[Purpose] We aimed to investigate the changes in the swallowing sounds of healthy adults during neuromuscular joint facilitation treatment using neck patterns. [Participants and Methods] A total of 20 healthy adults (10 males and 10 females; mean age, 29.2 ± 6.3 years) swallowed 10 mL of water four times under three conditions (after the neuromuscular joint facilitation neck-flexion resistance pattern, after the Shaker-type exercise, and during relaxed sitting without prior exercise [control]), randomly ordered with an interval greater than 3 days. Swallowing sounds for each water swallow were recorded using cervical auscultation. [Results] The mean amplitude of swallowing sound intensity and the mean spectral frequency were significantly higher after the neuromuscular joint facilitation neck-flexion resistance pattern and the Shaker-type exercise, in comparison with those in the control group. [Conclusion] Neuromuscular joint facilitation training with the neck-flexion resistance pattern influenced swallowing sounds to the same degree as the Shaker-type exercise, implying that this resistance pattern may enhance suprahyoid muscle contraction.

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神経疾患による睡眠障害は，脳内病変により睡眠と覚醒をコントロールする神経機構の障害，呼吸筋筋力低下や不随意運動といった神経症状，治療薬に起因するもの，疾患に対する不安などの心理的要因が組み合わさって生じる．レム睡眠行動障害はパーキンソン病，レビー小体病，多系統萎縮症の前駆症状のことがある．筋ジストロフィー症ではレム睡眠時の低呼吸が呼吸不全の初発症状となる．筋萎縮性側索硬化症では肺胞低換気が主症状で，進行に伴って睡眠呼吸障害が生じる．各種神経疾患の睡眠障害の発生機序を理解することで，初めて適切な治療が可能となる．

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Mutations of isocitrate dehydrogenase 1 (IDH1) and isocitrate dehydrogenase 2 (IDH2) have been reported in gliomas, cartilaginous tumors, and acute myeloid leukemias. IDH mutations are specific to a single codon in the conserved and functionally important arginine 132 residue (R132) of IDH1 or arginine 172 residue (R172) of IDH2 in gliomas. Although IDH1 and IDH2 catalyze the oxidative carboxylation of isocitrate to α-ketoglutarate in cytosol and mitochondria, respectively, mutated IDH1/2 proteins can possess the ability to change α-ketoglutarate to an oncometabolite R(−)-2-hydroxyglutarate. We have established several monoclonal antibodies (mAbs) specific for IDH1/2 mutations. However, no multi-specific mAb against IDH1/2 mutations has been reported. For this study, we immunized mice with an IDH1-R132G peptide of 19 amino acids (GGVKPIIIGGHAYGDQYRA), and established a novel mAb MsMab-1 that recognizes IDH1-R132G, but not wild type IDH1 in enzyme-linked immunosorbent assay (ELISA). It is particularly interesting that MsMab-1 recognizes all IDH1 mutants (R132H, R132C, R132S, R132G, R132L) in ELISA. Western blot analysis also revealed that MsMab-1 reacted with recombinant proteins of IDH1-R132H, IDH1-R132S, and IDH1-R132G, but not with wild type IDH1 and other IDH1 mutations, indicating that MsMab-1 is a multi-specific anti-mutated IDH1 mAb. Unexpectedly, MsMab-1 recognizes IDH2-R172M protein, despite that the IDH1-R132G peptide shows only 73.7% identity with the equivalent portion of IDH2-R172M (GGTKPITIGMHAHGDQYKA). Moreover, MsMab-1 stained the IDH1-R132S or IDH1-R132G-expressing glioma cells in immunohistochemistry. This report is the first to establish a multi-specific anti-mutated IDH1/2 mAb, that is expected to be useful for immunohistochemical determination of IDH1/2 mutation-bearing tumors.

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前十字靭帯（ACL）の損傷は、あらゆるレベルのアスリートが経験する可能性のある、最も発生頻度の高い傷害のひとつである。非常に多くの変数がかかわっているため、どのように、そしてなぜ損傷が生じるのかについては多くの論争がある。さらに、できるだけ早く、かつ安全にスポーツに復帰するために取るべき適切な手段についても、様々な提案がある。しかし、傷害からの回復とスポーツへの実際の復帰における大きな問題は、ACL損傷後にアスリートが実行すべきゴールドスタンダードや、一貫した活動指針がないことである。したがって、本稿の目的は、ACL再建術後の競技への復帰に関して、エビデンスに基づく方法を決定するための文献レビューを行ない、復帰のプロセスを導く実践的な助言を提供することである。

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