Biosciences Institute Research Articles

Research Misconduct in Japan and How It Is Covered by the Media

Cases of research misconduct (fabrication, falsification, and plagiarism) have been increasing worldwide, including in Japan. In particular, since 2006, many cases of research misconduct have been reported in Japan, and these cases have also been covered by the media. The 2014 case of the withdrawal of articles on STAP cells followed a rare course in which research misconduct became a full-blown social phenomenon. In recent years, even the University of Tokyo has experienced reported cases of research misconduct. In this report, I would like to introduce some representative cases of research misconduct in the field of life sciences over the past decade. These examples include studies conducted at Osaka University Graduate School of Medicine (2006), Osaka University Graduate School of Frontier Bioscience (2006), Ryukyu University School of Medicine (2010), Toho University School of Medicine (2012), The University of Tokyo Institute of Molecular and Cellular Biosciences (2013), and several cases outside of Japan. I will discuss what researchers should do to reduce the incidence of research misconduct. In addition, I will discuss how these cases were covered by the media, because the public's impression of research misconduct is formed by media coverage.

Cancer‐induced Metabolic Cardiotoxicity Characterized through Optical Metabolic Imaging

Heart disease is a primary contributor to mortality in the world and progressively develops by advancing age, obesity, and other disease states. Pathological hypertrophy, atrophy, apoptotic cell death, and fibrosis can all be contributing factors to heart failure but diminished oxidative capacity seems to be a universal characteristic. New applications of two‐photon excited fluorescence microscopy (TPEF) can aid in the characterization of cardiac metabolic alterations. Specifically, NADH and FAD are fluorescent metabolic cofactors that play important roles in metabolic pathways of the cytoplasm and the mitochondria. The optical reduction‐oxidation (redox) ratio (ORR) of FAD/(FAD+NADH) provides a validated method to quantify the redox state of a cell thus characterizing reliance on oxidative metabolism versus glycolytic utilization.PurposeTo utilize the ORR as a non‐destructive, label free marker of cardiac metabolism in a mouse model of cancer‐induced heart disease and in‐vitro genetically altered cardiomyocytes.Methods1×106 Lewis Lung Carcinoma (LLC) cells were injected into the flank of C57BL6/J mice and the tumor was allowed to develop for 4 wks and compared to PBS injected control. TPEF was performed on 10μm sections of the left ventricle to quantify ORR. Further histological analysis (Sirius Red, TUNEL, 2HG) and immunoblot analysis (mitochondrial turnover markers, apoptosis signaling) were performed to verify and characterize this unique form of cardiomyopathy. To examine if changes in ORR are indicative of a transition from oxidative to glycolytic metabolism, experiments were performed using H9c2 cardiomyocytes transfected with shRNA targeting mitochondrial translation initiation factor 2 (mtIF2). Oxidative capacity was measured using bioenergetics flux analysis and TPEF to verify decreased oxidative capacity resulting from impaired mitochondrial mRNA translation products.ResultsLLC hearts demonstrated ~15% lower ORR (FAD/FAD+NADH) indicating greater glycolytic reliance compared to PBS controls. LLC hearts had ~50% greater content in markers of mitochondrial content (COX‐IV, VDAC) likely due to ~50% lower PINK1/Parkin‐mediated mitophagy markers while biogenesis proteins PGC‐1α, PPARα, and PPARδ were unaffected. H9c2 cells transfected with mtIF2 shRNA had decreased basal, maximal, and reserve oxygen consumption rates, greater AMPK phosphorylation and a ~40% lower ORR.ConclusionsThese results demonstrate how TPEF of the optical redox state can identify metabolic characteristics associated with cardiomyopathy as demonstrated using cancer‐induced cardiac atrophy and in vitro genetic alteration of cardiomyocytes. Further research could use this non‐destructive, label‐free approach to screen for drugs contributing to cardiotoxic effects of cancer treatments as well as pharmaceuticals that may attenuate the development of cardiomyopathies.Support or Funding InformationThis study was supported by Arkansas Bioscience Institute (NR, NPG), American College of Sports Medicine Foundation Doctoral Student Research Grant (DEL) and National Institutes of Health R15AR069913 (NPG).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Leucine improves markers energy metabolism in C2C12 myotubes treated with palmitate

More than one‐third of adults and 17% of children in the United States are classified as obese. One contributor to the development of obesity is an increase energy intake accompanied by a decrease energy expenditure. Muscle plays an important role in energy utilization and production in human body. Excessive fat mass accumulation in muscle blunts energy production such as fatty acid oxidation. The objectives of this study were to: 1) determine if the branched‐chain amino acid leucine lowers intracellular fatty acid uptake, and 2) determine if mitochondria are involved in the leucine‐mediated effect on fatty acid uptake. C2C12 myotubes were used as a cell model for muscle. Cells were treated with palmitate for 24 hours in order create an obesogenic muscle model. All cells were serum and leucine starved for 24 hours before receiving one of the following four treatments: control (CON), palmitate (PALM, palmitate treated for 24h), palmitate + 0.5mM leucine (PALM+0.5mM LEU,, palmitate and 0.5mM leucine co‐treated for 24h), palmitate + 1.5mM leucine (PALM+1.5mM LEU,, palmitate and 1.5mM leucine co‐treated for 24h). Intracellular lipid deposition was measured using oil red o staining kit and quantified using ImageJ software. Both doses of leucine showed significant effect (p<0.05) on lowering the intake of intracellular lipid uptake in PALM treated cells. Real‐time PCR results showed higher (p<0.05) expression of uncoupling proteins (UCP2 and UCP3), which are involved in ATP synthesis, in both leucine treatment groups compared with PALM. There was no significant difference in gene expression of NRF1, SIRT1, Tfam, PPARγ and ANT1, all involved in mitochondria DNA transcription. In conclusion, these data suggest leucine promotes energy metabolism through regulating uncoupling protein in mitochondria in C2C12 myotubes, indicating a possible target for improving obesity.Support or Funding InformationArkansas Biosciences InstituteThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

IDH2 Deficiency Disrupts Energy Homeostasis and Skeletal Muscle Development by Upregulating UCP1 Expression in Mice

Isocitrate dehydrogenase 2 (IDH2) is a mitochondrial specific enzyme that catalyses the oxidative decarboxylation of isocitrate into α‐ketoglutarate with concurrent reduction of NADP+ to NADPH. We previous reported that IDH2 knock‐out (KO) increased obesity resistance via UCP1‐mediated enhanced energy expenditure in adipose and liver tissues. Since skeletal muscle is the most mitochondria abundant tissue and is a major site for energy expenditure, we here examined the effects of IDH2 KO on skeletal muscle energy homeostasis and its growth. Calf skeletal muscle samples (i.e., mixed part of soleus, gastrocnemius, and plantaris muscles) were harvested from 11‐week‐old male IDH2 KO (n=4) and wild type (WT; C57BL/6; n=4) mice, and a ratio of skeletal muscle weight to body weight was measured. Subsequently, marker of mitochondrial DNA to nucleic DNA ratio was measured by PCR analysis. In addition, mRNA expression levels involved in fatty acid β‐oxidation (CPT1 and FAT), adipogenesis (PPARγ, C/EBPα, C/EBPβ, aP2, and ZFP423), thermogenesis (UCP1, BMP7, and PRDM16), myogenesis (MRF4 and MyoD), and mitochondria biogenesis (PGC‐1α, TFAM, ERRα, and MFN2) were compared. Interestingly, a ratio of skeletal muscle weight to body weight was significantly lower in IDH2 KO mice compared to that of WT mice (P=0.0004). Further, mitochondrial content was relatively lower in skeletal muscle of IDH2 KO mice than the WT mice albeit it was not statistically significant (P=0.09). In consistent with the muscle mass, there were trends of decrease in the expressions of myogenesis (MyoD, P=0.07) as well as mitochondrial biogenesis genes in IDH2 KO mice (PGC‐1α, P<0.05; TFAM, P=0.07). Last, the expression level of UCP1, a hallmark of thermogenesis, was remarkably increased in skeletal muscle whereas adipogenesis pathway (PPARγ, P<0.005; C/EBPβ, P=0.06; ZFP423, P<0.05) was down‐regulated in skeletal muscle of IDH2 KO mice. However, UCP1 seems not directly regulated by the expression of BMP7 or PRDM16 as the expression of BMP7 and PRDM16 was also down‐regulated in IDH2 KO mice. Taken together, our study suggests that IDH2 deficiency may upregulate UCP1‐mediated thermogenesis possibly to adopt limited NADPH supply. In turn, the thermogenesis‐induced energy imbalance may cause suppression of myogenesis, mitochondria biogenesis, adipogenic signaling pathway, and skeletal muscle growth. Our study will provide scientific background to further studies on the mechanistic functions of IDH2 in skeletal muscle development.Support or Funding InformationThis work was supported by the University of Arkansas, VPRED Start‐up fund (KJK, and PJH). Support has been provided in part by the Arkansas Biosciences Institute, a partnership of scientists from Arkansas Children's Hospital, Arkansas State University, the University of Arkansas‐Division of Agriculture, the University of Arkansas, Fayetteville, and the University of Arkansas for Medical Sciences. The Arkansas Biosciences Institute is the major research component of the Arkansas Tobacco Settlement Proceeds Act of 2000 (JKK, JHP, KEB, and BCK).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Alterations in Hepatic Protein Synthetic Signaling During the Progression of Cancer Cachexia

Cancer and its associated co‐morbidities remain a significant public health concern. Specifically, cancer‐associated muscle wasting (cancer cachexia) is a strong predictor of cancer‐associated mortality. Cachexia is thought to be partially mediated by increased energy expenditure, as the liver is the predominant regulator of whole body energy expenditure, it is plausible that alterations in liver physiology may contribute to cachexia. More so, liver hypertrophy is a common pathological hepatic manifestation of cachexia, which has been demonstrated to directly relate to energy expenditure. Therefore, understanding the mechanisms underlying hepatic hypertrophy is critical for understanding hepatic pathologies of cachexia.PurposeTo examine alterations in hepatic protein synthetic pathways during the progression of cancer cachexia.MethodsC57BL/6J mice were injected with either phosphate buffered saline (CON) or 1×106 Lewis Lung Carcinoma (LLC) cells in the hind flank. Cancer progressed for 1, 2, 3, or 4 weeks, mice were then humanely euthanized, and livers collected for analysis (n=10–16/group). CON animals were age‐matched with 4 week animals. Subsets of each group (n=8/group) were analyzed by Western blot for measures of hepatic protein synthesis. Data were analyzed by oneway ANOVA with independent factors of cancer progression (CON, 1, 2, 3, or 4 weeks). When significant F‐ratios were found, a Dunnett's post hoc was used to compare differences between experimental groups and control. Significance was denoted at p<0.05.ResultsLivers from 4 week animals were 30% larger compared to CON with no other differences noted compared to CON (p<0.05). Total Akt protein content was ~8.5‐fold greater in 4 week animals compared to control (p<0.05). p‐AktSer473 was ~3.5‐fold greater in 4 week animals compared to control. However, p‐Akt Ser473/Akt ratio demonstrated a ~35–45% decrease in 1 week, 2 week, 3 week, and 4 week animals compared to control. There were no differences in total p70, p‐p70Thr389, or p‐p70Thr389/p70 content between groups. Total 4EBP1 was not different between groups, however, an apparent ~1.7‐fold greater p‐4EBP1Thr37/46 appeared in 4 week animals, approached statistical significance (p=0.08). There were no statistical differences on p‐4EBP1Thr37/46/4EBP1 ratio.ConclusionsCancer progression causes marked alterations in upstream signaling in hepatic protein synthesis, however these differences may not necessarily translate to alterations in downstream hepatic protein synthesis signaling. More research is necessary to identify the precise mechanisms of hepatic hypertrophy in the progression of cancer cachexia.Support or Funding InformationThis study was supported by The Arkansas Bioscience Institute and National Institutes of Health R15AR069913.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

IDH2 Deficiency Aggravates Fructose‐Induced NAFLD by Activating Inflammatory Signaling in Female Mice

Fructose is a strong risk factor of non‐alcoholic fatty liver disease (NAFLD), resulting from disruption of redox systems by excessive reactive oxygen species production in the liver cells. Importantly, recent epidemiological studies indicated that women are more prone to develop metabolic syndrome in response to fructose‐sweetened beverages. Here, we examined whether disruption of redox system exacerbates fructose‐induced NAFLD conditions in female mice. The redox system was disrupted by blocking NADPH supply through mitochondrial NADP+‐dependent isocitrate dehydrogenase knock‐out (IDH2 KO) in C57BL/6 female mice. After, wild type (WT) and IDH2 KO mice were treated with either water or 34% fructose water over six weeks. NAFLD phenotypes and key proteins and mRNAs involved in inflammatory pathway (e.g., NF‐κB p65 and IL‐1β) were assessed. As results, hepatic lipid accumulation was significantly increased in IDH2 KO mice fed fructose compared to its WT counterpart. Neutrophil infiltration was observed only in IDH2 KO mice fed fructose. Further, phosphorylation of NF‐κB p65 and expression of IL‐1β was remarkably upregulated in IDH2 KO mice fed fructose, and expression of IκBα was decreased by fructose treatment in both WT and IDH2 KO groups. For the first time, we report that IDH2 KO significantly aggravates fructose‐induced NAFLD phenotypes (fatty liver and neutrophil infiltration) and related inflammatory responses (i.e., NF‐κB p65 pathway). Collectively, this study provides evidence that IDH2 deficiency may have implications on fructose‐induced NAFLD through suppression of fatty acid β‐oxidation and/or activation of the NF‐κB pathway. Given our significant phenotypes in response to fructose intervention, the present study will provide a good justification for further characterization thus warrants additional investigations to clarify mechanistic roles of mice IDH2 in metabolic diseases.Support or Funding InformationThis work was supported by the University of Arkansas, VPRED Start‐up fund (KJK, and PJH). Support has been provided in part by the Arkansas Biosciences Institute, a partnership of scientists from Arkansas Children's Hospital, Arkansas State University, the University of Arkansas‐Division of Agriculture, the University of Arkansas, Fayetteville, and the University of Arkansas for Medical Sciences. The Arkansas Biosciences Institute is the major research component of the Arkansas Tobacco Settlement Proceeds Act of 2000 (JKK, JHP, KEB, and BCK).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Protein Synthesis throughout the Progression of Cancer Cachexia in Tumor‐Bearing Mice

Cancer cachexia occurs in approximately 80 percent of cancer patients and is a key contributor to cancer‐related death. The mechanisms controlling development of tumor‐induced muscle wasting are not fully elucidated. Specifically, the progression of cancer cachexia is underexplored. We have previously reported that muscle wasting occurs 4 wks following tumor implantation in these mice.PurposeTo examine the rate of muscle protein synthesis throughout the progression of cancer cachexia in tumor‐bearing mice.MethodsLewis Lung Carcinoma (LLC) was injected into the hind‐flank of C57BL6/J mice at 8 wks age with tumor allowed to develop for 1, 2, 3, or 4 wks and compared to PBS injected control. PBS control animals were age matched to the 4 wk tumor bearing group. Cumulative fractional protein synthetic rates (FSR) were determined using deuterium oxide (2H20). Briefly, a (20 μL/g body weight) bolus priming dose of deuterium oxide was injected intraperitoneally approximately 24 hours before tissue collection. Drinking water was thereafter supplemented with 4% deuterium oxide in order to maintain the plasma pool of deuterium oxide. Fractional synthetic rate (FSR) of mixed muscle fraction (soluble, mitochondria, sarcolemmal, and contractile) and myofibrillar (contractile) rich fraction from gastrocnemius muscle were measured us a GC/MS. Data were analyzed by one‐way ANOVA. When significant F‐ratios were found, a SNK post hoc was used to compare differences between experimental groups. Significance was established at p<0.05.ResultsPlasma enrichment of 2H20 for all groups was 2.91 ± 0.073% and no significant differences existed in means between groups. Mixed muscle FSR remained consistent in 1 wk and 2 wk animals and was ~40% lower 4 wks following tumor implantation (p<0.05) when compared to PBS control. The myofibrillar rich fraction of FSR followed a similar pattern, but changes did not reach statistical significance between groups.ConclusionsThese data indicate muscle protein synthesis decreases concomitantly with muscle loss and may be a major contributor of cancer cachexia in tumor‐bearing mice. More research needs to be conducted to analyze the mechanism for the loss of protein synthesis in cachectic mice.Support or Funding InformationThis study was supported by The Arkansas Bioscience Institute and National Institutes of Health R15AR069913.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Clausenidin suppresses the production of VEGF and inhibits angiogenesis of HepG2 cells

Event Abstract Back to Event Clausenidin suppresses the production of VEGF and inhibits angiogenesis of HepG2 cells Peter M. Waziri1*, Rasedee Abdullah2, Kartinee N. Kassim3 and Jaafar M. Sani4 1 Kaduna State University, Nigeria 2 Faculty of Veterinary Medicine, Putra Malaysia University, Malaysia 3 Faculty of Science, Putra Malaysia University, Malaysia 4 Universiti Putra Malaysia, Malaysia Background Metastasis of tumor cells is responsible for over 90% of cancer deaths globally. The production of vascular endothelial growth factor (VEGF) promotes metastasis and immortality of cancer cells. Up till date, there is still no clinical drug that effectively prevents the production of VEGF in tumor cells. Clausena excavata Burm. f (local name: cherek hitam) is a shrub that is used locally for the treatment of cancer tumors in Malaysia and other countries of South East Asia. The current study evaluated the effect of clausenidin isolated from the chloroform extract of C. excavata on the production of VEGF in liver cancer (HepG2) cells. Methods The anti-angiogenic effect (production of VEGF) in the clausenidin-treated cells was monitored using Western blot assay and the anti-apoptotic effect of the pure compound was monitored using transmission electron microscopy (TEM). Prior to Western blot analysis, the cells were treated with 5, 15, 30 and 40 µg/mL of clausenidin and in the TEM analysis, cells were treated with the IC50 (7.7 µg/mL) of clausenidin at 24, 48 and 72 h. Results The Western blot analysis showed that clausenidin treatment significantly reduced (p<0.05) the production of VEGF that causes metastasis of liver cancer cells in a dose-dependent manner. In addition, we observed apoptosis to be one of the routes of cell death in the clausenidin-treated cells. The TEM analysis revealed margination and condensation of chromatin, nuclear fragmentation, formation of lipid droplets and convolution of nuclear outline (at all treatment points) which confirmed apoptosis of the clausenidin-treated HepG2 cells. Conclusion Clausenidin can be used as an anti-angiogenic and anti-apoptotic agent for the treatment of liver cancer. Acknowledgements The authors are grateful to MAKNA Cancer Research Laboratory, Institute of Bioscience, Universiti Putra Malaysia. Keywords: Clausenidin, VEGF, Apoptosis, Angiogenesis, Cancer Conference: International Conference on Drug Discovery and Translational Medicine 2018 (ICDDTM '18) “Seizing Opportunities and Addressing Challenges of Precision Medicine”, Putrajaya, Malaysia, 3 Dec - 5 Feb, 2019. Presentation Type: Oral Presentation Topic: Cancer Citation: Waziri PM, Abdullah R, Kassim KN and Sani JM (2019). Clausenidin suppresses the production of VEGF and inhibits angiogenesis of HepG2 cells. Front. Pharmacol. Conference Abstract: International Conference on Drug Discovery and Translational Medicine 2018 (ICDDTM '18) “Seizing Opportunities and Addressing Challenges of Precision Medicine”. doi: 10.3389/conf.fphar.2018.63.00118 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 29 Nov 2018; Published Online: 17 Jan 2019. * Correspondence: Dr. Peter M Waziri, Kaduna State University, Kaduna, Nigeria, petermwaziri@gmail.com Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Peter M Waziri Rasedee Abdullah Kartinee N Kassim Jaafar M Sani Google Peter M Waziri Rasedee Abdullah Kartinee N Kassim Jaafar M Sani Google Scholar Peter M Waziri Rasedee Abdullah Kartinee N Kassim Jaafar M Sani PubMed Peter M Waziri Rasedee Abdullah Kartinee N Kassim Jaafar M Sani Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Dual compound loaded chitosan nanoparticles: synthesis and optimization

Event Abstract Back to Event Dual compound loaded chitosan nanoparticles: synthesis and optimization Nurhanisah Othman1, Mas Jaffri Masarudin2, 3, Cha Yee Kuen2, 3, Nurul Azira Dasuan1, Luqman Chuah Abdullah4 and Siti Nurul Ain Md Jamil1* 1 Department of Chemistry, Faculty of Science, Putra Malaysia University, Malaysia 2 Department of Cell and Molecular Biology, Faculty of Biotechnology and Biomolecular Sciences, Putra Malaysia University, Malaysia 3 MAKNA Cancer Research, Institute of Bioscience, University Putra Malaysia, Malaysia 4 Department of Chemical and Environmental Engineering, Faculty of Engineering, Universiti Putra Malaysia, Malaysia Introduction: Chitosan nanoparticles (CNP) have been tremendously studied for its excellent property as drug carrier. However, its hydrophilicity makes it more selective to certain pharmaceutical products. Encapsulation of both hydrophilic l-ascorbic acid (LAA) and hydrophobic thymoquinone (TQ) in CNP were investigated to augment its potential in delivering compounds. Method: CNP loaded with antioxidant LAA and TQ were synthesized via harmless ionic gelation routes. They were then characterized by using Fourier-Transform Infrared Spectroscopy (FTIR), nanosizer, UV-vis spectrophotometer and Field Emission Scanning Electron Microscope (FESEM). Result: The optimum CNP-LAA-TQ size produced was 141.5 ± 7.8 nm. The encapsulation efficiency of CNP-LAA-TQ was 22.8 ± 3.2 % for LAA and 35.6 ± 3.6 % for TQ. Conclusion: The incorporation of hydrophilic LAA and hydrophobic TQ in a single CNP organization contributes in the advancement of multidrug therapy, especially in treating tuberculosis and cancers. The emergence of this dual compound nanoparticles is hoped to solve the issue of multitudinous potent drugs with low systemic uptake. Keywords: antioxidant, Chitosan, Hydrophobic-hydrophilic, Ionic gelation, Nanoparticles Conference: International Conference on Drug Discovery and Translational Medicine 2018 (ICDDTM '18) “Seizing Opportunities and Addressing Challenges of Precision Medicine”, Putrajaya, Malaysia, 3 Dec - 5 Feb, 2019. Presentation Type: Oral Presentation Topic: Miscellaneous Citation: Othman N, Masarudin M, Kuen C, Dasuan N, Abdullah L and Md Jamil S (2019). Dual compound loaded chitosan nanoparticles: synthesis and optimization. Front. Pharmacol. Conference Abstract: International Conference on Drug Discovery and Translational Medicine 2018 (ICDDTM '18) “Seizing Opportunities and Addressing Challenges of Precision Medicine”. doi: 10.3389/conf.fphar.2018.63.00040 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 30 Oct 2018; Published Online: 17 Jan 2019. * Correspondence: Dr. Siti Nurul Ain Md Jamil, Department of Chemistry, Faculty of Science, Putra Malaysia University, Serdang, Selangor, 43400, Malaysia, ctnurulain@upm.edu.my Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Nurhanisah Othman Mas Jaffri Masarudin Cha Yee Kuen Nurul Azira Dasuan Luqman Chuah Abdullah Siti Nurul Ain Md Jamil Google Nurhanisah Othman Mas Jaffri Masarudin Cha Yee Kuen Nurul Azira Dasuan Luqman Chuah Abdullah Siti Nurul Ain Md Jamil Google Scholar Nurhanisah Othman Mas Jaffri Masarudin Cha Yee Kuen Nurul Azira Dasuan Luqman Chuah Abdullah Siti Nurul Ain Md Jamil PubMed Nurhanisah Othman Mas Jaffri Masarudin Cha Yee Kuen Nurul Azira Dasuan Luqman Chuah Abdullah Siti Nurul Ain Md Jamil Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

First Report of Maize yellow mosaic virus Infecting Panicum miliaceum and Sorghum bicolor in South Korea

Maize yellow mosaic virus (MaYMV) is a tentative new Polerovirus, which was recently identified from maize (Zea mays) in China (Chen et al. 2016). MaYMV has also been reported to infect sugarcane (Saccharum spp.) and itch grass (Rottboellia cochinchinensis), and it has been reported in Asia, Africa and South America (Goncalves et al. 2017; Palanga et al. 2017; Yahaya et al. 2017). In this study, MaYMV was detected in Panicum miliaceum and Sorghum bicolor using Illumina HiSeq2500 system by Theragen Etex Bio Institute (Suwon, Korea) and SG-VIPdb by SeqGenesis (Daejeon, Korea), as described by Lim et al. (2015). Twenty samples of P. miliaceum and sixty three samples of S. bicolor were collected from July to September and from June to October, 2016, respectively, in South Korea. The high-throughput RNA sequencing of the samples mixed into one pool resulted in a single large contig (5606-nt) with nearly complete MaYMV genome coverage. The contig was assembled from a total of 234,537 reads; the maximum, minimum...

Confronting Climate Change: The Uneasy Alliance of Scientists and Nonscientists in a Neoliberal World

Confronting Climate Change: The Uneasy Alliance of Scientists and Nonscientists in a Neoliberal World

Enzyme harnesses light to make alkanes

Although many organisms respond to light, very few enzymes inside those organisms use light directly as an energy source for catalysis. Researchers now report a new light-driven enzyme: Christened fatty acid photodecarboxylase (FAP), it uses blue light to drive the removal of carboxyl groups from fatty acids to form alkanes or alkenes (Science 2017, DOI: 10.1126/science.aan6349). FAP joins a select group of so-called photoenzymes, including DNA-repair enzymes called photolyases, that use light for catalysis on their own rather than functioning as part of a larger complex such as photosystems I or II, which are used by plants and algae for photosynthesis. The team that identified FAP was led by Fred Beisson, a scientist in the Biosciences & Biotechnologies Institute of the French Alternative Energies & Atomic Energy Commission. Beisson and colleagues knew that some species of microalgae could convert long-chain fatty acids to alkanes or alkenes through a light-dependent mechanism

Myogenic And Atrophic Signaling In The Progression Of Cancer-cachexia

Cancer is a major public health problem in the U.S. and the world. In 2013 there were an estimated 1,660,290 new cases of cancer in the U.S. Severe weight and muscle loss in cancer (cancer-cachexia [CC]) is accepted as a common effect of many cancers, and is directly responsible for 20-40% of cancer-related deaths. The mechanisms that control the development of CC are not well understood. In order for muscle wasting to occur, there must be either a decrease in myogenic factors or an increase in catabolic factors. Most investigations of CC focus on the post-cachectic state and do not examine the progression of the condition. PURPOSE: The purpose of this study is to determine the roles of classical myogenic factors (Pax7, MyoD and Myogenin; markers of satellite cell content and regulators of myocyte proliferation and differentiation, respectively), and catabolic factors (Atrogin and MuRF; E3 ubiquitin ligases regulating ubiquitin-mediated protein degradation) in the onset of CC. METHODS: : 1x106 Lewis Lung Carcinoma cells (LLC) or Phosphate Buffered Saline (PBS, control) were injected into the hind-flank of normal wildtype C57BL6/J mice at 8 wks of age, and tumor allowed to develop for 1, 2, 3, or 4 wks, gastrocnemius muscle weights were measured to assess CC. MyoD, Myogenin, Atrogin, MuRF, and Pax7 were analyzed using RT-PCR for all 5 groups (1, 2, 3, 4 wk LLC and PBS). Data were analyzed by one-way ANOVA, Student-Newman-Keuls test was used to determine differences among means, significance was set at P<0.05. RESULTS: Gastrocnemius muscle weights were only lower than PBS control at 4 wk post tumor-implantation. Pax7 was ~30% lower at all timepoints following tumor implantation. MyoD and Myogenin were ~50% lower in wks 1 and 2 post-tumor implantation, and returned to baseline for wks 3 and 4. Atrogin was ~3.5-fold greater in wk 4, while MuRF was ~2.3-fold higher in wk 3 and ~3.8-fold in wk 4 post-tumor implantation. CONCLUSIONS: Our data suggest a reduction in satellite cell content shortly after tumor implantation in mice which is tied to an early reduction in markers of myogenic differentiation and proliferation though muscle loss is not evident until 4 wk post tumor implantation; while MuRF and atrogin mediated protein degradation does not seem to be altered until later in tumor progression. Supported by Arkansas Bioscience Institute

The Effects of Exercise Training on Cardiorespiratory Fitness in Obese Sedentary Pregnant Women

PURPOSE: Maternal obesity has profound detrimental effects on the offspring’s risk of obesity and cardiometabolic health. Although pre-conception interventions are preferable, exercise during pregnancy can potentially mitigate the effects of maternal obesity on metabolic health in both the mothers and the offspring. The Expecting study is an ongoing RCT in obese sedentary women aiming to determine if combined resistance and aerobic exercise during pregnancy improves maternal health and decreases the risk of obesity in the offspring. The purpose of the current analysis was to assess the effects of 11 weeks of exercise training on markers of cardiorespiratory health in women participating in the study for whom data are available at gestation week (GW) 12 and 24. METHODS: Women (n=40) were recruited at GW 12. Body composition and submaximal aerobic capacity were assessed at GWs 12 and 24 using air displacement plethysmography and an incremental treadmill test, respectively. Twenty-one women were randomized to receive standard of care (SOC) and 19 received a combined exercise intervention (EX) 3 times/week. Oxygen consumption (VO2, ml·kg-1·fat-free-mass-1) and oxygen pulse [OP, ml/beat, (VO2/heart rate)] are reported for the work load corresponding to a rate of perceived exertion of 15 on Borg’s scale (RPE-15). The intervention effect was assessed using analysis of covariance where baseline measurements and incline were used as covariates. Data are presented as mean ±SE. RESULTS: at GW 12, groups were comparable in terms of age (EX=30±4 vs. SOC=29±4 years, NS), BMI (37.4±5.2 vs. 37.8±6.6, NS), body fat mass (48.8±5.4 vs. 47.8±5.2%, NS), and body fat free mass (51.1±5.9 vs. 51.4±7.5 kg, NS). Mean attendance to EX sessions was 80±9% (2.4±0.3 visits/wk.) After 11 weeks of training, the EX group had higher VO2 (34.0±0.8 vs. 30.3±0.7, p=0.002) than the SOC group. Oxygen pulse was also higher in the EX group compared to the SOC group (11.6±0.3 vs. 10.6±0.3). CONCLUSION: A structured exercise intervention during pregnancy in obese sedentary women is not only well-received and easy to adhere to, but also results in improved aerobic fitness. Supported by USDA-ARS # 6026-51000-010-05S, ACRI, and Arkansas Biosciences Institute, the major research component of the Arkansas Tobacco Settlement Proceeds Act of 2000.

Docosahexaenoic Acid (DHA), not Leucine, May Protect HepG2 Cells from Palmitate‐Induced Non‐Alcoholic Fatty Liver Disease

Non‐alcoholic fatty liver disease (NAFLD) is the leading cause of chronic liver disease in the United States, affecting 70 million adults and ~3% of young children. NAFLD is characterized by an accumulation of fat in the liver cells that is not caused by alcohol. NAFLD is closely associated with obesity and insulin resistance, which are precursors for development of type 2 diabetes. Recent data suggests that the PPARs (PPARα and PPARγ may be connected to the development and progression of NAFLD, which make them potential biomarkers for treating and diagnosing NAFLD. Currently, there are several approaches to treating NAFLD, including nutrition therapy and specific food recommendations. Diets high in protein, high in the branched‐chain amino acid leucine, and diets high in polyunsaturated fatty acids, such as DHA, have been linked with weight reduction and improved insulin resistance. However, neither has been evaluated as a treatment for NAFLD. Therefore, the objective of this study was to analyze the ability of leucine and DHA to act either synergistically or alone to reduce markers of NAFLD using HepG2 cells treated with palmitate as an in vitro model. HepG2 cells (80% confluent) received one of 6 treatments for 48 hours: control, vector control, 0.75 mM palmitate, 5 mM leucine + palmitate, 0.1 mM DHA + palmitate, or leucine + DHA + palmitate. Lipid deposition and markers of energy metabolism were measured. Data was analyzed using one‐way ANOVA with P &lt; 0.05 indicating significance. There was no effect of leucine on cellular lipid deposition. However, cells treated with DHA had significantly less lipid deposition compared to cells treated with palmitate or palmitate + leucine. Palmitate increased Tfam expression compared to controls, however, there was no further effect of leucine. Palmitate + DHA and palmitate + leucine + DHA significantly increased Tfam expression compared to control, palmitate and palmitate + leucine. Palmitate significantly lowered PGC1a and PPARg expression, however treatment with DHA further decreased PGC1α and PPARγ compared to controls and palmitate, alone. Preliminary data shows no treatment effect on SIRT1 or mTOR phosphorylation. Taken together, these data suggest that DHA, not leucine, has the potential to reduce markers of NAFLD in HepG2 cells.Support or Funding InformationArkansas Biosciences Institute. University of Arkansas State Undergraduate Research Fellowship.

Educational Messaging at Breakfast, Not Protein Source, Influences Appetite Response, Food Preferences, and Food Intake in Men and Women

Early adulthood is a vulnerable time for weight gain. A primary contributor to weight gain and obesity is an increase in unhealthy eating habits, such as skipping breakfast, which has been strongly associated with overeating, weight gain, and obesity. Studies have shown that breakfasts high in protein enhance feelings of fullness compared a carbohydrate‐based breakfast. However, very few studies have examined the effect of protein quality at breakfast on postprandial appetite response, food preference and food intake, and, to our knowledge, no data exists regarding educational messaging at breakfast and subsequent food intake. Therefore, the objectives of this study were to 1) determine if protein source at breakfast impacts appetite response, food preference and food intake, and 2) determine if educational messaging presented at breakfast impacts appetite response, food preference and food intake. This was a randomized, crossover study in which each participant received two different breakfasts (plant protein‐based and animal protein‐based) with a minimum one‐week washout period between breakfasts. Each participant was randomly assigned to either the educational messaging (EM; n=17; 13 females, 4 males; 24 ± 1 y) or non‐messaging (NM; 9 females, 6 males; 23 ± 1 y) group. Each test breakfast was 280 kcal, 59% protein, 27% carbohydrate, and 14% fat. At the beginning of each breakfast, participants in the EM group received 5 messages about dietary protein, which they read and kept visible during the 3‐hour testing period. Participants had 7 minutes to consume the breakfast and appetite was assessed for the following 120 min. At 120 min, participants were presented with a variety of healthy or unhealthy snacks and advised to eat as much or as little as they desired. The snacking period lasted 60 min. Data was analyzed using two‐way, repeated measures ANOVA, P&lt;0.05 was considered significant. Participants preferred (P&lt;0.05) the animal protein‐ versus plant protein‐based breakfast. There was no difference in protein source or EM or NM in appetite response. Protein source did not influence snack intake. However, participants in the NM group consumed more snacks and more unhealthy snacks compared to participants in the EM group (P&lt;0.05). These data suggest that educational nutritional messaging at breakfast can reduce snack intake and encourage healthy snack choices later in the day.Support or Funding InformationArkansas Biosciences Institute. University of Arkansas Honors College Grant.

Erratum to: Titanium scaffold osteogenesis in healthy and osteoporotic rats is improved by the use of low-level laser therapy (GaAlAs).

Department of Bioscience and Oral Diagnosis Institute of Science and Technology Univ Estadual Paulista (UNESP), Av. Engenheiro Francisco Jose Longo, 777

Factors affecting eating quality of beef

The most important factors known to influence the eating quality of beef are well established and include both pre- and post-slaughter events with many of the determinants interacting with each other. A substantial programme of work has been conducted by the Agri-Food and Biosciences Institute in Northern Ireland aimed at quantifying those factors of most importance to the local beef industry. Post-slaughter effects such as carcase chilling and electrical stimulation, ageing, carcase hanging and cooking method have been shown to have a significant impact on eating quality when compared with pre-slaughter activities such as animal handling and lairage time in the Northern Ireland studies. However, the effect of animal breed, particularly the use of dairy breed animals, was shown to significantly improve eating quality. Many of these factors were found to interact with each other.

Inovações Didáticas na Disciplina Introdução ao Ensino de Biologia: Conversas entre Ensino, Pesquisa e Extensão

A formação de professores ainda é um desafio para universidades e outros centros formadores. Tendo em vista uma de suas principais metas, a de garantir maior encadeamento entre as unidades de formação dos cursos para professores, o Instituto de Biociências da Universidade de São Paulo desenvolveu seu Projeto Pedagógico, buscando garantir disciplinas e ações comuns às habilitações de bacharelado e licenciatura de seu curso de Ciências Biológicas. Uma das disciplinas oferecidas no Núcleo Básico aborda aspectos introdutórios ao ensino de Biologia e busca articular as dimensões do tripé universitário: ensino, pesquisa e extensão. Neste relato, serão apresentados a estrutura básica de tal disciplina, os principais recursos e estratégias utilizados e as ferramentas de avaliação

Raspberry-like poly(γ-glutamic acid) hydrogel particles for pH-dependent cell membrane passage and controlled cytosolic delivery of antitumor drugs.

In this research, we synthesized bioderived poly(amino acid) hydrogel particles that showed pH-dependent membrane-disrupting properties and controlled cytosolic delivery of antitumor drugs. Poly(γ-glutamic acid) (γ-PGA) that has been produced extensively using bacteria, especially those of Bacillus subtilis species, was modified with cholesterol (γ-PGA/Chol), and the γ-PGA/Chol conjugates were used to form polymeric nanoparticles the size of 21.0±1.1 nm in aqueous solution. When the polymeric nanoparticles were mixed with doxorubicin (Dox), raspberry-like hydrogel particles (RBHPs) were formed by the electrostatic interaction between the cationically charged Dox and the anionically charged nanoparticles. The average size and surface charge of the RBHPs in aqueous solution were 444.9±122.5 nm and −56.44 mV, respectively. The loaded amount of Dox was approximately 63.9 μg/mg of RBHPs. The RBHPs showed controlled drug release behavior in both in vitro and ex vivo cell-based experiments. Through fluorescence microscopy and fluorescence-activated cell sorting, the cellular uptake of RBHPs into human cervical cancer cells (HeLa) was analyzed. The cytotoxic effect, evaluated by the methyl tetrazolium salt assay, was dependent on both the concentration of RBHPs and the treatment time. The pH-dependent membrane-disrupting properties of the RBHPs and the subsequent cytosolic delivery of Dox were evaluated using a standard hemolysis assay. Upon an increase in hydrophobicity at the lysosomal acidic pH, RBHPs could easily interact, penetrate cell membranes, and destabilize them. Taken together, the data suggested that RBHPs could be used as drug delivery carriers after loading with other therapeutic drugs, such as proteins or small interfering RNA for cancer therapy.