bluuebunny/crossref_metadata_2025_split huggingface dataset:
Audio–visual and olfactory–visual integration in healthy participants and subjects with autism spectrum disorder
Authors: Stickel Susanne , Weismann Pauline , Kellermann Thilo , Regenbogen Christina , Habel Ute , Freiherr Jessica , Chechko Natalya 
Published: July 2019

AbstractThe human capacity to integrate sensory signals has been investigated with respect to different sensory modalities. A common denominator of the neural network underlying the integration of sensory clues has yet to be identified. Additionally, brain imaging data from patients with autism spectrum disorder (ASD) do not cover disparities in neuronal sensory processing. In this fMRI study, we compared the underlying neural networks of both olfactory–visual and auditory–visual integration in patients with ASD and a group of matched healthy participants. The aim was to disentangle sensory‐specific networks so as to derive a potential (amodal) common source of multisensory integration (MSI) and to investigate differences in brain networks with sensory processing in individuals with ASD. In both groups, similar neural networks were found to be involved in the olfactory–visual and auditory–visual integration processes, including the primary visual cortex, the inferior parietal sulcus (IPS), and the medial and inferior frontal cortices. Amygdala activation was observed specifically during olfactory–visual integration, with superior temporal activation having been seen during auditory–visual integration. A dynamic causal modeling analysis revealed a nonlinear top‐down IPS modulation of the connection between the respective primary sensory regions in both experimental conditions and in both groups. Thus, we demonstrate that MSI has shared neural sources across olfactory–visual and audio–visual stimulation in patients and controls. The enhanced recruitment of the IPS to modulate changes between areas is relevant to sensory perception. Our results also indicate that, with respect to MSI processing, adults with ASD do not significantly differ from their healthy counterparts.
Home enteral nutrition may prevent myelosuppression of patients with nasopharyngeal carcinoma treated by concurrent chemoradiotherapy
Authors: Li Xuemei , Zhou Jidan , Chu Ci , You Qian , Zhong Renming , Rao Zhiyong , Hu Wen 
Published: July 2019

AbstractBackgroundThe aim of this study is to assess the effect of home enteral nutrition (HEN) on the myelosuppression of patients with nasopharyngeal cancer (NPC) during the course of concurrent chemoradiotherapy (CCRT).MethodsA total of 18 outpatients with NPC administered oral nutritional supplementation intervention at home during the course of CCRT were designated as the HEN group, whereas 36 patients with NPC who had previously completed CCRT were retrospectively included as the control group. Patient Generated Subjective Global Assessment, body mass index (BMI), and blood test were evaluated prior to CCRT. During the course of CCRT, blood test was assessed every 2 weeks.ResultsIn male patients, hemoglobin (HB) and red blood cell were decreased (P < .05) in both HEN and control group after CCRT, whereas white blood cell (WBC) started to decrease since week 2 of CCRT in the control group but maintained in the HEN group which was significantly higher than the control (5.05 ± 1.29 vs 3.77 ± 1.5, P < .05). In female patients, HB and WBC were reduced in control group during CCRT, whereas these indicators also maintained in the HEN group. Surprisingly, all patients with lower BMI (<24 kg/m2) had a significant increase in platelet (PLT) after CCRT (200.78 ± 58.03 vs 253.00 ± 69.82, P < .05), while had steady HB and WBC values in the HEN group. At the end of CCRT, WBC and PLT of the HEN group were both higher than those in the control group (5.21 ± 1.07 vs 3.37 ± 1.52), (253.00 ± 69.82 vs 165.57 ± 59.56) (P < .05 for both). Our findings suggest that HEN is effective in preventing myelosuppression during CCRT for patients with NPC.ConclusionOur findings suggest that HEN is effective in preventing myelosuppression during CCRT for patients with NPC.
Balanced synaptic currents underlie low‐frequency oscillations in the subiculum
Authors: Royzen Feliks , Williams Sylvain , Fernandez Fernando R. , White John A. 
Published: July 2019

AbstractNumerous synaptic and intrinsic membrane mechanisms have been proposed for generating oscillatory activity in the hippocampus. Few studies, however, have directly measured synaptic conductances and membrane properties during oscillations. The time course and relative contribution of excitatory and inhibitory synaptic conductances, as well as the role of intrinsic membrane properties in amplifying synaptic inputs, remains unclear. To address this issue, we used an isolated whole hippocampal preparation that generates autonomous low‐frequency oscillations near the theta range. Using 2‐photon microscopy and expression of genetically encoded fluorophores, we obtained on‐cell and whole‐cell patch recordings of pyramidal cells and fast‐firing interneurons in the distal subiculum. Pyramidal cell and interneuron spiking shared similar phase‐locking to local field potential oscillations. In pyramidal cells, spiking resulted from a concomitant and balanced increase in excitatory and inhibitory synaptic currents. In contrast, interneuron spiking was driven almost exclusively by excitatory synaptic current. Thus, similar to tightly balanced networks underlying hippocampal gamma oscillations and ripples, balanced synaptic inputs in the whole hippocampal preparation drive highly phase‐locked spiking at the peak of slower network oscillations.
Place cell firing cannot support navigation without intact septal circuits
Authors: Bolding Kevin A. , Ferbinteanu Janina , Fox Steven E. , Muller Robert U. 
Published: July 2019

AbstractThough it has been known for over half a century that interference with the normal activity of septohippocampal neurons can abolish hippocampal theta rhythmicity, a definitive answer to the question of its function has remained elusive. To clarify the role of septal circuits and theta in location‐specific activity of place cells and spatial behavior, three drugs were delivered to the medial septum of rats: Tetracaine, a local anesthetic; muscimol, a GABA‐A agonist; and gabazine, a GABA‐A antagonist. All three drugs disrupted normal oscillatory activity in the hippocampus. However, tetracaine and muscimol both reduced spatial firing and interfered with the rat's ability to navigate to a hidden goal. After gabazine, location‐specific firing was preserved in the absence of theta, but rats were unable to accurately locate the hidden goal. These results indicate that theta is unnecessary for location‐specific firing of hippocampal cells, and that place cell activity cannot support accurate navigation when septal circuits are disrupted.
Degeneracy in hippocampal physiology and plasticity
Authors: Rathour Rahul K. , Narayanan Rishikesh 
Published: July 2019

AbstractDegeneracy, defined as the ability of structurally disparate elements to perform analogous function, has largely been assessed from the perspective of maintaining robustness of physiology or plasticity. How does the framework of degeneracy assimilate into an encoding system where the ability to change is an essential ingredient for storing new incoming information? Could degeneracy maintain the balance between the apparently contradictory goals of the need to change for encoding and the need to resist change towards maintaining homeostasis? In this review, we explore these fundamental questions with the mammalian hippocampus as an example encoding system. We systematically catalog lines of evidence, spanning multiple scales of analysis that point to the expression of degeneracy in hippocampal physiology and plasticity. We assess the potential of degeneracy as a framework to achieve the conjoint goals of encoding and homeostasis without cross‐interferences. We postulate that biological complexity, involving interactions among the numerous parameters spanning different scales of analysis, could establish disparate routes towards accomplishing these conjoint goals. These disparate routes then provide several degrees of freedom to the encoding‐homeostasis system in accomplishing its tasks in an input‐ and state‐dependent manner. Finally, the expression of degeneracy spanning multiple scales offers an ideal reconciliation to several outstanding controversies, through the recognition that the seemingly contradictory disparate observations are merely alternate routes that the system might recruit towards accomplishment of its goals.
Nanofluid flow over three different geometries under viscous dissipation and thermal radiation using the local linearization method
Authors: Shaw Sachin , Motsa Sandile S. , Sibanda Precious 
Published: July 2019

AbstractThis study deals with the transfer of mass and heat of nanofluid flow over three different geometries of the non‐Darcy permeable vertical cone/wedge/vertical plate. Influence of the Brownian motion and thermophoresis takes place due to the nanofluid. Boundary condition on the temperature is introduced at the surface where the thermal conductivity of the fluid obeys a linear relation with the temperature. The local linearization method is introduced for solving the governing equations, and is based on spectral discretization. To verify the numerical scheme, we compared our results with those in the existing literature. The impact of the governing parameters on the fluid velocity, temperature distribution, and concentration distribution of nanoparticles along with the Nusselt number and Sherwood number is discussed. Some important outcomes of the present study are that the Nusselt number is higher for the plane plate than that for the vertical cone and it significantly decreases with introduction of the radiation parameter. The nanofluid Lewis number decreases the diffusivity of mass of the nanofluid, and as a result it helps enhance the Sherwood number.
Free convective MHD micropolar fluid flow with thermal radiation and radiation absorption: A numerical study
Authors: Pradhan S. R. , Baag S. , Mishra S. R. , Acharya M. R. 
Published: July 2019

AbstractAn analysis is carried out for the free convective flow of an electrically conducting micropolar fluid through permeable stretching sheet in the presence of porous medium. Inclusion of thermal radiation to the energy equation enhances the thermal properties of polar fluid. In addition to that the radiation absorption parameter occurs due to the interaction of solutal concentration difference also considered in the heat transfer equation. Suitable similar transformation is used to convert the governing partial differential equations to ordinary differential equations. Furthermore, though analytical solutions of these complex nonlinear coupled equations are more complicated therefore, numerical solution such as Runge‐Kutta fourth order method associated with shooting technique is adopted. Behavior of characterizing parameters for the flow phenomena are presented via graphs and computed values of physical quantities of interest are obtained and shown in tabular form. Present result validates with that of earlier results in particular case which confirms the existence of present solution methodology. However, the main findings of contributing parameters are laid down as; angular velocity profile contributes a dual character from the point of contact at the middle of the channel. Fluid temperature is affected by the inclusion of absorption coefficient.
P2Y11 receptor antagonist NF340 ameliorates inflammation in human fibroblast‐like synoviocytes: An implication in rheumatoid arthritis
Authors: Gao Feng , Li Xin 
Published: July 2019

AbstractRheumatoid arthritis is a common chronic inflammatory joint disease. Fibroblast‐like synoviocytes‐mediated inflammation is closely associated with the development of rheumatoid arthritis. In this study, we report that P2Y11 receptor activity is required for cytokine‐induced inflammation in primary fibroblast‐like synoviocytes (FLS). P2Y11R is fairly expressed in primary FLS isolated from healthy subjects and is elevated to around three‐ to four‐fold in rheumatoid arthritis‐derived FLS. The expression of P2Y11R is inducible upon IL‐1β treatment. Blockage of P2Y11R by its antagonist suppresses IL‐1β‐induced TNF‐α and IL‐6 induction and ameliorates oxidative stress as determined by levels of cellular ROS and the oxidative byproduct 4‐HNE. Moreover, blockage of P2Y11R by NF340 inhibits IL‐1β‐induced matrix metalloproteinase protein expression as indicated by the levels of MMP‐1, MMP‐3, and MMP‐13. Mechanistically, blockage of P2Y11R mitigates IL‐1β‐activated NFκB signaling, which was revealed by reduced IκBα phosphorylation, nuclear p65 accumulation, and NFκB promoter activity. Our study provides evidence of a protective mechanism of P2Y11R antagonist NF340 against cytokine‐induced inflammation. Therefore, targeting P2Y11R could have potential therapeutic implication in the treatment of RA.
Cholinergic and peptidergic neurotransmission in the adrenal medulla: A dynamic control of stimulus‐secretion coupling
Authors: Guérineau Nathalie C. 
Published: July 2019

AbstractSynaptic neurotransmission at the splanchnic nerve‐chromaffin cell synapse is a chief element of the stimulus‐secretion coupling in the adrenal medullary tissue, managing and regulating the secretion of catecholamines. Making the state of play more intricate than initially envisioned, the synaptic vesicles of nerve terminals innervating the medulla contain various compounds, including various neurotransmitters and neuropeptides. Under basal conditions associated with a low splanchnic nerve discharge rate, neurotransmission is ensured by the synaptic release of the primary neurotransmitter acetylcholine (ACh). Under sustained and repetitive stimulations of the splanchnic nerve, as triggered in response to stressors, the synaptic release of neuropeptides, such as the pituitary adenylate cyclase‐activating polypeptide PACAP, supplants ACh release. The anatomical and functional changes that occur presynaptically at the preganglionic splanchnic nerve, combined with changes occurring postsynaptically at nicotinic acetylcholine receptors (nAChRs), confer the adrenomedullary synapses a solid and persistent aptitude to functional remodeling, from birth to aging. The present review focuses on the composite cholinergic and noncholinergic nature of neurotransmission occurring at the splanchnic nerve‐chromaffin cell synapse and its remodeling in response to physiological or pathological stimuli.
Secreted frizzled‐related protein 4 and its implication in obesity and type‐2 diabetes
Authors: Bukhari Shazia Anwer , Yasmin Aysha , Zahoor Muhammad Asif , Mustafa Ghulam , Sarfraz Iqra , Rasul Azhar 
Published: July 2019

AbstractSecreted frizzled‐related protein 4 (SFRP4) is a member of secreted protein family with sequence similarity to frizzled receptors of wingless‐related integration site (Wnt) signaling pathways. These proteins control diverse functions from embryonic development to adults in many organisms including humans. Initially, SFRPs were recognized as antagonists of Wnt signaling and supposed to interact with Wnts. Further research demonstrated their interactions to frizzled receptors and a functional diversity was related to these proteins, Wnt signaling potentiation in addition to modulation. SFRP4 is the largest member of SFRP family and is implicated in many diseases including obesity, type 2 diabetes (T2D), and cancer. SFRP4 acts as a biomarker for T2D and was expressed several years before clinical diagnosis of disease. This review mainly focusses on the role of SFRP4 in obesity and how it can lead to β‐cell failure and ultimately to T2D. The role of SFRP4 in adipose tissues causing increased production of adipokines lead to the oxidative stress in pancreas that particularly have low amount of antioxidant enzymes in pancreatic β‐cells leading to failure in exocytosis of insulin containing granules causing T2D. Obesity‐induced inflammation is a principal factor in pathogenesis of insulin resistance as well as metabolic syndrome. Pro‐inflammatory cytokines have potential to cause insulin resistance in skeletal muscles, adipose tissue, and liver via inhibition of insulin signal transduction. Secretion of SFRP4 is mediated by interleukin 1‐β (IL1‐β). This review highlights the molecular mechanisms by which SFRP4 leads to T2D. Understanding of molecular mechanism and targeting SFRP4 could help to eradicate or reduce chances of developing T2D.
Potential role of circulating long noncoding RNA MALAT1 in predicting disease risk, severity, and patients' survival in sepsis
Authors: Geng Feng , Liu Wei , Yu Li 
Published: July 2019

AbstractBackgroundThis study aimed to investigate the plasma long noncoding RNA metastasis‐associated lung adenocarcinoma transcript 1 (lncRNA MALAT1) expression with risk, severity, inflammation level, and prognosis in sepsis.MethodsOne hundred and ninety sepsis patients and 190 health controls (HCs) were consecutively recruited. Blood samples within 24 hours after admission of sepsis patients and those on enrollment of HCs were collected, and then, plasma was separated for lncRNA MALAT1 and miR‐125b expressions detections by RT‐qPCR. In sepsis patients, clinical data and 28‐day mortality were recorded, and plasma inflammatory cytokines expressions were detected by ELISA.ResultsPlasma lncRNA MALAT1 expression was elevated in sepsis patients than HCs (P < 0.001), and ROC curve disclosed that it had a good value in predicting sepsis risk with an area under curve (AUC) of 0.823 (95% CI: 0.783‐0.864). Additionally, lncRNA MALAT1 expression was positively correlated with Scr (P = 0.005), WBC (P = 0.017), CRP (P < 0.001), PCT (P < 0.001), TNF‐α (P < 0.001), IL‐8 (P < 0.001), IL‐17 (P = 0.001), APACHE II score (P < 0.001), and SOFA score (P < 0.001). LncRNA MALA1 expression was elevated in deaths compared with survivors (P < 0.001) and could predict the risk of 28‐day mortality with an AUC of 0.755 (95% CI: 0.682‐0.828). Accumulating survival was worse in patients with lncRNA MALAT1 high expression compared with patients who had lncRNA MALAT1 low expression (P < 0.001). Moreover, lncRNA MALAT1 expression was negatively correlated with miR‐125b level in both sepsis patients (P < 0.001) and HCs (P < 0.001).ConclusionLncRNA MALAT1 could be developed as a potential biomarker for facilitating diagnosis and management in sepsis patients.
Preactivation of β‐catenin in osteoblasts improves the osteoanabolic effect of PTH in type 1 diabetic mice
Authors: Chen Sixu , Yang Lei , He Sihao , Yang Jiazhi , Liu Daocheng , Bao Quanwei , Qin Hao , Du Wenqiong , Zhong Xin , Chen Can , Zong Zhaowen 
Published: July 2019

AbstractType 1 diabetes (T1D) is correlated with osteopenia primarily due to low bone formation. Parathyroid hormone (PTH) is a known anabolic agent for bone, the anabolic effects of which are partially mediated through the Wnt/β‐catenin signaling pathway. In the present study, we first determined the utility of intermittent PTH treatment in a streptozotocin‐induced T1D mouse model. It was shown that the PTH‐induced anabolic effects on bone mass and bone formation were attenuated in T1D mice compared with nondiabetic mice. Further, PTH treatment failed to activate β‐catenin signaling in osteoblasts of T1D mice and was unable to improve osteoblast proliferation and differentiation. Next, the Col1–3.2 kb‐CreERTM; β‐cateninfx(ex3) mice were used to conditionally activate β‐catenin in osteoblasts by injecting tamoxifen, and we addressed whether or not preactivation of β‐catenin boosted the anabolic action of PTH on T1D‐related bone loss. The results demonstrated that pretreatment with activation of osteoblastic β‐catenin followed by PTH treatment outperformed PTH or β‐catenin activation monotherapy and led to greatly improved bone structure, bone mass, and bone strength in this preclinical model of T1DM. Further analysis demonstrated that osteoblast proliferation and differentiation, as well as osteoprogenitors in the marrow, were all improved in the combination treatment group. These findings indicated a clear advantage of developing β‐catenin as a target to improve the efficacy of PTH in the treatment of T1D‐related osteopenia.
Adenosine triphosphate enhances osteoblast differentiation of rat dental pulp stem cells via the PLC–IP3 pathway and intracellular Ca2+ signaling
Authors: Stovall Kelsie E. , Tran Tran D.N. , Suantawee Tanyawan , Yao Shaomian , Gimble Jeffrey M. , Adisakwattana Sirichai , Cheng Henrique 
Published: July 2019

AbstractIntracellular Ca2+ signals are essential for stem cell function and play a significant role in the differentiation process. Dental pulp stem cells (DPSCs) are a potential source of stem cells; however, the mechanisms controlling cell differentiation remain largely unknown. Utilizing rat DPSCs, we examined the effect of adenosine triphosphate (ATP) on osteoblast differentiation and characterized its mechanism of action using real‐time Ca
2+ imaging analysis. Our results revealed that ATP enhanced osteogenesis as indicated by Ca
2+ deposition in the extracellular matrix via Alizarin Red S staining. This was consistent with upregulation of osteoblast genes BMP2, Mmp13, Col3a1, Ctsk, Flt1, and Bgn. Stimulation of DPSCs with ATP (1–300 µM) increased intracellular Ca
2+ signals in a concentration‐dependent manner, whereas histamine, acetylcholine, arginine vasopressin, carbachol, and stromal‐cell‐derived factor‐1α failed to do so. Depletion of intracellular Ca
2+ stores in the endoplasmic reticulum by thapsigargin abolished the ATP responses which, nevertheless, remained detectable under extracellular Ca
2+ free condition. Furthermore, the phospholipase C (PLC) inhibitor U73122 and the inositol triphosphate (IP
3) receptor inhibitor 2‐aminoethoxydiphenyl borate inhibited the Ca
2+ signals. Our findings provide a better understanding of how ATP controls osteogenesis in DPSCs, which involves a Ca
2+‐dependent mechanism via the PLC‐IP
3 pathway. This knowledge could help improve osteogenic differentiation protocols for tissue regeneration of bone structures.
Umbilical cord‐derived mesenchymal stromal/stem cells expressing IL‐24 induce apoptosis in gliomas
Authors: Fan Shaochen , Gao Huasong , Ji Wei , Zhu Fengwei , Sun Lingzheng , Liu Yuankun , Zhang Siming , Xu Yanran , Yan Yaohua , Gao Yilu 
Published: July 2019

AbstractAlthough much progress has been made in the treatment of gliomas, the prognosis for patients with gliomas is still very poor. Stem cell‐based therapies may be promising options for glioma treatment. Recently, many studies have reported that umbilical cord‐derived mesenchymal stromal/stem cells (UC‐MSCs) are ideal gene vehicles for tumor gene therapy. Interleukin 24 (IL‐24) is a pleiotropic immunoregulatory cytokine that has an apoptotic effect on many kinds of tumor cells and can inhibit the growth of tumors specifically without damaging normal cells. In this study, we investigated UC‐MSCs as a vehicle for the targeted delivery of IL‐24 to tumor sites. UC‐MSCs were transduced with lentiviral vectors carrying green fluorescent protein (GFP) or IL‐24 complementary DNA. The results indicated that UC‐MSCs could selectively migrate to glioma cells in vitro and in vivo. Injection of IL‐24‐UC‐MSCs significantly suppressed tumor growth of glioma xenografts. The restrictive efficacy of IL‐24‐UC‐MSCs was associated with the inhibition of proliferation as well as the induction of apoptosis in tumor cells. These findings indicate that UC‐MSC‐based IL‐24 gene therapy may be able to suppress the growth of glioma xenografts, thereby suggesting possible future therapeutic use in the treatment of gliomas.