An in vitro method for the estimation of iron bioavailability was subjected to an interlaboratory trial. The method involved a simulated gastrointestinal digestion using pepsin for the gastric stage followed by pancreatin and bile salts for the intestinal stage. The proportion of iron diffused through a semi‐permeable membrane (molecular mass cut‐off 10 kDa) was used to measure the iron dialysability. An interlaboratory trial between nine laboratories was conducted to evaluate the repeatability and reproducibility of the agreed method. The reproducibility of the method among the participating laboratories was 20–30% and depended on the content of dialysable iron. Several factors contributing to the variation in the in vitro dialysability among laboratories are discussed. The pH adjustment in the intestinal digestion was identified as one of the critical parameters. The present in vitro method was used to evaluate the iron dialysability from three meals. The dialysability data were in reasonable agreement with human absorption data. The usefulness of the in vitro dialysability method is discussed.

Abstract. Collagen type XI α1 (COL11A1), a minor fibrillar collagen, has been demonstrated to be involved in cell proliferation, migration and the tumorigenesis of many human malignancies. Previous studies have shown that COL11A1 may be a valuable diagnostic marker for non-small cell lung carcinoma (NSCLC). However, its biological function in NSCLC progression remains largely unclear. In the present study, we investigated the expression levels of COL11A1 in different human NSCLC samples, and found that COL11A1 was overexpressed in NSCLC with lymph node metastasis and in recurrent NSCLC tissues. We also revealed that COL11A1 promoted the cell proliferation, migration and invasion of NSCLC cell lines in vitro. Furthermore, our results highlighted the importance of COL11A1 in chemoresistance to cisplatin. Mechanistically, we found that the effects of the overexpression of COL11A1 in NSCLC cells were mediated by Smad signaling. Collectively, our findings suggest that COL11A1 may sever as a biomarker for metastatic NSCLC, and can be used to predict recurrence after surgical resection. Therapeutic approaches targeting COL11A1 may facilitate the optimization of cisplatin treatment of NSCLC by overcoming chemoresistance. IntroductionLung cancer is the most common type of cancer, and is the leading cause of human cancer-related deaths (1,2). Non-small cell lung carcinoma (NSCLC) accounts for approximately 85% of all cases of human lung cancer, including all types of epithelial lung cancer except small cell lung carcinoma (SCLC) (3). Generally, the 5-year survival rate of lung cancer patients is approximately 15% (2). For patients with different stages of lung cancer, the 5-year relative survival rate varies dramatically from 49 to 2% (2,4). However, approximately 70% of patients with lung cancer were found to present with intrathoracic or extrathoracic metastasis at initial diagnosis (3,5). Thus, it is crucial to detect lung cancer at an early stage, and to suppress the spread of primary cancer.Currently, surgical resection remains the single most successful treatment for patients with early-stage NSCLC (6,7). However, despite optimal surgical treatment, approximately half of the patients with NSCLC develop recurrence and succumb to the disease, even though they present with histologically negative lymph nodes (8,9). While bone is the most common target of distant metastasis from lung cancer, recurrent NSCLC is often systemic (4,8). Although the mechanisms of recurrent NSCLC remain unclear, several molecules have been reported to predict the recurrence of NSCLC. These include EphA2 (EPH receptor A2) receptor tyrosine kinase, USP17 and DNA methylation markers (10-12).The collagen type XI α1 (COL11A1) gene encodes one of the two α chains of type XI collagen, a minor fibrillar collagen (13). As a major component of the extracellular matrix (ECM), collagens are involved in the regulation of multiple biological processes, including cell proliferation, differentiation and migration (14,15). Type XI collagen is a heterotrimer, ...

Transplantation of bone marrow stromal cells (BMSCs) is a promising therapy for ischemic stroke, but the poor oxygen environment in brain lesions limits the efficacy of cell-based therapies. Here, we tested whether hypoxic preconditioning (HP) could augment the efficacy of BMSC transplantation in a rat ischemic stroke model and investigated the underlying mechanism of the effect of HP. In vitro, BMSCs were divided into five passage (P0, P1, P2, P3, and P4) groups, and HP was applied to the groups by incubating the cells with 1% oxygen for 0, 4, 8, 12, and 24 h, respectively. We demonstrated that the expression of hypoxia-inducible factor-1α (HIF-1α) was increased in the HP-treated BMSCs, while their viability was unchanged. We also found that HP decreased the apoptosis of BMSCs during subsequent simulated ischemia-reperfusion (I/R) injury, especially in the 8-h HP group. In vivo, a rat transient focal cerebral ischemia model was established. These rats were administered normal cultured BMSCs (N-BMSCs), HP-treated BMSCs (H-BMSCs), or DMEM cell culture medium (control) at 24 h after the ischemic insult. Compared with the DMEM control group, the two BMSC-transplanted groups exhibited significantly improved functional recovery and reduced infarct volume, especially the H-BMSC group. Moreover, HP decreased neuronal apoptosis and enhanced the expression of BDNF and VEGF in the ischemic brain. Survival and differentiation of transplanted BMSCs were also increased by HP, and the quantity of engrafted BMSCs was significantly correlated with neurological function improvement. These results suggest that HP may enhance the therapeutic efficacy of BMSCs in an ischemic stroke model. The underlying mechanism likely involves the inhibition of caspase-3 activation and an increasing expression of HIF-1α, which promotes angiogenesis and neurogenesis and thereby reduces neuronal death and improves neurological function.

IntroductionHeparin-binding protein (HBP) is an antimicrobial protein stored in neutrophil granules and plays a role in endothelial permeability regulation. The aim was to assess the diagnostic and prognostic value of measuring HBP in patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS).MethodsPlasma HBP was collected from 78 patients with ALI/ARDS, 28 patients with cardiogenic pulmonary edema (CPE) and 20 healthy volunteers at enrollment. Levels of HBP were measured by ELISA.ResultsPatients with ALI/ARDS had significantly higher median levels of HBP compared with patients with CPE (17.15 (11.95 to 24.07) ng/ml vs. 9.50 (7.98 to 12.18) ng/ml, P <0.001) at enrollment. There was no significant difference between CPE patients and healthy subjects in terms of HBP value (P = 0.372). The HBP levels of nonsurvivors was significantly higher than that of survivors (23.90 (14.81 to 32.45) ng/ml vs. 16.01 (10.97 to 21.06) ng/ml, P = 0.012) and multivariate logistic regression showed HBP (odds ratio =1.52, P = 0.034) was the independent predictor for 30-day mortality in patients with ALI/ARDS.ConclusionsPlasma HBP levels of ALI/ARDS patients were significantly higher than that of CPE patients. HBP was a strong prognostic marker for short-term mortality in ALI/ARDS.