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Probiotics show great promise as alternative and environmentally friendly candidates to control microbial pathogens. Here, six isolated lactic acid bacteria (LAB) were chosen based on their anti-listerial activity. Anti-listerial LAB isolates were identified by 16S rRNA gene sequencing. The anti-listerial activities of these isolates were evaluated by Listeria monocytogenes biofilm inhibition assays on stainless-steel coupons (SS), lettuce, and a minimum biofilm eradication concentration (MBEC™) biofilm device. Results revealed that following co-culture with LAB for 24 h, L. monocytogenes biofilm cells were inhibited by up to 2.17 log CFU/cm2, 1.62 log CFU/cm2, and 1.09 log CFU/peg on SS, lettuce, and MBEC™, respectively. Although these LAB bacteria suppressed L. monocytogenes biofilm formation on both surfaces, the inhibitory effect on lettuce surfaces was lower than that on SS. These results support the potential use of LAB strains to inhibit biofilm formation by pathogenic bacteria on vegetable products and in the food industry, without associated risk to consumers.

Purpose c-Met is an attractive potential target for novel therapeutic inhibition of human cancer, and c-Met tyrosine kinase inhibitors (TKIs) are effective growth inhibitors of various malignancies. However, their mechanisms in anticancer effects are not clear. In the present study, we investigated the possibility that blocking c-Met signaling induces p53-mediated growth inhibition in lung cancer. Materials and Methods The growth inhibitory effects of c-Met TKI (SU11274) on lung cancer cells and a xenograft model were assessed using the MTT assay, flow cytometry, and terminal deoxyribonucleotide transferase-mediated nick-end labeling staining. The role of p53 protein in the sensitivity of c-Met TKI (SU11274) was examined by Western blot analysis and immunohistochemistry. Results SU11274 significantly induced apoptosis in A549 cells with wild-type p53, compared with that in Calu-1 cells with null-type p53. SU11274 increased p53 protein by enhancing the stability of p53 protein. Increased p53 protein by SU11274 induced up-regulation of Bax and PUMA expression and down-regulation of Bcl-2 expression, subsequently activating caspase 3. In p53 knock-out and knock-in systems, we confirmed that SU11274 caused apoptosis through the p53-mediated apoptotic pathway. Likewise, in the A549 xenograft model, SU11274 effectively shrank tumor volume and induced apoptosis via increased p53 protein expression. Blocking c-Met signaling increased the level of p53 protein. Conclusion Our finding suggested that p53 plays an important role in SU11274-induced apoptosis, and p53 status seems to be related to the sensitivity to SU11274 in lung cancer.

This research explored the importance of conflict resolution in communication between adolescents and their parents. A teaching and learning plan on communication using the Active listening, I-message method and no-lose conflict resolution method was developed and applied to teaching the `Communication among Family Members` unit in the middle school home economics and technology textbook. The experimental class of 203 students using the active listening, I message and no-lose conflict resolution method in communication was compared with a comparative class of 163 students using only the active listening and I message method, investigating the amounts of communication, conflicts, functional communication and degree of satisfaction the students perceived regarding relationships with their parents via pre and post tests. Both groups showed significant increases in their amounts of communication and functional communication. However, only the experimental class showed an increase in their degree of relationship satisfaction with their parents. Both groups evaluated the lesson positively.

Increased modification of proteins with O-linked N-acetylglucosamine (O-GlcNAc) has been implicated in the development of diabetic cardiomyopathy. We used the well-characterized ES cells (Nkx2.5GFP knock-in ES cells), to investigate the role of O-GlcNAcylation in cardiomyocyte development. O-GlcNAcylation decreased in differentiating ES cells, as did the expression of O-GlcNAc transferase. Increasing O-GlcNAcylation with glucosamine or by inhibiting N-acetylglucosaminidase (streptozotocin or PUGNAc) decreased the number of cardiomyocyte precursors and cardiac-specific gene expression. On the other hand, decreasing O-GlcNAcylation with an inhibitor of glutamine fructose-6-phosphate amidotransferase (6-diazo-5-oxo-norleucine) increased cardiomyocyte precursors. These results suggest that excessive O-GlcNAcylation impairs cardiac cell differentiation in ES cells.

The noninvasive imaging of dendritic cells (DCs) migrated into lymph nodes (LNs) can provide helpful information on designing DCs-based immunotherapeutic strategies. This study is to investigate the influence of transduction of human ferritin heavy chain (FTH) and green fluorescence protein (GFP) genes on inherent properties of DCs, and the feasibility of FTH as a magnetic resonance imaging (MRI) reporter gene to track DCs migration into LNs. FTH-DCs were established by the introduction of FTH and GFP genes into the DC cell line (DC2.4) using lentivirus. The changes in the rate of MRI signal decay (R-2*) resulting from FTH transduction were analyzed in cell phantoms as well as popliteal LN of mice after subcutaneous injection of those cells into hind limb foot pad by using a multiple gradient echo sequence on a 9.4 T MR scanner. The transduction of FTH and GFP did not influence the proliferation and migration abilities of DCs. The expression of co-stimulatory molecules (CD40, CD80 and CD86) in FTH-DCs was similar to that of DCs. FTH-DCs exhibited increased iron storage capacity, and displayed a significantly higher transverse relaxation rate (R-2*) as compared to DCs in phantom. LNs with FTH-DCs exhibited negative contrast, leading to a high R-2* in both in vivo and ex vivo T-2*-weighted images compared to DCs. On histological analysis FTH-DCs migrated to the subcapsular sinus and the T cell zone of LN, where they highly expressed CD25 to bind and stimulate T cells. Our study addresses the feasibility of FTH as an MRI reporter gene to track DCs migration into LNs without alteration of their inherent properties. This study suggests that FTH-based MRI could be a useful technique to longitudinally monitor DCs and evaluate the therapeutic efficacy of DC-based vaccines.

We describe a simple method for synthesizing superparamagnetic nanoparticles (SPIONs) as small, stable contrast agents for magnetic resonance imaging (MRI) based on sulfobetaine zwitterionic ligands. SPIONs synthesized by thermal decomposition were coated with zwitterions to impart water dispersibility and high in vivo stability through the nanoemulsion method. Zwitterion surfactant coating layers are formed easily on oleic acid-stabilized SPIONs via hydrophobic and van der Waals interactions. Our zwitterion-coated SPIONs (ZSPIONs) had ultrathin (∼5 nm) coating layers with mean sizes of 12.0 ± 2.5 nm, as measured by dynamic light scattering (DLS). Upon incubation in 1 M NaCl and 10% FBS, the ZSPIONs showed high colloidal stabilities without precipitating, as monitored by DLS. The T2 relaxivity coefficient of the ZSPIONs, obtained by measuring the relaxation rate on the basis of the iron concentration, was 261 mM(-1) s(-1). This value was much higher than that of the commercial T2 contrast agent because of the ultrathin coating layer. Furthermore, we confirmed that ZSPIONs can be used as MR contrast agents for in vivo applications such as tumor imaging and lymph node mapping.

The control of dendritic cell (DC) migration into lymph nodes (LNs) is important for the development of more effective DC-based immunotherapies. This study was undertaken to evaluate, dynamically and noninvasively, prostaglandin E2 (PGE2)-enhanced migration of DCs using a 1.5 T clinical MR scanner. DC2.4 cells were labeled with superparamagnetic iron oxide (SPIO), a clinically approved MRI contrast agent. DCs were stimulated with tumor necrosis factor-α and interferon-γ in the presence or absence of PGE2. Before and after subcutaneous injection of labeled DCs into the hind leg footpads of mice, MRI detailing the extent of DC migration into popliteal LNs was performed using a 1.5 T clinical MR scanner. SPIO labeling did not influence the viability, endocytic activity, migratory ability and/or co-stimulatory molecule expression of DCs. PGE2 enhanced significantly chemokine receptor-7 expression and the migration of DCs (p0.05). After subcutaneous injection of DCs, there were decreases in MR signal intensity in popliteal LNs at 24 h post-injection; in PGE2-treated cells, the MR signal intensity was significantly lower (decrease of 86.6 ± 2.5%) than in PGE2-untreated cells (decrease of 70.0 ± 4.2%) (p0.05). Histological analyses with the conventionally used Prussian blue stain demonstrated that the PGE2-treated DCs migrated more deeply into the center of LNs. PGE2-enhanced migration of SPIO-labeled DCs into LNs can be detected using a 1.5 T clinical MR scanner. Our results suggest that in vivo MRI of DC migration is a useful imaging method to predict DC therapy with a high rate of efficacy and to improve DC-based immunotherapy, thereby reducing costs compared with current treatments in clinical trials.

We report a case of insufficiency fracture of the sternum in a 70-year-old female patient with a review of the literature. She complained of sudden onset chest pain and aggravating dyspnea. She has been managed with corticosteroid due to chronic obstructive pulmonary disease for 15 years. Diagnosis of sternal insufficiency fracture presented with thoracic kyphosis was made on the basis of absence of trauma history, radiologic findings of lateral chest radiograph, bone scintigraphy and chest computed tomography. Thoracic kyphosis and osteoporosis secondary to menopause, corticosteroid therapy and limited mobility due to chronic obstructive pulmonary disease were considered as predisposing factors of the sternal insufficiency fracture in this patient.

A 52-year-old woman was presented with 2-week history of increasing dyspnea and dry cough. The chest radiograph revealed bilateral reticular infiltrates. Radiographic infiltrates were rapidly progressed and symptoms from hypoxemia were aggravated. The patient was intubated and bronchoscopy with transbronchial lung biopsies was performed. Biopsies revealed lymphatic vessels plugged by nests of metastatic adenocarcinoma. She died 11 days after admission despite of intensive ventilatory support. We had difficulties in the diagnosis of lymphangitic lung carcinomatosis at initial presentation of her illness because the progression was unusually rapid. Lymphangitic lung carcinomatosis shoud should be included in the differential diagnosis of patients showing rapidly progressive interstitial radiographic findings. Also, transbronchial biopsy may be a useful tool to confirm the diagnosis.