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Cell Biology

Virus expert and cancer biologist Harry Rubin dies at 93 – UC Berkeley

Harry Rubin in 1989. (UC Berkeley photo by Jane Scherr)

Harry Rubin, a leader in the search to understand how viruses cause cancer research that ultimately led to the discovery of cancer-causing genes called oncogenes died on Sunday, Feb. 2, at the age of 93. Rubin was a professor emeritus of molecular and cell biology at the University of California, Berkeley.

A veterinarian by training, Rubin began investigating in the 1950s how normal cells turn into cancer cells a process called transformation. This was at a time before genes could be cloned and sequenced, and much of his research relied on manipulating cultured cells in a petri dish.

Many labs were beginning to work with tumor viruses as the only tractable way to understand cancerous transformation, and Rubin chose to focus on a virus known since 1911 to cause cancer in chickens: the Rous sarcoma virus (RSV). RSV is an RNA virus, which means that it carries its genetic instructions in the form of RNA, not DNA. The virus tricks cells into reverse transcribing its RNA into DNA and integrating it into its own genome.

At that time, there was really no way of studying the molecular or genetic basis of cancer by studying cancer cells, because the genome of the cell is so enormous, said G. Steven Martin, one of Rubins former postdoctoral fellows and a UC Berkeley professor emeritus of molecular and cell biology. Before the advent of cloning and genetic sequencing, we couldnt look into the cancer cell and find the genes involved in cancer. Since tumor viruses have such small genomes and carry only a few genes, it was clear that studying tumor viruses would provide an entry point into the basic mechanisms of cancer.

Between 1953 and 1958, Rubin worked as a postdoctoral fellow and, later, as a research fellow in the lab of virologist Renato Dulbecco at the California Institute of Technology in Pasadena. In 1955, Rubin showed that every cell in an RSV-induced tumor was capable of releasing the virus, implying that RSV was permanently associated with the host cell and suggesting that it plays a direct and continuing role in perpetuating the cell in its malignant state.

Then, working with Caltech graduate student Howard Temin, Rubin developed a way to measure the amount of infectious virus using cultured fibroblast cells from chicken embryos. This opened the way for quantitative studies of the mechanism by which RSV transforms normal cells into cancerous cells.

Dulbecco and Temin later shared the 1975 Nobel Prize in Physiology or Medicine for their work on tumor-causing viruses.

When Rubin moved to UC Berkeley in 1958 to join the Department of Virology, he continued work on RSV and developed other assays, including one to detect avian leukosis virus in vaccines, such as the measles vaccine, that are produced in chicken cell cultures.

Harry Rubin and his wife Dorothy.

He also showed that one strain of RSV was a replication-defective virus that could transform normal cells into cancer cells, but required a leukosis virus a helper virus to replicate and spread. In other words, the RSV could transform, but not replicate, itself, while the helper virus could replicate, but not transform.

This was one of the very first observations to suggest that the virus might carry information about cell transformation and tumorigenesis that was separate from the information needed for the replication cycle of the virus, Martin said.

Rubins work on RSV earned him a prized Lasker Award in 1964.

The work of Drs. Rubin and Dulbecco proves that cells can carry, for many generations, a foreign nucleic acid, whether RNA or DNA, that is responsible for the malignant properties of these cells, the Lasker Foundation wrote in giving them the award in clinical research.

Rubin also received the 1961 Eli Lilly Award in Bacteriology and Immunology and the 1963 Merck Research Award for his work on RSV and was elected to the National Academy of Sciences in 1978.

In 1970, a viral gene responsible for cancerous transformation, now known as viral src, or v-src, was identified through genetic and biochemical studies on RSV carried out by Martin, who was then in the Rubin lab, Peter Vogt at the University of Washington in Seattle and Peter Duesberg at UC Berkeley. This allowed Harold Varmus and Michael Bishop of UC San Francisco to identify an analogous gene in the cellular genome a gene evidently stolen by the Rous sarcoma virus. Called cellular src, or c-src, it was the first known proto-oncogene, that is, a normal gene that, when mutated, can trigger cancer. Many more proto-oncogenes have been discovered since then. The discovery won Bishop and Varmus the 1979 Nobel Prize in Physiology or Medicine.

The significance of the work on the Rous sarcoma virus is that it led to the work on cellular genes that can cause cancer, Martin said. The idea that, by studying the virus, one could get an insight into the cellular and genetic mechanism of carcinogenesis was, in fact, vindicated.

Although Rubins research set the stage for the discovery of oncogenes, by the early 1970s he had switched his focus from viruses to the biology of transformed cells, looking at the mechanisms of growth control and, in particular, the role of inorganic ions in cellular regulation. In later years, he studied the origin of spontaneous transformation of animal cells in culture, using this system as a model for tumor progression.

Harry Rubin was born in New York City on June 23, 1926, the son of Russian Jewish immigrants. His father ran a grocery store in Manhattan. As a teenager, he worked on farms in upstate New York and at 16 enrolled in the veterinary school at Cornell University. Upon graduation in 1947 with a D.V.M. degree, he went to Mexico to help with an outbreak of hoof-and-mouth disease, then joined the U.S. Public Health Service in Montgomery, Alabama, to work on viral diseases, including rabies and Eastern equine encephalitis. In a 1991 profile in California Monthly magazine, he referred to it as time spent chasing cows and horses in Mexico and Louisiana.

Seeking new challenges, he enrolled at New York University and, a year later, in 1952, convinced Nobel Prize winner Wendell Stanley to let him work in his Virus Laboratory at UC Berkeley. Rubin transferred to Caltech in 1953, returning to join the UC Berkeley faculty in 1958, where he eventually occupied Stanleys old office. He retired as an emeritus professor in 2001.

Rubin is survived by his wife, Dorothy, of Berkeley; three children, Andrew, Janet and Clinton Rubin; six grandchildren; and six great-grandchildren. He and his wife were longtime members of Congregation Beth Israel in Berkeley.

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Virus expert and cancer biologist Harry Rubin dies at 93 - UC Berkeley

Cell Biology

When rocket blasts off for space station, EVMS will be along for the ride – Daily Press

Just days before a planned rocket launch, a crate the size of a dishwasher destined for the International Space Station had been routed to the wrong Norfolk address.

The mysterious wooden box held equipment for scientists at Eastern Virginia Medical School who needed to prepare it to be shot into orbit from Wallops Island on Sunday.

Instead, it sat at a senior high-rise, intriguing elderly residents with its many Hawaii labels.

The delivery mishap gave Northrop Grumman project manager JoElla Delheimer a dose of last-minute anxiety. The stress lifted when she learned that the box was only a couple of blocks away from the EVMS campus.

One thing about flying a rocket to space is that you cant be five minutes late, she said.

Through a multimillion-dollar contract, scientists are using the Norfolk medical schools laboratories and supplies to prepare experiments for astronauts. And while certain studies are done in orbit, scientists down below will conduct control experiments at EVMS.

The partnership with NASA contractor Northrop Grumman began with a mission last fall and will continue for at least three years, aiding five more space launches out of Wallops Island.

Weather permitting, Northrop Grumman plans to send up its unmanned Antares rocket and Cygnus spacecraft, carrying more than 8,000 pounds of cargo, at 5:39 p.m. Sunday from the Virginia flight facility.

So long as the Cygnus is on schedule, it will dock at the station Tuesday.

Bill Wasilenko, the vice dean of research at EVMS, said one reason the school got involved was that it would bring in researchers from around the world. On a later mission, for example, the school will host some Japanese scientists through the contract.

A lot of biomedical benefit is likely to come out of doing the research that we do up there, in terms of drug development. There are ways in which crystals develop in space that are different that could lead to new pharmaceuticals, new therapeutics, he said. The hope is our medical students will mingle around the scientists, learn about what were doing from mission to mission, come to our seminars. Maybe some of them will get interested in space medicine.

Two research teams were at the Norfolk campus this week preparing experiments and hardware for liftoff.

One group from Hawaii plans to run a tissue-culturing study in a device it developed called the Mobile SpaceLab. The equipment has a sort of set-it-and-forget-it capability: Once its at the space station, it will perform biology tests without crew. The device will take pictures of the cell activity every six minutes for four weeks.

Devin Ridgley, chief biologist for the Scorpio-V division of HNu Photonics, said the automation frees up the crew to work on other things and eliminates some of the potential for mistakes.

Weve been trained with this equipment and cell biology for many years now, but the crew may not be as well-trained, he said. Some are fighter pilots deservedly crew, but maybe not the best at doing cell biology experiments.

On Thursday at EVMS, Ridgley started growing a type of cancer cell, neuroblastoma, for the experiment. The study will look at the effects of microgravity the weak gravitational conditions of the space station at the subcellular level.

The second team, from BioServe Space Technologies based at the University of Colorado, was busy in a different lab preparing kits for another microgravity-related study. Mark Rupert, associate director of BioServe, said the hardware sort of like petri dishes that work without gravity will facilitate research on bone loss using osteoblast cells.

On Earth there is a way to levitate organisms with strong magnets, which may provide a way to study the bone loss that happens in space, he said. But its unclear if that simulation is a good substitute. The experiment, run by a researcher at the University of Minnesota, will compare the methods. If the magnet technique is suitable, it could be a cheaper way to study the problem in the future than running more tests at the space station.

Because astronauts experience bone loss in orbit, researchers want to learn more about it, not only to help future space travelers but to better understand a wide range of disorders, such as osteoporosis.

To get ready for its supporting role for NASA, EVMS sent staff down to the Kennedy Space Center in Florida to tour the facility and observe operations. There they saw things like researchers who were growing lettuce talk to an astronaut, who was also growing the leafy vegetable at the space station.

The laboratories that are needed for the pre-launch preparation of experiments primarily occur at the Kennedy Space Center, but theyre overwhelmed. They have a backlog of experiments, Wasilenko said.

That makes EVMS, a two-hour drive from the Wallops Island launchpad, well-positioned for providing similar services, especially for experiments that involve live tissue or rodents that must be packed at the last minute. Though no critters will board the Cygnus this time, about 40 mice, born and raised on campus, flew in the previous mission that took off in November.

Northrop Grumman said that no other place it considered was large enough or had the capabilities of EVMS.

One of the primary things that brought us here, of course, was the animal care facility, Delheimer said. Their reputation is tremendous.

Separate from the Northrop Grumman contract, EVMS has two NASA-funded studies. Richard Britten, an associate professor of radiation oncology and biophysics, is examining the effects of galactic cosmic radiation on brain function. And Larry Sanford, professor of pathology and anatomy, is studying in-flight stress and sleep disturbances on brain function.

EVMS administrators hope the schools new role will open opportunities for more of its own biomedical research. Wasilenko thinks its an interesting coincidence that a lot of the research coming out of EVMS right now happens to be on similar subjects as those being studied in the space station.

Diabetes, obesity, circadian rhythm work and now the bone thing, he said. "Theres a lot of overlap, and thats the appeal of researchers coming here and mingling with our researchers. If they hit it off, they could work together on some future projects.

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When rocket blasts off for space station, EVMS will be along for the ride - Daily Press

Cell Biology

Trillium Therapeutics Announces Changes to Its Board of Directors – BioSpace

CAMBRIDGE, Mass., Feb. 07, 2020 (GLOBE NEWSWIRE) -- Trillium Therapeutics Inc.. (Trillium or the Company) (NASDAQ/TSX: TRIL), a clinical stage immuno-oncology company developing innovative therapies for the treatment of cancer, today announced that Paul Walker has been appointed to the Companys Board of Directors, and Dr. Ali Behbahani has been appointed as a Board Observer, effective February 6, 2020.

We are delighted to welcome Mr. Walker to the Board of Directors and Dr. Behbahani as a Board Observer, and look forward to their guidance as we work to bring to patients our CD47 programs, stated Dr. Robert Kirkman, Executive Chair of Trillium Therapeutics.

We are excited about Trilliums recent progress and look forward to working with the leadership team as they expand their clinical development program, said Paul Walker.

Mr. Walker and Dr. Behbahani are general partners with New Enterprise Associates (NEA), a global venture capital firm with more than $20 billion of cumulative committed capital invested in healthcare and technology companies. Prior to joining NEA, Paul worked at MPM Capital as a General Partner with the MPM BioEquities Fund, where he specialized in public, PIPE and mezzanine-stage life sciences investing. Previously, he was a portfolio manager at Franklin Templeton Investments. Paul received a BS in Biochemistry and Cell Biology from the University of California at San Diego, and holds the Chartered Financial Analyst (CFA) designation.

Dr. Behbahanis previous positions include a consultant in business development at The Medicines Company, a Venture Associate at Morgan Stanley Venture Partners and as a Healthcare Investment Banking Analyst at Lehman Brothers. He concurrently earned his MD degree from The University of Pennsylvania School of Medicine and his MBA degree from The University of Pennsylvania Wharton School.

The Company also announced that Dr. Robert Uger, Trilliums Chief Scientific Officerhas resigned from the Board of Directors effective February 6, 2020.

About Trillium Therapeutics

Trillium is an immuno-oncology company developing innovative therapies for the treatment of cancer. The Companys two clinical programs, TTI-621 and TTI-622,target CD47, a do not eat signal that cancer cells frequently use to evade the immune system.

The Companys pipeline also includes a preclinical STING (stimulator of interferon genes) agonist program. As previously announced, the program is earmarked for out-licensing.

For more information visit: http://www.trilliumtherapeutics.com

Caution Regarding Forward-Looking Information

This press release contains forward-looking statements within the meaning of applicable United States securities laws and forward-looking information within the meaning of Canadian securities laws (collectively, forward-looking statements). Forward-looking statements in this press release include statements about, without limitation, the belief that Trilliums programs could achieve best-in-class status for CD47 blocking agents and Trilliums future plans and objectives for its CD47 programs. With respect to the forward-looking statements contained in this press release, Trillium has made numerous assumptions regarding, among other things: the effectiveness and timeliness of clinical trials; and the completeness, accuracy and usefulness of the data. While Trillium considers these assumptions to be reasonable, these assumptions are inherently subject to significant scientific, business, economic, competitive, market and social uncertainties and contingencies. Additionally, there are known and unknown risk factors that could cause Trilliums actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements contained in this press release. Factors that may cause such a difference include, without limitation, risks and uncertainties related to the reliance on positive results of preclinical and early clinical research as such results are not necessarily predictive of results of later-stage clinical trials. A further discussion of risks and uncertainties facing Trillium appears in Trilliums Form 20-F for the year ended December 31, 2018 is filed with Canadian securities authorities and with the U.S. Securities Exchange Commission, each as updated by Trilliums continuous disclosure filings, which are available at http://www.sedar.comand at http://www.sec.gov. Forward-looking statements are not guarantees of future performance and accordingly undue reliance should not be put on such statements due to the inherent uncertainty therein. All forward-looking statements herein are qualified in their entirety by this cautionary statement, and Trillium disclaims any obligation to revise or update any such forward-looking statements or to publicly announce the result of any revisions to any of the forward-looking statements contained herein to reflect future results, events or developments, except as required by law.

Company Contact:James ParsonsChief Financial OfficerTrillium Therapeutics Inc.416-595-0627 x232james@trilliumtherapeutics.com

Media Contact:Mike BeyerSam Brown Inc.312-961-2502mikebeyer@sambrown.com

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Trillium Therapeutics Announces Changes to Its Board of Directors - BioSpace

Cell Biology

Sonoma Biotherapeutics launches with $40 million in Series A funding to advance regulatory T cell therapy in autoimmune and degenerative diseases -…

Company founded by four pioneers of Treg cell biology and cell therapy and financed by a syndicate of leading biotech investors

SOUTH SAN FRANCISCO, Calif. and SEATTLE, Feb. 6, 2020 /PRNewswire/ -- Sonoma Biotherapeutics, a privately held company developing regulatory T cell (Treg) therapies for autoimmune and degenerative diseases, launched today in South San Francisco, CA and Seattle, WA with $40 million in its Series A financing. Sonoma brings together next-generation research, development and manufacturing capabilities in cell therapy and genetic engineering with an accomplished team of executives, scientists, board members and investors with extensive experience in the fields of cell therapy and drug discovery.

"With this team and our assembled expertise and technologies, we are in an ideal position to move adoptive cell therapy beyond cancer, to establish safe, effective and long-lasting treatments for a range of conditions where current drugs and biologics are simply not good enough," said founder and CEO Jeffrey Bluestone, PhD. "As the immune system's master regulators of protecting the body against self-destruction, Treg cell therapy is perhaps the ideal means to shut down unwanted immune reactions and provide meaningful treatment for patients."

The financing involves an investor syndicate that includes Lyell Immunopharma, ARCH Venture Partners, Milky Way Ventures and 8VC. "Treg therapies have the potential to transform the treatment of autoimmune and degenerative diseases," said Robert Nelsen, managing partner and co-founder of ARCH Ventures Partners. "Sonoma Biotherapeutics has assembled the team and capabilities required to make this vision a reality for patients and their families."

The goal of Treg therapy is to restore a state of self-tolerance by halting harmful inflammatory responses in autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease and multiple sclerosis, along with degenerative diseases including amyotrophic lateral sclerosis (ALS) and Alzheimer's. Over 50 million Americans currently live with an autoimmune disease, and millions more with some form of degenerative diseases. For many, existing therapies are ineffective at controlling their disease.

Tregs have a clear role in many of these conditions. These cells' natural ability to migrate to inflamed tissues and control harmful immune responses make them ideal for treating a range of conditions. In addition, the ability to engineer Treg cells to target specific disease-causing antigens reduces the potential for unwanted systemic effects. The role of Tregs in tissue maintenance and repair offers the potential for effective, durable and restorative treatments.

Sonoma Biotherapeutics is co-founded by four of the foundational scientists in the Treg field:

Collectively, the founding team brings expertise and proprietary methodologies across the Treg drug discovery and development process, including selection, manipulation, editing, regulation and translation for clinical use. Together, Drs. Bluestone and Tang have pioneered adoptive Treg cell therapy in some of its first clinical uses in type 1 diabetes, lupus and organ transplantation. Drs. Rudensky and Ramsdell co-discovered FOXP3, a critical transcription factor for Treg development and function, and in 2017 were awarded the Crafoord Prize by the Royal Swedish Academy of Sciences for their landmark studies. They are complemented by an experienced senior management team and seasoned board of directors.

"The Sonoma Biotherapeutics leadership are responsible for a significant portion of our understanding of the nature of Treg cells, their role in disease and their potential for use as a cell therapy," said Dr. Rick Klausner, CEO of Lyell Immunopharma and newly appointed Chair of the Sonoma Biotherapeutics Board of Directors. "Perhaps more importantly, they understand the requirements of a successful cell therapeutic and the corresponding challenges in defining the pathway to market. We look forward to a strong partnership between Lyell and Sonoma Biotherapeutics."

In this regard, Sonoma Biotherapeutics has entered into a strategic partnership with Lyell that provides both parties with access to technologies and know-how to enhance the durability, stability and specificity of cell therapies in their respective indications of focus. This partnership will further enable Sonoma's rapid translation of Treg therapies from target identification and discovery, through preclinical and clinical development.

Senior Management Team

Jeffrey Bluestone, PhD, Founder, CEO & PresidentFred Ramsdell, PhD, Founder & CSOPeter DiLaura, Chief Business & Strategy OfficerJoshua Beilke, MBA, PhD, VP Translational Development

Board of Directors

Rick Klausner, MD (Chair) Founder & CEO, Lyell Immunopharma, Inc.Maggie Wilderotter CEO, Grand Reserve Inn; former board member, Juno TherapeuticsToni Hoover, PhD Director, Strategy, Planning and Management for Global Health, Bill & Melinda Gates FoundationTerry Rosen, PhD CEO, Arcus BiosciencesDavid Moskowitz, PhD Principal, 8VC (observer)Jeffrey Bluestone, PhD, CEO & President, Sonoma Biotherapeutics

About Sonoma Biotherapeutics

Sonoma Biotherapeutics is a privately held, San Francisco and Seattle-based company leading the development of adoptive Treg therapies cell for autoimmune and degenerative diseases. Using next generation genome editing and target-specific cell therapy, Sonoma is focused on developing its best-in-class platform across the entire spectrum of Treg cell therapeutic capabilities. Founded by pioneers in Treg biology and cell therapy, the company brings together leading expertise and proprietary methodologies for the discovery and development of disease modifying and curative therapies.

Contact: media@sonomabio.com

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Sonoma Biotherapeutics launches with $40 million in Series A funding to advance regulatory T cell therapy in autoimmune and degenerative diseases -...

Cell Biology

Pedal to the Metal: Speeding Up Treatments for ALS – UANews

A therapeutic intervention for amyotrophic lateral sclerosis, better known as ALS or Lou Gehrig's disease, could be on the horizon thanks to unexpected findings by University of Arizona researchers.

ALS is the progressive degeneration of motor neurons that causes people to lose the ability to move and eventually speak, eat and breathe.

Within the neuronal cells of patients with ALS and other neurodegenerative diseases, two proteins TDP-43 and FUS are often found in bundles of molecular junk called aggregates, which can accumulate to deadly levels.

Its not clear yet if TDP-43 aggregates themselves are truly toxic or a sign that things have gotten really bad in a cell, and this is its last Hail Mary trying to keep things in order, said Ross Buchan, assistant professor of molecular and cellular biology and a member of the BIO5 Institute. These aggregates could possibly be toxic because they are trapping other useful molecules and not letting them do their job.

Buchan and his team set out to investigate how healthy cells clear harmful aggregates from the cell.

What they found was that the aggregates were being removed via endocytosis, which was surprising for two reasons. First, the textbook definition of endocytosis is a process in which proteins, nutrients and chemical signals from outside the cell are brought inside to be degraded and recycled by the lysosome. But in this case, endocytosis was working on aggregates that were already inside the cell. And second, theres already a mechanism, called autophagy, in place for recycling junk that originated from within a cell, yet endocytosis was doing what autophagy should have been doing instead.

Autophagy and also likely, although its still uncertain, endocytosis often slows as we age, and there are genes that are mutated in that pathway that are associated with some neurodegenerative diseases. So people thought the reason aggregates form when we get old, or when you have these diseases, is because that pathway isnt working very well, Buchan said.

Additionally, the accumulation of aggregates slows the endocytosis pathway further, creating a negative feedback loop within the cell.

If we genetically or chemically impede the pathway, then the TDP-43 protein accumulates and becomes super toxic. The cool thing, as far as a therapy for ALS is concerned, is that we can also do the reverse, Buchan said. We can make the endocytosis pathway work better by over-expressing parts of it, like putting the gas pedal down so it goes really fast. When we do that, then the TDP-43 aggregates are cleared really efficiently and its no longer toxic.

Many of the papers experiments were performed in yeast cells, but the general findings are likely translatable to human cells based on initial findings. Buchan called yeast a powerful genetic tool, for understanding cellular processes, including those in human disease.

While the results from Buchans lab are unexpected If I were to pull a textbook off the self, it would say endocytosis is for things that are outside the cell, not inside, so its still pretty heretical, he said there are other labs with data suggesting endocytosis can also clear already internalized proteins.

The next step is to determine how TPD-43 and FUS enter the endocytic pathway, and then to develop ways to make endocytosis work better in these cells.

There are genetic ways to do that, but not chemically at the moment, Buchan said. We think if we have a drug that inhibits the negative regulators of endocytosis, the pathway will go faster as a result. We have a couple ideas of where to start next.

The findings were published in the journal Molecular and Cellular Biology. Buchans co-authors include undergraduate Amanda Warner, former post-doctoral fellow Guangbo Liu, graduate student Aaron Byrd, former graduate student Fen Pei, assistant research scientist Eman Basha and former lab technician Allison Buchanan.

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Pedal to the Metal: Speeding Up Treatments for ALS - UANews

Cell Biology

Chopping Genes and Growing Brains – The LumberJack

Biology professor John Steele guided a cell biology lab his first year at HSU wherein he wanted to teach students that cells need nutrients to survive. After 48 hours, the lab discovered quite the opposite. James Gomez, a current student in the lab, had the opportunity to research more into the groundbreaking discovery.

In science, youre kinda looking for that unexpected stuff, Gomez said. Right after I came in, I was really excited to be a part of that. There was this thing that was happening that we particularly cant fully explain, and Im actually in the lab doing that science.

Steeles experiment for his class involved students starving the cells of nutrients to trigger a state of autophagy, which is when the cell starts to consume itself. Steele meant to emphasize that cells needed nutrients like amino acids and lipids to survive. It was assumed that starving cells of key nutrients eventually killed them.

Steele said the experiment was common, and was usually shut down after six to eight hours. Steele decided to run it for 48 hours instead, since that was the time between lab sections. When his class returned returned to the lab, rather than seeing a bunch of dead cells, they were decidedly more alive. The lab had made a discovery.

Despite the cells being in autophagy in Steeles experiment, they had stopped dividing and took on a strange morphology. Their metabolic rate was highthey were very much not dead.

Now the lab, including Gomez, are deep in research. The lab is introducing pathway inhibitors, or drugs, to block basic cell functions, narrowing down the essential and non-essential. The project is open-ended, as students methodically look at every cellular pathway to determine the needs of cells.

What I love about this project is that it was born here, Steele said. Nobody else that I know of is working on this, outside of HSU. Thats an awesome process to be a part of, where students get hands-on training in phenotypic genetic screening and drug screening, and we get to learn about the basic biology of cells in doing this.

Steele encourages the students in his lab to explore the boundaries of their knowledge. CRISPR, Cas9 and stem cell cultures are unique tools available to these students, and they offer an opportunity to think outside the box and do creative science.

Steeles lab combines bio-technologies using unique stem cell cultures and genome editing techniques. The lab cultures stem cellscells which can grow into any cell typeand chops up DNA using CRISPR, a revolutionary gene-clipping tool, to learn how rare neurodegenerative diseases develop in the brain.

There have been some really cool applications of CRISPR out there. And theyre just because somebody said, I wonder if we could do that? and they did.

Steeles graduate student Kyle Anthoney, on the other hand, is working on making a model of a rare disease called progressive supernucleogical palsy, which looks like a combination of Parkinsons and Alzheimers diseases. The disease is a tauopathic disease because a main characteristic of the disease is a buildup of the tau protein, which blocks some necessary cell functions. To understand the finer details of the disease, Anthoney developed a new method for growing neurosphere cell types into what is, effectively, a miniature brain.

Scientifically named 3D neural sphere cultures, these miniature brains offer a platform for researchers to study three types of brain cells at the same time. Anthoneys method allowed him to organically grow neurons, oligodendrocytes and astrocytes, three dominant cell types in the brain, from human stem cells, so they would develop naturally like they would in a growing brain.

Anthoneys research is up for review in a number of scientific publications and his name is on some breakthrough scientific papers. He is contributing to research about progressive supernucleogical palsy and other tauopathic diseases. His research concentrates the tau protein in a miniature brain to simulate the symptoms of progressive supernucleogical palsy, and he is exploring how the protein and disease impact his lab-grown brain cells.

There have been some really cool applications of CRISPR out there, Steele said. And theyre just because somebody said, I wonder if we could do that? and they did.

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Cell Biology

ID Literature and the Great Evolutionary Firewall – Discovery Institute

Peer-reviewed literature is supposed to be the gold standard in any given scientific field, though it both lets through junk science at times, and at others, excludes solid science, whether for ideological or other reasons. The gatekeepers are only human, prone to bias or wish fulfillment. The humans who police the gatekeepers are also prone to hallucinate. See a couple of posts on that subject from earlier this week, here and here.

These provisos having been stated, there is of course value in this literature. Thats why Evolution News spends so much time analyzing it. We havent talked about this in a while, but the body of peer-reviewed articles supporting intelligent design is impressive. You can find an extensive discussion of it here. Remember, this is just the literature supportive of ID. Criticism is valuable and significant too. Weve got a file of a hundred mainstream scientific papers that cite Michael Behe and his ID work. Yes, many are negative, but many are positive too.

In any case, as recent email inquiries have made clear, this body of published writing calls for some additional commentary.

First, do all of these articles use the term intelligent design explicitly? No. But dont let anyone tell you that that somehow disqualifies the articles in our bibliography as directly supporting ID. All of these papers are by ID sympathizers (at least one author, in each case) and they all make ID arguments or explicitly support ID. Some of them do use the term intelligent design but some use terms like teleological or goal-directed rather than explicitly saying intelligent design. The intended meaning is the same. Also, many of the articles provide explicit support for core ID concepts like complex and specified information, irreducible complexity, prescriptive information, and the like, even if they dont call it intelligent design.

Second, its true that not every journal is respected equally. But the fact that ID proponents are publishing legitimate ID-oriented ideas in journals at all is what counts. Journals like Cell, Nature, Science, and many other high-level publications are never going to publish an article not in this corner of the multiverse that is pro-ID or positively cites Michael Behe or Stephen Meyer or William Dembski, no matter how strong the evidence and no matter how good the article is. Those in the ID community are well aware that you can sometimes publish modest critiques of certain evolutionary ideas, but the moment that you suggest that intelligent design might be involved or that you speak favorably of an ID proponents work, the great evolutionary firewall goes up and it blocks the paper. Many ID-friendly scientists who have tried to publish have had such experiences. Biologist Jonathan Wells recalls an exchange with a journal editor:

In 2003 I submitted an article on an aspect of cell biology to a very prominent biology journal in the U.K. My article did not mention ID or cite ID authors, but it presented a hypothesis based on an ID perspective. The article successfully passed peer review after I responded to some questions by the reviewers, and the editor wrote to me that he was ready to publish it. But then he asked me whether I was the Jonathan Wells of intelligent design fame. When I answered in the affirmative he sent the article out for one last review, which was a contemptuous hatchet job from start to finish. With that in hand the editor rejected my article.

Even having been cited positively by ID advocates can harm a papers chances. Thats why Evolution News hesitates to discuss preprint articles like those at bioRxiv. An article there, that has not yet been peer-reviewed or published formally, can be rendered ritually impure if Darwinists see that ID proponents have praised it. The perversity and unfairness of this situation hardly needs underlining.

Third, remember the phenomenon in social media that is called subtweeting. This refers to criticizing people without naming them, often compared with talking about them covertly behind their back. From the Urban Diction: Indirectlytweetingsomething about someone without mentioning their name. Eventhoughtheir name is not mentioned, it isclearwho the person tweeting is referring to. It often happens that science journals subtweet about ID arguments, those of Meyer or Behe or Dembski, without having the courage, frankly, to name them. As an example, the many desperate attempts to offer theories explaining the Cambrian explosion, the geologically sudden eruption of animal phyla into the fossil record, evidently have Stephen Meyers book, Darwins Doubt, on their mind.

The point is this: If youre going to engage people on the topic of ID publications, dont let them force two false assumptions on you:

And these observations apply not only to intelligent design but to other terms that tend to start arguments. Cast your mind back to the famous Dover trial. The ACLU and anti-ID plaintiffs cited a paper, Long et al., 2003, which they told Judge John Jones showed how new genetic information could evolve. The problem? The paper did not contain the phrase new genetic information. It didnt even contain the term genetic information! Judge Jones cited the paper anyway to claim that the plaintiffs had demonstrated that evolution could produce new genetic information.

But that was OK. In fact, this is not a criticism of what they did because the paper certainly was relevant to discussing the origin of new genetic information, and the fact that the paper did not contain the term genetic information did not prevent it from bearing on the subject, which it did.

That having been said, in reality, the paper by Long and his colleagues is not very successful in showing how new information arises, although it is certainly relevant from an evolutionary perspective. If you would like to see some critiques of the paper, please read Chapter 11 of Darwins Doubt.We see again that word searches often say very little about the implications of a paper for evolution or ID. Whats needed, always, is honest, critical analysis, as we try to provide here.

Photo credit:Andrew Martin viaPixabay.

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ID Literature and the Great Evolutionary Firewall - Discovery Institute

Cell Biology

Sonoma Bio Launches With $40M to Take Cell Therapy Beyond Cancer – Xconomy

XconomySan Francisco

Cell therapies have reached the market as a new treatment option for some cancers. But the scientists of Sonoma Biosciences say this approach also holds promise for autoimmune disorders, and the biotech startup has unveiled $40 million in financing to develop its technology.

The investors in Sonomas Series A round of funding include Lyell Immunopharma, ARCH Venture Partners, Milky Way Ventures, and 8VC.

Cell therapy involves removing a patients immune cells, engineering them, and then infusing them back into the patient to perform their therapeutic tasks. The cancer cell therapies that have been approved by the FDA are made by engineering T cells, the frontline defenders of the immune system.

Sonoma, which splits its operations between South San Francisco and Seattle, is working with a different immune cell called a regulatory T cell (Treg). Whereas T cells target pathogens, Tregs target other immune cells, suppressing excessive immune responses, CEO and co-founder Jeff Bluestone tells Xconomy. Research by Sonomas scientific co-founders uncovered evidence, in studies in mice and humans, that the absence of these cells sparked the development of some autoimmune diseases. Those diseases led to death in about one year without a bone marrow transplant, Bluestone adds.

Sonoma is developing Treg therapies intended to shut down unwanted immune responses. The approach involves harvesting these cells from patients and engineering them with features that make them stable, durable, and targeted specifically to the site of inflammation. Those cells would then be infused into the patient to stop the autoimmune response. Bluestone says its too soon to talk about a lead disease target, but he adds that this approach has potential applications in rheumatoid arthritis, inflammatory bowel disease, and multiple sclerosis.

The hope is that a Sonoma cell therapy is a one-time treatment. Bluestone says that because these therapies are cells that multiply, they should survive in the patient on standby until theyre needed again to address an autoimmune response.

Theres another feature that could contribute to the longevity of a Treg treatment. When these cells shut down an autoimmune response, they influence other cells in the vicinity to join in, Bluestone explains. By educating these other cells to take up this immunosuppressive role, Bluestone says the effect of these therapies could be long lasting. But he cautions that the durability of a Treg therapy wont be known until more tests are done in humans.

Bluestones knowledge about Tregs stems from his own research. He and another Sonoma co-founder, Qizhi Tang, studied Tregs at the University of California, San Francisco, for 12 years. Their research included diabetes, organ transplantation, and lupus, among other conditions. That work led to small patient studies testing the technology for safety.

In addition to his UCSF research, Bluestone was the president and CEO of the Parker Institute for Cancer Immunotherapy. Over the course of a career that has bridged academia and industry, Bluestones immunology research has led to the development and commercialization of immunotherapies for organ transplants and cancer. He says he is joining Sonoma now because theres only so far that you can get in an academic lab if you want to impact peoples lives. Cell therapy could be the next major medicine for humans, he adds, and he wants to be involved as part of a company developing these treatments.

The other co-founders are Chief Scientific Officer Fred Ramsdell who, like Bluestone, joined Sonoma from the Parker Institute, and Alexander Rudensky, an immunologist at the Memorial Sloan Kettering Cancer Center. Ramsdell and Rudensky are credited as co-discoverers of the FOXP3 gene that is critical to the development and function of Tregs.

Bluestone says that Sonoma continues the Treg research that he and the other co-founders had done. The company also builds on the successes and failures in cancer cell therapy research. While those therapies can treat blood cancers, its been much harder to use them to treat solid tumors. Bluestone hopes that Lyell, a South San Francisco cell therapy company, can help the company get its therapies into tissues. In addition to being a Sonoma investor, Bluestone says Lyell will be a research partner, providing access to its technology and cell therapy insights.

Sonoma also aims to go beyond autoimmune diseases. Bluestone says the companys approach could potentially address degenerative disorders, such as amyotrophic lateral sclerosis and Alzheimers disease. In the nearer term, Bluestone says the company will use the funding to better understand Tregs.

The way were approaching this field is not to be in a hurry, in a sense of feeling this pressure or need to get into the clinic with these engineered cells as quickly as possible, he says. We want to spend the time to make sure were working with the best cells possible, that we understand the science and the biology, so that it has the best chance of success.

Public domain image by Flickr user NIH Image Gallery

Frank Vinluan is an Xconomy editor based in Research Triangle Park. You can reach him at fvinluan [[at]] xconomy.com.

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Sonoma Bio Launches With $40M to Take Cell Therapy Beyond Cancer - Xconomy

Cell Biology

Postdoctoral Research Associate – Department of Biosciences job with DURHAM UNIVERSITY | 195812 – Times Higher Education (THE)

The Role

Applications are invited for a Postdoctoral Research Associate to work on a project entitled

"Skin model engineering by harnessing the biomechanical forces exerted on skin cell nuclei".

As a collaboration between Drs Akis Karakesisoglou and Martin Goldberg, Department of Biosciences, Durham University and Steven Hyde, Oxford University we have designed new methodology to generate high quality in vitroskin models. The methodology works through using genetic engineering tools that re-program the biomechanical properties of skin cells.

We have gained funds from the Northern Accelerator (a research commercialisation collaboration between four North East Universities) to further develop the in vitro skin model and to commercialise the underlying technology.

The role of the post holder is to research and implement solutions in the fields of skin tissue engineering, skin tissue/cell biology and microscopy. The project will involve the creation and development of skin equivalent cell culture models using novel methods, then testing and analysing their structural and functional properties. The postholder will be helped by Drs Karakesisoglou, Goldberg and Hyde to find solutions and the candidate will need experience in the above fields to implement the solutions.

The post requires good skills in reporting research progress verbally, and in writing.

This post is fixed term for 9 months which is the extent of the currently available funding.

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Postdoctoral Research Associate - Department of Biosciences job with DURHAM UNIVERSITY | 195812 - Times Higher Education (THE)

Human Behavior

Human Behavior: The Complete Pocket Guide – iMotions

Introduction to Human Behavior

Academic and commercial researchers alike are aiming towards a deeper understanding of how humans act, make decisions, plan, and memorize. Advances in wearable sensor technology along with procedures for multi-modal data acquisition and analysis have lately been enabling researchers all across the globe to tap into previously unknown secrets of the human brain and mind.

Still, as emphasized by Makeig and colleagues (2009), the most pivotal challenge lies in the systematic observation and interpretation of how distributed brain processes support our natural, active, and flexibly changing behavior and cognition.

We all are active agents, continuously engaged in attempting to fulfill bodily needs and mental desires within complex and ever-changing surroundings, while interacting with our environment. Brain structures have evolved that support cognitive processes targeted towards the optimization of outcomes for any of our body-based behaviors.

N.B. this post is an excerpt from our Human BehaviorGuide. You can download your free copy below and get even more insights into human behavior.

In scientific research, human behavior is a complex interplay of three components: actions, cognition, and emotions.

Sounds complicated? Lets address them one by one.

An action denotes everything that can be observed, either with bare eyes or measured by physiological sensors. Think of an action as an initiation or transition from one state to another at a movie set, the director shouts action for the next scene to be filmed.

Behavioral actions can take place on various time scales, ranging from muscular activation to sweat gland activity, food consumption, or sleep.

Cognitions describe thoughts and mental images you carry with you, and they can be both verbal and nonverbal. I have to remember to buy groceries, or Id be curious to know what she thinks of me, can be considered verbal cognitions. In contrast, imagining how your house will look like after remodeling could be considered a nonverbal cognition.

Cognitions comprise skills and knowledge knowing how to use tools in a meaningful manner (without hurting yourself), sing karaoke songs or being able to memorize the color of Marty McFlys jacket in Back to the Future (its red).

Commonly, an emotion is any relatively brief conscious experience characterized by intense mental activity, and a feeling that is not characterized as resulting from either reasoning or knowledge. This usually exists on a scale, from positive (pleasurable) to negative (unpleasant).

Other aspects of physiology that are indicative of emotional processing such as increased heart rate or respiration rate caused by increased arousal are usually hidden to the eye. Similar to cognitions, emotions cannot be observed directly. They can only be inferred indirectly by tracking facial electromyographic activity (fEMG),analyzing facial expressions, monitoring arousal using ECG, galvanic skin response (GSR), respiration sensors, or self-reported measures, for example.

Actions, cognitions and emotions do not run independently of each other their proper interaction enables you to perceive the world around you, listen to your inner wishes and respond appropriately to people in your surroundings. However, it is hard to tell what exactly is cause and effect turning your head (action) and seeing a familiar face might cause a sudden burst of joy (emotion) accompanied by an internal realization (cognition):

action = emotion (joy) + cognition (hey, theres Peter!)

In other cases, the sequence of cause and effect might be reversed: Because youre sad (emotion) and ruminating on relationship issues (cognition), you decide to go for a walk to clear your head (action).

emotion (sadness) + cognition (I should go for a walk) = action

Humans are active consumers of sensory impressionsYou actively move your body to achieve cognitive goals and desires, or to get into positive (or out of negative) emotional states. In other words: While cognition and emotion cannot be observed directly, they certainly drive the execution of observable action. For example, through moving your body to achieve cognitive goals and desires, or to get into positive (or out of negative) emotional states.

Cognitions are specific to time and situationsNew information that you experience is adapted, merged and integrated into your existing cognitive mindset. This allows you to flexibly adapt to and predict how events in the current environment may be influenced by your actions. Whenever you decide to carry out an action, you accomplish the decision in a timely, environment- and situation-appropriate manner. Put differently: Your cognitive system has to manage the dynamic interplay of flexibility and stability.

The former is important as you have to couple responses dynamically to stimuli, dependent on intentions and instructions. This allows you to respond to one and the same stimulus in near-unlimited ways. Stability, by contrast, is crucial for maintaining lasting stimulus-response relationships, allowing you to respond consistently to similar stimuli.

Imagination and abstract cognition are body-basedEven abstract cognitions (devoid of direct physical interaction with the environment) are body-based. Imagining limb movements triggers the same brain areas involved when actually executing the movements. When you rehearse material in working memory, the same brain structures used for speech perception and production are activated (Wilson, 2001).

When we talk about behavior, we need to consider how it is acquired. Learning denotes any acquisition process of new skills and knowledge, preferences, attitudes and evaluations, social rules and normative considerations.

You surely have heard of the nature nurture debate in the past, there has been quite some fighting about whether behavior was solely driven by genetic predispositions (nature) or environmental factors (nurture).

Today, its no longer a question of either/or. There simply is too much evidence for the impact of nature and nurture alike behavior is considered to be established by the interplay of both factors.

Current theoretical frameworks also emphasize the active role of of the agent in acquiring new skills and knowledge. You are able to develop and change yourself through ongoing skill acquisition throughout life, which can have an impact on a neurological level. Think of it as assigning neuroscientific processes to the phrase practice makes perfect.

Classical conditioning refers to a learning procedure in which stimulus-response pairings are learned seeing tasty food typically triggers salivation (yummy!), for example. While food serves as unconditioned stimulus, salivation is the unconditioned response.

Unconditioned stimulus -> unconditioned response

Seeing food -> salivation

If encountering food is consistently accompanied by a (previously) neutral stimulus such as ringing a bell, a new stimulus-response pairing is learned.

unconditioned stimulus + conditioned stimulus -> unconditioned response

seeing food + hearing bell -> salivation

The bell becomes a conditioned stimulus and is potent enough to trigger salivation even in absence of the actual food.

conditioned stimulus > response

hearing bell -> salivation

Described as generalization, this learning process was first studied by Ivan Pavlov and team (1927) through experiments with dogs, which is why classical conditioning is also referred to as Pavlovian conditioning.

Today, classical conditioning is one of the most widely understood basic learning processes.

Operant conditioning, also called instrumental conditioning, denotes a type of learning in which the strength of a behavior is modified by the consequences (reward or punishment), signaled via the preceding stimuli.

In both operant and classical conditioning behavior is controlled by environmental stimuli however, they differ in nature. In operant conditioning, behavior is controlled by stimuli which are present when a behavior is rewarded or punished.

Operant conditioning was coined by B.F. Skinner. As a behaviorist, Skinner believed that it was not really necessary to look at internal thoughts and motivations in order to explain behavior. Instead, he suggested to only take external, observable causes of human behavior into consideration.

According to Skinner, actions that are followed by desirable outcomes are more likely to be repeated while those followed by undesirable outcomes are less likely to be repeated. In this regard, operant conditioning relies on a fairly simple premise: Behavior that is followed by reinforcement will be strengthened and is more likely to occur again in the future.

The key concepts of operant conditioning are:

These learning theories give guidance for knowing how we gather information about the world. The way in which we learn is both emotionally and physiologically appraised. This will have consequences for how we act, and carry out behaviors in the future what we attend to, and how it makes us feel.

While behavior is acquired through learning, whether the acting individual decides to execute an action or withhold a certain behavior is dependent on the associated incentives, benefits and risks (if Peter was penalized for doing this, I certainly wont do it!).

But which are the factors driving our decisions? Theories such as social learning theory provide a base set of features, but one of the most influential psychological theoriesaboutdecision-makingactually has its origins in an economics journal.

In 1979, Daniel Kahneman & Amos Tversky published a paper proposing a theoretical framework called the Prospect Theory. This laid the foundations for Kahnemans later thoughts and studies on human behavior, that was summarized in his bestselling bookThinking, Fast and Slow.

Kahnemans theories were also concerned with how people process information. He proposed that there are two systems which determine how we make decisions: System 1 which is fast but relatively inaccurate, and system 2 which is slow but more accurate.

The theory suggests that our everyday decisions are carried out in one of these two ways, from buying our morning coffee, to making career choices. We will use different approaches depending on the circumstances.

Human behavior and decision-making are heavily affected by emotions even in subtle ways that we may not always recognize. After making an emotionally-fueled decision, we tend to continue to use the imperfect reasoning behind it, and a mild incidental emotion in decision-making can live longer than the emotional experience itself as pointed out by Andrade & Ariely (2009).

An example of mood manipulation affecting decision making was completed by researchers who wanted to know how a willingness to help could be affected by positive feelings.

To study their question, they placed a Quarter (25ct) clearly visible in a phone booth (yes, these things actually existed!) and waited for passers-by to find the coin. An actor working on behalf of the psychologist stepped in, asking to take an urgent phone call. Study participants who actually found the coin were significantly happier, allowing the confederate to take the call, while those who didnt find the coin were unaffected, and more likely to say no (Isen & Levin, 1972).

Research on human behavior addresses how and why people behave the way they do. However, as you have seen in the previous sections, human behavior is quite complex as it is influenced, modulated and shaped by multiple factors which are often unrecognized by the individual: Overt or covert, logical or illogical, voluntary or involuntary.

Conscious vs. unconscious behaviorConsciousness is a state of awareness for internal thoughts and feelings as well for proper perception for and uptake of information from your surroundings.

A huge amount of our behaviors are guided by unconscious processes. Just like an iceberg, there is a great amount of hidden information, and only some of it is visible with the naked eye.

Overt vs. covert behaviorOvert behavior describes any aspects of behavior that can be observed, for example body movements or (inter-)actions. Also, physiological processes such as blushing, facial expressions or pupil dilation might be subtle, but can still be obeserved. Covert processes are thoughts (cognition), feelings (emotion) or responses which are not easily seen. Subtle changes in bodily processes, for instance, are hidden to the observers eye.

In this case, bio- or physiological sensors are used to aid the observation with quantitative measures as they uncover processes that are covert in the first place. Along this definition, EEG, MEG, fMRI and fNIRS all monitor physiological processes reflecting covert behavior.

Rational vs. irrational behaviorRational behavior might be considered any action, emotion or cognition which is pertaining to, influenced or guided by reason. In contrast, irrational behavior describes actions that are not objectively logical.

Patients suffering from phobias often report an awareness for their thoughts and fears being irrational (I know that the spider cant harm me) albeit they still cannot resist the urge to behave in a certain way.

Voluntary vs. involuntary behaviorVoluntary actions are self-determined and driven by your desires and decisions. By contrast, involuntary actions describe any action made without intent or carried out despite an attempt to prevent it.In cognitive-behavioral psychotherapy, for example, patients are exposed to problematic scenarios, also referred to as flooding, such as spiders, social exhibition or a transatlantic plane ride.

Many of our behaviors appear to be voluntary, rational, overt, and conscious yet they only represent the tip of the iceberg for normal human behavior. The majority of our actions are involuntary, potentially irrational, and are guided by our subconscious. The way to access this other side of behavior is to examine the covert behaviors that occur as a result.

In order to describe and interpret human behavior, academic and commercial researchers have developed intricate techniques allowing for the collection of data indicative of personality traits, cognitive-affective states and problem solving strategies.

In experimental setups, specific hypotheses about stimulus-response relationships can be clarified. Generally, research techniques employed by scientists can be classified into qualitative and quantitative procedures.

Qualitative studiesgather non-numerical insights, for example by analyzing diary entries, using open questionnaires, unstructured interviews or observations. Qualitative field / usability studies, for example, aim towards understanding how respondents see the world and why they react in a specific way rather than counting responses and analyzing the data statistically.

Quantitative studies characterize statistical, mathematical or computational techniques using numbers to describe and classify human behavior. Examples for quantitative techniques include structured surveys, tests as well as observations with dedicated coding schemes. Also, physiological measurements from EEG, EMG, ECG, GSR and other sensors produce quantitative output, allowing researchers to translate behavioral observations into discrete numbers and statistical outputs.

Behavioral observation is one of the oldest tools for psychological research on human behavior. Researchers either visit people in their natural surroundings (field study) or invite individuals or groups to the laboratory.

Observations in the field have several benefits. Participants are typically more relaxed and less self-conscious when observed at home, at school or at the workplace. Everything is familiar to them, permitting relatively unfiltered observation of behavior which is embedded into the natural surroundings of the individual or group of interest.

However, theres always the risk of distraction shouting neighbors or phones ringing. Field observations are an ideal starting point of any behavioral research study. Just sitting and watching people offers tremendous amounts of insights if youre able to focus on a specific question or aspect of behavior.

Observation in the laboratory, by contrast, allows much more experimental control. You can exclude any unwanted aspects and completely ban smart phones, control the room layout and make sure to have everything prepared for optimal recording conditions (correct lighting conditions, ensuring a quiet environment, and so on).

You can create near-realistic laboratory environments building a typical family living room, office space or creative zone, for example, to make respondents feel at ease and facilitating more natural behavior.

Surveys and questionnaires are an excellent tool to capture self-reported behaviors and skills, mental or emotional states or personality profiles of your respondents. However, questionnaires are always just momentary snapshots and capture only certain aspects of a persons behavior, thoughts and emotions.

Surveys and questionnaires typically measure what Kahneman would describe as system 2 processes thoughts that are carried out slowly and deliberately. System 1 processes thoughts that are fast and automatic can be measured by other methods that detect quick physiological changes.

In market research, focus groups typically consist of a small number of respondents (about 415) brought together with a moderator to focus on beliefs and attitudes towards a product, service, concept, advertisement, idea or packaging. Focus groups are qualitative tools as their goal is to discuss in the group instead of coming to individual conclusions.

What are the benefits of a product, what are the drawbacks, where could it be optimized, who are ideal target populations? All of these questions can be addressed in a focus group.

While surveys and focus groups can be instrumental in understanding our conscious thoughts and emotions, there is more to human behavior than meets the eye. The subconscious mind determines how our behavior is ultimately carried out, and only a small fraction of that is accessible from traditional methodologies using surveys and focus groups.

As some researchers have claimed, up to 90% of our actions are guided by the subconscious. While the other 10% is important, it is clear that there is much to gain by probing further than what is tested by traditional methods.

Modern approaches aim to explore the hidden and uncharted territory of the subconscious, by measuring reliable outputs that provide deeper information about what someone is really thinking.

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Human Behavior: The Complete Pocket Guide - iMotions