Isotropic negative permeability resulting from Mie resonance is demonstrated in a three-dimensional (3D) dielectric composite consisting of an array of dielectric cubes. A strong subwavelength magnetic resonance, corresponding to the first Mie resonance, was excited in dielectric cubes by electromagnetic wave. Negative permeability is verified in the magnetic resonance area via microwave measurement and the dispersion properties. The resonance relies on the size and permittivity of the cubes. It is promising for construction of novel isotropic 3D left-handed materials with a simple structure.

This study demonstrated the feasibility of printing three-dimensional (3D) hybrid objects based on acrylic photocurable formulations, with an additional function of thermochromic (TC) performance. In fact, directly mixing TC pigments into an acrylic resin (AR), led to a decrease of the mechanical properties like tensile strength and elongation. In order to address this problem, TC was modified by γ-methacryloxypropyltrimethoxysilane before added into an AR (modified thermochromic [mTC] pigment). Compared with pure AR and TC/resin composite structures (TC/AR), the final mTC/acrylic resin (mTC/AR) exhibited a better performance of tensile strength and Young's modulus. Besides, they could be successfully fabricated into 3D structures by stereolithography method. More interestingly, mTC/AR 3D composite structures demonstrated a unique tunable TC property, which could be responsive to external temperature fields reversely. Thus, their TC property could find novel applications in smart temperature sensor technology, and other related technological applications.

No abstract

of aspartate transaminase and alanine aminotransferase (grade II CTCAE5.0). Patient B was diagnosed as adenocarcimoma with clinical stage III A (T1bN2M0). The evaluation of CT was stable disease (SD)(Fig. 1(e)(f)(g)(h)). The pathological response rate was 30%. Pathological stage reduced to stage II B (pT1cN1M0). Treat-related AE was leukopenia (grade II CTCAE5.0). All adverse reactions can be returned to normal after symptomatic treatment. Conclusion:Neoadjuvant Sintilimab plus chemotherapy showed a bright efficacy with no intolerable adverses. It may improve the downstage rate and pathologic remission rate of patients with NSCLC. Whether it can improve the DFS and OS of patients remains to be further observed with experimental data.

Type 2 diabetes mellitus (T2DM) is worldwide epidemic, which challenges the health of the public. The pathological hyperactivity of cyclin-dependent kinase 5 (Cdk5) contributes to the pathogenesis of T2DM. P5, a peptide derived from the Cdk5 activator p35, shows excellent performance as a Cdk5 activity inhibitor.However, its inhibitory effect and functional regulation on Cdk5 activity needs to be con rmed. In this study, we conjugated P5 with a uorescein isothiocyanate (FITC) tag at the N-terminus and a TAT protein transduction domain, an 11-amino acid peptide, at the C-terminus to synthesize TFP5, which was used to inhibits Cdk5 activity. We then evaluated the e ciency of TFP5 in treating T2DM. We demonstrated that TFP5 effectively penetrated pancreatic β-cells, inhibited the pathological hyperactivity of Cdk5, enhanced insulin secretion, and protected penetrated pancreatic β-cells (MIN6 cells) from apoptosis in pancreatic tissues of db/db mice (type II diabetes mice). Furthermore, we found that TFP5 reduced in ammation in pancreatic islets by reducing the expression of in ammatory cytokines, including TGF-β1, TNF-α, and IL-1β. These data indicates that the TFP5 peptide is a promising candidate for T2DM treatment. Impact StatementWe conjugated P5 with a Fluorescein Isothiocyanate (FITC) tag at the N-terminus and a TAT protein transduction domain containing an eleven amino acids peptide at the C-terminus to form TFP5, to explore the e ciency of TFP5 as T2DM therapy. TFP5 effectively penetrated pancreatic β-cells, inhibited the hyperactivity of Cdk5, enhanced insulin secretion, and protected pancreatic β-cells from apoptosis in pancreatic tissues of db/db mice. TFP5 also reduced in ammation in pancreatic islets by reducing the level of in ammatory cytokines, including TGF-β1, TNF-α, and IL-1β.