Essential Elements as Biomarkers of Acute Kidney Injury and Spontaneous Reversion.

Acute kidney injury (AKI) is an important health problem and can be caused by number of factors. The use of aminoglycosides, such as gentamicin, is one of these factors. Recently, an effort has been made to find biomarkers to guide treatment protocols. Inductively coupled plasma optical emission spectroscopy (ICP-OES) was used to estimate the contents of Ca, Cu, Fe, K, Mg, Mn, Na, P, and Zn in serum and urine of the healthy, AKI, and spontaneous recovery (SR) groups of animals. The animal model of AKI and SR was validated by measuring serum and urinary urea and creatinine. The quantitative determination of the elements showed a decrease in serum levels of Ca, and Fe in the AKI group (P<0.01 vs. healthy), with a return to normal levels in the SR group, without a significant difference between the healthy and SR groups. In the urine samples, there was a decrease in P and Na levels in the AKI group (P<0.001 and P<0.01 vs. healthy), but Ca levels were increased in this group compared with the healthy and SR groups (P<0.01). These findings indicate that mineral elements might be useful as biomarkers for AKI.

Knockdown of NF-κB1 by shRNA Inhibits the Growth of Renal Cell Carcinoma In Vitro and In Vivo.

Renal cell carcinoma (RCC) accounts for approximately 2%-3% of human malignancies and is the most aggressive among urologic tumors. Biological heterogeneity, drug resistance, and chemotherapy side effects are the biggest obstacles to the effective treatment of RCC. The NF-κB transcription factor is one of several molecules identified to be responsible for the aggressive phenotype of this tumor. In the past decade, several studies have demonstrated the activation of NF-κB in RCC, and many have implicated NF-κB1 (p50) as an important molecule in tumor progression and metastasis. In the present study, a lentivirus was used to deliver shRNA targeting NF-κB1 into mouse RCC (Renca) cells. It was determined that the knockdown of the NF-κB1 gene led to a reduction in cell proliferation and late apoptosis/necrosis in vitro. Flow cytometry analysis demonstrated G2/M arrest in the cells. In addition, immunoblotting analysis revealed a significant increase in cyclin B1 and Bax. In vivo experiments showed that Renca-shRNA-NF-κB1 cells have significantly diminished tumorigenicity. Moreover, immunohistochemical analysis revealed an increase in necrotic areas of Renca-shRNA-NF-κB1 tumors. Thus, this study indicates that downregulation of NF-κB1 can suppress RCC tumorigenesis by inducing late apoptosis/necrosis. Therefore, NF-κB1 may be a potential therapeutic target for RCC.

Knockdown of NF-kB1 by shRNA Inhibits the Growth of Renal Cell Carcinoma In Vitro and In Vivo

Renal cell carcinoma (RCC) accounts for approximately 2%-3% of human malignancies and is the most aggressive among urologic tumors. Biological heterogeneity, drug resistance, and chemotherapy side effects are the biggest obstacles to the effective treatment of RCC. The NF-kappa B transcription factor is one of several molecules identified to be responsible for the aggressive phenotype of this tumor. In the past decade, several studies have demonstrated the activation of NF-kappa B in RCC, and many have implicated NF-kappa B1 (p50) as an important molecule in tumor progression and metastasis. In the present study, a lentivirus was used to deliver shRNA targeting NF-kappa B1 into mouse RCC (Renca) cells. It was determined that the knockdown of the NF-kappa B1 gene led to a reduction in cell proliferation and late apoptosis/necrosis in vitro. Flow cytometry analysis demonstrated G(2)/M arrest in the cells. In addition, immunoblotting analysis revealed a significant increase in cyclin B1 and Bax. In vivo experiments showed that Renca-shRNA-NF-kappa B1 cells have significantly diminished tumori genicity. Moreover, immunohistochemical analysis revealed an increase in necrotic areas of Renca-shRNA-NF-kappa B1 tumors. Thus, this study indicates that downregulation of NF-kappa B1 can suppress RCC tumorigenesis by inducing late apoptosis/necrosis. Therefore, NF-kappa B1 may be a potential therapeutic target for RCC.

Knockdown of NF-kB1 by shRNA Inhibits the Growth of Renal Cell Carcinoma In Vitro and In Vivo

Renal cell carcinoma (RCC) accounts for approximately 2%-3% of human malignancies and is the most aggressive among urologic tumors. Biological heterogeneity, drug resistance, and chemotherapy side effects are the biggest obstacles to the effective treatment of RCC. The NF-kappa B transcription factor is one of several molecules identified to be responsible for the aggressive phenotype of this tumor. In the past decade, several studies have demonstrated the activation of NF-kappa B in RCC, and many have implicated NF-kappa B1 (p50) as an important molecule in tumor progression and metastasis. In the present study, a lentivirus was used to deliver shRNA targeting NF-kappa B1 into mouse RCC (Renca) cells. It was determined that the knockdown of the NF-kappa B1 gene led to a reduction in cell proliferation and late apoptosis/necrosis in vitro. Flow cytometry analysis demonstrated G(2)/M arrest in the cells. In addition, immunoblotting analysis revealed a significant increase in cyclin B1 and Bax. In vivo experiments showed that Renca-shRNA-NF-kappa B1 cells have significantly diminished tumori genicity. Moreover, immunohistochemical analysis revealed an increase in necrotic areas of Renca-shRNA-NF-kappa B1 tumors. Thus, this study indicates that downregulation of NF-kappa B1 can suppress RCC tumorigenesis by inducing late apoptosis/necrosis. Therefore, NF-kappa B1 may be a potential therapeutic target for RCC.