Category Archives: BioEngineering

Public release date: 25-Apr-2012 [ | E-mail | Share ]

Contact: LaKisha Ladson lakisha.ladson@UTDallas.edu 972-883-4183 University of Texas at Dallas

Dr. Mathukumalli Vidyasagar, an internationally known expert in control and system theory, has been elected a Fellow of The Royal Society, the oldest continuously operating scientific society in the world.

Vidyasagar, head of the Department of Bioengineering at The University of Texas at Dallas, joins the ranks of the most distinguished international scientists drawn from all areas of science, engineering and medicine.

Vidyasagar's selection recognizes his contributions to various aspects of control and system theory, robotics, statistical learning theory and computational biology. His citation reads: "He has combined probability theory, combinatorics, and artificial intelligence to produce a beautiful unified theory of statistical learning, and used it to solve NP-hard design problems."

Vidyasagar's pattern in life has been to master a subject area, write a book about it, and then move to a different research problem at the forefront of the field. Two of his books co-authored with Dr. Mark W. Spong, dean of UT Dallas' Erik Jonsson School of Engineering and Computer Science, are among the most popular textbooks on robot dynamics and control.

"Joining the Fellowship of the Royal Society is the proudest moment of my career. The joy and satisfaction this election brings is immeasurable."

Vidyasagar holds the Cecil H. and Ida Green Chair in Systems Biology Science at UT Dallas and leads the bioengineering department in the Jonsson School. The department collaborates with other schools within the University, UT Southwestern Medical Center and the University of Texas at Arlington.

"Dr. Vidyasagar has made many fundamental contributions in several areas of engineering, including control theory, robotics, and learning theory, which have earned him numerous awards and an international reputation as an outstanding scientist," Spong said. "His latest work in the area of computational biology, in collaboration with UT Southwestern Medical Center, has the potential to greatly advance our knowledge of the causes of cancer and the effectiveness of new drugs for the treatment of cancer. Election to the Royal Society is a very high honor and brings distinction to him, the Jonsson School, and to UT Dallas."

A native of India, Vidyasagar attended the University of Wisconsin and earned a bachelor's degree in electrical engineering by age 17. At 21, he completed his doctorate and by age 35, he was given an Institute of Electrical and Electronics Engineers fellowship for "contributions to the stability analysis of linear and nonlinear distributed systems."

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UT Dallas bioengineering head to be inducted as Fellow of Royal Society

Despite decades of cancer research, cancer remains a leading cause of death worldwide, accounting for 7.6 million deaths in 2008, and breast cancer is one of the most common causes of cancer deaths each year . In Singapore, more than 1,400 women are diagnosed with breast cancer and more than 300 die as a result of breast cancer each year . The high fatality rate of cancer is partially attributed to the invasive ability of malignant tumors to spread throughout the human body, and the ineffectiveness of conventional therapies to eradicate the cancer cells.

A team of researchers led by IBN Group Leader, Dr Shu Wang, has made a landmark discovery that neural stem cells (NSCs) derived from human induced pluripotent stem (iPS) cells could be used to treat breast cancer. The effectiveness of using NSCs, which originate from the central nervous system, to treat brain tumors has been investigated in previous studies. This is the first study that demonstrates that iPS cell-derived NSCs could also target tumors outside the central nervous system, to treat both primary and secondary tumors.

To test the efficiency of NSCs in targeting and treating breast cancer, the researchers injected NSCs loaded with a suicide gene (herpes simplex virus thymidine) into mice bearing breast tumors. They did this using baculoviral vectors or gene carriers engineered from an insect virus (baculovirus), which does not replicate in human cells, making the carriers less harmful for clinical use. A prodrug (ganciclovir), which would activate the suicide gene to kill the cancerous cells upon contact, was subsequently injected into the mice. A dual-colored whole body imaging technology was then used to track the distribution and migration of the iPS-NSCs.

The imaging results revealed that the iPS-NSCs homed in on the breast tumors in the mice, and also accumulated in various organs infiltrated by the cancer cells such as the lung, stomach and bone. The survival of the tumor-bearing mice was prolonged from 34 days to 39 days. This data supports and explains how engineered iPS-NSCs are able to effectively seek out and inhibit tumor growth and proliferation.

Dr Shu Wang shared, "We have demonstrated that tumor-targeting neural stem cells may be derived from human iPS cells, and that these cells may be used in combination with a therapeutic gene to cripple tumor growth. This is a significant finding for stem cell-based cancer therapy, and we will continue to improve and optimize our neural stem cell system by preventing any unwanted activation of the therapeutic gene in non-tumor regions and minimizing possible side effects."

"IBN's expertise in generating human stem cells from iPS cells and our novel use of insect virus carriers for gene delivery have paved the way for the development of innovative stem cell-based therapies. With their two-pronged attack on tumors using genetically engineered neural stem cells, our researchers have discovered a promising alternative to conventional cancer treatment," added Professor Jackie. Y. Ying, IBN Executive Director.

Compared to collecting and expanding primary cells from individual patients, IBN's approach of using iPS cells to derive NSCs is less laborious and suitable for large-scale manufacture of uniform batches of cellular products for repeated patient treatments. Importantly, this approach will help eliminate variability in the quality of the cellular products, thus facilitating reliable comparative analysis of clinical outcomes.

Additionally, these iPS cell-derived NSCs are derived from adult cells, which bypass the sensitive ethical issue surrounding the use of human embryos, and since iPS cells are developed from a patient's own cells, the likelihood of immune rejection would be reduced.

References: 1. J. Yang, D. H. Lam, S. S. Goh, E. X. L. Lee, Y. Zhao, F. Chang Tay, C. Chen, S. Du, G. Balasundaram, M. Shahbazi, C. K. Tham, W. H. Ng, H. C. Toh and S. Wang, "Tumor Tropism of Intravenously Injected Human Induced Pluripotent Stem Cell-derived Neural Stem Cells and their Gene Therapy Application in a Metastatic Breast Cancer Model," Stem Cells, (2012) DOI: 10.1002/stem.1051.

2. E. X. Lee, D. H. Lam, C. Wu, J. Yang, C. K. Tham and S. Wang, "Glioma Gene Therapy Using Induced Pluripotent Stem Cell-Derived Neural Stem Cells," Molecular Pharmaceutics, 8 (2011) 1515-1524.

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IBN Discovers Human Neural Stem Cells with Tumor Targeting Ability - A Promising Discovery for Breast Cancer Therapy

Probiotics are an enormous field and even bigger market but and as interesting as they are an, arguably, more interesting biotic is starting to gain traction as more innovative researchers explore its possibilities. This is the field of designer probiotics.

The central idea is this, certain pathogenic bacteria (and I am speaking exclusively within the gut) use host sugars to facilitate binding or toxin targeting and by doing so cause disease. However, if we expressed these host sugars on something else, a harmless strain of Escherichia coli for example, we would create more sites for the attachment of pathogens and their weapons. This dilutes the effect these pathogenic bacteria can have on our insides and either prevents disease or certainly reduces the severity of it and the harmless E. coli,ladenwith pathogen and toxin, passes out of the body before they can cause any problems.

Additionally, there is little chance that the pathogens will evolve around this therapeutic strategy as doing so would comprimise their capacity to recognise the target receptor that has been copied and expressed on our harmless E. coli strain and therefore would reduce their capacity to cause disease as part of their lifecycle.

Then of course there is money. Currently, host sugars have been developed synthetically to be used in isolation to attempt prevention of pathogen binding but are not optimally successful as these sugar structures must survive the stomache and early gut before reaching the distal gut where much disease occurs. Making these sugars alone is not cheap but you know what is cheap, bacteria and broth. Vats of drug can be grown in labs much faster than the sugars can be synthesised making it a much more cost effective approach. Of course then there is also the problem of hostmetabolismof the synthesised sugars. By the time the distal gut is reached the gastro-intestinal system has done what it does best and broken much of the sugar down into its component parts rendering it ineffective as a therapeutic. The probiotic approach secures the expression of the host sugars deep into the distal gut as long as the bacteria survive, which they have been shown to do. Once they get there they grow and divide increasing the amount of drug in the system for free.

I am aware of three such bioengineered bugs capable of doing this work, one for Shiga toxigenic E. coli (STEC) infections, one for enterotoxigenic E. coli (ETEC) infections and one for cholera. Together these three species account for a large proportion of the 2 million deaths that occur each year due to enteric infections, not including the significant morbidity that occurs at the hands of these species.

STEC produces, as you would expect, a shiga toxin which is a very powerful toxin that causes breakdown of cell membranes leading to haemorrhagic colitis (bleeding gut) and the significantly worse haemolytic uraemic syndrome where the patient develops haemolytic anaemia (not enough blood cells because they keep popping), thrombocytopenia (not enough platelets so your blood cant clot) and renal failure (kidneys shut down). Importantly, in this case at least, the shiga toxin is made in the gut before binding to a host sugar called GB3 which facilitates absorption into the body where it does its damage. When GB3 was expressed on a harmless E. coli strain and fed twice daily to STEC infected mice it was found to be 100% effective in preventing disease as the toxin was being soaked up before reaching the gut wall. For the cautious out there the use of dead GB3 expressing E. coli was also tested and found to be just as effective if the dosage was increased to three times daily. Dead bacteria do not mutate and are not technically genetically modified organismsany moreso this approach has long term promise to treat STEC infection in the future.

ETEC is behind travellersdiarrhoea but should not be underestimated. This bacteria is endemic in developingcountriesand is the major killer of young children in these areas. It kills by messing around with the way your body controls water loss in the gut. The toxin made by ETEC binds to the host sugar GM1 and then is internalised by the cell. The target cells are those that line the gut surface and are responsible for absorbing nutrients, ions and water. Once inside the cell the toxin modifies a biochemical pathway to ensure a protein called adenyl cyclase is constantly stimulated which in turn causes aninterruptionto ion movement resulting in ions moving out of the cell into the gut but not back in again. A general rule in gut physiology is where the ions go water will follow and so water flows straight of the body into the gut causing watery diarrhoea. This diarrhoea facilitates the spread of the ETEC into water supplies and then into new hosts as they consume the contaminated water. The production of a harmless E. coli strain capable of binding the ETEC toxin was performed and the result was a bacterial strain that could bind 5% of its own weight in toxin! There is the suggestion that the administration of this strain prophylactically to travellers from developed coutries before travel to the developing world may eliminate a good proportion of disease cases and the ease in growing high quantities of drug would make treating the developing world significantly easier and cheaper providing some additional hope in these areas.

Finally, cholera. Vibrio cholera is endemic to Asia and causes epidemics all over the world. Usually as a result of eating undercooked fish the pathogen enters the system, colonises the small intestine and releaases its toxin which works in the same way as the ETEC toxin. If no treatment is made available, as is the case for many where cholera is endemic, the chance of death rockets up to 50%. Treatment here is tricky as antibiotics can actually make the disease worse as toxin leeches from the dying pathogens and overwhelms the patient so most are treated with fluid therapy, keep drinking salty water (made using sachets of important salts which can be added to sterilised water) until you get better, or not. A GM1 expressing E. coli was developed and shown to be very effective in preventing disease. Mice given V. cholera infections were treated with the harmless GM1 expressing strain 1 or 4 hours post infection and 12/12 survived compared to 1/12 for the post 1 hour treatment, 8/12 compared to 2/12 for the post 4 hour treatment. In this case it was found that the GM1 producing strain could remain stable when freeze dried and so could be made, stored, then added to the oral rehydration salts as part of the current therapeutic strategy which would keep costs significantly down.

This is but the start. Similar approaches could be applied to Clostridium difficile, Helicobacter pylori and Schistosoma mansonii infections as this novel approach is developed.

So thats it. The problem of antibiotic resistance is solved right? We just dont use antibiotics and instead use these cleverly designed genetically modified organisms that cant be evolved aroundwithoutthe pathogenreducingits ability to infect at all. We produceenormousquantities cheaply in vats where the drug grows itself on $10 worth ofingredientsand then treat the whole world.

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Bioengineering the bugs

NEWARK, N.J., April 6, 2012 /PRNewswire-Asia-FirstCall/ -- American Oriental Bioengineering, Inc. (NYSE: AOB - News) (the "Company") today announced that the New York Stock Exchange (the "NYSE") has notified the Company that it is not in compliance with NYSE rules due to the Company's failure to timely file its Annual Report on Form 10-K with the Securities and Exchange Commission.

Under NYSE rules, when a Company does not comply with annual report filing requirements, the NYSE allows a company an additional six months to file its annual report in order to regain compliance. In the case of the Company, the annual report would be due on or before October 29, 2012. If the Company fails to file its annual report within that time period, the NYSE may, in its sole discretion, allow the Company's securities to remain listed for up to an additional six months or may, in its sole discretion, commence suspension and delisting procedures.

As previously announced, during the performance of the annual audit of the Company's financial statements for the fiscal year 2011, the Company's auditors, Ernst & Young Hua Ming's (E&Y), noted certain inconsistencies. As a result, the Audit Committee has commenced an independent investigation into the matters identified by E&Y. Although the Company cannot know at this time how long the investigation will take, the Company will endeavor to file the Form 10-K as soon as possible upon the completion of the investigation.

About American Oriental Bioengineering, Inc.

American Oriental Bioengineering, Inc. is a pharmaceutical company dedicated to improving health through the development, manufacture and commercialization of a broad range of prescription and over the counter products.

Safe Harbor Statement

Statements made in this press release are forward-looking and are made pursuant to the safe harbor provisions of the Securities Litigation Reform Act of 1995. Such statements involve risks and uncertainties that may cause actual results to differ materially from those set forth in these statements. The economic, competitive, governmental, technological and other factors identified in the Company's filings with the Securities and Exchange Commission may cause actual results or events to differ materially from those described in the forward looking statements in this press release. The Company undertakes no obligation to publicly update or revise any forward-looking statements, whether because of new information, future events, or otherwise.

Contact:

American Oriental Bioengineering, Inc.

Hong Zhu

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American Oriental Bioengineering Inc. Receives NYSE Notice of Delisting or Failure to Satisfy a Continued Listing Rule ...

Researchers led by Jinfeng Liu from the State Key Lab of Seedling Bioengineering in Yinchuan, China, describe in the Journal of Molecular Diagnostics their method to determine gene copy number. First, the researchers amplified a target and a control gene using PCR, which were quantified before being mixed at different molar ratios. Then, using real-time PCR, the researchers measured the quantification cycle value of the mixture. "A standard curve was constructed to correlate the differences between the Cq values and the logarithmic ratios of the target gene to the internal control gene," the researchers say, adding that "this method was validated by a set of internal control genes and a foreign gene in transgenic alfalfa, demonstrating the utility of this method in the determination of gene copy number for various applications."

Also in the Journal of Molecular Diagnostics, Manchester Cancer Research Centre's John Radford and his colleagues report that archival FFPE samples are useful for a number of microarray experiments, including molecular classification projects. Radford and his team compared fresh-frozen archival diffuse large B-cell lymphoma biopsy samples for use in such experiments. "Enrichment for NF-B genes was appropriately seen in ABC-DLBCL FFPE tissues," the researchers report. "The top discriminatory genes expressed in FFPE separated cases with high statistical significance and contained novel biology with potential therapeutic insights, warranting further investigation."

Originally posted here:
This Week in the Journal of Molecular Diagnostics

Replacing the Osterizer as standard lab equipment

By Kate Rix

Lina Nilsson, Tekla Labs founder. KAP STANN PHOTO

Imagine a research laboratory relying on little more than old phonographs and kitchen blenders. This is what Lina Nilsson, a post-doctoral researcher in the bioengineering lab of professor Daniel Fletcher, saw in Bolivian labs, inspiring her to develop alternatives to expensive laboratory equipment.

After a year in Asia and South America visiting labs that lacked the basics, Nilsson and a team of engineering colleagues brainstormed about how to develop low-cost, accessible tools that could produce research-grade results. They created protocols for making do-it-yourself laboratory equipment, along with detailed how-to blueprints available for free online.

The team evolved into Tekla Labs, a cooperative of ten partners from Berkeley Engineering and UCSF. Their idea won first place for social entrepreneurship in the 2010-11 Big Ideas @ Berkeley contest.

A lot of basic equipment is really expensive, but it doesnt have to be, says Nilsson. She adds that while many charitable organizations make contributions to labs in developing countries, most donated equipment consists of larger and more costly machines.

A sample rotator designed and built by Berkeley student Anthony Fernando for Tekla Labs. LINA NILSSON PHOTO

Each semester, Tekla Labs researchers help individual students build equipment. They also team up with Engineering World Health on a DeCal (student-run) course that tasks undergraduate students with designing inexpensive product prototypes. In one case, a student was sent to Radio Shack for supplies to build a magnetic stirrer; she returned with a light-switch circuit box, which ended up serving quite nicely as housing for the stirrer.

Where the outlet would have plugged in we placed the speed dial, Nilsson says. The core requirement is that the parts must be cheap and easy to find. My lab has four magnetic stirrers and they cost $250 and up. We built one for $30 that runs off a battery.

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Turning kitchen gadgets (and more) into low-cost lab equipment