Longitudinal change of Th1, Th2, and Th17 cells and their relationship between cognitive impairment, stroke recurrence, and mortality among acute ischemic stroke patients.

BACKGROUND: T-helper (Th) cells regulate immunity and inflammation, and modulate cognitive impairment in both cardio-cerebrovascular and neurological diseases. This study aimed to explore the correlation of longitudinal change of Th1/2/17 cells with cognitive impairment and prognosis in acute ischemic stroke (AIS). METHODS: Th1/2/17 cells were detected by flow cytometry in peripheral blood samples from 150 AIS patients at admission (baseline), Day (D)1, D3, and D7 after admission, and from 30 controls. Mini-Mental State Examination (MMSE) score among AIS patients at discharge was assessed. Stroke recurrence and mortality were evaluated. RESULTS: Th1 (p = 0.013) and Th17 cells (p < 0.001) but not Th2 cells (p = 0.105) were elevated in AIS patients versus controls. Th1 cells (p = 0.027) and Th17 cells (p < 0.001) but not Th2 cells (p = 0.227) were positively correlated with NIHSS score in AIS patients. Furthermore, Th1 and Th17 cells elevated from baseline to D3 and then decreased on D7 after AIS onset, while Th2 cells illustrated an opposite trend (all p < 0.001). Th17 cells on D1 (p = 0.011), D3 (p = 0.014), and D7 (p < 0.001) were correlated with lower MMSE score, and their levels on D3 (p = 0.033) and D7 (p = 0.004) were related to elevated cognitive impairment. Th1 and Th2 cells were not related to cognitive function (all p > 0.05). Additionally, Th17 cells at baseline, D1, D3, and D7 (all p < 0.05) were increased in recurrent patients versus non-recurrent patients, and in survived patients versus dead patients, but Th1 or Th2 cells did not vary (all p > 0.05). CONCLUSION: Th17 cells correlate with increased cognitive impairment, stroke recurrence, and mortality among AIS patients.

Environment-friendly dual-network hydrogel dust suppressant based on xanthan gum, polyvinyl alcohol and acrylic acid.

Hydrogen bonding interactions among poly vinyl alcohol (PVA), xanthan gum (XG) and acrylic acid (AA) molecules have been utilized to prepare an environment-friendly interpenetrating double-network hydrogel dust suppressant (PVA-XG-PAA/SDBS) with the aim of enhancing the poor mechanical performance of current hydrogel dust suppressants. A single factor test was used to determine the optimal formulation conditions for the PVA-XG-PAA/SDBS, and the viscosity, surface tension, compression strength, wind resistance, water retention and biodegradability of the samples were measured. The results showed that the hydrogel with optimal usage contained 1.5 g, 0.1 g, and 6 g of PVA, XG and AA, respectively and the optimal reaction temperature was 55 °C. Under the optimal conditions, the viscosity was 45 mPa s, the surface tension was 30 mN/m, the compression strength of the dust suppressant-solidified coal pillar reached 126 kPa, and the degradation rate at the 8th cycle (40 days) after being buried in soil was 34%. Compared with a conventional hydrogel dust suppressant, like poly acrylic acid (PAA), and the dust suppressant sodium dodecyl benzene sulfonate (SDBS), the PVA-XG-PAA/SDBS showed better water retention, wind erosion resistance, and dust-solidifying properties. On the basis of these remarkable properties, the PVA-XG-PAA/SDBS is applicable for dust prevention during coal mining, transport, and storage, which enhances the dust suppression efficiency obviously and has significant meaning to the sustainable development of the coal mining industry while protecting the environment.

A green, environment-friendly, high-consolidation-strength composite dust suppressant derived from xanthan gum.

To solve issues of low consolidation strength, poor dust suppression effect, and secondary pollution of the current coal dust suppressors, a greener and higher-consolidation-strength composite dust suppressor was synthesized by the radical polymerization of xanthan gum (XG) as the graft substrate, methyl acrylate (MA), and vinyl acetate (VAc) as the graft monomers. Taking compressive strength as the main optimization index and viscosity and surface tension as the secondary indices, the optimum ratio of MA:VAc was 3:5 and the optimum solid content was 2%. Experiments reveal that the prepared dust suppressant can naturally infiltrate into coal to form a hard solidified layer. At a wind speed of 10 m/s, the solidified layer still maintained structural integrity, indicating that the dust suppressant exhibits a good dust fixation effect. The dust suppressant can not only maintain relatively stable performance for a period of time but also degrade naturally. Furthermore, molecular dynamics simulation reveals not only the interaction mechanism between coal molecules and the dust suppressor but also the wetting mechanism of the dust suppressor. Experimental and simulation results reveal that as a multifunctional dust suppressor with excellent performance, the as-prepared dust suppressor demonstrates the immense potential for the control of coal dust. Graphical abstract.

The effect of propofol on hypoxia- and TNF-α-mediated BDNF/TrkB pathway dysregulation in primary rat hippocampal neurons.

AIMS: Hypoxia and inflammation may lead to BDNF/TrkB dysregulation and neurological disorders. Propofol is an anesthetic with neuroprotective properties. We wondered whether and how propofol affected BDNF/TrkB pathway in hippocampal neurons and astrocytes. METHODS: Primary rat hippocampal neurons and astrocytes were cultured and exposed to propofol followed by hypoxia or TNF-α treatment. The expression of BDNF and the expression/truncation/phosphorylation of TrkB were measured. The underlying mechanisms were investigated. RESULTS: Hypoxia and TNF-α reduced the expression of BDNF, which was reversed by pretreatment of 25 µM propofol in hippocampal neurons. Furthermore, hypoxia and TNF-α increased the phosphorylation of ERK and phosphorylation of CREB at Ser142, while reduced the phosphorylation of CREB at Ser133, which were all reversed by 25 µM propofol and 10 µM ERK inhibitor. In addition, hypoxia or TNF-α did not affect TrkB expression, truncation, or phosphorylation in hippocampal neurons and astrocytes. However, in hippocampal neurons, 50 µM propofol induced TrkB phosphorylation, which may be mediated by p35 expression and Cdk5 activation, as suggested by the data showing that blockade of p35 or Cdk5 expression mitigated propofol-induced TrkB phosphorylation. CONCLUSIONS: Propofol modulated BDNF/TrkB pathway in hippocampal neurons via ERK/CREB and p35/Cdk5 under the condition of hypoxia or TNF-α exposure.