Objective This study aimed to explore the therapeutic effect of high-frequency repetitive transcranial magnetic stimulation (HF-rTMS) with two different inter-train intervals (ITIs) on upper limb motor function in the early period of stroke. Methods We recruited 48 post-stroke patients in the early period and randomly divided them into three cohorts: the sham group, the short ITI (8 s) group, and the long ITI (28 s) group. HF-rTMS was delivered at 20 Hz. The amplitude of motor evoked potentials at the affected cortical region, representing the abductor pollicis brevis muscle, reflected cortical excitability. At baseline, immediately after treatment, and 1 month after treatment, we evaluated the recovery of upper limb motor function using Brunnstrom recovery stages (BRSs) and the Fugl–Meyer Assessment for upper extremity (FMA-UE), and assessed functional independence using the Barthel Index (BI). Results HF-rTMS with two different ITIs significantly improved upper limb functional recovery relative to the sham group, but there was no significant difference in cortical excitability changes or BRS, FMA-UE, or BI scores between the different ITI groups. Conclusions At the early post-stroke stage, HF-rTMS with short ITIs generates a similar therapeutic effect to HF-rTMS with long ITIs, suggesting that treatment times can be decreased.

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Hepatocellular carcinoma (HCC) is one of the major causes of cancer-related death worldwide. AHSA1 as a chaperone of HSP90 promotes the maturation, stability, and degradation of related cancer-promoting proteins. However, the regulatory mechanism and biological function of AHSA1 in HCC are largely unknown. Actually, we found that AHSA1 was significantly upregulated in HCC tissues and cell lines and was notably correlated with the poor clinical characteristics and prognosis of HCC patients in this study. Furthermore, both in vitro and in vivo, gain- and loss-of-function studies demonstrated that AHSA1 promoted the proliferation, invasion, metastasis, and epithelial-mesenchymal transition (EMT) of HCC. Moreover, the mechanistic study indicated that AHSA1 recruited ERK1/2 and promoted the phosphorylation and inactivation of CALD1, while ERK1/2 phosphorylation inhibitor SCH772984 reversed the role of AHSA1 in the proliferation and EMT of HCC. Furthermore, we demonstrated that the knockdown of CALD1 reversed the inhibition of proliferation and EMT by knocking AHSA1 in HCC. We also illustrated a new molecular mechanism associated with AHSA1 in HCC that was independent of HSP90 and MEK1/2. In summary, AHSA1 may play an oncogenic role in HCC by regulating ERK/CALD1 axis and may serve as a novel therapeutic target for HCC.

It is shown that great progress was recently made in the treatment of repetitive transcranial magnetic stimulation (rTMS) for neurological and psychiatric diseases. This study aimed to address how rTMS exerted it therapeutic effects by regulating competitive endogenous RNAs (ceRNAs) of lncRNA-miRNA-mRNA. The distinction of lncRNA, miRNA and mRNA expression in male status epilepticus (SE) mice treated by two different ways, low-frequency rTMS (LF-rTMS) vs. sham rTMS, was analyzed by high-throughput sequencing. The Gene Ontology (GO) functional enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were carried out. Gene–Gene Cross Linkage Network was established; pivotal genes were screened out. qRT-PCR was used to verify gene–gene interactions. Our results showed that there were 1615 lncRNAs, 510 mRNAs, and 17 miRNAs differentially which were expressed between the LF-rTMS group and the sham rTMS group. The expression difference of these lncRNAs, mRNAs, and miRNAs by microarray detection were consistent with the results by qPCR. GO functional enrichment showed that immune-associated molecular mechanisms, biological processes, and GABA-A receptor activity played a role in SE mice treated with LF-rTMS. KEGG pathway enrichment analysis revealed that differentially expressed genes were correlated to T cell receptor signaling pathway, primary immune deficiency and Th17 cell differentiation signaling pathway. Gene–gene cross linkage network was established on the basis of Pearson’s correlation coefficient and miRNA. In conclusion, LF-rTMS alleviates SE through regulating the GABA-A receptor activity transmission, improving immune functions, and biological processes, suggesting the underlying ceRNA molecular mechanisms of LF-rTMS treatment for epilepsy.