bluuebunny/crossref_metadata_2025_split huggingface dataset:
A New Housing Concept for the Karl Friedrich Schinkel Collection: Chemical and Mechanical Aspects
Authors: Meyer Fabienne , Volland Gerhard 
Published: September 2016

AbstractThis paper describes the measures taken to rehouse the collection of drawings and prints by Karl Friedrich Schinkel in the Kupferstichkabinett Berlin. Previously, the collection had been exposed to high concentrations of volatile organic compounds (VOCs). Housing the artworks in piles inside portfolios had caused mechanical damage. The VOC concentration in the object’s environment was reduced by replacing the main emission sources with low-emissive materials, by increasing the air exchange rate of the cabinets, and by sealing emission sources that could not be removed from the cabinets. It was decided to dispense with the application of any chemisorbents since they proved to be ineffective for the given storage situation. To avoid further mechanical damage, the objects were inserted into folders made either from cardboard or, depending on the characteristics and sensitivity of the object, from a combination of cardboard and polyester film. Groups of artworks were stored in new, lightweight enclosures that combine the advantages of the Solander box, the corrugated cardboard box, and the four-flap portfolio. Crosswise bonding of the corrugated boards provides sufficient stability. The joints that are particularly subjected to stress were reinforced with fabric. These new enclosures protect the objects from slipping and lateral impact. The historic portfolios were preserved as documentary material and are now stored in a separate place.
Optimization of biogas generation using anaerobic digestion models and computational intelligence approaches
Authors: Enitan Abimbola M. , Adeyemo Josiah , Swalaha Feroz M. , Kumari Sheena , Bux Faizal 
Published: September 2016

Abstract
Anaerobic digestion (AD) technology has become popular and is widely used due to its ability to produce renewable energy from wastes. The bioenergy produced in anaerobic digesters could be directly used as fuel, thereby reducing the release of biogas to the atmosphere. Due to the limited knowledge on the different process disturbances and microbial composition that are vital for the efficient operation of AD systems, models and control strategies with respect to external influences are needed without wasting time and resources. Different simple and complex mechanistic and data-driven modeling approaches have been developed to describe the processes taking place in the AD system. Microbial activities have been incorporated in some of these models to serve as a predictive tool in biological processes. The flexibility and power of computational intelligence of evolutionary algorithms (EAs) as direct search algorithms to solve multiobjective problems and generate Pareto-optimal solutions have also been exploited. Thus, this paper reviews state-of-the-art models based on the computational optimization methods for renewable and sustainable energy optimization. This paper discusses the different types of model approaches to enhance AD processes for bioenergy generation. The optimization and control strategies using EAs for advanced reactor performance and biogas production are highlighted. This information would be of interest to a dynamic group of researchers, including microbiologists and process engineers, thereby offering the latest research advances and importance of AD technology in the production of renewable energy.
Examining Fundamental Movement Competency and Closed-Chain Upper-Extremity Dynamic Balance in Swimmers
Authors: Bullock Garrett S. , Brookreson Nate , Knab Amy M. , Butler Robert J. 
Published: September 2016

Abstract
Bullock, GS, Brookreson, N, Knab, AM, and Butler, RJ. Examining fundamental movement competency and closed-chain upper-extremity dynamic balance in swimmers. J Strength Cond Res 31(6): 1544–1551, 2017—Abnormal fundamental movement patterns and upper-quarter dynamic balance are proposed mechanisms affecting athletic performance and injury risk. There are few studies investigating functional movement and closed-chain upper-extremity dynamic stability in swimmers. The purpose of this study was to determine differences in fundamental movement competency and closed-chain upper-extremity dynamic balance, using the Functional Movement Screen (FMS) and Upper-Quarter Y Balance Test (YBT-UQ), of high school (HS; n = 70) and collegiate (COL; n = 70) swimmers. Variables included the individual movement tests on the FMS and the average normalized reach (percent limb length [%LL]) for each direction, with the YBT-UQ. Statistical analysis was completed using a chi square for the independent test scores on the FMS while independent samples t-test to examine performance on the YBT-UQ (p ≤ 0.05). HS swimmers exhibited a statistically significant greater percentage of below average performance (score of 0 or 1) on the following FMS tests: lunge (HS: 22.9%, COL: 4.3%), hurdle step (HS: 31.4%, COL: 7.1%), and push-up (HS: 61.4%, COL: 31.4%). Furthermore, COL males performed worse in the lunge (male: 9%, female: 0%), whereas COL females had poorer efficiency in the push-up (male: 17.6%, female: 44%). Significant effects of competition level and sex were observed in YBT-UQ medial reach (HS: female 92.06, male 101.63; COL: female 101.3, male 101.5% LL). Individual fundamental movement patterns that involved lumbopelvic neuromuscular control differed between HS and COL swimmers. General upper-extremity dynamic balance differed between competition levels. These data may be helpful in understanding injury and performance-based normative data for participation and return to swimming.
The Effects of Accentuated Eccentric Loading on the Drop Jump Exercise and the Subsequent Postactivation Potentiation Response
Authors: Bridgeman Lee A. , McGuigan Michael R. , Gill Nicholas D. , Dulson Deborah K. 
Published: September 2016

Abstract
Bridgeman, LA, McGuigan, MR, Gill, ND, and Dulson, DK. The effects of accentuated eccentric loading on the drop jump exercise and the subsequent postactivation potentiation response. J Strength Cond Res 31(6): 1620–1626, 2017—The aims of this study were (a) to investigate the acute effects of different drop jump (DJ) accentuated eccentric loading (AEL) protocols and (b) to investigate the effect of these AEL DJ protocols on subsequent countermovement jump (CMJ) performance. The subjects were 12 strength-trained athletes; initially, baseline CMJ performance was assessed and individual optimal DJ drop height identified. In subsequent weeks, subjects completed 1 set of 5 DJs with no additional load or an AEL of 10, 20, or 30% of their individual body mass (BM) using dumbbells to provide the extra load. After the AEL DJ protocols, 3 CMJs were completed after 2, 6, and 12 minutes rest. A generalized linear mixed model was used to investigate the effects of AEL load and time post-DJs on CMJ height, peak power, and ground reaction force. The 20% AEL condition resulted in greater CMJ height in comparison with all other conditions (p < 0.001). CMJ height was significantly greater after 2 and 6 minutes rest compared with 12 minutes (p < 0.001 and p ≤ 0.05 respectively). Greater peak power was also found during the CMJs after the 20% AEL condition compared with baseline, BM, and 10% AEL (p ≤ 0.05). In conclusion, 5 DJs with 20% AEL followed by a 2 minutes recovery period resulted in significant enhancement in CMJ height and peak power.
The Training Octagon: Training the Anterior and Posterior Serape
Authors: Santana Juan C. , Brown Lee E. , Ferrigno Vance A. 
Published: September 2016

ABSTRACT
THE PURPOSE OF THIS ARTICLE IS TO EXPLAIN HOW THE ANTERIOR AND POSTERIOR SERAPE (APS) CAN BE SYSTEMATICALLY TRAINED USING A SIMPLE MOVEMENT MODEL; THE TRAINING OCTAGON (TO). THE DIRECTIONS OF THE MUSCLES ARE ASSOCIATED WITH THE DIRECTIONS OF THE TO, AND A SYSTEM OF FIVE BASIC CABLE/BAND EXERCISES IS PROVIDED FOR TRAINING. TABLES AND FIGURES ORGANIZING AND CLASSIFYING THE MUSCLES, MOVEMENTS, AND EXERCISES FURTHER ASSOCIATE THE TRAINING AND BIOMECHANICAL MODELS OF THE APS. THE MODEL PRESENTED IN THIS ARTICLE IS A TOOL FOR STRENGTH AND CONDITIONING PROFESSIONALS TO USE WHEN TRAINING THE CORE MUSCULATURE.
Ventral Tegmental Area Dopamine Cell Activation during Male Rat Sexual Behavior Regulates Neuroplasticity and d-Amphetamine Cross-Sensitization following Sex Abstinence
Authors: Beloate Lauren N. , Omrani Azar , Adan Roger A. , Webb Ian C. , Coolen Lique M. 
Published: September 2016

Experience with sexual behavior causes cross-sensitization of amphetamine reward, an effect dependent on a period of sexual reward abstinence. We previously showed that ΔFosB in the nucleus accumbens (NAc) is a key mediator of this cross-sensitization, potentially via dopamine receptor activation. However, the role of mesolimbic dopamine for sexual behavior or cross-sensitization between natural and drug reward is unknown. This was tested using inhibitory designer receptors exclusively activated by designer drugs in ventral tegmental area (VTA) dopamine cells. rAAV5/hSvn-DIO-hm4D-mCherry was injected into the VTA ofTH::Creadult male rats. Males received clozapine N-oxide (CNO) or vehicle injections before each of 5 consecutive days of mating or handling. Following an abstinence period of 7 d, males were tested for amphetamine conditioned place preference (CPP). Next, males were injected with CNO or vehicle before mating or handling for analysis of mating-induced cFos, sex experience-induced ΔFosB, and reduction of VTA dopamine soma size. Results showed that CNO did not affect mating behavior. Instead, CNO prevented sexual experience-induced cross-sensitization of amphetamine CPP, ΔFosB in the NAc and medial prefrontal cortex, and decreases in VTA dopamine soma size. Expression of hm4D-mCherry was specific to VTA dopamine cells and CNO blocked excitation and mating-induced cFos expression in VTA dopamine cells. These findings provide direct evidence that VTA dopamine activation is not required for initiation or performance of sexual behavior. Instead, VTA dopamine directly contributes to increased vulnerability for drug use following loss of natural reward by causing neuroplasticity in the mesolimbic pathway during the natural reward experience.SIGNIFICANCE STATEMENTDrugs of abuse act on the neural pathways that mediate natural reward learning and memory. Exposure to natural reward behaviors can alter subsequent drug-related reward. Specifically, experience with sexual behavior, followed by a period of abstinence from sexual behavior, causes increased reward for amphetamine in male rats. This study demonstrates that activation of ventral tegmental area dopamine neurons during sexual experience regulates cross-sensitization of amphetamine reward. Finally, ventral tegmental area dopamine cell activation is essential for experience-induced neural adaptations in the nucleus accumbens, prefrontal cortex, and ventral tegmental area. These findings demonstrate a role of mesolimbic dopamine in the interaction between natural and drug rewards, and identify mesolimbic dopamine as a key mediator of changes in vulnerability for drug use after loss of natural reward.
The Role of Primary Motor Cortex (M1) Glutamate and GABA Signaling in l-DOPA-Induced Dyskinesia in Parkinsonian Rats
Authors: Lindenbach David , Conti Melissa M. , Ostock Corinne Y. , George Jessica A. , Goldenberg Adam A. , Melikhov-Sosin Mitchell , Nuss Emily E. , Bishop Christopher 
Published: September 2016

Long-term treatment of Parkinson's disease withl-DOPA almost always leads to the development of involuntary movements termedl-DOPA-induced dyskinesia. Whereas hyperdopaminergic signaling in the basal ganglia is thought to cause dyskinesia, alterations in primary motor cortex (M1) activity are also prominent during dyskinesia, suggesting that the cortex may represent a therapeutic target. The present study used the rat unilateral 6-hydroxydopamine lesion model of Parkinson's disease to characterizein vivochanges in GABA and glutamate neurotransmission within M1 and determine their contribution to behavioral output. 6-Hydroxydopamine lesion led to parkinsonian motor impairment that was partially reversed byl-DOPA. Among sham-lesioned rats,l-DOPA did not change glutamate or GABA efflux. Likewise, 6-hydroxydopamine lesion did not impact GABA or glutamate among rats chronically treated with saline. However, we observed an interaction of lesion and treatment whereby, among lesioned rats,l-DOPA given acutely (1 d) or chronically (14–16 d) reduced glutamate efflux and enhanced GABA efflux. Site-specific microinjections into M1 demonstrated thatl-DOPA-induced dyskinesia was reduced by M1 infusion of a D1antagonist, an AMPA antagonist, or a GABAAagonist. Overall, the present study demonstrates thatl-DOPA-induced dyskinesia is associated with increased M1 inhibition and that exogenously enhancing M1 inhibition may attenuate dyskinesia, findings that are in agreement with functional imaging and transcranial magnetic stimulation studies in human Parkinson's disease patients. Together, our study suggests that increasing M1 inhibitory tone is an endogenous compensatory response designed to limit dyskinesia severity and that potentiating this response is a viable therapeutic strategy.SIGNIFICANCE STATEMENTMost Parkinson's disease patients will receivel-DOPA and eventually develop hyperkinetic involuntary movements termed dyskinesia. Such symptoms can be as debilitating as the disease itself. Although dyskinesia is associated with dynamic changes in primary motor cortex physiology, to date, there are no published studies investigatingin vivoneurotransmitter release in M1 during dyskinesia. In parkinsonian rats,l-DOPA administration reduced M1 glutamate efflux and enhanced GABA efflux, coincident with the emergence of dyskinetic behaviors. Dyskinesia could be reduced by local M1 modulation of D1, AMPA, and GABAAreceptors, providing preclinical support for the notion that exogenously blunting M1 signaling (pharmacologically or with cortical stimulation) is a therapeutic approach to the treatment of debilitating dyskinesias.
Adult Brain Serotonin Deficiency Causes Hyperactivity, Circadian Disruption, and Elimination of Siestas
Authors: Whitney Meredith Sorenson , Shemery Ashley M. , Yaw Alexandra M. , Donovan Lauren J. , Glass J. David , Deneris Evan S. 
Published: September 2016

Serotonin (5-HT) is a crucial neuromodulator linked to many psychiatric disorders. However, after more than 60 years of study, its role in behavior remains poorly understood, in part because of a lack of methods to target 5-HT synthesis specifically in the adult brain. Here, we have developed a genetic approach that reproducibly achieves near-complete elimination of 5-HT synthesis from the adult ascending 5-HT system by stereotaxic injection of an adeno-associated virus expressing Cre recombinase (AAV-Cre) into the midbrain/pons of mice carrying a loxP-conditionaltryptophan hydroxylase 2 (Tph2) allele. We investigated the behavioral effects of deficient brain 5-HT synthesis and discovered a unique composite phenotype. Surprisingly, adult 5-HT deficiency did not affect anxiety-like behavior, but resulted in a robust hyperactivity phenotype in novel and home cage environments. Moreover, loss of 5-HT led to an altered pattern of circadian behavior characterized by an advance in the onset and a delay in the offset of daily activity, thus revealing a requirement for adult 5-HT in the control of daily activity patterns. Notably, after normalizing for hyperactivity, we found that the normal prolonged break in nocturnal activity (siesta), a period of rapid eye movement (REM) and non-REM sleep, was absent in all animals in which 5-HT deficiency was verified. Our findings identify adult 5-HT as a requirement for siestas, implicate adult 5-HT in sleep–wake homeostasis, and highlight the importance of our adult-specific 5-HT-synthesis-targeting approach in understanding 5-HT's role in controlling behavior.SIGNIFICANCE STATEMENTSerotonin (5-HT) is a crucial neuromodulator, yet its role in behavior remains poorly understood, in part because of a lack of methods to target specifically adult brain 5-HT synthesis. We developed an approach that reproducibly achieves near-complete elimination of 5-HT synthesis from the adult ascending 5-HT system. Using this technique, we discovered that adult 5-HT deficiency led to a novel compound phenotype consisting of hyperactivity, disrupted circadian behavior patterns, and elimination of siestas, a period of increased sleep during the active phase. These findings highlight the importance of our approach in understanding 5-HT's role in behavior, especially in controlling activity levels, circadian behavior, and sleep–wake homeostasis, behaviors that are disrupted in many psychiatric disorders such as attention deficit hyperactivity disorder.
Reduced Efficacy of Anti-Aβ Immunotherapy in a Mouse Model of Amyloid Deposition and Vascular Cognitive Impairment Comorbidity
Authors: Weekman Erica M. , Sudduth Tiffany L. , Caverly Carly N. , Kopper Timothy J. , Phillips Oliver W. , Powell Dave K. , Wilcock Donna M. 
Published: September 2016

Vascular cognitive impairment and dementia (VCID) is the second most common form of dementia behind Alzheimer's disease (AD). It is estimated that 40% of AD patients also have some form of VCID. One promising therapeutic for AD is anti-Aβ immunotherapy, which uses antibodies against Aβ to clear it from the brain. While successful in clearing Aβ and improving cognition in mice, anti-Aβ immunotherapy failed to reach primary cognitive outcomes in several different clinical trials. We hypothesized that one potential reason the anti-Aβ immunotherapy clinical trials were unsuccessful was due to this high percentage of VCID comorbidity in the AD population. We used our unique model of VCID-amyloid comorbidity to test this hypothesis. We placed 9-month-old wild-type and APP/PS1 mice on either a control diet or a diet that induces hyperhomocysteinemia (HHcy). After being placed on the diet for 3 months, the mice then received intraperotineal injections of either IgG2a control or 3D6 for another 3 months. While we found that treatment of our comorbidity model with 3D6 resulted in decreased total Aβ levels, there was no cognitive benefit of the anti-Aβ immunotherapy in our AD/VCID mice. Further, microhemorrhages were increased by 3D6 in the APP/PS1/control but further increased in an additive fashion when 3D6 was administered to the APP/PS1/HHcy mice. This suggests that the use of anti-Aβ immunotherapy in patients with both AD and VCID would be ineffective on cognitive outcomes.SIGNIFICANCE STATEMENTDespite significant mouse model data demonstrating both pathological and cognitive efficacy of anti-Aβ immunotherapy for the treatment of Alzheimer's disease, clinical trial outcomes have been underwhelming, failing to meet any primary endpoints. We show here that vascular cognitive impairment and dementia (VCID) comorbidity eliminates cognitive efficacy of anti-Aβ immunotherapy, despite amyloid clearance. Further, cerebrovascular adverse events of the anti-Aβ immunotherapy are significantly exacerbated by the VCID comorbidity. These data suggest that VCID comorbidity with Alzheimer's disease may mute the response to anti-Aβ immunotherapy.
Calpain Activation in Alzheimer's Model Mice Is an Artifact of APP and Presenilin Overexpression
Authors: Saito Takashi , Matsuba Yukio , Yamazaki Naomi , Hashimoto Shoko , Saido Takaomi C. 
Published: September 2016

Intraneuronal calcium stimulates the calpain-dependent conversion of p35 to p25, a CDK5 activator. It is widely believed that amyloid β peptide (Aβ) induces this conversion that, in turn, has an essential role in Alzheimer's disease pathogenesis. However,in vivostudies on p25 generation used transgenic mice overexpressing mutant amyloid precursor protein (APP) and presenilin (PS). Here, using singleAppknock-in mice, we show that p25 generation is an artifact caused by membrane protein overexpression. We show that massive Aβ42accumulation without overexpression of APP or presenilin does not produce p25, whereas p25 generation occurred with APP/PS overexpression and in postmortem mouse brain. We further support this finding using mice deficient for calpastatin, the sole calpain-specific inhibitor protein. Thus, the intracerebral environment of the APP/PS mouse brain and postmortem brain is an unphysiological state.SIGNIFICANCE STATEMENTWe recently estimated using singleAppknock-in mice that accumulate amyloid β peptide without transgene overexpression that 60% of the phenotypes observed in Alzheimer's model mice overexpressing mutant amyloid precursor protein (APP) or APP and presenilin are artifacts (Saito et al., 2014). The current study further supports this estimate by invalidating key results from papers that were published inCell. These findings suggest that more than 3000 publications based on APP and APP/PS overexpression must be reevaluated.
Dysregulated NMDA-Receptor Signaling Inhibits Long-Term Depression in a Mouse Model of Fragile X Syndrome
Authors: Toft Anna Karina Hugger , Lundbye Camilla Johanne , Banke Tue G. 
Published: September 2016

Fragile X syndrome (FXS) is a neurodevelopmental disease. It is one of the leading monogenic causes of intellectual disability among boys with most also displaying autism spectrum disorder traits. Here we investigated the role of NMDA receptors on mGluR-dependent long-term depression (mGluR-LTD), a key biomarker in the disease, at four different developmental stages. First, we applied the mGluR agonist 3,5-dihydroxyphenylglycine in the absence or presence of the NMDAR blocker, APV, hereby unmasking the NMDAR component in this process. As expected, in the presence of APV, we found more LTD in the mouse KO than in WT. This, however, was only observed in the p30–60 age group. At all other age groups tested, mGluR-LTD was almost identical between KO and WT. Interestingly, at p60, in the absence of APV, no or very little LTD was found in KO that was completely restored by application of APV. This suggests that the underlying cause of the enhanced mGluR-LTD in KO (at p30) is caused by dysregulated NMDAR signaling. To investigate this further, we next used NMDAR-subunit-specific antagonists. Inhibition of GluN2B, but not GluN2A, blocked mGluR-LTD only in WT. This was in contrast in the KO where blocking GluN2B rescued mGluR-LTD, suggesting GluN2B-containing NMDARs in the KO are hyperactive. Thus, these findings suggest strong involvement of GluN2B-containing-NMDARs in the pathophysiology of FXS and highlight a potential path for treatment for the disease.SIGNIFICANCE STATEMENTThere is currently no cure for fragile X, although medications targeting specific FXS symptoms do exist. The FXS animal model, theFmr1knock-out mouse, has demonstrated an increased mGluR5-mediated long-term depression (LTD) leading to several clinical trials of mGluR5 inhibitors/modulators, yet all have failed. In addition, surprisingly little information exists about the possible role of other ion channels/receptors, including NMDA receptors (NMDAR), in mGluR-LTD. Here we focus on NMDARs and their regulation of mGluR-mediated LTD at different developmental stages using several different NMDAR blockers/antagonists. Our findings suggest dysregulated NMDARs in the pathophysiology of FXS leading to altered mGluR-mediated LTD. Together, these data will help to develop new drug candidates that could lead to reversal of the FXS phenotype.