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Poly(ethylene 2,6-naphthalate) (PEN) nanocomposites reinforced with silica nanoparticles were prepared by direct melt compounding. Dynamic thermogravimetric analysis was conducted on the PEN/silica nanocomposites to clarify the effect of silica nanoparticle on the thermal decomposition behavior of the resultant nanocomposites. There is a significant dependence of thermal decomposition behavior for PEN/silica nanocomposites on the content of silica nanoparticles and heating rate. The variation of the activation energy for thermal decomposition reflected the improvement of the thermal stability of the PEN/silica nanocomposites. The unique characteristics of silica nanoparticles resulted in physical barrier effect against the thermal decomposition, leading to the enhancement of the thermal stability of the PEN/silica nanocomposites. The incorporation of silica nanoparticles into the PEN matrix increased the storage modulus of the PEN/silica nanocomposites and made it possible for them to sustain higher modulus at higher temperature relative to pure PEN. POLYM. COMPOS.a Values obtained from the DSC heating traces at 108C/min. b The crystallization temperature measured from the DSC cooling traces at 108C/min. c The degree of supercooling, DT ¼ T m 2 T c . FIG. 4. SEM image of the residues of PEN/silica 2.0 nanocomposite after thermal decomposition. FIG. 5. Dynamic mechanical properties of pure PEN and the PEN/ silica 1.0 nanocomposites as a function of temperature (open circles represent PEN and the solid circles represent PEN/silica nanocomposites).

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Pancreatic ductal adenocarcinoma (PDAC) has a poor 5-year overall survival rate. Patients with PDAC display limited benefits after undergoing chemotherapy or immunotherapy modalities. Herein, we reveal that chemotherapy upregulates placental growth factor (PlGF), which directly activates cancer-associated fibroblasts (CAFs) to induce fibrosis-associated collagen deposition in PDAC. Patients with poor prognosis have high PIGF/VEGF expression and an increased number of PIGF/VEGF receptor-expressing CAFs, associated with enhanced collagen deposition. We also develop a multi-paratopic VEGF decoy receptor (Ate-Grab) by fusing the single-chain Fv of atezolizumab (anti-PD-L1) to VEGF-Grab to target PD-L1-expressing CAFs. Ate-Grab exerts anti-tumor and anti-fibrotic effects in PDAC models via the PD-L1-directed PlGF/VEGF blockade. Furthermore, Ate-Grab synergizes with gemcitabine by relieving desmoplasia. Single-cell RNA sequencing identifies that a CD141+ CAF population is reduced upon Ate-Grab and gemcitabine combination treatment. Overall, our results elucidate the mechanism underlying chemotherapy-induced fibrosis in PDAC and highlight a combinatorial therapeutic strategy for desmoplastic cancers.