Lifeboat Foundation

Cell freezing (cryopreservation)—which is essential in cell transfusions as well as basic biomedical research—can be dramatically improved using a new polymeric cryoprotectant, discovered at the University of Warwick, which reduces the amount of ‘anti-freeze’ needed to protect cells.

The ability to freeze and store cells for cell-based therapies and research has taken a step forward in the paper “A synthetically scalable poly(ampholyte) which dramatically Enhances Cellular Cryopreservation.” published by the University of Warwick’s Department of Chemistry and Medical School in the journal Biomacromolecules. The new polymer material protects the cells during freezing, leading to more cells being recovered and less solvent-based antifreeze being required.

Cryopreservation of cells is an essential process, enabling banking and distribution of cells, which would otherwise degrade. The current methods rely on adding traditional ‘antifreezes’ to the cells to protect them from the cold stress, but not all the cells are recovered and it is desirable to lower the amount of solvent added.

Scientists are “extremely concerned” by a bacterium resistant to antibiotics of last resort.

Victoria Gray, 34, of Forest, Miss., has volunteered for one of the most anticipated medical experiments in decades: the first attempt to use the gene-editing technique CRISPR to treat a genetic disorder in the U.S. Meredith Rizzo/NPR hide caption.

The art of tattooing may have found a diagnostic twist. A team of scientists in Germany have developed permanent dermal sensors that can be applied as artistic tattoos. As detailed in the journal Angewandte Chemie, a colorimetric analytic formulation was injected into the skin instead of tattoo ink. The pigmented skin areas varied their color when blood pH or other health indicators changed.

Researchers from the Beijing Institute of Brain Disorders have discovered a new method of using exosomes to deliver aptamers that prevent the accumulation of α-synuclein aggregates, which are the cause of Parkinson’s disease [1].

α-Synuclein Aggregates

Like Alzheimer’s, Parkinson’s disease is characterized by protein aggregation caused by a loss of proteostasis, one of the hallmarks of aging. In order for the brain to function properly, non-aggregated α-synuclein proteins are needed in order to facilitate the release of dopamine, a neurotransmitter, in nerve cell synapses. α-synuclein only becomes a problem when proteostasis fails and the proteins misfold, aggregate, and accumulate.

Most soft robots are controlled manually or pre-programmed but the lenses mimic the natural electric signals in the human eyeball that are active even when the eye itself is closed.

But getting human cells to grow in another species is not easy. Nakauchi and colleagues announced at the 2018 American Association for the Advancement of Science meeting in Austin, Texas that they had put human iPS cells into sheep embryos that had been engineered not to produce a pancreas. But the hybrid embryos, grown for 28 days, contained very few human cells, and nothing resembling organs. This is probably because of the genetic distance between humans and sheep, says Nakauchi.

The research could eventually lead to new sources of organs for transplant, but ethical and technical hurdles need to be overcome.

Medicine has a “Goldilocks” problem. Many therapies are safe and effective only when administered at just the right time and in very precise doses – when given too early or too late, in too large or too small an amount, medicines can be ineffective or even harmful. But in many situations, doctors have no way of knowing when or how much to dispense.

Now, a team of bioengineers led by UC San Francisco’s Hana El-Samad, PhD, and the University of Washington’s David Baker, PhD, have devised a remarkable solution to this problem – “smart” cells that behave like tiny autonomous robots which, in the future, may be used to detect damage and disease, and deliver help at just the right time and in just the right amount.

Skeletal muscle is important not only for locomotion but also for regulating metabolic function. Lahiri et al. studied the interactions between the gut microbiota and skeletal muscle in mice. They identified genes and signaling pathways involved in the regulation of skeletal muscle mass and function that responded to cues from the gut microbiota. Additional biochemical and functional analysis also revealed the influence of the gut microbiota on the function of neuromuscular junctions. These findings open the door to a better understanding of the role of the gut microbiota in the mechanisms underlying loss of muscle mass.

The functional interactions between the gut microbiota and the host are important for host physiology, homeostasis, and sustained health. We compared the skeletal muscle of germ-free mice that lacked a gut microbiota to the skeletal muscle of pathogen-free mice that had a gut microbiota. Compared to pathogen-free mouse skeletal muscle, germ-free mouse skeletal muscle showed atrophy, decreased expression of insulin-like growth factor 1, and reduced transcription of genes associated with skeletal muscle growth and mitochondrial function. Nuclear magnetic resonance spectrometry analysis of skeletal muscle, liver, and serum from germ-free mice revealed multiple changes in the amounts of amino acids, including glycine and alanine, compared to pathogen-free mice. Germ-free mice also showed reduced serum choline, the precursor of acetylcholine, the key neurotransmitter that signals between muscle and nerve at neuromuscular junctions.