Positive predictors for the extension of SSBE were presence of hiatal hernia and reflux symptoms, but not age.

CD5 expression was the only significant prognostic factor among the biomarkers examined in this study. Further studies with larger numbers are warranted to confirm the prognostic significance of CD5 expression for patients with DLBCL receiving rituximab-containing chemotherapy.

SummaryProteasome inhibition induces the accumulation of aggregated misfolded/ ubiquitinated proteins in the aggresome; conversely, histone deacetylase 6 (HDAC6) inhibition blocks aggresome formation. Although this rationale has been the basis of proteasome inhibitor (PI) and HDAC6 inhibitor combination studies, the role of disruption of aggresome formation by HDAC6 inhibition has not yet been studied in multiple myeloma (MM). The present study aimed to evaluate the impact of carfilzomib (CFZ) in combination with a selective HDAC6 inhibitor (ricolinostat) in MM cells with respect to the aggresome-proteolysis pathway. We observed that combination treatment of CFZ with ricolinostat triggered synergistic anti-MM effects, even in bortezomib-resistant cells. Immunofluorescent staining showed that CFZ increased the accumulation of ubiquitinated proteins and protein aggregates in the cytoplasm, as well as the engulfment of aggregated ubiquitinated proteins by autophagosomes, which was blocked by ricolinostat. Electron microscopy imaging showed increased autophagy triggered by CFZ, which was inhibited by the addition of ACY-1215. Finally, an in vivo mouse xenograft study confirmed a decrease in tumour volume, associated with apoptosis, following treatment with CFZ in combination with ricolinostat. Our results suggest that ricolinostat inhibits aggresome formation, caused by CFZ-induced inhibition of the proteasome pathway, resulting in enhanced apoptosis in MM cells.

Human neutrophil antigens (HNAs) play an important role in a variety of clinical conditions including immune‐mediated neutropenia, non‐hemolytic transfusion reactions, and transfusion‐related acute lung injury. The aim of this study was to investigate the frequency distribution of HNAs‐1 to ‐5 among the Japanese population. We analyzed samples from 570 healthy Japanese by molecular and serologic techniques to estimate the gene frequencies of HNAs‐1 to ‐5. DNA samples were obtained and typed for the HNA‐1 (n = 523), ‐3 (n = 570), ‐4 (n = 570), and ‐5 (n = 508), by molecular techniques. The HNA‐1 genotype was determined by using a commercial polymerase chain reaction‐reverse sequence‐specific oligonucleotide probes (PCR‐rSSOP) kit. The HNA‐3 to ‐5 genotypes were determined by the PCR‐sequence specific primer (PCR‐SSP), previously described, with a small modification. The HNA‐2a phenotype was determined in 301 donors by granulocyte immunofluorescence test. In Japanese, the gene frequencies of HNA‐1a, ‐1b, and ‐1c were 0.623, 0.377, and 0.000, respectively. The frequency of HNA‐2a phenotype was 0.987, and the gene frequencies of HNA‐3a and ‐3b were 0.654 and 0.346, respectively. HNA‐4a and ‐4b were found at 1.000 and 0.000, respectively, and HNA‐5a and ‐5b at 0.840 and 0.160, respectively. We describe, for the first time, the frequencies of all HNAs (HNA‐1 to ‐5) among the Japanese population. This study will be helpful for the prediction of the risk of alloimmunization to HNA, especially to determine the risk of HNA alloantibody production by transfusion of HNA incompatible blood and feto‐maternal incompatibility.