Up next will be Dr. Gerry Shaw.  Gerry is the founder and head of EnCor Biotechnology, Inc. His company is recognized for creating markers that are engines of Neuroscience and Stem Cell Research.

Dr. Gerry Shaw with Triumph MC

I am pleased to represent his company’s reagents. They are well designed, thoroughly tested and proven to work in my customers’ many application.

They have proven especially effective in working in cell based assays using our eSC derived hNP1 human neurons and e18 primary rat hippocampal neurons.

Applications include the study of TBI, SCI, ALS, AD, MS and PD.

Image:  hN2 cells stained with our chicken polyclonal antibody to Vimentin, in red. Islands of Hn2 cells form after 4 days in culture forming beautiful flower like structures. Vimentin is a well established marker of early differentiating neuronal lineage cells. Taken with a 10X objective lens. Blue staining is the nuclear DNA.

hN2 Cells stained with Vimentin

These assays represent best in class solutions for detecting and measuring cell viability, functionality, growth, proliferation and cytotoxicity of stem and progenitor cells for stem cell and basic research, cellular therapy, in vitro toxicity testing and veterinary applications.

 

2000-Present- Hemogenix-CEO
and Chairman

1996-2000-Palmetto Richland Memorial Hospital

 1995-Second Thesis in Experimental Hematology, University of Ulm

1981-1983-Post Doc University of Chicago

1973-1978-Ph.D. University of Ulm, Biology

Ivan’s journey leading to founding of HemoGenix provided him a unique blend of scientific, entrepreneurial and operational expertise.  These traits are the drivers that enable him to invent, successfully commercialize and continuously improve cell based assay systems. These systems meet a wide range of demanding requirements. These include, for example, meeting the requirement by Standards Organizations and Regulatory Agencies for “appropriate” and “validated” assays that can be used by cord blood banks and stem cell transplantation centers to determine whether a stem cell product has the necessary potency characteristics and can be released for transplantation into a patient…high standards indeed!

The Back Story-Hematology and Hemopoietic Stem Cells

Ivan received his PhD from the University of Ulm, in Germany in 1973 in Human Biology. He then completed a second thesis in 1995 in experimental hematology.  Our story starts here.  As a background we need to understand:  the hemopoietic stem cell compartment consists of cells which are responsible for maintaining the steady-state production of some two million red blood cells and two hundred thousand white blood cells every second of a person’s life!

Beginning in 1973, he worked extensively with “classic” colony-forming cell (CFC) assay.  At the same time, He also gained experience in culturing erythropoietic progenitor cells (BFU-E and CFU-E) under low oxygen tension. His group was the first to demonstrate that macrophages grown in vitro could respond to low oxygen tension by regulating erythropoietin production at a local level. His group also demonstrated the role of HOXB6 in erythropoietic development as well as the role of the Na/H exchanger in hematopoiesis. “Necessity being the mother of invention”, Ivan began developing these assays into miniaturized format.  Assays necessary for fully understanding the potential and associated risks of using of these cells for human therapies.

This opened the door for him to do a post doc with the late Dr. Eugene Goldwasser at the University of Chicago. Dr. Goldwasser was renowned for discovering the first partial amino acid sequence of erythropoietin (EPO). This discovery eventually led to the production of human recombinant EPO by Amgen and the development of first EPO related therapeutic (Epogen). It is used to treat anemia from kidney disease and certain cancers.

We now move to Palmetto Richland Memorial Hospital in South Carolina where Ivan served as Director of Basic Research for Transplantation Medicine. From this research,  we learn that the most primitive stem cells have the greatest potential for proliferation and long-term reconstitution of the hemopoietic system, while the most mature stem cells have only short-term reconstitution potential. These primitive cells then become the most excellent candidates for future therapies. BUT how do we know the population of cells derived from cord blood or bone marrow contain the required population of potent and safe (phenotypically stable) primitive stem cells for effective therapies? We can ask the same questions for other stem cell populations that are candidates for therapies. These include mesenchymal stem cells, neural stem cells and others.

Introducing Quantitative, Accurate and Proven High Throughput (HTS) Stem Cell Assays

Ivan and HemoGenix began answering these questions in 2002 with help from National Cancer Insitute (NCI) SBIR grants. This led to the successful launch of the HALO® family of kits. These kits are based on Bioluminomics™ which is the science of using the cell’s energy source in the form of ATP (adenosine triphosphate) to provide us with a wealth of information. The production of ATP is an indicator of the cell’s cellular and mitochondrial integrity, which, in turn, is an indicator of its viability and cellular functionality. ATP also changes in proportion to cell number, proliferation status and potential, its cytotoxicity and even its apoptotic status.

HemoGenix continues to develop and evolve kits key to developing effective and safe stem cell related drugs and cell based therapies.

Practical Applications

Here are examples of the kits in action.

• HemoGenix and Vitro Diagnostic-Via this partnership, LUMENESC kits for mesenchymal stem cells include high performance growth media for research, quality control or potency or cytotoxicity to the mesenchymal stem cell system
• LumiSTEM™ for testing  hNP1™ Human Neural Progenitors Expansion Kit-enables  fast, accurate and multiplex detection system for hastening advances in drug safety and discovery as well as environmental toxicology. . LumiSTEM™[now LumiCYTE-HT]  kits are used for in vitro detection of liver toxicity, with an overall reduction in drug development cost for drug candidates
• High Throughput (HTS) Screening of Multiple Compounds using HALO®-(to learn more see: TOXICOLOGICAL SCIENCES 87(2), 427–441 (2005) doi:10.1093/toxsci/kfi25). Eleven reference compounds from the Registry of Cytotoxicity (RC) and eight other compounds, including anticancer drugs, were studied over an 8- to 9-log dose range for their effects on seven cell populations from both human and mouse bone marrow simultaneously. The cell populations studied included a primitive (HPP-SP) and mature (CFC-GEMM) stem cell, three hematopoietic (BFU-E, GM-CFC, Mk-CFC) and two lymphopoietic (T-CFC, B-CFC) populations. The results reveal a five-point prediction paradigm for lympho-hematotoxicity.

HSC Toxicity Data

Futures

The dawn is breaking for stem cells therapies. These cells are the reparative engines for damaged cells in our bodies. These therapies have the potential to alleviate the world’s most insidious, chronic and costly diseases. Tools that enable us to understand the true properties and potency of these cells lower the cost of discovering drugs and cell based therapies.

I look for more tools to spring from the vision of Dr. Ivan Rich that will play an ever increasing and important role in the world of basic stem cell research, stem cell based therapies and regenerative medicine. I plan to keep you updated on the evolution and capabilities of these inventions.

Mahesh C. Dodla, Amber Young, Alison Venable, Kowser Hasneen1, Raj R. Rao, David W. Machacek, Steven L. Stice. Differing Lectin Binding Profiles among Human Embryonic Stem Cells and Derivatives Aid in the Isolation of Neural Progenitor Cells. PLoS ONE 6(8): e23266. doi:10.1371/journal.pone.0023266.

Abstract: Identification of cell lineage specific glycans can help in understanding their role in maintenance, proliferation and differentiation. Furthermore, these glycans can serve as markers for isolation of homogenous populations of cells. Using a panel of eight biotinylated lectins, the glycan expression of hESCs, hESCs-derived human neural progenitors (hNP) cells, and hESCs-derived mesenchymal progenitor (hMP) cells was investigated. Our goal was to identify glycans that are unique for hNP cells and use the corresponding lectins for cell isolation. Flow cytometry and immunocytochemistry were used to determine expression and localization of glycans, respectively, in each cell type. These results show that the glycan expression changes upon differentiation of hESCs and is different for neural and mesenchymal lineage. For example, binding of PHA-L lectin is low in hESCs (14±4.4%) but significantly higher in differentiated hNP cells (99±0.4%) and hMP cells (90±3%). Three lectins: VVA, DBA and LTL have low binding in hESCs and hMP cells, but significantly higher binding in hNP cells. Finally, VVA lectin binding was used to isolate hNP cells from a mixed population of hESCs, hNP cells and hMP cells. This is the first report that compares glycan expression across these human stem cell lineages and identifies significant differences. Also, this is the first study that uses VVA lectin for isolation for human neural progenitor cells.

Figure 1. Defining the stem cell phenotype using immunocytochemistry and flow cytometry.Phase contrast image of hESCs (A), hNPs (B), and hMPs (C). hESCs express pluripotency markers: Oct 4 (D,GG, JJ), SSEA-4 (G), and Sox 2 (J,GG); lack expression of Nestin (M, JJ), CD 166 (P,DD), CD73 (DD), and CD105 (AA). hNPs have low expression of pluripotency markers: Oct 4 (E,KK), SSEA-4 (H); and mesenchymal markers CD 166 (Q,EE), CD73 (EE), and CD105 (BB). hNPs express neural markers: Sox 2 (J,HH) and Nestin (N,HH,KK). hMPs lack expression of pluripotency markers: Oct 4 (F,LL), SSEA-4 (I), and Sox 2 (L,II); however, hMPs express Nestin (O,II,LL), CD 166 (R,FF), CD73 (FF), CD90 (CC) and CD105 (CC). All the cells have been stained with the nuclear marker DAPI (blue) in panels D- P. Scale bar: 10 µm. In the dot plots, red dots indicate isotype control or secondary antibody only; black dots indicate the antigen staining. doi:10.1371/journal.pone.0023266.g001

 By comparing hESCs, hNP cells and hMP cells, we have identified glycan structures that are unique to hNP cells: GalNac end groups (VVA), α-linked N-acetylgalactosamine (DBA), and fucose moieties α-linked to GlcNAc (LTL). Future studies help in identifying the roles of these glycans in cell maintenance, proliferation and differentiation fate.

I will keep you posted on these future Studies.

In Search of Remyelination Therapies

Multiple Sclerosis (MS) is an inflammatory disease with no known cure. It affects over 400,000 people in the US and over 2.5 million people worldwide and is the leading cause of non-traumatic neurological disability in North America.

It is a chronic and brutal disease that attacks the brain and spinal cord. MS symptoms are due to the damage or loss of myelin sheath that surrounds, isolates and protects axons of brain and spinal cord. The results are often debilitating and afflict most sufferers in the prime of their lives. The annual costs to slow the disease and treat related
symptoms are in the billions of dollars and rising. There are currently no therapies to reverse damage of MS. At this point, there are only immune suppressive therapies that slow attack on the myelin sheath.

It is with hope and optimism that I present Dr. Satish Medicetty and his company, Renovo Neural Inc. (RNI) in this edition of the “News Behind the Neuroscience News”.

I became aware of Satish and his company in my search for Stem Cells that would broaden Neuromics ability to serve early phase Neuroscience Drug Discovery.

Satish Medicetty

Apr 2010 – Present: President and Board Director Renovo Neural Inc.

June 2008 – Mar 2010: Director of Stem Cell Research and Lab Operations
NeoStem Inc

July 2005 – June 2008: Senior Scientist Athersys

2006 – 2008: MBA, Case Western University

2002 – 2005: PhD, Kansas State University

After my first conversation with him, I was impressed with the capabilities RNI offered.

RNI

The company, founded in 2008 with a$3 million grant from the State of Ohio’s Third Frontier Commission, is leveraging cutting edge research from Dr. Bruce Trapp’s lab at the Cleveland Clinic.

At the core, RNI offers pioneering and propriety assays that give Drug Discovery Companies the ability to screen small molecules and compounds that could be lead therapy candidates for MS and other myelin-related diseases. These screens use a type of stem cell called adult oligodendrocyte precursor cells (OPCs).

The Power of OPCs

So what makes these OPCs an engine for finding cures for MS?  Inflammation associated with MS attacks destroys cells called oligodendrocytes that produce myelin. The only way to reverse this autoimmune related process is for the brain to produce healthy cells that can catalyze re-myelination. Enter OPCs.

OPCs are the raw material for processes the central nervous system uses to manufacture oligodendrocytes.  The brain’s inability to produce enough healthy cells to keep up with the destruction is a root cause of the disease. Understanding how to kick start and keep the oligodendrocyte factory running is a key to reversing this relentless destruction.

Delivering Value

RNI has the capabilities to the decrease time required and increase the odds for discovering potential MS therapies.  They have the raw material (OPCs) and the know how to encourage their transformation into myelinating cells. This expertise can be utilized can be used then to rapidly test new compounds both in vitro and in vivo.

In Vitro Assays Example

The features of their in vitro assays include:

• Stringent protocols to generate relatively homogeneous (>85% pure) and consistent population of OPCs as a reliable starting material for HCS assays
• Relatively high throughput primary screen to identify potential candidates that promote OPC proliferation and/or differentiation
• Secondary screen to confirm and qualify compounds for further pharmacological testing
• Positive and negative controls that demonstrate the utility of HCS assays to identify lead candidates that promote OPC proliferation and differentiation.

The features of their in vivo cuprizone assays include:

• Stringent protocols to generate highly reproducible demyelination/remyelination cuprizone model
• Cuprizone model recapitulates the in vivo process of demyelination and remyelination in the brain.
• Cuprizone model provides consistent and accurate results for key regions of the brain that are affected in MS patients including both white and gray matter regions – corpus callosum, hippocampus and cortex.
• Proof of concept studies demonstrate the utility of our in vivo remyelination assays to evaluate preclinical efficacy of potential remyelination therapies

The end goal is to discover therapies that repair neurons damaged by MS via remyelination and to get them in the hands of people that need them. I will keep you posted on their progress.

When differentiated, these  neural progenitors express subunits of glutamatergic,  GABAergic, nicotinic, purinergic and transient receptor potential receptors. In addition, sodium  and calcium channel subunits were also expressed. Functionally, virtually all the NP cells exhibited delayed rectifier potassium channel currents and some differentiated cells exhibited  tetrodotoxin sensitive, voltage-dependent sodium channel current under whole-cell voltage clamp and action potentials could be elicited by current injection under whole-cell current clamp.  These results indicate that removing basic fibroblast growth factor from the neural progenitor cell cultures leads to a post-mitotic state, and also results in the capability to produce excitable cells that can generate action potentials. This is the first data demonstrating capabilitiesof these cells for ionotrophic receptor assays and ultimately for electrically active human neural cell assays for drug discovery.

Images: Glutamate receptor expression in hNP cells and differentiated hNP cells The expression of ionotropic glutamate receptors might also be an indicator of neuronal maturation. These receptors are composed of three distinct families: NMDA, kainate and AMPA receptors. The hNP cells and differentiated hNP cells cultured in the absence of bFGF for 2 weeks were analyzed for mRNA expression of subunits of each glutamate receptor subtype relative to hESCs. Significant increases (p<0.05) in Grin2b were seen in hNP cells (20 fold) and differentiated hNP cells (25 fold) relative to hESCs (Figure 3A). Additionally, Grin1 and Grin2d were significantly increased (p<0.05) only in differentiated hNP cells relative to hESCs, but not in undifferentiated hNP cells (Figure 3A). Of the kainate receptors, Grik4 and Grik5 were significantly (p<0.05) increased only in undifferentiated hNP cells relative to hESCs (Figure 3B); whereas, Grik2 was significantly (p<0.05) increased only in hNP cells where bFGF had been removed (Figure 3B). AMPA receptor subunits were also examined. Gria1 and Gria4 were up regulated in hNP cells relative to hESCs (Figure 3C). Two week differentiated hNP cells showed significant (p<0.05) up regulation of Gria2 and Gira4 relative to hESCs (Figure 3C). To determine if functional glutamate channels exist in differentiated hNP cells, calcium influx in response to AMPA, kainic acid or NMDA application was measured on hNP cells, 14 days after the removal of bFGF. Figure 3G indicates that NMDA could not depolarize differentiated or undifferentiated hNP cells enough to cause significant calcium influx above background. In contrast, AMPA and kainic acid can cause calcium influx which can be potentiated by AMPA receptor specific modulator, cyclothiazide (50 μM, Figure 3G).Calcium influx was detected in the presence of cyclothiazide in calcium activity as measured (Figure 3H).

I would like to highlight a poster based on research Steve and his Team conducted with Platypus Technologies.

Obesity Energy, Thermogenesis and Appetite

Dr. Richard Rogers

In my routine follow up with researchers using our reagents, I started to get an appreciation on how these complex energy pathways are being unraveled and better understood. That appreciation forms the roots of this “News Behind the Neuroscience News” story. It is a story that has the hormones Leptin and TRH playing a starring role supported by hindbrain neuro/glial-circuitry and brown adipose tissue (BAT).

The Rogers Lab

I became aware of the Richard Rogers Lab in my follow up with Montina Van Meter checking on our  LepRb/OBRb antibody. She shared that it was giving them results better than most others they has used. She then gave me an overview of her research involved with  the control of feeding behavior and energy utilization including thermogenesis (“heat generation”) catalyzed in BAT.  Cool…this was a lab we wanted to make sure we served and served well.

Tina not only kept me informed on how our reagents were working, but also generously alerted to me publications referencing use of our reagents:
·        Maria J. Barnes, Richard C. Rogers, Montina J. Van Meter and Gerlinda E. Hermann. Co-localization of TRHR1 and LepRb
receptors on neurons in the hindbrain of the rat. doi:10.1016/j.brainres.2010.07.094…Included are excellent images of stained LepRb (OB-Rb)-(Dilution 1:500) and  GAD1-Dilution (2ug/ml) expressing neurons localized in loose clusters of cells in the DMN, NST, and the VLM…
·        Hung Hsuchou, Yi He, Abba J. Kastin, Hong Tu, Emily N. Markadakis, Richard C. Rogers, Paul B. Fossier, and Weihong Pan. Obesity induces functional astrocytic leptin receptors in hypothalamus. Brain, Mar 2009; doi:10.1093/brain/awp029…unique sequence of ObRb at its cytoplasmic tail (CH14104, Neuromics, Edina, MN, USA). This antibody was raised
against rat ObRb…

I found this research to be unique and intriguing. This led me to an interview with Dr. Rogers. Here is his backstory.

Beginnings

Dr. Rogers credits serendipity as a driving force in his interest in Neuroscience. It started with a bike ride and chance introduction with a ham radio operator when he was a youngster. This catalyzed his interest in electronics and circuitry.

This interest morphed to a passion for Neuroscience (circuits and signaling). He entered the first college program devoted to Neuroscience studies at UCLA.  He received his Ph. D. in 1979. His post-doc focused on digestive regulation. Here, he  investigated the neural circuitry involved in the normal control of gastric function.

Evolutions

In collaboration with his wife Dr. Gerlinda Hermann, his work evolved to solving the mystery of why we don’t eat (abnormal gastric function). What causes gastro-intestinal shutdown?  The breakthrough was their ability to show cross-talk between the immune system and nervous system. This research is a foundation for the discovery of therapies for sufferers of appetite shut down cause by cancer therapies and certain immune related pathologies.

The main culprit is TNF-α. The blood level of this peptide is elevated as a consequence of immune activation caused by infection, cancer, radiation exposure and chronic autoimmune disease. The breakthrough was showing that  TNF-α receptors are on neurons in the brainstem that control gastric functions, including emesis.  Neurons in the nucleus of the solitary tract (NST) respond to TNF-α greatly increasing the sensitivity of gastric vagal control circuitry.  This causes emptying of the gut to dramatically slow,l leading to nausea, vomiting and cessation of appetite.

Currently, they are delving into the complexities of  TNF-α signaling processes. This includes the role of astrocytes and glia.

See: Gerlinda E Hermann and Richard C Rogers.  TNF activates astrocytes and catecholaminergic neurons in the solitary nucleus: implications for autonomic control. doi: 10.1016/j.brainres.2009.03.059.

 Energy,Obesity and Thermogenesis-Active Astrocytes

Recently, the lab took another road less traveled. Dr. Gerlinda Hermann discovered interesting aspects of leptin and thyrotropin releasing hormone (TRH) signaling.  This research looks at signaling in thermogenesis and feeding behavior. A most interesting aspect includes conclusions concerning the role of astrocytes.  Their colleague Dr. Weihong Pan  showed that adult obese mice, (2 months after being placed on a high-fat diet) showed a striking increase of leptin receptor (+) astrocytes, most prominent in the dorsomedial hypothalamus and arcuate nucleus. Agouti viable yellow mice with their adult-onset obesity showed similar changes, but the increase of leptin receptor (+) astrocytes was barely seen in ob/ob or db/db mice with their early-onset obesity and defective leptin systems. The results indicate that metabolic changes in obese mice can rapidly alter leptin receptor expression and astrocytic activity, and that leptin receptor is responsible for leptin-induced calcium signalling in astrocytes. This novel and clinically relevant finding opens new avenues in astrocyte biology (doi: 10.1093/brain/awp029).

Non-shivering thermogenesis usually occurs in BAT. It uncouples the ATP energy producing process by generating heat rather than driving the conversion of ADP to ATP. This creates an ingenious way to untangle complex processes related to Leptin signaling. What happens when there is sufficient energy for the thermogenic process? Conversely, what happens when there is insufficient energy?

 Leptin and TRH act synergistically in the hindbrain to drive thermogenesis. However, in a starving condition there is a subsequent drop in Leptin and thermogenesis. Behind these simple facts are complex processes that occur in the hindbrain. The team is providing important insights including location of events and relevant signaling molecules. (doi:10.1016/j.brainres.2010.07.094).

The Future-Caged Compounds and Live Cell Signaling

Caged compounds are bioactive molecules attached to photolabile groups, that release the active component on contact with photons of the right energy level – the process of photolysis. Photolysis is now widely applied in biology to induce neurotransmitter and otherm ligand-receptor interactions in conditions that are otherwise subject to poor diffusional access and receptor desensitization, as well as for labile ligands.

This novel technology affords Dr. Rogers and his team the capability do live cell imaging of calcium signaling. From these they will help us gain a deeper understanding of what is happing and where. Specifically, we will more exactly learn the role that astrocytes and glia play in controlling the role of   Leptin and related signaling molecules in controlling energy, metabolism and feeding behavior. This could lead to important target for future therapies.

Getting Started with Alphagenix                     Steve is an advisor, collaborator and friend. He has the innate ability to bring his his scientific expertise and entrepreneural insticts together in a way that anticipates emerging needs of the research community we both serve. He is an expert in immunology, neuroscience, virology and regenerative medicine (stem cells).  Most notably, he is the sole inventor on the patent that formed the basis for using the Nodaviruses as vaccine and gene therapy vectors U.S. Patent 6,171,591. These vaccines are in various stages of preclinical development as are protoype therapeutic vaccines for neurodegenerative diseases.  Our two companies first worked together to identify and manufacture several important stem cell markers. We tested potency on our STEMEZ hNP1TM Human Neural Progenitors. They proved to be effective. This confirmed Steve’s ability to identify, design and make these markers. The demand for them continues to grow. These successes were a prelude of good things to come. Current Focus Steve is currently  developing novel products and technologies for basic and clinical research with a particular emphasis on stem cell markers, biomaterials and regenerative medicine. The biomaterials product focus involves the design and application of 3-dimensional biomaterials comprised of extracellular matrix components and peptide nanofibers that have cell culture and tissue engineering applications. In addition, the company conducts regenerative medicine research that involves basic science and translational preclinical research using stem cell regulatory network discoveries and novel preclinical studies utilizing animal models with a focus on neurological disease and diabetes. He is a contributor to: Stem Cell Therapy for Neurological Diseases Stem cell therapy for the treatment of acute and chronic neurological diseases

2001-Present-President-Alphagenix 2006-2007-CSO-Neuromics 2000-2001-President-AmProx, Inc 1996-2004-President and CSO-Pentamer Pharmaceuticals 1996-1997-Sr. Research Fellow-Medical Biology Institute. 1995-1997-Research Associate-Scripps Research Institute 1995 PhD Purdue University Musashi-1 Antibody Image: Musashi (green) staining of neural rosettes(human). Nuclei are counterstained blue (DAPI). Image courtesy of Dr. Steve Stice and Dr. Patricia Wilson, University of Georgia.

Harting, Matthew T., Cox, Charles S. and Hall, Stephen G.  Adult Stem Cell Therapy for Neurological Disease: Preclinical evidence for cellular therapy as a treatment for neurological disease. In Vemore and Vinoglo (eds): Regulatory Networks in Stem Cells. Humana Press, pp 561-573, (2009). More information.

Specific Projects

1. Steve has 3 major projects underway:
   In collaboration with Dr.  Charles Cox , Distinguished Professor, UT Medical School @ Houston, Steve has been using stem cells to treat  Traumtaic Brain Injury (TBI) in Rat. Neural stem cells transplanted into the site of injury. In this model, treated rats showed injury significantly improved motor skills with a moderate recovery in cognitive ability. This research forms the base for eventually repairing damage in humans suffering TBI. Methods and reagents developed also could be useful for basic research and drug discovery.
2. Steve is working with Burnham Institute to develop methods for using  Human Mesenchymal Stem Cells to regenerate beta cells. This research holds promise for type 1 diabetics.
3. Steve developing biomaterials including extracellular matrix proteins in novel cell culture systems and synthetic peptide nanofibers for these purposes.  It is investigating stem cells and genetically engineered cells and their interaction with these biomaterials, which has the ability to increase the efficacy of cell therapy. This is highlighted by a human laminin sytem that shows promise in restoring function in Muscular Dystophry.

The last project is promising enough that it could lead to funding for phase 1 testing.

I will continue to keep you posted on progress. I am excited about the new regeants and method that evolve from Steve’s Research. As these prove to work in unique and novel ways, the will become available to Neuromics.

STEMEZ hN2 Primary Human Neurons

I have profiled Steve Stice’s research here. The focus has been the excellent research results he and his team at ArunA Biomedical have generated with STEMEZ(TM) hN2 Human Neurons and hNP1 Human Neural Progenitors.

The story continues. He will be presenting the latest at the 9th Annual World Pharmaceutical Congress in Philadelphia, June 14. Topics include: using these neural cell lines to study neurotoxicity in cell-based assays and disease modeling.  Recent work conducted in outside laboratories demonstrates that these lines are more sensitive to environmental toxicants than traditional cellular models.

Sample high throughput assay applications:

• Cell morphology and neurite outgrowth
• Cell signaling and transcription factor expression
• Receptor and ion channel function
• Cytotoxicity
• Apoptosis, genotoxicity and DNA damage

These capabilities has been confirmed by our customers. I look for the use of the STEMEZ cell lines to continue to grow as researchers discover their value in Drug Discovery and Basic Neuroscience capabilities.