Background Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive cognitive and memory impairment. It is the most common neurological disease that causes dementia. Soluble amyloid-beta oligomers (AβO) in blood or cerebrospinal fluid (CSF) are the pathogenic biomarker correlated with AD. Methods A simple electrochemical biosensor using graphene oxide/gold nanoparticles (GNPs) hydrogel electrode was developed in this study. Thiolated cellular prion protein (PrP C ) peptide probe was immobilized on GNPs of the hydrogel electrode to construct an AβO biosensor. Electrochemical impedance spectroscopy was utilized for AβO analysis. Results The specific binding between AβO and PrP C probes on the hydrogel electrode resulted in an increase in the electron-transfer resistance. The biosensor showed high specificity and sensitivity for AβO detection. It could selectively differentiate AβO from amyloid-beta (Aβ) monomers or fibrils. Meanwhile, it was highly sensitive to detect as low as 0.1 pM AβO in artificial CSF or blood plasma. The linear range for AβO detection is from 0.1 pM to 10 nM. Conclusion This biosensor could be used as a cost-effective tool for early diagnosis of AD due to its high electrochemical performance and bionic structure.

No abstract

No abstract

: Leukaemia is the most common malignant tumor in childhood and can be cured by chemotherapy. Infection is an important cause of treatment-related death and treatment failure in childhood leukaemia. Recent studies have shown that the correlation between the occurrence of leukaemia infection and the intestinal flora has attracted more and more attention. Intestinal flora can affect the body's physiological defense and immune function. When intestinal microflora disorder occurs, metabolites/microorganisms related to intestinal flora alterations and even likely the associated morpho-functional alteration of the epithelial barrier may be promising diagnostic biomarkers for the early diagnosis of leukaemia infection. This review will focus on the interaction between leukaemia infection and intestinal flora, and the influence of intestinal flora in the occurrence and development of leukaemia infection.

BACKGROUND: The severity and mortality of sepsis is related to excessive inflammation and cytokine storm. Nevertheless, little is known about why sepsis has a significant increase in proinflammatory cytokine production, which leads to more severe inflammatory damage. METHOD: Mesenchymal stem cells have achieved certain results in the treatment of sepsis, but the specific mechanism remains to be further clarified. RESULT: Therefore, this paper will elaborate on the currently recognized mechanism of mesenchymal stem cells in the treatment of sepsis, protein phosphorylation mechanism of sepsis inflammatory response and the possibility that mesenchymal stem cells may block the occurrence and development of sepsis by regulating relevant pathways or protein phosphorylation. CONCLUSION: It provides a novel target for mesenchymal stem cells to prevent intervention or therapeutically block the development of sepsis.

No abstract