Version up-date: The CDKN2B-AS1/ MIR497/TXNIP axis regulated macrophages

The polarization of macrophages plays a critical role in the pathophysiology of rheumatoid arthritis. The macrophages can have pro-inflammatory M1 polarization and various types of alternative anti-inflammatory M2 polarization. Our preliminary results showed that the CDKN2B-AS1/MIR497/TXNIP axis might regulate macrophages of rheumatoid arthritis patients. Therefore, we hypothesized that this axis regulated the polarization of rheumatoid macrophages. Flow cytometry was used to determine the surface polarization markers in M1 or M2 macrophages from healthy donors and rheumatoid arthritis patients. The QPCR and Western Blotting were used to compare the expression of the CDKN2B-AS1/MIR497/TXNIP axis in these macrophages. We Knocked down and overexpressed the axis in the macrophage cell line MD to test its roles in macrophage polarization. Compared to cells from healthy donors, cells from rheumatoid arthritis patients expressed higher levels of CD40 and CD80 and lower levels of CD16, CD163, CD206, and CD200R after polarization, they also expressed higher CDKN2B-AS1, lower MIR497, and higher TXNIP. In macrophages from healthy donors, there was no correlation among CDKN2B-AS1, MIR497, and TXNIP. But in macrophages from patients, there were significant correlations. The CDKN2B-AS1 knockdown, MIR497 mimics suppressed the M1 polarization but promoted the M2 polarization in MD cells, while the MIR497 knockdown and the TXNIP overexpression did the opposite. This study demonstrated that elevated CDKN2B-AS1 in macrophages promotes the M1 polarization and inhibited the M2 polarization of macrophages by the CDKN2B-AS1/ MIR497/TXNIP axis.

Simulating fouling impact on the permeate flux in high-pressure membranes

Porous high-pressure membranes have been widely used for saline water desalination. However, fouling (concentration polarization) extensively reduces permeate flux in reverse osmosis (RO) and/or nanofiltration (NF) modules. Fouling arises from pore blocking, organic adsorption, cake formation, inorganic or biological precipitation reducing water flux. Herein, we investigated the effect of feed water with various NaCl concentrations on fouling of RO and/or NF and the permeate water flux. A parabolic (or diffusion) partial differential equation (PDE) was used to model salt concentration profile or gradient inside the membrane. Subsequently, the numerical PDE equation, solved by the forward finite difference (FFD) explicit method, estimated flux decline rates resulted from NaCl fouling. It was found that salt accumulation occurs at the feed-side with a noticeable decrease in flux as fouling increases. Previous works reported similar findings as those identified from our analysis: (1) fouling increases with feed concentration and surface roughness, (2) fouling becomes intensified with higher pressure and flux, (3) fouling from long operation times can reduce flux by 65% within 24 h, (4) NaCl fouling can decrease flux rates by 70% (67-22 LMH) for brackish water with an initial concentration of 10000 ppm, and (5) reversible organic fouling may be avoided from lowering flux rates below the membrane critical flux. Results showed fouled RO modules would decrease flux rates from the increased surface polarization, where reverse flow (negative flux) was estimated for feed-side accumulations >10000 ppm for waters with an initial NaCl concentration of 10000 ppm and average diffusivity of 1.3×10-6 cm2/s.

The CDKN2B-AS1/ MIR497/TXNIP axis regulated macrophages

Abstract The polarization of macrophages plays a critical role in the pathophysiology of rheumatoid arthritis. The polarization states include pro-inflammatory M1 polarization and various alternative anti-inflammatory M2 polarization. Our preliminary results showed that CDKN2B-AS1/MIR497/TXNIP axis might play a role in macrophages extracted from rheumatoid arthritis patients. Therefore, we hypothesized that this axis regulated the polarization of rheumatoid macrophages. Flow cytometry was used to determine the surface polarization markers in M1 or M2 macrophages from healthy donors and rheumatoid arthritis patients. QPCR and western blotting were used to compare the expression of the CDKN2B-AS1/MIR497/TXNIP axis in these macrophages. We interfered with the expression and function of the axis from upstream to downstream in the macrophage cell line MD to test its roles in macrophage polarization. Compared to cells from healthy donors, cells from rheumatoid arthritis patients expressed a higher level of CD40 and CD80 and a lower level of CD16, CD163, CD206, and CD200R after polarization, they also expressed higher CDKN2B-AS1, lower MIR497, and higher TXNIP. In macrophages from healthy donors, there was no correlation among CDKN2B-AS1, MIR497, and TXNIP. But in macrophages patients, they showed significant correlations. The CDKN2B-AS1 knockdown, MIR497 mimics suppressed M1 polarization but promoted M2 polarization in MD cells, while MIR497 knockdown and TXNIP overexpression did the opposite. This study demonstrated that elevated CDKN2B-AS1 in macrophages promotes M1 polarization and inhibits M2 polarization of macrophage by negatively regulating MIR497, thereby upregulated the expression of TXNIP.

Polarization of rheumatoid macrophages is regulated by the CDKN2B-AS1/ MIR497/TXNIP axis

The polarization of macrophages plays a critical role in the pathophysiology of rheumatoid arthritis. The polarization states include pro-inflammatory M1 polarization and various alternative anti-inflammatory M2 polarization. Our preliminary results showed that CDKN2B-AS1/MIR497/TXNIP axis might play a role in macrophages extracted from rheumatoid arthritis patients. Therefore, we proposed that this axis regulated the polarization of rheumatoid macrophages. Flow cytometry was used to determine the surface polarization markers in M1 or M2 macrophages from healthy donors and rheumatoid arthritis patients. QPCR and western blotting were used to compare the expression of CDKN2B-AS1/MIR497/TXNIP axis in these macrophages. We interfered with the expression and function of the CDKN2B-AS1/ MIR497/TXNIP axis from upstream to downstream in the macrophage cell line MD to test its roles in macrophage polarization. Compared to cells from healthy donors, cells from rheumatoid arthritis patients expressed a higher level of CD40 and CD80 and a lower level of CD16, CD163, CD206, and CD200R after polarization, they also expressed higher CDKN2B-AS1, lower MIR497, and higher TXNIP. In macrophages from healthy donors, there was no correlation among CDKN2B-AS1, MIR497, and TXNIP. But in macrophages patients, they showed significant correlations. The CDKN2B-AS1 knockdown, MIR497 mimics suppressed M1 polarization but promoted M2 polarization in MD cells, while MIR497 knockdown and TXNIP overexpression did the opposite. Elevated CDKN2B-AS1 in macrophages promotes M1 polarization and inhibits M2 polarization of macrophage by negative regulating MIR497, thereby upregulated the expression of TXNIP.