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BACKGROUND.The authors investigated the prevalence of hepatitis B virus (HBV) infection by using serologic markers in non‐Hodgkin lymphoma (NHL) compared with other types of cancers in Chinese patients.METHODS.In this case‐control study, HBV and other hepatitis markers were compared between a study group and a control group. The study group included 587 patients with NHL (age range, 16–86 years), and the control group included 1237 patients (age range, 16–89 years) who were diagnosed with other cancers except liver cancer. An enzyme‐linked immunosorbent assay was used to test serum samples from both groups for HBV markers and other hepatitis markers.RESULTS.Logistic regression analysis showed that there was a higher prevalence of HBV infection in patients with the B‐cell subtype of NHL (30.2%) than in patients with other cancers (14.8%; odds ratio [OR], 2.6; 95% confidence interval [95% CI], 2.0–3.4); however, in patients with the T‐cell subtype of NHL, the HBV infection rate (19.8%) was similar to that among patients with other cancers (OR, 1.2; 95% CI, 0.8–1.8). A significant difference in HBV prevalence was found between B‐cell and T‐cell NHL (OR, 2.3; 95% CI, 1.4–3.6). In the patients with B‐cell NHL, those who were infected with HBV had a significantly earlier disease onset (9.5 years) than those who were not infected with HBV.CONCLUSIONS.The current results demonstrated that patients with B‐cell NHL, but not patients with T‐cell NHL, had a higher prevalence of HBV infection. HBV infection was associated with a significantly earlier disease onset (P < .001), a finding that suggested the possibility that HBV may play an etiologic role in the induction of B‐cell NHL. Cancer 2007. © 2007 American Cancer Society.

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Our study aimed to investigate the effects of acupuncture on diabetic peripheral neuropathy. We compared 42 cases treated with acupuncture with 21 cases exposed to sham acupuncture and observed the effects on nerve conduction velocity and a variety of subjective symptoms associated with diabetic peripheral neuropathy. Three of the six measures of motor nerves, and two measures of sensory function, demonstrated significant improvement (p < 0.05) over the 15-day treatment period in the acupuncture group, while no motor or sensory function significantly improved in the sham acupuncture group. There were also significant differences in vibration perception threshold between the groups (p < 0.05) and when compared to the baseline levels (p < 0.01) in the acupuncture group. Acupuncture was significantly more effective than sham for treatment of numbness of the lower extremities, spontaneous pain in the lower extremities, rigidity in the upper extremities and alterations in temperature perception in the lower extremities after therapy. Our pilot study has, therefore, provided evidence that acupuncture may be clinically useful for the radical treatment of diabetic peripheral neuropathy.

Supraphysiological concentrations of cholecystokinin (CCK) induce chemokine expression in rat pancreatic acini through the activation of the transcription factor NF-kappaB. In the current study, the intracellular signals involved in these pathophysiological effects of CCK were investigated. CCK induction of mob-1 expression in isolated rat pancreatic acini was blocked by the protein kinase C (PKC) inhibitors GF-109203X and Ro-32-0432 and by the intracellular Ca(2+) chelator BAPTA. CCK induced NF-kappaB nuclear translocation, and DNA binding was also blocked by GF-109203X and BAPTA. Direct activation of PKC with TPA induced mob-1 chemokine expression and activated NF-kappaB DNA binding to a similar extent as did CCK. Increasing intracellular Ca(2+) using ionomycin had no effect on mob-1 mRNA levels or NF-kappaB activity. Both CCK and TPA treatments decreased inhibitory kappaB-alpha (IkappaB-alpha) levels, whereas ionomycin had no effect. However, the effects of TPA on IkappaB-alpha degradation were less complete than for CCK. In combination, TPA and ionomycin degraded IkappaB-alpha to a similar extent as CCK. Therefore, activation of NF-kappaB and mob-1 expression by supraphysiological CCK is likely mediated by both PKC activation and elevated intracellular Ca(2+).

Inflammatory mediators are involved in the early phase of acute pancreatitis, but the cellular mechanisms responsible for their generation within pancreatic cells are unknown. We examined the role of nuclear factor-κB (NF-κB) in cholecystokinin octapeptide (CCK-8)-induced mob-1 chemokine expression in pancreatic acinar cells in vitro. Supraphysiological, but not physiological, concentrations of CCK-8 increased inhibitory κB (IκB-α) degradation, NF-κB activation, and mob-1 gene expression in isolated pancreatic acinar cells. CCK-8-induced IκB-α degradation was maximal within 1 h. Expression of mob-1 was maximal within 2 h. Neither bombesin nor carbachol significantly increased mob-1 mRNA or induced IκB-α degradation. Thus the concentration, time, and secretagogue dependence of mob-1 gene expression and IκB-α degradation were similar. Inhibition of NF-κB with pharmacological agents or by adenovirus-mediated expression of the inhibitory protein IκB-α also inhibited mob-1 gene expression. These data indicate that the NF-κB signaling pathway is required for CCK-8-mediated induction of mob-1 chemokine expression in pancreatic acinar cells. This supports the hypothesis that NF-κB signaling is of central importance in the initiation of acute pancreatitis.

Current evidence, though limited, suggests that there is a possible increase in risk of colorectal cancer because of H. pylori infection.

SUMMARY BackgroundThe current standard of care in proton pump inhibitor failure is to double the proton pump inhibitor dose, despite limited therapeutic gain.