Comparison of the effects of sustained contractions in different positions of the upper extremity and different degrees of resistance by pinch on the active range of motion

無作為に選択した健常者10名を対象に,上肢静止性収縮時における肩・肘関節の肢位と負荷の相違が,手関節屈曲の自動関節可動域と手関節屈曲の主動筋と拮抗筋の表面筋電図に及ぼす影響を検討した.肩・肘関節の肢位は固有受容性神経筋促通(PNF)肢位(肩135°屈曲,45°内転,中等度外旋位,肘軽度屈曲,前腕90°回外)の上肢PNF肢位と非PNF 肢位(肩90°屈曲,内外旋中間位,肘伸展,前腕90°回内)の2種を選択し,負荷はピンチ力の最大随意収縮の30～40%(軽負荷)および70～80%(重負荷)の2種とした.重負荷・PNF 肢位の組み合わせによる静止性収縮後の手関節屈曲の自動関節可動域改善率が重負荷・非PNF 肢位の自動関節可動域改善率より有意に大きかった(p < 0.05).軽負荷と比較し重負荷で主動筋の積分筋電図値が有意に大きな値を示したが,PNF 肢位では認められなかった.積分筋電図値の指標と自動関節可動域改善との関連性は認められなかった.This study aimed to compare the effects of sustained contractions in different positions of the upper extremity and different degrees of load on both the active range of motion (AROM) of wrist flexion and the surface electromyographic (EMG) activity of wrist agonist and antagonist for ten healthy subjects randomly selected. The positions of the upper extremity were the non-PNF position (shoulder flexion (90°) and elbow extension with forearm pronation) and the PNF position (shoulder flexion-adductionexternal rotation and elbow extension with supination). The target loads by fingertip force spanned a range from 30% to 40% of maximal voluntary contraction (light load) to 70% to 80% (heavy load). The improvement percentage of AROM after each sustained contraction was calculated in comparison with AROM before the contractions, and each integrated EMG (IEMG) ratio was normalized to the IEMG of each maximal voluntary contraction. The results of this study showed that the improvement of AROM by a sustained contraction combined with the PNF position and a heavy load was significantly larger (P < 0.05) compared with the non-PNF position combined with a light load. The IEMG ratio of the agonist during heavy load was greater than for the light load, which may be explained by the observation that the facilitation of the agonist in the heavy load, but there was no facilitation of the agonist in the PNF position of the upper extremity. Because of the non-significant correlation coefficient between improvement of AROM and IEMG, there was no relation between AROM and facilitation of the agonist activity

Genetic Association between Akt1 Polymorphisms and Alzheimer's Disease in a Japanese Population

A recent paper reported that Aβ oligomer causes neuronal cell death through the phosphatidylinositol-3-OH kinase (PI3K)-Akt-mTOR signaling pathway. Intraneuronal Aβ, a main pathological finding of Alzheimer's disease (AD), is also known as inhibiting activation of Akt. This study aims to investigate whether single nucleotide polymorphisms (SNPs) of the Akt1 gene are associated with AD. SNPs genotyped using TaqMan technology was analyzed using a case-control study design. Our case-control dataset consisted of 180 AD patients and 130 age-matched controls. Although two SNPs showed superficial positive, Hardy-Weinberg equilibrium (HWE) tests, and linkage disequilibrium (LD) analyses suggested that genetic regions of the gene are highly polymorphic. We failed to detect any synergetic association among Akt1 polymorphisms, Apolipoprotein E (APO E), and AD. Further genetic studies are needed to clarify the relationship between the Akt1 and AD

Oxidation behaviour of lattice oxygen in Li-rich manganese-based layered oxide studied by hard X-ray photoelectron spectroscopy

The oxidation/reduction behaviours of lattice oxygen and transition metals in a Li-rich manganese-based layered oxide Li[Li0.25Ni0.20Mn0.55]O1.93 are investigated by using hard X-ray photoelectron spectroscopy (HAX-PES). By making use of its deeper probing depth rather than in-house XPS analyses, we clearly confirm the formation of O- ions as bulk oxygen species in the active material. They are formed on the 1st charging process as a charge compensation mechanism for delithiation and decrease on discharging. In particular, the cation-anion dual charge compensation involving Ni and O ions is suggested during the voltage slope region of the charging process. The Ni ions in the material are considered to increase the capacity delivered by a reversible anion redox reaction with the suppression of O2 gas release. On the other hand, we found structural deterioration in the cycled material. The O- species are still observed but are electrochemically inactive during the 5th charge-discharge cycle. Also, the oxidation state of Ni ions is divalent and inactive, although that of Mn ions changes reversibly. We believe that this is associated with the structural rearrangement occurring after the activation process during the 1st charging, leading to the formation of spinel- or rocksalt-like domains over the sub-surface region of the particles

Overexpression of TEAD4 in atypical teratoid/rhabdoid tumor: New insight to the pathophysiology of an aggressive brain tumor

BackgroundAtypical teratoid/rhabdoid tumor (AT/RT) is a highly malignant embryonal brain tumor that occurs mainly in early childhood. Although most of the tumors are characterized by inactivating mutations of the tumor suppressor gene, SMARCB1, the biological basis of its tumorigenesis and aggressiveness is still unknown.ProcedureWe performed high‐throughput copy number variation analysis of primary cell lines generated from primary and relapsed tumors from one of our patients to identify new genes involved in AT/RT biology. The expression of the identified gene was validated in 29 AT/RT samples by gene expression profiling, quantitative real‐time polymerase chain reaction, and immunohistochemistry (IHC). Furthermore, we investigated the function of this gene by mutating it in rhabdoid tumor cells.ResultsTEAD4 amplification was detected in the primary cell lines and its overexpression was confirmed at mRNA and protein levels in an independent cohort of AT/RT samples. TEAD4’s co‐activator, YAP1, and the downstream targets, MYC and CCND1, were also found to be upregulated in AT/RT when compared to medulloblastoma. IHC showed TEAD4 and YAP1 overexpression in all samples. Cell proliferation and migration were significantly reduced in TEAD4‐mutated cells.ConclusionsWe report the overexpression of TEAD4 in AT/RT, which is a key component of Hippo pathway. Recent reports revealed that dysregulation of the Hippo pathway is implicated in tumorigenesis and poor prognosis of several human cancers. Our results suggest that TEAD4 plays a role in the pathophysiology of AT/RT, which represents a new insight into the biology of this aggressive tumor.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/137309/1/pbc26398_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/137309/2/pbc26398.pd

Giant Cell Tumor of the Temporal Bone with Direct Invasion into the Middle Ear and Skull Base: A Case Report

Giant cell tumor (GCT) is classified as a benign bone tumor, and it is frequently identified at the epiphysis of long bones and relatively rare in the temporal bone. For orthopedists expert at recognizing bone and soft tissue tumors, the diagnosis of GCT is relatively easy; however, since head and neck surgeons experience few cases of GCT, it may be difficult to diagnose when it occurs in the temporal bone. A 32-year-old man complained of left hearing loss, aural fullness, and tinnitus. Examination of the ear revealed a bulging tumor. Audiologic examination demonstrated conductive hearing loss of the left ear. Computer tomograph of the temporal bone showed a soft-tissue-density specification indicating bone destruction at the left temporal bone. The tumor invaded the skull base. Imaging examinations using magnetic resonance imaging revealed a nonhomogenous isosignal intensity area on T1 at the left temporal bone. After intravenous gadolinium, the mass showed unequal enhancement. This patient subsequently underwent surgery to remove the lesion using transmastoid and middle fossa approach. Pathological examinations from specimens of the tumor revealed characteristic of GCT. No clinical or radiological evidence of tumor recurrence was detected for 4 years

Insight into the migratory history using otolith Sr : Ca ratio of the anadromous masu salmon Oncorhynchus masou masou from the Tonegawa River

利根川上流域で採集した大型ヤマメ8個体の回遊性を耳石Sr:Ca比分析を用い検証した。その結果，3個体が降海型，5個体が非回遊型と推定された。最も上流で釣獲された検体（降海型）は，4つの堰を通過し，利根川河口から243km遡上していた。利根川には降海型サクラマスと非回遊型の大型ヤマメが生息しており，環境に応じて柔軟に回遊パターンを変化させている可能性が示唆された。The migratory histories of Oncorhynchus masou masou in the Tonegawa River were evaluated from the ontogenetic changes in otolith Sr:Ca ratios. We sampled 8 fish at 180-243 km upstream from the river mouth. Three fish were categorized as anadromous whereas five individual were categorized as nonanadromous life mode with the constantly low Sr:Ca ratios. Intraspecific variation in the migration modes recorded for O. masou masou suggest a plasticity strategy for anadromous behaviors

Effects of xylitol on metabolic parameters and visceral fat accumulation

Xylitol is widely used as a sweetener in foods and medications. Xylitol ingestion causes a small blood glucose rise, and it is commonly used as an alternative to high-energy supplements in diabetics. In previous studies, a xylitol metabolite, xylulose-5-phosphate, was shown to activate carbohydrate response element binding protein, and to promote lipogenic enzyme gene transcription in vitro; however, the effects of xylitol in vivo are not understood. Here we investigated the effects of dietary xylitol on lipid metabolism and visceral fat accumulation in rats fed a high-fat diet. Sprague-Dawley rats were fed a high-fat diet containing 0 g (control), 1.0 g/100 kcal (X1) or 2.0 g/100 kcal (X2) of xylitol. After the 8-week feeding period, visceral fat mass and plasma insulin and lipid concentrations were significantly lower in xylitol-fed rats than those in high-fat diet rats. Gene expression levels of ChREBP and lipogenic enzymes were higher, whereas the expression of sterol regulatory-element binding protein 1c was lower and fatty acid oxidation-related genes were significantly higher in the liver of xylitol-fed rats as compared with high-fat diet rats. In conclusion, intake of xylitol may be beneficial in preventing the development of obesity and metabolic abnormalities in rats with diet-induced obesity