Lifeboat Foundation

A NIAID-funded study suggests a strategy to mitigate harmful side effects of nanoparticles in medicine. The researchers showed in animal models that a lab-made molecule safely prevented nanomedicines from activating a set of immune-system proteins called the complement system and causing negative side effects. This is significant because when nanoparticles activate complement, the resulting immune response can not only cause an adverse reaction, but also reduce the efficacy of nanomedicines.

More than 60,000 women in the U.S. get this type of cancer each year. Find out more about the symptoms and how it’s diagnosed and treated.

Breast changes are very common, and most breast changes are not cancer. Our health guide for women explains:

A breast lump may be benign or a symptom of breast cancer. Learn about follow-up after an abnormal mammogram. See pictures of breast cancer, cysts, and calcifications. Find out symptoms for benign breast conditions, precancers, and DCIS.

It’s been a month since a Maryland man became the second person to receive a transplanted heart from a pig — and hospital video released Friday shows he’s working hard to recover.

Lawrence Faucette was dying from heart failure and ineligible for a traditional heart transplant when doctors at the University of Maryland School of Medicine offered the highly experimental surgery.

In the first glimpse of Faucette provided since the Sept. 20 transplant, hospital video shows physical therapist Chris Wells urging him to push through a pedaling exercise to regain his strength.

Unfortunately, these precise cell arrangements are also why artificial muscles are difficult to recreate in the lab. Despite being soft, squishy, and easily damaged, our muscles can perform incredible feats—adapt to heavy loads, sense the outside world, and rebuild after injury. A main reason for these superpowers is alignment—that is, how muscle cells orient to form stretchy fibers.

Now, a new study suggests that the solution to growing better lab-grown muscles may be magnets. Led by Dr. Ritu Raman at the Massachusetts Institute of Technology (MIT), scientists developed a magnetic hydrogel “sandwich” that controls muscle cell orientation in a lab dish. By changing the position of the magnets, the muscle cells aligned into fibers that contracted in synchrony as if they were inside a body.

The whole endeavor sounds rather Frankenstein. But lab-grown tissues could one day be grafted into people with heavily damaged muscles—either from inherited diseases or traumatic injuries—and restore their ability to navigate the world freely. Synthetic muscles could also coat robots, providing them with human-like senses, flexible motor control, and the ability to heal after inevitable scratches and scrapes.

A study published today by scientists from Harvard University and epigenetic research company TruDiagnostic has shed light on the reasons why our bodies are aging on a cellular level, laying the foundations for medical based treatment options to reduce the risk of age-related death and disease in highly targeted ways.

Longevity. Technology: Age is the number one risk factor for most chronic diseases and death across the world. Epigenetics (or the way our genes are put to use throughout our bodies) has emerged as a crucial method of evaluating health, and while previous DNA methylation clocks could determine how advanced one’s body has aged, they have not yet been able to provide information to the reasons why someone might have accelerated or decelerated aging outcomes.

“In our research, we set out to create the best method to quantify the biological aging process. However, aging is extremely complex,” explains Harvard Medical School Associate Professor Dr Jessica Lasky-Su. “To solve this issue of complexity, our approach was to gather data across multiple sources of information. We chose to do this by building one of the most robust aging datasets in the world by quantifying patients’ proteomics, metabolomics, clinical histories and DNA methylation.”

Neurons, the main cells that make up our brain and spinal cord, are among the slowest cells to regenerate after an injury, and many neurons fail to regenerate entirely. While scientists have made progress in understanding neuronal regeneration, it remains unknown why some neurons regenerate and others do not.

Using single-cell RNA sequencing, a method that determines which genes are activated in individual cells, researchers from University of California San Diego School of Medicine have identified a new biomarker that can be used to predict whether or not neurons will regenerate after an injury. Testing their discovery in mice, they found that the biomarker was consistently reliable in… More.

Researchers from University of California San Diego have identified a new biomarker that can predict whether or not neurons will regenerate after an injury. The findings could help scientists develop regenerative therapies for spinal cord injuries and other neurological conditions.

Before epilepsy was understood to be a neurological condition, people believed it was caused by the moon, or by phlegm in the brain. They condemned seizures as evidence of witchcraft or demonic possession, and killed or castrated sufferers to prevent them from passing tainted blood to a new generation.

Today we know epilepsy is a disease. By and large, it’s accepted that a person who causes a fatal traffic accident while in the grip of a seizure should not be charged with murder.

That’s good, says Stanford University neurobiologist Robert Sapolsky. That’s progress. But there’s still a long way to go.

Continue reading “Stanford scientist, after decades of study, concludes: We don’t have free will” »

Researchers from University of California San Diego School of Medicine have used single-cell RNA sequencing (scRNA-seq) to identify a pattern of gene expression that can be used to predict whether or not neurons will regenerate after an injury. Tests in mice showed that this “Regeneration Classifier” was consistently reliable in predicting the regeneration potential of neurons across the nervous system and at different developmental stages. Conditional gene deletion then validated a role for NFE2L2 (or NRF2), a master regulator of antioxidant response, in corticospinal tract regeneration.

“Single-cell sequencing technology is helping us look at the biology of neurons in much more detail than has ever been possible, and this study really demonstrates that capability,” said senior author Binhai Zheng, PhD, professor in the Department of Neurosciences at UC San Diego School of Medicine. “What we’ve discovered here could be just the beginning of a new generation of sophisticated biomarkers based on single-cell data.” Zheng and colleagues reported on their findings in Neuron, in a paper titled “Deep scRNA sequencing reveals a broadly applicable Regeneration Classifier and implicates antioxidant response in corticospinal axon regeneration.” In their paper the team concluded, “Our data demonstrate a universal transcriptomic signature underlying the regenerative potential of vastly different neuronalpopulations and illustrate that deep sequencing of only hundreds of phenotypically identified neurons has the power to advance regenerative biology.”

Neurons are among the slowest cells to regenerate after an injury. While scientists have made progress in understanding neuronal regeneration, it remains unknown why some neurons regenerate and others do not.