28 research outputs found

    The Relationship between Peripheral Nerve Conduction Velocity and Ophthalmological Findings in Type 2 Diabetes Patients with Early Diabetic Retinopathy

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    Purpose. Nerve conduction velocity (NCV) is an indicator of neuronal damage in the distal segment of the peripheral nerves. Here, we determined the association between NCV and other systemic and ocular clinical findings, in type 2 diabetes patients with early diabetic retinopathy (DR). Methods. This study included 42 eyes of 42 type 2 diabetes patients (median age: 54 years) with no DR or with mild nonproliferative DR. Standard statistical techniques were used to determine associations between clinical findings. Results. Sural sensory conduction velocity (SCV) and tibial motor conduction velocity (MCV) were significantly lower in mild nonproliferative DR patients than patients with no DR (P=0.008 and P=0.01, resp.). Furthermore, logistic regression analyses revealed that sural SCV and tibial MCV were independent factors contributing to the presence of mild nonproliferative DR (OR 0.83, P=0.012 and OR 0.69 P=0.02, resp.). Tibial MCV was correlated with choroidal thickness (CT) (P=0.01), and a multiple regression analysis revealed that age, tibial MCV, and carotid intima-media thickness were independent associating factors with CT (P=0.035, P=0.015, and P=0.008, resp.). Conclusions. Our findings suggest that reduced NCV may be closely associated with early DR in type 2 diabetes patients. Thus, reduced nerve conduction is a potential early biomarker of DR

    Canonical Wnt signaling and its antagonist regulate anterior-posterior axis polarization by guiding cell migration in mouse visceral endoderm

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    The mouse embryonic axis is initially formed with a proximal-distal orientation followed by subsequent conversion to a prospective anterior-posterior (A-P) polarity with directional migration of visceral endoderm cells. Importantly, Otx2, a homeobox gene, is essential to this developmental process. However, the genetic regulatory mechanism governing axis conversion is poorly understood. Here, defective axis conversion due to Otx2 deficiency can be rescued by expression of Dkk1, a Wnt antagonist, or following removal of one copy of the beta-catenin gene. Misexpression of a canonical Wnt ligand can also inhibit correct A-P axis rotation. Moreover, asymmetrical distribution of beta-catenin localization is impaired in the Otx2-deficient and Wnt- misexpressing visceral endoderm. Concurrently, canonical Wnt and Dkk1 function as repulsive and attractive guidance cues, respectively, in the migration of visceral endoderm cells. We propose that Wnt/beta-catenin signaling mediates A-P axis polarization by guiding cell migration toward the prospective anterior in the pregastrula mouse embryo.info:eu-repo/semantics/publishedVersio

    Circadian regulation of intracellular G-protein signalling mediates intercellular synchrony and rhythmicity in the suprachiasmatic nucleus

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    Synchronous oscillations of thousands of cellular clocks in the suprachiasmatic nucleus (SCN), the circadian centre, are coordinated by precisely timed cell–cell communication, the principle of which is largely unknown. Here we show that the amount of RGS16 (regulator of G protein signalling 16), a protein known to inactivate Gαi, increases at a selective circadian time to allow time-dependent activation of intracellular cyclic AMP signalling in the SCN. Gene ablation of Rgs16 leads to the loss of circadian production of cAMP and as a result lengthens circadian period of behavioural rhythm. The temporally precise regulation of the cAMP signal by clock-controlled RGS16 is needed for the dorsomedial SCN to maintain a normal phase-relationship to the ventrolateral SCN. Thus, RGS16-dependent temporal regulation of intracellular G protein signalling coordinates the intercellular synchrony of SCN pacemaker neurons and thereby defines the 24 h rhythm in behaviour

    Relationship between Eccentric-Exercise-Induced Loss in Muscle Function to Muscle Soreness and Tissue Hardness

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    It is well-known that unusual exercise, especially eccentric contraction (ECC), could cause delayed-onset muscle soreness. However, the factors related to the loss of muscle strength and range of motion (ROM) caused by eccentrically damaged muscle, such as increases in muscle soreness, tissue hardness, and pain threshold, have not been investigated in detail. Thus, this study was conducted to investigate the factors related to the loss of muscle strength and ROM caused by eccentrically damaged muscle in a large sample. Fifty-six sedentary healthy young male volunteers were instructed to perform 60 repetitions of ECC exercise. The outcome variables were measured before and 48 h after the ECC exercise. The results showed that a decrease in ROM was correlated to an increase in tissue hardness, whereas a decrease in muscle strength was correlated to an increase in muscle soreness. Our results suggested that tissue hardness must be controlled for ROM loss, and muscle soreness must be controlled for muscle-strength loss

    The Effect of Static Compression via Vibration Foam Rolling on Eccentrically Damaged Muscle

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    Previous research has shown that vibration foam rolling (VFR) on damaged muscle can result in improvements in muscle soreness and range of motion (ROM). Furthermore, static compression via VFR (i.e., VFR without rolling) can increase the ROM and decrease the muscle stiffness of non-damaged muscle. Therefore, it is likely that static compression via VFR on eccentrically damaged muscle can mitigate muscle soreness and the decrease in ROM, and the decrease in muscle strength. The purpose of this study was to investigate the acute effects of a 90 s bout of VFR applied as a static compression on an eccentrically damaged quadriceps muscle, measuring ROM, muscle soreness, muscle strength, and jump performance. This study was a single-arm repeated measure design. Study participants were sedentary healthy male volunteers (n = 14, 20.4 ± 0.8 years) who had not performed habitual exercise activities or any regular resistance training for at least 6 months before the experiment. All participants performed a bout of eccentric exercise of the knee extensors with the dominant leg and then received a 90 s bout of static compression via VFR of the quadriceps 48 h after the eccentric exercise. The knee flexion ROM, muscle soreness at palpation, and countermovement jump height were measured before the eccentric exercise (baseline), before (pre-intervention) and after the VFR intervention (post-intervention), and 48 h after the eccentric exercise. The results showed that the static compression via VFR significantly (p < 0.05) improved the knee flexion ROM (6.5 ± 4.8%, d = 0.76), muscle soreness at palpation (−10.7 ± 8.6 mm, d = −0.68), and countermovement jump height (15.6 ± 16.0%, d = 0.49). Therefore, it can be concluded that static compression via VFR can improve muscle soreness and function