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ObjectiveTo summarize and analyze the protocols of repetitive transcranial magnetic stimulation (rTMS) in the treatment of post-stroke lower limb dysfunction. MethodsLiterature about rTMS for lower limb dysfunction of patients post stroke were retrieved from Web of Science, PubMed, CNKI, and Wanfang Data from inception to August 17, 2022. The quality of the literature was evaluated with Physiotherapy Evidence Database (PEDro) scale. Literature quality, data extraction and scoping review were performed by two researchers. ResultsA total of 21 studies were included, in which 20 studies suggested that rTMS treatment could promote the recovery of lower limb motor function after stroke. One study showed negative result. rTMS interventions were reported safe, with no serious adverse reactions. There were great heterogeneity in the demographic and clinical information, study protocols, stimulation parameters, coil types, targets of stimulation, and motor-evoked potential measurement in the included studies. ConclusionThe future protocols of rTMS need to be combined with stroke stage and severity of injury. There is a demand for more real vs. sham rTMS studies, reporting similar designs with sufficient information, to achieve a significant level of evidence regarding the use of rTMS in post-stroke patients.
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A new wave of engineered antibodies, leading to increased effectiveness of functions such as antibody-dependent cell-mediated cytotoxicity or complement-dependent cytotoxicity, is being evaluated in clinical settings. Several, such as immunotoxins, are expected to receive approval for usage soon. In this study, using a cognate heavy framework region (HFR2), two complementarity-determining regions (CDRs, i.e., LCDR1 and HCDR3) were fused to the first 388 amino acid residues of diphtheria toxin (DT388) to establish the immunotoxin IT-87. It was found that the mimetics of LCDR1-HFR2-HCDR3 retained the antigen recognition of their parent antibody. The immunotoxin IT-87 could especially kill the U87 MG glioblastoma cell line, the targets of the parent antibody, in vitro; however, the IT-87 could not kill Rajicells. In SCID mice bearing both U87 and Raji cells, the IT-87 directly targeted the U87-induced tumors (via tumor-specific surface markers) and inhibited the growth of the cells in vivo over a 20-day daily IT-87 treatment period. It is believed that the design of this particular immunotoxin could be the basis for even more promising molecules to be used in the treatment of human cancers.
