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Circa 2017


Insulin-producing cells have been restored in mouse models of type 1 diabetes using a new genetic engineering technique.

American scientists adapted the gene editing technology known as CRISPR (clustered, regularly interspaced, short palindromic repeat) to successfully treat mouse models of type 1 diabetes, kidney disease and muscular dystrophy.

CRISPR enables scientists to edit the genetic material of an organism allowing for DNA sequences to be easily altered and gene function to be modified.

Circa 2019


Researchers at Hanyang University, South Korea, have used the gene-editing technology CRISPR-Cas9 to treat obesity and type 2 diabetes in mice, a development that could eventually benefit humans. The therapy specifically reduced fat tissue and reversed obesity-related metabolic disease in the animals.

Circa 2013

These patents form part of Regeneron’s global patent portfolio, which together protect fundamental inventions behind Regeneron’s VelocImmune humanized mice. The two patents listed above specifically contain claims covering genetically modified mice that have unrearranged human immunoglobulin variable region gene segments at endogenous mouse immunoglobulin loci. The VelocImmune mice contain the full repertoire of human heavy chain immunoglobulin genes and kappa light chain genes, each linked to endogenous mouse constant regions. As a result, VelocImmune mice generate a normal and robust immune response which many believe is becoming the gold standard for making human antibody therapeutics. VelocImmune is also proving to be one of the most valuable technologies in biotechnology history, in terms of the licensing and collaboration revenues it has helped generate.


TARRYTOWN, N.Y., Aug. 7, 2013 /PRNewswire/ — Regeneron Pharmaceuticals, Inc. (NASDAQ: REGN) today announced that the United States Patent and Trademark Office granted U.S. Patent No. 8,502,018 relating to methods of genetically modifying a mouse to make human antibodies. A similar European.

Study charts the “incipient supernova” of COVID-19 through genetic mutations as it spread from China and Asia to Australia, Europe and North America. Researchers say their methods could be used to help identify undocumented infection sources.

Working around the clock for two weeks, a large team of Stanford Medicine scientists has developed a test to detect antibodies against the novel coronavirus, SARS-CoV-2, in blood samples.

In contrast to current diagnostic tests for COVID-19, which detect genetic material from the virus in respiratory secretions, this test looks for antibodies to the virus in plasma, the liquid in blood, to provide information about a person’s immune response to an infection.

The test was launched April 6 at Stanford Health Care. It differs from an externally developed test that Stanford researchers used for a prevalence study during recent community screening events.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes the infectious disease COVID-19, which was first reported in Wuhan, China in December, 2019. Despite the tremendous efforts to control the disease, COVID-19 has now spread to over 100 countries and caused a global pandemic. SARS-CoV-2 is thought to have originated in bats; however, the intermediate animal sources of the virus are completely unknown. Here, we investigated the susceptibility of ferrets and animals in close contact with humans to SARS-CoV-2. We found that SARS-CoV-2 replicates poorly in dogs, pigs, chickens, and ducks, but ferrets and cats are permissive to infection. We found experimentally that cats are susceptible to airborne infection. Our study provides important insights into the animal models for SARS-CoV-2 and animal management for COVID-19 control.

In late December 2019, an unusual pneumonia emerged in humans in Wuhan, China, and rapidly spread internationally, raising global public health concerns. The causative pathogen was identified as a novel coronavirus (116) that was named Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) on the basis of a phylogenetic analysis of related coronaviruses by the Coronavirus Study Group of the International Committee on Virus Taxonomy (17); the disease it causes was subsequently designated COVID-19 by the World Health Organization (WHO). Despite tremendous efforts to control the COVID-19 outbreak, the disease is still spreading. As of March 11, 2020, SARS-CoV-2 infections have been reported in more than 100 countries, and 118,326 human cases have been confirmed, with 4,292 fatalities (18). COVID-19 has now been announced as a pandemic by WHO.

Although SARS-CoV-96.2% identity at the nucleotide level with the coronavirus RaTG13, which was detected in horseshoe bats (Rhinolophus spp) in Yunnan province in 2013 (3), it has not previously been detected in humans or other animals. The emerging situation raises many urgent questions. Could the widely disseminated viruses transmit to other animal species, which then become reservoirs of infection? The SARS-CoV-2 infection has a wide clinical spectrum in humans, from mild infection to death, but how does the virus behave in other animals? As efforts are made for vaccine and antiviral drug development, which animal(s) can be used most precisely to model the efficacy of such control measures in humans? To address these questions, we evaluated the susceptibility of different model laboratory animals, as well as companion and domestic animals to SARS-CoV-2.

Researchers from Kumamoto University have found that Melinjo seed extracts may help to improve diabetes and obesity by stimulating the production of adiponectin which is a hormone that works to help improve both conditions; individual genotype differences were also discovered that were responsible for variations in its efficacy.

Melinjo fruit contain high levels of antioxidant and antibacterial properties as well as high levels of polyphenols such as resveratrol that has been shown to induce adiponectin and may help to improve lifestyle related diseases such as metabolic syndrome. A type of resveratrol called Gnetin C which is found in MSE has higher antioxidant activity and has been shown to stay in the blood longer than resveratrol, but the exact mechanisms of how they exert their biological activity remains unknown.

Genetic analysis was used to find that differences in the type of DsbA-L gene affects adiponectin activation; meaning that DsbA-L induction may promote adiponectin activation and help to improve lifestyle related diseases. Their recent research has attempted to determine whether MSE enhances the function of DsbA-L; whether MSE promotes adi[onectin activation; and whether MSE has a therapeutic effect on either obesity and diabetes.

As we enter our third decade in the 21st century, it seems appropriate to reflect on the ways technology developed and note the breakthroughs that were achieved in the last 10 years.

The 2010s saw IBM’s Watson win a game of Jeopardy, ushering in mainstream awareness of machine learning, along with DeepMind’s AlphaGO becoming the world’s Go champion. It was the decade that industrial tools like drones, 3D printers, genetic sequencing, and virtual reality (VR) all became consumer products. And it was a decade in which some alarming trends related to surveillance, targeted misinformation, and deepfakes came online.

For better or worse, the past decade was a breathtaking era in human history in which the idea of exponential growth in information technologies powered by computation became a mainstream concept.

New research shows that resveratrol, a chemical found in red wine, contributes to genomic stability by reducing the occurrence of DNA double-strand breaks and prolongs lifespan in genetically modified mice that are prone to carcinogenic mutations [1].

DSBs and genomic instability

Genomic instability, one of the hallmarks of aging, is a condition characterized by frequent mutations within the genome, and it has long been associated with cancer [2]. The authors of this study state that one of its major causes is the erroneous repair of DNA double-strand breaks (DSBs). High numbers of DSBs have been found in pre-cancerous cells, and DNA lesions caused by unrepairable DSBs accumulate with time, both in organisms and in cultured cells. One of the possible culprits is the degradation of DNA repair mechanisms in aged cells [3].