bluuebunny/crossref_metadata_2025_split huggingface dataset:
Electromyographical Comparison of Pike Variations Performed With and Without Instability Devices
Authors: Snarr Ronald L. , Hallmark Ashleigh V. , Nickerson Brett S. , Esco Michael R. 
Published: May 2016

Abstract
Snarr, RL, Hallmark, AV, Nickerson, BS, and Esco, MR. Electromyographical comparison of pike variations performed with and without instability devices. J Strength Cond Res 30(12): 3436–3442, 2016—Instability devices are primarily used with the intent of increasing the intensity of traditional exercises by providing further muscular demands of the abdominal wall by decreasing stability. Although there are multiple studies examining these devices, most often they only compare one such device to a stable movement and overlook the comparison among multiple devices. The purpose of this investigation was to compare the electromyographical differences of the rectus abdominis (RA), external oblique (EO), erector spinae (LSES), and rectus femoris (RF) during pike variations performed on various surfaces. Twenty men and women volunteered for this study. All subjects performed 5 variations of a pike on varying surfaces (i.e., stable ground [PK], Swiss ball [SB], suspension training device [ST], BOSU ball [BOSU], and Core Coaster [CC]). Normalized (%MVC) values were recorded for each muscle during 5 repetitions of each pike variations. For the RA, EO, LSES, and RF, the PK elicited significantly lower values compared with the instability devices. In terms of the EO, the ST was significantly higher than the BOSU, SB, and CC. Results of this investigation demonstrated significant differences between the instability devices and the stable pike. These results indicate that with more freely moving instability devices (e.g., suspension device, Swiss ball, etc.), core musculature may require greater muscular demands. Practitioners should take note that traditional stable pikes may not offer a core musculature challenge to resistance-trained individuals.
Effects of 16 Weeks of Concurrent Training on Resting Heart Rate Variability and Cardiorespiratory Fitness in People Living With HIV/AIDS Using Antiretroviral Therapy: A Randomized Clinical Trial
Authors: Pedro Rafael E. , Guariglia Débora A. , Okuno Nilo M. , Deminice Rafael , Peres Sidney B. , Moraes Solange M.F. 
Published: May 2016

Abstract
Pedro, RE, Guariglia, DA, Okuno, NM, Deminice, R, Peres, SB, and Moraes, SMF. Effects of 16 weeks of concurrent training on resting heart rate variability and cardiorespiratory fitness in people living with HIV/AIDS using antiretroviral therapy: a randomized clinical trial. J Strength Cond Res 30(12): 3494–3502, 2016—The study evaluated the effects of concurrent training on resting heart rate variability (HRVrest) and cardiorespiratory fitness in people living with HIV/AIDS undergoing antiretroviral therapy (ART). Fifty-eight participants were randomized into 2 groups (control and training group); however, only 33 were analyzed. The variables studied were HRVrest indices, submaximal values of oxygen uptake (V̇o
2sub) and heart rate (HR5min), peak speed (Vpeak), and peak oxygen uptake (V̇o
2peak). The training group performed concurrent training (15–20 minutes of aerobic exercise plus 40 minutes of resistance exercise), 3 times per week, for 16 weeks. Posttraining V̇o
2peak and Vpeak increased, and HR5min decreased. Resting heart rate variability indices did not present statistical differences posttraining; however, the magnitude-based inferences demonstrated a “possibly positive effect” for high frequency (HF) and low frequency (LF) plus high frequency (LF + HF) and a “likely positive effect” for R-Rmean posttraining. In conclusion, concurrent training was effective at improving cardiorespiratory fitness and endurance performance. Moreover, it led to probably a positive effect on HF and a likely positive effect on R-Rmean in people living with HIV/AIDS undergoing ART.
Maximal Aerobic Frequency of Ball Hitting: A New Training Load Parameter in Tennis
Authors: Baiget Ernest , Iglesias Xavier , Rodríguez Ferran A. 
Published: May 2016

Abstract
Baiget, E, Iglesias, X, and Rodríguez, FA. Maximal aerobic frequency of ball hitting: a new training load parameter in tennis. J Strength Cond Res 31(1): 106–114, 2017—This study aimed (a) to evaluate a new training load parameter in tennis based on the ball-hitting frequency (Ballf) at V̇o
2max occurs (maximal aerobic frequency of ball hitting, MAF) and (b) to assess the accuracy of a specific endurance tennis test (SET-Test) for predicting MAF. Thirty-five male competitive tennis players performed the SET-Test and selected physiological and performance parameters at maximal workload (MAX), and last completed stage (LS) and MAF were compared. Performance parameters (Ballf, time, stage, and hits per test) at LS were higher than at MAF (20.2 ± 1.7 vs. 18.1 ± 1.5 shots·min−1, 6.6 ± 0.8 vs. 5.6 ± 0.8 stages, and 189 ± 33 vs. 147 ± 27 hits; p < 0.001), and highly correlated (r = 0.72−0.77; p < 0.001). The mean difference between Ballf and stage at MAF and LS were 2.1 ± 1.1 shots·min−1 and 1.1 ± 0.6 stages, respectively. The main physiological parameters (heart rate, V̇o
2, and V̇c
o
2 at LS) were higher than at MAF (191 ± 9 vs. 186 ± 8 beats·min−1, 55.5 ± 5.9 vs. 55.0 ± 6.0 ml·kg−1·min−1 and 4,724 ± 880 vs. 4,253 ± 739 ml·min−1; p < 0.005), and were very strongly correlated (r = 0.93−0.99; p < 0.001). We conclude that MAF can be used as a practical performance parameter to prescribe tennis-specific training, and that the SET-Test is a valid method for assessing MAF. Gas exchange measurements not being available, as a rule of thumb, most players reach their MAF at ∼1 stage (95% confidence interval: 0.9−1.2) and ∼2 shots·min−1 (95% confidence interval: 1.7−2.5) less than their completed LS. A model for specific on-court training protocols for optimizing aerobic fitness in competitive tennis player is proposed.
Effect of Time-of-Day on Biochemical Markers in Response to Physical Exercise
Authors: Ammar Achraf , Chtourou Hamdi , Souissi Nizar 
Published: May 2016

Abstract
Ammar, A, Chtourou, H, and Souissi, N. Effect of time-of-day on biochemical markers in response to physical exercise. J Strength Cond Res 31(1): 272–282, 2017—It is well established that many physiological functions are time-of-day (TOD) dependent, and their circadian rhythms are well documented in healthy populations at resting state. In fact, greater rate of oxidative stress, white blood cell, homocysteine, and muscle damage markers were shown in the early evening (≈18:00 hours), and more efficient antioxidant activity was observed in the early morning (≈06:00 hours). During physical tasks, the majority of the above-mentioned physiological functions increase from pre to post physical exercise with different rates of increases from morning to evening. These different rates of increases are suggested to alter the physiological resting diurnal variation. In this context, given the possible significant interaction “TOD × physical exercise,” circadian rhythms of the physiological responses during physical activity are still not well established in trained subjects. Otherwise, it was suggested that the diurnal variation of these biochemical parameters could, in part, explain the typical diurnal fluctuation of physical performance. Therefore, the aim of this review was to summarize the currently available studies investigating the circadian rhythms of physiological functions at rest and after physical exercise and to establish their possible effect on the diurnal variation of sport performance. Although studies in this field are limited, the available information shows that compared with sedentary subjects, trained population maintained similar diurnal variations of hematological parameters, homocysteine, and some biochemical markers at rest and even after physical exercise. However, after strength exercises, the circadian rhythms for the majority of oxidative stress and muscle damage markers were altered because of the higher rate of increased pre-post exercises registered in the morning compared with the afternoon and evening. The available studies reveal that the significant circadian variation observed for sport performances could be more likely explained by the alteration of ionic movement and the diurnal fluctuation of homocysteine, lactate, muscle damage, and antioxidant markers.
Progressive Changes in a Distributed Neural Circuit Underlie Breathing Abnormalities in Mice Lacking MeCP2
Authors: Huang Teng-Wei , Kochukov Mikhail Y. , Ward Christopher S. , Merritt Jonathan , Thomas Kaitlin , Nguyen Tiffani , Arenkiel Benjamin R. , Neul Jeffrey L. 
Published: May 2016

Rett syndrome (RTT) is a neurodevelopmental disorder caused by mutations inMethyl-CpG-binding protein 2(MECP2). Severe breathing abnormalities are common in RTT and are reproduced in mouse models of RTT. Previously, we found that removing MeCP2 from the brainstem and spinal cord in mice caused early lethality and abnormal breathing. To determine whether loss of MeCP2 in functional components of the respiratory network causes specific breathing disorders, we used the Cre/LoxP system to differentially manipulate MeCP2 expression throughout the brainstem respiratory network, specifically within HoxA4-derived tissues, which include breathing control circuitry within the nucleus tractus solitarius and the caudal part of ventral respiratory column but do not include more rostral parts of the breathing control circuitry. To determine whether respiratory phenotypes manifested in animals with MeCP2 removed from specific pons medullary respiratory circuits, we performed whole-body plethysmography and electrophysiological recordings fromin vitrobrainstem slices from mice lacking MeCP2 in different circuits. Our results indicate that MeCP2 expression in the medullary respiratory network is sufficient for normal respiratory rhythm and preventing apnea. However, MeCP2 expression within components of the breathing circuitry rostral to the HoxA4 domain are neither sufficient to prevent the hyperventilation nor abnormal hypoxic ventilatory response. Surprisingly, we found that MeCP2 expression in the HoxA4 domain alone is critical for survival. Our study reveals that MeCP2 is differentially required in select respiratory components for different aspects of respiratory functions, and collectively for the integrity of this network functions to maintain proper respiration.SIGNIFICANCE STATEMENTBreathing abnormalities are a significant clinical feature in Rett syndrome and are robustly reproduced in the mouse models of this disease. Previous work has established that alterations in the function of MeCP2, the protein encoded by the gene mutated in Rett syndrome, within the hindbrain are critical for control of normal breathing. Here we show that MeCP2 function plays distinct roles in specific brainstem regions in the genesis of various aspects of abnormal breathing. This provides insight into the pathogenesis of these breathing abnormalities in Rett syndrome, which could be used to target treatments to improve these symptoms. Furthermore, it provides further knowledge about the fundamental neural circuits that control breathing.
Pin1 Modulates the Synaptic Content of NMDA Receptors via Prolyl-Isomerization of PSD-95
Authors: Antonelli Roberta , De Filippo Roberto , Middei Silvia , Stancheva Stefka , Pastore Beatrice , Ammassari-Teule Martine , Barberis Andrea , Cherubini Enrico , Zacchi Paola 
Published: May 2016

Phosphorylation of serine/threonine residues preceding a proline regulates the fate of its targets through postphosphorylation conformational changes catalyzed by the peptidyl-prolylcis-/transisomerase Pin1. By flipping the substrate between two different functional conformations, this enzyme exerts a fine-tuning of phosphorylation signals. Pin1 has been detected in dendritic spines and shafts where it regulates protein synthesis required to sustain the late phase of long-term potentiation (LTP). Here, we demonstrate that Pin1 residing in postsynaptic structures can interact with postsynaptic density protein-95 (PSD-95), a key scaffold protein that anchors NMDA receptors (NMDARs) in PSD via GluN2-type receptor subunits. Pin1 recruitment by PSD-95 occurs at specific serine-threonine/proline consensus motifs localized in the linker region connecting PDZ2 to PDZ3 domains. Upon binding, Pin1 triggers structural changes in PSD-95, thus negatively affecting its ability to interact with NMDARs. In electrophysiological experiments, larger NMDA-mediated synaptic currents, evoked in CA1 principal cells by Schaffer collateral stimulation, were detected in hippocampal slices obtained from Pin1−/−mice compared with controls. Similar results were obtained in cultured hippocampal cells expressing a PSD-95 mutant unable to undergo prolyl-isomerization, thus indicating that the action of Pin1 on PSD-95 is critical for this effect. In addition, an enhancement in spine density and size was detected in CA1 principal cells of Pin1−/−or in Thy-1GFP mice treated with the pharmacological inhibitor of Pin1 catalytic activity PiB.Our data indicate that Pin1 controls synaptic content of NMDARs via PSD-95 prolyl-isomerization and the expression of dendritic spines, both required for LTP maintenance.SIGNIFICANCE STATEMENTPSD-95, a membrane-associated guanylate kinase, is the major scaffolding protein at excitatory postsynaptic densities and a potent regulator of synaptic strength and plasticity. The activity of PSD-95 is tightly controlled by several post-translational mechanisms including proline-directed phosphorylation. This signaling cascade regulates the fate of its targets through postphosphorylation conformational modifications catalyzed by the peptidyl-prolylcis-/transisomerase Pin1. Here, we uncover a new role of Pin1 in glutamatergic signaling. By interacting with PSD-95, Pin1 dampens PSD-95 ability to complex with NMDARs, thus negatively affecting NMDAR signaling and spine morphology. Our findings further emphasize the emerging role of Pin1 as a key modulator of synaptic transmission.
Identification of a Circadian Clock in the Inferior Colliculus and Its Dysregulation by Noise Exposure
Authors: Park Jung-sub , Cederroth Christopher R. , Basinou Vasiliki , Meltser Inna , Lundkvist Gabriella , Canlon Barbara 
Published: May 2016

Circadian rhythms regulate bodily functions within 24 h and long-term disruptions in these rhythms can cause various diseases. Recently, the peripheral auditory organ, the cochlea, has been shown to contain a self-sustained circadian clock that regulates differential sensitivity to noise exposure throughout the day. Animals exposed to noise during the night are more vulnerable than when exposed during the day. However, whether other structures throughout the auditory pathway also possess a circadian clock remains unknown. Here, we focus on the inferior colliculus (IC), which plays an important role in noise-induced pathologies such as tinnitus, hyperacusis, and audiogenic seizures. Using PER2::LUC transgenic mice and real-time bioluminescence recordings, we revealed circadian oscillations of Period 2 protein in IC explants for up to 1 week. Clock genes (Cry1,Bmal1,Per1,Per2,Rev-erbα, andDbp) displayed circadian molecular oscillations in the IC. Averaged expression levels of early-induced genes and clock genes during 24 h revealed differential responses to day or night noise exposure.Rev-erbα andDbpgenes were affected only by day noise exposure, whereasPer1andPer2were affected only by night noise exposure. However, the expression ofBdnfwas affected by both day and night noise exposure, suggesting that plastic changes are unlikely to be involved in the differences in day or night noise sensitivity in the IC. These novel findings highlight the importance of circadian responses in the IC and emphasize the importance of circadian mechanisms for understanding central auditory function and disorders.SIGNIFICANCE STATEMENTRecent findings identified the presence of a circadian clock in the inner ear. Here, we present novel findings that neurons in the inferior colliculus (IC), a central auditory relay structure involved in sound processing, express a circadian clock as evidenced at both the mRNA and protein levels. Using a reporter mouse that expresses a luciferase protein coupled to the core clock protein PERIOD2 (PER2::LUC), we could observe spontaneous circadian oscillations in culture. Furthermore, we reveal that the mRNA profile of clock-related genes in the IC is altered differentially by day or night noise exposure. The identification of a clock in the IC is relevant for understanding the mechanisms underlying dysfunctions of the IC such as tinnitus, hyperacusis, or audiogenic seizures.
Bcl-xL Is Essential for the Survival and Function of Differentiated Neurons in the Cortex That Control Complex Behaviors
Authors: Nakamura Ayumi , Swahari Vijay , Plestant Charlotte , Smith Ikuko , McCoy Eric , Smith Spencer , Moy Sheryl S. , Anton E. S. , Deshmukh Mohanish 
Published: May 2016

Apoptosis plays an essential role during brain development, yet the precise mechanism by which this pathway is regulated in the brain remains unknown. In particular, mammalian cells are known to express multiple anti-apoptotic Bcl-2 family proteins. However, the cells of the developing brain could also exist in a primed state in which the loss of a single anti-apoptotic Bcl-2 family protein is sufficient to trigger apoptosis. Here, we examined the critical role of Bcl-xL, an anti-apoptotic protein, during brain development. Using conditional knock-out mice in which Bcl-xL is deleted in neural progenitor cells (Bcl-xLEmx1–Cre), we show that the loss of Bcl-xL is not sufficient to trigger apoptosis in these proliferating progenitors. In contrast, specific populations of postmitotic neurons derived from these progenitors, including upper layer cortical neurons and the CA1–CA3 regions of the hippocampus, were acutely dependent on Bcl-xL. Consistent with this finding, deletion of Bcl-xL selectively in the postmitotic neurons in the brain (Bcl-xLNex–Cre) also resulted in similar patterns of apoptosis. This Bcl-xL deficiency-induced neuronal death was a consequence of activation of the apoptotic pathway, because the cell death was rescued with codeletion of the proapoptotic proteins Bax and Bak. Importantly, the loss of these Bcl-xL-dependent neurons led to severe neurobehavioral abnormalities, including deficits in motor learning, hyperactivity, and increased risk-taking and self-injurious behaviors. Together, our results identify a population of neurons in the developing brain that are acutely dependent on Bcl-xL during the peak period of synaptic connectivity that are important for the establishment of higher-order complex behaviors.SIGNIFICANCE STATEMENTAlthough Bcl-xL is known to inhibit apoptosis, exactly which cells in the brain are dependent on Bcl-xL has remained unclear because of the embryonic lethality of mice globally deleted for Bcl-xL. Here, we conditionally deleted Bcl-xL in the brain and found that this did not result in widespread apoptosis in the proliferating progenitors. Instead, Bcl-xL deficiency induced apoptosis in a select population of differentiated neurons predominantly in the early postnatal stages. Importantly, these Bcl-xL-dependent neurons are not essential for survival of the organism but instead regulate complex behaviors. Our results show that the selective loss of these Bcl-xL-dependent neurons results in mice exhibiting severe neurobehavioral abnormalities, including self-injurious and risk-taking behaviors, hyperactivity, and learning and memory defects.
Pathogenic Upregulation of Glial Lipocalin-2 in the Parkinsonian Dopaminergic System
Authors: Kim Byung-Wook , Jeong Kyoung Hoon , Kim Jae-Hong , Jin Myungwon , Kim Jong-Heon , Lee Maan-Gee , Choi Dong-Kug , Won So-Yoon , McLean Catriona , Jeon Min-Tae , Lee Ho-Won , Kim Sang Ryong , Suk Kyoungho 
Published: May 2016

Lipocalin-2 (LCN2) is a member of the highly heterogeneous secretory protein family of lipocalins and increases in its levels can contribute to neurodegeneration in the adult brain. However, there are no reports on the role of LCN2 in Parkinson's disease (PD). Here, we report for the first time that LCN2 expression is increased in the substantia nigra (SN) of patients with PD. In mouse brains, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment for a neurotoxin model of PD significantly upregulated LCN2 expression, mainly in reactive astrocytes in both the SN and striatum. The increased LCN2 levels contributed to neurotoxicity and neuroinflammation, resulting in disruption of the nigrostriatal dopaminergic (DA) projection and abnormal locomotor behaviors, which were ameliorated in LCN2-deficient mice. Similar to the effects of MPTP treatment, LCN2-induced neurotoxicity was also observed in the 6-hydroxydopamine (6-OHDA)-treated animal model of PD. Moreover, treatment with the iron donor ferric citrate (FC) and the iron chelator deferoxamine mesylate (DFO) increased and decreased, respectively, the LCN2-induced neurotoxicityin vivo. In addition to thein vivoresults, 1-methyl-4-phenylpyridinium (MPP+)-induced neurotoxicity in cocultures of mesencephalic neurons and astrocytes was reduced by LCN2 gene deficiency in the astrocytes and conditioned media derived from MPP+-treated SH-SY5Y neuronal enhanced glial expression of LCN2in vitro. Therefore, our results demonstrate that astrocytic LCN2 upregulation in the lesioned DA system may play a role as a potential pathogenic factor in PD and suggest that inhibition of LCN2 expression or activity may be useful in protecting the nigrostriatal DA system in the adult brain.SIGNIFICANCE STATEMENTLipocalin-2 (LCN2), a member of the highly heterogeneous secretory protein family of lipocalins, may contribute to neuroinflammation and neurotoxicity in the brain. However, LCN2 expression and its role in Parkinson's disease (PD) are largely unknown. Here, we report that LCN2 is upregulated in the substantia nigra of patients with PD and neurotoxin-treated animal models of PD. Our results suggest that LCN2 upregulation might be a potential pathogenic mechanism of PD, which would result in disruption of the nigrostriatal dopaminergic system through neurotoxic iron accumulation and neuroinflammation. Therefore, inhibition of LCN2 expression or activity may be useful in protecting the nigrostriatal dopaminergic projection in PD.