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Category: biotech/medical – Page 2,716

NAD+ Regulates the Creation of Fat Cells

After NAD+ is consumed, it is broken down into nicotinamides and ADP-ribose; the researchers concluded that this means that NAD+ must be resynthesized following this in order for normal cellular functions to continue. This converges with previous studies, which suggest that NAD+ decline leads to changes in metabolism and an increased risk factor for some diseases; this typically happens as the result of aging, as NAD+ levels begin to fall.

With this in mind, the research team thought that cellular metabolism and gene regulation were potentially connected to NAD+ synthesis. They discovered evidence suggesting that compartmentalized NAD+ synthesis and the subsequent consumption are integrated with glucose metabolism and adipogenic transcription as part of the adipocyte differentiation process.

NAD+ synthesis acts as a mediator of PARP-1-regulated transcription during the differentiation of adipocytes, linking cellular metabolism and the adipogenic transcription process. During adipogenesis, nuclear NAD+ levels fall, causing the induction of NMNAT-2, the cytoplasmic NAD+ synthase. This increased level of NMNAT-2 then reduces the availability of NMN and leads to a reduction of nuclear NAD+ synthesis via NMNAT-1. The drop in NAD+ levels then results in decreased PARP-1 activity, which then reduces levels of inhibitory ADP-ribosylation of the adipogenic transcription factor C/EBPβ. Reduced ADP-ribosylation of C/EBPβ means that it is able to bind its target genes, thus promoting the differentiation of preadipocytes into adipocytes. In other words, a decline of NAD+ encourages an increase of preadipocytes turning into adipocyte fat cells.

Ignore the hype over big tech. Its products are mostly useless

Despite this, a regular ritual of hype and hysteria is now built into the news cycle. Every now and again, at some huge auditorium, a senior staff member at one of the big firms based in northern California – ordinarily a man – will take the stage dressed in box-fresh casualwear, and inform the gathered multitudes of some hitherto unimagined leap forward, supposedly destined to transform millions of lives. (There will be whoops and gasps in response, and a splurge of media coverage – before, in the wider world, a palpable feeling of anticlimax sets in.)

It’s years since Silicon Valley gave us a game-changer. Instead, from curing disease to colonies on Mars, we’re fed overblown promises, says Guardian columnist John Harris.

Bioprinting is the next medical revolution — C2 Montreal

Erik Gatenholm is Co-Founder and CEO here at CELLINK. In 2017, he founded CELLINK to revolutionize the way that we conduct medical research worldwide. He led a workshop at the C2 Montreal conference called “Need a tissue, Bioprinting is the next Medical Revolution”

At C2 Montreal – There was a presentation on bioprinting and Cellink technology. Then there was an activity where people in groups looked at a sample of bioprinted tissue and people worked on exercises of what people thought was possible or preposterous in the future.

There was a forecast of increased tissue engineering enhanced plastic surgery.

The Hallmarks of Aging: Loss of Proteostasis

Today, as part of our series of articles that cover the Hallmarks of Aging, we are going to take a look at the role of proteins in cellular function and how they play a key role in aging.

Proteins are essential for cellular function

Proteins are large, complex molecules that regulate almost everything in your body, either directly or indirectly. They do the majority of the work in cells and are critical for the function, regulation, and structure of tissues and organs.

Novel organ-on-chip platform for drug screening

Imec, the world-leading research and innovation hub in nano-electronics and digital technologies, presents this week at its technology forum ITF 2018 (Antwerp, May 23–24), a novel organ-on-chip platform for pharmacological studies with unprecedented signal quality. It fuses imec’s high-density multi-electrode array (MEA)-chip with a microfluidic well plate, developed in collaboration with Micronit Microtechnologies, in which cells can be cultured, providing an environment that mimics human physiology. Capable of performing multiple tests in parallel, the new device aims to be a game-changer for the pharmaceutical industry, offering high quality data in the drug development process.

Every year a handful of new drugs make it to the market, but in their wake tens of thousands of candidate drugs didn’t make the cut. Nevertheless, this journey will have taken a decade and costs billions. The fact that is so time-consuming and costly, is because of the insufficiency of the existing methodologies for screening assays. These current assays are based on poor cell models that limit the quality of the resulting data, and result in inadequate biological relevance. Additionally, there is a lack of spatial resolution of the assays, resulting in the inability to screen single cells in a cell culture. Imec’s novel organ-on-chip platform aims to address these shortcomings and challenges.

Imec’s solution packs 16,384 electrodes, distributed over 16 wells, and offers multiparametric analysis. Each of the 1,024 electrodes in a well can detect intracellular action potentials, aside from the traditional extracellular signals. Further, ’s chip is patterned with microstructures to allow for a structured cell growth mimicking a specific organ.

Triggering Autophagy to Potentially Combat Neurodegenerative Diseases

Researchers at Brown University have discovered a way to stimulate cellular autophagy, which is a natural recycling system built into every cell in the body. This has the potential to combat many age-related neurodegenerative diseases.

What is autophagy?

Autophagy means “eating of self” (from Ancient Greek “auto” = self, “phagein” = to devour). Autophagy is how cells break down broken or dysfunctional organelles and proteins in the cell [1,2]. This essentially means that autophagy can consume organelles, such as mitochondria, peroxisomes, and the endoplasmic reticulum, as part of this process. There is also evidence to support that high levels of autophagy are linked to longevity.

Physical exercise doesn’t slow down dementia once it appears, study shows

Physical exercise is a key piece of the brain health puzzle, but certainly not a magic pill.

___ Exercise ‘doesn’t slow’ progression of dementia (NHS Choices): A trial in which people with dementia took part in a moderately intense exercise programme for 4 months found their mental decline did not slow and may even have worsened faster than in people who did not take part in the programme…While the exercise.

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