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In this study, we explorethe synthesis of binaphthyl-based chiral macrocyclic hosts for the first time. They exhibited the selective recognition abilities of iodide anions which can be favored over those of other anions (AcO−, NO3−, ClO4−, HSO4−, Br−, PF6−, H2PO4−, BF4−, and CO3F3S−), as confirmed by UV-vis, HRMS, and 1H NMR spectroscopy experiments, as well as DFT calculations. Neutral aryl C–H···anion interactions play an important role in the formation complexes. The recognition process can be observed by the naked eye.

Background The Escherichia coli expression system is widely used for recombinant protein production, but its utility is often limited by the formation of insoluble inclusion bodies. Although fusion tags can enhance solubility, their effectiveness varies unpredictably across different target proteins, and the optimal tag must typically be determined empirically. Results We developed a standardized set of pX fusion tag vector system for the high-throughput screening of soluble protein expression in E. coli . This system consists of eight medium-sized, TEV-cleavable fusion tags (ArsC, Crr, DsbA, Ecotin, MsyB, SlyD, Snut, and YjgD) cloned into a standardized pET-28b(+) backbone. We systematically evaluated the impact of these tags on the solubility and function of three model proteins (eGFP, EcFabG, and Mals) and six proteins known to be challenging to express in E. coli (PulA, NodE, FabF1XL, FabF2XL, FabZXL, and FabGXL). Our results demonstrated that the efficacy of each tag was highly protein-dependent. Notably, tags such as MsyB and Snut dramatically increased the soluble proportion of eGFP from 15% to over 85%, while the SlyD tag significantly enhanced both the solubility and activity of Mals. For several difficult-to-express proteins, soluble expression was only achieved with specific tags, highlighting the critical importance of tag selection. Conclusions Our study presents a versatile and efficient parallel cloning and screening system for the rapid production of soluble recombinant proteins. By enabling parallel screening of multiple fusion partners, this system facilitates the identification of optimal conditions for enhancing protein solubility and function, thereby addressing a key bottleneck in recombinant protein applications.

Embryonic stem (ES) cell self‐renewal efficiency is determined by the Nanog protein level. However, the protein partners of Nanog that function to direct self‐renewal are unclear. Here, we identify a Nanog interactome of over 130 proteins including transcription factors, chromatin modifying complexes, phosphorylation and ubiquitination enzymes, basal transcriptional machinery members, and RNA processing factors. Sox2 was identified as a robust interacting partner of Nanog. The purified Nanog–Sox2 complex identified a DNA recognition sequence present in multiple overlapping Nanog/Sox2 ChIP‐Seq data sets. The Nanog tryptophan repeat region is necessary and sufficient for interaction with Sox2, with tryptophan residues required. In Sox2, tyrosine to alanine mutations within a triple‐repeat motif (S X T/S Y) abrogates the Nanog–Sox2 interaction, alters expression of genes associated with the Nanog‐Sox2 cognate sequence, and reduces the ability of Sox2 to rescue ES cell differentiation induced by endogenous Sox2 deletion. Substitution of the tyrosines with phenylalanine rescues both the Sox2–Nanog interaction and efficient self‐renewal. These results suggest that aromatic stacking of Nanog tryptophans and Sox2 tyrosines mediates an interaction central to ES cell self‐renewal. This paper features a comprehensive proteomic view on the Nanog interactome. Further, it molecularly and functionally defines the intimate interplay of Nanog with another pluripotency determinant Sox2.

A turn-on fluorescent probe, cage 1, was efficiently self-assembled by condensing 4,4′-(benzothiadiazole-4,7-diyl)dibenzaldehyde and TREN in chloroform. The formation of cage 1 was characterized and confirmed by NMR spectroscopy, mass spectrometry, and theoretical calculations. The yield of cage 1 could be controlled by tuning the reaction conditions, such as the precursor concentration. Interestingly, the addition of 10 equiv of Cd2+ relative to cage 1 could increase the fluorescence almost seven-fold. 1H NMR and fluorescence experiments indicating fluorescence enhancement may be caused by the decomposition of cage 1. Such a high selectivity toward Cd2+ implies that the cage could potentially be employed in cadmium detection.

To explore the main active components and effects of cell cycle regulation mechanism of Astragali radix (AR) and Angelicae sinensis radix (ASR) on oxidative damage in vascular endothelial cells, a model of oxidative damage in human umbilical vein endothelial cells (HUVECs) induced by oxidized low-density lipoprotein (ox-LDL) treatment was developed. Based on the “knock-out/knock-in” model of the target component, cell viability, intracellular reactive oxygen species (ROS), and lactate dehydrogenase (LDH) leakage were assessed by Cell Counting Kit-8 assay, fluorescent probe 2,7-dichlorodihydrofluorescein diacetate (DCFH-DA), and colorimetric assay, respectively, to evaluate the protective effect of the active components of AR and ASR (astragaloside IV (AS IV), astragaloside I (AS I), formononetin (FRM), calycosin (CAL), calycosin-7-O-β-D glucoside (CLG), and ferulic acid (FRA)) against oxidative damage. The cell cycle and expression of genes encoding cyclins and cyclin-dependent kinases (CDKs) were observed using flow cytometry and quantitative real-time polymerase chain reaction. The results showed that the combination of active components (ACC) significantly inhibited the decrease in cell viability as well as the increase in ROS and LDH release in HUVECs induced by ox-LDL treatment. AS IV and FRM promoted the proliferation of HUVECs but the proliferation index was decreased in the AS I and FRA groups; this inhibitory effect was counteracted by the ACC. The ACC reduced and increased the proportion of positive cells in G1 and S phases, respectively, followed by the upregulation of cyclin A (CCNA), cyclin E (CCNE), and CDK2 mRNA expression and downregulation of cyclin B (CCNB), cyclin D1 (CCND1), CDK1, CDK4, and CDK6 mRNA expression, which significantly mitigated inhibition of HUVECs proliferation induced by ox-LDL treatment. Taken together, AS IV, AS I, FRM, CAL, CLG, and FRA were the primary pharmacodynamic substances of AR and ASR that alleviated oxidative injury in HUVECs. ACC mitigated the upregulation of intracellular ROS levels and LDH release induced by ox-LDL treatment, which promoted the cell cycle procession of HUVECs by regulating the expression of genes encoding cyclins and CDKs and thus preventing oxidative damage in HUVECs.

Taking the DSC as the control core and the IPM as the driver,this paper design a highly practical brushless DC motor control system with CAN bus . The system use CANopen as the application layer communication protocol, which can simultaneously control the plurality of brushless DC motor efficiently.

Objective: To study the effect of salvianolic acid B (SAB) and curcumin, the extracts ofSalvia Miltiorrhiza andCurcuma Longa, on the proliferation and activation of hepatic stellate cell (HSC), and the extracellular signal regulated kinase (ERK) expression in it.Methods: Rat’s HSC-T6 were cultured and treated by SAB or curcumin. The inhibitory effect on cell proliferation was determined by 3-(4,5-dimthyl-2-2-thiazoly)-2,5-diphenyl-2H-tetrazolium bromide (MTT) colorimetry, and the expression levels of α smooth actin (α-SMA), collagen type I, and ERK were determined by Western blot.Results: SAB and curcumin inhibited the proliferation and activation of rat’s HSC-T6 in dose-dependent fashion and significantly reduced the expression level of a-SMA (P < 0.01). Curcumin significantly reduced the expression of collagen type I (P < 0.05). Both SAB and curcumin showed insignificant effect on the ERK expression level, but they could significantly reduce the level of phosphorylated-ERK expression, showing significant difference as compared with that in the control group (P < 0. 01 andP < 0. 05 respectively).Conclusion: SAB and curcumin could significantly inhibit the proliferation, activation of HSC, and the production of type I collagen in HSC, the mechanism may be associated with their inhibition on ERK phosphorylation.

Aim： To improve and validate an analytical method based on liquid chromatography and electrospray ionization tandem mass spectrometry （LC-ESI-MS/MS） for the quantitative measurement of ilaprazole and its two metablites in human plasma. Methods： Separation of analytes and the internal standard （IS）, omeprazole, was performed on a Thermo HyPURITY C18 column （150×2.1 mm, 5 um） with a mobile phase consisting of 10 mmol/L ammonium formate water-acetonitrile solution （50：50, v/v） at a flow rate of 0.25 mL/min. The API4000 triple quadruple mass spectrometer was operated in multiple reactions monitoring mode via positive electrospray ionization interface using the transition m/z 367.2 → m/z 184.0 for ilaprazole, m/z 383.3 → m/z 184.1 for ilaprazole sulfone, m/z 351.2 → m/z 168.1 for ilaprazole thiol ether and m/z 346.2 → m/z 198.0 for omeprazole. Results： The method was linear over the concentration range of 0.23-2400.00 ng/mL for ilaprazole, 0.05-105.00 ng/mL for ilaprazole thiol ether and 0.06-45.00 ng/mL for ilaprazole sulfone. The intra- and inter-day precisions were all less than 15% in terms of relative standard deviation （RSD）, and the accuracy was within 15% in terms of relative error （RE） for ilaprazole, ilaprazole sulfone and ilaprazole thiol ether. The lower limit of quantification （LLOQ） was identifiable and reproducible at 0.23, 0.05 and 0.06 ng/mL with acceptable precision and accuracy for ilaprazole, ilaprazole sulfone and ilaprazole thiol ether, respectively. Conclusion： The validated method offered sensitivity and a wide linear concentration range. This method was successfully applied for the evaluation of the pharmacokinetics of ilaprazole and its two metabolites after single oral doses of 5 mg ilaprazole to 12 healthy Chinese volunteers.

Autophagy, a conserved cellular degradation and recycling process, can be enhanced by nutrient depletion, oxidative stress or other harmful conditions to maintain cell survival. 6-Hydroxydopamine/ascorbic acid (6-OHDA/AA) is commonly used to induce experimental Parkinson’s disease (PD) lesions by causing oxidative damage to dopaminergic neurons. Activation of autophagy has been observed in the 6-OHDA-induced PD models. However, the mechanism and exact role of autophagy activation in 6-OHDA PD model remain inconclusive. In this study, we report that autophagy was triggered via mucolipin 1/calcium/calcineurin/TFEB (transcription factor EB) pathway upon oxidative stress induced by 6-OHDA/AA. Interestingly, overexpression of TFEB alleviated 6-OHDA/AA toxicity. Moreover, autophagy enhancers, Torin1 (an mTOR-dependent TFEB/autophagy enhancer) and curcumin analog C1 (a TFEB-dependent and mTOR-independent autophagy enhancer), significantly rescued 6-OHDA/AA-induced cell death in SH-SY5Y cells, iPSC-derived DA neurons and mice nigral DA neurons. The behavioral abnormality of 6-OHDA/AA-treated mice can also be rescued by Torin 1 or C1 administration. The protective effects of Torin 1 and C1 can be blocked by autophagy inhibitors like chloroquine (CQ) or by knocking down autophagy-related genes TFEB and ATG5. Taken together, this study supports that TFEB-mediated autophagy is a survival mechanism during oxidative stress and pharmacological enhancement of this process is a neuroprotective strategy against oxidative stress-associated PD lesions.

Background Depression is on the rise globally. Additionally, the United States has a high level of population mobility. The main aim of this study was to provide a reference for improving the mental health of internal migrants by investigating the relationship between internal migration experience and depressive symptoms. Methods We analysed data from the Panel Study of Income Dynamics (PSID). We included PSID data from the 2005 to 2019 waves in which all respondents were asked about their internal migration experience and depressive symptoms. This study included 15,023 participants. T tests, chi-square tests, multiple logistic regression methods were performed and fixed effects model. Results In the sample, the prevalence of depressive symptoms was 4.42%. The risk of depression in internal migrants was 1.259 times (OR = 1.259, 95% CI = (1.025–1.547, p  < 0.05) that of nonmigrants. Internal migration experience was significantly positively associated with female depressive episodes (OR = 1.312, 95% CI = 1.010–1.704, p  < 0.05) and increased risk of becoming depressed at a young age (OR = 1.304, 95% CI = 1.010–1.684, p  < 0.05). The association between internal migration experience and depressive symptoms was more significant for participants who might move (OR = 1.459, 95% CI = 1.094–1.947, p  < 0.05). In addition, different internal migratory causes are associated with depressive symptoms to varying degrees. Conclusions Our findings highlight the need for greater policy attention to mental health inequalities between Internal migrants and those who never move away from their hometown in the United States. Our study provides a foundation for further research.