Search

OBJECTIVE: To investigate the impact of time interval from symptoms onset to vestibular rehabilitation on the recovery of patients in the acute phase of vestibular neuritis. METHODS: Thirty-one patients with vestibular neuritis treated in outpatient and inpatient settings from December 2019 to July 2021 were selected and randomly divided into vestibular rehabilitation group and general treatment group. The vestibular rehabilitation group was subdivided into early-intervention group (1-week after symptom onset) and late-intervention group (2-week after symptom onset) according to the interval from the onset to vestibular rehabilitation. The differences in DP, UW, VOR, DHI, BBS and SAS values at 1 month and 3 months after treatment were compared among early-intervention group(11 cases), late-intervention group (10 cases) and general treatment group(10 cases). RESULTS: For patients in the vestibular rehabilitation group and the general treatment group, DP, UW, VOR gain, DHI score and SAS score were significantly different after treatment (P < 0.05) and no significant difference was found in BBS score (P>0.05). Pairwise comparisons between early-intervention and late-intervention group showed that the DP, UW and VOR gain were significantly different (P < 0.05), while the score of DHI and SAS were not significantly different (P>0.05). CONCLUSION: Vestibular rehabilitation therapy can accelerate vestibular compensation, relieve vertigo symptoms and anxiety symptoms in patients with vestibular neuritis. It is better to be carried out within 1 week after symptom onset.

The attack of vertigo and balance disorder affects individual quality of life among all age, while brings high medical burden. Vestibular rehabilitation plays an important role in the treatment for balance disorder. Early active and systematic rehabilitation treatment will be more conducive to symptom relief, functional recovery, and prevent the occurrence of chronic vestibular syndrome. There were no criteria for the methods, influencing factors and evaluation of vestibular rehabilitation in the treatment of peripheral vestibular vertigo yet, and the clinical application is diversified. This paper reviewed and summarized the related studies of vestibular rehabilitation in peripheral vestibular vertigo in recent years.

Beta-amyloid (Aβ) oligomers are the reliable molecular biomarkers and crucial targets for the diagnosis and therapy of Alzheimer's disease (AD). In this work, we reported on a fluorescent platform for the selective detection of Aβ oligomers with polydopamine nanospheres (PDANS) as the nanoquencher. The carboxyfluorescein (FAM)-labeled DNA aptamers specific to Aβ oligomers showed poor fluorescence signal when absorbed onto the surface of PDANS. The specific binding of Aβ oligomer to the FAM-DNA caused the conformation change of the aptamer into a hairpin structure, thus inducing the release of FAM-DNA from the PDANS surface and making the fluorophore far away from the nanoquencher. Aβ oligomers were thus determined based on the increase in the fluorescence signal. The “signal on” fluorescent platform could be used for sensing of Aβ oligomers, but not for the monomers and fibrils. The detection limit was found to be 12.5 nM. More intriguingly, we found that PDANS efficiently prevented the aggregation of Aβ monomers. We believe that the two-in-one PDANS as both the nanoquencher and the inhibitor would found many applications for determination of Aβ oligomers in bodily fluids and drug-therapy of AD.

Beta-amyloid (Aβ) peptides are the major constituents of senile plaques in the brains of Alzheimer's disease (AD) patients. Aβ monomers (AβMs) can coalesce to form small, soluble oligomers (AβOs), followed by reorganization and assembly into long, thread-like fibrils (AβFs). Recently, soluble AβOs have been regarded as reliable molecular biomarkers for the diagnosis of AD because of their high toxicity for neuronal synapse and high concentration levels in the brains of AD patients. In this work, we reported a label-free, sensitive and selective method for visual and fluorescent detection of AβOs based on the inner filter effect (IFE) of gold nanoparticles (AuNPs) on the fluorescence of CdTe quantum dots (QDs). Specifically, the fluorescence of CdTe QDs was quenched significantly by AuNPs through the IFE. PrP(95-110), an AβOs-specific binding peptide from cellular prion protein, triggered the aggregation and color change of AuNPs suspension; thus, the IFE of AuNPs on the fluorescence of CdTe QDs was weakened and the fluorescence intensity was recovered. However, in the presence of AβOs, the specific interaction of AβOs and PrP(95-110) prevented the absorption of PrP(95-110) onto the surface of AuNPs. As a result, the aggregation of AuNPs was inhibited and the fluorescence intensity of CdTe QDs was quenched again. This label-free method is specific for detection of AβOs but not for AβMs and AβFs. The detection limits were found to be 0.5nM for the visual assay and 0.2nM for the fluorescent detection. We believe that this work would be valuable for many investigations related to AD diagnosis and drug discovery.

Soluble amyloid-β oligomer (AβO) is believed to be a reliable molecular biomarker for the diagnosis of Alzheimer's disease (AD) because of its high toxicity for neuronal synapse and higher concentration level in cerebrospinal fluid sample from AD patient than from control individual. At present, it is critical to develop a simple method for AβO detection with low cost as well as high sensitivity and selectivity. In this work, we reported an antibody-free electrochemical method for the detection of AβO based on the specific interaction between AβO and PrP(95–110) peptide, a segment of cellular prion protein. Specifically, cysteine-containing PrP(95–110) peptide was first immobilized on a gold electrode for the capture of AβO. Then, alkaline phosphatase-conjugated PrP(95–110) was used for the recognition of the captured AβO and the generation of electroactive species. Furthermore, an “outer-sphere to inner-sphere” electrochemical–chemical–chemical (ECC) redox cycling using ferrocene methanol as the redox mediator was employed to enhance the detection sensitivity. As a result, a detection limit of 3 pM for equivalent monomer was achieved. The amenability of this method to AβO analysis in a biological matrix was demonstrated by assays of AβO in serum samples.

This work presented a simple, sensitive and label-free electrochemical method for the detection of microRNAs (miRNAs). It is based on the boronate ester covalent interaction between 4-mercaptophenylboronic acid (MPBA) and cis-diol at the 3′-terminal of miRNAs and the MPBA-induced in situ formation of citrate-capped silver nanoparticles (AgNPs) aggregates as labels on the electrode surface. In this design, MPBA acted as the cross-linker of AgNPs assembly. Specifically, the thiolated hairpin-like DNA probe was assembled onto the gold nanoparticles (nano-Au) modified electrode surface through the Ag-S interaction. After hybridization with the target miRNAs, MPBA was anchored onto the 3′-terminal of miRNAs through the formation of a boronate ester bond and then captured AgNP via the Ag-S interaction. Meanwhile, free MPBA molecules in solution induced the in situ assembly of AgNPs on electrode surface through the covalent interactions between α-hydroxycarboxylate of citrate and boronate of MPBA and the formation of Ag-S bonds. The electrochemical signal was therefore amplified due to the formation of AgNPs network architecture. To demonstrate the feasibility and analytical performances of the method, miRNA-21 was determined as a model analyte. The detection limit was found to be 20 aM. The viability of our method for biological sample assays was demonstrated by measuring the miRNA-21 contents in three human serum samples. In contrast to other signal-amplified electrochemical strategies for miRNAs detection, our method requires simple detection principle and easy operation procedure and obviates the specific modification of nanoparticles and capture/detection probes.