bluuebunny/crossref_metadata_2025_split huggingface dataset:
Parental Bonding and Hostility: Examining the Links Between Sex Differences, Hostility, Anger, and Aggression
Authors: Ingram Rick , Balderas Jessica , Hagan Kelsey , Kohnle Kendall 
Published: August 2019

Introduction: Although parental bonding that is characterized by overprotection and low care is associated with adult depression and anxiety, less is known about its association with other mood states. Additionally, few studies differentiate between maternal and paternal bonding or evaluate sex differences in offspring's emotional responding as a function of bonding. Method: The current study examined parental bonding as it relates to hostility, anger, and verbal and physical aggression in young adults. Participants reported their mood state, perception of parenting behaviors, and their experience of hostility and its correlates. Results: After controlling for current mood, paternal care modulated males' anger and verbal aggression, whereas maternal care modulated females' physical aggression. Maternal overprotection predicted hostility in males. Discussion: Findings suggest that less parental care and greater parental overprotection precipitate angry and aggressive responding later in life, and these results are linked to sex differences in both parents and in young adult males and females.
Cognitive and Neuroanatomic Accounts of Referential Communication in Focal Dementia
Authors: Healey Meghan , Spotorno Nicola , Olm Christopher , Irwin David J. , Grossman Murray 
Published: August 2019

AbstractThe primary function of language is to communicate—that is, to make individuals reach a state of mutual understanding about a particular thought or idea. Accordingly, daily communication is truly a task of social coordination. Indeed, successful interactions require individuals to (1) track and adopt a partner’s perspective and (2) continuously shift between the numerous elements relevant to the exchange. Here, we use a referential communication task to study the contributions of perspective taking and executive function to effective communication in nonaphasic human patients with behavioral variant frontotemporal dementia (bvFTD). Similar to previous work, the task was to identify a target object, embedded among an array of competitors, for an interlocutor. Results indicate that bvFTD patients are impaired relative to control subjects in selecting the optimal, precise response. Neuropsychological testing related this performance to mental set shifting, but not to working memory or inhibition. Follow-up analyses indicated that some bvFTD patients perform equally well as control subjects, while a second, clinically matched patient group performs significantly worse. Importantly, the neuropsychological profiles of these subgroups differed only in set shifting. Finally, structural MRI analyses related patient impairment to gray matter disease in orbitofrontal, medial prefrontal, and dorsolateral prefrontal cortex, all regions previously implicated in social cognition and overlapping those related to set shifting. Complementary white matter analyses implicated uncinate fasciculus, which carries projections between orbitofrontal and temporal cortices. Together, these findings demonstrate that impaired referential communication in bvFTD is cognitively related to set shifting, and anatomically related to a social-executive network including prefrontal cortices and uncinate fasciculus.
Preserving Inhibition during Developmental Hearing Loss Rescues Auditory Learning and Perception
Authors: Mowery Todd M. , Caras Melissa L. , Hassan Syeda I. , Wang Derek J. , Dimidschstein Jordane , Fishell Gord , Sanes Dan H. 
Published: August 2019

Transient periods of childhood hearing loss can induce deficits in aural communication that persist long after auditory thresholds have returned to normal, reflecting long-lasting impairments to the auditory CNS. Here, we asked whether these behavioral deficits could be reversed by treating one of the central impairments: reduction of inhibitory strength. Male and female gerbils received bilateral earplugs to induce a mild, reversible hearing loss during the critical period of auditory cortex development. After earplug removal and the return of normal auditory thresholds, we trained and tested animals on an amplitude modulation detection task. Transient developmental hearing loss induced both learning and perceptual deficits, which were entirely corrected by treatment with a selective GABA reuptake inhibitor (SGRI). To explore the mechanistic basis for these behavioral findings, we recorded the amplitudes of GABAAand GABABreceptor-mediated IPSPs in auditory cortical and thalamic brain slices. In hearing loss-reared animals, cortical IPSP amplitudes were significantly reduced within a few days of hearing loss onset, and this reduction persisted into adulthood. SGRI treatment during the critical period prevented the hearing loss-induced reduction of IPSP amplitudes; but when administered after the critical period, it only restored GABABreceptor-mediated IPSP amplitudes. These effects were driven, in part, by the ability of SGRI to upregulate α1 subunit-dependent GABAAresponses. Similarly, SGRI prevented the hearing loss-induced reduction of GABAAand GABABIPSPs in the ventral nucleus of the medial geniculate body. Thus, by maintaining, or subsequently rescuing, GABAergic transmission in the central auditory thalamocortical pathway, some perceptual and cognitive deficits induced by developmental hearing loss can be prevented.SIGNIFICANCE STATEMENTEven a temporary period of childhood hearing loss can induce communication deficits that persist long after auditory thresholds return to normal. These deficits may arise from long-lasting central impairments, including the loss of synaptic inhibition. Here, we asked whether hearing loss-induced behavioral deficits could be reversed by reinstating normal inhibitory strength. Gerbils reared with transient hearing loss displayed both learning and perceptual deficits. However, when animals were treated with a selective GABA reuptake inhibitor during or after hearing loss, behavioral deficits were entirely corrected. This behavioral recovery was correlated with the return of normal thalamic and cortical inhibitory function. Thus, some perceptual and cognitive deficits induced by developmental hearing loss were prevented with a treatment that rescues a central synaptic property.
GABAergic Inhibition Gates Perceptual Awareness During Binocular Rivalry
Authors: Mentch Jeff , Spiegel Alina , Ricciardi Catherine , Robertson Caroline E. 
Published: August 2019

Binocular rivalry is a classic experimental tool to probe the neural machinery of perceptual awareness. During rivalry, perception alternates between the two eyes, and the ebb and flow of perception is modeled to rely on the strength of inhibitory interactions between competitive neuronal populations in visual cortex. As a result, rivalry has been suggested as a noninvasive perceptual marker of inhibitory signaling in visual cortex, and its putative disturbance in psychiatric conditions, including autism. Yet, direct evidence causally implicating inhibitory signaling in the dynamics of binocular rivalry is currently lacking. We previously found that people with higher GABA levels in visual cortex, measured using magnetic resonance spectroscopy, have stronger perceptual suppression during rivalry. Here, we present direct causal tests of the impact of GABAergic inhibition on rivalry dynamics, and the contribution of specific GABA receptors to these dynamics. In a crossover pharmacological design with male and female adult participants, we found that drugs that modulate the two dominant GABA receptor types in the brain, GABAA(clobazam) and GABAB(arbaclofen), increase perceptual suppression during rivalry relative to a placebo. Crucially, these results could not be explained by changes in reaction times or response criteria, as determined through rivalry simulation trials, suggesting a direct and specific influence of GABA on perceptual suppression. A full replication study of the GABABmodulator reinforces these findings. These results provide causal evidence for a link between the strength of inhibition in the brain and perceptual suppression during rivalry and have implications for psychiatric conditions including autism.SIGNIFICANCE STATEMENTHow does the brain accomplish perceptual gating? Here we use a direct and causal pharmacological manipulation to present insight into the neural machinery of a classic illusion of perceptual awareness: binocular rivalry. We show that drugs that increase GABAergic inhibition in the brain, clobazam (GABAAmodulator) and arbaclofen (GABABmodulator), increase perceptual suppression during rivalry relative to a placebo. These results present the first causal link between GABAergic inhibition and binocular rivalry in humans, complementing classic models of binocular rivalry, and have implications for our understanding of psychiatric conditions, such as autism, where binocular rivalry is posited as a behavioral marker of disruptions in inhibitory signaling in the brain.
Promiscuous G-Protein-Coupled Receptor Inhibition of Transient Receptor Potential Melastatin 3 Ion Channels by Gβγ Subunits
Authors: Alkhatib Omar , da Costa Robson , Gentry Clive , Quallo Talisia , Mannebach Stefanie , Weissgerber Petra , Freichel Marc , Philipp Stephan E. , Bevan Stuart , Andersson David A. 
Published: August 2019

Transient receptor potential melastatin 3 (TRPM3) is a nonselective cation channel that is inhibited by Gβγ subunits liberated following activation of Gαi/oprotein-coupled receptors. Here, we demonstrate that TRPM3 channels are also inhibited by Gβγ released from Gαsand Gαq. Activation of the Gs-coupled adenosine 2B receptor and the Gq-coupled muscarinic acetylcholine M1 receptor inhibited the activity of TRPM3 heterologously expressed in HEK293 cells. This inhibition was prevented when the Gβγ sink βARK1-ct (C terminus of β-adrenergic receptor kinase-1) was coexpressed with TRPM3. In neurons isolated from mouse dorsal root ganglion (DRG), native TRPM3 channels were inhibited by activating Gs-coupled prostaglandin-EP2 and Gq-coupled bradykinin B2 (BK2) receptors. The Gi/oinhibitor pertussis toxin and inhibitors of PKA and PKC had no effect on EP2- and BK2-mediated inhibition of TRPM3, demonstrating that the receptors did not act through Gαi/oor through the major protein kinases activated downstream of G-protein-coupled receptor (GPCR) activation. When DRG neurons were dialyzed with GRK2i, which sequesters free Gβγ protein, TRPM3 inhibition by EP2 and BK2 was significantly reduced. Intraplantar injections of EP2 or BK2 agonists inhibited both the nocifensive response evoked by TRPM3 agonists, and the heat hypersensitivity produced by Freund's Complete Adjuvant (FCA). Furthermore, FCA-induced heat hypersensitivity was completely reversed by the selective TRPM3 antagonist ononetin in WT mice and did not develop inTrpm3−/−mice. Our results demonstrate that TRPM3 is subject to promiscuous inhibition by Gβγ protein in heterologous expression systems, primary neurons andin vivo, and suggest a critical role for this ion channel in inflammatory heat hypersensitivity.SIGNIFICANCE STATEMENTThe ion channel TRPM3 is widely expressed in the nervous system. Recent studies showed that Gαi/o-coupled GPCRs inhibit TRPM3 through a direct interaction between Gβγ subunits and TRPM3. Since Gβγ proteins can be liberated from other Gα subunits than Gαi/o, we examined whether activation of Gs- and Gq-coupled receptors also influence TRPM3 via Gβγ. Our results demonstrate that activation of Gs- and Gq-coupled GPCRs in recombinant cells and sensory neurons inhibits TRPM3 via Gβγ liberation. We also demonstrated that Gs- and Gq-coupled receptors inhibit TRPM3in vivo, thereby reducing pain produced by activation of TRPM3, and inflammatory heat hypersensitivity. Our results identify Gβγ inhibition of TRPM3 as an effector mechanism shared by the major Gα subunits.
Electronic Nicotine Delivery Systems Marketing and Initiation Among Youth and Young Adults
Authors: Loukas Alexandra , Paddock Ellen M. , Li Xiaoyin , Harrell Melissa B. , Pasch Keryn E. , Perry Cheryl L. 
Published: August 2019

BACKGROUND AND OBJECTIVES:
Electronic nicotine delivery systems (ENDS) have become the most popular tobacco products among young people, yet ENDS marketing remains unregulated, and its effects on ENDS use behavior across age groups is poorly understood. In this study, using a longitudinal design, we examined how recall of ENDS marketing through 5 different channels predicted subsequent ENDS initiation up to 2.5 years later among youth (ages 12–17 years) and young adults (ages 18–29 years).

METHODS:
Data were drawn from 2 large cohort studies in Texas. The analysis included school-going youth (n = 2288) and college-going young adults (n = 2423) who reported never having used ENDS at baseline in 2014. Logistic regression was used to assess the influence of recalled ENDS marketing exposure via television (TV), radio or Internet radio, billboards, retail stores, and the Internet on subsequent ENDS initiation, with adjustment for these channels, baseline sociodemographics, other past-30-day tobacco use, sensation seeking, and peer ENDS use.

RESULTS:
Recall of retail store–based ENDS marketing at baseline was associated with significantly higher odds of subsequent ENDS initiation among youth (adjusted odds ratio [aOR] = 1.99; 95% confidence interval [CI]: 1.25–3.17) and young adults (aOR = 1.30; 95% CI: 1.05–1.61) up to 2.5 years later. Young adult initiation was also associated with recalled ENDS marketing on TV at baseline (aOR = 1.29; 95% CI: 1.03–1.63).

CONCLUSIONS:
Marketing of ENDS at retail stores predicts youth and young adult ENDS initiation, and marketing on TV predicts young adult initiation. Future research and regulation should be used to address the most influential marketing channels.
Cell-Autonomous Hedgehog Signaling Is Not Required for Cyst Formation in Autosomal Dominant Polycystic Kidney Disease
Authors: Ma Ming , Legué Emilie , Tian Xin , Somlo Stefan , Liem Karel F. 
Published: August 2019

Significance StatementPolycystin proteins function in renal primary cilia to regulate a pathway important to kidney functional homeostasis. Autosomal dominant polycystic kidney disease (ADPKD) results when polycystin genes are mutated, but key cilia-based signaling pathways dysregulated by loss of polycystin function require elucidation. One cilia-dependent pathway suggested as playing a role in polycystic kidney diseases is the Hedgehog pathway, which is important in development, cancer, and ciliopathies. In mouse models of ADPKD, the authors used conditional control of gene expression to upregulate or inactivate Hedgehog in kidney cells that had undergone inactivation ofPkd1, the gene encoding Polycystin-1. They found that the Hedgehog pathway had no significant effect on polycystic kidney disease initiated byPkd1inactivation, excluding it as a functional cell-autonomous component of kidney cyst formation in these ADPKD models.BackgroundPKD1orPKD2, the two main causal genes for autosomal dominant polycystic kidney disease (ADPKD), encode the multipass transmembrane proteins polycystin-1 (PC1) and polycystin-2 (PC2), respectively. Polycystins localize to the primary cilium, an organelle essential for cell signaling, including signal transduction of the Hedgehog pathway. Mutations in ciliary genes that build and maintain the cilium also cause renal cystic disease through unknown pathways. Although recent studies have found alterations in Hedgehog signaling in ADPKD-related models and tissues, the relationship between Hedgehog and polycystic kidney disease is not known.MethodsTo examine the potential role of cell-autonomous Hedgehog signaling in regulating kidney cyst formationin vivoin both early- and adult-onset mouse models of ADPKD, we used conditional inactivation ofPkd1combined with conditional modulation of Hedgehog signaling components in renal epithelial cells, where mutations inPkd1initiate cyst formation. After increasing or decreasing levels of Hedgehog signaling in cells that underwent inactivation ofPkd1, we evaluated the effects of these genetic manipulations on quantitative parameters of polycystic kidney disease severity.ResultsWe found that inPkd1conditional mutant mouse kidneys, neither downregulation nor activation of the Hedgehog pathway in epithelial cells along the nephron significantly influenced the severity of the polycystic kidney phenotype in mouse models of developmental or adult-onset of ADPKD.ConclusionsThese data suggest that loss ofPkd1function results in kidney cysts through pathways that are not affected by the activity of the Hedgehog pathway.
Some results on free Euclidean self-dual codes over F2+vF2
Authors: AKSOY Refia , ÇALIŞKAN Fatma 
Published: August 2019

In this
paper, free Euclidean self-dual codes over the ring F2 + v F2 with v2 =v of order 4 are considered. A necessary and
sufficient condition for the form of the generator matrix of a free Euclidean
self-dual code is given. By using the distance preserving Gray map from F2 + v F2 to F2 x F2,
the generator matrix of the binary code which corresponds the code over the
ring F2 + v F2 is obtained. The codes of lengths up to 100 over
the ring F2 + v F2 are
found.
Notes on Papuasian and Malesian stingless bees, with the descriptions of new taxa (Hymenoptera: Apidae)
Authors: Engel Michael S. 
Published: August 2019

Two new species of the stingless bee genus Heterotrigona Schwarz (Apinae: Meliponini) are described and figured from Papua New Guinea: Heterotrigona (Sahulotrigona) tricholoma Engel, new species, lighter individuals of which superficially resemble the larger H. (Platytrigona) lamingtonia (Cockerell) and H. (P.) keyensis (Friese), and H. (S.) taraxis Engel, new species, a taxon generally misidentified as “Trigona atricornis Smith”. The western Malesian (Borneo) species H. hobbyi (Schwarz) is removed to Borneotrigona Engel, new subgenus, and distinguished from the otherwise eastern Platytrigona Moure, which occur in eastern Wallacea (east of Weber’s line) and Papuasia. The historically misidentified T. atricornis is a senior synonym of T. genalis Friese (new synonymy), the latter type species for the genus Papuatrigona Michener & Sakagami, resulting in the following nomenclatural change: Papuatrigona atricornis (Smith), new combination. Flavotetragonula Shanas is placed as a new synonym of Tetragonula Moure s.str. (new synonymy).
Öğretmen Adaylarının Okul, Öğretmen ve Öğrenci Kavramlarına İlişkin Metaforik Algıları
Authors: NEYİŞÇİ Nilay , ÖZDİYAR Özlenen 
Published: August 2019

Öğretmen
adaylarının hizmet öncesi eğitimleri sırasında sahip oldukları nitelikler hiç
kuşkusuz öğretmenlik mesleğine olumlu bir biçimde yansımaktadır. Bu nedenle
öğretmen adaylarının donanımlı birer öğretmen olabilmeleri için öğretim
hizmetinin niteliğinin artırılması önem taşımaktadır. Hizmet öncesi eğitim
sırasında öğrencilerin eğitim ile ilgili temel kavramlar bilgisine sahip olması,
ortak bir zeminde çalışılabilmesine olanak sağlayacaktır. Bu nedenle öncelikle
öğrencilerin zihninde yer alan metaforların belirlenmesi mesleki donanımlarının
sağlanması ve varolan donanımlarını güçlendirmek için bir çıkış noktası oluşturması
açısından önemlidir. Bu araştırmanın amacı öğretmen adaylarının “okul, öğretmen
ve öğrenci” kavramına ilişkin sahip oldukları algıları metaforlar aracılığıyla
ortaya çıkarmak ve böylelikle eğitim sisteminin temellerini oluşturan bu
kavramlara ilişkin algılarını çözümlemeyi kolaylaştırmaktır.

Bu
çalışmada olgubilim deseni kullanılmıştır. Açık uçlu anket yoluyla toplanan
veriler içerik analize tabi tutulmuştur. Araştırma sonucunda çalışmaya katılan
275 öğretmen adayı olumlu ve olumsuz anlam taşıyan geçerli 494 adet metafor
üretmişlerdir.

Kavramlar ile ilgili öne
çıkan olumlu ve olumsuz metaforlar şöyledir: Öğretmen adayları “okulu” hem
psiko-sosyal gelişime destek olan hem de fiziki güvenliği tehdit eden bir yer
olarak görmektedirler. Öğretmen adayları “öğretmeni” hem duyuşsal ve bilişsel
alanda öğrencilerin ihtiyaçlarını karşılayan hem de öğrencilerin ilgi ve
yeteneklerini sınırlandıran bireyler olarak algılamaktadırlar. Öğretmen
adaylarının bir kısmı “öğrenciyi” eğitim sistemine hevesle, bir kısmı ise isteksiz katılan bireyler olarak
algıladıkları sonucuna ulaşılmıştır.
Biochemical algorithms of early diagnostic of metabolic remodeling and cardiac hypertrophy in patients with diabetic mellitus and chronic heart failure cause by ischemic heart disease
Authors: Donetskaya O. P. , Shuldeshova N. V. , Tulupova V. A. , Sukoyan G. V. 
Published: August 2019

The aims of study– a development of biochemical algorithms of early diagnostic of severity of CHF in patients with DM and IHD and analyze interrelationships between plasma redox-potential, as a marker of progressive of tissues metabolic remodeling and cardiac hypertrophy and markers of progressive of DM, neurohumoral markers of severity of CHF, and frequency of heart rhythm disturbances.Materials and methods.172 patients, male / female (45–65 years), with diagnosis of DM (metabolic decompensation of carbohydrate metabolism, HbА1c – 7.4 ± 1.9 %) during 3–15 years, accompanied with IHD and symptoms of CHF I–IV NYHA functional class (FC). The first point of investigation was examined markers of DM progression HbА1c, changes in FC of HCHF and evidenced prognostic neurohumoral markers of myocardial dysfunction NT-proBNP, and as a second (surrogate) point – changes in redox-potential NAD / NADH and total pool of pyridine nucleotides.Results.Mean NYHA FC CHF in cohort of DM patients and IHD was 2.4 ± 1.2, mean point of CHF estimated by scale of symptoms of CHF was 6.7 ± 0.6, mean distance in 6-minute test was 212 ± 26 m, concentration of neurohumoral markers of myocardial dysfunction NT-proBNP 178 ± 26 fmol / l at the level of HbA1c = 7.8 ± 1.0 %, mean redox-potential of plasma, НАД / НАДН, 0.71 ± 0.06 and total pool of pyridine nucleotide 15.1 ± 1.2 μmol / mg protein of plasma. For the first time was shown that changes in redox-potential and sum of pyridine nucleotide coupled with severity of CHF (FC of CHF), eliminated the correlation between NAD / NADH and HbA1c (r = –0.79, p<0.001), and NTproBNP (r = –0.73; р <0.001), and increasing of tumor necrosis factor alpha (TNF-α, r = –0.73; р <0.001). Simultaneously maintenance decreasing of NAD / NADH and sum of pyridine nucleotide in plasma of patients with DM and IHD coupled with increasing of daily mean values of paired supraventricular and ventricular extrasystoles.Conclusions.In patients with DM and CHF with left ventricular dysfunction the decreasing of redox-potential level in plasma could be recommended as a markers of increasing of metabolic remodeling and progression of cardiac hypertrophy.