New research shows a new method for overcoming drug-resistance in cancer cells. Cells with acquired (de novo) resistance to kinase inhibitors characteristically show increased numbers of and/or longer cilia. Blocking cilia growth, the study illustrates, resensitizes the cells to anticancer drugs.

Scientists in the UK have shown that targeting the cilia of cancer cells could be a universal way to make resistant cancer cells sensitive to anticancer drugs. The recent study looks at the characteristics of resistant cancer cells, noting that cells with either acquired or de novo resistance to traditional kinase inhibitors have either increased quantities of and/or notably longer cilia. By blocking cilia growth or signaling, the cancer cells become receptive to anticancer drugs. On the flip side, increasing the length of cilia made previously drug-receptive cells become resistant to kinase inhibitors. Researchers hope that targeting cilia could be a way to universally strip cancer cells of their innate defenses, making treatments more effective.

Cilia and Drug Resistance

Many anticancer drugs inhibit proteins like epidermal growth factor receptor, platelet-derived growth factor receptor, and KRAS. While treatment with kinase inhibitors (like erlotinib) can be effective for some tumor types, it seems as though drug resistance eventually emerges.

With the link association between oncogenic proteins and cilia, the researchers wanted to discover whether changes in ciliogenesis could play a permissive role of sorts in the development of drug resistance, and wanted to test whether the characteristics of cilia (like number and length) would affect resistance to kinase inhibitors in different cell lines (including lung cancer and sarcoma cells).

Relationship between de novo drug resistance and ciliogenisis confirmed

Initial studies found that drug-resistant cancer cells showed greater numbers of and/or longer length of cilia. Downregulating the protein Kif7 (known to be involved in controlling cilia length) led to developing resistance to dasatinib, an anticancer drug, in cells that were previously sensitive to the drug. Blocking ciliogenesis by knocking down a structural protein or chemically inhibiting the Hedgehog pathway resensitized cancer cells to kinase inhibitor therapy.

The team was able to confirm an association between de novo drug resistance and ciliogenesis, and demonstrated that using a chemical FGFR inhibitor lead to increased cancer cell death when the cells were then exposed to a kinase inhibitor.

Further research will explore cilia changes in greater detail, with the goal of gaining more understanding of how they impact resistance to cancer drug therapies, and how they could be targeted to increase the effectiveness of treatment.

Further Reading & References:

Targeting Cilia Could Offer Universal Approach to Combat Anticancer Drug Resistance. GEN: Genetic Engineering & Biotechnology News. 06 June 2018.

Primary Cilia Mediate Diverse Kinase Inhibitor Resistance Mechanisms in Cancer. Cell Reports: Volume 23, Issue 10, p3042-3055, 5 June 2018.


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Scientists have developed a new laboratory technique that allows them to create engineered human pancreatic islets that are vascularized and secrete hormones like insulin. When transplanted into mice, these pancreatic islets develop a circulatory system and successfully treat sudden-onset type 1 diabetes.

Researchers from Japan and the US have created a new method for creating tissue-engineered human pancreatic islets, according to a new study. Not only are they able to grow this tissue in a laboratory setting, but when transplanted into mice, these engineered pancreatic islets develop a mature vascular/circulatory system and are able to secrete insulin. This transplant proved to be a successful treatment for mice with type 1 diabetes, effectively controlling blood sugar levels.

Self-Condensation Cell Culture

The scientists used a new process for bioengineering, which they are calling "self-condensation cell culture." This, researchers hope, brings us a step closer to one day finding a way to grow human organ tissues using an individual's own cells.

To test their processing system, the researchers used a combination of cells. They started with donated human organ cells, mouse organ cells, and induced pluripotent stem cells (iPS). They then added two forms of embryonic-stage progenitor cells, the purpose of which are to support the formation of the body and specific organs. In this case, the researchers used mesenchymal stem cells (MSNs) and human umbilical vascular endothelial cells (HUVECs).

Forming Pancreatic Islets

Together, the various biological "ingredients" condensed and formed pancreatic islets. When transplanted into humanized mouse models of type 1 diabetes, these islets appeared to resolve and control the disease.

It is already possible to transplant pancreatic islets into diabetic human patients for treatment, but until this point, the success rate has been relatively low because it has been difficult to develop pancreatic islets that have sufficient blood supply to nourish the transplanted tissue.

Functional, Effective Transplantation

Pancreatic islets engineered in this new way not only develop a mature vascular network after transplantation into animal models, but the transplanted tissue also functions effectively as part of the endocrine system. The transplanted tissue secretes hormones like insulin and stabilizes the animals' glycemic control. This marks the first time the team has been able to engineer tissue fragments from organ cells that are able to vascularize in the body.

This method is hoped to be a promising treatment for type 1 diabetes in humans, a disease that is currently seeing nearly 80k new diagnoses annually. There is currently no cure for type 1 diabetes, and the condition can be life-threatening. Finding a curative or permanent therapy would benefit millions of people worldwide.

Further Reading & References:

Tissue-engineered human pancreatic cells successfully treat diabetic mice. Science Daily. 08 May 2018.

Transplanted Human Islets Grow Blood Vessels and Secrete Insulin to Treat Diabetic Mice. GEN: Genetic Engineering & Biotechnology News. 08 May 2018.

Self-Condensation Culture Enables Vascularization of Tissue Fragments for Efficient Therapeutic Transplantation. Cell Reports. doi.org/10.1016/j.celrep.2018.03.123


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Much research has emerged recently when it comes to understanding and treating breast cancer. From better detection methods to better treatment options, our understanding of the cause, detection, and treatment of breast cancer is rapidly growing.

Approximately one in eight women will be diagnosed with breast cancer during her life, and one in thirty women will receive a fatal breast cancer diagnosis. Understanding the ways in which breast cancer metastasizes, how to better detect breast cancer in more treatable stages, and how to effectively treat the cancer while minimizing side effects is an area of research that is seeing significant progress.

A Protein found in Breast Cancer could be Essential to Metastasis

Investigators at the Montreal Clinical Research Institute and University of Montreal have uncovered an essential protein that, upon deactivation, could prevent aggressive HER2-positive breast cancer from metastasizing. Cancerous tumors develop when cells multiply at an abnormally high rate, clustering in otherwise healthy tissue.

Some of these cancerous cells are especially sneaky - leaving the tumor to move elsewhere in the body, spreading the disease to other healthy tissues and organs. Metastatic cells move throughout the body more easily by detaching from the tumor, entering the bloodstream, and making their way other organs. They are the most difficult cells to destroy, as they are not localized and tend to be more resistant to current treatments.

The researchers demonstrated that the protein AXL influences the occurrence of metastasis in HER2-positive breast cancer. When administering an AXL-inhibiting drug therapy to mice with HER2-positive tumors, metastases were less likely to develop. Further study is needed, but if the studies are successful, this could potentially become a treatment option in breast cancer patients, working as a complement to therapies targeting HER2-positive tumors.

Targeting the Mitochondria of Breast Cancer Cells

A small-molecule drug, called ONC201, is traditionally used to induce transcription of TNF-related apoptosis-inducing ligand (TRAIL) and destroy cancer cells by activating TRAIL death receptors. In breast cancer, however, ONC201 seems to have a different effect.

Independent of TRAIL transcription, investigators report that ONC201 induces cell death via cell stress mechanisms. In human breast cancer lines, researchers found that ONC201 inhibits mitochondrial respiration and induces mitochondrial structural damage. It also reduces the number of mitochondrial DNA copies.

The study also suggests that cancer cells dependent on glycolysis will be resistant to ONC201.

Treating otherwise unresponsive breast cancer with immunotherapy

Modified from adoptive cell transfer (ACT), experimental research uses a high-throughput method to identify mutations in a cancer that are recognized by the immune system. Scientists hope this will lead to the development of a "blueprint" of sorts that can be used for treating many types of cancer.

ACT has been traditionally effective in treating melanoma, which tends to have high levels of acquired mutations. It has been less effective in common epithelial cancers with lower levels of mutations, like breast cancer. Researchers are developing a form of ACT that uses tumor-infiltrating lymphocytes (TILs) that target mutations to try and shrink tumors in patients with these common epithelial cancers. This process involves growing the selected TILs to large numbers in a laboratory setting, and then infusing them back into the patient (who - in the meantime - has been treated to deplete remaining lymphocytes). This creates a stronger immune response against the tumor.

All cancers have mutations, and the scientific research team hopes that their research will create a "big picture" treatment that is not cancer-type specific. The mutations that cause the cancer could, in fact, become the best targets to treat the cancer.

Using Genetic Testing to Determine Breast Cancer Treatment

A commercially-available 21-gene test could help two of every three women with the most common type of early breast cancer avoid chemotherapy altogether. The new study shows that for women with tumors that are hormone-receptor-positive, HER2-negative, axillary node-negative, and that generate intermediate scores on the 21-gene Oncotype DX recurrence-score assay, hormone therapy is just as effective at preventing disease recurrence as hormone therapy that is coupled with chemotherapy.

While the ongoing trend of prescribing hormone therapy alongside chemotherapy has contributed to the declining rates of mortality for breast cancer, the majority of these patients may be undergoing chemotherapy unnecessarily.

Using the 21-gene assay could identify as many as 85% of women with early breast cancer who could safely skip the immediate chemotherapy, especially women over the age of 50 and with a recurrence score of 25 or lower, and women under the age of 50 with a recurrence score of 15 or lower.

This research is expected to have a big impact on doctors and patients, with the findings greatly expanding the number of patients who are able to safely forego chemotherapy without compromising their outcomes.

Further Reading & References:

Protein in Breast Cancer Found to Be Essential for Metastasis. GEN: Genetic Engineering & Biotechnology News. 07 May 2018.

For Breast Cancer, Targeting Mitochondria Could Be Key. GEN: Genetic Engineering & Biotechnology News. 09 May 2018.

Breast Cancer Genetic Test May Help Women Forgo Chemotherapy. GEN: Genetic Engineering & Biotechnology News. 04 June 2018.

New approach to immunotherapy leads to complete response in breast cancer patient unresponsive to other treatments. Science Daily. 04 June 2018.


Innovative Research was established in 1998 after the realization that dependable, high-quality, and affordable research materials were hard to come by. Starting with core products like human plasma and serum, Innovative Research has grown to be a trusted supplier of all lab reagents, including human biologicals and ELISA kits. Today, we manufacture and supply over 3,000 high-quality human and animal biologicals including plasma, serum, tissues, and proteins.

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In a medical advance that could lead to the development of more effective antimalarial drugs and vaccines, new research uncovers the full genome of Plasmodium falciparum, the parasite that makes malaria so deadly.

Each year, malaria infects some 220 million people across the globe, resulting in the death of about 500,000 people. 9 in 10 people who are killed by malaria are infected with the Plasmodium falciparum parasite. For the first time, a new research technique gives insight into what is essential in the parasite's genetic makeup, which could lead to the development of better treatments and vaccines.

Mutating the Genome

The research team created a technique that mutated most of P. falciparum's thousands of genes, leading to a better understanding of how each gene functions.

They were able to successfully target adenine and thymine (two of the four chemical "building blocks" of DNA), a significant accomplishment since P. falciparum has a high percentage of adenine and thymine, which has proven to be a limiting factor in previous efforts to manipulate its genome.

From Hundreds to Thousands

Until this point, the P. falciparum parasite has remained resistant to many of the modern genetics-modifying methods, and as a result, it has only been possible to identify the function of a few hundred of the more than 6,000 genes. Using the new genetics tool - dubbed "piggyBac mutagenesis" - the researchers were able to characterize the function of nearly all of the parasite's genes.

Advanced Analysis

With some advanced computational analysis, researchers were able to narrow in on the approximately 2,600 genes that are considered the most essential to growth and resistance to existing antimalarial drugs.

Knowing the parasite's vital genes and pathways, the team hopes, will help to guide and speed up the development of more effective drugs and vaccines.

Further Reading & References:

Min Zhang, Chengqi Wang, Thomas D. Otto, Jenna Oberstaller, Xiangyun Liao, Swamy R. Adapa, Kenneth Udenze, Iraad F. Bronner, Deborah Casandra, Matthew Mayho, Jacqueline Brown, Suzanne Li, Justin Swanson, Julian C. Rayner, Rays H. Y. Jiang, John H. Adams. Uncovering the essential genes of the human malaria parasitePlasmodium falciparumby saturation mutagenesis. Science, 2018; 360 (6388): eaap7847 DOI: 10.1126/science.aap7847

University of South Florida (USF Health). "Unlocking the genome of the world's deadliest parasite." ScienceDaily. ScienceDaily, 3 May 2018. www.sciencedaily.com/releases/2018/05/180503142722.htm.


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A new study shows that researchers were able to successfully treat obesity in patients whose obesity is caused by a genetic defect. The researcher also provides new information about the mechanics of how the brain receives signals of satiety.

A mutation in the leptin receptor (LEPR) gene can cause extreme hunger, beginning in the first months of life. Affected individuals develop extreme obesity during their childhood years, to the extent that increased exercise and reduced caloric intake are insufficient to stabilize body weight. Not only that, but other obesity treatments - like surgical options - fail to benefit these individuals, which serves to highlight the importance of finding a drug-based treatment approach.

Peptides and MC4R

Within the past couple of years, researchers have demonstrated that treatment using a peptide to activate the melanocortin 4 receptor (MC4R) could play a key role in how the body metabolizes energy and regulates body weight.

Leptin - also commonly referred to as the satiety or starvation hormone - normally binds to LEPR, which sets off a series of actions that lead up to the production of melanocyte-stimulating hormone (MSH). The MSH binds to its receptor (MC4R), sending the body signals indicating satiety/fullness.

For individuals for whom LEPR is defective, this chain of actions is interrupted, which means their body does not recognize when hunger is satisfied.

Activating Signals of Satiety

Researchers used a peptide that binds to MC4R in the brain, finding that this activation triggered the normal signals of fullness. Not only that, but the team was able to record significant weight loss in patients who had the genetic LEPR mutation.

The scientists were able to demonstrate that treatment in this way leads to the activation of a critical signaling pathway, the significance of which has previously been underestimated. Additionally, there were no observed severe side effects (in contract to other preparations with a similar mode of action).

Researchers hope that further research will determine if other patients with dysfunctions affecting the same signaling pathway could also be suitable candidates for this treatment.

Further Reading & References:

Karine Clment, Heike Biebermann, I. Sadaf Farooqi, Lex Van der Ploeg, Barbara Wolters, Christine Poitou, Lia Puder, Fred Fiedorek, Keith Gottesdiener, Gunnar Kleinau, Nicolas Heyder, Patrick Scheerer, Ulrike Blume-Peytavi, Irina Jahnke, Shubh Sharma, Jacek Mokrosinski, Susanna Wiegand, Anne Mller, Katja Wei, Knut Mai, Joachim Spranger, Annette Grters, Oliver Blankenstein, Heiko Krude, Peter Khnen. MC4R agonism promotes durable weight loss in patients with leptin receptor deficiency. Nature Medicine, 2018; DOI: 10.1038/s41591-018-0015-9

Charit - Universittsmedizin Berlin. "Switching off insatiable hunger: A new drug to help young patients with genetic obesity." ScienceDaily. ScienceDaily, 8 May 2018. www.sciencedaily.com/releases/2018/05/180508131029.htm.


Innovative Research was established in 1998 after the realization that dependable, high-quality, and affordable research materials were hard to come by. Starting with core products like human plasma and serum, Innovative Research has grown to be a trusted supplier of all lab reagents, including human biologicals and ELISA kits. Today, we manufacture and supply over 3,000 high-quality human and animal biologicals including plasma, serum, tissues, and proteins.

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Multiple sclerosis is a serious neurological condition for which there is no known cure. While the causes of the disease remain relatively unknown, we do know that, in individuals with MS, the immune system attacks the protective sheaths around nerve fibers. New research has uncovered how the formation of these myelin sheaths is regulated by protein molecules.

Think of the human brain as a computer in which the individual processors are efficiently connected using high speed cables. The approximately 100 billion nerve cells are the processors, and the nerve fibers (axons covered by myelin sheaths) are the fiber-optic cables. How quickly data can be passed is very dependent on the quality of the myelin sheaths. Damage to these - or to the cells that produce them - leads to serious disorders like MS that, eventually, destroy the nerve cells entirely.

Oligodendrocytes and Nfat Proteins

A team of researchers is looking at how oligodendrocytes regulate the formation of these myelin sheaths, with hope that this understanding will further develop knowledge of neurological disorders like MS. They have successfully identified protein molecules (like Sox10) that regulate the creation and preservation of myelin sheaths, but they wanted to go a step further and try to understand how the proteins interact when myelin is formed.

In the course of their research, they found that other molecules, called Nfat proteins, are necessary for the success of the interaction between the known molecules. The existence of Nfat proteins in oligodendrocytes allows the other required protein molecules to coexist without displacing one another.

Targeting Nfat Proteins

This research is closely linked with other research that aims to target stimulation of Nfat proteins in the hopes of promoting the formation of new myelin sheaths in MS patients. This type of stimulating substance is not yet available, however.

So far, only substances that inhibit the activity of these Nfat proteins have been developed, and are used in medicines like Cyclosporin A and Tacrolimus to keep the immune system in line to prevent organ rejection in transplant patients, for example. It is interesting to note that these patients often suffer from neurological disorders resulting from myelin sheath loss.

The new research suggests that serious side effects of current medications aimed at inhibiting Nfat proteins include myelin sheath loss, resulting in serious neurological conditions, making it absolutely critical that further research is performed as quickly as possible to improve existing medications.

These findings also show just how important Nfat proteins are for myelin formation, which opens up an entirely new approach to finding treatments to neurological disorders like MS that currently have no cure.

Further Reading & References:

Matthias Weider, Laura Julia Starost, Katharina Groll, Melanie Kspert, Elisabeth Sock, Miriam Wedel, Franziska Frb, Christian Schmitt, Tina Baroti, Anna C. Hartwig, Simone Hillgrtner, Sandra Piefke, Tanja Fadler, Marc Ehrlich, Corinna Ehlert, Martin Stehling, Stefanie Albrecht, Ammar Jabali, Hans R. Schler, Jrgen Winkler, Tanja Kuhlmann, Michael Wegner. Nfat/calcineurin signaling promotes oligodendrocyte differentiation and myelination by transcription factor network tuning. Nature Communications, 2018; 9 (1) DOI: 10.1038/s41467-018-03336-3

University of Erlangen-Nuremberg. "Our vulnerable nervous system: What affects its protective sheaths? Researchers shed light on a complex biochemical mechanism." ScienceDaily. ScienceDaily, 8 May 2018. www.sciencedaily.com/releases/2018/05/180508081453.htm.


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New research looks at the effectiveness of revolutionary "nanofiber" dressings - which make use of naturally-occurring proteins from plants and animals - to promote healing and regrow tissue.

New wound dressings, recently described in two separate research papers, seem to dramatically accelerate healing and improve tissue regeneration. What's the secret? Nanofiber dressings, which use naturally-occurring proteins found in both plants and animals.

Senior author of the research, Kit Parker - Tarr Family Professor of Bioengineering and Applied Physics at SEAS - served in Afghanistan. Witnessing battle wounds (and the healing process for those wounds) inspired his passion for researching new therapeutics for treating the wounds of war.

Early Developments in Wound Healing

Beginning nearly 50 years ago, scientists discovered that wounds incurred prior to the third trimester left no scars. This opened up a range of research possibilities for regenerative medicine, but the decades in between have proved challenging when it comes to replicating the distinctive characteristics of fetal skin.

Unlike adult skin, fetal skin contains high levels of fibronectin, a protein that promotes cell binding and adhesion. There are two main forms of fibronectin: globular, which is found in blood, and fibrous, which is found in tissue. While fibrous fibronectin seems to be the more promising option for wound healing, research up to now has mainly focused on the globular structure. This is likely due to the fact that globular fibronectin was easier to source, and fibrous fibronectin has been an engineering challenge.

Engineering New Methods

The research team was able to overcome this hurdle, however, by pioneering new methods of nanofiber engineering. By using a platform called Rotary Jet-Spinning (RJS), the scientists were able to use a liquid polymer solution (globular fibronectin dissolved in a solvent) that then gets "spun" in a way that is not dissimilar to a cotton candy machine. The resulting fibers, less than a single micrometer in diameter, can be collected to form a large-scale dressing or bandage.

A dressing made from these fibers integrates into the wound, creating a scaffold of sorts that is able to "recruit" relevant stems cells necessary for regenerating tissues. The bandage is able to assist in healing before it is absorbed by the body.

Early tests showed wounds treated with the fibronectin dressing have nearly normal epidermal thickness and dermal architecture and are even able to regrow hair follicles (which is often referenced as one of the biggest challenges in wound healing). This solution is much more straightforward than other existing treatment options.

Other Treatments and Advantages

Other research is looking at using a soy-based nanofiber produced in a similar way (using RJS to spin ultra-thin soy fibers into dressings). Early experiments are finding increased success in using soy-based nanofibers to aid in healing wounds.

Both types of nanofiber dressings have great advantages in wound-healing, and it's likely that both could find their niche in the market. Soy-based nanofibers are inexpensive, which could make them an excellent option for large-sale use like on burns. Fibronectin dressings could be especially helpful and useful where the prevention of scarring is important, as well.

Further Reading & References:

Christophe O. Chantre, Patrick H. Campbell, Holly M. Golecki, Adrian T. Buganza, Andrew K. Capulli, Leila F. Deravi, Stephanie Dauth, Sean P. Sheehy, Jeffrey A. Paten, Karl Gledhill, Yanne S. Doucet, Hasan E. Abaci, Seungkuk Ahn, Benjamin D. Pope, Jeffrey W. Ruberti, Simon P. Hoerstrup, Angela M. Christiano, Kevin Kit Parker. Production-scale fibronectin nanofibers promote wound closure and tissue repair in a dermal mouse model. Biomaterials, 2018; 166: 96 DOI: 10.1016/j.biomaterials.2018.03.006

Seungkuk Ahn, Christophe O. Chantre, Alanna R. Gannon, Johan U. Lind, Patrick H. Campbell, Thomas Grevesse, Blakely B. O'Connor, Kevin Kit Parker. Soy Protein/Cellulose Nanofiber Scaffolds Mimicking Skin Extracellular Matrix for Enhanced Wound Healing. Advanced Healthcare Materials, 2018; 1701175 DOI: 10.1002/adhm.201701175

Harvard John A. Paulson School of Engineering and Applied Sciences. "Drawing inspiration from plants and animals to restore tissue: Nanofiber dressings heal wounds, promote regeneration." ScienceDaily. ScienceDaily, 19 March 2018. www.sciencedaily.com/releases/2018/03/180319090743.htm.


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A Happy, Healthy Gut Microbiome

Written by InnovativeResearch on May 17, 2018. Posted in Blog

The gut microbiome is an exciting field of scientific research, as new studies continue to find links between the composition of the gut microbiome and an individual's overall health (and how this potentially ties in with disease). One of the lingering questions has been curiosity about how, exactly, an individual's microbiome is established. New research addresses this point, looking at the mechanisms used by gut bacteria to develop a healthy, thriving microbiome.

The gut is a happy habitat for bacterial growth - it is warm, moist, and offers an abundance of nutrients. The colonies of "good bacteria" that flourish in the gut are vital partners in helping the body perform important tasks like digesting fiber, extracting nutrients, and preventing disease. How is it that mammals are able to maintain such beneficial partnerships with gut bacteria, while the body typically has such a strong immune and/or illness response to pathogenic bacteria? What makes gut bacteria different?

A Closer Look at Bacteriodes fragilis

New research shows how one species of beneficial gut bacteria is able to harness the body's intrinsic immune response as a way to settle happily in the gut. Researchers looked closely at the Bacterioides fragilis microbe. This particular species is commonly found in the large intestines of a variety of mammals, including humans, and has been shown in previous research to prevent certain inflammatory and neurological disorders in mice (like inflammatory bowel disease and multiple sclerosis). Although there are various strains of B. fragilis, it is notable that healthy people tend to form a long-term relationship with only one strain throughout their lives.

The research team first looked at the specific locations where the bacteria took up residence. B. fragilis tends to cluster together within the thick layer of mucus that lines the gut (near the epithelial cells lining the surface of the intestine), which could be a necessary characteristic that allows for a single species to establish a strong presence.

Next, the team looked closer at the mechanisms that allow the bacteria to create their niche within the gut - they found that each B. fragilis bacterium is encased in a thick carbohydrate-based capsule, which may be a driving force in allowing the bacteria to dominate their niche within the gut.

Triggering the Immune System

Capsules like these are typically related to an immune response in pathogenic bacteria, a "trigger" that will often provoke an immune response. Sure enough, the researchers discovered that antibodies were binding to the B. fragilis capsules in the gut - but, unlike the imminent death that usually awaits pathogenic bacteria, immunoglobulin A (IgA) does not negatively impact most of the beneficial gut bacteria. In this particular case, it seems like IgA actually helped B. fragilis attach to epithelial cells.

The researchers believe the body's immune response is actually helpful to the "good bacteria" in the gut microbiome, allowing the bacteria to thrive - which then helps the host to thrive, as well. The research suggests that the immune system seems to function as more than just defense, and that antibodies can be useful in more ways than simply providing the body with a weapon against pathogens. Future research is expected to explore how to improve colonization by beneficial bacteria, an area of research that could lead to better probiotics and finding ways to use the gut microbiome as medicine for treating illness or disease.

Further Reading & References:

California Institute of Technology. "A gut bacterium's guide to building a microbiome: Unlike invading pathogens, which are attacked by the immune system, certain good bacteria in the gut invite an immune response in order to establish robust gut colonization." ScienceDaily. ScienceDaily, 4 May 2018. ww.sciencedaily.com/releases/2018/05/180504133624.htm.

G. P. Donaldson, M. S. Ladinsky, K. B. Yu, J. G. Sanders, B. B. Yoo, W. C. Chou, M. E. Conner, A. M. Earl, R. Knight, P. J. Bjorkman, S. K. Mazmanian. Gut microbiota utilize immunoglobulin A for mucosal colonization. Science, 2018; eaaq0926 DOI: 10.1126/science.aaq0926


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A recent article from TIME magazine takes a look at some exciting news from the scientific group Genome Project-write.

The scientists announced a new plan to develop cells that are resistant to viruses, as well as cells that could be resistant to other hazards like radiation, freezing, aging, and even cancer.

Highlights:

  • "There is a very strong reason to believe that we can produce cells that would be completely resistant to all known virusesIt should also be possible to engineer other traits, including resistance to prions and cancer." says Jef Boeke, director of the Institute for Systems Genetics at NYU Langone Medical Center and one of the GP-write leaders.
     
  • Biopharmaceutical company Cellectis will be providing the lab with its virus-targeting technology that uses the TALEN genome editing tool to make extremely precise changes to DNA.
     
  • This approach has proven feasible in testing genetic changes on the bacteria E. coli. A series of 321 changes to the bacteria's genome made the microbes resistant to certain viruses.
     
  • The researchers are hoping to complete their project - which could entail recoding every protein in the human genome, an effort that would require 400,000 changes - within 10 years.
     
  • The project has potential health implications that could help to make pharmaceuticals safer, cheaper, and more reliable.

You can read the full article, "Scientists Announce Plan to Create Virus-Proof Cells," on TIME.


Innovative Research was established in 1998 after the realization that dependable, high-quality, and affordable research materials were hard to come by. Starting with core products like human plasma and serum, Innovative Research has grown to be a trusted supplier of all lab reagents, including human biologicals and ELISA kits. Today, we manufacture and supply over 3,000 high-quality human and animal biologicals including plasma, serum, tissues, and proteins.

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Nausea and vomiting are never fun, and for some women, this can be an extreme and dangerous issue during pregnancy. New research suggests that there are two genes associated with this condition.

Experiencing morning sickness during pregnancy is not uncommon, but about 2% of pregnant women experience "hyperemesis gravidarum," a more severe form of nausea and vomiting that can sometimes lead to hospitalization. This is the condition that Kate Middleton, the Duchess of Cambridge, famously dealt with, and is the second leading cause of hospitalization during pregnancy.

Hormones? Nope. Genes.

New research, as recently reported in ScienceDaily, suggests that there are two genes associated with hyperemesis gravidarium. Known as GDF15 and IGFBP7, the two genes are both involved in placenta development and are important in both early pregnancy and appetite regulation.

Until now, it was assumed that hormones associated with pregnancy were to blame for extreme nausea and vomiting, but the new study found no evidence that hormones were the culprit. The two identified genes are also related to cachexia, which is a weight- and muscle-loss condition that leads to death in roughly 20% of cancer patients and has similar severe nausea and vomiting symptoms.

Finding the Cause

Past research indicates that hyperemesis gravidarum often runs in families, suggesting a genetic component. For this study, researchers compared DNA variations in pregnant women suffering no nausea and vomiting to that of those with hyperemesis gravidarum to identify variation between the two groups. The study's findings were then confirmed in an independent study of women with the condition.

Following up on that research, a separate study was conducted in which it was proven that the protein levels for GDF15 and IGFBP7 are abnormally high in women known to have hyperemesis gravidarum.

What's Next

These findings suggest new areas to look into to help a condition that has been notoriously difficult to treat. For example, is altering GDF15 and IGFBP7 protein levels safe during pregnancy, and does this lessen the severity of the symptoms? Researchers are hopeful that these findings will lead to the development of new medications and treatments that could offer relief for those suffering from hyperemesis gravidarum.

Further Reading & References:

Marlena S. Fejzo, Olga V. Sazonova, J. Fah Sathirapongsasuti, Ingileif B. Hallgrmsdttir, Vladimir Vacic, Kimber W. MacGibbon, Frederic P. Schoenberg, Nicholas Mancuso, Dennis J. Slamon, Patrick M. Mullin & 23andMe Research Team. Placenta and appetite genes GDF15 and IGFBP7 are associated with hyperemesis gravidarum. Nature Communications, 2018 DOI: 10.1038/s41467-018-03258-0

University of California - Los Angeles Health Sciences. "Two genes likely play key role in extreme nausea and vomiting during pregnancy: Study will help scientists better understand debilitating condition." ScienceDaily. ScienceDaily, 21 March 2018. www.sciencedaily.com/releases/2018/03/180321090849.htm.


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Spread by mosquitoes, malaria is responsible for 430,000 deaths per year. Scientists have not yet been able to develop a highly-effective, long-lasting vaccine that protects against contracting malaria.

A Deadly Parasite

New research, as reported in ScienceDaily, aims to bring us one step closer with the discovery of a human antibody that protects mice from infection with Plasmodium falciparum, the deadliest malaria parasite.

This new discovery could pave the way for future testing in humans to find out whether the antibody is able to provide short-term protection against malaria in people, and could prove helpful in the quest to develop an effective, long-term vaccine.

Discovering a Protective Antibody

Investigators at the National Institute of Allergy and Infectious Diseases (part of the National Institutes of Health) led the research, alongside researchers at the Fred Hutchinson Cancer Research Center in Seattle, were able to isolate an antibody called CIS43 from the blood of a volunteer who had been inoculated with an experimental vaccine. The vaccine was created using whole, weakened parasites (PfSPZ Vaccine-Sanaria). Following inoculation, the volunteer was (carefully, and under controlled conditions) exposed to infectious malaria-carrying mosquitos, and did not become infected.

In two different models looking at malaria infection in mice, the isolated CIS43 antibody proved to be highly effective at preventing the mice from becoming infected with malaria.

How it Works and What's Next

Looking at the CIS43 antibody in more detail shows that it works by binding to a specific portion of a key parasite surface protein, one that occurs only once along the length of the protein. Not only that, but the CIS43-binding epitope is conserved across 99.8% of all known strains of P. falciparum.

Because of this, the CIS43 antibody is an attractive target for researching next-generation experimental malaria vaccines, with the goal of producing this "neutralizing" antibody. If the results seen in mice are confirmed via human studies, CIS43 could be developed as a prophylactic measure designed to prevent infection long-term (for several months) following administration. If found to be effective at preventing malaria infection for six months, it could potentially work in combination with antimalarial drugs to help eliminate the disease in regions where malaria is endemic.

Scientists at the NIAID Vaccine Research Center are looking to assess the safety and efficacy of this new antibody in the coming year through controlled human malaria infection challenge trials.

Further Reading & References:

Neville K Kisalu, Azza H Idris, Connor Weidle, Yevel Flores-Garcia, Barbara J Flynn, Brandon K Sack, Sean Murphy, Arne Schon, Ernesto Freire, Joseph R Francica, Alex B Miller, Jason Gregory, Sandra March, Hua-Xin Liao, Barton F Haynes, Kevin Wiehe, Ashley M Trama, Kevin O Saunders, Morgan A Gladden, Anthony Monroe, Mattia Bonsignori, Masaru Kanekiyo, Adam K Wheatley, Adrian B McDermott, S Katie Farney, Gwo-Yu Chuang, Baoshan Zhang, Natasha Kc, Sumana Chakravarty, Peter D Kwong, Photini Sinnis, Sangeeta N Bhatia, Stefan H I Kappe, B Kim Lee Sim, Stephen L Hoffman, Fidel Zavala, Marie Pancera, Robert A Seder. A human monoclonal antibody prevents malaria infection by targeting a new site of vulnerability on the parasite. Nature Medicine, 2018; DOI: 10.1038/nm.4512

NIH/National Institute of Allergy and Infectious Diseases. "Newly described human antibody prevents malaria in mice: Research might help prevent malaria and aid design of next-generation vaccines." ScienceDaily. ScienceDaily, 19 March 2018. www.sciencedaily.com/releases/2018/03/180319215840.htm


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The dreaded "flu season" is never exciting. You can do everything right - wash your hands, get your annual flu shot - and still catch the virus. Why? A recent article from TIME takes a closer look.

Perfecting the Imperfect

Creating the annual flu vaccine is still, in part, a bit of a guessing game. The current shot is only 25% effective against this season's most frequently-identified strain, H3N2, because of issues like the required lead time in making a season's worth of vaccine.

Officials have to decide the makeup of the annual vaccine months ahead of the flu season, which typically results in 40%-60% effectiveness.

It's no easy feat to out-maneuver the stealthy flu virus, famous for continuously mutating.

There are hundreds of known variations, and each seasonal vaccine targets three or four versions that researchers believe will be the most common in a given year.

New Approaches to a Universal Problem

The goal of ongoing research is to create a "universal" vaccine that would work more like a measles vaccine, offering something along the lines of 90% protection for years (or even for life!) with a single inoculation.

Recent research has uncovered new and potentially promising approaches to bringing this "universal" dream closer to reality. One method, already in use by some pharmaceutical companies, uses cell cultures (instead of eggs) to reproduce viruses.

Other scientists are finding ways to use recombinant DNA technology in producing cell-based vaccines, which allows for identifying individual genes on a virus that are most likely to stimulate an immune response, and then using these particular genes in a different organism to create a more successful vaccine.

Other research targets components of the virus that remain more stable year-over-year, as opposed to current methods that target constantly-changing proteins on the surface of the flu virus.

Overcoming Hurdles

The two biggest issues in developing a universal flu vaccine are common issues that come as no surprise " time and money. Big Pharma's drugmaking giants " like GlaxoSmithKline PLC, Sanofi SA, and Johnson & Johnson " recognize the need for new innovations in vaccinating against influenza, and vaccines can be big business for pharmaceutical companies. But in order to capitalize on the potential, experts say there needs to be a push for increased investment and funding.

Overall, if you look at the resources being used toward developing a universal flu vaccine, the numbers are relatively small across the world. Mobilizing funding is the first step in increasing efforts " and lawmakers are jumping onboard. Senator Ed Markey, for example, has recently introduced the Flu Vaccine Act, which aims to provide 1 billion over five years to fund efforts by the National Institutes of Health.

Still, results are not going to magically appear overnight. In the meantime, the seasonal flu shot is as important as ever " but with more time, new research, and increases in funding " we will be ever-closer to developing better and more effective vaccinations.

Further Reading & References:

Why Flu Outbreaks Have Been the Worst in Nearly a Decade. TIME. 28 February 2018.


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Induced Pluripotent Stem Cells as Cancer Vaccine

Written by InnovativeResearch on February 20, 2018. Posted in Blog

cancer research - using stem cells as a possible vaccine

What, exactly, are iPS cells? And why are they so interesting?

In a lab setting, induced pluripotent stem cells (iPS cells, for short) can become various types of cells and tissues, making them a cornerstone of regenerative medicine with seemingly endless applications for repairing damage due to trauma or disease.

Now, as ScienceDaily reports, a study in mice suggests that iPS cells could be used to train the immune system to attack (or possibly even prevent) tumors, which could pave the way for the possibility of a "cancer vaccine" that is individually tailored using a person's own iPS cells to protect against various forms of cancer.

How iPS cells work against cancer

In general, iPS cells are similar (on their surface) to tumor cells. Both resemble developmentally immature progenitor cells — which means that both iPS and tumor cells are free from the growth restrictions that are seen in mature tissue cells.

Because of this, injecting iPS cells that genetically match the individual (but that are unable to replicate) can provide safe exposure to a range of cancer-specific targets, according to new research recently published by Stanford Medicine.

As part of a potential vaccine, iPS cells have strong immunogenic properties that are able to induce a systemic cancer-specific immune response.

Creating iPS cells

Researchers are able to create iPS cells from an easily-accessible source, like skin cells or blood cells. The collected cells then undergo genetic treatment which essentially turns back the clock, developmentally speaking, to a pluripotent stage — meaning that the cells are able to develop from that stage into nearly any tissue of the body.

How it worked in mouse testing

In comparing gene expression between iPS and cancer cells in both mice and humans, researchers identified remarkable similarities that suggested these types of cells both contain the same surface proteins (epitopes) that could serve as immune targets.

This was tested in four groups of mice — the first group was injected with a control, the second received iPS cells that were a genetic match and irradiated, the third received a generic immune-stimulating agent, and the fourth and final group received both irradiated iPS cells and the immune-stimulating agent. A mouse breast cancer cell line was transplanted into all mice involved in the study so that potential tumor growth could be observed.

A week later, all of the mice had developed breast cancer tumors at the injection site. In the control groups, these tumors proceeded to grow robustly. In 7 of the 10 mice from the fourth group (receiving both the iPS cells and the immune-stimulating agent), the tumors shrank in size, and two of these mice were able to reject the cancer cells completely and live for more than one year following the tumor transplant. Similar results occurred when tested with mouse melanoma and mesothelioma.

What's next

The scientists involve believe this approach is especially powerful since it allows for exposure to different types of cancer-specific epitopes at the same time, putting the immune system on alert and allowing it to target cancers as they begin to develop.

Next, the team would like to study if this approach would work with samples of human cancers and immune cells in a laboratory setting.

The future looks bright, if this research continues to perform as expected, for creating a personalized vaccine using an individual's own iPS cells to prevent cancer development for months or years. Additionally, this could potentially be used as part of cancer therapy, alongside surgery, chemotherapy, radiation, or a combination thereof.

While much research remains to be done, the concept is certainly exciting — and we may be just around the proverbial corner from the development of better cancer treatment and prevention.

Further Reading & References:

Nigel G. Kooreman, Youngkyun Kim, Patricia E. de Almeida, Vittavat Termglinchan, Sebastian Diecke, Ning-Yi Shao, Tzu-Tang Wei, Hyoju Yi, Devaveena Dey, Raman Nelakanti, Thomas P. Brouwer, David T. Paik, Idit Sagiv-Barfi, Arnold Han, Paul H.A. Quax, Jaap F. Hamming, Ronald Levy, Mark M. Davis, Joseph C. Wu. Autologous iPSC-Based Vaccines Elicit Anti-tumor Responses In Vivo. Cell Stem Cell, 2018; DOI: 10.1016/j.stem.2018.01.016

Stanford Medicine. "Induced pluripotent stem cells could serve as cancer vaccine." ScienceDaily. ScienceDaily, 15 February 2018. www.sciencedaily.com/releases/2018/02/180215125026.htm.


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Early Characteristics of Alzheimer's disease

As reported in ScienceDaily, one of the earliest events that occurs with Alzheimer's disease is an unusual buildup of beta-amyloid peptide, which then can form the characteristic amyloid plaques in the brain. These plaques disrupt the function of neuronal synapses. Beta-secretase (BACE1) is an enzyme that helps to produce the problematic beta-amyloid peptide.

A team of researchers from the Cleveland Clinic Lerner Research Institute have found that - in mice with Alzheimer's disease - gradually depleting the BACE1 enzyme completely reverses the formation of amyloid plaques in the brain. Not only that, but this reversal also led to improvements in the animals' cognitive function.

The new report, published this week in the Journal of Experimental Medicine, brings hope that scientists will be able to develop drugs that target this enzyme in a bid to find a successful treatment for Alzheimer's disease in people.

Testing BACE1 reduction in adult mice

BACE1 controls many important processes, so simply getting rid of the enzyme could have serious side effects. Mice completely lacking BACE1 have severe neurodevelopmental defects - but, researchers wondered, would inhibiting this enzyme in adults be less harmful?

To find out, the team of scientists generated mice that gradually lose the BACE1 enzyme as they age. These mice developed as expected and seemed to remain perfectly healthy throughout their lifespan. Next, the team bred these mice with a group of mice that begin to develop amyloid plaques and Alzheimers disease when they reach 75 days old. The resulting offspring formed plaques at the expected age, with BACE1 levels close to half what they would normally be at 75 days.

Incredibly, these plaques began to shrink and disappear as the mice continued aging (and as their BACE1 levels continued to fall). Even more remarkable, by the time these cross-bred mice reached 10 months of age, the plaques had entirely disappeared.

In addition, the lower BACE1 activity also led to lower beta-amyloid peptide levels and reversals in other benchmarks of Alzheimer's disease (like the activation of microglial cells and formation of abnormal neuronal processes). The memory of the mice with Alzheimers disease saw improvement with the loss of BACE1 - but the depletion of the enzyme only partially restored synaptic activity, which may point to BACE1 as necessary for optimal cognition.

More study is needed, but this groundbreaking research certainly suggests progress in identifying treatments for Alzheimers disease, something that has proved elusive thus far.

Further Reading & References

Xiangyou Hu, Brati Das, Hailong Hou, Wanxia He, Riqiang Yan. BACE1 deletion in the adult mouse reverses preformed amyloid deposition and improves cognitive functions. The Journal of Experimental Medicine, 2018; jem.20171831 DOI: 10.1084/jem.20171831

Rockefeller University Press. "Alzheimer's disease reversed in mouse model." ScienceDaily. ScienceDaily, 14 February 2018. www.sciencedaily.com/releases/2018/02/180214093712.htm.

Alzheimer's Disease Reversed in Mouse Model." Genetic Engineering & Biotechnology News. 14 February 2018. https://genengnews.com/gen-news-highlights/alzheimers-disease-reversed-in-mouse-model/81255493


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Transcribing DNA

In order to "read" the information from a gene - for purposes like mapping a human genome - the gene first needs to be copied.

This transcription process uses a factory molecule (RNA polymerase) that works much like a biological jump-drive: it attaches to the DNA at the beginning of a gene, "downloads" the genetic information into the RNA molecule, and then terminates the transcription process at the end of the gene.

Not surprisingly, it is critical to start and stop this transcription process at exactly the correct place or the data (in this case, the RNA transcript) may become corrupted, meaning that it might not make any sense or sometimes may even cause harm.

As ScienceDaily reports, new research published this month in Genes & Development looks at understanding how the transcription process is terminated.

In general, there have been two models that are used to explain how this transcription process stops.

Allosteric Model of Termination

The allosteric model suggests that the properties of RNA polymerase are changed after binding or losing some of its associated proteins, causing it to detach from the DNA. Essentially, termination can be attributed to structural change to the RNA polymerase unit.

Torpedo Model of Termination

The torpedo model proposes that at the ends of genes, a "molecular torpedo" jumps onto the RNA and chases the RNA polymerase, bumping it off the DNA when it catches it.

Looking for Answers with Gene Editing

In this study, the scientists used the approach of gene editing to identify this molecular torpedo.

The team of researchers was then able to eliminate strategic mechanisms in a short time frame, which in turn gave the scientists a better look at what, exactly, was occurring. They then took this modality and combined it with a technique that illustrates the exact position of RNA polymerase on all genes in a cell.

Gene editing technology has been making a lot of news cycles as of late, especially when it comes to the therapeutic potential of such technology. Research like this shows a different side of this progress, however, by using these advances as a biological tool to look more closely at cellular processes. Removing the molecular torpedo demonstrated that the RNA polymerase took much longer to stop, and this result was seen in most genes.

Further Reading & References:

Joshua D. Eaton, Lee Davidson, David L.V. Bauer, Toyoaki Natsume, Masato T. Kanemaki, and Steven West. Xrn2 accelerates termination by RNA polymerase II, which is underpinned by CPSF73 activity. Genes and Development, 2018

University of Exeter. "New insight into workings of building blocks of life." ScienceDaily. ScienceDaily, 12 February 2018. www.sciencedaily.com/releases/2018/02/180212105240.htm.


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Medical science has reached an exciting new milestone this month, when scientists were able to successfully produce human kidney tissue within a living organism. Not just any kidney tissue, though — this is FUNCTIONING kidney tissue with the ability to produce urine. This is widely regarded as a significant breakthrough in the path to creating treatments for kidney disease, as ScienceDaily reports.

The study was funded by the Medical Research Council and Kidney Research UK, and lead by Professors Sue Kimber and Adrian Woolf from the University of Manchester. The results were recently published in the journal Stem Cell Reports.

How'd They Do That?

Kidney glomeruli (microscopic parts of the organ) were created from human embryonic stem cells, grown in a laboratory setting using a culture medium that contained molecules promoting kidney development. These were combined with a gel-like substance (to mimic natural connective tissues), and the mixture was then injected under the skin of mice.

Three months later

After a 90-day wait, the team examined the tissues and found that nephrons — the core structural and functional feature of the kidney — had developed. These tissue samples included most of the nephrons found in humans, including proximal tubules, distal tubules, Bowmans capsule, and Loop of Henle. In addition, small human capillaries had developed inside the mice, providing nourishment to the new kidney tissues.

These new tissues lacked a key component, however — they did not develop a large artery, without which the organ will only function at a fraction of what would normally be expected. The researchers are working with surgeons to work on adding an artery to bring more blood to the kidney tissue.

When tested, it was determined that the tissue was functioning as kidney cells — the structure was filtering blood and producing urine, a medical first.

What's Next

While this is a significant step that certainly proves the concept, there is important research still to come. Scientists hope to build upon this breakthrough by determining an exit route for the urine that is produced, and from there, a way to deliver this technology to diseased kidneys.

Further Reading and Reference

Ioannis Bantounas, Parisa Ranjzad, Faris Tengku, Edina Silajdi, Duncan Forster, Marie-Claude Asselin, Philip Lewis, Rachel Lennon, Antonius Plagge, Qi Wang, Adrian S. Woolf, Susan J. Kimber. Generation of Functioning Nephrons by Implanting Human Pluripotent Stem Cell-Derived Kidney Progenitors. Stem Cell Reports, 2018; DOI: 10.1016/j.stemcr.2018.01.008

University of Manchester. "Scientists create functioning kidney tissue." ScienceDaily. ScienceDaily, 9 February 2018. www.sciencedaily.com/releases/2018/02/180209112402.htm.


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Could it really be so simple?

New research suggests that something as simple as a blood test could potentially reveal whether a person is at risk for developing Alzheimer's disease.

As ScienceNews reports, Alzheimer's patients will commonly begin developing a protein called amyloid-beta in their brain long before any outward sign of the disease develops. Detecting these A-beta buildups ("plaques") in the brain is traditionally done via brain scan or spinal tap, but research is showing that it may be possible to also use A-beta blood levels to predict the presence of these plaques.

A recent study published online in Nature outlines a test to successfully detect plaques as measured by the presence of A-beta in blood plasma with about 90% accuracy (as corroborated by PET brain scan). These results are in line with those from a smaller study that took place last year, performed by a different team of researchers.

Detecting A-beta levels in blood plasma

Developing a blood test for this has historically been challenging, as there are relatively tiny A-beta levels in the blood (as compared to the amounts that build up in the brain), and it has been difficult to find a consistent correlation between the presence of A-beta buildup in the brain and A-beta levels in the blood. This new study used a more sensitive measuring technique (mass spectrometry), allowing for the detection of minute amounts of the protein in blood plasma.

Interpreting A-beta results with ratios

Rather than looking at the total A-beta level found in the blood, the research team instead looked to the ratio between different types of A-beta. These ratios allowed the scientists to differentiate between those who had A-beta brain plaques and those who didn't.

The team created a composite biomarker score by combining two different ratios, which allowed them to predict the presence or absence of A-beta plaques in the brain with ~90% accuracy.

Looking Forward

Currently, there exists no known treatment for Alzheimer's that is able to slow or stop the progression of the disease, so detecting this early isn't able to improve patient outcome at the moment. However, researchers believe that a blood test like this could help to identify those who may be good candidates for clinical trials of early interventions.

While these results are promising, the test still needs to be researched and refined further before it would be ready for use. At the moment, it is not clear whether this blood test would eventually be more affordable than the traditional methods of detection, like brain scans and spinal taps.

Further Reading:

A. Nakamura et al. High performance plasma amyloid- biomarkers for Alzheimers disease. Nature Published online January 31, 2018. doi:10.1038/nature25456.

V. Ovod et al. Amyloid concentrations and stable isotope labeling kinetics of human plasma specific to central nervous system amyloidosis. Alzheimers & Dementia. Vol. 13, August 2017, p. 841. doi:10.1016/j.jalz.2017.06.2266.

L. Hamers. A blood test could predict the risk of Alzheimers disease. Science News. February 1, 2018. https://www.sciencenews.org/article/blood-test-could-predict-risk-alzheimers


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Although the first embryonic stem cells were developed from mice in 1981, and human embryonic stem cells were cultured in 1998, bovine embryonic stem cells have proved elusive until now, as reported in Science Mag.

What makes an embryonic stem cell so useful in research?

Key to successful embryonic stem cells is their pluripotency — the ability of the cells to differentiate into other cell types. In the case of pluripotent embryonic stem cells, they have no fixed developmental potential and the new bovine embryonic stem cells could make it easier to improve animal genetics.

Bovine stem cells have proved tricky to create, as stem cells cultured from cow embryos would quickly lose their pluripotency and develop into specific cell types when grown in a lab.

The beauty of embryonic stem cells is that they could become a wide variety of tissues, which (in the case of bovine embryonic stem cells) could make it easier to modify and/or preserve useful genetic traits of the various breeds of cattle. This could lead to animals that could theoretically produce more milk or higher-quality meat, have an easier time giving birth, or better resist common diseases. The possibilities are endless, really.

How'd they do that?

The research team used a unique culture medium that combined two key ingredients: a protein to boost cell growth and propagation, and a different molecule that inhibits cell development (so that the embryonic stem cells would be unable to differentiate into more mature cell types).

This combination both sped up and hampered cell development, resulting in stem cells that remained pluripotent in a laboratory setting over a long period of time.

How can this technology be used?

These cells could hypothetically make it possible for breeders to select more genetically-advantaged animals by testing embryonic stem cells from different embryos for desired genetic traits (and then even potentially creating clones from those cells).

Researchers are also looking at ways to develop these bovine embryonic stem cells into bovine sperm and egg cells, which would open up a method for creating embryos with new genetic combinations, isolating even more stem cells from the best ones. This sequence (stem cell, sperm/egg, embryo, stem cell) could then allow for livestock genetics companies to rapidly cycle through generations without needing to birth any animals, potentially fast-tracking genetic progress in an exponential way.

Access to a new species of embryonic stem cells could also open new research opportunities. For example, this may make it possible for creating large-animal models that could mimic human disease more closely than mice are able to.

Embryonic stem cells are still proving difficult to produce from most species — the new culture medium is showing early promise with sheep cells, and researchers are looking to test this with additional species in the near future.

Further Reading:

American Association for the Advancement of Science. "First cow embryonic stem cells could lead to healthier, more productive livestock." Science Magazine Vol 359, Issue 6375. doi:10.1126/science.aat2197


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