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Category: genetics – Page 184

Genetically Engineering Cells to Respond to Electricity

A paper published today in Nature Metabolism has described a method of genetically engineering cells to respond to electrical stimuli, allowing for on-demand gene expression.

Despite its futuristic outlook, this line of research is built upon previous work. The idea of an implantable gene switch to command cells in order to deliver valuable compounds into the human body is not new. The authors of this paper cite longstanding work showing that gene switches can be developed to respond to antibiotics [1] or other drugs, and the antibiotic doxycycline is used regularly for this purpose in mouse models. More recently, researchers have worked on cells that control their output based on green light [2], radio waves [3], or heat [4].

However, these mechanisms have their problems. A gene trigger that operates in response to a chemical compound requires that compound to have stable, controllable biological availability [5]. If it relies on any wavelength of electromagnetic radiation, that process may be triggered by mistake or require intense energy to function [3].

3D Animation Captures Viral Infection in Action

With the summer holiday season now in full swing, the blog will also swing into its annual August series. For most of the month, I will share with you just a small sampling of the colorful videos and snapshots of life captured in a select few of the hundreds of NIH-supported research labs around the country.

To get us started, let’s turn to the study of viruses. Researchers now can generate vast amounts of data relatively quickly on a virus of interest. But data are often displayed as numbers or two-dimensional digital images on a computer screen. For most virologists, it’s extremely helpful to see a virus and its data streaming in three dimensions. To do so, they turn to a technological tool that we all know so well: animation.

This research animation features the chikungunya virus, a sometimes debilitating, mosquito-borne pathogen transmitted mainly in developing countries in Africa, Asia and the Americas. The animation illustrates large amounts of research data to show how the chikungunya virus infects our cells and uses its specialized machinery to release its genetic material into the cell and seed future infections. Let’s take a look.

New genetic clues uncovered in largest study of families with multiple children with autism

UCLA Health researchers have published the largest-ever study of families with at least two children with autism, uncovering new risk genes and providing new insights into how genetics influence whether someone develops autism spectrum disorder.

The new study, published July 28 in the Proceedings of the National Academy of Sciences, also provides genetic evidence that language delay and dysfunction should be reconsidered as a core component of autism.

Most genetic studies of autism have focused on families with one child affected by the neurodevelopmental disorder, sometimes excluding families with multiple affected children. As a result, few studies have examined the role of rare inherited variation or its interaction with the combined effect of multiple common genetic variations that contribute to the risk of developing autism.

Clever DNA tricks

Every person starts as just one fertilized egg. By adulthood, that single cell has turned into roughly 37 trillion cells, many of which keep dividing to create the same amount of fresh human cells every few months.

But those cells have a formidable challenge. The average dividing cell must copy — perfectly — 3.2 billion base pairs of DNA, about once every 24 hours. The cell’s replication machinery does an amazing job of this, copying genetic material at a lickety-split pace of some 50 base pairs per second.

Scientists Create New Material Five Times Lighter and Four Times Stronger Than Steel

Materials possessing both strength and lightness have the potential to enhance everything from automobiles to body armor. But usually, the two qualities are mutually exclusive. However, researchers at the University of Connecticut, along with their collaborators, have now crafted an incredibly strong yet lightweight material. Surprisingly, they achieved this using two unexpected building blocks: DNA

DNA, or deoxyribonucleic acid, is a molecule composed of two long strands of nucleotides that coil around each other to form a double helix. It is the hereditary material in humans and almost all other organisms that carries genetic instructions for development, functioning, growth, and reproduction. Nearly every cell in a person’s body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).

Artificial intelligence vs. evolving super-complex tumor intelligence: critical viewpoints

Recent developments in various domains have led to a growing interest in the potential of artificial intelligence to enhance our lives and environments. In particular, the application of artificial intelligence in the management of complex human diseases, such as cancer, has garnered significant attention. The evolution of artificial intelligence is thought to be influenced by multiple factors, including human intervention and environmental factors. Similarly, tumors, being heterogeneous and complex diseases, continue to evolve due to changes in the physical, chemical, and biological environment. Additionally, the concept of cellular intelligence within biological systems has been recognized as a potential attribute of biological entities. Therefore, it is plausible that the tumor intelligence present in cancer cells of affected individuals could undergo super-evolution due to changes in the pro-tumor environment. Thus, a comparative analysis of the evolution of artificial intelligence and super-complex tumor intelligence could yield valuable insights to develop better artificial intelligence-based tools for cancer management.

Tumor evolution refers to the changes that occur in a cancerous tumor over time as it grows and spreads (Hanahan and Weinberg, 2011; Lyssiotis and Kimmelman, 2017). These changes are the result of genetic mutations and changes in gene expression that can give rise to new subpopulations of cells within the tumor (Lyssiotis and Kimmelman, 2017; Balaparya and De, 2018). Over time, these subpopulations may accumulate subsequent mutations that confer enhanced survival and heightened proliferative capacity, thereby culminating in the emergence of a more formidable tumor exhibiting either heightened aggressiveness or treatment resistance (Balaparya and De, 2018; Gui and Bivona, 2022; Shin and Cho, 2023). Tumor evolution can have important implications for cancer diagnosis and treatment.

FDA Approves First-Line Enzalutamide/Talazoparib Combo in Prostate Cancer

The U.S Food and Drug Administration (FDA) has approved a new drug combination for men with metastatic, castration-resistant prostate cancer (mCRPC) and certain DNA repair gene mutations, widening treatment options for this large patient population.

The androgen-receptor inhibitor enzalutamide plus the PARP inhibitor talazoparib can now be used as first-line treatment for mCRPC patients who have homologous recombination repair (HRR) gene alterations.

#MetastaticProstateCancer.

A new combination therapy for for metastatic prostate cancer that includes an already approved breast cancer drug was just approved by the FDA last month on June 20. It has many excited.

The FDA has approved a new drug combination therapy for metastatic castration-resistant prostate cancer and DNA repair gene mutations.

Oxidative Stress in Cancer Cell Metabolism

Reactive oxygen species (ROS) are important in regulating normal cellular processes whereas deregulated ROS leads to the development of a diseased state in humans including cancers. Several studies have been found to be marked with increased ROS production which activates pro-tumorigenic signaling, enhances cell survival and proliferation and drives DNA damage and genetic instability. However, higher ROS levels have been found to promote anti-tumorigenic signaling by initiating oxidative stress-induced tumor cell death. Tumor cells develop a mechanism where they adjust to the high ROS by expressing elevated levels of antioxidant proteins to detoxify them while maintaining pro-tumorigenic signaling and resistance to apoptosis.

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