Lens arrays are introduced to diminish the total internal reflection (TIR) that happens at chip-encapsulant and encapsulant-air interfaces of chip-on-board light-emitting diodes (COB-LEDs), so as to improve the light extraction efficiency (LEE) of the COB-LEDs. However, the LEE of COB-LEDs with lens array depends on the refractive index of the encapsulant layer n e n c a p and lens array n l e n s , which was rarely concerned so far. Optical simulations based on a Monte Carlo ray tracing method, and experiments were conducted to investigate the effect of n e n c a p and n l e n s on the LEE of COB-LEDs with millilens array. The simulated results show that the TIR at chip-encapsulant, encapsulant-lens, and lens-air interfaces can be significantly diminished by regulating the n e n c a p and n l e n s , and the LEE of COB-LEDs decreases as the refractive difference of encapsulant layer and lens array | n l e n s − n e n c a p | increases. Compared to the COB-LEDs with only a flat encapsulant layer, the LEEs of blue and white COB-LEDs with n l e n s = n e n c a p = n I T O = 2 are enhanced by 246.2% and 50.6%, where n I T O is the refractive index of the top layer of the conventional LED chip. The experimental results agree well with the simulated results with normalized LEE deviation within 7.3%.

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Quantum dots (QDs) are facing significant photoluminescence degradation in moisture environment. In QDs-silicone composites, the poor water resistance of silicone matrix makes it easy for water and oxygen molecules to erode QDs. To tackle this issue, we proposed a new QDs protection strategy by introducing short-chain silica precursors onto the QDs’ surface, so that a dense silica passivation layer could be formed onto the QDs nanoparticles. Sol-gel method based on 3-aminopropyl triethoxysilane (APTES), 3-mercaptopropyl trimethoxysilane (MPTMS), and 3-mercaptopropyl triethoxysilane (MPTES) were adopted to prepare the uniform and crack-free QDs-silica glass (QD-glass). Because of the crosslinking of short-chain precursors, the formed silica glass possesses 38.6% smaller pore width and 68.6% lower pore volume than silicone, indicating its denser cross-linked network surrounding QDs. After 360-hour water immersion, the QDs-glass demonstrated a 6% enhancement in red-light peak intensity, and maintained a stable full width at half maximum (FWHM) and peak wavelength, proving its excellent water-resistant ability. However, the conventional QDs-silicone composites not only showed a decrease of 75.3% in red-light peak intensity, but also a broadened FWHM and a redshifted peak wavelength after water immersion. QDs-glass also showed superior photostability after 132-hour exposure to blue light. Red-light peak intensity of QDs-glass remained 87.3% of the initial while that of QDs-silicone decreased to 19.8%. And the intensity of QDs-glass dropped to 62.3% of that under 20 ℃ after thermal treatment of 160 ℃. Besides, under increasing driving currents, the light conversion efficiency (LCE) drop of QDs-glass is only one fifth that of QDs-silicone. Based on the QDs-glass, the white light-emitting diodes was achieved with a high luminous efficiency (LE) of 126.5 lm/W and a high color rendering index (CRI) of 95.4. Thus, the newly proposed QD-glass has great significance in guaranteeing the working reliability of QDs-converted devices against moisture and high-power environment.

Background The Wnt planar cell polarity (PCP) pathway is implicated in osteoarthritis (OA) both in animals and in humans. Van Gogh-like 2 (Vangl2) is a key PCP protein that is required for the orientation and alignment of chondrocytes in the growth plate. However, its functional roles in OA still remain undefined. Here, we explored the effects of Vangl2 on OA chondrocyte in vitro and further elucidated the molecular mechanism of silencing Vangl2 in Wnt5a-overexpressing OA chondrocytes. Methods Chondrocytes were treated with IL-1β (10 ng/mL) to simulate the inflammatory microenvironment of OA. The expression levels of Vangl2, Wnt5a, MMPs, and related proinflammatory cytokines were measured by RT-qPCR. Small interfering RNA (siRNA) of Vangl2 and the plasmid targeting Wnt5a were constructed and transfected into ATDC5 cells. Then, the functional roles of silencing Vangl2 in the OA chondrocytes were investigated by Western blotting, RT-qPCR, and immunocytochemistry (ICC). Transfected OA chondrocytes were subjected to Western blotting to analyze the relationship between Vangl2 and related signaling pathways. Results IL-1β induced the production of Vangl2, Wnt5a, and MMPs in a time-dependent manner and the significantly increased expression of Vangl2. Vangl2 silencing effectively suppressed the expression of MMP3, MMP9, MMP13, and IL-6 at both gene and protein levels and upregulated the expression of type II collagen and aggrecan. Moreover, knockdown of Vangl2 inhibited the phosphorylation of MAPK signaling molecules (P38, ERK, and JNK) and P65 in Wnt5a-overexpressing OA chondrocytes. Conclusions For the first time, we demonstrate that Vangl2 is involved in the OA process. Vangl2 silencing can notably alleviate OA progression in vitro by inhibiting the expression of MMPs and increasing the formation of the cartilage matrix and can inhibit the proinflammatory effects of Wnt5a via MAPK and NF-κB pathway. This study provides new insight into the mechanism of cartilage inflammation.