Non-Hunner-type IC is characterized by severe fibrosis and increased mast cell infiltration, whereas Hunner-type IC is characterized by severe inflammation and urothelial denudation in the entire bladder. Fibrosis in the bladder of IC/BPS patients was correlated with increased urinary frequency and decreased bladder capacity.

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Abstract-Provable lower bounds are presented for the information rate I(X; X + S + N ) where X is the symbol drawn independently and uniformly from a finite-size alphabet, S is a discrete-valued random variable (RV) and N is a Gaussian RV. It is well known that with S representing the precursor intersymbol interference (ISI) at the decision feedback equalizer (DFE) output, I(X; X + S + N ) serves as a tight lower bound for the symmetric information rate (SIR) as well as capacity of the ISI channel corrupted by Gaussian noise. When evaluated on a number of well-known finite-ISI channels, these new bounds provide a very similar level of tightness against the SIR to the conjectured lower bound by Shamai and Laroia at all signalto-noise ratio (SNR) ranges, while being actually tighter when viewed closed up at high SNRs. The new lower bounds are obtained in two steps: First, a "mismatched" mutual information function is introduced which can be proved as a lower bound to I(X; X + S + N ). Secondly, this function is further bounded from below by an expression that can be computed easily via a few single-dimensional integrations with a small computational load.Index Terms-Channel capacity, decision feedback equalizer, information rate, intersymbol interference, lower bounds, mutual information.

Tyrosine kinase inhibitors (TKIs) are widely accepted as treatment for metastatic clear cell renal cell carcinoma (ccRCC). However, most patients eventually experience disease progression despite TKI treatment, even if the initial response is favorable. To define the underlying mechanism of TKI resistance, 10 TKI-treated metastatic ccRCC cases in which tumor samples were harvested before treatment and immediately after disease progression were examined. Gene expression profiles and copy number variations of matched pre-and post-treatment tumor samples were investigated. Altered biologic characteristics were confirmed in sunitinib-resistant ccRCC cell lines, which were generated by long-term treatment with sunitinib-containing media. Gene transcript levels related to the cell cycle and epithelial-mesenchymal transition (EMT) were significantly upregulated in the treated tumor samples compared with the pre-treatment samples. The mitotic count and sarcomatoid component were significantly increased in treated tumor samples. Alteration of EMT-related genes was also demonstrated in a sunitinib-resistant ccRCC cell line that showed enhanced migration and invasion compared to the parent cell line. siRNA-induced inhibition of EMT-related gene expression significantly suppressed the migration and invasion capacity of TKI-resistant cell lines. The present study shows that both ccRCC cases that progressed after TKI treatment and sunitinib-resistant ccRCC cell lines demonstrated alteration of EMT-related gene expression and enhancement of EMTrelated behavior. These results suggest that EMT may explain the aggressive behavior of TKI-resistant ccRCC.

TPS is a useful diagnostic system for urinary tract washing specimens by decreasing the number of AUC cases and increasing sensitivity. In this study, anisonucleosis and India ink nuclei improved the diagnostic accuracy of HGUC.

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