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5 (from 6.0 for the native enzyme) and temperature to 55°C (40°C for the native enzyme). During storage at 25°C, the immobilized enzyme retained 75.8% of initial activity after 60days compared to 29.2% retained by the free enzyme.

The immobilization method developed in this work enhanced enzyme stability during catalysis and storage. learn more Up to 12cycles of repeated use of the catalyst became feasible.

The simple and rapid immobilization strategy of this work is broadly applicable to enzymes used in diverse bioconversions.

The simple and rapid immobilization strategy of this work is broadly applicable to enzymes used in diverse bioconversions.The human cell line activation test (h-CLAT) is an OECD approved (Test No. 442E) assay to identify novel skin sensitizers. h-CLAT simulates dendritic cell activation in the skin sensitization pathway and is based on the measurement of CD54 and CD86 overexpression on monocytic, leukemic THP-1 cells. However, the current h-CLAT markers show inconsistent results with moderate and weak sensitizers. Moreover, these markers have accessory roles in cell adhesion and signaling rather than a direct role in cellular inflammation. Therefore, we have explored other inflammation-related markers in this study. PBMCs comprises a mixture of cells that resemble the complex immunological milieu in adults and were primarily used to identify markers. PBMCs (n = 10) and THP-1 cells were treated with 1-chloro-2,4-dinitrobenzene (DNCB, strong) and NiCl2 (Ni, moderate) sensitizers or DMSO (control) and incubated for 24 h. The samples were subjected to RNA sequencing to obtain log2fold change in gene expression. DNCB and NiCl2 significantly upregulated 80 genes in both cell types. Of these, CD109, CD181, CD183, CLEC5A, CLEC8A & CD354 were experimentally validated. DNCB and Ni but not isopropyl alcohol (non-sensitizer) significantly induced the expression of all novel markers except CLEC8A. Moreover, the percentage induction of all novel markers except CLEC8A satisfied the OECD acceptance criteria. In summary, we identified five novel markers that may supplement the current repertoire of h-CLAT markers.

Deterioration of neuromuscular function is a major mechanism of age-related strength loss. Resistance training (RT) improves muscle strength and mass. However, the effects of RT on neuromuscular adaptations in middle-aged and older adults are unclear.

Randomised controlled RT interventions (≥2weeks) involving adults aged ≥50years were identified. Primary outcome measures were voluntary activation (VA), electromyographic (EMG) activity during maximal voluntary contraction (MVC), and antagonist coactivation. Data were pooled using a weighted random-effect model. Sub-analyses were conducted by muscle or muscle group and health status of participants. Sensitivity analysis was based on study quality. P<0.05 indicated statistical significance.

Twenty-seven studies were included. An effect was found for VA (standardised mean difference [SMD] 0.54, 0.01 to 1.07, P=0.04), This result remained significant following sensitivity analysis involving only studies that were low risk of bias. Subgroup analyses showederalisability of these findings to clinical cohorts. Future research should determine the effects of RT on neuromuscular function in people with sarcopenia and age-related syndromes.

Mobility is a complex but crucial clinical outcome in older adults. Past observational studies have highlighted that cardiorespiratory fitness (CRF), energy cost of walking (ECW), and cognitive switching abilities are associated with mobility performance, making these key determinants of mobility intervention targets to enhance mobility in older adults. The objective of this study was to compare, in the same design, the impact of three training methods - each known to improve either CRF, ECW, or cognitive switching abilities - on mobility in healthy older adults.

Seventy-eight participants (69.28±4.85yo) were randomly assigned to one of three twelve-week interventions Aerobic Exercise (AE; n=26), Gross Motor Abilities (GMA; n=27), or Cognitive (COG; n=25) training. Each intervention was designed to improve one of the three key determinants of mobility (CRF, ECW, and cognitive switching). Primary outcomes (usual gait speed, and TUG performance) and the three mobility determinants were measured before and and professionals, more options to promote healthy ageing.

This study provides further support to the notion that multiple interventional approaches (aerobic, gross motor exercise, or cognitive training) can be employed to improve functional mobility in older adults, giving them, and professionals, more options to promote healthy ageing.Recently, there is evidence that long non-coding RNA p21 may play a regulatory role in the development of neuropathic pain (NPP), but it remains to be studied. In this study, we found that lncRNA p21 and tumor necrosis factor alpha-induced protein 1 (Tnfaip1) expression were up-regulated and miR-181b expression was down-regulated in lipopolysaccharide (LPS)-induced and activated BV-2 microglia. The results of flow cytometry and ELISA suggested that overexpression of lncRNA p21 or Tnfaip1 promoted apoptosis and inflammatory factors secretion, and miR-181b overexpression inhibited apoptosis and secretion of inflammatory factors. Luciferase reporter gene analysis validated the adsorption of miR-181b by lncRNA p21. In addition, the targeting relationship between miR-181b and Tnfaip1 was determined. Next, the up-regulation of lncRNA p21 and miR-181b was used as a reversal experiment, and the results suggested that the up-regulation of miR-181b attenuated the promoting effect of lncRNA p21 and Tnfaip1 on apoptosis and inflammatory response, which may be related to the activation of AKT/cAMP response element binding protein (CREB) axis. Finally, the rat model of SNL with lncRNA p21 knockdown was constructed, and the results of paw retraction mechanical threshold (PWMT) and paw retraction thermal latency (PWTL) measurements showed that knockdown of lncRNA p21 alleviated neuropathic pain in rats. In conclusion, our study found that the lncRNA p21/miR-181b/Tnfaip1 axis probably plays an important role in the progression of neuropathic pain, among which lncRNA p21 may become a new insight in the treatment of neuropathic pain.