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Tel Aviv-based D-ID released today the first multimodal generative AI video platform to combine text, image and animation in one interface. The self-service video platform integrates D-ID’s proprietary generative AI technology with GPT-3 from Open AI and Stable Diffusion from Stability AI, allowing users to generate digital composite faces and speech in 119 languages based on their text prompts.

“This is a game changer for creators,” says Gil Perry, D-ID co-founder and CEO. “It’s the bleeding edge of generative AI,” he asserts, touting the startup’s expertise in deep learning and computer vision. When I talked to Perry last year, he said that the company’s long-term vision is “to lead the next disruption in the video entertainment space by creating AI-generated synthetic media in a responsible way.”

In the rapidly evolving generative AI space, “long-term” means “next year,” so now Perry talks about providing “digital humans” to enterprises, “transforming the way we communicate with machines and elevating our capabilities as humans.” He hopes that sometime next year, we could chat with the digital humans we will create with D-ID’s help.

Hitting two targets at the same time may be the key to stopping the spread of aggressive cancers, according to new research from the University of East Anglia and the Quadram Institute.

Researchers have found that in mice could be stopped by simultaneously targeting two signaling switches that trigger growth of new blood vessels.

Their study, published in the journal Cancer Research Communications, points to new approaches for treating cancer in humans.

The BACE1 enzyme has a rate-limiting role in the amyloidogenic pathway (see Glossary) and has been extensively studied for its neuronal functions[1]. Since 2000, intensive efforts have focused on developing small-molecule BACE1 inhibitors to reduce amyloid β (Aβ) production in Alzheimer’s disease (AD) brains. However, human clinical trials involving most BACE1 inhibitors were stopped at Phase 2/3 due to limited therapeutic benefits[2]. BACE1 inhibitors act by reducing Aβ-related pathologies in AD brains, that is, they are used to treat the symptoms rather than the underlying disease.

Huntington’s disease (HD) is a neurological disorder that causes progressive loss of movement, coordination and cognitive function. It is caused by a mutation in a single gene called huntingtin (HTT). More than 200,000 people worldwide live with the genetic condition, approximately 30,000 in the United States. More than a quarter of a million Americans are at risk of inheriting HD from an affected parent. There is no cure.

But in a new study, published December 12, 2022 in Nature Neuroscience, researchers at University of California San Diego School of Medicine, with colleagues elsewhere, describe using RNA-targeting CRISPR/Cas13D technology to develop a new therapeutic strategy that specifically eliminates toxic RNA that causes HD.

CRISPR is known as a genome-editing tool that allows scientists to add, remove or alter genetic material at specific locations in the genome. It is based on a naturally occurring immune defense system used by bacteria. However, current strategies run the risk of off-target edits at unintended sites that may cause permanent and inheritable chromosomal insertions or genome alterations. Because of this, significant efforts have focused on identifying CRISPR systems that target RNA directly without altering the genome.

An international research team led by Dr. Ana Guadaño at the Alberto Sols Biomedical Research Institute (IIBM, a combined CSIC-UAM center) and involving the Complutense University of Madrid (UCM), used CRISPR gene editing techniques to incorporate into mice a mutation of the MCT8 protein responsible for transporting thyroid hormones to the interior of the cell.

Patients with mutations in this protein suffer from Allan-Herndon-Dudley syndrome, a that takes the form of serious neurological alterations, in which each patient may reveal a different mutation of MCT8.

This study, published in Neurobiology of Disease, describes the first avatar model for the disease—in other words, the first animal model with the same as various .

Summary: Researchers engineered cells containing customized adhesion molecules that bind to specific cell partners in predictable ways to form complex multicellular entities. The discovery is a major step toward building new tissue and organs.

Source: UCSF

Researchers at UC San Francisco (UCSF) have engineered molecules that act like “cellular glue,” allowing them to direct in precise fashion how cells bond with each other. The discovery represents a major step toward building tissues and organs, a long-sought goal of regenerative medicine.

Summary: Researchers have developed a new compound, dubbed FexD, that can prevent and reverse inflammation in mouse models of inflammatory bowel disease.

Source: Salk Institute.

A drug developed by Salk Institute researchers acts like a master reset switch in the intestines. The compound, called FexD, has previously been found to lower cholesterol, burn fat, and ward off colorectal cancer in mice.

Achieving a long-sought goal of regenerative medicine.

Researchers from the University of California, San Francisco, (UCSF) engineered molecules that function as “cellular glue,” enabling them to precisely direct how cells bond with each other. This is a significant step toward regenerative medicine’s long-term goal of creating new tissues and organs, according to a press release.

Adhesive molecules are naturally present in the body and keep the tens of trillions of cells together in organized patterns. They build neural networks, develop structures, and direct immune cells to specific areas of the body. Adhesion also makes cell communication easier to maintain the body functioning as a self-regulating whole.