To determine its diagnostic value, we evaluated glutathione S-transferase alpha (GST-alpha) expression in a large number of renal cell carcinomas (RCCs). GST-alpha messenger RNA (mRNA) levels from 70 renal neoplasms were analyzed with complementary DNA (cDNA) microarray chips containing 21,632 cDNA clones. Furthermore, 348 primary renal tumors and 24 metastatic RCCs were subjected to immunohistochemical analysis with a GST-alpha-specific antibody. GST-alpha mRNA was elevated significantly (11.4-fold) in a majority of clear cell RCCs (28/43 [65.1%]; 28/39 [71.8%] with adjustments for informative spots) compared with other kidney tumors (1/27 [3.7%]). Strong and diffuse GST-alpha immunoreactivity was demonstrated in a majority of clear cell (166/202 [82.2%]; mean intensity, 2.41) and metastatic clear cell RCCs (17/24 [70.8%]; mean intensity, 2.62). Other renal tumor types did not exhibit significant GST-alpha immunoreactivity, confirming mRNA results. Through cDNA microarrays and immunohistochemical analysis, we demonstrated GST-alpha as a biomarker for clear cell RCCs.

A case of ruptured intracranial mycotic aneurysm associated with acute subdural hematoma is presented. A 26-year-old woman with cardiac valve disease who had been intermittently febrile for 2 weeks suddenly became comatose. There had been no head injury. At the time of admission, a cardiac murmur was audible and petechiae were noted on the conjunctivae and fingers, suggesting a diagnosis of bacterial endocarditis. The blood culture yielded Streptococcus faecalis. The computed tomo graphic scan revealed an intracerebral hematoma and acute subdural hematoma. Angiography dis closed an aneurysm at the distal middle cerebral artery. Such a combination of intracranial mycotic aneurysm and acute subdural hematoma is very rare.

diagnosis. This tumor occurs exclusively in young patients with sickle cell trait or disease. To date, very little is known about the underlying molecular basis, nor is there effective treatment for patients with this tumor.METHODS: We analyzed the gene expression profiles of two renal medullary carcinomas from patients with sickle cell trait using microarrays containing 21,632 eDNA clones and compared it to the gene expression profiles of 27 renal tumors including 7 clear cell renal cell carcinomas (RCC), 6 papillary RCC, 6 chromophobe RCC, 5 Wilms tumors, and 3 urothelial carcinomas of the renal pelvis. Comparative Genomic Microarray Analysis (CGMA), a recently developed method to identify chromosomal loss or gain based on overall gene expression patterns, was then performed. A heat map of a given chromosomal arm was created for each tumor. Two renal medullary carcinomas were compared wtih 9 clear cell RCC and 5 papillary RCC. Immunohistochemistry was performed using monoclonal antibodies specific for DNA topoisomerase IIa (Topo IIa) and keration 19 respectively.RESULTS: We found a distinct molecular signature of renal medullary carcinoma and closer clustering with urothelial carcinoma of the renal pelvis than conventional renal cell carcinoma, based on global gene clustering with 3,560 selected cDNAs. Noticeably, overexpression ofTopo IIa, which has been reported in Wilms tumors but not any other renal tumors, was significantly increased. Keratin 19, which has been previously found in urothelial carcinoma, was also overexpressed in renal medullary carcinomas. With CGMA, renal medullary carcinomas did not demonstrate any significant chromosomal gain or loss, in contrast to clear cell RCC with a characteristic loss of chromosome 3p (VHL) and papillary RCC with gains of chromosomes 7, 16, and 17. The overexpression of Topo IIa and keratin 19 in renal medullary carcinoma cells was confirmed by immunohistochemistry.CONCLUSIONS: Gene expression profiling shows a distinct molecular signature of renal medullary carcinoma, and close clustering with urothelial carcinoma. The genes specifically expressed in this tumor could lead to not only a better understanding of its molecular pathways, but also discoveries of potential diagnostic markers and therapeutic targets.

Purpose This study aimed to evaluate cytokine levels in plasma samples over time from living-donor renal transplant recipients with no evidence of pathological and clinical rejection at least 1 year post-procedure. Methods We examined plasma cytokine levels in 15 living-donor renal transplant recipients who were treated at our hospital from 2015 to 2018 and who presented with no evidence of pathological or clinical rejection for 1 year or longer. We collected blood samples before renal transplantation and at 1 week and 1 year post-procedure. We evaluated levels of 40 cytokines in plasma using Bio-Plex Pro™ Human Chemokine Assay kit. Results We detected no increase in plasma cytokine levels at either the 1 week or the 1 year time points. Plasma levels of 22 cytokines remained stable throughout and levels of 18 cytokine decreased after transplantation. Conclusion Plasma cytokine levels remained unchanged or were decreased in our patient cohort that included stable cases of living-donor renal transplantation. Our results suggest that renal transplantation may promote amelioration of chronic inflammation associated with end-stage renal failure and dialysis.