Archive for the ‘Drug Toxicity’ Category

Activation of Efficient and Multiple Site-specific Nonstandard Amino Acid Incorporation

Posted in Biological Networks, Gene Regulation and Evolution, Biomarkers & Medical Diagnostics, Cell Biology, Signaling & Cell Circuits, Chemical Genetics, Cytoskeleton, De novo synthesis, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Drug Toxicity, Evolutionary cognition, Experimental validation, Glycobiology: Biopharmaceutical Production, Pharmacodynamics and Pharmacokinetics, Immunodiagnostics, Infectious Disease & New Antibiotic Targets, Infectious Disease Immunodiagnostics, Innovation in Immunology Diagnostics, Molecular Genetics & Pharmaceutical, Pharmaceutical Analytics, Pharmacologic toxicities, Population Health Management, Genetics & Pharmaceutical, Proteomics, Systemic Inflammatory Response Related Disorders, Technology Advance Assessment of, Technology Transfer: Biotech and Pharmaceutical, Translational Effectiveness, Translational Research, Translational Science, tagged activation of biosynthesis, amino acid incorporation, Cell-free Protein Synthesis, chemical and biological engineering, incorporation of nonstandard AAs, Multiple Site-specific Nonstandard Amino Acid Incorporation, Release Factor 1, Synthetic biology on June 20, 2014| Leave a Comment »

Larry Bernstein, MD, FCAP

http://pharmaceuticalintelligence.com/6-19-3014/larryhbern/Activation of Efficient and Multiple Site-specific Nonstandard Amino Acid Incorporation

 

Cell-free Protein Synthesis from a Release Factor 1 Deficient Escherichia coli Activates Efficient and Multiple Site-specific Nonstandard Amino Acid Incorporation

Seok Hoon Hong †‡, Ioanna Ntai ‡§, Adrian D. Haimovich #, Neil L. Kelleher ‡§, Farren J. Isaacs #, and Michael C. Jewett *†‡

^†Department of Chemical and Biological Engineering,^‡Chemistry of Life Processes Institute, ^§Department of Chemistry, and Department of Molecular Biosciences,Northwestern University, Evanston, Illinois 60208,United States of America

Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, Connecticut 06520, United States of America

^# Systems Biology Institute, Yale University, West Haven, Connecticut 06516, United States of America

Member, Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois 60611, United States of America

Institute of Bionanotechnology in Medicine, Northwestern University, Chicago, Illinois 60611, United States of America

ACS Synth. Biol., 2014, 3 (6), pp 398–409

DOI: 10.1021/sb400140t

Publication Date (Web): December 13, 2013

Copyright © 2013 American Chemical Society

*Tel: +1 847 467 5007. Fax (+1) 847 491 3728. E-mail: m-jewett@northwestern.edu

Site-specific incorporation of nonstandard amino acids (NSAAs) into proteins

 

 

 

 

 

 

 

 

 

Site-specific incorporation of nonstandard amino acids (NSAAs) into proteins enables the creation of biopolymers, proteins, and enzymes with new chemical properties, new structures, and new functions. To achieve this, amber (TAG codon) suppression has been widely applied. However, the suppression efficiency is limited due to the competition with translation termination by release factor 1 (RF1), which leads to truncated products. Recently, we constructed a genomically recoded Escherichia coli strain lacking RF1 where 13 occurrences of the amber stop codon have been reassigned to the synonymous TAA codon (rEc.E13.ΔprfA). Here, we assessed and characterized cell-free protein synthesis (CFPS) in crude S30 cell lysates derived from this strain. We observed the synthesis of 190 ± 20 μg/mL of modified soluble superfolder green fluorescent protein (sfGFP) containing a single p-propargyloxy-l-phenylalanine (pPaF) or p-acetyl-l-phenylalanine. As compared to the parentrEc.E13 strain with RF1, this results in a modified sfGFP synthesis improvement of more than 250%. Beyond introducing a single NSAA, we further demonstrated benefits of CFPS from the RF1-deficient strains for incorporating pPaF at two- and five-sites per sfGFP protein. Finally, we compared our crude S30 extract system to the PURE translation system lacking RF1. We observed that our S30 extract based approach is more cost-effective and high yielding than the PURE translation system lacking RF1, 1000 times on a milligram protein produced/$ basis. Looking forward, using RF1-deficient strains for extract-based CFPS will aid in the synthesis of proteins and biopolymers with site-specifically incorporated NSAAs.

Keywords: 

cell-free protein synthesis; PURE translation; nonstandard amino acid;release factor 1; genomically recoded organisms

 

 

 

 

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Tang Prize for 2014: Immunity and Cancer

Posted in CANCER BIOLOGY & Innovations in Cancer Therapy, Discovery process, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Drug Toxicity, Evolutionary cognition, Experimental validation, Human Immune System in Health and in Disease, International Global Work in Pharmaceutical, Monoclonal Immunotherapy, Pharmaceutical Analytics, Pharmacologic toxicities, Proteomics, Technology Transfer: Biotech and Pharmaceutical, Translational Effectiveness, Translational Research, Translational Science, tagged Cancer - General, Cancer immunology, chemical structure, chemo regimens, chemoresistance, immunosupression, research, T-cell biology, therapeutic toxicity reduction, Translational Research on June 20, 2014| Leave a Comment »

Tang Prize for 2014: Immunity and Cancer

Curator: Larry Bernstein, MD, FCAP

 

 

2014 Tang Prize in Biopharmaceutical Sciences awards to James P. Allison and Tasuku Honjo For the discoveries of CTLA-4 and PD-1 as immune inhibitory molecules that led to their applications in cancer immunotherapy 2014/06/19.

Founded by Dr. Samuel Yin in December 2012, the Tang Prize recognizes scholars conducting revolutionary research in the four major fields of Sustainable Development, Biopharmaceutical Science, Sinology, and the Rule of Law. The Prize is awarded with each category a cash reward of over US$1 million (NT$50 million). The Tang Prize Foundation hopes that recipients of the Prize will continue to innovate while cultivating and nurturing new talent in their respective fields.
Academia Sinica was commissioned by the Tang-Prize Foundation to administer the selection of Tang-Prize Laureates for the category of Biopharmaceutical Science, recognizing original biopharmaceutical or biomedical research that has led to significant advances towards preventing, diagnosing and/or treating major human diseases to improve human health.
James P. Allison and Tasuku Honjo were chosen among nearly a hundred nominees for their discoveries of CTLA-4 and PD-1 as immune inhibitory molecules, revealing ways to harness our incredibly powerful immune system to fight cancer and marking the beginning of the immunotherapy revolution.
A critical process in the immune response involves presentation of antigens to T cells by antigen-presenting cells, two key cell types in our immune system. This process is highly regulated by molecules that stimulate the response to ensure our mounting a sufficient immune response, especially in the event of invasion by pathogens, but also by molecules that inhibit the process to ensure the response is not excessive. Indeed, there is now a family of proteins on T cells involved in this regulatory process, which is designated the “CD28 receptor family” co-receptors, as CD28 is the first protein identified to have such function. They are divided into co-receptors transmitting stimulatory signals and co-receptors transmitting inhibitory signals. Each of these has its counterpart (ligand) on antigen-presenting cells belonging to the “B7 family”. Two most prominent inhibitory receptors on T cells are called CTLA-4 (cytotoxic T lymphocyte antigen-4, as it is first identified on cytotoxic T lymphocytes) and PD-1 (program death-1, as it is first identified to be associated with a type of cell death process called programmed cell death). Their ligands are designated as B7-1/B7-2 and PD-L1/PD-L2, respectively. These are also referred to as immune checkpoint receptors and ligands.
Our immune system is not perfect and at times, the regulatory mechanisms might be faulty, which in fact may be the basis of a variety of diseases. For example, autoimmune diseases may be related to the suppressive mechanism becoming weak and the individuals can mount excessive immune responses even to their own cells and tissues. Also, our immune system is capable of recognizing cancer cells and attacking them, in a process called immune surveillance. However, cancer cells are also equipped with machineries to evade the host anti-tumor activity, which is described as immune escape. For example, cancer cells can also express B7 family ligands on their surfaces and, by engaging the co-receptors transmitting inhibitory signals on T cells, they can inhibit the host anti-tumor T cell activity. By recognizing how cancer cells escape the immune surveillance, scientists have developed novel approaches to interfere with the ability of cancer cells to suppress the immune response, thus enhancing the ability of the host immune system to inhibit cancer cell growth.
Dr. James Allison, Chairman, Department of Immunology and Executive Director, Immunotherapy Platform at the University of Texas, MD Anderson Cancer Center, is one of two scientist to identify CTLA-4 as an inhibitory receptor on T-cells in 1995 and was the first to recognize it as a potential target for cancer therapy.  His team then developed an antibody that blocks CTLA-4 activity and showed in 1996 that this antibody is able to help reject several different types of tumors in mouse models. This subsequently led to development of a monoclonal antibody drug, which has undergone clinical trials against stage 4 melanoma and been approved for treatment of melanoma by the U.S. FDA in 2011.
Dr. Tasuku Honjo, Professor, Department of Immunology and Genomic Medicine, Kyoto University, discovered PD-1 in 1992. His group subsequently established that PD-1 is an inhibitor regulator of the T cell response. Additional studies from his and other laboratories established that this protein plays a critical role in the regulation of tumor immunity and stimulated many groups to generate its blocker for the treatment of cancer. Antibodies against PD-1 have been approved by the U.S. FDA as an investigational new drug and developed for the treatment of cancer. One such antibody produced complete or partial responses in non-small-cell lung cancer, melanoma, and renal-cell cancer in clinical trials, and is predicted to be launched in 2015 for treatment of non-small cell lung cancer; this has been stated by some as having the potential to “change the landscape” of the treatment for lung cancer. Another antibody, shown to achieve a substantial response rate also in patients with non-small cell lung cancer, is currently in clinical trial for many types of cancers. In addition, combination therapy (anti-CTLA-4 plus anti-PD-1) has been shown to dramatically improve the long-term survival rates in cancer patients.
This is an exciting time in our fight against cancer. The discoveries by Dr. Allison and Dr. Honjo have spurred additional development of therapeutic approaches along the line of immunotherapy and brought new hope that many types of cancers can be cured.
In addition, dysregulation in immune checkpoint pathways may be intimately involved in other illnesses, such as allergy, infectious diseases, and autoimmune diseases. Thus, the approach of targeting immune stimulatory and inhibitory molecules also promises to lead to the development of new therapies for these diseases.
Dr. Allison’s and Dr. Honjo’s discoveries have opened a new therapeutic era in medicine.

 

Supplementary figure:

unleashes immune system to attack cancer cells

 

 

 

 

 

 

 

 

 

 

 

 

 

Dr. Samuel Yin, founder of the Tang Prize, is currently chairman of the Ruentex Group and chief development officer, chief technology officer, and chief engineer of Ruentex Construction & Development. He is also an adjunct professor in the department of civil engineering at National Taiwan University and a professor at Peking University, where he advises PhD students.

Dr. Yin read history at Chinese Culture University. He received a master’s degree in business administration at National Taiwan University and a doctorate in business administration at National Chengchi University.

In addition to his academic background in the humanities and business administration, Dr. Yin’s great interest in and devotion to interdisciplinary studies have made him an award-winning civil engineer and educator.

In 2004, Dr. Yin was named fellow of the Chinese Institute of Civil and Hydraulic Engineering. In 2008, he was invited to join Russia’s International Academy of Engineering and also awarded the Engineering Prowess Medal, the academy’s highest honour. In 2010, Dr. Yin received the Henry L. Michel Award for Industry Advancement of Research by the prestigious American Society of Civil Engineers (ASCE) for his contribution in the area of construction technology research. He was the first person without an academic background in engineering to receive the award.

Driven by a firm belief that he should give back to the society that has enabled him to achieve so much, Dr. Yin has been investing in philanthropy and education for a long time, in the hope of creating a positive force in society and making a better world.

Dr. Yin’s biggest dream was to set up an international award. He has long had great respect and admiration for the Nobel Prize, so he established an award modeled on the Nobel. The Tang Prize rewards excellent research in the areas of Sustainable Development, Biopharmaceutical Science, Sinology (excluding literary works), and Rule of Law. Dr. Yin hopes to encourage experts to dedicate themselves to innovative research in these fields and to spur human development with first-class research.

Dr. Yin’s relentless enthusiasm for philanthropy was instilled through his upbringing, particularly the example set by his late father Yin Shu-Tien. Dr. Yin established a foundation in memory of his grandfather, Yin Xun-Ruo, to provide scholarships to students of families originating in Shandong Province to study Chinese literature and history. When Yin senior passed away, Dr. Yin also set up the Kwang-Hua Education Foundation to help with China’s higher education programs.

In the past few years, Dr. Yin has set up a number of foundations to serve people on both sides of the Taiwan Strait and to foster more talented people for the nation (the Yin Xun-Ruo Educational Foundation, the Yin Shu-Tien Medical Foundation, the Kwang-Hua Education Foundation, and the Guanghua School of Management of Peking University). In 2012, Dr. Yin set up a global award, the Tang Prize, to spread his philanthropy across the world.

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The Discovery and Properties of Avemar – Fermented Wheat Germ Extract: Carcinogenesis Suppressor

Posted in Anaerobic Glycolysis, Biomedical Measurement Science, Ca2+ triggered activation, CANCER BIOLOGY & Innovations in Cancer Therapy, Discovery process, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Drug Toxicity, Experimental validation, FDA, CE Mark & Global Regulatory Affairs: process management and strategic planning - GCP, GLP, ISO 14155, Historical relevance, Intellectual Property, Innovations, Commercialization, Investment in technological breakthrough, International Global Work in Pharmaceutical, Interviews with Scientific Leaders, ISO 10993 for Product Registration: FDA & CE Mark for Development of Medical Devices and Diagnostics, Metabolomics, Nutrition, Oxidative phosphorylation, Phosphorylation, Population Health Management, Nutrition and Phytochemistry, Proteomics, Scientific & Biotech Conferences: Press Coverage, Signaling, Translational Science, Ubiquitinylation, tagged alternative medicine, Avemar, Chemotherapy, complementary medicine, Dietary supplement, experimental cancer research, fermented wheat germ extract, functional foods, gene expression, glucose consumption, pancreatic carcinoma, regulation of metabolism, RNA, tyrosine phosphorylation on June 7, 2014| Leave a Comment »

Larry H Bernstein, MD, FCAP, Contributor

Article ID #143: The Discovery and Properties of Avemar – Fermented Wheat Germ Extract: Carcinogenesis Suppressor. Published on 6/7/2014

WordCloud Image Produced by Adam Tubman

http://pharmaceuticalintelligence.com/5-6-2014/larryhbern/ The Discovery_and_Properties_of_Avemar – Fermented_ Wheat_Germ_Extract:_Carcinogenesis_Suppressor

The following discussion will be a review of the current interest in Avemar, a nontoxic, fermentation product of wheat germ extract, garnering interest with respect to alternative and complementary medicinal use.

Extracts from an interview by Sandra Cascio with Mate Hidvegi

Mate’s Transylvania Professor Lajos David was the organizer of the Department of Pharmacy of the University of Szeged in the 1920’s. He was elected as the Dean of the Faculty of Medicine, the first and only pharmacist who reached this high position at the University since. Dr. Hidvegy’s grandfather was a devout Roman catholic, who publicly opposed Nazi persecution of Jews during the Holocaust. One of his colleagues and, perhaps his best friend, was Albert Szent­Gyorgyi, the Nobel laureate who discovered vitaminC. Szent­Gyorgyi moved to the United States after World War II, where he turned to studies of muscle biochemistry. In his later years he turned to cancer research. He  theorized that a revolutionary anticancer drug could be based upon vitamin C combined with methoxy­substituted benzoquinones, the precursors of which can be found in wheat germ. After completion of the PhD, Dr. Hidvegi spent two years with the Wheat Grain Trust in Winnipeg, Canada, before returning to Hungary in 1990.  He decided to followthepathwaythat Szent­Gyorgyi was now engaged intocompletehisgoals.He contacted anoldfriend,GaborFodor, a brilliantchemist, also a collaborator withSzent­Gyorgyiincancerresearch.

He wasinvited by Hermann Esterbauer, the head of the Institute of Biochemistry at the University of Graz, to work in his laboratory. Thanks to the generosity of Professor Esterbauer,  he accomplished much at Graz  together with his student, Dr. Rita Farkas.  It was soon after Szent­-Gyorgyi’s death when, with the help of Dr. Fodor, they prepared the chemicals to make the drug Szent­-Gyorgyi had intended to make, with encouragement from the great quantum­ biochemist, Janos Ladik.  They made wheat germ extracts with the highest free benzoquinone content.This required a  fermentation process to liberate the benzoquinone moieties from the chemical bonds which keep them in natural forms: in glycosides. He recalls the purple colored active molecules in the fermentation liquid. Living cells with their exo­ and endo­enzymes are used to split bonds and make new molecules. This is also true for the manufacturing process of Avemar. This extract contains new molecules which cannot be found elsewhere.

“WhenAvemar was voted by the majority of the more than 50,000 professionals for NutrAward, it became obvious that this product is of biological efficacy  plus safety, and it is based on good science.” It received the financial support needed. From this, he was able to complete the experiments and get the approval for the registration. The time arrived when he really had to give a name to the product which had only had a code name. One late night it just came: Avemar, from the Latin prayer: Ave Maria.

Avemar with widely used chemotherapeutic drugs completely inhibited the development of metastases. Exploring its whole activity profile might even take a lifetime of research. So far he has supervised Avemar research done in Hungary, Israel, the United States, Austria, Italy, Spain, Slovakia, the Czech Republic, Germany,the United Kingdom, Russia, Australia, Korea, Vietnam. It has been a good experience to see the scientific interest it has generated worldwide. In 2009, Dr. Hidvegy received an invitation from the Nobel laureate, James Watson, co­discoverer of DNA’s double helix. It was a great honor. Avemar, he hopes,will be a significant cancer drug.

Mate Hidvegi was born in Budapest, Hungary, in 1955. He studied, then  taught at what is now Budapest University of Technology  and Economics.  After finishing university, he worked in the cereal industry and was co­developer of patented feed advisory system based on near infrared ingredient      data. In Hungary, Hidvegi was one of the pioneers in the development of           technologies for large ­scale production of instantized extracts for  therapeutic use.

 

Carcinogenesis vol.22 no.10 pp.1649–1652, 2001

Wheat germ extract inhibits experimental colon carcino-genesis in F-344 rats

Attila Zalatnai, Karoly Lapis, Bela Szende, Erzsebet Raso, Andros Telekes, Akos Resetar, and Mate Hidvegi

 

It has been demonstrated for the first time that a wheat germ extract prevents colonic cancer in laboratory animals. Four-week-old inbred male F-344 rats were used in the study. Colon carcinogenesis was induced by azoxy-methane (AOM). Ten rats served as untreated controls (group 1). For the treatment of the animals in group 2, AOM was dissolved in physiologic saline and the animals were given three weekly subcutaneous injections at 15 mg/kg body weight (b/w). In two additional groups Avemar (MSC), a fermented wheat germ extract standardized to 2,6-dimethoxy-p-benzoquinone was administered as a tentative chemo-preventive agent. MSC was dissolved in water and was given by gavage at a dose of 3 g/kg b/w once a day. In group 3, animals started to receive MSC 2 weeks prior to the first injection of AOM daily and continuously thereafter until they were killed 32 weeks later. In group 4 only the basal diet and MSC were administered. At the end of the experiment all the rats were exsanguinated under a light ether anesthesia and necropsied. Percentage of animals developing colon tumors and number of tumors per animals: group 1 – 0 and 0; group 2– 83.0 and 2.3; group 3 – 44.8 (P ≤ 0.001) and 1.3 (P ≤ 0.004); group 4 – 0 and 0. All the tumors were histologically neoplastic. The numbers of the aberrant crypt foci (ACF) per area (cm2) in group 2 were 4.85 while in group 3 the ACF numbers were 2.03 only (P ≤ 0.0001).

Table I. Macroscopic findings in the large intestines of F-344 rats treated with MSC or MSC +  AOM No. of animals     w/tumorw   Average # tumors Average diameter N 1 Untreated controls (10) 0/10 0/10 2.  AOM (47) 39/47 (83.0%) 2.3 ­+ 0.21 (range 1–8) 2.35 + 0.25 3.   MSC + AOM (29) 13/29 (44.8%) 1.3 + 0.17 (range 1–3) 2.21 + 0.12 4.  MSC (9) 0/9 0/9

Fig. 1. Experimental schedule. Colon carcinogenesis was induced by three consecutive s.c. doses of AOM 1 week apart in F-344 rats. Oral administration of MSC was started 2 weeks before the carcinogen treatments. All the animals were killed at the end of the experiment, e.g. on the 32nd week.  (not shown)

 

Summing up, although the chemoprevention of colon cancers (and their pre-neoplastic lesions) has well and long been established and could be achieved by totally different compounds, the mechanisms have still remained to be clarified. This is also true for MSC.

The exact mechanism by which the fermented wheat germ concentration can prevent colon cancer is still partly unknown. MSC did inhibit the AOM-induced ACF and colon neoplasm formation, the multiplicity of the tumors, apparently acting in the initiation phase. Regarding this, we can hypothesize that MSC acts as an immunomodulator.

 

Wheat Germ Extract Decreases Glucose Uptake and RNARibose Formation but Increases Fatty Acid Synthesis in MIAPancreatic Adenocarcinoma Cell

LG Boros, K Lapis, B Szende, R Tömösközi-Farkas, Ádám Balogh, …., and M Hidvégi

UCLA School of Medicine, Harbor-UCLA Research and Education Institute, Torrance, Ca.; First Institute of Pathology and Experimental Cancer Research, Semmelweis  Medical University, Budapest, Hungary; Central Food Research Institute, Budapest, Hungary; Department of Surgery, Albert Szent-Gyorgyi Medical and Pharmaceutical Center, School of General Medicine, University of Szeged, Szeged, Hungary; Department of Biochemistry and Molecular Biology, Institut d’Investigacions Biomediques August Pi i Sunyer, University of Barcelona, Barcelona, Spain; andDepartment of Biochemistryand Food Technology, Technical University of Budapest and Biromedicina Company, Budapest, Hungary

Pancreas 2001; 23 (2), pp. 141–147

Summary: The fermented wheat germ extract with standardized composition has potent tumor inhibitory properties. The fermented wheat germ extract controls tumor propagation. The authors show that this extract induces profound metabolic changes in cultured MIA pancreatic adenocarcinoma cells when the [1,2- ¹³C₂] glucose isotope is used as the single tracer with biologic gas chromatography–mass spectrometry.

MIA cells treated with 0.1, 1, and 10 mg/mL wheat  germ extract showed a dose-dependent decrease in cell glucose consumption, consumption, uptake of isotope into ribosomal RNA (2.4%, 9.4%, and 8.0%), and release of ¹³CO₂ . Conversely, direct glucose oxidation and ribose recycling in the pentose cycle showed a dose-dependent increase of 1.2%, 20.7%, and 93.4%. The newly synthesized fraction of cell palmitate and the ¹³C enrichment of acetyl units were also increased with all doses of wheat germ extract.

The fermented wheat germ extract controls tumor propagation primarily by regulating glucose carbon redistribution between cell proliferation–related and cell differentiation–related macromolecules. Wheat germ extract treatment is likely associated with the phosphor-ylation and transcriptional regulation of metabolic enzymes that are involved in glucose carbon redistribution between cell the direct oxidative degradation of glucose,proliferation–related structural and functional macromolecules(RNA, DNA) and the direct oxidative degradation and survival of pancreatic adenocarcinoma cells in culture.

Key Words: Pentose cycle—Ribose synthesis—Fermented wheat germ extract—Nonoxidative glucose metabolism—Cell proliferation—Avemar.

 

Fig 1 glu consumption of MIA pancreatic carcinoma cells in response to WGE

 

 

 

 

 

 

 

 

 

 

 

Figure 1. Glucose consumption of MIA pancreatic adenocarcinoma cells in response to increasing doses of fermented wheat germ extract (Avemar) treatment after 72 hours of culture. Glucose consumption (measured in milligrams) was estimated by the difference in media glucose content between Avemar-treated and control cultures. MIA cell glucose consumption was significantly inhibited in the presence of either 1 mg/mL (*p < 0.05) or 10 mg/mL (**p < 0.01) Avemar (x + SD;  n = 6).

 

fig-3-rna-syn-of-mia-pancreatic-carcinoma-cells-in-response-to-wge.jpg

 

 

 

 

 

 

 

 

 

 

 

Figure 3. Ribosomal RNA synthesis of MIA pancreatic adenocarcinoma cells in response to increasing doses of fermented wheat germ extract (Avemar) treatment after 72 hours of culture. Glucose carbon incorporation into ribose isolated from ribosomal RNA is expressed as molar enrichment. The dose-dependent decrease in of rRNA after Avemar treatment indicates that ribosomal RNA synthesis is the primary site significantly affected by all doses of Avemar treatment with a maximum decrease of 29% after 10 mg/mL treatment (x + SD; n = 9; *p < 0.05, **p < 0.01).

changes in metabolic activity indicate that Avemar treatment affects cell metabolism primarily by decreasing glucose uptake and nucleic acid ribose synthesis while increasing glucose oxidation through the oxidative reactions of the pentose cycle and fatty acid  synthesis from glucose carbon. The effect of Avemar treatment on lactate production and TCA cycle anapleurotic flux compared with glucose oxidation is less prominent

 

Fermented wheat germ extract induces apoptosis and downregulation of major histocompatibility complex class I proteins in tumor T and B cell lines

R FAJKA-BOJA, M HIDVÉGI, Y SHOENFELD, G  ION, D DEMYDENKO, R TÖMÖSKÖZI-FARKAS, et al.

INTL J ONCOLOGY 2002; 20: 563-570.

Lymphocyte Signal Transduction Laboratory, Institute of Genetics, and Cytokine Group, Institute of Biochemistry, Biological Research Center of the Hungarian Academy of Sciences, Szeged; Department of Biochemistry and Food Technology, Budapest University of Technology and Economics, Budapest, Hungary; Department of Medicine ‘B’, Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel; Central Food Research Institute; National Institute of Oncology; Biromedicina Co., Budapest, Hungary
Abstract. The fermented wheat germ extract (code name:  on cyto-fluorimeter using a monoclonal antibody to the  MSC, trade name: Avemar), with standardized benzoquinone non-polymorphic region of the human MHC class I. MSC  content has been shown to inhibit tumor propagation and stimulated tyrosine phosphorylation of intracellular proteins metastases formation in vivo. The aim of this study was to  understand the molecular and cellular mechanisms of the anti-tumor effect of MSC. Therefore, we have designed in vitro model experiments using T and B tumor lymphocytic cell lines. As a result of the MSC treatment, cell surface MHC class I proteins was downregulated by 70-85% compared to the non-stimulated control.

Prominent apoptosis of and the influx of extracellular Ca²⁺ resulted in elevation of the amount of the intracellular Ca²⁺ concentration. 20-40% was detected upon 24 h of MSC treatment of the cell lines. Apoptosis was measured with cytofluorimetry by staining the DNA with propidium iodide and detecting the ‘sub-G ’ cell population.

Tyrosine phosphorylation of intra-cellular proteins and elevation of the intracellular Ca²⁺ concentration were examined using immunoblotting with anti-phosphotyrosine antibody and cytofluorimetry by means of Ca²⁺ sensitive fluorescence dyes, Fluo-3AM and FuraRed-AM, respectively. MSC did not induce a similar degree of apoptosis in healthy peripheral blood mononuclear cells.

Inhibition of the cellular tyrosine phosphatase activity or Ca²⁺ influx resulted in the opposite effect – increasing or diminishing the Avemar induced apoptosis as well as the MHC class I downregulation. The level of the cell surface MHC class I molecules was analysed with indirect immunofluorescence. The benzoquinone component (2,6-dimethoxi-p-benzoquinone) in MSC induced similar apoptosis and downregulation of the MHC class I molecules in the tumor T and B cell lines to that of MSC. These results suggest that MSC acts on lymphoid tumor cells by reducing MHC class I expression and selectively promoting apoptosis of tumor cells on a tyrosine phosphorylation and Ca²⁺ influx dependent way.  One of the components in MSC, 2,6-dimethoxi-p-benzoquinone was shown to be an important factor in MSC mediated cell response.

 

Abbreviations:MHC, major histocompatibility complex;NK, natural killer;DMBQ, 2,6-dimethoxi-p-benzoquinone; FCS, fetal calf serum;PBMC, peripheral bloodmononuclear cells; TCR, T cell receptor;BCR, B cell receptor; mAb, monoclonal antibody;PMSF,phenylmethyl-sulfonylfluoride;pNPP, para-nitrophenyl-phosphate; PHA,phytohemagglutinineKey words: fermented wheat germ extract, Avemar, MSC, 2+ benzoquinone, tyrosine phosphorylation, intracellular Ca , CD45, tyrosine phosphatase, MHC class I downregulation, apoptosis

 

fig-4-apoptosis-of-t-cell-lines-induced-by-avamer.jpg

 

 

 

 

 

Figure 4. Apoptosis of tumor T cell lines and healthy lymphocytes upon MSC treatment. Jurkat cells were treated with 1 mg/ml MSC or .3 µg/ml DMBQ and PBMC were treated with 1 mg/ml
MSC for 24 h (A) or Jurkat cells were treated for 12 h (thick line in panel B). Control cells were left unstimulated (black bars in panel A or thin line on panel B). Apoptotic cells were enumerated
with the DNA analysis of the ‘sub-G ’ population (A) or with staining the cells with FITC1 labeled Annexin V
(B). Representative experiments are shown. The difference between the % of apoptosis in the case of treated and non-treated Jurkat cells was significant (MSC, p<0.001, n=14; DMBQ, p<0.05, n=3,
using  paired, two-tailed t-test). No difference was found for PBMC (n=2).

MSC treatment causes prominent apoptosis in lymphoid tumor cells but it does not induce apoptosis of healthy resting mononuclear cells. Moreover, although MSC blocks the proliferation of PBM cells stimulated with PHA, it does not induce apoptosis in PHA stimulated cells (data not shown).

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Cancer Labs at School of Medicine @ Technion: Janet and David Polak Cancer and Vascular Biology Research Center

Posted in Academic Publishing, Autologous Cell Therapy, Bio Instrumentation in Experimental Life Sciences Research, BioBanking, Biological Networks, Gene Regulation and Evolution, Biomarkers & Medical Diagnostics, Biomedical Measurement Science, BioSimilars, CANCER BIOLOGY & Innovations in Cancer Therapy, Cardiac muscle regeneration, Cardiovascular Pharmacogenomics, Cell Biology, Signaling & Cell Circuits, Chemical Biology and its relations to Metabolic Disease, Chemical Genetics, Circulating Progenitor Cells, Computational Biology/Systems and Bioinformatics, Cytoskeleton, Diagnostic Immunology, Drug Delivery Platform Technology, Drug Toxicity, Frontiers in Cardiology and Cardiovascular Disorders, Genome Biology, Genomic Testing: Methodology for Diagnosis, Human Immune System in Health and in Disease, Immunodiagnostics, Innovation in Immunology Diagnostics, Intellectual Property, Innovations, Commercialization, Investment in technological breakthrough, Interviews with Scientific Leaders, Personalized and Precision Medicine & Genomic Research, Pharmaceutical Analytics, Pharmaceutical R&D Investment, Pharmacogenomics, Pharmacologic toxicities, Population Health Management, Genetics & Pharmaceutical, Proteomics, Regenerative Biology and Medicine, Regulated Clinical Trials: Design, Methods, Components and IRB related issues, Scientist: Career considerations, Signaling, Stem Cells for Regenerative Medicine, Technology Transfer: Biotech and Pharmaceutical, Translational Science, Ubiquitinylation on May 28, 2014| Leave a Comment »

Cancer Labs at School of Medicine @ Technion

Reporter: Aviva Lev-Ari, PhD, RN

Article ID #139: Cancer Labs at School of Medicine @ Technion: Janet and David Polak Cancer and Vascular Biology Research Center. Published on 5/28/2014

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Janet and David Polak Cancer and Vascular Biology Research Center. The Rappaport Faculty of Medicine Research Institute and Faculty of Medicine, Technion – Israel Institute of Technology, Haifa, Israel

The center was established in 2003 to promote an in-depth interdisciplinary basic and clinical research on the control of cellular and molecular processes that are involved in cancer initiation and progression. We strongly believe that the understanding of basic biological processes that underlie normal development and their deregulation in cancer, is crucial for our ability to identify molecular targets for early detection, intervention, and cure of the disease. We are interested in a broad view of cancer – from the single malignantly transformed cell and its microenvironment, through the entire tumor in the animal. We focus on targeted ubiquitin-mediated degradation of key regulatory proteins that are involved in malignant transformation [Prof. Aaron Ciechanover (Nobel Prize in Chemistry 2004)], angiogenesis and cancer progression (Prof. Gera Neufeld), metastasis and tumor microenvironment (Prof. Israel Vlodavsky), as well as genetic and genomic dissection of embryonic and cancer transcriptional networks (Dr. Amir Orian). Towards these objectives, we combine molecular, biochemical, cell biological with Drosophila genetic and genomics experimental approaches, as well as employing advanced models of angiogenesis and metastasis.

We believe that scientific excellence and collegiality go together. Therefore, the center has an open and friendly atmosphere, creating a highly stimulating environment. The center is located in the 11th Floor of the Rappaport Faculty of Medicine building. It currently trains 45 graduate students, post-doctoral fellows, clinicians and researchers that are at the heart of our research. Formal and informal collaborations between individuals and laboratories are on-going and encouraged. We are running a series of joint seminars to which we invite researchers from Israel and abroad. The Center has advanced state-of-the-art microscopic and image analysis equipment, as well as other shared pieces of infrastructural equipment . The center is an integral part of the Faculty of Medicine and the Rappaport Research Institute which are home for excellent research groups, and enjoys their advanced Interdepartmental Equipment Unit. It is also adjacent to the Rambam Medical Center – the major hospital in the north of Israel – which provides us with access to rich clinical material and collaboration with clinicians. Many of them spend active research periods in our laboratories and bring the bench closer to the patient bed and vice versa. The Center is in an active phase of growth, and offers excellent research opportunities, space and facilities for students, post-doctoral fellows, and physicians.

Research Groups The Ubiquitin System and Cellular Protein Turnover and Interactions Immunity and Host Defense Cardiovascular Biology The Central Nervous System in Health and Disease Developmental Biology and Cancer Research Genetics

SOURCE 

http://www.rappaport.org.il/Rappaport/Templates/ShowPage.asp?DBID=1&TMID=842&FID=76

The cancer and vascular biology research center was established in 2003 to promote an in-depth interdisciplinary basic and clinical research on the control of cellular and molecular processes that are involved in cancer development and progression. Our goal is to advance knowledge in fundamental biological questions that are highly relevant for cancer.

	The cancer and vascular biology research center was established in 2003 to promote an in-depth interdisciplinary basic and clinical research on the control of cellular and molecular processes that are involved in cancer development and progression. Our goal is to advance knowledge in fundamental biological questions that are highly relevant for cancer.

SOURCE

http://www.technioncancer.co.il/index.php

Home  >>  Research Groups

Aaron Ciechanover Protein Turnover Intracellular protein degradation and mechanisms of cancer Israel Vlodavsky Cancer Biology Impact of heparanase and the tumor microenvironment on cancer progression: Basic aspects and clinical implications Gera Neufeld Tumor Progression & Angiogenesis Blood vessels and tumor progression: The neuropilin connection Amir Orian Genetic Networks Genetic networks in development and cancer

Home About the Cancer Centers Research Groups Administration / Contact Join – Us Seminars and Events Links Beyond Science Friends and supporters Ms. Sigal Alfasi – Izrael, Center’s coordinator e-mail: gsigal@tx.technion.ac.il Tel: +972-4-829-5424 Fax: +972-4-852-3947

SOURCE

http://www.technioncancer.co.il/ResearchGroups.php

Yuval Shaked, PhD

Publications by Yuval Shaked, PhD

Assistant Professor of Molecular Pharmacology

PhD, 2004 – Hebrew University, Israel

Understanding host – tumor interactions during cancer therapy

Personalized medicine holds promise of better cures with fewer side effects for many diseases. Individualized cancer therapy is sometimes utilized after multiple attempts of standard therapies and is based on several considerations, such as tumor type, acquired resistance to a specific therapy, previous treatment protocols, and other tumor-related factors. We have recently demonstrated that many cancer therapies can induce pro-tumorigenic or metastatic effects that derive not only from the tumor cells themselves, but also from host cells within the tumor microenvironment. The focus of research in my laboratory is to identify, characterize, and seek ways to block such pro-tumorigenic host effects observed after anti-cancer therapy, and thus potentially improve the outcome of current cancer therapies. Our findings may foster a paradigm shift in cancer therapy by minimizing the gap between preclinical findings and the clinical setting, laying the foundation for development of entirely new strategies for improving cancer therapy.

SOURCE

http://www.rappaport.org.il/Rappaport/Templates/ShowPage.asp?DBID=1&TMID=610&FID=77&PID=0&IID=1268

 

Other Related articled published on this Open Access Online Scientific Journal included the following:

D&D NT’s Solution: Galectin Proteins for Therapy and Diagnosis of Autoimmune Inflammatory and Cancer Diseases, Dr. Itshak Golan, CEO

http://pharmaceuticalintelligence.com/2014/05/28/dd-nts-solution-galectin-proteins-for-therapy-and-diagnosis-of-autoimmune-inflammatory-and-cancer-diseases-dr-itshak-golan-ceo/

MaimoniDex RA:  Monoclonal Antibodies for Therapy and Diagnosis of Cancer and Autoimmune Inflammatory Diseases – Dr. Itshak Golan, CEO

http://pharmaceuticalintelligence.com/2014/05/28/maimonidex-ra-monoclonal-antibodies-for-therapy-and-diagnosis-of-cancer-and-autoimmune-inflammatory-diseases-dr-itshak-golan-ceo/

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Immunity and Host Defense – A Bibliography of Research @Technion

Posted in Biological Networks, Gene Regulation and Evolution, Biomarkers & Medical Diagnostics, Biomedical Measurement Science, CANCER BIOLOGY & Innovations in Cancer Therapy, Cancer Prevention: Research & Programs, Cell Biology, Signaling & Cell Circuits, Chemical Biology and its relations to Metabolic Disease, Chemical Genetics, Diagnostic Immunology, Drug Delivery Platform Technology, Drug Toxicity, FDA Regulatory Affairs, Genome Biology, Genomic Testing: Methodology for Diagnosis, Human Immune System in Health and in Disease, Immunodiagnostics, Innovation in Immunology Diagnostics, Intellectual Property, Innovations, Commercialization, Investment in technological breakthrough, Interviews with Scientific Leaders, Medical and Population Genetics, Molecular Genetics & Pharmaceutical, Personalized and Precision Medicine & Genomic Research, Pharmaceutical Analytics, Pharmaceutical R&D Investment, Pharmacogenomics, Pharmacologic toxicities, Population Health Management, Genetics & Pharmaceutical, Proteomics, Regulated Clinical Trials: Design, Methods, Components and IRB related issues, Scientist: Career considerations, Signaling, Technology Transfer: Biotech and Pharmaceutical, Translational Science on May 27, 2014| Leave a Comment »

Immunity and Host Defense – A Bibliography of Research @Technion

Reporter: Aviva Lev-Ari, PhD, RN

Article ID #138: Immunity and Host Defense – A Bibliography of Research @Technion. Published on 5/27/2014

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Antigen-Dependent Integration of Opposing Proximal TCR-Signaling Cascades Determines the Functional Fate of T Lymphocytes 2014 Shai Shen-Orr, PhD Authors : Wolchinsky R, Hod-Marco M, Oved K, Shen-Orr SS, Bendall SC, Nolan GP, Reiter Y. J Immunol. 2014 Mar 1;192(5):2109-19.

Identification of functionally important conserved trans-membrane residues of bacterial P(IB) -type ATPases 2013 Oded Lewinson, PhD Authors : Zhitnitsky D, Lewinson O. Mol Microbiol. 2013 Dec 19. doi: 10.1111/mmi.12495. [Epub ahead of print] PubMed PMID: 24350798.

Variability in the immune system: of vaccine responses and immune states 2013 Shai Shen-Orr, PhD Authors : Shen-Orr SS, Furman D. Curr Opin Immunol. 2013 Aug;25(4):542-7.

Computational deconvolution: extracting cell type-specific information from heterogeneous samples. 2013 Shai Shen-Orr, PhD Authors : Shen-Orr SS, Gaujoux R. Curr Opin Immunol. 2013 Oct 19. [Epub ahead of print] PubMed PMID: 24148234.

Challenges and promise for the development of human immune monitoring. 2013 Shai Shen-Orr, PhD Authors : Shen-Orr S. Rambam Maimonides Med J. 2012 Oct 31;3(4):e0023.

Homeostatic regulation of aging and rejuvenation in the B lineage cells 2013 Doron Melamed, PhD Authors : Melamed D. Crit Rev Immunol. 2013;33(1):41-56.

Variability in the immune system: of vaccine responses and immune states 2013 Shai Shen-Orr, PhD Authors : Shen-Orr S, Furman D. Curr Opin Immunol. 2013 Aug 13. doi:pii: S0952-7915(13)00113-1.

A single intact ATPase site of the ABC transporter BtuCD drives 5% transport activity yet supports full in-vivo vitamin B12 utilization. 2013 Oded Lewinson, PhD Authors : Tal N, Ovcharenko E, Lewinson O. Proc Natl Acad Sci U S A. (March 19 Epub ahead of print)

Apoptosis and other immune biomarkers predict influenza vaccine responsiveness. 2013 Shai Shen-Orr, PhD Authors : Furman D, Jojic V, Kidd B, Shen-Orr S, Price J, Jarrell J, Tse T, Huang H, Lund P, Maecker HT, Utz PJ, Dekker CL, Koller D, Davis MM. Molecular Systems Biology. 9, 659

The dual roles of inflammatory cytokines and chemokines in the regulation of autoimmune diseases and their clinical implications. 2013 Nathan Karin, PhD Authors : Shachar, I., and N. Karin. J Leukoc Biol 93:51-61.

Two molybdate/tungstate ABC transporters that interact very differently with their substrate binding proteins. 2013 Oded Lewinson, PhD Authors : Vigonsky, Ovcharenko E, Lewinson O. Proc Natl Acad Sci U S A. (March 19 Epub ahead of print)

Dissecting the Autocrine and Paracrine Roles of the CCR2-CCL2 Axis in Tumor Survival and Angiogenesis. 2012 Nathan Karin, PhD Authors : Izhak, L., G. Wildbaum, S. Jung, A. Stein, Y. Shaked, and N. Karin. PloS one 7:e28305

Dose-related effects of hyperoxia on the lung inflammatory response in septic rats 2012 Nitza Lahat, PhD Authors : Waisman D, Brod V, Rahat MA, Amit-Cohen BC, Lahat N, Rimar D, Menn-Josephy H, David M, Lavon O, Cavari Y, Bitterman H. Shock. 2012 Jan;37(1):95-102.

Robust and sensitive analysis of xMap bead arrays using SAxCyB. 2012 Shai Shen-Orr, PhD Authors : Won JH, Goldberger O, Shen-Orr SS, David MM, Olshen RA. Proc Natl Acad Sci U S A. 109, 2848-53.

The Entamoeba histolytica methylated LINE-binding protein EhMLBP provides protection against heat shock 2012 Serge Ankri, PhD Authors : Katz S, Kushnir O, Tovy A, Siman Tov R, Ankri S. Cell Microbiol. 2012 Jan;14(1):58-70

Hypoxia increases membranal and secreted HLA-DR in endothelial cells, rendering them T-cell activators. 2011 Nitza Lahat, PhD Authors : Lahat N, Bitterman H, Weiss-Cerem L, Rahat MA. Transpl Int. 2011 Oct;24(10):1018-26.

The Entamoeba histolytica methylated LINE-binding protein EhMLBP provides protection against heat shock. 2011 Serge Ankri, PhD Authors : Katz S, Kushnir O, Tovy A, Siman Tov R, Ankri S. Cell Microbiol. 2011 Sep 8. [Epub ahead of print]

Dose-Related Effects of Hyperoxia on the Lung Inflammatory Response in Septic Rats. Shoc 2011 Nitza Lahat, PhD Authors : Waisman D, Brod V, Rahat MA, Amit-Cohen BC, Lahat N, Rimar D, Menn-Josephy H, David M, Lavon O, Cavari Y, Bitterman H. 2011 Sep 3. [Epub ahead of print]

Glucose starvation boosts Entamoeba histolytica virulence. 2011 Serge Ankri, PhD Authors : Tovy A, Hertz R, Siman-Tov R, Syan S, Faust D, Guillen N, Ankri S. PLoS Negl Trop Dis. 2011 Aug;5(8):e1247.

The binding activity of Mel-18 at the Il17a promoter is regulated by the integrated signals of the TCR and polarizing cytokines. 2011 Eur J Immunol. 2011 Aug;41(8):2424-35.

phosphorylation of SLP-76 at tyrosine 173 is required for activation of T and mast cells. 2011 Deborah Yablonski, PhD Authors : Sela M, Bogin Y, Beach D, Oellerich T, Lehne J, Smith-Garvin JE, Okumura M, Starosvetsky E, Kosoff R, Libman E, Koretzky G, Kambayashi T, Urlaub H, Wienands J, Chernoff J, Yablonski D. Sequential EMBO J. 2011 Jul 1;30(15):3160-72.

The binding activity of Mel-18 at the Il17a promoter is regulated by the integrated signals of the TCR and polarizing cytokines. 2011 Orly Avni, PhD Authors : Hod-Dvorai R, Jacob E, Boyko Y, Avni O. Eur J Immunol. 2011 Jun 15. [Epub ahead of print]

MMP expression in leaking filtering blebs and tears after glaucoma filtering surgery. 2011 Nitza Lahat, PhD Authors : Mathalone N, Marmor S, Rahat MA, Lahat N, Oron Y, Geyer O. Graefes Arch Clin Exp Ophthalmol. 2011 Mar 31. [Epub ahead of print]

B cell depletion reactivates B lymphopoiesis in the BM and rejuvenates the B lineage in aging. 2011 Doron Melamed, PhD Authors : Keren Z, Naor S, Nussbaum S Golan K, Itkin T, Sasaki Y, Schmidt-Supprian M, Lapidot T, Melamed D. Blood 117, 3104 – 3112.

Chronic B cell deficiency from birth prevents age-related alterations in the B lineage J. 2011 Doron Melamed, PhD Authors : Keren Z, Averbuch D, Shahaf G, Zisman-Rozen S, Golan K, Itkin T, Lapidot T, Mehr R, Melamed D. Immunol 187, 2140 – 2147.

Epigenetics in the unicellular parasite Entamoeba histolytica. 2010 Serge Ankri, PhD Authors : Tovy A, Ankri S. Future Microbiol. 2010 Dec;5:1875-84.

The MAPK/ERK and PI3K pathways additively coordinate the transcription of recombination-activating genes in B lineage cells 2010 Orly Avni, PhD Authors : Novak R, Jacob E, Haimovich J, Avni O, Melamed D. J Immunol. 2010 Sep 15;185(6):3239-47

A fusion protein encoding the second extracellular domain of CCR5 arrests chemokine-induced cosignaling and effectively suppresses ongoing experimental autoimmune encephalomyelitis 2010 Nathan Karin, PhD Authors : Sapir Y, Vitenshtein A, Barsheshet Y, Zohar Y, Wildbaum G, Karin N. J Immunol. 2010 Aug 15;185(4):2589-99.

Antigen-specific CD25- Foxp3- IFN-gamma(high) CD4+ T cells restrain the development of experimental allergic encephalomyelitis by suppressing Th17 2010 Nathan Karin, PhD Authors : Wildbaum G, Zohar Y, Karin N. Am J Pathol. 2010 Jun; 176(6):2764-75.

Circulating interleukin-10: association with higher mortality in systolic heart failure patients with elevated tumor necrosis factor-alpha 2010 Nitza Lahat, PhD Authors : Amir O, Rogowski O, David M, Lahat N, Wolff R, Lewis BS. Isr Med Assoc J. 2010 Mar;12(3):158-62.

In vitro tRNA Methylation Assay with the Entamoeba histolytica DNA and tRNA Methyltransferase Dnmt2 (Ehmeth) Enzyme 2010 Serge Ankri, PhD Authors : Tovy A, Hofmann B, Helm M, Ankri S. J Vis Exp. 2010 Oct 19;(44). pii: 2390. doi: 10.3791/2390.

Circulating interleukin-10: association with higher mortality in systolic heart failure patients with elevated tumor necrosis factor-alpha 2010 Nitza Lahat, PhD Authors : Amir O, Rogowski O, David M, Lahat N, Wolff R, Lewis BS Isr Med Assoc J. 2010 Mar;12(3):158-62

A distinct mechanism for the ABC transporter BtuCD-BtuF revealed by the dynamics of complex formation. 2010 Oded Lewinson, PhD Authors : Lewinson O, Lee AT, Locher KP, Rees DC. Nat Struct Mol Biol. 17, 332-8.

Extracting Cell-Type-Specific Gene Expression Differences from Complex Tissues. 2010 Shai Shen-Orr, PhD Authors : Shen-Orr SS*, Tibshirani R*, Khatri P, Bodian DL, Staedtler F, Perry NM, Hastie T, Sarwal MM, Davis MM*, Butte AJ*. Nature Methods 7, 287-9.

The MAPK/ERK and PI(3)K Pathways Additively Coordinate the Transcription of Recombination-Activating Genes in B Lineage Cells. 2010 Doron Melamed, PhD Authors : Novak R, Jacob E, Haimovich J, Avni O, Melamed D. Immunol 185, 3239 – 3247.

Protein denitrosylation: enzymatic mechanisms and cellular functions 2009 Moran Benhar, PhD Authors : Benhar, M., Forrester, M.T., Stamler, J.S. Nat. Rev. Mol. Cell Biol. 10:721-32.

Psoriasis patients generate increased serum levels of autoantibodies to tumor necrosis factor-alpha and interferon-alpha 2009 Nathan Karin, PhD Authors : Bergman R, Ramon M, Wildbaum G, Avitan-Hersh E, Mayer E, Shemer A, Karin N. J Dermatol Sci. 2009 Oct 1. Epub

The role of macrophage-derived IL-1 in induction and maintenance of angiogenesis 2009 Nitza Lahat, PhD Authors : Carmi Y, Voronov E, Dotan S, Lahat N, Rahat MA, Fogel M, Huszar M, White MR, Dinarello CA, Apte RN. J Immunol. 2009 Oct 1;183(7):4705-14.

Insights into the mechanism of DNA recognition by the methylated LINE binding protein EhMLBP of Entamoeba histolytica 2009 Serge Ankri, PhD Authors : Lavi T, Siman-Tov R, Ankri S. Mol Biochem Parasitol. 2009 Aug;166(2):117-25. Epub 2009 Mar 20.

A novel recombinant fusion protein encoding a 20-amino acid residue of the third extracellular (E3) domain of CCR2 neutralizes the biological activity of CCL2 2009 Nathan Karin, PhD Authors : Izhak L, Wildbaum G, Zohar Y, Anunu R, Klapper L, Elkeles A, Seagal J, Yefenof E, Ayalon-Soffer M, Karin N J Immunol. 2009 Jul 1;183(1):732-9

Selective autoantibody production against CCL3‭ ‬is associated with human type 1‭ ‬diabetes mellitus and serves as a novel biomarker for its diagnosis 2009 Nathan Karin, PhD Authors : Shehadeh N‭, ‬Pollack S‭, ‬Wildbaum G‭, ‬Zohar Y‭, ‬Shafat I‭, ‬Makhoul R‭, ‬Daod E‭,‬ J Immunol‭. ‬2009‭ ‬Jun 15‭;‬182‭(‬12‭):‬8104-9

The effect of 100% oxygen on intestinal preservation and recovery following ischemia-reperfusion injury in rats 2009 Nitza Lahat, PhD Authors : Sukhotnik I, Brod V, Lurie M, Rahat MA, Shnizer S, Lahat N, Mogilner JG, Bitterman H. Crit Care Med. 2009 Mar;37(3):1054-61.

Transcriptional regulation of GATA3 in T helper cells by the integrated activities of transcription factors downstream of the interleukin-4 receptor and T cell receptor 2009 Orly Avni, PhD Authors : Scheinman EJ, Avni O. J Biol Chem. 2009 30;284(5):3037-48.

TOLL-like receptor ligands stimulate aberrant class switch recombination in early B cell precursors 2008 Doron Melamed, PhD Authors : Edry E, Azulay-Debby H, Melamed D. Int Immunol. 2008 Dec;20(12):1575-85. Epub 2008 Oct 29.

EhMLBP is an essential constituent of the Entamoeba histolytica epigenetic machinery and a potential drug target 2008 Serge Ankri, PhD Authors : Lavi T, Siman-Tov R, Ankri S. Mol Microbiol. 2008 Jul;69(1):55-66. Epub 2008 May 12

Hypoxia enhances lysosomal TNF-α degradation in mouse peritoneal macrophages 2008 Nitza Lahat, PhD Authors : Lahat, N., Rahat, M. A., Kinarty, A., Weiss-Cerem, L., Pinchevski, S., Bitterman, H. Am J Physiol Cell Physiol 295, C2-12.

What do unicellular organisms teach us about DNA methylation? 2008 Serge Ankri, PhD Authors : Harony H Trends Parasitol. 2008 May;24(5):205-9. Epub 2008 Apr 9. PMID: 18403268 [PubMed – in process]

Regulated protein denitrosylation by cytosolic and mitochondrial thioredoxins 2008 Moran Benhar, PhD Authors : Benhar, M., Forrester, M.T., Hess, D.T., Stamler, J.S. Science 320:1050-4

Trichostatin A regulates peroxiredoxin expression and virulence of the parasite Entamoeba histolytica. 2008 Serge Ankri, PhD Authors : Isakov E, Siman-Tov R, Weber C, Guillen N Mol Biochem Parasitol. 2008 Mar;158(1):82-94.

Progress and prospects of gene inactivation in Entamoeba histolytica. 2008 Serge Ankri, PhD Authors : Abed M Exp Parasitol. 2008 Feb;118(2):151-5

Class switch recombination: a friend and a foe. 2007 Doron Melamed, PhD Authors : Edry E. Clin Immunol. 2007 Jun;123(3):244-51.

Native and fragmented fibronectin oppositely modulate monocyte secretion of MMP-9 2007 Nitza Lahat, PhD Authors : Marom, B., Rahat, M. A., Lahat, N., Weiss-Cerem, L., Kinarty, A., Bitterman, H. J Leukoc Biol 81, 1466-1476.

SLP-76 mediates and maintains activation of the Tec family kinase ITK via the T cell antigen receptor-induced association between SLP-76 and ITK. 2007 Deborah Yablonski, PhD Authors : Bogin Y, Ainey C, Beach D Proc Natl Acad Sci U S A. 2007 Apr 17;104(16):6638-43.

Dual role of SLP-76 in mediating T cell receptor-induced activation of phospholipase C-gamma1. 2007 Deborah Yablonski, PhD Authors : Beach D, Gonen R, Bogin Y, Reischl IG J Biol Chem. 2007 Feb 2;282(5):2937-46. Epub 2006 Dec 4. Read the Article

B cell receptor editing in tolerance and autoimmunity. 2007 Doron Melamed, PhD Authors : Azulay-Debby H. Front Biosci. 2007 Jan 1;12:2136-47.

Genome-wide analysis of mRNA polysomal profiles with spotted DNA microarrays. 2007 Doron Melamed, PhD Authors : Arava Y. Methods Enzymol. 2007;431:177-201

Coadministration of plasmid DNA constructs encoding an encephalitogenic determinant and IL-10 elicits regulatory T cell-mediated protective immunity in the central nervous system. 2006 Nathan Karin, PhD Authors : Schif-Zuck S, Wildbaum G, Karin N. J Immunol. 2006 Dec 1;177(11):8241-7.

Sensing DNA methylation in the protozoan parasite Entamoeba histolytica. 2006 Serge Ankri, PhD Authors : Lavi T, Isakov E, Harony H, Fisher O, Siman-Tov R. Mol Microbiol. 2006 Dec;62(5):1373-86. Read the Article:

Modulation of matrix metalloproteinase-9 (MMP-9) secretion in B lymphopoiesis. 2006 Doron Melamed, PhD Authors : Melamed D, Messika O, Glass-Marmor L, Miller A. Int Immunol. 2006 Sep;18(9):1355-62.

A Pak- and Pix-dependent branch of the SDF-1alpha signalling pathway mediates T cell chemotaxis across restrictive barriers. 2006 Deborah Yablonski, PhD Authors : Volinsky N, Gantman A, Yablonski D. Biochem J. 2006 Jul 1;397(1):213-22. PMID: 16515536 [PubMed – in process] Read more

DNA methylation and targeting of LINE retrotransposons in Entamoeba histolytica and Entamoeba invadens. 2006 Serge Ankri, PhD Authors : Harony H, Bernes S, Siman-Tov R, Ankri S. Mol Biochem Parasitol. 2006 May;147(1):55-63. Epub 2006 Feb 23. PMID: 16530279 [PubMed � in process] Read more

Pleiotropic phenotype in Entamoeba histolytica overexpressing DNA methyltransferase (Ehmeth). 2006 Serge Ankri, PhD Authors : Fisher O, Siman-Tov R, Ankri S. Mol Biochem Parasitol. 2006 May;147(1):48-54. Epub 2006 Feb 9. PMID: 16497397 [PubMed � in process] Read more

Hypoxia reduces the output of matrix metalloproteinase-9 (MMP-9) in monocytes by inhibiting its secretion and elevating membranal association 2006 Nitza Lahat, PhD Authors : Rahat, M. A., Marom, B., Bitterman, H., Weiss-Cerem, L., Kinarty, A., Lahat, N. J Leukoc Biol 79, 706-718.

Antisense inhibition of Entamoeba histolytica cysteine proteases inhibits colonic mucus degradation 2006 Serge Ankri, PhD Authors : Moncada D, Keller K, Ankri S, Mirelman D, Chadee K. Gastroenterology. 2006 Mar;130(3):721-30. PMID: 16530514 [PubMed � indexed for MEDLINE] Read more

Beneficial autoimmunity participates in the regulation of rheumatoid arthritis. 2006 Nathan Karin, PhD Authors : Zohar Y, Wildbaum G, Karin N. Front Biosci. 2006 Jan 1;11:368-79. Review. PMID: 16146738 [PubMed – indexed for MEDLINE] Read more

The RNA polymerase II subunit Rpb4p mediates decay of a specific class of mRNAs. 2005 Doron Melamed, PhD Authors : Lotan R, Bar-On VG, Harel-Sharvit L, Duek L, Melamed D, Choder M. Genes Dev. 2005 Dec 15;19(24):3004-16. PMID: 16357218 [PubMed – indexed for MEDLINE] Read more

Single point mutations in the zinc finger motifs of the human immunodeficiency virus type 1 nucleocapsid alter RNA binding specificities of the gag protein and enhance packaging and infectivity. 2005 Doron Melamed, PhD Authors : Mark-Danieli M, Laham N, Kenan-Eichler M, Castiel A, Melamed D, Landau M, Bouvier NM, Evans MJ, Bacharach E. J Virol. 2005 Jun;79(12):7756-67. PMID: 15919928 [PubMed – indexed for MEDLINE] Read more

Molecular characterization of Entamoeba histolytica Rnase III and AGO2, two RNA interference hallmark proteins. 2005 Serge Ankri, PhD Authors : Abed M, Ankri S. Exp Parasitol. 2005 Jul;110(3):265-9. Epub 2005 Apr 7. PMID: 15955322 [PubMed � indexed for MEDLINE] Read more

Targeted overexpression of IL-18 binding protein at the central nervous system overrides flexibility in functional polarization of antigen-specific Th2 cells. 2005 Nathan Karin, PhD Authors : Schif-Zuck S, Westermann J, Netzer N, Zohar Y, Meiron M, Wildbaum G, Karin N. Immunol. 2005 Apr 1;174(7):4307-15. PMID: 15778395 [PubMed – indexed for MEDLINE] Read more

T cell receptor-induced activation of phospholipase C-gamma1 depends on a sequence-independent function of the P-I region of SLP-76. 2005 Deborah Yablonski, PhD Authors : Gonen R, Beach D, Ainey C, Yablonski D. J Biol Chem. 2005 Mar 4;280(9):8364-70. Epub 2004 Dec 28. PMID: 15623534 [PubMed – indexed for MEDLINE] Read more

Naive, effector, and memory T lymphocytes efficiently scan dendritic cells in vivo: contact frequency in T cell zones of secondary lymphoid organs does not depend on LFA-1 expression and facilitates 2005 Nathan Karin, PhD Authors : Westermann J, Bode U, Sahle A, Speck U, Karin N, Bell EB, Kalies K, Gebert A. J Immunol. 2005 Mar 1;174(5):2517-24. PMID: 15728457 [PubMed – indexed for MEDLINE] Read more

Antigen receptor signaling competence and the determination of B cell fate in B-lymphopoiesis. 2005 Doron Melamed, PhD Authors : Keren Z, Melamed D. Histol Histopathol. 2005 Jan;20(1):187-96. Review. PMID: 15578437 [PubMed – indexed for MEDLINE] Read more

CD19 regulates positive selection and maturation in B lymphopoiesis: lack of CD19 imposes developmental arrest of immature B cells and consequential stimulation of receptor editing. 2005 Doron Melamed, PhD Authors : Diamant E, Keren Z, Melamed D. Blood ;105:3247-3254.

Entamoeba histolytica DNA methyltransferase (Ehmeth) is a nuclear matrix protein that binds EhMRS2, a DNA that includes a scaffold/matrix attachment region (S/MAR). 2005 Serge Ankri, PhD Authors : Banerjee S, Fisher O, Lohia A, Ankri S. Mol Biochem Parasitol. 2005 Jan;139(1):91-7. PMID: 15610823 [PubMed � indexed for MEDLINE] Read more

Epigenetic and classical activation of Entamoeba histolytica heat shock protein 100 (EHsp100) expression. 2005 Serge Ankri, PhD Authors : Bernes S, Siman-Tov R, Ankri S. FEBS Lett;579:6395-6402.

T cell receptor-induced activation of phospholipase C-γ1 depends on a sequence-independent function of the P-I region of SLP-76. 2005 Deborah Yablonski, PhD Authors : Gonen R, Beach D, Ainey C, Yablonski D. J Biol Chem ;280:8364-8370.

Characterization of cytosine methylated regions and 5-cytosine DNA methyltransferase (Ehmeth) in the protozoan parasite Entamoeba histolytica. 2004 Serge Ankri, PhD Authors : Fisher O, Siman-Tov R, Ankri S. Nucleic Acids Res ;1:287-297.

Modification of ligandindependent B cell receptor tonic signals activates receptor editing in immature B lymphocytes. 2004 Doron Melamed, PhD Authors : Keren Z, Diamant E, Ostrovsky O, Bengal E, Melamed D. J Biol Chem ;279:13418-13424.

A failsafe mechanism for negative selection of isotype-switched B cell precursors is regulated by the Fas/FasL pathway 2003 Doron Melamed, PhD Authors : Seagal J, Edry E, Keren Z, Leider N, Benny O, Machluf M, Melamed D. J Exp Med ;198:1609-1619.

Beneficial autoimmunity to proinflammatory mediators restrains the consequences of self-destructive immunity. 2003 Nathan Karin, PhD Authors : Wildbaum G, Nahir MA, Karin N. Immunity;19:679-688.

T(H) cell differentiation is accompanied by dynamic changes in histone acetylation of cytokine genes. 2002 Orly Avni, PhD Authors : Avni O, Lee D, Macian F, Szabo SJ, Glimcher LH, Rao A. Nat Immunol ;3:643-651.

Tr1 cell-dependent active tolerance blunts the pathogenic effects of determinant spreading. 2002 Nathan Karin, PhD Authors : Wildbaum G, Netzer N, Karin N. J Clin Invest ;110:701-710.

A PAK1-PIX-PKL complex is activated by the T-cell receptor independent of Nck, Slp-76 and LAT. 2001 Deborah Yablonski, PhD Authors : Ku GM, Yablonski D, Manser E, Lim L, Weiss A. EMBO Journal ;20:457-465.

Identification of a phospholipase C-γ1 (PLC- γ1) SH3 domain-binding site in SLP-76 required for T-cell receptor-mediated activation of PLC-γ1 and NFAT 2001 Deborah Yablonski, PhD Authors : Yablonski D, Kadlecek T, Weiss A. Mol Cell Biol ;21:4208-4218.

C-C chemokineencoding DNA vaccines enhance breakdown of tolerance to their gene products and treat ongoing adjuvant arthritis. 2000 Nathan Karin, PhD Authors : Youssef S, Maor G, Wildbaum G, Grabie N, Gour-Lavie A, Karin N. J Clin Invest ;106:361-371.

Cell-type-restricted binding of the transcription factor NFAT to a distal IL-4 enhancer in vivo. 2000 Orly Avni, PhD Authors : Agarwal S, Avni O, Rao A. Immunity ;12:643-652.

T cell differentiation: a mechanistic view. 2000 Orly Avni, PhD Authors : Avni O, Rao A. Curr Opin Immunol; 12:654-659.

A systemic cytokine response defect stratifies older adults into distinct immune profiles. 1900 Shai Shen-Orr, PhD Authors : Shen-Orr SS*, Furman D*, Kidd BA, Morgan A, Lovelace P, Rosenberg-Hasson Y, Maecker H, Mackey S, Dekker C, Butte AJ, Davis MM. Submitted.

 

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Summary of Translational Medicine – e-Series A: Cardiovascular Diseases, Volume Four – Part 1

Posted in Academic Publishing, Acute Myocardial Infarction, Advanced Drug Manufacturing Technology, Alzheimer's Disease, Atherogenic Processes & Pathology, Autologous Cell Therapy, Automated Cell Processing, Bio Instrumentation in Experimental Life Sciences Research, Biological Networks, Gene Regulation and Evolution, Biomarkers & Medical Diagnostics, Biomedical Measurement Science, Bone Disease and Musculoskeletal Disease, Bone marrow derived cells, Ca2+ triggered activation, Ca2+ triggered activation, Cachexia, Calcium Signaling, Calmodulin, Calmodulin Kinase and Contraction, Cardiac & Vascular Repair Tools Subsegment, Cardiac and Cardiovascular Surgical Procedures, Cardiac muscle regeneration, Cardiomyopathy, Cardiovascular Pharmacogenomics, Cell Biology, Signaling & Cell Circuits, Chemical Biology and its relations to Metabolic Disease, Chemical Genetics, Chronic Thromboembolic Pulmonary Hypertension (CTEPH) and Pulmonary Arterial Hypertension (PAH), Circulating Progenitor Cells, Coagulation Therapy and Internal Bleeding, Competition in regenerative stem cell science, Computational Biology/Systems and Bioinformatics, Curation, Cytoskeleton, Diabetes Mellitus, Disease Biology, Small Molecules in Development of Therapeutic Drugs, Drug Delivery Platform Technology, Drug Toxicity, Electrophysiology, Endothelial cells, Epigenetics and Cardiovascular Risks, Etiology, Evolutionary cognition, Frontiers in Cardiology and Cardiovascular Disorders, Genome Biology, Genomic Expression, Health Economics and Outcomes Research, Human Immune System in Health and in Disease, International Global Work in Pharmaceutical, Interviews with Scientific Leaders, Medical and Population Genetics, Medical Device Therapies for Altzheimer’s Disease, Medical Devices R&D Investment, Medical Imaging Technology, Image Processing/Computing, MRI, CT, Nuclear Medicine, Ultra Sound, Metabolomics, Molecular Genetics & Pharmaceutical, Myocardial metabolism, Myocardial ischemia, myocardial perfusion, Myocardial adenine nucleotide metabolism, Na-K transport, Na-K-ATPase, Neurohumoral Transmission, Nitric Oxide in Health and Disease, Nutrition, Nutritional Supplements: Atherogenesis, lipid metabolism, Origins of Cardiovascular Disease, Oxidative phosphorylation, Personalized and Precision Medicine & Genomic Research, Pharmaceutical Analytics, Pharmacologic toxicities, Pharmacotherapy of Cardiovascular Disease, Phosphorylation, PKC, Population Health Management, Genetics & Pharmaceutical, Population Health Management, Nutrition and Phytochemistry, Proteomics, Regenerative Biology and Medicine, S-nitrosylation, Signaling, Skeletal muscle regeneration, Statistical Methods for Research Evaluation, Stem Cells for Regenerative Medicine, Stents & Tools, Synaptic vesicle, Systemic Inflammatory Response Related Disorders, Technology Advance Assessment of, Translational Effectiveness, Translational Science, Ubiquitinylation, Water Transporters, tagged bioengineering, Cardiovascular Disorders, computational biology, Coronary artery disease, DNA Sequencing, functional proteomics, gene expression, gene silencing, genetic engineering, Heart Failure, Human Genome Project, Hypertension, MicroRNA, mtRNA, myocardial infarction, nitric oxide, Nitric oxide synthase, Personalized medicine, protein modifications, Proteomics, reverse engineering, RNA, signaling pathways, Stem cell, synbiology on April 28, 2014| Leave a Comment »

Summary of Translational Medicine – e-Series A: Cardiovascular Diseases, Volume Four – Part 1

Author and Curator: Larry H Bernstein, MD, FCAP

and

Curator: Aviva Lev-Ari, PhD, RN

Article ID #135: Summary of Translational Medicine – e-Series A: Cardiovascular Diseases, Volume Four – Part 1. Published on 4/28/2014

WordCloud Image Produced by Adam Tubman

 

Part 1 of Volume 4 in the e-series A: Cardiovascular Diseases and Translational Medicine, provides a foundation for grasping a rapidly developing surging scientific endeavor that is transcending laboratory hypothesis testing and providing guidelines to:

• Target genomes and multiple nucleotide sequences involved in either coding or in regulation that might have an impact on complex diseases, not necessarily genetic in nature.
• Target signaling pathways that are demonstrably maladjusted, activated or suppressed in many common and complex diseases, or in their progression.
• Enable a reduction in failure due to toxicities in the later stages of clinical drug trials as a result of this science-based understanding.
• Enable a reduction in complications from the improvement of machanical devices that have already had an impact on the practice of interventional procedures in cardiology, cardiac surgery, and radiological imaging, as well as improving laboratory diagnostics at the molecular level.
• Enable the discovery of new drugs in the continuing emergence of drug resistance.
• Enable the construction of critical pathways and better guidelines for patient management based on population outcomes data, that will be critically dependent on computational methods and large data-bases.

What has been presented can be essentially viewed in the following Table:

 

Summary Table for TM – Part 1

 

 

 

There are some developments that deserve additional development:

1. The importance of mitochondrial function in the activity state of the mitochondria in cellular work (combustion) is understood, and impairments of function are identified in diseases of muscle, cardiac contraction, nerve conduction, ion transport, water balance, and the cytoskeleton – beyond the disordered metabolism in cancer.  A more detailed explanation of the energetics that was elucidated based on the electron transport chain might also be in order.

2. The processes that are enabling a more full application of technology to a host of problems in the environment we live in and in disease modification is growing rapidly, and will change the face of medicine and its allied health sciences.

 

Electron Transport and Bioenergetics

Deferred for metabolomics topic

Synthetic Biology

Introduction to Synthetic Biology and Metabolic Engineering

Kristala L. J. Prather: Part-1    <iBiology > iBioSeminars > Biophysics & Chemical Biology >

http://www.ibiology.org Lecturers generously donate their time to prepare these lectures. The project is funded by NSF and NIGMS, and is supported by the ASCB and HHMI.
Dr. Prather explains that synthetic biology involves applying engineering principles to biological systems to build “biological machines”.

http://synthetic_biology/Introduction_to_Synthetic_Biology_and_Metabolic_Engineering/Kristala_ L.J._Prather/E2/iBiology.htm#/sthash.71kZ0ofr.dpuf

Dr. Prather has received numerous awards both for her innovative research and for excellence in teaching.  Learn more about how Kris became a scientist at

http://science360.gov/obj/video/753bb4fa-aafb-4315-848e-51066ed9799a/finding-way-kristala-l-jones-prather-phd 

Prather 1: Synthetic Biology and Metabolic Engineering  2/6/14IntroductionLecture Overview In the first part of her lecture, Dr. Prather explains that synthetic biology involves applying engineering principles to biological systems to build “biological machines”. The key material in building these machines is synthetic DNA. Synthetic DNA can be added in different combinations to biological hosts, such as bacteria, turning them into chemical factories that can produce small molecules of choice. In Part 2, Prather describes how her lab used design principles to engineer E. coli that produce glucaric acid from glucose. Glucaric acid is not naturally produced in bacteria, so Prather and her colleagues “bioprospected” enzymes from other organisms and expressed them in E. coli to build the needed enzymatic pathway. Prather walks us through the many steps of optimizing the timing, localization and levels of enzyme expression to produce the greatest yield. Speaker Bio: Kristala Jones Prather received her S.B. degree from the Massachusetts Institute of Technology and her PhD at the University of California, Berkeley both in chemical engineering. Upon graduation, Prather joined the Merck Research Labs for 4 years before returning to academia. Prather is now an Associate Professor of Chemical Engineering at MIT and an investigator with the multi-university Synthetic Biology Engineering Reseach Center (SynBERC). Her lab designs and constructs novel synthetic pathways in microorganisms converting them into tiny factories for the production of small molecules. Dr. Prather has received numerous awards both for her innovative research and for excellence in teaching.

VIEW VIDEOS

https://www.youtube.com/watch?feature=player_embedded&v=ndThuqVumAk#t=0

https://www.youtube.com/watch?feature=player_embedded&v=ndThuqVumAk#t=12

https://www.youtube.com/watch?feature=player_embedded&v=ndThuqVumAk#t=74

https://www.youtube.com/watch?feature=player_embedded&v=ndThuqVumAk#t=129

https://www.youtube.com/watch?feature=player_embedded&v=ndThuqVumAk#t=168

https://www.youtube.com/watch?feature=player_embedded&v=ndThuqVumAk

 

David Bartel: micro-RNAs

 

I. Introduction to microRNAs

https://www.youtube.com/watch?feature=player_embedded&v=dupzE66J8u4#t=0

– See more at: http://www.ibiology.org/ibioseminars/genetics-gene-regulation/david-bartel-part-1.html#sthash.nGGr1tIt.dpuf

II. Regulatory Effects of Mammalian microRNAs

https://www.youtube.com/watch?feature=player_embedded&v=TcZK_A_wcWQ#t=0

https://www.youtube.com/watch?feature=player_embedded&v=TcZK_A_wcWQ

Calcium Cycling in Synthetic and Contractile Phasic or Tonic Vascular Smooth Muscle Cells

in INTECH
Current Basic and Pathological Approaches to
the Function of Muscle Cells and Tissues – From Molecules to HumansLarissa Lipskaia, Isabelle Limon, Regis Bobe and Roger Hajjar
Additional information is available at the end of the chapter
http://dx.doi.org/10.5772/48240

1. Introduction
Calcium ions (Ca ) are present in low concentrations in the cytosol (~100 nM) and in high concentrations (in mM range) in both the extracellular medium and intracellular stores (mainly sarco/endo/plasmic reticulum, SR). This differential allows the calcium ion messenger that carries information
as diverse as contraction, metabolism, apoptosis, proliferation and/or hypertrophic growth. The mechanisms responsible for generating a Ca signal greatly differ from one cell type to another.

In the different types of vascular smooth muscle cells (VSMC), enormous variations do exist with regard to the mechanisms responsible for generating Ca signal. In each VSMC phenotype (synthetic/proliferating and contractile [1], tonic or phasic), the Ca signaling system is adapted to its particular function and is due to the specific patterns of expression and regulation of Ca.
For instance, in contractile VSMCs, the initiation of contractile events is driven by mem- brane depolarization; and the principal entry-point for extracellular Ca is the voltage-operated L-type calcium channel (LTCC). In contrast, in synthetic/proliferating VSMCs, the principal way-in for extracellular Ca is the store-operated calcium (SOC) channel.
Whatever the cell type, the calcium signal consists of  limited elevations of cytosolic free calcium ions in time and space. The calcium pump, sarco/endoplasmic reticulum Ca ATPase (SERCA), has a critical role in determining the frequency of SR Ca release by upload into the sarcoplasmic
sensitivity of  SR calcium channels, Ryanodin Receptor, RyR and Inositol tri-Phosphate Receptor, IP3R.
Synthetic VSMCs have a fibroblast appearance, proliferate readily, and synthesize increased levels of various extracellular matrix components, particularly fibronectin, collagen types I and III, and tropoelastin [1].
Contractile VSMCs have a muscle-like or spindle-shaped appearance and well-developed contractile apparatus resulting from the expression and intracellular accumulation of thick and thin muscle filaments [1].

Schematic representation of Calcium Cycling in Contractile and Proliferating VSMCs

 

Figure 1. Schematic representation of Calcium Cycling in Contractile and Proliferating VSMCs.

Left panel: schematic representation of calcium cycling in quiescent /contractile VSMCs. Contractile re-sponse is initiated by extracellular Ca influx due to activation of Receptor Operated Ca (through phosphoinositol-coupled receptor) or to activation of L-Type Calcium channels (through an increase in luminal pressure). Small increase of cytosolic due IP3 binding to IP3R (puff) or RyR activation by LTCC or ROC-dependent Ca influx leads to large SR Ca IP3R or RyR clusters (“Ca -induced Ca SR calcium pumps (both SERCA2a and SERCA2b are expressed in quiescent VSMCs), maintaining high concentration of cytosolic Ca and setting the sensitivity of RyR or IP3R for the next spike.
Contraction of VSMCs occurs during oscillatory Ca transient.
Middle panel: schematic representa tion of atherosclerotic vessel wall. Contractile VSMC are located in the media layer, synthetic VSMC are located in sub-endothelial intima.
Right panel: schematic representation of calcium cycling in quiescent /contractile VSMCs. Agonist binding to phosphoinositol-coupled receptor leads to the activation of IP3R resulting in large increase in cytosolic Ca calcium pumps (only SERCA2b, having low turnover and low affinity to Ca depletion leads to translocation of SR Ca sensor STIM1 towards PM, resulting in extracellular Ca influx though opening of Store Operated Channel (CRAC). Resulted steady state Ca transient is critical for activation of proliferation-related transcription factors ‘NFAT).
Abbreviations: PLC – phospholipase C; PM – plasma membrane; PP2B – Ca /calmodulin-activated protein phosphatase 2B (calcineurin); ROC- receptor activated channel; IP3 – inositol-1,4,5-trisphosphate, IP3R – inositol-1,4,5- trisphosphate receptor; RyR – ryanodine receptor; NFAT – nuclear factor of activated T-lymphocytes; VSMC – vascular smooth muscle cells; SERCA – sarco(endo)plasmic reticulum Ca sarcoplasmic reticulum.

 

Time for New DNA Synthesis and Sequencing Cost Curves

By Rob Carlson

I’ll start with the productivity plot, as this one isn’t new. For a discussion of the substantial performance increase in sequencing compared to Moore’s Law, as well as the difficulty of finding this data, please see this post. If nothing else, keep two features of the plot in mind: 1) the consistency of the pace of Moore’s Law and 2) the inconsistency and pace of sequencing productivity. Illumina appears to be the primary driver, and beneficiary, of improvements in productivity at the moment, especially if you are looking at share prices. It looks like the recently announced NextSeq and Hiseq instruments will provide substantially higher productivities (hand waving, I would say the next datum will come in another order of magnitude higher), but I think I need a bit more data before officially putting another point on the plot.

 

cost-of-oligo-and-gene-synthesis

Illumina’s instruments are now responsible for such a high percentage of sequencing output that the company is effectively setting prices for the entire industry. Illumina is being pushed by competition to increase performance, but this does not necessarily translate into lower prices. It doesn’t behoove Illumina to drop prices at this point, and we won’t see any substantial decrease until a serious competitor shows up and starts threatening Illumina’s market share. The absence of real competition is the primary reason sequencing prices have flattened out over the last couple of data points.

Note that the oligo prices above are for column-based synthesis, and that oligos synthesized on arrays are much less expensive. However, array synthesis comes with the usual caveat that the quality is generally lower, unless you are getting your DNA from Agilent, which probably means you are getting your dsDNA from Gen9.

Note also that the distinction between the price of oligos and the price of double-stranded sDNA is becoming less useful. Whether you are ordering from Life/Thermo or from your local academic facility, the cost of producing oligos is now, in most cases, independent of their length. That’s because the cost of capital (including rent, insurance, labor, etc) is now more significant than the cost of goods. Consequently, the price reflects the cost of capital rather than the cost of goods. Moreover, the cost of the columns, reagents, and shipping tubes is certainly more than the cost of the atoms in the sDNA you are ostensibly paying for. Once you get into longer oligos (substantially larger than 50-mers) this relationship breaks down and the sDNA is more expensive. But, at this point in time, most people aren’t going to use longer oligos to assemble genes unless they have a tricky job that doesn’t work using short oligos.

Looking forward, I suspect oligos aren’t going to get much cheaper unless someone sorts out how to either 1) replace the requisite human labor and thereby reduce the cost of capital, or 2) finally replace the phosphoramidite chemistry that the industry relies upon.

IDT’s gBlocks come at prices that are constant across quite substantial ranges in length. Moreover, part of the decrease in price for these products is embedded in the fact that you are buying smaller chunks of DNA that you then must assemble and integrate into your organism of choice.

Someone who has purchased and assembled an absolutely enormous amount of sDNA over the last decade, suggested that if prices fell by another order of magnitude, he could switch completely to outsourced assembly. This is a potentially interesting “tipping point”. However, what this person really needs is sDNA integrated in a particular way into a particular genome operating in a particular host. The integration and testing of the new genome in the host organism is where most of the cost is. Given the wide variety of emerging applications, and the growing array of hosts/chassis, it isn’t clear that any given technology or firm will be able to provide arbitrary synthetic sequences incorporated into arbitrary hosts.

 TrackBack URL: http://www.synthesis.cc/cgi-bin/mt/mt-t.cgi/397

 

Startup to Strengthen Synthetic Biology and Regenerative Medicine Industries with Cutting Edge Cell Products

28 Nov 2013 | PR Web

Dr. Jon Rowley and Dr. Uplaksh Kumar, Co-Founders of RoosterBio, Inc., a newly formed biotech startup located in Frederick, are paving the way for even more innovation in the rapidly growing fields of Synthetic Biology and Regenerative Medicine. Synthetic Biology combines engineering principles with basic science to build biological products, including regenerative medicines and cellular therapies. Regenerative medicine is a broad definition for innovative medical therapies that will enable the body to repair, replace, restore and regenerate damaged or diseased cells, tissues and organs. Regenerative therapies that are in clinical trials today may enable repair of damaged heart muscle following heart attack, replacement of skin for burn victims, restoration of movement after spinal cord injury, regeneration of pancreatic tissue for insulin production in diabetics and provide new treatments for Parkinson’s and Alzheimer’s diseases, to name just a few applications.

While the potential of the field is promising, the pace of development has been slow. One main reason for this is that the living cells required for these therapies are cost-prohibitive and not supplied at volumes that support many research and product development efforts. RoosterBio will manufacture large quantities of standardized primary cells at high quality and low cost, which will quicken the pace of scientific discovery and translation to the clinic. “Our goal is to accelerate the development of products that incorporate living cells by providing abundant, affordable and high quality materials to researchers that are developing and commercializing these regenerative technologies” says Dr. Rowley

 

Life at the Speed of Light

http://kcpw.org/?powerpress_pinw=92027-podcast

NHMU Lecture featuring – J. Craig Venter, Ph.D.
Founder, Chairman, and CEO – J. Craig Venter Institute; Co-Founder and CEO, Synthetic Genomics Inc.

J. Craig Venter, Ph.D., is Founder, Chairman, and CEO of the J. Craig Venter Institute (JVCI), a not-for-profit, research organization dedicated to human, microbial, plant, synthetic and environmental research. He is also Co-Founder and CEO of Synthetic Genomics Inc. (SGI), a privately-held company dedicated to commercializing genomic-driven solutions to address global needs.

In 1998, Dr. Venter founded Celera Genomics to sequence the human genome using new tools and techniques he and his team developed.  This research culminated with the February 2001 publication of the human genome in the journal, Science. Dr. Venter and his team at JVCI continue to blaze new trails in genomics.  They have sequenced and a created a bacterial cell constructed with synthetic DNA,  putting humankind at the threshold of a new phase of biological research.  Whereas, we could  previously read the genetic code (sequencing genomes), we can now write the genetic code for designing new species.

The science of synthetic genomics will have a profound impact on society, including new methods for chemical and energy production, human health and medical advances, clean water, and new food and nutritional products. One of the most prolific scientists of the 21st century for his numerous pioneering advances in genomics,  he  guides us through this emerging field, detailing its origins, current challenges, and the potential positive advances.

His work on synthetic biology truly embodies the theme of “pushing the boundaries of life.”  Essentially, Venter is seeking to “write the software of life” to create microbes designed by humans rather than only through evolution. The potential benefits and risks of this new technology are enormous. It also requires us to examine, both scientifically and philosophically, the question of “What is life?”

J Craig Venter wants to digitize DNA and transmit the signal to teleport organisms

http://pharmaceuticalintelligence.com/2013/11/01/j-craig-venter-wants-to-digitize-dna-and-transmit-the-signal-to-teleport-organisms/

2013 Genomics: The Era Beyond the Sequencing of the Human Genome: Francis Collins, Craig Venter, Eric Lander, et al.

http://pharmaceuticalintelligence.com/2013/02/11/2013-genomics-the-era-beyond-the-sequencing-human-genome-francis-collins-craig-venter-eric-lander-et-al/

Human Longevity Inc (HLI) – $70M in Financing of Venter’s New Integrative Omics and Clinical Bioinformatics

http://pharmaceuticalintelligence.com/2014/03/05/human-longevity-inc-hli-70m-in-financing-of-venters-new-integrative-omics-and-clinical-bioinformatics/

 

 

Where Will the Century of Biology Lead Us?

By Randall Mayes

A technology trend analyst offers an overview of synthetic biology, its potential applications, obstacles to its development, and prospects for public approval.

• In addition to boosting the economy, synthetic biology projects currently in development could have profound implications for the future of manufacturing, sustainability, and medicine.
• Before society can fully reap the benefits of synthetic biology, however, the field requires development and faces a series of hurdles in the process. Do researchers have the scientific know-how and technical capabilities to develop the field?

Biology + Engineering = Synthetic Biology

Bioengineers aim to build synthetic biological systems using compatible standardized parts that behave predictably. Bioengineers synthesize DNA parts—oligonucleotides composed of 50–100 base pairs—which make specialized components that ultimately make a biological system. As biology becomes a true engineering discipline, bioengineers will create genomes using mass-produced modular units similar to the microelectronics and computer industries.

Currently, bioengineering projects cost millions of dollars and take years to develop products. For synthetic biology to become a Schumpeterian revolution, smaller companies will need to be able to afford to use bioengineering concepts for industrial applications. This will require standardized and automated processes.

A major challenge to developing synthetic biology is the complexity of biological systems. When bioengineers assemble synthetic parts, they must prevent cross talk between signals in other biological pathways. Until researchers better understand these undesired interactions that nature has already worked out, applications such as gene therapy will have unwanted side effects. Scientists do not fully understand the effects of environmental and developmental interaction on gene expression. Currently, bioengineers must repeatedly use trial and error to create predictable systems.

Similar to physics, synthetic biology requires the ability to model systems and quantify relationships between variables in biological systems at the molecular level.

The second major challenge to ensuring the success of synthetic biology is the development of enabling technologies. With genomes having billions of nucleotides, this requires fast, powerful, and cost-efficient computers. Moore’s law, named for Intel co-founder Gordon Moore, posits that computing power progresses at a predictable rate and that the number of components in integrated circuits doubles each year until its limits are reached. Since Moore’s prediction, computer power has increased at an exponential rate while pricing has declined.

DNA sequencers and synthesizers are necessary to identify genes and make synthetic DNA sequences. Bioengineer Robert Carlson calculated that the capabilities of DNA sequencers and synthesizers have followed a pattern similar to computing. This pattern, referred to as the Carlson Curve, projects that scientists are approaching the ability to sequence a human genome for $1,000, perhaps in 2020. Carlson calculated that the costs of reading and writing new genes and genomes are falling by a factor of two every 18–24 months. (see recent Carlson comment on requirement to read and write for a variety of limiting  conditions).

Startup to Strengthen Synthetic Biology and Regenerative Medicine Industries with Cutting Edge Cell Products

http://pharmaceuticalintelligence.com/2013/11/28/startup-to-strengthen-synthetic-biology-and-regenerative-medicine-industries-with-cutting-edge-cell-products/

Synthetic Biology: On Advanced Genome Interpretation for Gene Variants and Pathways: What is the Genetic Base of Atherosclerosis and Loss of Arterial Elasticity with Aging

http://pharmaceuticalintelligence.com/2013/05/17/synthetic-biology-on-advanced-genome-interpretation-for-gene-variants-and-pathways-what-is-the-genetic-base-of-atherosclerosis-and-loss-of-arterial-elasticity-with-aging/

Synthesizing Synthetic Biology: PLOS Collections

http://pharmaceuticalintelligence.com/2012/08/17/synthesizing-synthetic-biology-plos-collections/

Capturing ten-color ultrasharp images of synthetic DNA structures resembling numerals 0 to 9

http://pharmaceuticalintelligence.com/2014/02/05/capturing-ten-color-ultrasharp-images-of-synthetic-dna-structures-resembling-numerals-0-to-9/

Silencing Cancers with Synthetic siRNAs

http://pharmaceuticalintelligence.com/2013/12/09/silencing-cancers-with-synthetic-sirnas/

Genomics Now—and Beyond the Bubble

Futurists have touted the twenty-first century as the century of biology based primarily on the promise of genomics. Medical researchers aim to use variations within genes as biomarkers for diseases, personalized treatments, and drug responses. Currently, we are experiencing a genomics bubble, but with advances in understanding biological complexity and the development of enabling technologies, synthetic biology is reviving optimism in many fields, particularly medicine.

BY MICHAEL BROOKS    17 APR, 2014     http://www.newstatesman.com/

Michael Brooks holds a PhD in quantum physics. He writes a weekly science column for the New Statesman, and his most recent book is The Secret Anarchy of Science.

The basic idea is that we take an organism – a bacterium, say – and re-engineer its genome so that it does something different. You might, for instance, make it ingest carbon dioxide from the atmosphere, process it and excrete crude oil.

That project is still under construction, but others, such as using synthesised DNA for data storage, have already been achieved. As evolution has proved, DNA is an extraordinarily stable medium that can preserve information for millions of years. In 2012, the Harvard geneticist George Church proved its potential by taking a book he had written, encoding it in a synthesised strand of DNA, and then making DNA sequencing machines read it back to him.

When we first started achieving such things it was costly and time-consuming and demanded extraordinary resources, such as those available to the millionaire biologist Craig Venter. Venter’s team spent most of the past two decades and tens of millions of dollars creating the first artificial organism, nicknamed “Synthia”. Using computer programs and robots that process the necessary chemicals, the team rebuilt the genome of the bacterium Mycoplasma mycoides from scratch. They also inserted a few watermarks and puzzles into the DNA sequence, partly as an identifying measure for safety’s sake, but mostly as a publicity stunt.

What they didn’t do was redesign the genome to do anything interesting. When the synthetic genome was inserted into an eviscerated bacterial cell, the new organism behaved exactly the same as its natural counterpart. Nevertheless, that Synthia, as Venter put it at the press conference to announce the research in 2010, was “the first self-replicating species we’ve had on the planet whose parent is a computer” made it a standout achievement.

Today, however, we have entered another era in synthetic biology and Venter faces stiff competition. The Steve Jobs to Venter’s Bill Gates is Jef Boeke, who researches yeast genetics at New York University.

Boeke wanted to redesign the yeast genome so that he could strip out various parts to see what they did. Because it took a private company a year to complete just a small part of the task, at a cost of $50,000, he realised he should go open-source. By teaching an undergraduate course on how to build a genome and teaming up with institutions all over the world, he has assembled a skilled workforce that, tinkering together, has made a synthetic chromosome for baker’s yeast.

 

Stepping into DIYbio and Synthetic Biology at ScienceHack

Posted April 22, 2014 by Heather McGaw and Kyrie Vala-Webb

We got a crash course on genetics and protein pathways, and then set out to design and build our own pathways using both the “Genomikon: Violacein Factory” kit and Synbiota platform. With Synbiota’s software, we dragged and dropped the enzymes to create the sequence that we were then going to build out. After a process of sketching ideas, mocking up pathways, and writing hypotheses, we were ready to start building!

The night stretched long, and at midnight we were forced to vacate the school. Not quite finished, we loaded our delicate bacteria, incubator, and boxes of gloves onto the bus and headed back to complete our bacterial transformation in one of our hotel rooms. Jammed in between the beds and the mini-fridge, we heat-shocked our bacteria in the hotel ice bucket. It was a surreal moment.

While waiting for our bacteria, we held an “unconference” where we explored bioethics, security and risk related to synthetic biology, 3D printing on Mars, patterns in juggling (with live demonstration!), and even did a Google Hangout with Rob Carlson. Every few hours, we would excitedly check in on our bacteria, looking for bacterial colonies and the purple hue characteristic of violacein.

Most impressive was the wildly successful and seamless integration of a diverse set of people: in a matter of hours, we were transformed from individual experts and practitioners in assorted fields into cohesive and passionate teams of DIY biologists and science hackers. The ability of everyone to connect and learn was a powerful experience, and over the course of just one weekend we were able to challenge each other and grow.

Returning to work on Monday, we were hungry for more. We wanted to find a way to bring the excitement and energy from the weekend into the studio and into the projects we’re working on. It struck us that there are strong parallels between design and DIYbio, and we knew there was an opportunity to bring some of the scientific approaches and curiosity into our studio.

 

 

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  • List of Articles included in the Article SELECTION from Collection of Aviva Lev-Ari, PhD, RN Scientific Articles on PULSE on LinkedIn.com for Training Small Language Models (SLMs) in Domain-aware Content of Medical, Pharmaceutical, Life Sciences and Healthcare by 15 Subjects Matter January 10, 2026
  • Article SELECTION from Collection of Aviva Lev-Ari, PhD, RN Scientific Articles on PULSE on LinkedIn.com for Training Small Language Models (SLMs) in Domain-aware Content of Medical, Pharmaceutical, Life Sciences and Healthcare by 15 Subjects Matter January 10, 2026
  • Collection of Aviva Lev-Ari, PhD, RN Scientific Articles on PULSE on LinkedIn.com January 10, 2026
  • The youngest leader in AI in Health: Tanishq Mathew Abraham, Ph.D. (@iScienceLuvr) January 8, 2026
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