bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cardiovagal baroreflex gain relates to sensory but not neurological level of spinal cord injury
Authors: Draghici Adina E , Taylor J. Andrew 
Published: June 2021

The arterial baroreflex is a primary regulator of autonomic outflow to effectively regulate acute blood pressure changes. After a spinal cord injury (SCI), damage to the autonomic nervous system results in cardiovascular dysregulation. Higher level of injury results in greater loss of sympathetic control, while cardiac parasympathetic control remains intact regardless of injury level. Thus, it is possible that those with high level SCI, and hence extensive sympathetic disruption, will require greater cardiac parasympathetic compensation to control blood pressure. However, the effect of an SCI on cardiovagal baroreflex gain remains unclear. Baroreflex control of blood pressure in those with SCI has been reported to be greater, lesser, and no different compared to able‐bodied individuals. Moreover, the effect of injury level on baroreflex gain remains unclear as most studies that examined the effect of lesion level treated it as a discrete variable – high, usually cervical level lesions, and low, usually thoracic level lesions. Therefore, we assessed baroreflex sensitivity using the neck chamber techniques in those with SCI (N = 29) across a range of injury levels (neurological level of injury C1 – T10, sensory score C4 – S4/5), within 2 years of injury, and compared them to able‐bodied (N = 14). Injury level was assessed by both neurological level of injury and sensory score. We assessed baroreflex gain during 5 trials of 4 levels of neck chamber pressure (corresponding to −15, −25, −35, and −45 mmHg). We found no difference in baroreflex gain between those with SCI and able‐bodied (p>0.1). Neurological level of injury was not correlated to baroreflex gain, but sensory score and resting RR‐interval were (r = 0.47, p<0.01; r = 0.57, p<0.01). Multiple regression showed that both sensory score and resting RR‐interval were strongly predictive of baroreflex gain (r2 = 0.47, p<0.01): gain increased with lower sensory score and higher resting RR‐interval. Moreover, baroreflex gain was not different between those with high and low neurological level of injury; but higher in those with lower compared to higher sensory score (both p<0.01). Hence, sensory score is more predictive of baroreflex gain than the widely used neurological level of injury. This might be understood in the context of vagal‐sympathetic accentuated antagonism: those with high level injuries have the lowest likelihood of intact cardiac sympathetic innervation depressing cardiac vagal responsiveness.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Work in the Cold: A Systematic Review of How the Chronic Exposure to Low Temperatures May Explain Painful Soft Tissue Disorders
Authors: Remigio Wilton , Trygar Michael Y , Schweiger Jacob , Fairchild Mary 
Published: June 2021

Movement disorders presenting with pain carry a significant economic and rehabilitative burden which is more predominantly in the working age population. Amongst the many causative factors suggested, cold exposure has been implicated as an important, albeit, unrecognized etiology in the development of painful movement related conditions. To this date no reviews have focused on the effects of cold exposure and its association with the appearance of musculoskeletal pain. The purpose of this systematic review aims to delineate and characterize this relationship.An electronic search was conducted using PubMed, Google Scholar, Academic Search Premier, and Oxford Journals. The following search terms were used to conduct this study: “Cold exposure and musculoskeletal injury” “Cold and injury risk” “Cold climate and workplace injury” “Cold exposure and pain” “Cold and arthritis”, “Cold physiology” “Effects of cold on musculoskeletal disorders” “ Effects of cold on pain perception” “Effects of cold exposure on injury risk” “Musculoskeletal manifestations and diseases due to environmental cold exposure.” A hand search of each reference list was performed to improve the quality of the literature review. Fourteen relevant articles were gathered from the literature review and used in this study.A consistent relationship between cold environment exposure and painful somatic manifestations was noted throughout the literature in the past 15 years. The most frequently reported manifestations included low back pain, finger pain, shoulder pain, neck pain as well as diagnoses of epicondylitis, tenosynovitis, and peri‐tendonitis. This relationship was stronger in subjects exposed to cold environments in their workplace when compared to controls. Chronic cold exposure in workplace environments appears to be a primary determinant in the etiopathogenesis of painful disorders affecting the body with important implications for productivity and work enjoyment.Support or Funding InformationMIsericordia UniversityCollege of Health Professions and EducationPhysical Therapy DepartmentThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Inhibition of the RNA binding protein HuR protects against cardiac ischemia/reperfusion injury by reducing inflammatory gene expression
Authors: Slone Samuel , Fleifil Salma , Anthony Sarah , Green Lisa , Nieman Michelle L , Lorenz John , Tranter Michael 
Published: June 2021

Despite medical advances, cardiac ischemia/reperfusion (I/R) injury remains a leading cause of morbidity and a huge economic burden in the United States. RNA binding proteins are becoming recognized as potential mediators of cardiac physiology and pathology, but the role of HuR, an RNA binding protein highly expressed in myocytes, in acute cardiac I/R injury is unknown. HuR has been shown in other tissues to be a critical post‐transcriptional mediator of pro‐inflammatory chemokine and cytokine gene expression, and our lab has shown HuR to be activated (nuclear‐to‐cytoplasmic translocation) in cardiomyocytes 2 hours post‐ischemia/reperfusion injury.To address the functional role of HuR in I/R, cardiomyocyte‐specific HuR deletion mice (iCM‐HuR−/−) were subjected to 30 minutes of LAD (left anterior descending) coronary artery ligation followed by 24 hours of reperfusion. In parallel, a separate group of wild‐type mice were subjected to 30 minutes ischemia with a pharmacological inhibitor of HuR given just prior to reperfusion. Analysis of infarct size showed a smaller infarct with both HuR genetic deletion (41% infarct/risk in iCM‐HuR−/− vs. 51% infarct/risk in control, N=3, P<0.05) and pharmacological inhibition (~11% decrease in infarct size compared to vehicle, N=4, P=0.069). We were also able to recapitulate this protection in vitro using neonatal rat ventricular myocytes (NRVMs) and H9C2s (myoblast derived rat left ventricular cardiomyocytes) subjected to 6 hrs of simulated ischemia (glucose deprivation and hypoxia at ≤1% O2) followed by 2 or 24 hrs of reperfusion (reoxygenation and reintroduction of glucose/serum) by showing that siRNA‐mediated knockdown or pharmacological inhibition of HuR significantly reduced cell death and caspase‐3 activation. Analysis of inflammatory gene expression demonstrates a significant blunting of IL‐6 expression at just two hours post‐reperfusion both in vivo and in vitro, suggesting that HuR activity is necessary for the early induction of inflammatory gene expression networks.In conclusion, our results suggest that inhibition of HuR is protective against cardiac I/R injury through a reduction in inflammatory gene expression. Work is still ongoing to identify the specific means by which HuR is activated and mediating expression of inflammatory cytokines and chemokines.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
PPARα interacts with PHD proteins on Renal Fibrosis in a Mouse Unilateral Ureteral Obstruction Model of Chronic Kidney Disease
Authors: Choi Myung , Oyekan Adebayo 
Published: June 2021

Peroxisome proliferator activated receptor (PPAR)α and prolyl hydroxylase domain‐containing protein (PHD), “sensors” of cellular energy and oxygen have protective effects in the kidney and potentially act in a complimentary fashion but the mechanisms involved are not fully known. This study examined the effects of PPARa and its interaction with PHD in a mouse model of renal fibrosis induced by unilateral ureteral obstruction (UUO). UUO increased hydroxyl proline in PPARa WT and KO kidneys (P<0.05) but to a greater extent in KO kidneys. Dimethyl oxallyl glycine (DMOG), a PHD inhibitor, markedly blunted the effect only in WT kidneys (P<0.05). TGFβ expression was also increased (~ 3‐fold, P<0.05) in both WT and KO kidneys. However, DMOG blunted UUO‐induced increase in TGFb expression only in WT kidneys (P<0.05). Bilirubin, an index of heme oxygenase activity, was lower in KO kidneys at basal level (P<0.05) and was reduced in WT kidneys (P<0.05) following UUO but paradoxically increased in KO kidneys (P<0.05). DMOG blunted the reduction in bilirubin in WT (P<0.05) but was without effect in KO kidneys. Serum arginase activity, an index of cellular content of L‐Arginine, was increased in WT mice (P<0.05) but there was no change in KO mice following UUO. DMOG abolished the effect in WT but not KO mice. These data suggest that PPARα plays a protective role against UUO that appears to be coupled to PHD proteins by mechanisms related to heme oxygenase and arginase.Support or Funding InformationThis study was supported by the National Institutes of Health grant G12MD007605.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The stable and unstable function of Bioenergy, in the immunological and neuronal environment of cancer, viral infection and bacteria
Authors: Einstein George P , Tulp Orien L , Konyk Carla M , Rahman Michael S 
Published: June 2021

There has been long established that biophysical & biochemical reactions in the cellular communication of neuronal messaging. Specific Quantum Photonics Energy have been shown to stimulates these Biophysical/Biochemical Reactions. Systems Biology model representing regulation.Biophotonics therapy uses the harnessing and application of light for immune stimulation and antibacterial and antiviral properties.Biophysical Neural Networks examines the interface between systems theory and experiment at a multi‐hierarchical level of neural organization.The Immune stimulation matrix may be understood as a interplay of the milieu of the biochemical and physical parameters that ultimately move the organism to health and homeostasis, or to disease. The GP Einstein model of Coherence – Congruence can be used to understand the parameters and relations that have been obtained from previous independent experiments using specific quantum photonic energy conducted at Einstein Medical Institute. The experiments have included published applications of treatment of HIV/HVC therapy.This stability model can them be used to predict immunological phenomenon as a summation towards regulation or not and can further the impetus to design corresponding experiments.Support or Funding InformationSupported by Institutional Resources of USAT, UHH, and EMIThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
HEPATIC REGENERATION INDICES AND BEST PERIOD POST 70% HEPATECTOMY TREATMENT: AN EXPERIMENTAL MODEL
Authors: DE ARAUJO OLIVEIRA LUZ MARINA GONÇALVES , LEME PEDRO LUIZ SCHILACCI , CHAVANTES MARIA CRISTINA G 
Published: June 2021

BACKGROUNDHepatic regeneration represents a protection mechanism against the loss of hepatic tissue functional or by partial hepatectomy.OBJECTIVESThe present study analyzed morphological, histomorphometric and immunohistochemical characteristics for monitoring hyperplasia and hypertrophy liver regeneration in rats post partial hepatectomy as same as the best time regeneration.METHODSTwenty‐eight male adult Wistar rats were divided into four groups: Sham (SG), 3 (H3), 7 (H7) and 14 (H14) days, according to observation time post surgical procedure. The Sham group underwent just to laparotomy. The groups H3, H7 and H14 underwent to 70 % partial hepatectomy. According to each time treatment each group were euthanized. The regenerated livers were removed and were submitted to morphological calculations (weight, volume and hepatosomatic index), histomorphometric (mitotic index and quantification by PAS) and immunohistochemical analysis (quantification of mitosis by PCNA).RESULTSThere were no statistical differences in the morphological indices after the experimental period. There were differences of the Mitotic Index among the sham group and the three study groups. Comparing to H14 group in the percentage of positive area for PAS were not found differences among the sham, H3 and H7 groups. The Hepatocyte Proliferation Index showed differences by immunohistochemical study among to the sham group, comparing to the three study groups.CONCLUSIONThe histomorphometric and immunohistochemical indices showed the importance for the liver regeneration process, by the number of mitosis and the hepatic glycogen presence. The best regeneration time were in 7 days, due to the positive correlation into all indices.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Leptin Induced Satiety and the Contribution of Brainstem Astrocytes
Authors: Stein Lauren , Lhamo Rinzin , Cao Anh , Tinsley Ian , Doyle Robert , Hayes Matthew 
Published: June 2021

The staggering prevalence of obesity worldwide poses major public health concerns. Since energy balance regulation is coordinated by CNS centers, investigation into the underlying homeostatic, brain mechanisms controlling feeding behavior and weight management is critical to the development of novel and efficacious obesity therapeutics. While the vast majority of studies have investigated neuronal processing of satiety hormone signaling, little is known about the contribution of non‐neuronal cells such as astrocytes. Using fluorescent in situ hybridization we observed colocalization of fluorescently labeled leptin (Cy5‐lep) on both human and rodent brain stem astrocytes that express the leptin receptor (LepRb). These findings suggest that brainstem astrocytes are involved in leptin mediated energy balance control. To test this hypothesis, rats maintained on chow or high fat diet (HFD) for 4 weeks were pretreated with vehicle or 5nmol fluorocitrate (FC; transient inhibitor of astrocyte metabolism) followed by vehicle or 5μg/μL leptin (all administered into the 4th ventricle). FC pretreatment significantly attenuated 24h hypophagic and body weight suppressive effects of leptin in chow‐ but not in HFD‐maintained rats. Collectively, these findings support the hypothesis that DVC astrocytes express LepRb and acts as critical modulators of the anorectic effects of leptin ‐ an effect that is blunted in HFD‐induced obesity and may contribute to the perpetuation of obesity. Further experiments are underway to investigate the direct action of leptin signaling on DVC astrocytes to promote satiety.Support or Funding InformationNIH NIDDK R01DK116762 NIH NIDDK F32DK118818 TOS Early Career FellowshipThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The Role of Respiratory Noradrenergic Neurons Projecting to the Basal Lateral Amygdala in Anxiety‐related Behavior
Authors: Martinez Vena , Sun Jenny , McKinney Andrew , Jiang Xiaolong , Ray Russell 
Published: June 2021

The most commonly reported symptom of panic attacks is respiratory dysfunction, such as hyperventilation. It has been shown that subsets of patients with anxiety disorders show a lower threshold for carbon dioxide level imbalances and exposure to high levels of carbon dioxide (hypercapnia) can induce anxiety‐like behavior such as panic attacks. The false suffocation alarm hypothesis posits that inappropriate activation of respiratory chemoreceptors in response to benign indices triggers an alarm of suffocation danger and may contribute to anxiety and panic disorders. Two potential candidates that may link anxiogenic and respiratory circuitry are the central noradrenergic (NA) system and the amygdala, both of which have been shown to play roles in both breathing and anxiety. Therefore, we hypothesize that projections from the brainstem NA nuclei to the amygdala play a functional role in modulating the hypercapnic ventilatory response and anxiety‐like behavior in mice.To test this hypothesis, we targeted NA projections to the amygdala by using a Cre‐expressing retrograde virus applied to the amygdala of our intersectional DBH‐p2a‐FLPo; RR5, multicolor reporter line to conduct projection mapping of NA neurons to the amygdala and DBH‐p2a‐FLPo; RR1 and RR2 DREADD mice to specifically inhibit or stimulate NA neurons that project to the amygdala. In these mice, we measured respiratory output using whole‐body plethysmography and anxiety‐like behavior using open field, light dark, and elevated plus maze.Preliminary results indicate that DREADD mediated inhibition of NA neurons projecting to the amygdala may result in a decreased hypercapnic ventilatory response. However, upon stimulation of the NA neurons that project to the amygdala, there was no change in the hypercapnic ventilatory response. Inhibition and stimulation of NA neurons projecting to the amygdala result in a possible decrease in anxiety‐like behavior. Our preliminary results demonstrate the feasibility of delineating and accessing NA neurons based on the their projection target and suggest that NA neurons that project to the amygdala may play a role in the hypercapnic ventilatory response, as well as anxiety‐related behavior. Future directions will include the role of amygdala‐projecting NA neurons in behavior, such as fear learning and anxiety‐related behavior, under higher CO2 concentrations.Support or Funding InformationMcNair Medical InstituteR01HL130249R01HL130249‐02S1This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
5‐hydroxymethyl‐2‐furfural (5HMF) Improves Exercise Capacity During Normoxia and Preserves Cardiovascular Function During Severe Hypoxia in Exercising Swine
Authors: Williams Brian T , Ciarlone Geoffrey E , Mahon Richard T , Swift Joshua M 
Published: June 2021

BACKGROUNDModern military operations at high altitudes >5,000m result in reduced warfighter performance due to a lack of acclimatization. The exercise performance decrements are attributed to acute exposure to hypobaric hypoxia (HH), characterized by reduced arterial oxygen content and oxygen tissue delivery. The compound 5‐hydroxymethyl‐2‐furfural (5HMF), facilitates oxygen binding to hemoglobin (HgB) at low FiO2. Recent swine experiments in our lab demonstrated that 5HMF can increase oxygen‐HgB affinity, reduce cardiopulmonary decrements, and improve survival time during normobaric hypoxia (10% FiO2) exposure. The experiment determined if prophylactic treatment with 5HMF would mitigate hypoxia‐dependent decrements in exercise performance.METHODSCastrated Yorkshire swine (30–35kg, n=9) completed a one week treadmill familiarization protocol, followed by a baseline maximal exercise test (BET) consisting of staged increases in speed at a fixed 19% grade. Animals were randomized to receive IV infusion of either normal saline (VEH) or 5HMF (20mg/kg; 2hrs pre‐testing) and completed two additional maximal exercise tests during exposure to normoxic air (21% FiO2) (NET) and hypoxia (12% FiO2) (HET) on successive days. The same three tests (BET, NET, and HET) were completed the following week with the other IV treatment not used during the first testing week, allowing each animal to serve as its own control. Physiological parameters collected included cardiovascular and exercise performance during baseline, exercise, and recovery phases.RESULTSHET led to ~40% lower total exercise time compared to both normoxic tests [BET (p=0.001) and NET (p=0.001)] regardless of treatment. During NET, 5HMF resulted in a 7% greater peak workload (METS) than BET (p=0.02) that was not seen with VEH (p=0.07). During HET, 5HMF resulted in a similar mean workload as VEH (p=0.6), but reduced peak heart rate by 12% (p=0.04, n=4). Average heart rate during recovery from HET was 6% lower in swine administered 5HMF compared to recovery following NET (p=0.02).CONCLUSIONSThis study developed an exercise model in swine exposed to acute hypoxia that reliably reduced exercise performance. Using our model, we observed that 5HMF increased exercise capacity under normoxic conditions and preserved cardiovascular function during and immediately after exercising in severe hypoxic conditions. This work further demonstrates the utility of using an oxygen‐HgB affinity increasing compound (5HMF) to improve operational effectiveness and capabilities in high altitude environments without the need for prior acclimatization.Support or Funding InformationOffice of Naval Research, USUHS Grant, HU0001‐14‐1‐0008This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.