Description: Background: The appearance of smear-positivity but culture-negativity (SPCN) for acid-fast bacilli among sputum specimen is frequently found in pulmonary tuberculosis (TB) patients during treatment. This study aimed to investigate clinical risk factors, impacts on treatment course, and relapse pattern associated with sputum SPCN. Methods: We retrospectively enrolled 800 patients with culture-proven pulmonary TB who were receiving standard treatment and follow-up at six TB-referral hospitals in Taiwan between January 2006 and December 2007. Relevant patient characteristics and chemotherapy data were analyzed for associations with incidence of SPCN. Data from patients who relapsed within 3 years after completing treatment were analyzed for associations with SPCN during treatment. Results: Of the 800 subjects, 111 (13.8%) had sputum SPCN during treatment. Three factors were found to predict the development of SPCN; namely, high initial acid-fast staining grading (OR, 3.407; 95% CI, 2.090–5.553), cavitation on chest-X ray films (OR, 2.217; 95% CI, 1.359–3.615), and smoking (OR, 1.609; 95% CI, 1.006–2.841). Patients with SPCN had longer treatment duration (rifampicin: 284 ± 91 vs. 235 ± 69 days, P

Description: Background: Resistin, adipocyte-secreting adipokine, may play critical role in modulating cancer pathogenesis. The aim of this study was to investigate the effects of resistin on HCC adhesion to the endothelium, and the mechanism underlying these resistin effects. Methods: Human SK-Hep1 cells were used to study the effect of resistin on intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions as well as NF-kappaB activation, and hence cell adhesion to human umbilical vein endothelial cells (HUVECs). 5-Aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, was used to determine the regulatory role of AMPK on HCC adhesion to the endothelium in regard to the resistin effects. Results: Treatment with resistin increased the adhesion of SK-Hep1 cells to HUVECs and concomitantly induced NF-kappaB activation, as well as ICAM-1 and VCAM-1 expressions in SK-Hep1 cells. Using specific blocking antibodies and siRNAs, we found that resistin-induced SK-Hep1 cell adhesion to HUVECs was through NF-kappaB-regulated ICAM-1 and VCAM-1 expressions. Moreover, treatment with AICAR demonstrated that AMPK activation in SK-Hep1 cells significantly attenuates the resistin effect on SK-Hep1 cell adhesion to HUVECs. Conclusions: These results clarify the role of resistin in inducing HCC adhesion to the endothelium and demonstrate the inhibitory effect of AMPK activation under the resistin stimulation. Our findings provide a notion that resistin play an important role to promote HCC metastasis and implicate AMPK may be a therapeutic target to against HCC metastasis.