bluuebunny/crossref_metadata_2025_split huggingface dataset:
Behavioral Thermoregulation of Antarctic Teleosts With and Without Hemoglobin in Response to Acute Thermal Challenge
Authors: Ismailov Iskander I. , Scharping Jordan B. , Andreeva Iraida E. , Friedlander Michael J. 
Published: June 2021

Antarctic teleosts C. aceratus (lack hemoglobin, Hb−) and N. coriiceps (possess hemoglobin, Hb+) are extremely stenothermic and live in the Southern Ocean at temperatures near 0°C. While survival of both species is threatened by anthropogenic activities, it is thought to be more so for Hb− fishes which are less tolerant to temperature elevation than Hb+ animals. To examine behavioral thermoregulation of these fishes, freely swimming in a tank, we studied their responses to acute thermal stress. We found that both Hb+ and Hb− species follow generally similar strategy ‐ avoidance‐ and escape‐like transient bursts of locomotion interleaved by periods of relative motionless (possibly, an energy saving maneuver), with some species‐specific differences in onset, duration and intensity. Survival strategy of both species also includes a repertoire of respiratory modularity behaviors, some of which have been previously attributed to parental care in other species of fish. We also found that thermally triggered escape‐like fast S‐starts and C‐turns in N.coriiceps (but not slow C‐turns and withdrawals in C.aceratus) are lateralized. At high temperatures, total reversal (followed by a gradual loss) of lateralization was observed, which may indicate the onset of nervous system malfunction. We conclude that both Hb+ and Hb− Antarctic fishes undergo a variety of ambulatory and respiratory behaviors that appear to represent attempts to avoid and/or escape hazardous temperatures (and, possibly, to adapt to elevated temperatures within a limited range), all similarly sensitive and well‐orchestrated by the nervous system to prevent malfunction, that occurs only when rise in temperature is extreme and unescapable.Support or Funding InformationSupported by NSF ANT‐1341602.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Body Mass‐Specific Na, K‐ATPase Activity in the Medullary Thick Ascending Limb – Implications for Species‐Dependent Urine Concentrating Mechanisms
Authors: Aw Mun , Armstrong Tamara M. , Nawata Michele , Bodine Sarah N. , Oh Jeeeun J. , Wei Guojun , Evans Kristen K. , Shahidullah Mohammad , Rieg Timo , Pannabecker Thomas 
Published: June 2021

In general, the mammalian whole body mass‐specific metabolic rate correlates positively with maximal urine concentration (Umax), irrespective of whether or not the species have adapted to arid or mesic habitat. Accordingly, we hypothesized that the thick ascending limb (TAL) of a rodent with markedly higher whole body mass‐specific metabolism than rat exhibits a substantially higher TAL metabolic rate as estimated by Na, K‐ATPase activity and Na, K‐ATPase α1 gene and protein expression. The kangaroo rat inner stripe of the outer medulla exhibits significantly higher mean Na, K‐ATPase activity (~70%) compared to two rat strains (Sprague‐Dawley and Munich‐Wistar), extending prior studies showing rat activity exceeds rabbit. Furthermore, higher expression of Na, K‐ATPase α1 protein (~4–6‐fold) and mRNA (~13‐fold) and higher TAL mitochondrial volume density (~20%) were seen in the kangaroo rat compared to both rat strains. Rat TAL Na, K‐ATPase α1 protein expression is relatively unaffected by body hydration status or, as shown previously, by dietary Na, arguing against confounding effects from two unavoidably dissimilar diets: grain‐based diet without water (kangaroo rat) or grain‐based diet with water (rat). We conclude that higher TAL Na, K‐ATPase activity contributes to relationships between whole body mass‐specific metabolic rate and high Umax. With the combination of 70% greater Na, K‐ATPase activity and 50% greater total kidney mass:body mass ratio for the kangaroo rat compared to the rat, and assuming all other factors remain equal, the contribution of TAL Na, K‐ATPase activity to overall whole body metabolism would be about 2.5‐fold greater in the kangaroo rat compared to the rat. More vigorous TAL Na, K‐ATPase activity in the kangaroo rat than in the rat may contribute to its steeper Na and urea axial concentration gradients, adding support to a revised model of the urine concentrating mechanism, which hypothesizes a leading role for vigorous active transport of NaCl, rather than countercurrent multiplication, in generating the outer medullary axial osmotic gradient.Support or Funding InformationNIDDK DK083338 (TP) and DK110621 (TR), NSF IOS‐0952885 (TP), Joint DMS/NIGMS‐NSF DMS‐1263943 (TP), APS/NSF Fellowships (MA).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
AMPK affects thermal tolerance in decapod crustaceans
Authors: Lancor Pierce , Bucicchia Christina , Frederich Markus 
Published: June 2021

AMP‐activated protein kinase (AMPK) is a cellular master regulator of energy metabolism, that is activated during stress to ensure a stable ATP pool in the cell. Additional to substantial work on the role of AMPK in mammals, especially humans, it becomes increasingly clear that AMPK is also involved in multiple processes in marine invertebrates, like crustaceans. Following the Oxygen and Capacity‐Limited Thermal Tolerance Hypothesis (OCLTT) marine invertebrates' thermal tolerance is dependent on sufficient oxygen delivery to the tissues and subsequent cellular ATP supply. Recent work has shown AMPK activation during heat stress in the rock crab, Cancer irroratus and the lobster, Homarus americanus. However, heat stress did not activate AMPK in the green crab Carcinus maenas. In the current project we tested whether pharmaceutically activating AMPK prior to a heat stress affects subsequent thermal tolerance. We injected Metformin in C. irroratus and activated AMPK about 3 fold above control levels, without affecting HSP70 protein levels or glucose levels in the hemolymph, indicating that this treatment did not trigger a broader stress response. A subsequent progressive temperature challenge between 11 and 32°C led in the Metformin treated animals to a drop in the maximum heart rate from 150 to 100 BPM at 29 and 23°C (control vs. Metformin treated, respectively), and a drop of the critical temperature, indicated by a switch to anaerobic metabolism and lactate accumulation, from 30 to 26°C. Therefore, AMPK activation diminished thermal tolerance in C. irroratus. Injecting Metformin into C. maenas showed a 30% increase in AMPK activity in the gills, with no substantial increase in AMPK activity in the hepatopancreas or heart. First results on the effect on injecting another AMPK activator, AICAR, don't lead to a substantial increase in AMPK activity yet, and require further adjustments of the treatment protocol.Pharmaceutically activating AMPK and investigating the subsequent effect on stress tolerance will contribute to a mechanistic understanding of energy allocations during stress in the context of the dynamic energy budget framework.Support or Funding InformationSupported by a summer research fellowship from the American Physiological Society to P.L., and NSF grant DUE 1431955 to M.F.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Enteroglial adenosine A2B receptor signaling contributes to local cytokine production and delays functional recovery following acute inflammation in the mouse colon
Authors: Grubisic Vladimir , Eltzschig Holger K. , Gulbransen Brian D. 
Published: June 2021

Glial cells in the enteric nervous system (ENS) contribute to regulation of gut functions by modulating neural reflexes that control motility and secretion. Intestinal inflammation leads to gut dysfunction by inducing neuroplasticity in the ENS. The mechanisms that control local inflammation in the ENS are poorly understood. Resolution coincides with a thousand‐fold increase in adenosine production. Enteric glia express functional adenosine A2B receptors (A2BRs), but the role of glial activation by adenosine is unknown. We hypothesized that enteroglial A2BRs play a role in the progression of the ENS neuroinflammation. We tested our hypothesis by utilizing molecular genetics to ablate A2BRs in glial cells in Sox10::CreERT2+/−/A2BRf/f mice and acute colitis was induced by 2% dextran sodium sulfate (DSS) in drinking water for 7 days. We performed experiments 1 and 3 weeks post DSS treatment to assess the peak and recovery of inflammation. The degree of inflammation was evaluated by body weight change, macroscopic tissue damage, and immunohistochemistry to examine cellular changes in the ENS. Colonic epithelial functions and cytokine/chemokine production were assayed by Ussing chambers and plate array. At peak‐inflammation weight loss, macroscopic tissue damage, and infiltration of CD45+ cells at the level of the myenteric plexus were comparable between the Sox10::CreERT2+/−/A2BRf/f mice and their littermate controls (A2BRf/f). During the recovery, colon wall permeability of DSS‐treated A2BRf/f animals was significantly increased in comparison to their water treated controls, but not in colons from the Sox10::CreERT2+/−/A2BRf/f mice (P = 0.03 and 0.72, respectively, 2‐way ANOVA, water‐to‐DSS comparison). In addition, the ablation of enteroglial A2BRs protected against the DSS‐induced increase in colonic production of cytokines/chemokines at the peak of inflammation (G‐CSF, IL‐1a, IL‐6, IP‐10, MIG), during recovery (IL‐17), or both phases (eotaxin‐1, KC) [P ≤ 0.07 (A2BRf/f) vs P > 0.3 (Sox10::CreERT2+/−/A2BRf/f), 2‐way ANOVA, water‐to‐DSS comparison]. Together, our findings indicate that glial A2BR signaling modulates endogenous immune responses during acute colitis. Glial‐immune interactions mediated downstream of glial A2BR signaling could contribute to gut dysfunction following inflammation. These novel findings could be used in the design of new therapeutics for inflammatory bowel disease.Support or Funding InformationDr. Gulbransen's research is currently supported by grants from the Crohn's and Colitis Foundation (CCF; Senior Research Award) and the National Institutes of Health (NIH; RO1DK103723).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Case Study: A Possible Accessory Muscle of the Serratus Posterior Superior Muscle
Authors: Lashley Kerrie Samantha , Granite‐Cohn Guinevere 
Published: June 2021

Anatomical variation is defined as the normal range of possibilities in the topography and morphology of body structures. In contrast, congenital anomaly is any structural or functional anatomical finding beyond the normal range of possibilities. This case study describes a congenital anomaly found in a 73‐year old preserved Caucasian male.This individual presents an atypical left accessory neck muscle originating from the transverse process of the C1 (Atlas) vertebrae. It inserts at more than 90 degrees onto the serratus posterior superior (SPS) proximal attachment at the C7 level.Head and neck anatomical variations are also present in this individual, which include 4‐headed levator scapulae and 3‐headed splenius muscles bilaterally.It is thought that this anomaly is a result of embryologic development and it is hypothesize that the atypical neck muscle may reinforce the action of the SPS. Due to the rarity of this finding, a description of such a case is very infrequent in the literature. Identifying anatomical head and neck anomalies are important in understanding pathological and evolutionary implications in our species.Support or Funding InformationThe opinions or assertions contained herein are the private ones of the author/speaker and are not to be construed as official or reflecting the views of the Department of Defense, the Uniformed Services University of the Health Sciences or any other agency of the U.S. Government.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
L‐Arginine Prevents Heme‐Induced Acute Lung Injury (ALI) in a Rat Model of Trauma/Hemorrhage and Resuscitation with Transfusion
Authors: Johnson Fruzsina K. , Durante William , Johnson Robert A. , Rhodes Spencer A. , Stewart Ronald M. 
Published: June 2021

Resuscitation with long (> 28 days) stored packed red blood cells (PRBC) promotes acute lung injury (ALI) in our rat model of trauma/hemorrhage. Low nitric oxide (NO) production has been implicated in the development of ALI. Arginase can decrease NO production by decreasing L‐arginine availability for endothelial NO synthase (eNOS). We found that arginase, released from red blood cells (RBC) during prolonged storage, contributes to ALI in our rat model of trauma/hemorrhage. Prolonged storage also increases levels of free hemoglobin (Hb). Heme, a breakdown product of Hb, is metabolized by heme oxygenase to form carbon monoxide (CO). We were the first to report that heme‐derived CO inhibits endothelial nitric oxide (NO) synthase and promotes vasoconstriction in a manner that can be prevented by L‐arginine administration. This study tests the hypothesis that the hemolysis product, heme, promotes ALI in our rat model of trauma/hemorrhage and resuscitation with transfusion in a manner that is exacerbated by limited L‐arginine availability. Fresh PRBC were prepared from rat whole blood. Male Lewis rats were implanted with femoral arterial and venous catheters (trauma), subjected to a 30% hemorrhage and resuscitated with crystalloids and fresh PRBC containing heme alone or with L‐arginine or L‐lysine (competitive inhibitor of L‐arginine uptake). ALI was assessed by pulmonary protein leak (Evans blue dye ‐ EBD) and cytokine‐induced neutrophil chemoattractant‐1 (CINC‐1; rat homologue of human interleukin (IL)‐8) accumulation in bronchoalveolar lavage fluid (BALF). Heme alone caused a 5.6‐fold increase in pulmonary protein leak and 3.5‐fold increase in CINC‐1 accumulation. Co‐administration of L‐arginine decreased heme‐induced pulmonary protein leak by 77% and CINC‐1 accumulation by 32.4%. In contrast, L‐lysine, a competitive inhibitor of L‐arginine uptake, increased heme‐induced pulmonary protein leak by 102% and CINC‐1 accumulation by 106.4%. These data show that the Hb breakdown product, heme, promotes ALI in our rat model of trauma/hemorrhage and resuscitation with transfusion. L‐Arginine co‐administration protects against heme‐induced ALI, while blocking L‐arginine transport by L‐lysine exacerbates heme‐induced ALI. These results suggest that the other hemolysis product, heme, also contributes to ALI in a manner that is greatly exacerbated by decreased L‐arginine bioavailability. We conclude that hemolysis products arginase and heme work in concert to promote ALI during trauma/hemorrhage and resuscitation with transfusion.Support or Funding InformationSupported by grants AHA 0865241F (FKJ), NIH HL074966 (WD) and USAMRC DOD W81XWH‐07‐1‐0717 (RAJ, RMS).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Inhibitors Targeting IGF‐1r and mTOR Induce Synergistic Cell Growth Inhibition and Enhance Apoptotic Activity in Cancer Cell Lines
Authors: Warshamana‐Greene Gnana (Saku) , Panthi Asmita 
Published: June 2021

Insulin‐like growth factor I (IGF‐1) and its cognate receptor (IGF‐1r) show prominent molecular irregularities in many tumor types. Autocrine function for the growth factor is documented in multiple cancers and cell lines. In experimental settings the cell lines show a spectrum of dependency on IGF‐1. Presence of IGF‐1 inhibits programmed cell death with its activation of Akt through the PI3‐Akt‐mTOR signaling pathway. The inhibition extends to chemotherapy‐induced cell death as reported in instances where mammalian target of Rapamycin (mTOR) inhibitors are used pharmacologically for induction of apoptosis. We investigated the effects of concurrent targeting of IGF‐1r and mTOR with potent small molecule inhibitors in cancer cell lines that are dependent on IGF‐1 for cell growth. We show that the drug combination synergistically inhibited cell growth and induced apoptosis at inhibitor concentrations that are minimally toxic to normal lung fibroblast cells but potently inhibits PI3‐Akt activation.Support or Funding InformationUSDA/NIFA # SCX‐311‐17‐14 (1890 research program @SCSU)NIGMS/NIH IDeA SC INBRE P20 RR‐016461This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Intercellular junctions and endothelial permeability are regulated by cell chirality
Authors: Fan Jie , Ray Poulomi , Lu Yao Wei , Kaur Gurleen , Schwarz John J. , Wan Leo Q. 
Published: June 2021

Cell chirality is newly discovered as an intrinsic cell property characterized by the bias of cell polarizing along the left‐right axis. We have recently reported that the endothelial phenotype is right biased; however, little is known about its implications in vascular physiology. In this study, we measured chirality and permeability of human umbilical vein endothelial cells by utilizing micropatterning and transwell culture. Even with low‐level PKC activation, we observed a remarkable reversal of endothelial cell chirality, accompanied by a non‐monotonic change in the monolayer permeability. Using a co‐culture model and immunofluorescence‐based image analysis, we found that uniformity in cell chirality was important for endothelial barrier function such that chirality mismatch between adjacent cells resulted in disrupted cell‐cell junctions leading to increased permeability, which peaked when cell chirality was randomized in the endothelial monolayer. Pharmacological and genetic studies allowed us to determine that PKCα and PI3K/AKT mediated the switch of cell chirality, while other known vascular permeability factors such as VEGF, PAF, and histamine regulated permeability independent of cell chirality. Our study has demonstrated for the first time the role of endothelial cell chirality in vascular permeability regulation and provides unique opportunities for drug delivery across tightly connected cellular sheets.Support or Funding InformationThis work was supported by the National Institutes of Health (OD/NICHD DP2HD083961), National Science Foundation (CAREER CMMI‐1254656), American Heart Association (13SDG17230047), March of Dimes (MOD 5‐FY14‐111). Leo Q. Wan is a Pew Scholar in Biomedical Sciences (PEW 00026185), supported by the Pew Charitable Trusts.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Effects of Phenolic‐Enriched Raspberry Extracts and Raspberry Ketone (4‐(4‐ hydroxyphenyl)‐2‐butanone) on Obesity Prevention in a Mouse Model of Diet‐Induced Obesity
Authors: Kshatriya Dushyant , Yeomans Bryn L. , Li Xinyi , Guinta Gina , Bello Nicholas T. 
Published: June 2021

IntroductionRed raspberries (Rubus idaeus) contain numerous phenolic compounds with documented positive health benefits. One naturally occurring phenolic, raspberry ketone (4‐(4‐ hydroxyphenyl)‐2‐butanone), is considered the principle flavor component of red raspberries. Raspberry ketone, either as a sole or mixed ingredient, has been marketed as a weight loss supplement.ObjectiveTo investigate the metabolic signature associated with the weight preventative actions of a phenolic‐enriched raspberry extract compared with raspberry ketone in a diet‐induced obese mouse model.MethodsMale C57BL/6 mice (8 wk old) received a daily oral dose of vehicle (Veh; 50% propylene glycol, 40% water, and 10% DMSO), raspberry extract low (REL; 0.2g/kg), raspberry extract high (REH; 2g/kg) or raspberry ketone (RK; 0.2g/kg). Coincident with daily dosing mice were placed on a high fat diet (45% Fat kcal) for 4 wks. Feeding, hormonal, and metabolic endpoints were assessed.ResultsFor body weight gain, there was treatment effect [F (3, 59) = 5.7, p < 0.005] and treatment × time effect [F (81, 1593) = 5.5, p < 0.005]. On days 20–28, the RK had lower body weights (~9%) compared with Veh (p < 0.05 for all). On days 24–28, the REH had lower body weights (~7%) compared with the Veh (p < 0.05 for all). At the end of the 4 weeks, retroperitoneal [F (3, 55) = 4.8, p < 0.005], epidydimal [F (3, 55) = 10.6, p < 0.005], and inguinal [F (3, 55) = 6.8, p < 0.005] fat masses were lower (~25%) in the RK and REH compared with REL and Veh (p < 0.05 for all). There were no treatment differences in cumulative intake nor in meal patterns. Terminal plasma ghrelin levels [F (3, 57) = 3.5, p< 0.05] were lower (~44%) in REL, REH, and RK compared with Veh (p < 0.05), whereas corticosterone levels [F (3, 57) = 4.4, p <0.005] were elevated (~85%) in the REL compared with Veh (p < 0.05). Indirect calorimetry indicated the RER (VCO2/VO2) [F (3, 28) = 7.4, p < 0.01] was lower (~5%) in REL, REH, REH compared with Veh (p < 0.005 for all). Mean blood pressure [F (3, 148) = 3.0, p < 0.05] was increased in the RK (~19%) and REH (~14%) compared with Veh (p < 0.05 for both). In addition, heart rate [F (3, 148) = 4.2, p < 0.05] was increased in the REH (~30%), REL (~34%), and RK (~38%) compared with Veh (p < 0.05 for all).ConclusionRaspberry ketone and phenolic‐enriched extracts of red raspberries have potential to prevent diet‐induced weight gain by alterations in metabolism.Support or Funding InformationNIH R01 AT008933; USDA‐NIFA NJ06280This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.