Influence of electrohydrodynamics on the drying characteristics and volatile components of iron stick yam.

The drying characteristics, rehydration capacity, color, infrared spectra and volatile components of iron stick yam slices were investigated under different alternating current (AC) voltages (13, 17, 21 kV), hot air drying (HAD) (60 °C) and natural drying (AD) by electrohydrodynamic (EHD) drying and HAD experimental devices. The results showed that slices of iron stick yam dried the quickest with HAD, which also had the fastest drying rate; while drying the slices of iron stick yam with EHD led to a better rehydration capacity, higher brightness L* and whiteness, a more stable protein secondary structure, and a greater variety and content of volatile components compared with AD and HAD. These finding indicated that EHD is a more promising method for drying iron stick yam.

[Retracted] MicroRNA-33b suppresses the proliferation and metastasis of hepatocellular carcinoma cells through the inhibition of Sal-like protein 4 expression.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the Transwell cell migration data shown in Figs. 2D and 4C were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to International Journal of Molecular Medicine, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in International Journal of Molecular Medicine 38: 1587­1595, 2016; DOI: 10.3892/ijmm.2016.2754].

Spectral characteristics on increasing hydrophilicity of Alfalfa seeds treated with alternating current corona discharge field.

In this study, corona discharge at atmospheric pressure under an alternating current (AC) field with a multi-needle plate electrode structure was used as mutagen to study the effects of corona discharge field on the hydrophilicity of alfalfa seeds, especially the effects of non-uniform electric field that is frequently ignored. Alfalfa seed were divided into two groups, one group was covered with 1 mm-thick polypropylene petri dish cover that can be approximated as a single factor effect of non-uniform electric field, the other group was directly irradiated by corona discharge field under different parameters. Fourier transform infrared spectroscopy (FTIR) and dual-index sequence analysis were used to detect and compare the spectra of alfalfa seed coats with different treatments. Results showed that the peaks of the seed coat at 2856 and 1727 cm-1 in the treatment group changed, indicating that hydrophobic wax, lipid, and cellulose may be cracked or degraded. Corona discharge field treatment can change the chemical structure of alfalfa seed coats, resulting in the changes in their hydrophilicity. The results of the apparent contact angle and scanning electron microscopy (SEM) and other experiments showed that the change in 19 kV non-covered treatment group was greatest, the petri dish cover can effectively reduce the physicochemical etching of ionic wind, the hydrophilicity of alfalfa seeds improved after corona discharge field treatment regardless of whether there is an ionic effect during irradiation, and the ionic wind has a greater influence on the hydrophilicity of alfalfa seeds than the non-uniform electric field. This study revealed the biological effect mechanism of corona discharge field from the perspective of spectral characteristics and provided experimental data support for the analysis of alfalfa seed surface modification and chemical structure after corona discharge field treatment.

THBS2 is a biomarker for AJCC stages and a strong prognostic indicator in colorectal cancer.

PURPOSE: To investigate the expression of thrombospondin 2 (THBS2) in colorectal cancer (CRC) and its relationship with clinicopathological features and prognosis. METHODS: THBS2 expression was evaluated with tissue microarrays (TMAs) immunohistochemistry (IHC) staining in 100 CRC samples. RESULTS: High THBS2 expression was found in 73 patients (45 male and 28 female). THBS2 expression was significantly correlated to TNM stages (p=4.1×10-5), T classification (p=0.005), lymph node metastasis (p=3×10-4) and AJCC stages (p=0), while no significant association was found in gender, age, distant metastasis or tumor size. In both univariate and multivariate analyses, THBS2 showed statistically prognostic significance [p<0.001, HR (hazard ratio) = 0.237, 95% CI (0.101-0.557) and p<0.001, HR=0.158, 95% CI (0.062-0.401)]. Kaplan-Meier survival analysis further confirmed that THBS2 expression was significantly correlated with clinical outcomes (p<0.001). CONCLUSIONS: All the results indicated THBS2 expression might become a prognostic marker for CRC.

MicroRNA-33b suppresses the proliferation and metastasis of hepatocellular carcinoma cells through the inhibition of Sal-like protein 4 expression.

MicroRNAs (miRNAs or miRs) have been found to participate in the development and malignant progression of human cancers by negatively mediating the expression of their target genes. Recently, miR­33b has been reported to be involved in multiple types of human cancer, including hepatocellular carcinoma (HCC). However, the underlying regulatory mechanisms of miR­33b in HCC cell growth and metastasis remain largely unclear. In the present study, RT-qPCR revealed that miR­33b was significantly downregulated in HCC tissues compared to their matched adjacent normal tissues. Moreover, the miR­33b level was significantly lower in advanced-stage HCC (stages T3-T4) compared to early-stage HCC (stages T1-T2). Furthermore, it was also downregulated in the HCC cell lines, LH86, HepG2, LMH and PLHC-1, when compared with the THLE-3 normal human liver cells. We further demonstrated that the overexpression of miR­33b led to a significant decrease in the proliferation, migration and invasion of HepG2 and LH86 cells. Luciferase reporter assay identified Sal-like protein 4 (SALL4) as a target gene of miR­33b, and its protein expression was negatively regulated by miR­33b in HepG2 and LH86 cells. Moreover, the restoration of SALL4 expression markedly reversed the inhibitory effect of miR­33b overexpression on the proliferation, migration and invasion of HepG2 and LH86 cells, indicating that SALL4 is involved in miR­33b-mediated malignant phenotypes of HCC cells. Furthermore, we found that SALL4 was significantly upregulated in HCC tissues compared to their matched adjacent normal tissues, and its increased expression was significantly associated with the advanced malignancy of HCC. Moreover, SALL4 was also upregulated in HCC cell lines compared to the THLE-3 normal human liver cells. Finally, we found that the SALL4 expression inversely correlated with the miR­33b level in HCC tissues. On the whole, the findings of our study demonstrate that miR­33b suppresses the proliferation and metastasis of HCC cells through the inhibition of SALL4 expression. Therefore, miR­33b/SALL4 may become a potential therapeutic target for the treatment of HCC.

C323 of SR-BI is required for SR-BI-mediated HDL binding and cholesteryl ester uptake.

Scavenger receptor BI (SR-BI) is an HDL receptor. It binds HDL and mediates the uptake of cholesteryl ester from HDL. Early studies have pointed out that the extracellular domain of SR-BI is critical for SR-BI-mediated cholesteryl ester uptake. However, the extracellular loop of SR-BI is large: it contains 403 amino acids. The HDL binding site and the modulation of SR-BI-mediated cholesteryl ester uptake remain to be identified. In this study, using C323G mutant SR-BI, we showed that C323G mutant SR-BI lost its HDL binding and cholesteryl ester uptake activity, indicating that the highly conserved C323 is required for SR-BI-mediated HDL binding and cholesteryl ester uptake. Using a blocking antibody against C323 region, we demonstrated that C323 is directly involved in HDL binding and likely an HDL binding site. Using C323G mutant transgenic mouse model, we further demonstrated that C323 of SR-BI is required for regulating plasma cholesterol levels in vivo. Using redox reagents, we showed that physiological relevant levels of H(2)O(2) upregulated the SR-BI-mediated cholesteryl ester uptake activity by 65%, whereas GSH or DTT significantly downregulated SR-BI-mediated cholesteryl ester uptake activity by 45%. C323 of SR-BI is critical for SR-BI-mediated HDL binding and cholesteryl ester uptake, and changes in redox status may be a regulatory factor modulating SR-BI-mediated cholesterol transport.

Caveolin-1 protects against sepsis by modulating inflammatory response, alleviating bacterial burden, and suppressing thymocyte apoptosis.

Sepsis is a leading cause of death, which is characterized by uncontrolled inflammatory response. In this study, we report that caveolin-1, a major component of caveolae, is a critical survival factor of sepsis. We induced sepsis using a well established sepsis animal model, cecal ligation and puncture (CLP). CLP induced 67% fatality in caveolin-1 null mice, but only 27% fatality in wild type littermates (p = 0.015). Further studies revealed that mice deficient in caveolin-1 exhibited marked increase in tumor necrosis factor-alpha and interleukin-6 production 20 h following CLP treatment, indicating uncontrolled inflammatory responses in the absence of caveolin-1. Caveolin-1 null mice also had a significant increase in bacteria number recovered from liver and spleen, indicating elevated bacterial burdens. In addition, caveolin-1 null mice had a 2-fold increase in thymocyte apoptosis compared with wild type littermates, indicating caveolin-1 as a critical modulator of thymocyte apoptosis during sepsis. In conclusion, our findings demonstrate that caveolin-1 is a critical protective modulator of sepsis in mice. Caveolin-1 exerts its protective function likely through its roles in modulating inflammatory response, alleviating bacterial burdens, and suppressing thymocyte apoptosis.

Scavenger Receptor BI Protects against Septic Death through Its Role in Modulating Inflammatory Response.

Sepsis is a leading cause of death that is characterized by uncontrolled inflammatory response. In this study, we report that scavenger receptor BI (SR-BI), a high density lipoprotein receptor, is a critical survival factor of sepsis. We induced sepsis using an established septic animal model, cecal ligation and puncture (CLP). CLP induced 100% fatality in SR-BI-null mice but only 21% fatality in wild type littermates. SR-BI-null mice exhibited aberrant inflammatory responses with delayed inflammatory cytokine generation at the early stage of sepsis and highly elevated inflammatory cytokine production 20 h after CLP treatment. To understand the mechanisms underlying SR-BI protection, we elucidated the effect of macrophage SR-BI on inflammatory cytokine generation. Macrophages from SR-BI-null mice produced significantly higher levels of inflammatory cytokines than those of wild type controls in response to LPS. Importantly, transgenic mice overexpressing SR-BI were more resistant to CLP-induced septic death. Using an HEK-Blue(TM) cell system, we demonstrated that expression of SR-BI suppressed TLR4-mediated NF-kappaB activation. To understand why SR-BI-null mice had a delayed inflammatory response, we elucidated the effect of SR-BI on LPS clearance during sepsis. Compared with wild type controls, SR-BI-null mice had lower plasma LPS levels in the early stage of sepsis and elevated plasma LPS levels 20 h following CLP treatment. In conclusion, our findings demonstrate that SR-BI is a critical protective modulator of sepsis in mice. SR-BI exerts its protective function through its role in modulating inflammatory response in macrophages and facilitating LPS recruitment and clearance.