Successful development of safe and effective nanoprobes for tumor targeting and selective therapy is a challenging task. Although gold nanorods(GNRs) have the potential to perform such a role, the toxicity of surfactant cetyltrimethylammonium bromides (CTAB) on their surfaces limits their applications. Here, polyamidoamine dendrimer was applied to replace CTAB molecules on the surface of gold nanorods. When the resultant dendrimer-modified gold nanorods conjugated with arginine-glycine-aspartic acid (RGD) peptides, they showed highly selective targeting and destructive effects on the cancer cells and solid tumors under near-infrared laser irradiation. Also, we successfully observed the disappearance of tumors implanted in four sample mice from test group of ten. High-performance RGD-conjugated dendrimer-modified GNR nanoprobes exhibit great potential in applications such as tumor targeting, imaging, and selective photothermal therapy.

There are disagreements among researchers about the association between vitamin D deficiency during pregnancy and preterm birth (PTB). Therefore, we conducted a meta-analysis of observational studies to evaluate this association. We performed a systematic literature search of PubMed, MEDLINE and the Cochrane Library through August 2015 with the following keywords: “vitamin D” or “cholecalciferol” or “25-hydroxyvitamin D” or “25(OH)D” in combination with “premature birth” or “preterm birth” or “PTB” or “preterm delivery” or “PTD” or “prematurity”. Our meta-analysis of 10 studies included 10,098 participants and found that pregnant women with vitamin D deficiency (maternal serum 25 (OH) D levels < 20 ng/mL) experienced a significantly increased risk of PTB (odds ratio (OR) = 1.29, 95% confidence intervals(CI): 1.16, 1.45) with low heterogeneity (I2 = 25%, p = 0.21). Sensitivity analysis showed that exclusion of any single study did not materially alter the overall combined effect. In the subgroup analyses, we found that heterogeneity was obvious in prospective cohort studies (I2 = 60%, p = 0.06). In conclusion, pregnant women with vitamin D deficiency during pregnancy have an increasing risk of PTB.

Background: Non-coding RNA molecules, such as microRNAs, may play an important role in carcinogenesis. Recent studies have indicated that microRNAs are involved in initiation and progression of various malignancies. However, little work has been done to compare the microRNA expression patterns in oral cancer. In this study, we constructed an animal model of oral squamous cell carcinoma to investigate expression profiles of microRNAs in oral carcinogenesis.

These results suggested that the ERK, JNK and p38 pathways mediate TGF-beta(1)/Smad signal transduction and might be considered as specific targets of drug therapy for keloids.

A novel molecular axis of LINC00511/miR-765/LAMC2 was investigated to regulate the tumor development of TSCC. LINC00511 promoted the expression of LAMC2 via the ceRNA mechanism of sponging miR-765. The ceRNA regulatory network provided a novel understanding of TSCC pathogenesis and also shed light on exploiting the new field of lncRNA-directed therapy against TSCC.

We have demonstrated that Valpha24(+)Vbeta11(+) invariant (Valpha24(+)i) NKT cells from patients with allergic asthma express CCR9 at high frequency. CCR9 ligand CCL25 induces chemotaxis of asthmatic Valpha24(+)i NKT cells but not the normal cells. A large number of CCR9-positive Valpha24(+)i NKT cells are found in asthmatic bronchi mucosa, where high levels of Th2 cytokines are detected. Asthmatic Valpha24(+)i NKT cells, themselves Th1 biased, induce CD3(+) T cells into an expression of Th2 cytokines (IL-4 and IL-13) in cell-cell contact manner in vitro. CD226 are overexpressed on asthmatic Valpha24(+)i NKT cells. CCL25/CCR9 ligation causes directly phosphorylation of CD226, indicating that CCL25/CCR9 signals can cross-talk with CD226 signals to activate Valpha24(+)i NKT cells. Prestimulation with immobilized CD226 mAb does not change ability of asthmatic Valpha24(+)i NKT cells to induce Th2-cytokine production, whereas soluble CD226 mAb or short hairpin RNA of CD226 inhibits Valpha24(+)i NKT cells to induce Th2-cytokine production by CD3(+) T cells, indicating that CD226 engagement is necessary for Valpha24(+)i NKT cells to induce Th2 bias of CD3(+) T cells. Our results are providing with direct evidence that aberration of CCR9 expression on asthmatic Valpha24(+)i NKT cells. CCL25 is first time shown promoting the recruitment of CCR9-expressing Valpha24(+)i NKT cells into the lung to promote other T cells to produce Th2 cytokines to establish and develop allergic asthma. Our findings provide evidence that abnormal asthmatic Valpha24(+)i NKT cells induce systemically and locally a Th2 bias in T cells that is at least partially critical for the pathogenesis of allergic asthma.

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The occurrence of highly pathogenic avian influenza virus H5N1 highlights the urgent need for new classes of antiviral drugs. Inhibition of H5N1 entry into cells may be an effective strategy. We report the first three small molecule inhibitors saponins with 3-O-beta-chacotriosyl residue, which showed potent inhibitory activity with IC(50) of 7.22-9.25 microM. The subsequent SAR studies showed the 3-O-beta-chacotriosyl residue was essential for the activity, and the aglycone structure also affected the activity.