exPlants

Dr. Maria Somleva (Metabolix Inc., Cambridge, MA) has received funding from the DOE (Award Number: DE-EE0004943) for 6 million dollars for the grant titled “Renewable Enhanced Feedstocks for Advanced Biofules and Bioproducts (REFABB)”. Dr. Somleva has also recently published the paper titled “PHA bioplastics, biochemicals, and energy from crops” in the Plant Biotechnology Journal. Please use the attached link to read the abstract of the paper http://www.ncbi.nlm.nih.gov/pubmed/23294864.


Dr. Dwight Tomes retired from Pioneer Hi-Bred at the end of January, 2013.

 

 

Dr. Jerry Ranch retired from Pioneer Hi-Bred at the end of February, 2013.

Both Dwight and Jerry are involved with Pioneer on a part-time basis so they are not “fully retired”.

Submitted by David Songstad


Dr. Joseph Petolino (Dow AgroSciences) has published the paper titled “Activation domains for controlling plant gene expression using designed transcription factors” in the Plant Biotechnology Journal. Please use the attached link to read the abstract of the paper http://www.ncbi.nlm.nih.gov/pubmed/23521778 .


Özge Çelik, received the title of Assoc. Prof. Dr. on February 21, 2014. On June 26, 2014, she made an oral presentation which was entitled as “An Investigation On Regulation on Trichome Metabolism Related Genes Against Salt Stress In Soybean (Glycine max L. Merr.)” in Biotechnology

sciNews2

Update from Dr. Robert Stevenson

After retiring as Director of the ATCC, I spent several years traveling, renovating old houses and painting landscapes. In 2001 I was employed by the American Association of Tissue Banks to revamp their accreditation program for tissue banks and when that was accomplished to serve as a consultant inspector of tissue banks. During this period I also served on the AATB Standards Committee and was a member of a committee to write the first standards for non- transplant tissue banks that were published in 2012 along with the 13th edition of Standards for Tissue Banking.

In 2004 the AATB conferred their highest award, the George W Hyatt Award on me for contributions to the field.

In 2012 I reached the age of 86 and decided it was time to retire again.

Since 1951, when I became a member of the Tissue Culture Association, I have had the privilege of knowing many wonderful people in that organization and learning from the pioneers in the field. I wish for the continuation of that tradition and your future success.

Submitted by Dr. Robert Stevenson


Dr. Wallace McKeehan (Texas A&M Health Sciences Center Institute of Biosciences and Technology) and his research team were recently featured in an article published in the Texas Medical Center News Online (Vol. 35(7), 2013) for their research demonstrating the importance of adipocyte FGFR1 receptors as a potential therapeutic target for alleviating obesity.

To read the entire article please use the provided link http://tmcnews.org/articles/liver-hormone-targets-fat-cells-discovery-may-help-develop-new-obesity-treatments/.


Dr. James Trosko (Michigan State University) was invited by Health Canada and the Canadian Institute of Health Research to speak at the CIHR Best Brain Exchange: Integrating Epigenetic Effects of Food and Environmental Contaminants into Risk Assessments Meeting on Tuesday March 19, 2013 in Ottawa, Ontario. A summary of Dr. Trosko’s presentation titled “Integrating Epigenetic Effects of Food and Environmental Contaminants into Risk Assessments” is included below.

Canadian Institutes of Health Research, Ottawa Ca, March 19, 2013:

“Integrating Epigenetic Effects of Food and Environmental Contaminants into Risk Assessments”

The Role of Nutritional/Dietary “Epigenetics” in Modulating the Risk to Acute & Chronic Human Diseases.

James E. Trosko, Ph.D., Center for Integrative Toxicology, Institute for International Health, Dept. Pediatrics/Human Development, College of Human Medicine, and Reza Nassiri, D.Sc., FACCP, Director of International Institute of Health, College of Osteopathic Medicine, Michigan State University, East Lansing, Michigan 48824, USA In the context of finite global resources for sustained healthy human survival, population explosion, increased environmental pollution, decreased clean air, water, food distribution, climate changes, changing gut microbiome, diminishing opportunities for human self-esteem, increased median life span, and interconnected causes of acute infectious and chronic diseases, the need to understand the factors leading to human diseases will be necessary for both the long term prevention and for managing short-term crises heath problems. There are but three mechanisms that can affect the pathogenesis of human diseases, such as birth defects, behavioral disorders, cardiovascular diseases, cancers, reproductive-and neuro-toxicological effects, and immune-reactions.

Those three mechanisms are: (a) mutations or “genotoxicity”, caused by either “errors in DNA repair or by “errors in DNA replication”; (b) cell death or cytotoxicity, caused by necrosis, apoptosis , etc. and (c) alteration in gene expression at the transcriptional ( DNA methylation; histone acetylation, etc,); translational levels ( m-RNA splice variants) or posttranslational levels ( mi-RNA effects and protein phosphorylation) or “Epigenetic toxicity”. Both natural agents (hormones, cytokines, growth factors; neurotransmitters, food components, products of food processing, biological toxins) and synthetic agents ( pesticides, food additives, pharmaceuticals, cosmetics) can trigger “epigenetic “ events. These epigenetic agents , by interacting with an organism, ultimately interact by extra-cellular communication with the three types of cells ( stem, transit amplifying cells and differentiated cells) , differentially, to trigger intracellular communication that either turn on or turn off genes, which, in turn, modulate gap junctional inter-cellular communication. These three integrated communication mechanisms exist in all organs of our body to regulate, homeostatically, the 5 choices a cell has when its internal physiology is altered by epigenetic agents. They can (a) proliferate; (b) differentiate; (c) apoptose; (d) senescence or (e) adaptively respond.[ 1]These are mutually exclusive choices a cell makes depending on the intracellular changes induced by the extracellular communicating molecule.(Figure 1)

Figure 1.

These epigenetic agents can be species-specific, gender specific, developmentally specific, organ –specific. They also work at threshold levels. They are effective in the absence of anti-epigenetic agents; they can work with other agents, additively, synergistically, or antagonistically. Depending on the biological context, they can have “good news-bad news” characteristics (retinoids, thalidomide, genistein, ATBC and CARET trials).

On a completely different level, the role of nutritional/food epigenetic effects must be viewed from an interaction of our biological and culturally evolutionary history. [2, 3] The transition of our pre-human geographical-determined biological evolutionary- nutritional requirements for survival to our current unequal and culturally- shaped diet has created a biologically mis-matched human nutritional experience. While genetic, gender, and developmental stage factors contribute to human diseases, various environmental and culturally-determined factors are now contributing to both acute and chronic diseases. The transition from the hunter-gatherer to an agricultural -dependent human being has brought about a global crisis in human health. Initially, early humans ate seasonally-dependent and calorically-restricted foods, during the day, in a “feast or famine” manner. Today, modern humans eat diets of caloric abundance, at all times of the day, with foods of all seasons and from all parts of the world, that have been processed and which have been contaminated by all kinds of factors, due to a diaspora of crops and global climate changes. No longer can one view, as distinct, infectious agent –related human acute diseases from chronic diseases. Given the predicted increase in the number of new births before the end of this century, a serious effort must be made to provide a healthy in utero environment for the most vulnerable stage of human development in order to prevent alterations in organ-specific adult stem cell numbers and stem cell –based diseases later in life. This new concept provides a mechanistic explanation for how pre-natal maternal environmental or dietary exposures can now affect diseases later in life (Barker Hypothesis). Studies of the atomic bomb survivors should illustrate this insight.

REFERENCES

  1. Upham, B.L. and Trosko, J.E., “Carcinogenic tumor promotion, induced oxidative stress signaling, modulated gap junction function and altered gene expression”. Antioxidants & Redox Signaling 11: 297-308, 2009.
  2. Trosko, J.E., “The gap junction as a ‘Biological Rosetta Stone’: Implications of evolution, stem cells to homeostatic regulation of health and disease in the Barker Hypothesis”. J. Cell Commun & Signaling, 5; 53-66, 2011.
  3. Trosko, J.E. “Pre-natal Epigenetic influences on acute and chronic diseases later in life, such as cancer : Global health crises resulting from a collision of biological and cultural evolution.. J. Food Science & Nutrition 16: 394-407, 2011.

 

 

The following Biotechnology training courses are being offered at the National Institutes of Health in Bethesda, MD.  These Workshops are sponsored by the Foundation for Advanced Education in the Sciences.  For more information on these workshops please visit www.biotrac.com.

 

October Workshops

Small Interfering RNA (siRNA) & Functional Genomics, September 30 – October 4, 2013
Vaccines: Development and Evaluation of Efficacy, October 7-11, 2013
Bioinformatic Analysis of Next Generation Sequencing Data, October 8-11, 2013
miRNA: Tools and Techniques for the Quantitative and Functional Analysis in Mammalian Cells, October 15 – 17, 2013
Protein Informatics, October 16 – 18, 2013
Stem Cell: Principles & Applications, October 21-25, 2013
iPSC II: Induced Human Pluripotent Stem Cells (hiPSC); Differentiation to Neural Lineages, October 28 – November 1, 2013

November Workshops

Protein-DNA Interactions: Gene Specific and Epigenetic Regulation of Expression of the Mammalian Genome, November 4-8, 2013
Super Resolution Microscopy: Principles and Methods, November 6-8, 2013
Flow Cytometry: Principles and Methods, November 12-15, 2013
Expression, Detection & Purification of Recombinant Proteins in Prokaryotic & Eukaryotic Cells, November 20-22, 2013

December Workshops

Epigenetics, December 11-13, 2013
Proteomics: Principles and Methods, December 9-13, 2013
Digital Imaging, December 11-13, 2013

January Workshops

Laser Capture Microdissection: Methods for Microgenomic Analysis, January 13-17, 2014
Immunofluorescence & Confocal Microscopy, January 21-24, 2014
Real Time and Quantitative PCR, January 27-31, 2014

February Workshops

Principles and Applications of DNA Microarrays, February 3-7, 2014
Genome Analysis and Mutation Detection, February 10-14, 2014
Vaccines: Development and Evaluation of Efficacy, February 18-21, 2014
Cellular Immunology: Principles and Methods, February 24-28, 2014

March Workshops

Stem Cell: Principles & Applications, March 3-7, 2014
iPSC II: Induced Human Pluripotent Stem Cells (hiPSC); Differentiation to Neural Lineages, March 10-14, 2014
Immunohistochemistry, March 19-21, 2014
Proteomics: Principles and Methods, March 24-28, 2014

April Workshops

Epigenetics, April 1-4, 2014
Nanotechnology in Medicine, April 9-11, 2014
Hybridization Techniques: Labeling, Detection & Applications, April 14-17, 2014
Cellular Immunology: Principles and Methods, April 21-25, 2014
miRNA: Tools and Technologies for the Quantitative and Functional Analysis in Mammalian Cells, April 28-30, 2014
Protein Informatics, April 29 – May 1, 2014

May Workshops

Flow Cytometry: Principles and Methods, May 6-9, 2014
Advanced Microarray Analysis and Pathway Integration, May 12-15, 2013
Mitochondrial Molecular Biology and Pathology Workshop, May 13-15, 2014
Animal and Human Cell Culture: Method and Applications, May 19-23, 2014

June Workshops

Recombinant DNA Methodology, June 2-6, 2014
Clinical Proteomics and Biomarker Discovery, June 16-20, 2014

July Workshops

PCR Methodology: Principles, Optimization and Applications, July 7-11, 2014
Bioinformatic Analysis of Next Generation Sequencing Data, July 8 – 11, 2014
Real Time and Quantitative PCR, July 14-18, 2014
Using TALENs for Gene Engineering, July 28-30, 2014