonatal urinary tract obstruction is a very difficult task requiring confirmation of reduced renal function and hydronephrosis. In this study we followed a series of consecutive patients with intrauterine hydronephrosis that persisted during post-natal life.
METHODS:116 newborns with antenatal hydronephrosis diagnosed by ultrasound and submitted to a specific post-natal evaluative protocol with a follow-up period of 6 years.
RESULTS:In 45 (38.8%) of 116 patients, ureteropelvic junction (UPJ) obstruction was confirmed and surgical correction of the UPJ obstruction was done in 19 patients. From 26 children who were initially submitted to non-surgical treatment, only 6 (23%) needed a surgical approach during follow up. Overall analysis showed that surgery was performed in 25 patients with UPJ obstruction, and the others 20 patients were kept under clinical observation, since normal renal function was confirmed by scintigraphy scans.
CONCLUSION:Fetal hydronephrosis due to UPJ obstruction deserves careful postnatal evaluation. UPJ obstruction is the most frequent anomaly and its surgical treatment has very precise indications. The evaluative protocol was useful in identify patients that could be followed-up with a non-surgical approach.Key words: Hydronephrosis. Prenatal Diagnosis. Radionuclide Imaging.
RESUMO OBJETIVO:Com a ampla utilização dos exames ultrassonográficos na avaliação pré-natal, é frequente o diagnóstico da hidronefrose fetal. A definição de obstrução do trato urinário no periodo pós-natal necessita da confirmação de redução da função renal além da hidronefrose. Neste estudo, acompanhamos uma série de pacientes consecutivos com hidronefrose intra-útero que persistiu no periodo pós-natal.
MÉTODOS:116 recém-nascidos com hidronefrose pré-natal diagnosticada pela ultrassonografia foram submetidos a protocolo específico de avaliação e companhados pelo periodo de 06 anos. inicialmente para observação clínica, apenas 6 (23%) necessitaram cirurgia durante o seguimento ambulatorial. Na análise geral, o procedimento cirúrgico para correção da estenose da JUP foi indicado em 25 pacientes. Nas outras 20 crianças não houve necessidade da realização da cirurgia.
RESULTADOS:CONCLUSÃO: a hidronefrose fetal requer cuidadosa avaliação pós-natal. A estenose da junção pielo-ureteral é a anomalia mais frequente como causa da hidronefrose, e sua correção cirúrgica tem indicações precisas. O protocolo aplicado foi útil em diferenciar pacientes que não necessitaram cirurgia para tratamento da estenose da JUP.
Descritores:Hidronefrose. Diagnóstico Pré-natal. Cintilografia.
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