Monday, November 2, 2015

Development of Ti-Nb-Zr alloys with high elastic admissible strain for temporary orthopedic devices

Journal Reference

Acta Biomater. 2015;20:176-87. doi: 10.1016/j.actbio.2015.03.023.

Ozan S¹, Lin J², Li Y³, Ipek R⁴, Wen C⁵.

Show Affiliations

Faculty of Engineering and Industrial Sciences, Swinburne University of Technology, Hawthorn, Victoria 3122, Australia; Department of Mechanical Engineering, Ege University, 35100 Bornova, Izmir, Turkey.
Advanced Material Research andDevelopment Center, Zhejiang Industry & Trade Vocational College, Wenzhou, Zhejiang 325003, China; Department of Materials Science and Engineering, Jilin University, Changchun, Jilin 130025, China.
School of Aerospace, Mechanical and Manufacturing Engineering, RMIT University, Melbourne, Victoria 3083, Australia.
Department of Mechanical Engineering, Ege University, 35100 Bornova, Izmir, Turkey.
Faculty of Engineering and Industrial Sciences, Swinburne University of Technology, Hawthorn, Victoria 3122, Australia; School of Aerospace, Mechanical and Manufacturing Engineering, RMIT University, Melbourne, Victoria 3083, Australia. Electronic address: cuie.wen@rmit.edu.au.

Abstract

A new series of beta Ti-Nb-Zr (TNZ) alloys with considerable plastic deformation ability during compression test, high elastic admissible strain, and excellent cytocompatibility have been developed for removable bone tissue implant applications. TNZ alloys with nominal compositions of Ti-34Nb-25Zr, Ti-30Nb-32Zr, Ti-28Nb-35.4Zr and Ti-24.8Nb-40.7Zr (wt.% hereafter) were fabricated using the cold-crucible levitation technique, and the effects of alloying element content on their microstructures, mechanical properties (tensile strength, yield strength, compressive yield strength, Young’s modulus, elastic energy, toughness, and micro-hardness), and cytocompatibilities were investigated and compared. Microstructural examinations revealed that the TNZ alloys consisted of β phase. The alloy samples displayed excellent ductility with no cracking, or fracturing during compression tests. Their tensile strength, Young’s modulus, elongation at rupture, and elastic admissible strain were measured in the ranges of 704-839 MPa, 62-65 GPa, 9.9-14.8% and 1.08-1.31%, respectively. The tensile strength, Young’s modulus and elongation at rupture of the Ti-34Nb-25Zr alloy were measured as 839 ± 31.8 MPa, 62 ± 3.6 GPa, and 14.8 ± 1.6%, respectively; this alloy exhibited the elastic admissible strain of approximately 1.31%. Cytocompatibility tests indicated that the cell viability ratios (CVR) of the alloys are greater than those of the control group; thus the TNZ alloys possess excellent cytocompatibility.

Go To Acta Biomater.

About The Author

Dr Sertan Ozan received his MSc and PhD degrees in Mechanical Engineering from Ege University, Turkey. During his PhD study, he has spent 18 months at Swinburne University of Technology, Australia as a visiting research student under supervision of Professor Cuie Wen. Currently, he is a research fellow in the Department of Mechanical Engineering of Bozok University, Turkey. His research focuses on the mechanical behaviour of metallic biomaterials and developing new Ti alloys.

About The Author

Mr Jixing Lin received his BS (2004) and MS (2007) degrees from Jiangxi university of Science and Technology, China. He is currently a PhD candidate under supervision of Professor Guanyu Li at Jilin University and Professor Cuie Wen at RMIT University. Since 2015, he has been appointed as Associate Professor in the Advanced Material Research & Development Center, Zhejiang Industry and Trade Vocational College, China. His research interests include biocompatible titanium alloys, biodegradable magnesium alloys, corrosion and surface modification for metals and alloys.

About The Author

Dr Yuncang Li obtained his PhD in Materials Engineering from Deakin University, Australia in 2004 and then took up a research fellow position in Biomaterials Engineering at Deakin University to the end of 2014. He joined RMIT University as a Senior Research Fellow of Biomaterials Engineering in the beginning of 2015. His research focuses on the developing of biomaterials, amorphous and nano-structured materials, titanium based shape memory alloys, biodegradable magnesium alloys, nano particulate-reinforced titanium composites and surface functionalisation on metallic implant materials. He has published more than 140 peer-reviewed articles: ttps://scholar.google.com.au/citations?user=1DlmTHgAAAAJ&hl=en.

About The Author

Dr Cuie Wen is Professor of Biomaterials Engineering at RMIT University and leads the biomaterials research team. This team’s research focuses on biocompatible titanium alloys and scaffolds, shape memory alloys and surface modification, biodegradable magnesium alloys, nanostructured metals, alloys and composites, metal foams and nanolaminates. Cuie was Professor of Surface Engineering at Swinburne University of Technology from 2010 to 2014. She joined Deakin University as a Research fellow 2003 and was appointed senior researcher 2007 and associate professor 2010. She worked in the National Institute of Advanced Industrial Science and Technology (Japan) before she moved to Australia. She has published over 300 refereed articles: http://ift.tt/1l3JxKa

Age-dependent alterations in the inflammatory response to pulmonary challenge

Significance Statement

Changes in pulmonary physiology, pathology, and function are common in older populations, and lead to altered responses and increased morbidity and mortality associated with lung infections. However, in many respects, the reasons for the altered susceptibility remain unclear. Our previous studies have revealed that age influences early changes (6hrs after pulmonary challenge) in lung water and oxygen saturation (Lee et al Shock 2013, 40:Suppl 1, 27), and temperature control, hemodynamics and myocardial proteasome activity (Linge et al Exp Lung Res 2015, 41:4, 216-227). Understanding age-related changes in the immune response within the pulmonary compartment and its impact on lung host defense and systemic responses, is of critical importance for developing effective therapeutic strategies for the treatment of the older patient. The current study highlights age-related changes and the possible interactions between inflammatory (MIF) and metabolic pathways (thyroxine) that are not immediately obvious (Al-Abed et al PNAS 2011, 108:20, 8224–8227). It also underlines the importance of using age-appropriate models for studying clinical conditions.

The research team brought together individuals with a variety of ethnic backgrounds (Sweden, Pakistan, China, S. Korea and England) and specialties/interests (host response, internal medicine, analytical chemistry, pulmonary critical care, bio/clinical chemistry). A diverse group can result in different approaches to a single problem, and differences in interpretation of data achieved. This has led to a series of interesting studies and publications (including the current manuscript) that have revealed some aspects of disease pathogenesis that have not previously been considered.

Journal Reference

Immunol Res. 2015 Aug 29.

Linge HM, Ochani K, Lin K, Lee JY, Miller EJ.

Center for Heart and Lung Research, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY, 11030, USA.

Abstract

The aging lung is increasingly susceptible to infectious disease. Changes in pulmonary physiology and function are common in older populations, and in those older than 60 years, pneumonia is the major cause of infectious death. Understanding age-related changes in the innate and adaptive immune systems, and how they affect both pulmonary and systemic responses to pulmonary challenge are critical to the development of novel therapeutic strategies for the treatment of the elderly patient. In this observational study, we examined age-associated differences in inflammatory responses to pulmonary challenge with cell wall components from Gram-positive bacteria. Thus, male Sprague-Dawley rats, aged 6 months or greater than 18 months (approximating humans of 20 and 55-65 years), were challenged, intratracheally, with lipoteichoic acid and peptidoglycan. Cellular and cytokine evaluations were performed on both bronchoalveolar lavage fluid (BAL) and plasma, 24 h post-challenge. The plasma concentration of free thyroxine, a marker of severity in non-thyroidal illness, was also evaluated. The older animals had an increased chemotactic gradient in favor of the airspaces, which was associated with a greater accumulation of neutrophils and protein. Furthermore, macrophage migration inhibitory factor (MIF), an inflammatory mediator and putative biomarker in acute lung injury, was increased in both the plasma and BAL of the older, but not young animals. Conversely, plasma free thyroxine, a natural inhibitor of MIF, was decreased in the older animals. These findings identify age-associated inflammatory/metabolic changes following pulmonary challenge that it may be possible to manipulate to improve outcome in the older, critically ill patient.

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Upregulation of miR-125b by estrogen protects against non-alcoholic fatty liver in female mice

Significance Statement

Non-alcohol fatty liver disease (NAFLD) is considered to be the hepatic manifestation of the metabolic syndrome. NAFLD occurs mainly due to the fat accumulation in the liver, and can lead to cirrhosis, which is not reversible and may ultimately progress to hepatocellular carcinoma.

The previous reports showed that estrogen protects against hepatic steatosis. The risk of developing NAFLD markedly increases in postmenopausal women and men. The hormone (estrogen) replacement therapy might be one consideration for prevention or treatment of NAFLD, but estrogen may lead to side effects like breast cancer. And we can’t treat men with estrogen against NAFLD.

Here, we firstly demonstrated that estrogen could regulate miR-125b expression via estrogen receptor alpha and that miR-125b could inhibit lipid accumulation in vitro and in vivo. Notably, we discovered FAS as a novel functional target of miR-125b. We demonstrated the function of miR-125b on limiting fat accumulation and inflammatory insults in the liver of both male and females, providing new understanding of a molecular mechanism underlying hepatic steatosis.

We identify a novel mechanism that estrogen protects against hepatic steatosis in female mice by miR-125b and provide a potential treatment strategy for metabolic disorders.

Journal Reference

J Hepatol. 2015. pii: S0168-8278(15)00541-3.

Zhang ZC¹, Liu Y¹, Xiao LL¹, Li SF¹, Jiang JH¹, Zhao Y¹, Qian SW¹, Tang QQ², Li X³.

Show Affiliations

Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, Fudan University Shanghai Medical College, Shanghai 200032, PR China.
Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, Fudan University Shanghai Medical College, Shanghai 200032, PR China; Institute of Stem Cell and Regenerative Medicine, Institutes of Biomedical Sciences, Fudan University, Shanghai 200032, PR China.
Key Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, Fudan University Shanghai Medical College, Shanghai 200032, PR China. Electronic address: lixi@shmu.edu.cn.

ABSTRACT

BACKGROUND & AIMS:
Due to the protective effect of estrogen against hepatic fat accumulation, the prevalence of non-alcoholic fatty liver disease (NAFLD) in premenopausal women is lower than that in men at the same age and in postmenopausal women. Our study was to further elucidate an underlying mechanism by which estrogen prevents NAFLD from miRNA perspective in female mice.

METHODS:
miRNA expression was evaluated by TaqMan miRNA assay. Luciferase and ChIP assay were done to validate regulation of miR-125bby estrogen via estrogen receptor alpha (ERα). Nile red and Oil red O staining were used to check lipid content. Overexpressing or inhibiting the physiological role of miR-125b in the liver of mice through injecting adenovirus were used to identify the function of miR-125b in vivo.

RESULTS:
miR-125b expression was activated by estrogen via ERα in vitro and in vivo. miR-125b inhibited lipid accumulation both in HepG2 cells and primary mouse hepatocytes. Consistently, ovariectomized or liver-specific ERα knockdown mice treated with miR-125b overexpressing adenoviruses were resistant to hepatic steatosis induced by high-fat diet, due to decreased fatty acid uptake and synthesis and decreased triglyceride synthesis. Conversely, inhibiting the physiological role of miR-125b with a sponge decoy slightly promoted liver steatosis with a high-fat diet. Notably, we provided evidence showing that fatty acid synthase was a functional target of miR-125b.

CONCLUSION:
Our findings identify a novel mechanism by which estrogen protects against hepatic steatosis in female mice via upregulating miR-125b expression.

Go To J Hepatol.

About The Author

Xi Li: Prof. Li is a Professor in Department of Biochemistry and Molecular Biology at Fudan University Basic Medical School, with a Ph.D. in Physiology from Nanjing University, and post-doctoral training at Johns Hopkins University Medical School. Dr. Li‘s research interests are transcriptional and epigenetic regulation of adipogenesis, and the molecular mechanism of obesity related disease.

Mechanistic Insights into R776H Mediated Activation of Epidermal Growth Factor Receptor Kinase

Significance Statement

Epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase that is frequently mutated in a variety of human cancers. Researchers from the University of Georgia characterized a novel recurrent oncogenic mutation (R776H) in the hinge region of EGFR kinase domain through a combination of cell-based assays and molecular dynamics simulations. The authors show that the R776H mutation activates the kinase domain by enhancing EGFR dimerization, a critical step in EGFR activation, and the mutant form preferentially adopts the acceptor position in the asymmetric dimer. The authors also demonstrate that the asymmetric dimer can phosphorylate monomeric EGFR, providing insights into lateral phosphorylation and downstream signaling. Using molecular modeling and molecular dynamics simulations, the authors propose a mechanistic model in which loss of key auto-inhibitory interactions with the regulatory αC-helix results in constitute activation. These findings have implications for the design of mutant-specific EGFR inhibitors for personalized cancer therapy

About The Author

Dr. Natarajan Kannan is an Associate Professor in the Department of Biochemistry & Molecular Biology and Institute of Bioinformatics at the University of Georgia, Athens, GA. He obtained his PhD at the Indian Institute of Science, Bangalore in 2001, and post-doctoral training at University of California, San Diego and Cold Spring Harbor Laboratory, New York. Dr. Kannan is a Georgia Cancer Coalition Distinguished Cancer Scholar.

About The Author

Zheng Ruan is a PhD student at The University of Georgia in Athens, GA. He finished his undergraduate study at Huazhong Agricultural University, Wuhan, China. ZhengRuan’s current research focuses on understanding the dynamics and functions of protein kinases using computational and experimental approaches.

Journal Reference

Biochemistry. 2015;54(27):4216-25.

Ruan Z, Kannan N.

Department of Biochemistry & Molecular Biology and ^‡Institute of Bioinformatics, University of Georgia, Athens, Georgia, United States

Abstract

The epidermal growth factor receptor (EGFR) kinase is activated by a variety of mutations in human cancers. R776H is one such recurrent mutation (R752H in another numbering system) in the αC-β4 loop of the tyrosine kinase domain that activates EGFR in the absence of the activating EGF ligand. However, the mechanistic details of how R776H contributes to kinase activation are not well understood. Here using cell-based cotransfection assays, we show that the R776H mutation activates EGFR in a dimerization-dependent manner by preferentially adopting the acceptor position in the asymmetric dimer. The acceptor function, but not the donor function, is enhanced for the R776H mutant, supporting the “superacceptor” hypothesis proposed for oncogenic mutations in EGFR. We also find that phosphorylation of monomeric EGFR is increased by R776H mutation, providing insights into EGFR lateral phosphorylation and oligomerization. On the basis of molecular modeling and molecular dynamics simulation, we propose a model in which loss of key autoinhibitory αC-helix capping interaction and alteration of coconserved cis regulatory interactions between the kinase domain and the flanking regulatory segments contribute to mutational activation. Since the R776 equivalent position is mutated in ErbB2 and ErbB4, our studies have implications for understanding kinase mutational activation in other ErbB family members as well.

Go To Biochemistry

Figure legend

Background: DNA sequences of EGFR with the R776 codon highlighted in red. Upper left panel: WT EGFR adopts αC-helix “out” conformation, whereas R776H favors αC-helix “in” conformation. Right panel: R776H mutant adopts the “acceptor” position in the asymmetric dimer. Lower left panel: R776H mutant exerts lateral phosphorylation of monomeric EGFR.

An Early and Robust Activation of Caspases Heads Cells for a Regulated Form of Necrotic-like Cell Death

Journal Reference

J Biol Chem. 2015;290(34):20841-55.

Garcia-Belinchón M¹, Sánchez-Osuna M¹, Martínez-Escardó L², Granados-Colomina C², Pascual-Guiral S², Iglesias-Guimarais V¹, Casanelles E¹, Ribas J³,Yuste VJ⁴.

Show Affiliations

From the Cell Death, Senescence and Survival group, Departament de Bioquímica i Biologia Molecular-Unitat de Medicina and Institut de Neurociències, Facultat de Medicina, Universitat Autònoma de Barcelona, Campus de Bellaterra, 08193 Cerdanyola del Vallès, Barcelona, Spain, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Universitat Autònoma de Barcelona, Campus de Bellaterra, 08193 Cerdanyola del Vallès, Barcelona, Spain, and.
From the Cell Death, Senescence and Survival group, Departament de Bioquímica i Biologia Molecular-Unitat de Medicina and Institut de Neurociències, Facultat de Medicina, Universitat Autònoma de Barcelona, Campus de Bellaterra, 08193 Cerdanyola del Vallès, Barcelona, Spain.
Celldeath regulation by non-coding RNA group, Pharmacology Unit, Departament de Medicina Experimental, Universitat de Lleida/Institut de Recerca Biomèdica de Lleida, Avinguda Rovira Roure 80, 25198 Lleida, Spain.
From the Cell Death, Senescence and Survival group, Departament de Bioquímica i Biologia Molecular-Unitat de Medicina and Institut de Neurociències, Facultat de Medicina, Universitat Autònoma de Barcelona, Campus de Bellaterra, 08193 Cerdanyola del Vallès, Barcelona, Spain, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Universitat Autònoma de Barcelona, Campus de Bellaterra, 08193 Cerdanyola del Vallès, Barcelona, Spain, and victor.yuste@uab.cat

Abstract

Apoptosis is triggered by the activation of caspases and characterized by chromatin condensation and nuclear fragmentation (type II nuclear morphology). Necrosis is depicted by a gain in cell volume (oncosis), swelling of organelles, plasma membrane leakage, and subsequent loss of intracellular contents. Although considered as different cell death entities, there is an overlap between apoptosis and necrosis. In this sense, mounting evidence suggests that both processes can be morphological expressions of a common biochemical network known as “apoptosis-necrosis continuum.” To gain insight into the events driving the apoptosis-necrosis continuum, apoptotically proficient cells were screened facing several apoptotic inducers for the absence of type II apoptotic nuclear morphologies. Chelerythrine was selected for further studies based on its cytotoxicity and the lack of apoptotic nuclear alterations. Chelerythrine triggered an early plasma membrane leakage without condensed chromatin aggregates. Ultrastructural analysis revealed that chelerythrine-mediated cytotoxicity was compatible with a necrotic-like type of cell death. Biochemically, chelerythrine induced the activation of caspases. Moreover, the inhibition of caspases prevented chelerythrine-triggered necrotic-like cell death. Compared with staurosporine, chelerythrine induced stronger caspase activation detectable at earlier times. After using a battery of chemicals, we found that high concentrations of thiolic antioxidants fully prevented chelerythrine-driven caspase activation and necrotic-like celldeath. Lower amounts of thiolic antioxidants partially prevented chelerythrine-mediated cytotoxicity and allowed cells to display type II apoptotic nuclear morphology correlating with a delay in caspase-3 activation. Altogether, these data support that an early and pronounced activation of caspases can drive cells to undergo a form of necrotic-like regulated cell death.

Go To J Biol Chem.

Par6G suppresses cell proliferation and is targeted by loss-of-function mutations in multiple cancers

Journal Reference

Oncogene. 2015 Jun 15 (Advance online publication).

Marques E¹, Englund JI¹, Tervonen TA¹, Virkunen E¹, Laakso M², Myllynen M¹, Mäkelä A¹, Ahvenainen M¹, Lepikhova T³, Monni O³, Hautaniemi S², Klefström J¹.

Show Affiliations

Cancer Cell Circuitry Laboratory, Research programs unit, Translational Cancer Biology and Institute of Biomedicine, University of Helsinki, Finland.
Systems Biology Laboratory, Genome-Scale Biology Program and Institute of Biomedicine, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland.
Genome-Scale Biology Program and Institute of Biomedicine, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland.

Abstract

Differentiated epithelial structure communicates with individual constituent epithelial cells to suppress their proliferation activity. However, the pathways linking epithelial structure to cessation of the cell proliferation machinery or to unscheduled proliferation in the context of tumorigenesis are not well defined. Here we demonstrate the strong impact of compromised epithelial integrity on normal and oncogenic Myc-driven proliferation in three-dimensional mammary epithelial organoid culture. Systematic silencing of 34 human homologs of Drosophila genes, with previously established functions in control of epithelial integrity, demonstrates a role for human genes of apico-basal polarity, Wnt and Hippo pathways and actin dynamics in regulation of the size, integrity and cell proliferation in organoids. Perturbation of these pathways leads to diverse functional interactions with Myc: manifested as a RhoA-dependent synthetic lethality and Par6-dependent effects on the cell cycle. Furthermore, we show a role for Par6G as a negative regulator of the phosphatidylinositol 3′-kinase/phosphoinositide-dependent protein kinase 1/Akt pathway and epithelial cell proliferation and evidence for frequent inactivation of Par6G gene in epithelial cancers. The findings demonstrate that determinants of epithelial structure regulate thecell proliferation activity via conserved and cancer-relevant regulatory circuitries, which are important for epithelial cell cycle restriction and may provide new targets for therapeutic intervention.

Go To Oncogene.

About The Author

Juha Klefström, PhD, is a Research Director in Research Programs Unit, Medical Faculty, University of Helsinki and in Biomedicum Functional Genomics Unit. Klefström’s primary research interests are in breast cancer biology, genetically engineered mouse models of breast cancer, mammary gland reconstitution techniques, ex vivo organoid cultures and recombinant viral gene transfer methods. His laboratory has established variety of three-dimensional culture systems for primary mammary epithelial and tumor organoids to explore roles and targetability of Myc, Lkb1 and cell polarity pathways in breast cancer

About The Author

Elsa Marques, MSc, is a PhD student in Research Programs Unit/ Translational Cancer Biology, University of Helsinki. She graduated from University of Coimbra, Portugal and followed her interests in cancer biology to Finland where she joined the laboratory of Juha Klefström. Her current main research interests are in the role of apicobasal polarity genes in development of breast cancer.

Friday, October 23, 2015

List of Medical Research Papers featured as Key Scientific Articles on Global Medical Discovery (23rd October 2015)

The following research papers were selected as high impact medical research and featured on Global Medical Discovery (https://globalmedicaldiscovery.com/) on October 23rd 2015:

A new key Nanotechnology article: Nanostructured Biointerfaces: Nanoarchitectonics of Thermoresponsive Polymer Brushes Impact Protein Adsorption and Cell Adhesion on Global Medical Discovery. https://globalmedicaldiscovery.com/key-nanotechnology-articles/nanostructured-biointerfaces-nanoarchitectonics-of-thermoresponsive-polymer-brushes-impact-protein-adsorption-and-cell-adhesion/

A new key stem cell research article: Dietary restriction mitigates age-related accumulation of DNA damage, but not all changes in mouse corneal epithelium has just been featured on Global Medical Discovery. https://globalmedicaldiscovery.com/key-stem-cells-research-articles/dietary-restriction-mitigates-age-related-accumulation-dna-damage-but-not-all-changes-mouse-corneal-epithelium/

A new key drug discovery article: Antitumor and cytotoxic properties of a humanized antibody specific for the GM3(Neu5Gc) ganglioside is now featured on Global Medical Discovery. https://globalmedicaldiscovery.com/key-drug-discovery-articles/antitumor-cytotoxic-properties-humanized-antibody-specific-for-gm3neu5gc-ganglioside/

A new key scientific article: Monoclonal Antibodies Targeting LecLex-Related Glycans with Potent Antitumor Activity is now featured on Global Medical Discovery. https://globalmedicaldiscovery.com/key-scientific-articles/monoclonal-antibodies-targeting-leclex-related-glycans-with-potent-antitumor-activity/

A new key scientific article: Involvement of the Tyro3 receptor and its intracellular partner Fyn signaling in Schwann cell myelination is now featured on Global Medical Discovery. https://globalmedicaldiscovery.com/key-scientific-articles/involvement-of-tyro3-receptor-intracellular-partner-fyn-signaling-schwann-cell-myelination/

A new key scientific article: Genetic and epigenetic trends in telomere research: a novel way in immunoepigenetics is now featured on Global Medical Discovery. https://globalmedicaldiscovery.com/key-scientific-articles/genetic-and-epigenetic-trends-in-telomere-research-a-novel-way-in-immunoepigenetics/

A new key scientific article: The Anti-Proliferative Effect of Boron Neutron Capture Therapy in Prostate Cancer Xenograft Model is now featured on Global Medical Discovery. https://globalmedicaldiscovery.com/key-scientific-articles/anti-proliferative-effect-boron-neutron-capture-therapy-prostate-cancer-xenograft-model/