bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cortical voluntary activation adjustments induced by non‐exhausting eccentric exercise (1125.2)
Authors: Girard Olivier , Racinais Sébastien , Banzet Sébastien , Koulmann Nathalie , Chennaoui Mounir , Drogou Catherine , Chalabi Hakim 
Published: June 2021

We tested the hypothesis that an eccentric exercise would exacerbate fatigue‐induced impairments in cortical voluntary activation and delay the recovery process, compared with a concentric‐matched trial. Fourteen males randomly performed two 30‐min walking exercises (velocity: 1 m.s‐1; grade: 25%; load: 12% of body weight), one downhill (DW) and one uphill (UP). Neuromuscular test sessions including tibial nerve and motor cortex stimulations during maximal isometric voluntary contractions of the plantar flexors were performed before and 3 min, 24 h, 48 h and 72 h post‐exercise. DW immediately reduced voluntary torque by 14.1% (P<0.001), while smaller strength losses occurred after UP (‐6.0%; P=0.15). Torque remained significantly depressed at least 3 days into recovery post‐DW (‐14.1%, ‐11.5% and ‐7.2% after 24 h, 48 h and 72 h, respectively; P<0.05). After exercise, cortical voluntary activation (‐15.9% vs. ‐8.5%; P<0.05) and resting twitch (‐42.6% vs. ‐30.2%; P=0.06) values were reduced below baseline with larger reductions after DW compared to UP, and were restored near baseline within 24 h. The capacity of the motor cortex to optimally drive the plantar flexors that accompanies peripheral fatigue is acutely impaired by non‐exhaustive eccentric exercise, but recovers within 24 h, and is therefore unlikely to explain the persisting reductions in voluntary strength capacity with the development of muscle soreness.Grant Funding Source: Supported by Aspetar and the French Délégation Générale pour l’Armement under contracts 07ca704
Systemic inhibition of AT1 receptors does not alter respiratory‐sympathetic synchronization in anesthetized rats (1130.13)
Authors: Favero Michele , Menezes Miguel , Yamamoto Kenta , de Paula Patricia , Menani Jose , Mifflin Steve 
Published: June 2021

Sympathetic nerve discharge contains a respiratory‐related rhythm.Arterial chemoreceptors possess angiotensin AT1 receptors which have been reported to increase chemoreceptor afferent discharge. To determine if angiotensin might modulate respiratory‐sympathetic interactions, we tested if synchronization between phrenic nerve activity (PNA) and renal sympathetic nerve activity (RSNA) would be altered by systemic blockade of AT1 receptors. Spectral analysis and cross correlation were used to examine the synchronization in anesthetized, vagotomized and mechanically ventilated Sprague‐Dawley rats (300‐400g, n=5). Intravenous injections of losartan (a selective angiotensin II type‐1 receptor (AT1)antagonist, 1 mg/ml/kg body weight) inhibited the increase in blood pressure following iv. angiotensin II injection (50 ng/0.1 ml) from 40±7 mmHg to ‐6±8 mmHg (n=5, P<0.05). Following losartan, we estimated coherence between spectral power of PNA and RSNA at central respiratory drive frequency, defined as frequency of the main peak in PNA before and after losartan injection. Losartan did not alter the spectral power of either PNA or RSNA (P>.05). Coherence did not differ before (0.78 ± 0.21) compared to after (0.72 ± 0.34) losartan. Phase difference also did not change before (0.21 ± 0.25) and after (0.20 ± 0.24) losartan. These results suggest that systemic inhibition of AT1 receptors does not alter respiratory‐sympathetic synchronization.Grant Funding Source: HL088052; CAPES (18890‐12‐1); FAPESP; CNPq
Reduced GABAergic synaptic transmission in the nucleus tractus solitarius in Mecp2‐null mice (1130.20)
Authors: Chen Chao‐Yin , Lin Yen‐Chu , Rogawski Michael , Lien Cheng‐Chang , Maezawa Izumi , Jin Lee‐Way 
Published: June 2021

Rett syndrome (RTT), a devastating neurodevelopmental disorder, is caused by loss‐of‐function mutations in the X‐linked methyl‐CpG binding protein 2 (Mecp2) gene. Respiratory dysfunction is one of the major clinical features, presumably due to defective GABAergic function because enhancing GABAergic transmission improved the respiratory phenotype and prolonged survival in RTT mice. We test the hypothesis that deficiency in Mecp2 gene reduces GABAergic signal transmission in the NTS where respiratory information is first received and integrated. Spontaneous inhibitory postsynaptic currents (sIPSCs) and miniature IPSCs (mIPSCs) were recorded from NTS neurons in brainstem slices obtained from age‐matched male Mecp2‐null mice and wild‐type littermates. Compared to those from wild‐type mice (n = 11 neurons), NTS neurons from Mecp2‐null mice (n = 12 neurons) had a left‐ward shift in cumulative probability of sIPSC amplitudes (p < 0.05) without significant changes in inter‐event intervals (p > 0.05). Similarly, there was a significant left‐ward shift in mIPSC cumulative probability of amplitudes (p < 0.05) but not inter‐event intervals (p > 0.05). The data are consistent with the hypothesis and suggest that reduced GABAergic signaling via post‐synaptic mechanism(s) in the NTS contributes to respiratory dysfunction in RTT.Grant Funding Source: supported by: 1R01 HD064817, International Rett Syndrome Foundation
Effect of an emetic gastrointestinal input on the processing of labyrinthine inputs by cerebellar rostral fastigial nucleus neurons (1130.7)
Authors: Catanzaro Michael , Miller Daniel , Cotter Lucy , McCall Andrew , Yates Bill 
Published: June 2021

Multiple inputs can elicit nausea and vomiting, including ingested toxins and vestibular signals. Amongst the nervous system regions believed to participate in generating motion sickness is the cerebellar rostral fastigial nucleus (rFN). In addition, there is evidence that gastrointestinal inputs are transmitted to rFN through a variety of pathways, including projections from the dorsal motor nucleus of the vagus and area postrema. These observations raise the hypothesis that GI inputs could change motion sickness susceptibility by altering the processing of labyrinthine inputs by rFN neurons. To test this hypothesis, we recorded activity from rFN neurons in decerebrate cats, and compared their responses to whole‐body rotations before and after the intragastric infusion of the emetic compound copper sulfate (CuSO4). Some (18%) rFN neurons had complex responses to vestibular stimulation, particularly responses to only one direction of rotation (known as STC behavior). Such complex responses would be expected in a brain area that participates in generating motion sickness. The spatial and temporal characteristics of these responses changed little after injection of CuSO4. Although infusion of CuSO4 affected gains of responses to rotations of ~25% rFN neurons, the effects were inconsistent (CuSO4 augmented responses in some cells and decremented responses in others). CuSO4 resulted in pronounced changes in responses to rotations of a significantly larger fraction (Chi‐squared test, p<0.05) of neurons in other brain regions that mediate nausea and vomiting, including the parabrachial nucleus and the “vomiting center” (caudal medullary lateral tegmental field). These data suggest that integration of vestibular and GI inputs by rFN neurons plays a limited role in affecting motion sickness susceptibility.Grant Funding Source: NIH grant R01‐DC03732
Femoral artery occlusion amplifies TRPA1 function in skeletal muscle sensory neurons (1132.5)
Authors: Xing Jihong , Lu Jian , Li Jianhua 
Published: June 2021

A prior study showed that transient receptor potential channel A1 (TRPA1) in thin‐fiber muscle afferents contributes to the amplified reflex autonomic responses observed in rats with femoral artery ligation. Thus, in this study we characterized current responses induced by activation of TRPA1 in skeletal muscle dorsal root ganglion (DRG) neurons of control limbs and limbs with 24 hrs of femoral ligation using whole‐cell patch clamp methods. Our results show that AITC (a TRPA1 agonist, 50‐200 µM) produced a dose‐dependent increase of amplitudes of inward current responses. Also, the peak current amplitude induced by AITC is significantly larger in DRG neuron of ligated limbs. There is no difference in size distribution of DRG neurons with AITC‐induced current responses between two groups. However, arterial occlusion increases the percentage of the AITC‐sensitive DRG neurons compared with control. AITC‐induced currents in DRG neurons are significantly attenuated by exposure to 10 µM of HC‐030031, a selective inhibitor of TRPA1. In addition, capsaicin (a TRPV1 agonist) evokes a greater increase in the amplitude of AITC‐currents in DRG neurons of ligated limbs. Overall, our data suggest that a greater TRPA1 function is developed in muscle afferent nerves with the hindlimb ischemia and TRPV1 is partly responsible for augmented TRPA1 responses induced by arterial occlusion.Grant Funding Source: NIH P01 HL096570 and AHA EIA 0840130N
Prenatal steroid exposure promotes expression of renal injury indices in African American females (1134.11)
Authors: Gwathmey TanYa , Chappell Mark , Nixon Patricia , Washburn Lisa 
Published: June 2021

Administration of steroids to expectant mothers at risk for pre‐term delivery is standard practice, but may have detrimental effects on kidney development and function in the offspring. African‐Americans (AA) experience higher rates of both pre‐term birth and kidney disease than other racial and ethnic groups, and the onset of kidney disease occurs much earlier in life for AA. This study examined the expression of specific markers of renal injury in a cohort of AA females (age 14) either born prematurely (<32weeks gestation) and exposed in utero to betamethasone (BMX; N=12), born prematurely but not exposed (PRE; N=18) or born at term (>37 weeks; N=12). In comparison to term AA, the oxidative stress marker 8‐Isoprostane tended to be higher in PRE [10.9 + 1.0 vs. 8.9 + 1.9 pg/g creatinine; P = 0.06], but was higher in the BMX cohort [13.1+ 1.6 pg/g creatinine; P < 0.05]. Angiotensinogen excretion, a biomarker for glomerular damage and precursor to the fibrotic and inflammatory peptide angiotensin II, did not differ between BMX and PRE [0.14+0.04 vs. 0.12+0.04 ng/g creatinine], but was higher than in term subjects [0.06+0.01 ng/g creatinine; P<0.05]. While urinary angiotensin II tended to be higher in BMX [0.20+0.09 pg/g creatinine], no significant differences were observed between groups [PRE: 0.07+0.01 vs. Term: 0.11+0.06 pg/ g creatinine]. The microalbumin/creatinine ratio was higher in PRE [0.25+0.18 mg/g] and BMX [0.25+0.13 mg/g] as compared to term [0.04+0.01 mg/g]. In summary, we show that pre‐term birth is associated with increased expression of urinary 8‐Isoprostane, angiotensinogen and microalbumin, and is exacerbated by prenatal exposure to betamethasone. These findings suggest preterm birth and the accompanying prenatal steroid exposure may result in an increased susceptibility to renal injury and that indices of damage can be detected early during adolescence.Grant Funding Source: Supported by AHA 12CRP9390000 and HD047584
Podocyte NLRP3 inflammasome activation and glomerular injury by adipokine visfatin: in vitro and in vivo evidence (1134.7)
Authors: Boini Krishna , Xia Min , Abais Justine , Li Pin‐Lan 
Published: June 2021

NLRP3 inflammasome formation and activation have recently been reported to be an important early mechanism responsible for glomerular inflammation and injury in obese mice. However, the precise mechanism of obesity‐induced NLRP3 inflammasome activation remains unknown. The present study explored whether adipokine visfatin mediates obesity‐induced podocyte NLRP3 inflammasome activation and consequent glomerular injury in in vitro and in vivo models. Confocal microscopic analysis showed that visfatin treatment increased the colocalization of NLRP3 with Asc or caspase‐1 in podocytes indicating the formation of NLRP3 inflammasomes. This visfatin‐induced inflammasome formation was abolished by pretreatment of podocytes with Asc siRNA. Correspondingly, visfatin treatment significantly increased the caspase‐1 activity and IL‐1β production in podocytes, representing activation of NRLP3 inflammasomes, which was significantly attenuated by Asc siRNA. Further RT‐PCR and confocal microscopic analysis demonstrated that visfatin treatment significantly decreased the podocin expression (podocyte damage), and Asc siRNA transfection attenuated this visfatin‐induced podocin reduction. Similar findings were observed in mouse model in vivo. It was shown that visfatin infusion induced NLRP3 inflammasome formation and activation in glomeruli of Asc+/+ mice, but not in Asc‐/‐ mice. Further functional studies found that visfatin infusion significantly increased the urinary albumin and protein excretion in Asc+/+ mice compared to Asc‐/‐ mice. Fluorescent immunohistochemical examinations using podocin and desmin as podocyte injury markers showed that the inflammasome formation induced by the visfatin were mostly located in podocytes as demonstrated by co‐localization of NLRP3 with podocin or desmin. Based on these results, it is concluded that visfatin induces NLRP3 inflammasome formation and activation in podocytes and thereby results in glomerular injury and sclerosis.Grant Funding Source: supported by NIH grants DK54927 and HL‐75316
The endoplasmic reticulum stress inhibitor, 4‐phenylbutyrate, attenuates chronic kidney disease induced by a model of cardiorenal syndrome (1136.12)
Authors: Carlisle Rachel , Ask Kjetil , Dickhout Jeffrey 
Published: June 2021

Endoplasmic reticulum stress has been identified as a feature of chronic kidney disease and appears to be associated with proteinuria. We have found the endoplasmic reticulum stress inhibitor, 4‐phenylbutyrate (4‐PBA), reduced renal damage in a mouse model of acute kidney injury. Therefore, we hypothesized that inhibition of endoplasmic reticulum stress through augmenting protein folding with a low molecular weight chemical chaperone, 4‐PBA, would attenuate chronic kidney disease. Chronic kidney disease was induced in uninephrectomized wild type mice. After recovery from uninephrectomy, an angiotensin II infusion pump (1.5 ng/min/g) and a deoxycorticosterone (DOCA) pellet were subcutaneously implanted and mice were provided with 1% NaCl in the drinking water for three weeks. Blood pressure was measured and animals were placed in metabolic cages for 24 h urine collection bi‐weekly, starting one week prior to uninephrectomy. Co‐treatment with 4‐PBA (1 g/kg/day) prevented angiotensin II/DOCA/salt‐induced hypertension, cardiac hypertrophy, proteinuria, and kidney injury, as demonstrated by reduced α‐smooth muscle actin expression, protein cast formation and damaged glomeruli. However, 4‐PBA‐treated mice suffered from significantly higher mortality rates. Inhibition of cardiac hypertrophy by 4‐PBA may have been the cause of the increased mortality through congestive heart failure. Despite the higher mortality rate in 4‐PBA‐treated mice, we conclude that 4‐PBA prevents hypertension, proteinuria, cardiac hypertrophy, and chronic kidney disease in this angiotensin II/DOCA/salt model of cardiorenal syndrome.Grant Funding Source: Supported by CIHR OSO‐115895.
Minimal piggyBac vectors for chromatin integration (1138.12)
Authors: Solodushko Victor , Troyanovsky Boris , Bitko Vira , Fouty Brian 
Published: June 2021

We describe novel transposon piggyBac vectors engineered to deliver transgenes as efficiently as currently available piggyBac systems, but with significantly less helper DNA co‐delivered into the host genome. To generate these plasmids, we identified a previously unreported aspect of transposon biology, that the full‐length terminal domains required for successful plasmid‐to‐chromatin transgene delivery can be repositioned from the transgene delivery cassette to the other (helper) parts of the plasmid. This design decreased the size of the required terminal domains within the delivered gene cassette of the piggyBac vector from about 1,500 to just 98 base pairs. Herein we tested the transposition efficiency of these minimal piggyBac transposons on different cell types: HEK293, HeLa, L929, and primary pulmonary artery smooth muscle cells. Transposition efficiency was defined as transgene (RFP) positivity at 28 days. The specificity of integration was determined by PCR and qPCR. Conclusion: Relocating most of the long terminal‐repeat sequences from the delivered gene cassette of minimal piggyBac vectors into the helper region of the same plasmid decreased the amount of non‐essential (helper) DNA incorporated into the host cell genome without a significant decrease in transposition efficiency. This may reduce the risk of target cell transformation.Grant Funding Source: Supported by the American Heart Association to V.S. (12GRNT12070291)
Levels of antioxidant activity and oxidative stress in metabolic syndrome Puerto Rican participants (1138.9)
Authors: Collazo‐Roman Marielys , Muñoz‐Forti Kevin , Gonzalez Adrian , Jimenez Giselle , Mangual Roberto , Perez Yamilette , Quintana Xiomara , Rodriguez Juan , Pérez‐Cardona Cynthia , Ferder Leon , Suarez‐Martinez Edu B. 
Published: June 2021

Metabolic syndrome (MetS) is defined as a of cluster factors that increase the risk of cardiovascular diseases. The criteria for diagnosis for MetS include increased triglycerides, reduced HDL cholesterol levels, raised plasma glucose concentration, and body mass index > 30 kg/m2. In the Puerto Rican population the prevalence of MetS is estimated in approximately 43.3%. Some studies suggested that MetS is linked to higher levels of oxidative stress (OxS). However, there is no data available using OxS markers at Puerto Rican community. Our objective was to determine levels of oxidized lipids and the activity of antioxidant enzymes Glutathione Peroxidase (GPx) and lipid peroxidation. We further expect to evaluate if there is there exist an association between the obtained levels and the presence of MetS in a Puerto Rican population. We hypothesized GPx activity will be significantly lower in participants with MetS and that lipid peroxidation will be higher in these persons. Data was analyzed using Prism Graph Pad and SPSSv12.0 Softwares. Our preliminary results showed no significant differences in plasma lipid peroxidation (n=224; p=0.229) and GPx (n=70; p=0.163). This study is important because excessive accumulation of oxidative molecules may be prevented by ingesting antioxidant supplements and this may create awareness of the consequences of the MetS and the potential benefit of intaking antioxidants.Grant Funding Source: Support by R25GM096955 (NIH RISE Program)
Peculiarities of trichophytia epidemiology in Astana (1139.4)
Authors: Batpenova Gulnar , Kazieva Aliya , Dzhetpisbaeva Zulfiya , Pshembaeva Saule 
Published: June 2021

To study the epidemiological aspects of the trichophytia in Astana Materials: The analysis of reported cases of Trichophytia in Astana from 2007 to 2011.It should be noted that since 2007 (23 cases) to 2010 (267 cases) there was an increasing of more than 10 times, and in 2011 the number of patients has decreased to 151. Analysis of gender showed an absolute predominance among male patients, almost 2 times. For example, in 2007, men were infected trichophytia ‐ 15 and women 8. In 2010: men ‐ 172, women ‐ 95, in 2011 there were 100 male patients, 51 woman. The average age of the patients was ‐ 20 years. 10%(62) of the patients were married. It is should be noted prevalence of sexual infection in 39% (243), 14%(87) were infected when caring for pets and cattle. In 31% (193) the source of infection is not known. 6%(37) were infected through household items from patients trichophytia.Social status of the patients was as follows : 174 ( 28 %) ‐ the unemployed, 124 (20%) employees, about the same workers, and 15% (93)‐ pupils and students, reported cases of Trichophytia among the private entrepreneurs and military ‐ 2 (0.3 %) and 1 (0.16%), respectively.Thus, the current trend towards an increased incidence of Trichophytia preserved. This pathology is most often affects children and young adults . Among the modes of transmission, in recent years, often indicates a sexual way, which requires strengthening health education among young people.
Aliskiren effects upon prorrenin/renin receptor expression on heart and kidney in 5/6 nephrectomy‐induced hypertension in rats (1140.12)
Authors: Lopez Pedro , Anguiano‐Robledo Liliana , Avila‐Ramirez Massiel Alfonsina 
Published: June 2021

Prorrenin / renin receptor (PRR), a new element of the renin‐angiotensin system has been implicated in development and progression of cardiovascular and renal diseases. Recently, Aliskiren, a direct renin inhibitor, has been used to treat these diseases. The aim of this work was to study Aliskiren effects upon PRR expression in cardiac and renal tissue during 5/6 nephrectomy‐induced hypertension. Male Wistar rats underwent 5/6 nephrectomy (5/6 Nx) or sham operation (S). Both groups received Aliskiren, 10 mg/kg/day, po, throughout the experiment. Control groups received vehicle. Seven days later, 24‐hour urine was collected and blood pressure was measured. PRR expression was determined by immunoblot. Our results showed that, compared to sham animals, 5/6 Nx rats treated with Aliskiren had lowered blood pressure and improved creatinine seric values, proteinuria and creatinine clearance. We found in nephrectomized rats that PRR increased seven days after surgery in heart and kidney, and aliskiren reduced PRR expression in both tissues. These results confirm the antihypertensive and renoprotective effects of aliskiren and interestingly, showed that aliskiren modifies PRR expressionGrant Funding Source: Supported by SIP20130546
α1D‐Adrenoceptors blockade revert angiotensin II‐dependent vascular remodeling in rats (1140.7)
Authors: Gallardo‐Ortíz Itzell , Rodríguez‐Hernández Sandra , López‐Guerrero Juan , Villalobos‐Molina Rafael 
Published: June 2021

We explored the cardiovascular effects of angiotensin II (Ang II) continuous infusion focusing on α1A/1D‐adrenoceptors (α1‐ARs) functional expression, and hypertrophy in aorta and tail arteries of Wistar rats. Minipumps filled with Ang II (200 ng/kg/min), were implanted in male Wistar rats during 4 weeks. Some rats were co‐treated Ang II+losartan, AT1R blocker, or Ang II+BMY7378, α1D‐AR antagonist starting after 2 weeks maintaining the Ang II infusion for 2 more weeks. The systolic blood pressure (SBP) was measured by tail‐cuff; at 4 weeks aorta (α1D‐AR vessel) and tail (α1A‐AR vessel) were isolated for functional and structural analyses. Ang II increased SBP (209±8 vs 115±2 mmHg). Phenylephrine‐induced contraction in aorta was ≍45% higher in Ang II‐treated rats; while in tail responses were similar among all groups. Ang II hypertrophied aorta, whereas no change occurred in tail artery. Losartan reversed hypertension and hypertrophy in aorta; while BMY reversed hypertrophy without modifying hypertension. Data indicate that Ang II‐induced hypertrophy in aorta involves AT1R and α1D‐AR, but not α1A‐AR. Ang II‐induced α1D‐AR‐mediated vascular remodeling occurs independently of hypertension. These findings identify a α1D‐AR‐sensitive mechanism in the hypertrophy induced by Ang II; however, this effect is independent of blood pressure elevation.Grant Funding Source: Grant IN214812 PAPIIT, DGAPA, U.N.A.M.