Summary. Background: Data on venous thromboembolism (VTE) in gastric cancer (GC) are very scarce. Objective: To investigate the incidence, risk factors and prognostic implications of VTE in Asian GC patients. Methods: Prospective databases containing clinical information on GC patients (n = 2,085) were used. Results: The 2-year cumulative incidences of all VTE events were 0.5%, 3.5% and 24.4% in stages I, II-IV(M0) and IV(M1), respectively. Advanced stage, older age and no major surgery were independent risk factors for developing VTE. When the VTE cases were classified into extremity venous thrombosis (EVT), pulmonary thromboembolism (PTE) or intra-abdominal venous thrombosis (IVT), IVTs (62%) were more common than EVTs (21%) or PTEs (17%). Although peri-operative pharmacologic thromboprophylaxis was not routinely administered, the VTE incidence after major surgery was only 0.2%. During chemotherapy, EVT/PTE developed more frequently than IVT (54% vs. 19%); however, during untreated or treatment-refractory periods, IVT developed more frequently than EVT/PTE (69% vs. 36%). In multivariate models, the development of EVT/PTE was a significant predictor of early death when compared with no occurrence of VTE (P < 0.05). However, IVT did not affect survival. Conclusion: This is the largest study that specially focused on VTE in GC and the VTE incidence in Asian GC patients was first demonstrated. Considering the low incidence of post-operative VTE development, the necessity of perioperative pharmacologic thromboprophylaxis should be evaluated separately in Asian patients. The clinical situation of the development of EVT/PTE and IVT differed. Only EVT/PTE had an adverse effect on survival and IVT had no prognostic significance.

Background: The incidence and risk factors of central nervous system (CNS) involvement in peripheral T-cell lymphomas (PTCLs) are still unclear. Patients and methods: We analyzed 228 patients with PTCLs, excluding cases of extranodal natural killer/T-cell lymphoma and primary cutaneous T-cell lymphoma, by retrospectively collecting the clinical features and outcomes of the patients. Results: Twenty events (8.77%, 20/228) of CNS involvement were observed during a median follow-up period of 13.9 months (range 0.03–159.43). Based on univariate analysis, elevated serum lactate dehydrogenase (LDH) level [ P = 0.019, relative risk (RR) 5.904, 95% confidence interval (CI) 1.334–26.123] and involvement of the paranasal sinus ( P = 0.032, RR 3.137, 95% CI 1.105–8.908) adversely affect CNS involvement. In multivariate analysis, both were independently poor prognostic factors for CNS relapse [elevated LDH level: P = 0.011, hazard ratio (HR) 6.716, 95% CI 1.548–29.131; involvement of the paranasal sinus: P = 0.008, HR 3.784, 95% CI 1.420–10.083]. The survival duration of patients with CNS involvement was significantly shorter than that of the patients without CNS involvement ( P = 0.009), with median overall survival of 7.60 months (95% CI of 4.92–10.28) versus 27.43 months (95% CI of 0.00–57.38), respectively. Conclusions: Elevated LDH level and involvement of the paranasal sinus are two risk factors for CNS involvement in patients with PTCLs. Considering the poor prognoses after CNS relapse, prophylaxis should be considered with the presence of any risk factor.

High-mobility group box 1 (HMGB1) mediates various functions according to the location. We tried to investigate the role of HMGB1 in upper airway under hypoxic conditions. We cultured primary normal human nasal epithelium (NHNE) cells under hypoxic conditions and evaluated the movement of HMGB1 by western blotting, immunofluorescence, and enzyme-linked immunosorbent assay (ELISA). Reactive oxygen species (ROS) level was evaluated to estimate the translocation mechanism of HMGB1. The role of secreted HMGB1 was evaluated by ELISA assay. Furthermore, we collected human nasal mucosa samples and nasal lavage fluids from patients conditioned under hypoxic and non-hypoxic environment, and compared the expression of HMGB1 in human nasal mucosa samples by immunohistochemistry and the levels of HMGB1 in lavage fluids using ELISA assay. Hypoxia induced translocation of HMGB1 into the extracellular area and it was dependent on ROS produced by dual oxidase 2. Secreted HMGB1 was involved in the upregulation of interleukin (IL)-8. In human samples, HMGB1 was translocated from nucleus to the cytoplasm in hypoxic-conditioned nasal mucosa. HMGB1 was increased in nasal lavage samples of chronic rhinosinusitis patients, whose sinus mucosa was supposed to be hypoxic as compared with controls. We suggest that HMGB1 is secreted in hypoxic condition via ROS-dependent mechanism and secreted HMGB1 participates in IL-8 upregulation mediating inflammatory response.

An unusual and rare gastric mucosal lesion histologically consisting of a localised accumulation of Russell bodies and Russell body-containing plasma cells, the so-called Mott cells, has been recognised only recently and termed as “Russell body gastritis”. This lesion, despite its densely monomorphous appearance is easily confirmed to be non-neoplastic by its polyclonal immunoreactive pattern to immunoglobulin light chains. However, the aetiology of Russell body gastritis is controversial and hence the optimal treatment for this disease has not been established. Two cases of Russell body gastritis associated withHelicobacter pyloriinfection are reported, and the possible role ofH pyloriinfection in the pathogenesis is discussed.

Based on the observed response rate and TTP, XP combination chemotherapy showed modest antitumor efficacy in patients with metastatic HCC as systemic first-line treatment. However, XP combination chemotherapy showed tolerable toxicity and demonstrated favorable OS time.