More Precise Control Over Stem Cells Using Material Screening Method

When it comes to delivering genes to living human tissue, the odds of success come down the molecule. The entire therapy – including the tools used to bring new genetic material into a cell – must have predictable effects.

Now, a new screening process will simplify non-viral transfection, providing a method researchers and clinicians use to find an optimal set of biomaterials to deliver genes to cells.


Developed by William Murphy, the Harvey D. Spangler professor of biomedical engineering at the University of Wisconsin-Madison, the method gives researchers greater control over how cells react to the gene delivery mechanism. The broader implication is more nuanced, effective control over cell behavior. “We’ve been exploring using this concept for reprogramming of adult cells, as well as controlling differentiation of stem cell types,” Murphy says.


Murphy and his collaborators published news of their advance in a recent issue of Nature Scientific Reports.*


In a current successful approach, researchers use specialized viruses to deliver genetic material to cells. While efficient, that method also carries a greater risk of turning on unwanted genes or provoking an immune response from the body – making it less attractive for sensitive biomedical applications like controlling stem cell behavior, says Murphy.


His team has developed a process that does not rely on viruses. Rather, the researchers can grow specific calcium phosphate coatings that serve as a medium via which genetic material can be delivered to cells more efficiently. By matching a coating to a specific application for delivering genes, Murphy has seen up to a 70-fold increase in successful expression of those genes in human stem cells.


“From an application standpoint, the advance could be really impactful, and could enable gene delivery to become an integral part of medical device design and tissue engineering applications,” says Murphy.


The process could be critical to further advances in regenerative medicine. Since researchers can apply it to any size or shape of tissue engineering structure, it could help provide engineers with a simpler way to build the complex tissue structures required to deliver next-generation drug screening and patient therapies.


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The Affordable Care Act and Reproductive Health

The new Journal of Health Politics, Policy, and Law appeared in my mailbox. It includes a useful symposium on the policy and politics of reproductive health:

Lynn Paltrow and Jeanne Flavin, “Arrests of and Forced Interventions on Pregnant Women in the United States, 1973–2005: Implications for Women’s Legal Status and Public Health.”

Miranda Waggoner, “Motherhood Preconceived: The Emergence of the Preconception Health and Health Care Initiative.”

Amanda Dennis, Kelly Blanchard, Denisse Córdova, Britt Wahlin, Jill Clark, Karen Edlund, Jennifer McIntosh, and Lenore Tsikitas, “What Happens to the Women Who Fall through the Cracks of Health Care Reform? Lessons from Massachusetts.”

Amy Dworsky, Kym Ahrens, and Mark Courtney. “Health Insurance Coverage and Use of Family Planning Services among Current and Former Foster Youth: Implications of the Health Care Reform Law.”

Debra Stulberg. “The Patient Protection and Affordable Care Act and Reproductive Health: Harnessing Data to Improve Care.”

Oh yeah. Here’s one more: Adam Sonfield and Harold Pollack on reproductive health issues here:

After nearly a century of failed or incomplete legislative efforts, the Patient Protection and Affordable Care Act (PPACA), enacted by Congress in March 2010, establishes the principle that every American is entitled to affordable and effective health insurance coverage regardless of income or health status. Although many aspects of the act have received broad attention, its impact on reproductive health has received considerably less scrutiny, except when debated through the specific lens of particularly polarized ideological concerns. If fully implemented as planned, the PPACA has the potential to improve reproductive health in the United States in at least three ways: increasing the number of women and men with insurance coverage; increasing the value of insurance coverage for addressing reproductive health needs; and improving access to reproductive health services and information more generally. Several PPACA provisions stand out as having particular importance for reproductive health, including Medicaid family planning expansions, standards for an essential health benefits package, expanded coverage for contraception and other clinical preventive services, and teen pregnancy prevention programs. All these potential gains, however, are threatened by political, economic, and logistical challenges to the PPACA and by flaws in the legislation itself.

Our piece was almost two years in the making on the slow academic brew. I’m struck by the number of issues here that never reached the public discourse. The abortion issue dominated during the legislative debate. Then religious institutions’ coverage of contraception consumed much of the oxygen during the 2012 campaign. Much more was going on. And there were many more reproductive health provisions contained within the apparent junk DNA of the health reform bill.

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Relationship Between Obesity, Heart Disease And Hypertension

Obesity, heart disease, and high blood pressure (hypertension) are all related, but understanding the molecular pathways that underlie cause and effect is complicated.

A new University of Iowa study identifies a protein within certain brain cells as a communications hub for controlling blood pressure, and suggests that abnormal activation of this protein may be a mechanism that links cardiovascular disease and obesity to elevated blood pressure.


“Cardiovascular diseases are the leading cause of death worldwide, and hypertension is a major cardiovascular risk factor,” says Kamal Rahmouni, UI associate professor of pharmacology and internal medicine, and senior study author. “Our study identifies the protein called mTORC1 in the hypothalamus as a key player in the control of blood pressure. Targeting mTORC1 pathways may, therefore, be a promising strategy for the management of cardiovascular risk factors.”


The hypothalamus is a small region of the brain that is responsible for maintaining normal function for numerous bodily processes, including blood pressure, body temperature, and glucose levels. Signaling of mTORC1 protein in the hypothalamus has previously been shown to affect food intake and body weight.


The new study, which was published in the journal Cell Metabolism, shows that the mTORC1 protein is activated by small molecules and hormones that are associated with obesity and cardiovascular disease, and this activation leads to dramatic increases in blood pressure.


Leucine is an amino acid that we get from food, which is known to activate mTORC1. The UI researchers showed that activating mTORC1 in rat brains with leucine increased activity in the nerves that connect the brain to the kidney, an important organ in blood pressure control. The increased nerve activity was accompanied by a rise in blood pressure. Conversely, blocking this mTORC1 activation significantly blunted leucine’s blood pressure-raising effect.


This finding may have direct clinical relevance as elevated levels of leucine have been correlated with an increased risk of high blood pressure in patients with cardiovascular disease.


“Our new study suggests a mechanism by which leucine in the bloodstream might increase blood pressure,” Rahmouni says.


Previous work has also suggested that mTORC1 is a signaling hub for leptin, a hormone produced by fat cells, which has been implicated in obesity-related hypertension.


Rahmouni and his colleagues showed that leptin activates mTORC1 in a specific part of the hypothalamus causing increased nerve activity and a rise in blood pressure. These effects are blocked by inhibiting activation of mTORC1.


“Our study shows that when this protein is either activated or inhibited in a very specific manner, it can cause dramatic changes in blood pressure,” Rahmouni says. “Given the importance of this protein for the control of blood pressure, any abnormality in its activity might explain the hypertension associated with certain conditions like obesity and cardiovascular disease.”


Rahmouni and his team hope that uncovering the details of the pathways linking mTORC1 activation and high blood pressure might lead to better treatments for high blood pressure in patients with cardiovascular disease and obesity.


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Gene Evolution Accelerated By Head-On Collisions Between DNA-Code Reading Machineries

Bacteria appear to speed up their evolution by positioning specific genes along the route of expected traffic jams in DNA encoding. Certain genes are in prime collision paths for the moving molecular machineries that read the DNA code, as University of Washington scientists explain in the journal Nature.

The spatial-organization tactics their model organism, Bacillus subtilis, takes to evolve and adapt might be imitated in other related Gram-positive bacteria, including harmful, ever-changing germs like staph, strep, and listeria, to strengthen their virulence or cause persistent infections. The researchers think that these mechanisms for accelerating evolution may be found in other living creatures as well.


Replication – the duplicating of the genetic code to create a new set of genes – and transcription – the copying of DNA code to produce a protein – are not separated by time or space in bacteria. Therefore, clashes between these machineries are inevitable. Replication traveling rapidly along a DNA strand can be stalled by a head-on encounter or same-direction brush with slower-moving transcription.


The senior authors of the study, Houra Merrikh, UW assistant professor of microbiology, and Evgeni Sokurenko, UW professor of microbiology, and their research teams are collaborating to understand the evolutionary consequences of these conflicts. The major focus of Merrikh and her research team is on understanding mechanistic and physiological aspects of conflicts in living cells – including why and how these collisions lead to mutations.


Impediments to replication, they noted, can cause instability within the genome, such as chromosome deletions or rearrangements, or incomplete separation of genetic material during cell division. When dangerous collisions take place, bacteria sometimes employ methods to repair, and then restart, the paused DNA replication, Merrikh discovered in her earlier work at the Massachusetts Institute of Technology.


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Point vs. plane

OK, so the position of the sign implies that at MIT, it’s some kind of bizarro world where hordes of drunk people stumble out of labs, rather than hordes of drunk people bumbling into labs from the main campus. Wouldn’t you expect it to be more the latter?

Heck, maybe not. It’s been some time since I’ve been in school. But if I were at MIT, I’d be more likely to knock a few beers back at the Cambridge Brewing Company and then stagger into some engineering lab.

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