85 research outputs found
Interferon-γ Inducible Protein (IP-10) Expression Is Mediated by CD8+ T Cells and Is Regulated by CD4+ T Cells During the Elicitation of Contact Hypersensitivity
To investigate the potential roles of CD4+ and CD8+ T cells during contact hypersensitivity, we examined the T-cell-dependent expression of proinflammatory cytokine genes in the responses to dinitrofluorobenzene and oxazolone. Whole cell RNA was isolated from challenged ear tissue and analyzed for level of cytokine gene expression by Northern blot and densitometry analysis. Expression of interleukin 1β and the three chemokine genes (IP-10, JE, and KC) examined was dependent on the hapten dose used for sensitization and correlated with the immune response, i.e., ear swelling, elicited. Antibody-mediated depletion of CD8+ T cells before sensitization resulted in the absence of IP-10 expression following hapten challenge, indicating the ability of immune CD8+ T cells to mediate IP-10 expression. Depletion of CD4+ T cells resulted in higher levels of IP-10 and KC expression during elicitation of contact sensitivity, suggesting CD4+ T cells inhibit the expression of these proinflammatory genes. Depletion of CD4+ T cells resulted in contact hypersensitivity responses of higher magnitude and depletion of CD8+ T cells resulted in responses of lower magnitude. Transfer of CD8+ T-cell-depleted immune cells resulted in low, but detectable levels of IP-10 expression, indicating the ability of some oxazolone-immune CD4+ T cells to mediate IP-10 expression. These results indicate the differential induction of proinflammatory cytokine gene expression during elicitation of contact hypersensitivity in which expression of IP-10 is primarily mediated by immune CD8+ T cells and inhibited by immune CD4+ T cells
Evaluation of First-Line Sorafenib Treatment for Metastatic Renal Cell Carcinoma in Kidney Transplant Patients: A Single-Center Experience With Four Cases
Effect of Systemic Inflammation on Survival in Patients With Metastatic Renal Cell Carcinoma Receiving Second-line Molecular-targeted Therapy
Sarcopenia and the Modified Glasgow Prognostic Score are Significant Predictors of Survival Among Patients with Metastatic Renal Cell Carcinoma Who are Receiving First-Line Sunitinib Treatment.
外科的に切除しえた, 肝硬変を伴う維持透析患者に発症した右腎癌下大静脈腫瘍塞栓の1例
症例は54歳, 男性。1900年, CGNにて血液透析導入となった。2005年2月に肉眼的血尿が出現。CTにて右腎癌を指摘され, 3月9日当科紹介。当科にて施行したCTでは直径7cm大の右腎腫瘍とともに下大静脈内の肝静脈流入部まで達する腫瘍塞栓を認めた。右腎腫瘍, 下大静脈塞栓, T3bN0M0 stage IIIの診断で4月28日, 根治的右腎摘除ならびに腫瘍塞栓摘除術を施行した。手術時間4時間28分, 出血量1, 400ml, 摘出標本は重量800g, 病理所見はrenal cell carcinoma, G2, pT3bであった。術前の凝固系検査は異常を認めなかったが, 肝硬変が原因と考えられる出血時間の延長と血小板数の低下を認めたため, 周術期は血小板輸血などにて対応した。術後経過は良好で, 後出血などの術後合併症もなく, 術後18日目に退院した。現在IFNα投与にて後療法を施行中であるが, 再発を認めていない。透析患者における下大静脈腫瘍塞栓を伴う腎癌に対して外科的治療を施行した症例についての報告例については比較的少なく, 文献的考察も含めて報告する。(著者抄録)A 54-year-old man who had been under hemodialysis therapy for 16 years presented with gross hematuria at our department in February 2005. Imaging findings revealed right renal tumor of8.2 cm in diameter. In addition, the tumor extended into inferior vena cava at the level of the hepatic vein. There were no findings of distant metastasis. Right radical nephrectomy and thrombectomy were performed on April 2006. Histopathological analysis showed that the tumor was renal cell carcinoma of clear cell type, grade 2. Postoperative course was uneventful, and the adjuvant therapy with interferon alpha was initiated. He has been free from recurrence for 22 months after surgery
Preoperative controlling nutritional status (CONUT) score as a novel predictive biomarker of survival in patients with localized urothelial carcinoma of the upper urinary tract treated with radical nephroureterectomy
Evaluation of relative dose intensity during the early phase of first-line sunitinib treatment using a 2-week-on/1-week-off regimen for metastatic renal cell carcinoma
Immediate Progressive Disease in Patients with Metastatic Renal Cell Carcinoma Treated with Nivolumab: a Multi-Institution Retrospective Study
Evaluation of renal function change during first-line tyrosine kinase inhibitor therapy for metastatic renal cell carcinoma
Efficacy and safety of third-line molecular-targeted therapy in metastatic renal cell carcinoma resistant to first-line vascular endothelial growth factor receptor tyrosine kinase inhibitor and second-line therapy
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