Anjeni Keswani

Hypoxia inducible factor-alpha activation in lymphoma and relationship to the thioredoxin family.

Hypoxia inducible factors (HIFs) activate oncogenic pathways, while thioredoxins (Trx), including Trx1 and Trx reductases‐1 and ‐2 (TrxR1 and TrxR2), promote HIF‐α stabilization. In immunoblotting studies in lymphoma cell lines we found that Raji and SUDHL4 cells exhibited normoxic HIF‐2α protein stabilization. Five cell lines showed increased TrxR1 expression, while only Namalwa, HF1 and SUDHL4 had Trx1 and TrxR2 activation. Tissue microarrays in diffuse large B‐cell lymphoma (DLBCL) and follicular lymphoma (FL) identified different HIF expression among histological subgroups (e.g. 44% DLBCL vs. 11% of FL cases with moderate‐to‐high expression of HIF‐1α and HIF‐2α, P = 0·0017). These data demonstrate that HIF and the thioredoxin family are abnormally activated in lymphoma.

Role of interleukin-32 in chronic rhinosinusitis.

Purpose of reviewIL-32 is a recently described proinflammatory cytokine and has been reported to be involved in inflammatory diseases. The purpose of this review is to discuss the role of IL-32 in chronic rhinosinusitis (CRS). Recent findingsTwo groups have recently reported data regarding the expression of IL-32 in CRS. IL-32 was induced by IFN-&ggr;, TNF-&agr;, dsRNA, and incubation with Th1 cells in primary nasal epithelial cells. IL-32 may be elevated in epithelial cells from patients with CRS without nasal polyps. IL-32 was significantly elevated in whole sinonasal tissue samples of nasal polyps compared with control tissue. IL-32 mRNA expression positively correlated with mRNA for CD3 and macrophage mannose receptor in nasal polyp tissue. Immunohistochemical studies demonstrated localization of IL-32 in epithelium, CD3+ and CD68+ cells, suggesting that epithelial cells, T cells, and macrophages are the major IL-32-producing cells in CRS. Activation of these cell types may trigger IL-32-related inflammation in CRS. SummaryElevated levels of IL-32 may play a role in the pathogenesis of CRS through its role as a proinflammatory cytokine and as an endogenous enhancer of pathogen-dependent cytokine production.

Sinusitis in patients on tumor necrosis factor alpha inhibitors

Tumor necrosis factor alpha (TNF‐α) inhibitors have revolutionized treatment of many inflammatory diseases. Sinusitis after initiation of TNF‐α inhibitors has been observed, but has not been well described in the literature. We aim to characterize the clinical features of sinusitis in patients on anti‐TNF‐α therapy.

Complications of Rhinitis

Chronic rhinitis involves inflammation of the upper airways. An association with comorbid conditions, such as rhinosinusitis, asthma, and chronic obstructive pulmonary disease, has been commonly observed in epidemiologic studies. The underlying pathogenesis of these disorders may be similar. Complications of rhinitis include sleep disturbances, learning impairment, and decreased quality of life. It is vital to recognize the complications of rhinitis so that treatment strategies can address rhinitis as well as its comorbidities and complications in a coordinated manner.