bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of a short‐term group fitness intervention on body composition and exercise motivation in college students
Authors: Hamre Megan , Hongu Nobuko , Lee Vinson R. , Welter Gale S. , Farr Joshua Nicholas , Going Scott B. 
Published: June 2021

The purpose of this study was to test the impact of a short‐term group fitness intervention on body weight, percent body fat, and attitude toward physical activity in college students. Twenty sedentary students (mean age 20.4±1.4 yr) were classified as healthy or overweight (BMI >25 kg/m2) and, then randomized into exercise and control groups. The exercise group participated in four aerobic fitness classes per week for 4 weeks, while the control subjects remained sedentary. Percent body fat was measured by BodPod and attitude toward physical activity was measured via questionnaire at baseline and the end of the study. Using univariate analysis of variance, we found significant differences in change in percent body fat between the healthy‐control and overweight‐control groups (−1.1 ± 0.8 vs. 1.8 ± 0.9%, P=0.034) and between the healthy‐exercise and the overweight‐control groups (−2.2 ± 1.0 vs. 1.8 ± 0.9%, P=0.010). These findings support the notion that even at a young age, overweight individuals are more susceptible to weight gain and may need increased amounts of exercise or encouragement in addition to restricted diets to produce weight loss. Using the motivation questions, 80% of participants reported that group fitness provided motivation to continue exercise.Supported by the University of Arizona Honors College and The Marshall Foundation.
Dietary vitamin D3 at 10 fold the adequate intake may attenuate disease severity in the transgenic G93A mouse model of ALS
Authors: Gianforcaro Alexandro , Hamadeh Mazen J 
Published: June 2021

BackgroundAmyotrophic lateral sclerosis (ALS) is a paralytic and fatal neurodegenerative disease due to motor neuron death. Vitamin D3 mitigates the severity of autoimmune and neurodegenerative diseases that share some common pathophysiologies with ALS.ObjectiveTo determine the effects of dietary vitamin D3 on functional and disease outcomes and lifespan in the transgenic G93A mouse model of ALS.MethodsStarting at age 40 d, 24 G93A mice (7 F, 17 M) were assigned to a diet with either adequate (AI; 1 IU D3/g feed) or high (HiD; 10 IU D3/g feed) vitamin D3.Preliminary ResultsAround disease onset, HiD‐F had 60% higher ability to move and 40% higher body condition vs AI‐F (P < 0.001, for both). HiD‐F (19 ± 4 d) had 26% prolonged progression to endpoint from onset vs AI‐F (15 ± 0 d), albeit not significant (P = 0.179). HiD mice had 26% lower cumulative clinical scores vs AI mice (28 ± 2 vs 38 ± 1; P = 0.072). Within females, HiD had 43% lower cumulative clinical scores vs AI (21 ± 6 vs 36 ± 8; P = 0.097). Males reached disease onset 2.8 fold faster (HR, 95% CI: 2, 11; P = 0.004) and endpoint 2.4 fold faster (HR, 95% CI: 1, 12; P = 0.025) vs females.ConclusionVitamin D3 at 10 fold the adequate intake may attenuate disease severity in the transgenic G93A mouse model of ALS, and improve functional outcomes in females. Supported by NSERC and Faculty of Health‐YORK U.
Bowel Carcinoma Proliferative Activity in a model of experimental
Authors: Carvalho Sa Pedro , Cavalcanti Karen , Coelho Nuno , Souza Ivone Antonia , Cabrita Antonio Silverio 
Published: June 2021

Insecticide 1‐naphtyl N‐methylcarbamate (1NC) has a wide spectrum action and is considered of low toxicity when applied according with the good practice rules. The present work was designed to evaluate morphology and proliferation rates of experimentally induced adenocarcinomas.30 Wistar 8 weeks old male rats were randomly distributed into three groups to be submitted to dimethylhydrazine (DMH) 15mg/week during 8week. Group II, to 1NC 60mg/l in drinking water during 8weeks. Group III, and without manipulation â€“ Group I. All the animals were sacrificed by the end of the 28th week.Group I rats had no colonic adenocarcinomas while groups II and III exhibited exophytic lesions with wider diameter between 2 and 4 cm. All were well differentiated adenocarcinomas except for one case 1NC induced that was moderately differentiated. Proliferation rate validated by PCNA immunohistochemical study showed to be higher in Group III: 6 negative cases in Group II against 3 negative cases in Group III; the cut off applied + (< 25% positive nuclei), ++ (25 % –75% positive nuclei) and 3+ (> 75% positive nuclei) demonstrated 5 cases of ++ and 3+ in Group III and 1 case 3+ in Group II as the other 3 cases had proliferation rate of +. Despite the small sample explored in this preliminary study, 1NC revealed to induce more aggressive adenocarcinomas validated by higher proliferation rate when compared with the DMH induced cases.
Colon Carcinogenesis p53 Dependent
Authors: Coelho Nuno , Sa Pedro , Alarcao Ana , Teixeira Lia , Cabrita Antonio Silverio 
Published: June 2021

Insecticide 1‐naphtyl N‐methylcarbamate (1NC) has a wide spectrum action and is considered of low toxicity when applied according with the good practice rules. The present work was designed to evaluate morphology and proliferation rates of experimentally induced adenocarcinomas.Thirty Wistar 8 weeks old male rats were randomly distributed into three groups (10 rats each), to be submitted to dimethylhydrazine (DMH) 15mg/week during 8weeks – Group II, to 1NC 60mg/liter in drinking water during 8weeks – Group III, and without manipulation – Group I. All the animals were sacrificed by the end of the twentyeighth week.Group I rats had no colonic adenocarcinomas while groups II and III exhibited exophytic lesions with wider diameter between 2 and 4 cm. All were well differentiated adenocarcinomas except for one case 1NC induced that was moderately differentiated. Apoptosis was validated by p53/DO7 immunohistochemistry and showed to be higher in Group III cases (1NC induced): 6 positive cases against 1 positive case in Group II; the cut off applied + (< 25% positive nuclei), ++ (25 – 75% positive nuclei) and +++ (> 75% positive nuclei) demonstrated to be useful but only one case was ++ in Group III.Despite the small sample explored in this preliminary study, 1NC carcinogenesis has to be someway related with apoptosis blockage.
Effect of Nigella Sativa on Carbon Tetrachloride and Paracetamol Induced hepatotoxicity: Role of Antioxidant Enzymes and Cytokines
Authors: Barakat Mervat kamel , Oda Naglaa Raafat , Bayoumy Fatehia Ali , Bayoumy Fatehia Ali 
Published: June 2021

ObjectiveTo investigate the possible protective effect of Nigella Sativa oil (NSO) on carbon tetrachloride (CCL4) and paracetamol (Para) induced hepatotoxicity in view of correlation with antioxidant enzymes and cytokines.Material and Method40 male albino rats (150–200 gm) were divided equally into 5 groups:group A (control), B (Para treated), C (Para+ NSO treated), D (CCL4 treated), E (CCL4+ NSO treated). Blood samples for estimation of liver enzymes. Liver tissues were used for histopathology study and biochemical assays of antioxidant enzymes Superoxide dismutase (SOD), Catalase (CAT), and Glutathione S‐transferase (GST), and proinflammatory cytokine (IL‐1á).ResultsThe plasma activity of Liver enzymes was significantly increased after treatment with CCL4, and Para. Their level was statistically decreased in rats pretreated with NSO. Tissue activity of GST was significantly higher in group of C as compared to B while SOD and Cat were significantly increased group E as compared to D. IL‐1 á was significantly increased in group E as compared to all groups.Conclusionsour results suggest the potential protective role of NSO in CCL4 and Paracetamol induced hepatotoxicity through selective increase of antioxidant enzymes.
A novel proadrenergic effect of cardiac natriuretic peptides: inhibition by histamine H3‐receptor activation
Authors: Chan Noel Yan‐Ki , Seyedi Nahid , Levi Roberto 
Published: June 2021

Natriuretic peptides (NP) are generally viewed as cardioprotective. Yet, NP were recently found to increase myocardial infarct size in mice, while their deletion decreased it. Further, a recombinant NP (nesiritide) was shown to increase death risk in heart failure patients. Excessive norepinephrine release may have been pivotal in these unexpected events. Thus, we questioned by which mechanisms NP could exert a pro‐adrenergic effect and whether this could be inhibited by histamine H3‐receptor (H3R) activation. NP treatment of sympathetic nerve endings isolated from guinea‐pig hearts (cardiac synaptosomes) and NGF‐differentiated PC12 cells markedly increased cAMP levels and PKA activity, thus promoting catecholamine exocytosis. These pro‐adrenergic effects derived from a cGMP/PKG‐mediated prevention of cAMP hydrolysis by PDE3. Activation of H3R, constitutively expressed in synaptosomes and permanently transfected in PC12 cells, inhibited NP‐induced catecholamine release and prevented the increases in cAMP levels and PKA activity. These effects most likely resulted from a H3R‐mediated enhancement of PDE3 activity and/or PKG inhibition. These findings elucidate new means to control catecholamine exocytosis in the heart, and may foster the design of new agents (e.g., selective H3R agonists) to enable a safe and effective treatment of congestive heart failure with NP.This work was supported by NIH Grant HL 034215 and by a PhRMA Pre‐doctoral fellowship.
Hypothalamic‐Pituitary‐Adrenal Feedback Regulation
Authors: GOVINDAN MANJAPRA VARIATH 
Published: June 2021

The hypothalamic‐pituitary‐adrenal axis (HPA) is regulated by corticotrophin‐releasing hormone (CRH), arginine vasopressin (AVP) and by glucocorticoids. In response to stress, the neuroendocrine system releases CRH and AVP to regulate adrenocorticotropin (ACTH) hormone secretion from the anterior pituitary and glucocorticoids from the adrenal cortex. Increasing levels of circulating glucocorticoids downregulate the synthesis of the glucocorticoid receptor (GR) in various tissues in an endocrine feedback loop and produce inhibitory effects on the secretion of CRH and ACTH (4, to bring back the system to its resting state. Despite this wealth of information, the precise mechanism of feedback regulation remains elusive.We have identified FBR sequences in the human GR gene promoter and examined the roles of GR, CREB and HDAC‐6 in the negative feedback regulation associated with promoter elements of the human GR gene. We have demonstrated that the enhancer and suppression activities contained within the promoter elements of the GR gene occur through the interaction of GR and the active recruitment of HDAC‐6 and phosphorylated CREB (CREB‐P) by the ligand bound GR. We demonstrated a direct involvement between GR, CREB and HDAC‐6 in the feedback regulation.In the cortisol depleted state, phosphorylated CREB binds to the CRE in the composite feedback regulatory element and CBP/p/CAF complexes. This interaction results in the acetylation of core histones and chromatin decondensation which turns the GR gene on. In the presence of active glucocorticoids, nGRE recruits GR‐ligand complexes which tether HDAC‐6 and phosphatase complexes. The GR‐DEX bound HDAC‐6 deacetylates core histones and the GR‐DEX tethered phosphatase dephosphorylates CREB‐P. Deacetylation leads to chromatin condensation and dephosphorylation of CREB‐P which results in its removal from the CRE which turns GR gene off.
Triarylmethane‐34 (TRAM‐34), inhibitor of Ca2+‐activated K+ channels of intermediate conductance, is a potent blocker of gap junctions
Authors: Figueroa Xavier F , Gaete Pablo S , Sáez Juan C , Riquelme Manuel 
Published: June 2021

Ca2+‐activated K+ channels of intermediate conductance (IKCa) and gap junctions (GJs) between endothelial and smooth muscle cells have been proposed to play a central role in the vasodilator response mediated by the endothelium‐derived hyperpolarizing factor (EDHF). Although TRAM‐34, the IKCa channels blocker, has emerged as an important pharmacological tool for studying EDHF‐mediated responses, its effect on GJs has not been described. We analyzed intercellular communication and cellular distribution of the GJ protein subunit, connexins (Cxs), in HeLa cells transfected with Cx43 or Cx43 conjugated to EGFP. Treatment with 10μM TRAM‐34 induced a time dependent reduction in dye coupling to Lucifer yellow; the average number of coupled cells observed in positive tests was reduced by ~50% after 20 min and abolished after 70 min. Dye coupling was recovered to control 30 min after TRAM‐34 wash out. The reduction in GJ communication was not associated with changes in levels or distribution of Cx43‐EGFP. Therefore, TRAM‐34, in addition to inhibit IKCa channels, also potently blocks the cell‐to‐cell communication mediated by the GJ protein Cx43 that is an important connexin involved in the coordination of resistance vessel function.VRAID 15/2009, FONDEF D07I1086.
AcSDKP Reduces Collagen Crosslinking, MMP and NFKB Expression in Angiotensin II Induced Hypertension
Authors: Gonzalez German Esteban , Nakagawa Pablo , Liu Yunhe , Liao Tang‐Dong , Yang Xiao‐Ping , Rhaleb Nour‐Eddine , Carretero Oscar A. 
Published: June 2021

We hypothesized that N‐acetyl‐Ser‐Asp‐Lys‐Pro AcSDKP not only reduces fibrosis but also crosslinking. Moreover we tested whether it increases MMP, which has antifibrotic effects and whether it reduces NFκB in the heart. Lewis rats were divided in 4 groups (n=6, each): 1 (control); 2 (AngII 750…g/kg/day); 3 (AcSDKP 800…g/kg/day); and 4 (AngII+AcSDKP). Systolic blood pressure (mmHg) was recorded for 3 weeks. After 3 weeks crosslinking was quantified by measuring total (TC), insoluble (IC) and soluble (SC) collagen (μg/mg dry weight tissue) and MMP2 activity (% respect to 1) in cardiac tissue. NFκB activity was quantified (EMSA assay).Results(X±SEM)

Control
AngII
AcSDKP
AcSDKP+AngII

BP
125±3
202±15*
122±3
205±8*

TC
11.7±1.3
19.0±1.8*
12.5±1.5
13.0±0.9#

IC
9.5±1.3
16.3±1.6*
10.7±1.3
10.0±0.9#

SC
2.0±0.2
2.7±0.7
1.7±0.4
2.9±0.7

MMP2
100.0±19.2
101.9±13.0
74.9±13.1
139.6±19.5†

NFκB
11.5±1.4
24.4±1.8*
15.0±3.5
15.7±2.0#

p<.05 vs G1 and 2 respectively;
p=.094vsG2

ConclusionAcSDKP decreased crosslinked collagen which is important for reducing myocardial stiffness in hypertension. MMP2 activity tends to increase, and may have a small role in the antifibrotic effect of AcSDKP. Also, AcSDKP decreased NFκB suggesting that its antiinflammatory effect may be mediated by reducing this factor. Grant#: NIH HL028982 to OAC
Using team‐based learning (TBL) approach in teaching cardiovascular physiology to first‐year osteopathic medical students
Authors: Ioudina Marina V , Guadagnoli Jutta , Miller Terrence 
Published: June 2021

BackgroundTUNCOM physiology is a lecture based course augmented by small group exercises and class presentations. Group exercises were deemed ineffective: they did not lend themselves to objective student assessment, and did not develop integration and application skills.PurposeTBL was implemented to address group exercise shortcomings.MethodsThe cardiovascular (CV) system for the past 2 years consisted of lectures, self‐ and group‐ study of objectives, and a TBL session utilizing traditional tools: individual and group readiness assurance tests (IRAT, GRAT); group application problems (GAP); and peer evaluation. Multiple faculty members developed each TBL tool. The system concluded with a multiple choice exam.ResultsGRAT (88%) and GAP (86%) scores were significantly higher than IRAT (68%), P<0.001. The mean system exam score did not differ from that of the exam given in the year preceding TBL (P= 0.611).ConclusionStudents learned objectives equally well before and after TBL implementation as evidenced by system exam results, but GRAT and GAP performance indicated that TBL improved integration and application skills. TBL offered objective, measurable outcomes for student assessment.
Differential regulatory response for the Δ9 desaturase in Saccharomyces cerevisiae based on fatty acid species and intracellular amount (1000.3)
Authors: Schriemer Clara , Willey Marshall , Ochs Matthew , Hillers Lauren , McDonough Virginia 
Published: June 2021

The OLE1 gene in Saccharomyces cerevisiae encodes the ∆9 desaturase, which inserts a double bond in saturated fatty acids to create unsaturated fatty acids (UFAs). OLE1 expression is controlled in part through the transcriptional regulators Mga2p and Spt23p in response to supply of UFAs. We investigated whether the regulation was uniform in response to different UFAs and at different concentrations. We found that in wild type cells, reporter gene assays show a stronger decrease in expression of OLE1 when fed 16:1∆9 or 18:2∆9, 12 as opposed to 18:1∆9 or 17:1∆10. Concentration of the fed fatty acid also impacted the regulation of OLE1 with higher levels of each UFA impacting expression to a greater degree. Fatty acid profiles of wild type cells show cells accumulate a higher concentration of 16:1∆9 and 18:2∆9, 12 than fed 18:1∆9 or 17:1∆10. This leads to the conclusion that the expression of OLE1 is dependent both on properties of fed fatty acids and the amount in the cell. While our initial hypothesis was that OLE1 is regulated in response to membrane fluidity, subsequent work does not support that idea. We have found that conditions that would affect membrane fluidity (besides UFA species and amount), such as growth temperature and saturated or trans fatty acid supplementation do not regulate OLE1 in the direction predicted by fluidity changes. Recently our lab has isolated a mutant that is deficient in regulation of OLE1, called nro1 (no regulation of OLE1). The signaling mechanism for the NRO1 protein’s action is unknown. Tests using the OLE1 promoter‐reporter gene constructs suggest that Nro1p responds more strongly to the fatty acids 16:1∆9 and 18:2∆9, 12, than 18:1∆9 and 17:1∆10. Characterization of NRO1 is discussed.Grant Funding Source: Supported by NSF‐REU DBI‐0754293
Palmitate‐induced alterations in phospholipid composition promote ER stress and cellular dysfunction in hepatic lipotoxicity (1001.2)
Authors: Leamy Alexandra , Egnatchik Robert , Shiota Masakazu , Jacobson David , Young Jamey 
Published: June 2021

Lipotoxicity induced by saturated fatty acid (SFA) accumulation has been postulated as a contributing factor in the pathogenesis of diseases such as non‐alcoholic fatty liver disease (NAFLD) and type II diabetes. Our central hypothesis is that overexposure to SFAs results in increased saturation of ER membrane phospholipids, which induces ER stress marked by calcium efflux and CHOP overexpression, ultimately culminating in apoptosis. Our objective is to determine how perturbations of pathways involved in lipid metabolism modulate SFA‐induced lipotoxicity, as assessed by measurements of phospholipid (PL) composition, ER stress, reactive oxygen species (ROS) accumulation and apoptotic cell death. Using the calcium chelator BAPTA, we suppressed downstream markers of lipotoxicity such as ROS accumulation and caspase activation, but were unable to prevent ER dysfunction. Interventions designed to reduce PA incorporation into PLs by increasing triglyceride synthesis resulted in elevated levels of lipid accumulation but significantly reversed PA‐induced increases in PL saturation, abnormalities in ER membrane structure and homeostasis, and all other phenotypic markers of hepatic lipotoxicity. Our data indicate that by modulating alternative pathways of hepatic lipid metabolism upstream of PL incorporation, the lipotoxic effects of SFAs can be significantly reduced.Grant Funding Source: Supported by: National Science Foundation Career Award 0955251
Regulation of CCN2 and CCN3 in bone marrow through myloid zinc finger‐1 and its medical implication in hematopoiesis (1005.4)
Authors: Rozado André , Piszczatowski Richard , Rafferty Brian , Lents Nathan 
Published: June 2021

CCN2, also known as CTGF, the connective tissue growth factor, has recently been found to be in high abundance in platelets and released upon activation, an effect inhibited by aspirin, suggesting additional role in blood clotting and/or wound healing. It has been demonstrated that another member of the CCN family, the Nephroblastoma overexpressed gene (NOV, CCN3) functions in hematopoietic potential, blood cell formation, and helps to maintain a competent immune system. Taken together, these two CCN family members represent interesting new areas of research in blood cell biology, with dramatic clinical potential.Recent research in our lab discovered that the transcription factor MZF‐1 regulates both the CCN2 and CCN3 genes. Specifically, we found that MZF‐1 binds to the promoter of both CTGF (CCN2) and NOV (CCN3). It is known that both vitamin D (calcitriol) and vitamin A (all‐trans retinoic acid) stimulate transcription of the MZF1 gene. We have thus discovered a potential new pathway in which Vitamins A and D induce MZF‐1 to upregulate CCN3 and CCN2 resulting in increased hematopoietic potential and increased differentiation of HSCs and their progeny. It is known that the presence of CTGF in platelets is the result of endocytosis from extracellular environment. However, we have confirmed that treatments with either vitamin A or D activate the MZF‐1 pathway and results in increased production of CCN2 in stromal fibroblasts, which in turn results in enhanced loading of CCN2 into developing platelets in vitro.Furthermore, the regulation of CCN3 by MZF‐1 represents a testable new clinical treatment. We have observed that both vitamin A and vitamin D induce CCN3 expression, through MZF‐1, in multiple blood cell types. We are currently testing if this will lead to enhanced hematopoietic potential. This work could impact the efficacy of blood donation and transfusion, bone marrow transplants, and the treatment of bleeding and clotting diseases as well as lymphomas and leukemias.
Pulsed EPR distance measurements resolve the impact of site‐specific calmodulin methionine oxidation (1009.4)
Authors: Klein Jennifer , McCarthy Megan , Reuter Mitch , Olenek Michael , Moen Rebecca , Thomas David 
Published: June 2021

We have examined the structural impact of oxidizing specific protein methionine (Met) residues in the C‐ter lobe of calmodulin (CaM); these oxidation sites are known to abolish CaM regulation of the major calcium release channel, the ryanodine receptor complex (RyR). We have linked oxidation‐induced changes in RyR regulation to changes in CaM‐RyR structure using (1) protein mutagenesis to mimic oxidation at specific sites and (2) spectroscopy to resolve oxidation‐induced changes in protein structural dynamics.Protein oxidation by reactive oxygen species (ROS) is strongly associated with loss of strength in skeletal muscle and is proposed to play major roles in aging and degenerative muscle disease. Targeted interventions that block or repair specific oxidative damage, while supporting normal levels of oxidation, could decrease morbidity associated with muscle dysfunction_this level of discrimination demands molecular‐level insights into the mechanisms that underlie the decline in muscle force associated with oxidative stress.Pulsed EPR distance measurements across CaM’s lobes were sensitive to large‐scale conformational changes that accompany both calcium binding and RyR peptide binding. In the absence of calcium, CaM was highly disordered, populating a broad distribution of conformations. Calcium binding strongly stabilized an elongated conformation, while RyR peptide binding to calcium‐loaded CaM strongly stabilized the compact conformation. CaM conformation, particularly the distribution over structural states, was sensitive to Met to Gln substitutions (M109Q and M124Q) designed to mimic CaM Met oxidation. Structural sensitivity to M‐to‐Q mutations was observed in both the presence and absence of calcium, and in complex with RyR peptide. We conclude that Met oxidation alters CaM’s functional interaction with RyR through changes in the orientation and flexibility of CaM’s lobes.Grant Funding Source: This work is supported by a University of Wisconsin‐La Crosse Faculty Research Grant to JC Klein, NI