Hematopoietic Neoplasms of the Sinonasal Tract.

Hematologic malignancies are one of the more common neoplasms to occur in the sinonasal tract and include a wide range of entities, including mature and immature B cell and T cell neoplasms as well as plasma cell dyscrasias and histiocytic disorders. CD45 expression can be helpful in identifying many, but not all, hematopoietic neoplasms in the sinonasal tract, and more extensive immunophenotyping, including EBV in situ hybridization, as well as correlation with genetic results and clinical features may be required for diagnosis.

PTEN expression and morphological patterns in prostatic adenocarcinoma.

Aims: Cribriform morphology, which includes intraductal carcinoma (IDCP) and invasive cribriform carcinoma, is an indicator of poor prognosis in prostate cancer. Phosphatase and tensin homologue (PTEN) loss is a predictor of adverse clinical outcomes. The association between PTEN expression and morphological patterns of prostate cancer is unclear.

β-arrestin 2 attenuates cardiac dysfunction in polymicrobial sepsis through gp130 and p38.

Sepsis is an exaggerated systemic inflammatory response to persistent bacteria infection with high morbidity and mortality rate clinically. β-arrestin 2 modulates cell survival and cell death in different systems. However, the effect of β-arrestin 2 on sepsis-induced cardiac dysfunction is not yet known.

TLR2 Involved in Naive CD4+ T Cells Rescues Stress-Induced Immune Suppression by Regulating Th1/Th2 and Th17.

Stress, either physical or psychological, can have a dramatic impact on our immune system. There has been little progress, however, in understanding chronic stress-induced immunosuppression. Naive CD4+ T cells could modulate immune responses via differentiation to T helper (Th) cells.

Stimulatory Toll-like receptor 2 suppresses restraint stress-induced immune suppression.

Stress can enhance or suppress immune functions depending on a variety of factors. Our previous studies observed that Toll-like receptor 2 (TLR2) participates in chronic restraint stress-induced immune dysfunction. However, the mechanism by which TLR2 prevents immune suppression remains elusive.