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The intrinsic limits of conventional ultrasound microbubble contrast agent greatly promoted the development and application of various nanomaterials for more efficient cancer ultrasound theranostics. Considerable successes have been achieved in the field of ultrasound molecular imaging and targeted therapy for tumor based on nanoparticulate theranostic agents. This review summarizes and discusses the emerging development on exploring organic and inorganic nanomaterials for ultrasound-based tumor diagnositic applications, and as synergistic agents for ultrasound targeted therapy in fighting cancer. The relationship between structure/composition and functionality of nanomaterials for ultrasound theranostic is discussed and revealed in detail. Finally, the further development and challenges facing clinical implementation of ultrasound nanomedicine are discussed. As a highly promising and valuable tumor-specific theranostic methodology, it is believed that ultrasound nanomedicine would pave a novel but efficient way for combating cancer. [ABSTRACT FROM AUTHOR]

Abstract Background Gastric cancer (GC) severely threatens human life, and METase seemed to inhibit tumor growth. However, the potential mechanism underlying it is still unclear. Methods Both clinical tissues and cell lines were used in the present study. SNHG5 and miR-20a expressions were determined using real-time PCR. Western blot was performed to determine the expression of autophagy-related proteins. The interaction between miR-20a and SNHG5 was determined using luciferase reporter assay and RNA immunoprecipitation (RIP). Results The expression of SNHG5 was decreased in GC tissues and cell lines. Overexpressed METase significantly promoted cell apoptosis and autophagy, as well as the expression of SNHG5. SNHG5 directly regulated the expression of miR-20a. GC cells transfected with pcDNA-SNHG5 significantly promoted cell apoptosis and autophagy, while the co-transfected with miR-20a mimic dramatically reversed the effects of pcDNA-SNHG5. Overexpressed METase significantly promoted cell autophagy, which was abolished by down-regulated SNHG5. Conclusion Overexpressed METase promoted cell apoptosis and autophagy via up-regulating the expression of SNHG5 and down-regulating miR-20a in GC. [ABSTRACT FROM AUTHOR]

In this paper, a new discrete element method (DEM) containing particle flow code (PFC) is presented as an efficient-to-implement alternative to the existing finite element method (FEM) for simulating internal forces and deformations of a hot-rolled H-section steel beam subject to static loading. Unlike FEM, which is efficient to solve continuous problems, the PFC method can solve discontinuous problems, such as collapse procedure of structures, and the collapse procedure of the structure can be monitored at different times in a more time-saving way. First of all, a linear constitutive model in FEM was built to compare with the linear parallel bond model built in PFC, a hot-rolled H-section steel beam considering geometrically non-linearity subject to static loading was simulated and the simulation results were compared with theoretical solution and FEM results. Both internal forces and deformations before yielding were compared and good agreements were achieved. Secondly, with the object-oriented programming technique and the redeveloped interface of PFC, a user-defined parallel bond model was developed to consider material nonlinearity and compared with the bilinear constitutive model built in FEM. Both internal forces and deformations before and after yielding were compared and good agreements were observed. Thus, the DEM model adopted in this paper can be efficiently used to simulate the behavior of the H-section steel beam. In the future, the developed parallel bond model can be used to simulate the performance of H-section steel beam subject to vertical impact loading and three-dimensional steel framed structure subject to horizontal collision. [ABSTRACT FROM AUTHOR]

Seven new acylated C-glycosylflavones, oreocharioside A-G, together with two known compounds were isolated from the whole plant of Oreocharis auricula. Their structures were characterized by the comprehensive analysis of their NMR, IR, UV, CD spectra and HRESIMS data. All the new compounds were evaluated for the antioxidant and anti-inflammatory activities. The results showed that compounds 1 and 2 had significant DPPH and ABTS radical scavenging activities, with the IC 50 values of 0.32–3.20 μg/mL. Compounds 2 and 3 exhibited the higher potency among all the new compounds in reducing TNF-α production. [Display omitted] • Seven new acylated C-glycosylflavones (1 – 7) together with two known compounds were isolated from Oreocharis auricula. • All the new compounds were characterized by the comprehensive analysis of their NMR, IR spectra and HRESIMS data. • Compound 1 and 2 showed significant DPPH and ABTS radical scavenging activities, with IC 50 values of 0.32–3.20 μg/mL. • Compound 2 and 3 exerted weak anti-inflammatory effects by inhibiting TNF-α production in the inflammatory process. [ABSTRACT FROM AUTHOR]

• LncRNA HCG18 is highly expressed in Exos derived from GC and exosomal lncRNA HCG18 facilitate M2 macrophage polarization. • Exosomal lncRNA HCG18 promotes M2 macrophage polarization by negatively regulating miR-875-3p in macrophages. • Overexpression of miR-875-3p in macrophages restrains M2 macrophage polarization by decreasing KLF4 expression. • GCCs-sh-HCG18-Exos restrain the tumor growth of GC induced by M2 macrophages. Gastric cancer (GC) derived exosomes (Exos) aggravate GC development by facilitating M2 macrophage polarization and long non-coding RNA (lncRNA) HCG18 was highly expressed in GC. This study aimed to investigate whether the exosomal lncRNA HCG18 regulated the M2 macrophage polarization in GC and the possible mechanism. The isolated GC cells (GCCs)-Exos were identified using transmission electron microscopy, Nanoparticle Tracking Analysis and Western blot. The GCCs-Exos function was verified by enzyme-linked immunosorbent assay and flow cytometry. Meanwhile, the exosomal lncRNA HCG18 function was determined using the in vitro assays. Furthermore, the underlying mechanism of the exosomal lncRNA HCG18 that regulated M2 macrophage polarization in GC was investigated using dual-luciferase reporter gene assay and RNA pull-down. After the validation of GCCs-Exos, the GCCs-Exos facilitated the M2 macrophage polarization. The in vitro assays confirmed that the exosomal lncRNA HCG18 positively regulated the M2 macrophage polarization. Mechanistically, lncRNA HCG18 bound to miR-875-3p, miR-875-3p bound to KLF4. Furthermore, GCCs-exosomal lncRNA HCG18 elevated the KLF4 expression by decreasing miR-875-3p in macrophages to facilitate M2 macrophage polarization, thus alleviating GC. The in vivo assays clarified that the GCCs-exosomal lncRNA HCG18 restrained the tumor growth of GC induced by M2 macrophages. GCCs-exosomal lncRNA HCG18 elevated KLF4 expression by decreasing miR-875-3p in macrophages to facilitate the M2 macrophage polarization. [ABSTRACT FROM AUTHOR]

Purpose: To investigate, in a large cohort of patients, the immunophenotypic and clinical differences of nasal and extranasal extranodal nasal-type natural killer/T-cell lymphoma of the upper aerodigestive tract (UADT-NKTCL) and examine the relevance of the immunophenotype on the clinical behavior, prognosis, and treatment. Methods and Materials: A total of 231 patients with UADT-NKTCL were recruited. One hundred eighty-one patients had primary location in the nasal cavity (nasal UADT-NKTCL), and 50 patients had primary extranasal UADT-NKTCL. Results: Patients with extranasal UADT-NKTCL had more adverse clinical features, including advanced-stage disease, regional lymph node involvement, B symptoms, and poor performance status, than patients with nasal UADT-NKTCL. In addition, CD56 and granzyme B were less frequently expressed in extranasal UADT-NKTCL. The 5-year overall survival rate was 74.1% for the entire group and 76.0% for early-stage disease. The 5-year overall survival rate for extranasal UADT-NKTCL was similar or superior to that of nasal UADT-NKTCL for all disease stages (76.9% vs 73.4%, P=.465), stage I disease (75.9% vs 79.2%, P=.786), and stage II disease (83.3% vs 50.3%, P=.018). CD56 expression and a Ki-67 proliferation rate ≥50% predicted poorer survival for extranasal UADT-NKTCL but not for nasal UADT-NKTCL. Conclusions: Patients with nasal and extranasal UADT-NKTCL have significantly different clinical features, immunophenotypes, and prognosis. Extranasal UADT-NKTCL should be considered as a distinct subgroup apart from the most commonly diagnosed prototype of nasal UADT-NKTCL. [Copyright &y& Elsevier]

Purpose: Early stage peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS) is rare. The purpose of this study was to evaluate the outcome of treatment as well as the potential role of radiation therapy in PTCL-NOS. Methods and Materials: Thirty-five patients with early stage PTCL-NOS were included. There were 13 patients with stage I disease and 22 with stage II. All patients except 1 received doxorubicin-based chemotherapy alone (n=13) or a combination of chemotherapy and radiation therapy (CMT) (n=21). Results: The 3-year overall survival (OS) and progression-free survival (PFS) rates for the entire group were 41.3% and 25.7%, respectively. The addition of radiation therapy to chemotherapy significantly improved OS and PFS in early stage PTCL-NOS. The 3-year OS and PFS rates were 49.7% and 33.3% for CMT, compared with 23.1% (P=.042) and 15.4% (P=.035) for chemotherapy alone, respectively. The prognosis for patients who achieved a complete response (CR) was significantly better than that observed in those who did not achieve a CR. Conclusions: Despite the aggressive clinical course of early stage PTCL-NOS, additional radiation therapy has a significant impact on outcome. The integration of local radiation therapy into more effective systemic therapies may further improve survival. [Copyright &y& Elsevier]

The occurrence of recurrence and metastasis after treatment is a major challenge in the treatment of gastric cancer. This study was based on the methionine (Met)-dependent characteristics of gastric cancer cells to explore the effect of Met deficiency on the occurrence and development of gastric cancer. Human gastric cancer cell lines MKN45 and AGS and nude mice model were used to explore how Met affects gastric cancer by regulating lncRNA PVT1. The levels of lncRNA PVT1 in gastric cancer cells and human gastric cancer xenografts of nude mice were down-regulated under the condition of Met deficiency. The cell viability and cell proliferation were declined after MKN45 and SGC-790 cells were cultured in Met-deficient medium. LncRNA PVT1 could affect BNIP3 promoter DNA methylation level through its interaction with DNMT1. Moreover, the silence of lncRNA PVT1 and the up-regulation of BNIP3 level inhibited the gastric cancer cell proliferation. Met deficiency could up-regulate BNIP3 expression by inhibiting the binding of lncRNA PVT1 to DNMT1, and activate mitophagy, thus inhibiting gastric cancer cell proliferation. Our study suggested that Met deficiency could down-regulate the expression of lncRNA PVT1, further demethylated the promoter of BNIP3, thus inhibiting the proliferation of gastric cancer cells by activating mitophagy. [Display omitted] [ABSTRACT FROM AUTHOR]