Meiling Chen

This work aims to evaluate the antimicrobial potential of ethanolic and water extracts of roselle (Hibiscus sabdariffa), rosemary (Rosmarinus officin), clove (Syzygium aromaticum), and thyme (Thymus vulgaris) on some food pathogens and spoilage microorganisms. Agar well diffusion method has been used to determine the antimicrobial activities and Minimum Inhibitory Concentrations (MIC) of different plant extracts against Gram-positive bacteria (Bacillus cereus, Staphylococcus aureus), Gram-negative bacteria (Escherichia coli, Salmonella enteritidis, Vibrio parahaemolyticus, Pseudomonas aeruginosa), and one fungus (Candida albicans). The extracts exhibited both antibacterial and antifungal activities against tested microorganisms. Ethanolic roselle extract showed significant antibacterial activity (P<0.05) against all tested bacterial strains, while no inhibitory effect on Candida albicans (CA) was observed. Only the ethanolic extracts of clove and thyme showed antifungal effects against CA with inhibition zones ranging from 25.2±1.4 and 15.8±1.2 mm, respectively. Bacillus cereus (BC) appears to be the most sensitive strain to the aqueous extract of clove with a MIC of 0.315%. To enhance our understanding of antimicrobial activity mechanism of plant extracts, the changes in internal pH (pHin), and membrane potential were measured in Staphylococcus aureus (SA), and Escherichia coli (EC) cells after exposure to the plant extracts. The results indicated that the plant extracts significantly affected the cell membrane of Gram-positive and Gram-negative bacteria, as demonstrated by the decline in pHin as well as cell membrane hyperpolarization. In conclusion, plant extracts are of great value as natural antimicrobials and can use safely as food preservatives.

BACKGROUND: Biomarker changes that occur in the period between normal cognition and the diagnosis of sporadic Alzheimer's disease have not been extensively investigated in longitudinal studies. METHODS: We conducted a multicenter, nested case-control study of Alzheimer's disease biomarkers in cognitively normal participants who were enrolled in the China Cognition and Aging Study from January 2000 through December 2020. A subgroup of these participants underwent testing of cerebrospinal fluid (CSF), cognitive assessments, and brain imaging at 2-year-to-3-year intervals. A total of 648 participants in whom Alzheimer's disease developed were matched with 648 participants who had normal cognition, and the temporal trajectories of CSF biochemical marker concentrations, cognitive testing, and imaging were analyzed in the two groups. RESULTS: , 14 years; phosphorylated tau 181, 11 years; total tau, 10 years; neurofilament light chain, 9 years; hippocampal volume, 8 years; and cognitive decline, 6 years. As cognitive impairment progressed, the changes in CSF biomarker levels in the Alzheimer's disease group initially accelerated and then slowed. CONCLUSIONS: In this study involving Chinese participants during the 20 years preceding clinical diagnosis of sporadic Alzheimer's disease, we observed the time courses of CSF biomarkers, the times before diagnosis at which they diverged from the biomarkers from a matched group of participants who remained cognitively normal, and the temporal order in which the biomarkers became abnormal. (Funded by the Key Project of the National Natural Science Foundation of China and others; ClinicalTrials.gov number, NCT03653156.).

CD4(+)CD25(+) regulatory T cells (Tregs) are essential for maintaining self-tolerance and immune homeostasis. Here we characterize a novel subset of CD4(+)CD25(+) Tregs that express latency-associated peptide (LAP) on their cell surface (CD4(+)CD25(+)LAP(+) cells). CD4(+)CD25(+)LAP(+) cells express elevated levels of Foxp3 and Treg-associated molecules (CTLA4, glucocorticoid-induced TNFR-related gene), secrete TGFbeta, and express both cell surface TGFbeta and surface receptors for TGFbeta. In vitro, the suppressive function of CD4(+)CD25(+)LAP(+) cells is both cell contact and soluble factor dependent; this contrasts with CD4(+)CD25(+)LAP(-) cells, which are mainly cell contact dependent. In a model of experimental autoimmune encephalomyelitis, CD4(+)CD25(+)LAP(+) cells exhibit more potent suppressive activity than CD4(+)CD25(+)LAP(-) cells, and the suppression is TGFbeta dependent. We further show that CD4(+)CD25(+)LAP(+) cells suppress myelin oligodendrocyte glycoprotein-specific immune responses by inducing Foxp3 and by inhibiting IL-17 production. Our findings demonstrate that CD4(+)CD25(+) Tregs are a heterogeneous population and that the CD4(+)CD25(+) subset that expresses LAP functions in a TGFbeta-dependent manner and has greater in vivo suppressive properties. Our work helps elucidate the ambiguity concerning the role of TGFbeta in CD4(+)CD25(+) Treg-mediated suppression and indicates that LAP is an authentic marker able to identify a TGFbeta-expressing CD4(+)CD25(+) Treg subset.