Controlling the anisotropy of two-dimensional materials with orientation-dependent heat transfer characteristics is a possible solution to resolve severe thermal issues in future electronic devices. We demonstrate a dramatic enhancement in the in-plane thermal conductivity of stretchable poly(vinyl alcohol) (PVA) nanohybrid films containing small amounts (below 10 wt %) of hexagonal boron nitride ( h-BN) nanoplatelets. The h-BN nanoplatelets were homogeneously dispersed in the PVA polymer solution by ultrasonication without additional surface modification. The mixture was used to prepare thermally conductive nanocomposite films. The in-plane thermal conductivity of the resulting PVA/ h-BN nanocomposite films increased to 6.4 W/mK when the strain was increased from 0 to 100% in the horizontal direction. More specifically, the thermal conductivity of a PVA/ h-BN composite film with 10 wt % filler loading can be improved by up to 32 times as compared to pristine PVA. This outstanding thermal conductivity value is significantly larger than that of materials currently used in in-plane thermal management systems. This result is attributed to the anisotropic alignment of h-BN particles in the PVA chain matrix during stretching, enhancing phonon conductive paths and hence improving the thermal conductivity and thermal properties of PVA/ h-BN nanocomposite films. These polymer nanocomposites have low cost as the amount of expensive conductive fillers is reduced and can be potentially used as high-performance materials for thermal management systems such as heat sink and thermal interface materials, for future electronic and electrical devices.

Human adenovirus-based vectors have emerged as a new promising vehicle for in vivo gene transfer-mediated therapy. However, the full potential of this methodology has not been fully realized because of the nonspecific tissue distribution of adenoviral vectors. Adenovirus infection is initiated by forming a complex between the fiber protein and a ubiquitously expressed host cell membrane protein, coxsackie B virus and adenovirus receptor (CAR). Therefore, ablating the adenovirus vector's ability to bind to the CAR is the first step in redirecting adenoviral tropism. To ablate CAR binding, we mutated the Bbeta sheet of the fiber knob, generating CAR-binding ablated replication-incompetent (dl-K420A-Z) and replication-competent (YKLK420A) adenoviral vectors. The in vitro transduction efficiency of dl-K420A-Z was significantly reduced in comparison to dl-LacZ carrying the wild-type fiber in CAR-positive cells but not in CAR-negative cells, suggesting that the mutation introduced in the Bbeta sheet of the fiber knob could disable the CAR-dependent transduction pathway. The in vivo transduction was also dramatically reduced in the liver and other organs for mice treated with dl-K420A-Z, compared with a cognate control vector, dl-LacZ. Concomitant with this attenuated gene transfer efficiency in vivo was a substantial reduction in the amount of general toxicity observed in the YKL-K420A-treated mice. Diminished toxicity was surmised from quantitative measurement of serum level of enzymes for liver and kidney function, hematologic chemistries, histopathology, and differences in lethality. Significant decrease in serum transaminases (alanine transferase [ALT] and aspartate transferase [AST]) was observed in mice treated with YKL-K420A. In addition, the lethality was lower in the YKLK420A- treated groups compared to the YKL-1-treated groups at all doses examined. Furthermore, the hepatopathologic analysis revealed that YKL-1 induced focal zonal necrosis and hepatocyte degeneration, while YKL-K420A induced mild spotty necrosis. In summary, this decreased vector tropism of CAR-binding ablated adenoviruses in normal tissues may increase the amount of virus available for infecting tumor cells and thus increase the antitumor efficacy with fewer unwanted side effects.

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Cancer immunotherapy is a promising therapy to treat cancer patients with minimal toxicity, but only a small fraction of patients responded to it as a monotherapy. In this study, a strategy to boost therapeutic efficacy by combining an immunotherapy based on ex vivo expanded tumor‐reactive T cells is devised, or adoptive cell therapy (ACT), with photothermal therapy (PTT). Smart gold nanoparticles (sAuNPs), which aggregates to form gold nanoclusters in the cells, are loaded into T cells, and their photothermal effects within T cells are confirmed. When transferred into tumor‐bearing mice, large number of sAuNP‐carrying T cells successfully infiltrate into tumor tissues and exert anti‐tumor activity to suspend tumor growth, but over time tumor cells evade and regrow. Of note, ≈20% of injected doses of sAuNPs are deposited in tumor tissues, suggesting T cells are an efficient nanoparticle tumor delivery vehicle. When T cells no longer control tumor growth, PTT is performed to further eliminate tumors. In this manner, ACT and PTT are temporally coupled, and the combined immuno‐photothermal treatment demonstrated significantly greater therapeutic efficacy than the monotherapy.