bluuebunny/crossref_metadata_2025_split huggingface dataset:
Impact of cervical spinal contusion on the upper airway resistance in the rat
Authors: Xu Ke‐Jun , Lee Kun‐Ze 
Published: June 2021

Bronchopulmonary C‐fiber induced pulmonary chemoreflex is a critical component of the respiratory defense reflex and characterized by cessation of inspiratory airflow (i.e., apnea) and increase of upper airway resistance (i.e., laryngeal closure). Our previous reports demonstrated that apneic response was attenuated following cervical spinal cord injury; however, it remained unclear whether the upper airway response of pulmonary chemoreflex was also influenced by spinal injury. Accordingly, the present study was designed to investigate the response of laryngeal function to bronchopulmonary C‐fiber activation following unilateral high‐cervical spinal cord contusion in rats. Adult Sprague–Dawley male rats were received laminectomy or unilateral contusion at C2 spinal cord using the MASCIS Impactor (height: 6.25 mm). The respiratory airflow and subglottal pressure in response to intra‐jugular capsaicin (1.5 μg/kg)‐induced pulmonary chemoreflex were measured under spontaneously breathing condition at 3 days, 2 weeks or 6 weeks following spinal surgery. The result demonstrated that high cervical contusion caused a long‐term reduction in the tidal volume without alteration of laryngeal resistance at three time points after injury. However, capsaicin‐induced increase of subglottal pressure was substantially attenuated in contused animals at 3 days post‐injury, and partially recovered at 2 and 6 weeks post‐injury. These results suggested that cervical spinal cord injury not only influence the breathing pattern but also impact the upper airway function. The attenuated laryngeal closure response may unfavorably reduce the ability to prevent inhaling irritants and cause the pulmonary pathological condition following cervical spinal cord injury.Support or Funding InformationMOST 105‐2628‐B‐110‐002‐MY3This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Evidence that the preBotzinger complex does not participate in cough rhythmogenesis in the anesthetized cat.
Authors: Shen Tabitha Y. , Poliacek Ivan , Kotmanova Zuzana , Musselwhite M Nicholas , Rose Melanie J. , Bolser Donald C. 
Published: June 2021

The nucleus tractus solitarius (NTS) participates in cough phase timing in the anesthetized cat. The preBotzinger complex (preBotC) is key for breathing rhythmogenesis, but the role of this area in regulating cough rhythmogenesis is still unknown. We hypothesized that excitation of neurons in the preBotC would modulate shorten the duration of the inspiratory cough, consistent with the effects during breathing. To test this hypothesis, we unilaterally microinjected 5 mM DL‐Homocysteic acid (DLH) into the preBotC in anesthetized, spontaneously breathing adult cats (n=7). In 3 of these animals, 15 mM DLH also was injected into the preBotC. Criteria for data inclusion were multi‐unit inspiratory neuron recording at the injection site, apneusis or tachypnea as a result of DLH injection, and histological verification of the injection site. We recorded esophageal pressure (EsPr) and electromygrams (EMG) from inspiratory (parasternal and diaphragm) and expiratory (internal oblique) muscles. Tracheobronchial cough was induced via mechanical stimulation of the intrathoracic trachea. DLH microinjection significantly altered the breathing response: breathing frequency increased (18.0±1.4 to 46.9±7.4 bpm) due to changes in both inspiratory time (TI − 1.04±0.5 to 0.75±0.76 s) and expiratory time (TE −2.34±0.19 to 0.63±0.16 s). Diaphragm EMG magnitude did not change significantly. Microinjection of DLH (5 mM) into the preBotC did not alter cough phase timing (cough frequency: 23.3±4.0 to 22.9±4.4 coughs per minute; TI − 1.27±0.13 to 1.31±0.10 s; TE1 −0.26±0.7 to 0.26±0.07 s; TE2 − 1.35±0.24 to 1.29±0.49 s). While the magnitude of cough pressures and diaphragm EMGs were not altered (EsPr – control 49.4±5.8 to DLH 35.7±5.2 ; EMG amplitude ‐ control 70.8±3.5 to DLH 65.1±6.5), cough expiratory motor drive was significantly lower (abdominal – control 62.1±5.5 to DLH 40.0±5.9%, p <0.04). Microinjections of 15 mM DLH into the preBotC eliminated cough. In the 3 animals that had both 5 and 15 mM DLH injections, there was a trend for a longer recovery time for cough with the higher concentration of DLH (5 mM – 33.8±10.4 s; 15 mM – 66.8±27.5 s). Unlike for breathing, excitation of neurons via DLH in the region of the preBotC does not affect phase timing for cough, although DLH appears to exhibit a dose‐dependent cough suppression.Support or Funding InformationSupported by NIH HL 103415 and 1OT20D001983.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The influence of CO2 on spatiotemporal features of mechanically‐induced coughing in anesthetized cats
Authors: Musselwhite M Nicholas , Shen Tabitha Y. , Rose Melanie J. , Watts Joseph , Bolser Donald C. 
Published: June 2021

Cough results in a dramatic increase in ventilation in part due to large increases in tidal volume. This increase in ventilation can cause severe hyperventilation during repetitive cough bouts. The purpose of this study was to quantify how reversal of hyperventilation during repetitive coughing affects the cough motor pattern. Prior studies have shown that increasing CO2 well above eupneic levels can suppress cough in anesthetized humans (Nishino 1989) but the effects of hypocapnia on the behavior are less well understood. Cough was elicited in anesthetized, spontaneously breathing adult cats (n=9) via a flexible cannula inserted into the trachea for 60 seconds. Animals were subjected to both a control condition, where cough‐induced hyperventilation was not perturbed (ETCO2 12±1, arterial CO2 17±1 mm Hg), and an “isocapnic” condition, where inspired CO2 was increased so that ETCO2 during cough approximated eupneic levels (ETCO2 32±1, arterial CO2 28±1 mm Hg). There was no change in cough number between control (9±1) and isocapnic (11±1) conditions. Further, the magnitudes of diaphragm, internal oblique and parasternal EMGs were unchanged under isocapnic relative to control conditions. There also was no significant change in intrathoracic pressures between the two conditions (control 53±12 cm H2O vs isocapnic 47±12 cm H2O). However, there was a decrease in the intensity of the maximal cough effort during the addition of CO2 (control 71±13 cm H2O vs isocapnic 62±13 cm H2O, p<0.05). There was a trend for inspiratory time during cough to be slightly reduced with added CO2 (p=0.07). The E1 phase of cough (control 0.5±0.03 s vs isocapnic 0.5±0.02 s) and E2 phase of cough (control 2±0.5 s vs isocapnic 2±0.3 s) were unchanged under isocapnic conditions. There also was a significantly shorter decrease in the time to first breath following the cessation of coughing in the isocapnic trials (control 16±4 s vs isocapnic 5±1 s, p<0.02). The results indicate that CO2 at or below the eupneic range does not strongly alter the motor pattern of coughing in anesthetized cats. Cough‐induced hyperventilation appears to be solely a consequence of the acceleration of pulmonary gas to accomplish ejection of foreign materials from the airways, rather than an important regulatory feature that modulates the behavior.Support or Funding InformationSupported by NIH HL 103415 and 1OT20D001983.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
RESPIRATORY CHANGES IN OFFSPRING OF HIGH FAT DIET FED DAMS
Authors: Bassi Mirian , Barbosa Rafaela Moreira , de Sa Jessica M. , Menani Jose Vanderlei , Colombari Eduardo , de Almeida Colombari Debora Simoes 
Published: June 2021

Several studies have demonstrated that early life over‐nutrition, such as maternal obesity, is associated with increased risk of cardio‐metabolic diseases. In the present study respiratory changes were investigated in offspring of high fat diet (HFD) fed dams. Adult female Holtzman rats (250 g) were fed with standard diet (SD) or HFD during 6 weeks before, during gestation and lactation. After weaning, male offspring of SD dams (O‐SD, n = 7–12) or HFD dams (O‐HFD, n = 7–12) were fed with SD. The results showed that O‐HFD (P28–32) presented an increase in retroperitoneal adipose tissue (0.15 ± 0.01, vs O‐SD: 0.08 ± 0.01 g/100 g of bw, p < 0.05), a higher plasma triglycerides levels (141 ± 11, vs. O‐SD 49 ± 10 mg/dl, p < 0.05) and insulin intolerance (1.28 ± 0.30, vs O‐SD: 2.25 ± 0.15 % of glucose disappearance/min, p <0.05). At P40, baseline ventilation was higher in the O‐HFD group (1.200 ± 48, vs O‐SD: 924 ± 58, ml.kg‐1.min‐1, p <0.05) due to an increase in tidal volume (9.12 ± 0.29, vs O‐SD: 7.43 ± 0.47, ml.kg‐1, p <0.05). An increased response to hypoxia was also observed in O‐HFD (1.634 ± 80, vs O‐SD: 1.325 ± 50 mL.kg‐1.min‐1, p <0.05). The results demonstrated that young offspring of obese dams have metabolic dysfunctions. The data also demonstrated that these offspring have baseline ventilatory changes as well as an exaggerated response to peripheral chemoreflex activation.Support or Funding InformationFAPESP (2015/234677), CNPq (425586/2016‐2).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Intakes of vegetables and red meat in relation to circulating nitrate levels
Authors: Wu Tianying , Sonoda Samantha , Fan Guochang 
Published: June 2021

ObjectiveOur study aimed to determine the associations between intakes of vegetables and red meat (processed and unprocessed) and circulating nitrate levels.DesignUsing a cross‐sectional study design.Setting and ParticipantsA secondary analysis using data from the National Health and Nutrition Examination Survey (NHANES) and from the Health Professionals Follow‐up Study (HPFS). 5,058 adults (men and women) in the 2005–2006 NHANES and 1,260 men from HPFS were analyzed.MeasurementsThe non‐quantitative food frequency questionnaire (NFFQ) and two 24‐hr recalls were collected and urinary nitrate was measured in the NHANES. Plasma nitrate was measured and a semi‐quantitative FFQ (SFFQ) was collected in the HPFS.ResultsUsing three dietary assessment instruments (NFFQ, SFFQ and average 24‐hr recalls), we found a similar trend when assessing the associations of vegetables and red meat with circulating (plasma and urinary) nitrate. Across instruments, circulating nitrate levels were 15–33% higher for participants in the highest, when compared to the lowest, quintile of vegetable intake (p<0.001). Circulating nitrate levels were 8–16% lower for participants in the highest, when compared to the lowest, quintile of red meat intake (p<0.001).ConclusionOur study has demonstrated a positive association between vegetable and circulating nitrate and an inverse association between red meat and circulating nitrate. As nitrate has been demonstrated to be beneficial for preventing several chronic diseases, our results provide valuable information for studying dietary etiologic factors associated with nitrate and chronic diseases.Support or Funding InformationNCI KO7 awardThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
A Multiscale Analysis of Early Cardiogenesis Following VEGF Perturbations
Authors: Rongish Brenda J. , Aleksandrova Anastasiia , Filla Michael B. , Kosa Edina , Little Charles D. , Petersen Alan , Czirok Andras , Rugonyi Sandra , Rykiel Graham , Lansford Rusty 
Published: June 2021

Congenital Heart Defects (CHDs) are multi‐factorial in origin, and there is a critical need to identify other contributing factors in the development of CHDs. Endogenous factors that regulate development, such as altered levels of cardiovascular growth factors in the embryo/fetus, may initiate or contribute to CHDs. Our objective was to determine if alteration of Vascular Endothelial Growth Factor (VEGF) levels at key developmental periods leads to reproducible cardiovascular defects, which may be correlated with underlying altered cell behavior, physiological parameters and/or molecular signaling events. We used ex ovo culture and imaging systems that capitalize on the experimental accessibility of quail embryos, which, like humans, have four‐chambered hearts. In order to alter VEGF signaling, the following were introduced into quail embryos: recombinant human VEGF, exogenous VEGF‐GFP fusion protein, and inhibitors of VEGF receptor tyrosine kinase signaling and downstream effectors of VEGF. Time‐lapse imaging (KUMC) and optical coherence tomography (OHSU) revealed abnormal phenotypes between Hamburger and Hamilton (1951) stages 4 to HH38 – encompassing vasculogenic (pre‐circulatory) stages through primordial valve formation. Hemodynamic parameters were measured and related to structural defects at circulation stages. These studies showed the effects of altered VEGF signaling on cardiac and endothelial cellular behavior, organogenesis of four‐chambered hearts and great vessels, and cardiac function. Further, we identified potential molecular pathways involved in VEGF signaling. The ability to observe the behavior of endothelial, endocardial, and myocardial precursors, gross cardiac phenotypes and hemodynamic changes following experimental manipulation of VEGF allowed a careful analysis of the role of VEGF at multiple length scales, and over time, during cardiovascular morphogenesis. We conclude that VEGF signaling, when dysregulated, leads to detrimental cardiovascular malformations and altered cardiac cellular behavior and function. This work has helped to determine the underlying mechanisms of VEGF's role and actions in cardiac and vessel development, as well as identified structural and functional cardiovascular defects that are attributable to aberrant VEGF signaling; which are similar to CHDs observed in humans.Support or Funding InformationAmerican Heart Association 16GRNT29840002, the Molecular Regulation of Cell Development and Differentiation COBRE, P30 GM122731, and the University of Kansas School of Medicine Bridging 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.
Professional Identity: What is it, when is it formed, and what is the role of anatomy in this developmental process?
Authors: Byram Jessica N. 
Published: June 2021

Professional identity formation (PIF) has been described as an essential process by which medical students internalize knowledge, skills, and values of the profession to ultimately become physicians. This session will introduce the developmental process of PIF in medical students and will discuss its relationship to professionalism. The described model and its role in anatomy education is grounded in the results of a thematic analysis of nine medical students who shared how their training and anatomy education experiences shaped their professional identities and perceptions of professionalism. Overall, the evidence suggests anatomy educators can foster PIF by promoting a complex and reflective understanding of professionalism and by encouraging students to enact those professional values as components of their professional identities during team‐based experiences in both laboratory and didactic settings. Specifically, the values of respect, both for the patient (donor) and the team, duty, and good communication were found to be fostered through team‐based cadaveric dissection.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Nonsense‐mediated mRNA decay and human disease: Genome guardian and executor
Authors: Maquat Lynne E. 
Published: June 2021

Much progress has been made on how nonsense‐mediated mRNA decay (NMD), which we first described for humans in 1981, controls the quality of gene expression by detecting and rapidly degrading aberrant mRNAs that contain a premature termination codon1. Our studies of NMD have led to the discovery of the pioneer round of translation, the post‐splicing “mark” on newly synthesized mRNAs – later named the exon‐junction complex (EJC) with Melissa Moore – the mechanistically related and competing Staufen‐mediated mRNA decay pathway2,3, including new roles for SINEs4, and most recently a microRNA decay pathway5,6. We tracked individual cellular transcripts in collaboration with Rob Singer to confirm our results from the mid‐1990's indicating that NMD for a number of mRNAs occurs on the cytoplasmic side of the nuclear envelop7. Our data provide explicit evidence that proteins acquired by newly synthesized mRNAs in the nucleus, including the cap‐binding protein CBP80 and constituents of the EJC, are critical for mRNA quality control via translation in the cytoplasm. We have also described the molecular mechanism for how NMD targets are discriminated from other transcripts: the central NMD factor – the ATP‐dependent RNA helicase UPF1 – preferentially associates with mRNA 3′‐untranslated regions (3′ UTRs) in a way that correlates with 3′ UTR length and the presence of a 3′ UTR EJC8,9. Importantly, NMD also targets ~10% physiologic mRNAs that are key to maintaining cellular homeostasis in a changing environmental milieu. For example, we reported that a sufficient level of DNA damage induced by commonly used frontline chemotherapeutics inhibits NMD by triggering the caspase‐mediated cleavage of sub‐stochiometric amounts of UPF1, thereby upregulating the half‐lives of mRNAs that include those encoding proteins promoting apoptosis10. Notably, the modest inhibition of NMD promotes but is not sufficient for programmed cell death. These and other results will be discussed.Support or Funding InformationWork on nonsense‐mediated mRNA decay in the Maquat lab is supported by NIH R01 GM 059614 to L.E.M.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Chemoinformatics Profiling of the Bioactive Fraction of Bizzy Nut
Authors: Gray wesley , Philips Orville , Telles Caroline 
Published: June 2021

Bizzy Nut status as a traditional natural medicine resulted from its reputation as a stimulant, increasing energy and strength, staving off hunger and a multitude of biological activities such as anti‐oxidation, anti‐cancer, and prevention of certain diseases. We have developed a method for fingerprinting and quantifying the anti‐prostatic activity existing in Bizzy Nut using liquid chromatography (LC) with a diode array detector and LC‐MS. Using this method, the chemical fingerprint of Biz‐2Fr.3 extract was established, in which the separation of more than five analytes were realized in about 30 mins, and 6–8 distinctive peaks were identified by LC/MS analysis. The linearity, precision, stability, repeatability, and accuracy of the method will clearly reveal any variations of Bizzy Nut samples produced in Jamaica in different years. To provide clues to the chemical identity of bioactive peaks (Biz‐2Fr.3), we applied LC‐MS because of its sensitivity, reproducibility, speed, and versatility. Analysis of Biz‐2Fr.3 using an Agilent 6210 Quadrupole LC‐MS with an Agilent Ultra‐2 fused silica capillary MS column in the negative ion mode resulted in three major peaks with retention times of 1.1, 5.8 and 7.5 minutes. Characterization of the molecular ions in peak one revealed the presence of the analyte, with m/z ranging from 120 m/z to 445 m/z. Peaks two and three, on the other hand, contained a single molecular ion with m/z of 181. The 1H NMR spectrum of Biz‐2Fr.3 contained peaks with the following chemical shifts, in ppm, and assignments: a stretch of H between 3.5–4ppm indicating the presence of straight chains CH, CH2 or CH3. Methyl hydrogens that are bonded to oxygen (eg. ROCH3) were observed between chemical shifts between 2.9–3.6 ppm. There is a possibility of the presence of C=C (eg. R2C=CHR) due to the shift between 4.0–4.5 ppm. The absence of the chemical shift between 6–8ppm indicates the absence of any aromatic hydrogen. The LC‐MS and NMR data suggested that we have three groups of compounds in the Biz‐2Fr.3 fraction.Support or Funding InformationGrant support: U.S. Public Health Service grants R15AT006821, awarded by the National Center for Complementary and Integrative Health.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Connection between antimicrobial venom peptides and bacterial ATP Synthase
Authors: Syed Hiba , Ahmad Zulfiqar 
Published: June 2021

BackgroundAntibiotic resistance is becoming a huge threat with devastating effects on public health and the global economy. Therefore, finding new alternatives to combat antibiotic resistant microbes is of paramount importance. Selective inhibition of bacterial ATP synthase provides a fascinating opportunity to deal with this ongoing problem. ATP synthase is vital for cellular energy production in almost all organisms from bacteria to man. Inhibition of ATP synthase can deprive cells of ATP resulting in cell death. Many peptides are known to have antimicrobial and antitumor properties. Earlier some peptide were shown to inhibit Escherichia coli ATP synthase establishing that the antimicrobial effects of peptides can be connected to the blocking of ATP generation in bacterial cells. Currently, our lab is exploring the connection between a variety of antimicrobial venom peptides and E. coli ATP synthase.MethodThe growth properties of wild‐type and mutant E. coli strains along with null strains were verified on fermentable and non‐fermentable carbon sources before harvesting cells in minimal media to isolate ATP synthase. Membrane bound F1Fo ATP synthase inhibitory studies and E. coli cell growth assays were performed in presence of varied concentrations of natural and modified venom peptides. A null control with deleted ATPase gene was also used in all the studies.ResultsOur preliminary results show that the natural and modified venom peptides affected degree of inhibition. It seems that inhibitory potency of venom peptides can be enhanced by addition of a c‐terminal NH2 groups. We also observed that venom peptides follow a differential pattern of inhibition between wild type and mutant ATP synthase. Our initial results also indicate that incremental additions of positive charges can augment the extent of inhibition. Our early results suggest a feasible connection between the antimicrobial properties of venom peptides and bacterial ATP synthase. We are finalizing our preliminary results and we are investigating the synergetic effects of venom peptides on ATP synthase.ConclusionsApparently, antimicrobial venom peptides inhibit E. coli ATP synthase and bind at the βDELSEED‐motif of ATP synthase. Our preliminary data suggests that the inhibitory potency of venom peptides can be augmented through structural modification of venom peptides. Also, selective inhibition of ATP synthase by venom peptides offers a valuable alternative to combat antibiotic resistant bacterial infection.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.