136 research outputs found

    Can golfers choose low-risk routes in steep putting based on visual feedback of ball trajectory?

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    This study aims to clarify why the aiming method in golf putting in risky situations differs based on skill level. This study set up a difficult challenge (steep slopes and fast ball rolling greens), which required even professional golfers to change their aim. A total of 12 tour professionals and 12 intermediate amateurs were asked to perform a steep-slope task with no visual feedback of outcomes (no FB) followed by a task with visual feedback (with FB). The aim of the task was for the ball to enter the hole in one shot. Additionally, the participants were told that if the ball did not enter the hole, it was to at least stop as close to it as possible. The participant's aim (as an angle) and the kinematics of the putter head and ball were measured. The results indicated that professionals' highest ball trajectory points were significantly higher than that of amateurs, especially with FB. Additionally, professionals had higher ball-launch angles (the direction of the ball when the line connecting the ball and the center of the hole is 0 degrees) and lower peak putter head velocities than amateurs. Furthermore, the aim angle, indicating the golfer's decision-making, was higher for professionals under both conditions. However, even with FB, the amateurs' aim angles were lower and the difference between trials was smaller than that of professionals. Therefore, this study confirmed that the professionals made more drastic changes to their aim to find low-risk routes than the amateurs and that the amateurs’ ability to adjust their aim was lower than that of professionals. The results suggest that the reason for the amateurs' inability to find low-risk routes lies in their decision-making. The professionals found better routes; however, there were individual differences in their routes

    Immune Reactions Against Elongation Factor 2 Kinase: Specific Pathogenesis of Gastric Ulcer from Helicobacter pylori Infection

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    Helicobacter pylori (H. pylori) infection is a definite causative factor for gastric ulcers (GUs). In the present study we detected a specific antigen of gastric epithelial cells (HGC-27) using cell ELISA, which was recognized by the sera of GU patients (n = 20) but not in patients with chronic gastritis (CG; n = 20) or in healthy volunteers (HC; n = 10). This antigen was over-expressed by a stressful (heat-stressed) environment, and was identified as elongation factor 2 kinase (EF-2K) by western blotting. The GU patients' lymphocytes stimulated by H. pylori specifically disrupted heat-stressed HGC-27 cells in a cytotoxic assay. In flow cytometry, the effector cells (lymphocytes) from GU patients were significantly differentiated to T helper type 1 lymphocyte (Th1) and cytotoxic T lymphocyte (CTL) as opposed to those from CG patients. The target cells (HGC-27) expressed EF-2K and MHC-class I together with costimulatory molecules from heat stress. This antigen specific immune mechanism could have a prominent role in the pathogenesis of GU

    The Pharmacological Effects of Herbs on Catecholamine Signaling

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    Herbs have many biologically and pharmacologically active compounds such as flavonoids and stilbenes. They have been used in remedies for various disorders. Here we review the effects of herbs on catecholamine synthesis and secretion in cultured bovine adrenal medullary cells. Ikarisoside A (1.0–100 μM), a flavonol glycoside, inhibited the catecholamine secretion induced by acetylcholine (0.3 mM). This inhibition was associated with the suppression of 22Na+ and 45Ca2+ influx induced by acetylcholine. The ethanol extract (0.0003–0.005%) of matsufushi (extract of pine nodules) inhibited the catecholamine secretion induced by acetylcholine. SJ-2, one of the stilbene compounds isolated from matsufushi, inhibited acetylcholine-induced catecholamine secretion. Matsufushi extract and SJ-2 reversibly inhibited acetylcholine-induced Na+ currents in Xenopus oocytes expressed with α3β4nicotinic acetylcholine receptors. Sweet tea is the processed leaves of Hydrangea macrophylla. The extract of sweet tea (0.3–1.0 mg/ml) suppressed catecholamine secretion induced by acetylcholine (0.3 mM). Moreover, sweet tea (0.1–1.0 mg/ml), ikarisoside A (1.0–100 μM), and matsufushi (0.001–0.003%) or SJ-2 (10–30 μM) inhibited acetylcholine-induced 14C-catecholamine synthesis from 14C-tyrosine. These findings indicate that ikarisoside A, matsufushi (or SJ-2), and sweet tea inhibit the catecholamine secretion and synthesis induced by acetylcholine in cultured bovine adrenal medullary cells and probably in sympathetic neurons

    The first Japanese MDPL case

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    Mandibular hypoplasia, deafness, progeroid features and lipodystrophy (MDPL) syndrome is a rare autosomal dominant disorder caused by heterozygous POLD1 mutations. To date, 13 patients affected by POLD1 mutation-caused MDPL have been described. We report a clinically undiagnosed 11-year-old male who noted joint contractures at 6 years of age. Targeted exome sequencing identified a known POLD1 mutation [NM_002691.3:c.1812_1814del, p.(Ser605del)] that diagnosed him as the first Japanese/East Asian MDPL case

    The effects of caffeine on the human Somatosensory evoked potential (SEP), visual evoked potential (VEP) and EEG

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    The effects of caffeine on central nervous system were investigated with SEP and VEP (EPs). The subjects were 25 healthy male volunteers aged 24-44 with a mean caffeine consumption of 251.4 mg/day, and were divided into the light and heavy consumer groups according to DSM-IV criteria for caffeine intoxication. They were given 3 mg/kg of body weight of caffeine or placebo in a double-blind cross-over design. EEGs containing SEPs evoked by electric stimuli to the right median nerve and VEPs by flash stimuli were recorded before, 30, 60, 90 minutes after dosing. The consecutive changes in EPs and EEG power% were studied and the following results were obtained. 1. Overall subjects had few components with significant changes in latencies and amplitudes of SEP and VEP after administration of caffeine. 2. EEGs recorded together with EPs showed a significant increase in α1 power% and a significant decrease in δ, θ and β2 power%. 3. There were also no significant differences in EPs measures and EEGs between the light and heavy consumer groups, except for EEG power% of VEP with the heavy costumer group showing an earlier appearance of changes. In conclusion, 3 mg/kg of body weight of caffeine administered in the present study did not effect on SEP and VEP as well as EEGs

    Constant Current vs. Constant Voltage Systems for Temporal Spinal Cord Stimulation for Intractable Pain

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    Although spinal cord stimulation (SCS) is a useful treatment for chronic intractable pain, the optimal method of stimulation has not yet been established. In this prospective, crossover study, we compared the efficacy of using a constant current (CC) system with that of a constant voltage (CV) system for temporal SCS. Twenty patients were enrolled and divided into two groups. For 10 patients, a CV system was applied on Days 1-5, followed by the use of a CC system on Days 6-10. For the other 10 patients, a CC system was applied for the first five days, followed by a CV system for the subsequent five days. We evaluated the alteration of pain intensity using a visual analogue scale (VAS), the area of stimulation, the stability of effect, and patient satisfaction regarding treatment. The pain scores decreased significantly after the start of the SCS. There was no significant difference in the change in VAS between the two systems. The stimulation method used for temporal SCS did not affect the reduction of pain intensity. Patients felt a wider stimulation area by the CC system compared to the CV system

    Increased amygdala reactivity following early life stress : a potential resilience enhancer role

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    Background: Amygdala hyper-reactivity is sometimes assumed to be a vulnerability factor that predates depression; however, in healthy people, who experience early life stress but do not become depressed, it may represent a resilience mechanism. We aimed to test these hypothesis examining whether increased amygdala activity in association with a history of early life stress (ELS) was negatively or positively associated with depressive symptoms and impact of negative life event stress in never-depressed adults. Methods: Twenty-four healthy participants completed an individually tailored negative mood induction task during functional magnetic resonance imaging (fMRI) assessment along with evaluation of ELS. Results: Mood change and amygdala reactivity were increased in never-depressed participants who reported ELS compared to participants who reported no ELS. Yet, increased amygdala reactivity lowered effects of ELS on depressive symptoms and negative life events stress. Amygdala reactivity also had positive functional connectivity with the bilateral DLPFC, motor cortex and striatum in people with ELS during sad memory recall. Conclusions: Increased amygdala activity in those with ELS was associated with decreased symptoms and increased neural features, consistent with emotion regulation, suggesting that preservation of robust amygdala reactions may reflect a stress buffering or resilience enhancing factor against depression and negative stressful events

    Detection of Nε-(hexanoyl)lysine in the tropomyosin 1 protein in N-methyl-N'-nitro-N-nitrosoguanidine-induced rat gastric cancer cells

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    Nε-(Hexanoyl)lysine, formed by the reaction of lysine with n-6 lipid hydroperoxide, is a lipid peroxidation marker during the initial stage of oxidative stress. The aim of the present study is to indentify Nε-(hexanoyl)lysine-modified proteins in neoplastic transformed gastric mucosal cells by N-methyl-N'-nitro-N-nitrosoguanidine, and to compare the levels of these proteins between gastric mucosal cells and normal gastric cells. Much greater fluorescence of 2-[6-(4'-hydroxy)phenoxyl-3H-xanthen-3-on-9-yl]benzoic acid, an index of the intracellular levels of reactive oxygen species, was observed for gastric mucosal cells compared to normal gastric cells. Nε-(Hexanoyl)lysine-modified proteins were detected by SDS-PAGE or two-dimensional electrophoresis and Western blotting using anti-Nε-(hexanoyl)lysine polyclonal antibody, and a protein band of between 30–40 kDa was clearly increased in gastric mucosal cells compared to normal gastric cells. Two Nε-(hexanoyl)lysine-modified protein spots in gastric mucosal cells were identified as the tropomyosin 1 protein by mass spectrometry using a MASCOT search. The existence of Nε-(hexanoyl)lysine modification in tropomyosin 1 was confirmed by Western blotting of SDS-PAGE-separated or two-dimensional electrophoresis-separated proteins as well as by the immunoprecipitation with anti-tropomyosin 1 antibody. These data indicate that Nε-(hexanoyl)lysine modification of tropomyosin 1 may be related to neoplastic transformation by N-methyl-N'-nitro-N-nitrosoguanidine in gastric epithelial cells

    Effect of ipragliflozin on carotid intima-media thickness in type 2 diabetes patients

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    Aims To examine the effects of a 24-month treatment with ipragliflozin on carotid intima-media thickness (IMT) in type 2 diabetes patients. Methods and results In this multicenter, prospective, randomized, open-label, and blinded-endpoint investigator-initiated clinical trial, adults with type 2 diabetes and haemoglobin A1C (HbA1c) of 6.0–10.0% (42–86 mmol/mol) were randomized equally to ipragliflozin (50 mg daily) and non-sodium-glucose cotransporter-2 (SGLT2) inhibitor use of standard-care (control group) for type 2 diabetes and were followed-up to 24 months. The primary endpoint was the change in mean common carotid artery IMT (CCA-IMT) from baseline to 24 months. A total of 482 patients were equally allocated to the ipragliflozin (N = 241) and control (N = 241) groups, and 464 patients (median age 68 years, female 31.7%, median type 2 diabetes duration 8 years, median HbA1c 7.3%) were included in the analyses. For the primary endpoint, the changes in the mean CCA-IMT from baseline to 24 months were 0.0013 [95% confidence interval (CI), −0.0155–0.0182] mm and 0.0015 (95% CI, −0.0155–0.0184) mm in the ipragliflozin and control groups, respectively, with an estimated group difference (ipragliflozin-control) of −0.0001 mm (95% CI, −0.0191–0.0189; P = 0.989). A group difference in HbA1c change at 24 months was also non-significant between the treatment groups [−0.1% (95% CI, −0.2–0.1); P = 0.359]. Conclusion Twenty-four months of ipragliflozin treatment did not affect carotid IMT status in patients with type 2 diabetes recruited in the PROTECT study, relative to the non-SGLT2 inhibitor-use standard care for type 2 diabetes
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