bluuebunny/crossref_metadata_2025_split huggingface dataset:
Distinct Heat Stress Responses of Porcine Cumulus Cells and The Oocyte Is Associated With Disrupted Intercellular Communication
Authors: Yin Chao 
Published: June 2021

Cumulus cells (CCs) play critical roles in oocytes maturation through intercellular communication. The adverse effect of heat stress (HS) on oocyte maturation has been well documented, whereas the HS responses of CCs and the oocytes in association with cumulusoocyte communication remain unclear. In this study, cumulus‐oocyte complexes (COCs) were subjected to HS at 42°C for 24 h during in vitro maturation. Cumulus expansion was impaired and oocyte quality was reduced with lower survival rate, polar body extrusion rate and early embryo developmental potentials. Oocytes and cumulus cells isolated from COCs demonstrated distinct responses to HS. In oocytes, mitochondrial DNA (mtDNA)‐encoded genes and heat shock protein (HSP)‐related genes were significantly down‐regulated, with significantly lower ATP content yet higher mitochondria reactive oxygen species (mROS) and caspase 3 activity. In contrast, CCs isolated from heat‐exposed COCs showed significant activation of mtDNAencoded genes and HSP‐related genes, which was accompanied by increased ATP content and caspase 3 activity yet unaltered mROS content. When denuded oocytes and isolated CCs were subjected to HS separately, ATP content in denuded oocytes decreased more extensively than that in oocytes isolated from heat‐exposed COCs. Also, mROS was significantly increased in CCs but not in denuded oocytes, which coincided with less pronounced increase of caspase 3 in denuded oocytes. Moreover, F‐actin, a marker of trans‐zonal projections, and occludin, a tight junction protein, and their co‐localization, were significantly reduced in heat‐exposed COCs. These results indicate that cumulus cells and oocytes show distinct HS responses, indicating disrupted cumulus‐oocytes communication in heat‐exposed porcine oocytes.Support or Funding InformationThis work was supported by the National Key Research and Development Program of China (2016YFD0500502), the National Basic Research Program of China (2014CB138502), the Priority Academic Program Development of Jiangsu Higher Education Institutions, and Jiangsu Collaborative Innovation Center of Meat Production and Processing, Quality and Safety Control.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Regional Adipose Tissue Immune Cell Profiles in Childhood‐Onset and Adult‐Onset Obesity
Authors: Murphy Jessica , Dam Vi , Delaney Kerri , Morais José A. , Tsoukas Michael , Santosa Sylvia 
Published: June 2021

BackgroundWe do not understand why individuals who have had obesity since childhood are at greater risk of metabolic disease.ObjectiveTo examine the effects of obesity onset and adipose tissue region (upper vs. lower body) on the proportion of adipose tissue immune cells.MethodsWe used flow cytometry to quantify the proportion of immune cells in the stromovascular fraction of abdominal (AB) and femoral (TH) subcutaneous adipose tissue from adults with childhood‐onset (n = 16) or adult‐onset (n = 22) obesity.ResultsThe proportion of CD8+CD3+ T‐cells was greater in AB than TH in childhood‐onset obesity, while greater in TH than AB in adult‐onset obesity. There was no effect of obesity onset on other immune cell types. However, there was an overall effect of region where the proportion of CD45RA+CD8+CD3+ T‐cells was greater in TH than AB, and the proportion of CD206+CD68+ M2‐like macrophages was greater in AB than TH.ConclusionOur results show that there are regional differences in the adipose tissue immune cell profiles between childhood‐onset and adult‐onset obesity. It remains to be seen whether these differences are implicated in increasing the risk of metabolic disease.Support or Funding InformationThis research was funded by NSERC and the Heart and Stroke Foundation of CanadaThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Endothelial‐dependent activation of smooth muscle PDGF Receptors enhances PASMC proliferation in IPAH
Authors: Wu Kang , Tang Haiyang , Wu Xiaomin , Lin Ruizhu , Wang Ziyi , Zhang Qian , Ayon Ramon J. , Wang Jian , Makino Ayako , Yuan Jason X.‐J. 
Published: June 2021

Platelet‐derived growth factor (PDGF), is one of the major growth factors found in mammalian serum, which plays an important role in cell growth. It has been previously demonstrated that abnormal activation of the PDGF signaling pathway can contribute to aberrant pulmonary vascular remodeling and pulmonary hypertension via active PDGF receptors. The overall goal of this study was to examine the expression of the PDGFR isoforms in both pulmonary artery smooth muscle cells (PASMC) and pulmonary artery endothelial cells (PAEC) and to identify whether PDGF produced in PASMC or PAEC promotes PASMC cell proliferation. We observed that the protein and mRNA expression level of both PDGFRα and PDGFRβ were upregulated in IPAH patients in comparison to normal PASMC. However, expression of PDGFRα and PDGFRβ was not detected in PAEC. PDGF treatment enhanced the activity of PDGFRα and PDGFRβ, as determined by phosphorylation of PDGFRα and PDGFRβ in IPAH PASMC compared to control. Furthermore, the PDGF‐induced rise in cytosolic free Ca2+ was also increased in IPAH PASMC in comparison to normal PASMC. Treatment with normal PAEC cultured conditioned medium enhanced PDGFRα activation in IPAH PASMC than normal PASMC, while normal PASMC cultured conditioned medium had no effect on p‐PDGFRα and p‐PDGFRβ. We further found that the expression level of PDGFA and PDGFB were increased in IPAH PAEC compare to normal PAEC. Additionally, the expression level of PDGFA and PDGFB in PAEC were increased in normoxic condition compare to hypoxia. Normal PAEC cultured conditioned medium promotes cell proliferation in PASMC; proliferation was markedly higher in IPAH PAEC cultured conditioned medium, but not in PASMC cultured conditioned medium. The data showed that the expression and activity of PDGF receptor were increased in IPAH PASMC. Overall these results suggest that IPAH PAEC secret high‐levels of PDGF to the PASMC, which can affect active PDGF receptor, promoting PASMC proliferation which can lead to pulmonary hypertension.Support or Funding InformationThis study was supported in part by the grants from the National Heart, Lung, and Blood Institute of the National Institutes of Health (HL135807 and HL125208), the National Natural Science Foundation of China (81630004, 81470246, 81220108001 and 81520108001), the Guangzhou Department of Education Yangcheng Scholarship (12A001S), the Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme of China, China Scholarship Council (201608440324) and the Actelion ENTELLIGENCE Young Investigator Award.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Interaction of Chitosan Derivatives with Organic Cation Transporter 1 and 2
Authors: Soodvilai Sirima , Sajomsang Warayuth , Chatsudthipong Varanuj , Soodvilai Sunhapas , Opanasopit Praneet 
Published: June 2021

The present study was to investigate the interactions of chitosan derivatives including quaternized chitosan (QC), N‐benzyl‐N,O‐succinyl chitosan (BSCS), N‐naphthyl‐N,O‐succinyl chitosan (NSCS) and N‐octyl‐N,O‐succinyl chitosan (OSCS), with organic cation transporter 1 (OCT1) and OCT2. The transport function of OCT1 and OCT2 was monitored by measurement accumulation of radiolabeled methyl‐4‐phenylpyridinium acetate (3H‐MPP+) in OCT1 and OCT2 heterologous expressing cell and endogenous expressing cells (HepG2 cells and human renal proximal tubular; RPTEC/TERT1 cells). The results revealed that of BSCS, NSCS and OSCS at concentration of 1,000 μg/ml significantly reduced 3H‐MPP+ cellular accumulation compared with control whereas QC showed no effect on OCT1 or OCT2‐mediated 3H‐MPP+ accumulation. Among the chitosan derivatives, OSCS showed the highest inhibitory potency (for OCT1; IC50 = 395±1.10 μg/ml, for OCT2; IC50 = 1,241±1.22 μg/ml). BSCS, NSCS and OSCS significantly reduced maximal transport (Jmax) of OCT1 whereas they increased Kt of OCT2 indicating these compounds inhibited OCT1 and OCT2 transport function by non‐competitive and competitive binding mechanism, respectively. In addition, OSCS significantly reduced 3H‐MPP+ accumulation in HepG2 cells and RPTEC/TERT1 cells with the inhibitory potency of 1,208±1.09 μg/ml and 1,529±1.11 μg/ml, respectively. These results suggested that OSCS may alter OCT1‐ and OCT2‐mediated cationic drug clearances.Support or Funding InformationThis research was supported by the Commission of Higher Education (Thailand), the Thailand Research Fund (TRF) through the Royal Golden Jubilee Ph.D. Program (Grant No.PHD/0139/2557), the TRF through the Natural product‐based drug discovery and development (Grant No. IRN58W0004), Mahidol University (Thailand). The authors would like to thank Prof. Stephen H. Wright for providing rbOCTs‐CHO‐K1 cells.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Long‐term high‐intensity sound stimulation inhibits Ih in CA1 pyramidal neurons.
Authors: de Deus Júnia Lara , Cunha Alexandra Olímpio Siqueira , Ceballos César Celis , Leão Ricardo Xavier 
Published: June 2021

Afferent neurotransmission on hippocampal pyramidal cells can change their intrinsic membrane properties and affect many ion currents. One of the most plastic neuronal currents is the hyperpolarization activated cationic current (Ih), which changes in CA1 pyramidal cells in responseto many types of physiological and pathological processes. Several evidences demonstrated that hippocampal CA1 pyramidal neurons are affected by auditory stimulation. Recently we demonstrated that long‐term potentiation (LTP) is depressed by high‐intensity sound stimulation. Here we investigated if a long‐term high‐intensity sound stimulation could affect intrinsic membrane properties of CA1 pyramidal neurons. Our results showed that Ih is depressed by longterm (2 minutes per day, for 10 days) high intensity sound (110 dB) exposure. This resulted in a decreased resting membrane potential, increased membrane input resistance and time constant, and decreased action potential threshold. In contrast, CA1 pyramidal neurons from sound‐exposed animals fired more action potentials than neurons from control animals, but this effect was not caused by a decreased Ih. Interestingly, a single episode (1 minute) of 110 dB sound stimulation which also inhibits hippocampal LTP did not affect Ih and firing in pyramidal neurons, suggesting that these are long‐term responses to high intensity sound exposure. Our results show that prolonged exposure to high‐intensity sound affects intrinsic membrane properties of hippocampal pyramidal neurons mainly by decreasing the amplitude of Ih.Support or Funding InformationFAPESP, CNPQ and CapesThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Electroacupuncture Modulates Reflex Elevation in Blood Pressure through Adenosine Receptor A2A, but not A1 in Rostral Ventrolateral Medulla of Rats
Authors: Guo Zhi‐Ling , Malik Shaista 
Published: June 2021

Acupuncture potentially offers a non‐pharmacological approach to reduce high blood pressure (BP). Our previous studies have shown that electroacupuncture (EA) attenuates reflex elevation in BP induced by gastric distension (GD) through modulation by several transmitters (e.g., opioids and GABA) in the rostral ventrolateral medulla (rVLM). Although adenosine is released during neuronal activation in the rVLM, its role in acupuncture‐cardiovascular regulation is unknown. Adenosine primarily modulates neuronal function through P1 (specifically, A1, A2, and A3) receptors. Since selective activation of A1 and A2A rVLM receptors respectively induces pressor and depressor responses, we hypothesized that adenosine in the rVLM contributes to EA modulation of sympathoexcitatory reflexes through an A2A but not an A1 adenosine receptor mechanism. Repeated GD every 10 min was performed in Sprague‐Dawley male rats under ketamine and α‐chloralose anesthesia. EA (2 Hz, 0.5 ms, 1–4 mA) was applied at the P5–P6 acupoints, overlying the median nerve, for 30 min after establishing two consistent reflex responses to GDs. We found that repetitive GDs evoked consistent sympathoexcitatory pressor responses. EA (n=5) but not sham‐EA (n=5) at P5–6 (insertion of acupuncture needles into acupoints without electrical stimulation) significantly (P<0.05) attenuated GD‐induced elevations in BPs. EA modulation of sympathoexcitatory cardiovascular reflexes was reversed significantly after rVLM microinjection of SCH 58261 (1 mM in 50 nl; A2A receptor antagonist; n=8; P<0.05), but not by the vehicle (5% dimethylsulfoxide; n=6). Microinjection of DPCPX (3 mM in 50 nl; A1 receptor antagonist; n=4) into the rVLM did not influence EA inhibition of GD‐induced pressor responses. GD‐evoked sympathoexcitatory cardiovascular reflexes, in the absence of EA, were unaltered by administration of SCH 58261 into the rVLM. Neurons labeled with adenosine A2A receptors were co‐localized with neurons stained with tyrosine hydroxylase (i.e., catecholaminergic neurons) in the rVLM. These data suggest that EA modulates sympathoexcitatory cardiovascular responses through an A2A receptor mechanism in the rVLM.Support or Funding InformationNCCIH grant, AT009347.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Role of baroreflex during endotoxemic shock
Authors: Amorim Mateus Ramos , Borges Gabriela Silva , Mota Clarissa Maria Dias , de Siqueira Branco Luiz Guilherme 
Published: June 2021

Septic shock is a prevalent and life‐threatening condition which is often associated with major hypotension, resulting in multiple organs failure. The infusion of high doses of endotoxin lipopolysaccharide (LPS) is a well‐accepted experimental model of septic shock. Considering that baroreflex is a mandatory mechanism involved in the beat‐to‐beat hemodynamic regulation, we hypothesized herein that baroreflex plays a role buffering endotoxin‐induced hypothension in conscious freely moving rats. Thus, in the present study, we evaluated the cardiovascular outcomes of iv injection of endotoxin (1.5 mg.kg−1 or 2.5 mg.kg−1) or saline in male Wistar rats (280–350g, CEUA #2017.1.585.58.9). The baseline levels of mean arterial pressure and heart rate were not different among all groups. As expected, endotoxin induced hypotension (P<0.001) and tachycardia (P < 0.001). These effects were independent of dose. Interestingly, the drop of mean arterial pressure was significantly higher in rats previously submitted to baroreceptors afferents removal (4 days before recordings) than in (sham) rats with intact baroreceptor afferents (P<0.001). The present data are consistent with the notion that baroreflex is key lessening endotoxin‐induced hypothension. The neural mechanisms involved in this control deserve further investigation aiming new strategic therapeutic tools to revert this critical condition.Support or Funding InformationFinancial support: FAPESP, CAPES and CNPqThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The Orcokinin Neuropeptide NLP‐14 Regulates Sleep in C. elegans
Authors: Barrett Natalie , Riazati Niknaz , Buscemi Kristen , Brown Amelia , Nelson Matthew 
Published: June 2021

Caenorhabditis elegans displays two distinct sleep states: Developmentally timed sleep (DTS), which occurs during a life stage called lethargus (Raizen et al., 2008) and stress induced sleep (SIS), which occurs following exposure to environmental stress that damages cells. Both sleep states have been shown to be regulated by distinct neuropeptide signaling pathways. We have identified a new neuropeptide pathway that regulates SIS, neuropeptide‐like protein‐14 (NLP‐14). NLP‐14 shares sequence similarities (~69%) with a class of neuropeptides in arthropods called orcokinins (Nathoo et al., 2001), which are highly conserved within Ecdysozoans. In cockroaches, injection of exogenous orcokinin into the accessory medulla, a circadian pacemaker in the brain, results in a circadian phase shift (Hofer and Homberg, 2006). Interestingly, we have found that ectopic over‐expression of nlp‐14 during adulthood induces behavioral quiescence which resembles sleep. Specifically, when nlp‐14 over‐expression is induced under the control of a heat shock promoter, animals become quiescent for locomotion and show prolonged defecation cycles. Additionally, we find that nlp‐14(tm1880) reduction in function mutants display decreased SIS phenotype. Introduction of NLP‐14:GFP transgenes into this background rescues the SIS defects. The tm1880 allele eliminates 7 of the 12 encoded peptides in the NLP‐14 protein, leaving 5 peptides (NLP‐14‐2(2), NLP‐14‐4(2) and NLP‐14‐5(2)). We are currently attempting to remove the remaining peptides one at a time using the CRISPR‐cas9 system.Support or Funding InformationJohn P. McNulty Scholars ProgramThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Rare Case of an Accessory Left Vertebral Artery on the Aortic Arch
Authors: Granite Guinevere , Lashley Kerrie 
Published: June 2021

Vascular variations of the head and neck are common, but often go unnoticed because they generally do not present clear clinical symptoms. Unawareness of the presence and location of such variations may result in iatrogenic complications or even fatalities. Medical physicians and surgeons should be cognizant of such deviations due to their clinical significance.Vertebral artery variations are prevalent in both number and origin, but not frequently documented in the literature. In this case study, a White 65‐year‐old male presented with an accessory left vertebral artery originating on the aortic arch, between the left common carotid artery and the left subclavian artery. This is the most common place for variations of this type, however, this individual also presented a normal left vertebral artery branching off of the left subclavian artery. This accessory left vertebral artery courses cranially, entering the foramina transversarium at the C4‐C5 level. The left vertebral artery also has an atypical course. It enters into the foramina transversarium at a higher level than its aberrant analog. With a prevalence rate of 2.04%, this rare anatomical variant illustrates the clinical importance of extensive anatomical understanding of head and neck vascular variations.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Using a Virtual Reality Laboratory to Identify Methods for Improving Neuroanatomy Learning
Authors: Shermon Suzanna , Stout Randy 
Published: June 2021

Virtual reality (VR) is a 3‐dimensionsal (3D) digitally‐created environment that is widely used as a training and instructional tool (e.g. surgical preparation, space mission rehearsal, flight training, and even museum exhibits). With the use of a headset and handheld controllers, the user can explore, move around in, and interact with the virtual environment. Of importance to our research, the newest generation of consumer VR systems allows the participant to use their hands to manipulate virtual objects in a very intuitive manner.The goal of our research is to eventually use VR to improve neuroanatomy instruction for medical students. In particular, we hypothesize that with proper application of VR technology, students could learn structures more efficiently, gain deeper understanding of how structure is related to function, and enhance the interactions between students and course leaders (instructors). To test how the design of the virtual learning process and environment affect retention, motivation, and depth of learning for complex concepts in neuroanatomy, we are constructing a virtual laboratory with the use of Blender and Unity softwares. We are adapting a 3D model of the human brain to use as the learning materials for the virtual learning laboratory (VLL) that we are developing with Unity™. Our current build of the Virtual Learning Laboratory is accessed via Oculus Rift+Touch™, in which the students will participate in gamified and active learning by manipulating virtual brain anatomical models using the Touch Controllers ™. We have assembled a 3D brain in Blender, built a prototype VLL, and are currently refining the interface in preparation for testing human participants.VR and Augmented Reality (AR) are already being used as tools in neuroanatomy education. We expect that the virtual learning laboratory that we have developed will allow optimization of the benefits that VR can provide to the learning process. This tool for pedagogical research will be important as improved VR technology and user interfaces are being rapidly developed.Support or Funding InformationThe Academic Medicine Scholars Program at New York Institute of Technology, College of Osteopathic Medicine.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
ACE Inhibitor Reaction‐Induced Acute Angioedema Leading to Macroglossia: Two Case Studie
Authors: Kesterke Matthew John , Stigall Garret , Carmichael Ryan , Bhattacharjee Ritesh , Reddy Likith V 
Published: June 2021

Macroglossia, either congenital or acquired enlargement of the tongue, is a rare condition that leads to functional deficiencies in speech, mastication/deglutition, and airway patency. Acute‐acquired cases of macroglossia are potentially life threatening and have myriad etiologies. Presented here are two cases of macroglossia in adults caused by acute angioedema resulting from reaction to angiotensin‐converting enzyme (ACE) inhibitors. The mechanism of ACE inhibitor‐induced angioedema is attributed to dysfunction in the kallikrien‐kinin system, a protease pathway converting high molecular weight kininogens to kinins such as bradykinin, which can lead to inflammation of the cardiovascular system. This condition, while rare in adults, is more easily diagnosed, monitored, and treated if detected early. However, many clinicians fail to educate patients on the warning signs of acute angioedema: swelling of the tongue, submandibular and pharyngeal spaces, and/or difficulty breathing. Furthermore, patients often do not recognize the symptoms of ACE inhibitor reactions, leading to delays in diagnosis and treatment. Management of acute angioedema and subsequent macroglossia includes hospitalization and intubation for airway maintenance, partial glossectomy, and subsequent glossal rehabilitation and speech therapy. Both cases presented here led to anoxic brain injury and necessitated intensive surgical intervention, demonstrating the need for better patient‐clinician communication for positive outcomes of ACE inhibitor use. Current research on the kinin system and its role in the cardiovascular system is limited, so baseline clinician‐patient education represents the best first‐line defense against life‐threatening cases of acute angioedema.Support or Funding InformationThis research is supported in part by funding from the Texas A&M University College of Dentistry and the Baylor University Medical Center at Dallas.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.