A toddler is thriving after doctors in the U.S. and Canada used a novel technique to treat her before she was born for a rare genetic disease that caused the deaths of two of her sisters.
Ayla Bashir, a 16-month-old from Ottawa, Ontario, is the first child treated as a fetus for Pompe disease, an inherited and often fatal disorder in which the body fails to make some or all of a crucial protein.
Scientists at the University of Pittsburgh School of Medicine have discovered the missing puzzle piece in the mystery of how melanoma tumors control their mortality.
In a paper published in Science this week, Jonathan Alder, Ph.D. and his team describe how they discovered the perfect combination of genetic alterations that tumors use to promote explosive growth and prevent their own demise, a development that could change the way oncologists understand and treat melanoma.
“We did something that was, in essence, obvious based on previous basic research and connected back to something that is happening in patients,” said Alder, assistant professor in the Division of Pulmonary, Allergy and Critical Care Medicine at Pitt’s School of Medicine.
A continuation of the enlightenment values that freed mankind of superstition.
Anders Sandberg discusses achieving a transhumanist utopia.
Watch more from Anders Sandberg at https://iai.tv/player#utm_source=YouTube&utm_medium=description.
Several proteins have been identified in hosts that interact with Ebola virus and primarily function to inhibit the production of viral genetic material in cells and prevent Ebola virus infection, according to a study led by the Institute for Biomedical Sciences at Georgia State University.
Zaire ebolavirus or Ebola virus, an RNA virus pathogen that belongs to the filovirus family, causes outbreaks of severe disease in humans. This public health threat has produced outbreaks where reported case fatality rates ranged up to 90 percent.
The West Africa Ebola virus epidemic from 2013–2016 resulted in more than 28,000 infections and more than 11,000 deaths. Four outbreaks occurred in the Democratic Republic of Congo from 2017–2021 and Ebola virus reemerged in Guinea in 2021.
The human genome has just over 20,000 genes coding for proteins. Yet, it produces at least ten times that many different non-coding RNA molecules, which can often take on more than one shape. At least some of this RNA structurome is functional in physiology or pathophysiology.
In an invited review for Nature Reviews Genetics, Danny Incarnato, a molecular geneticist from the University of Groningen (The Netherlands), and his colleague Robert C. Spitale from the University of Irvine in California (USA) describe ways to develop the, as yet, largely untapped potential of RNA structures.
RNA is perhaps best known as the intermediate between genome and protein synthesis: messenger RNA molecules copy the genetic code of a gene in the cell’s nucleus and transport it to the cytoplasm, where ribosomes translate the code into a protein. However, RNA is also a key regulator of almost every cellular process and the structures that are adopted by RNA molecules are thought to often be key to their functions.
Based on marketing activation events the company ran over the summer in Seattle, Austin, and Palo Alto, the outlook for their first product looks pretty rosy. They gave away bags of salad (which were clearly labeled as being gene-edited) consisting of red-and green-leaf mustard greens, and asked people to complete a short survey about it. Adams estimated that more than 6,000 people tried the salads, and over 90 percent responded that they were “very motivated” or “somewhat motivated” to buy the product.
A New Green Revolution?
Helping people make healthier dietary choices is just one benefit that CRISPR could bring to produce. Its possibilities are wide-ranging, as evidenced by PairWise’s work to create fruit trees that can grow in different climates and yield food that’s easier to harvest. It’s not unlike Norman Borlaug’s work back in the 1940s to create a high-yield wheat seed that was resistant to stem rust—a project that ended up saving millions of people from hunger and famine.
Ribonucleic acid (RNA) is a polymeric molecule similar to DNA that is essential in various biological roles in coding, decoding, regulation and expression of genes. Both are nucleic acids, but unlike DNA, RNA is single-stranded. An RNA strand has a backbone made of alternating sugar (ribose) and phosphate groups. Attached to each sugar is one of four bases—adenine (A), uracil (U), cytosine ©, or guanine (G). Different types of RNA exist in the cell: messenger RNA (mRNA), ribosomal RNA (rRNA), and transfer RNA (tRNA).” RNA is an important information transmitter in our cells and acts as a blueprint for protein production. When freshly formed RNA is processed, introns are removed to produce mature mRNA coding for protein. This cutting is known as “splicing,” and it is controlled by a complex known as the “spliceosome.”
“We found a gene in worms, called PUF60, that is involved in RNA splicing and regulates life span,” says Max Planck scientist Dr. Wenming Huang who made the discovery.
This gene’s mutations resulted in inaccurate splicing and the retention of introns within certain RNAs. As a result, less of the corresponding proteins were produced from this RNA. Surprisingly, worms with the PUF60 gene mutation survived significantly longer than normal worms.
In Switzerland, cancer is the second-leading cause of death. Non-small cell lung cancer (NSCLC) is the cancer form that kills the most people and is still mostly incurable. Unfortunately, only a small percentage of patients survive the metastatic stage for a long time, and even recently approved therapies can only prolong patients’ lives by a few months. As a result, researchers are looking for innovative cancer treatments. Researchers from the University of Bern and the Insel Hospital identified new targets for drug development for this cancer type in a recent study published in the journal Cell Genomics.
They searched for novel targets in the poorly understood class of genes known as “long noncoding RNAs (Ribonucleic acids)” (lncRNAs). LncRNAs are abundant in the “Dark Matter,” or non-protein-coding 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).
Even more daring, biology’s “mirror dimension” may be a springboard to engineer synthetic life forms that exist outside of nature, but are literal reflections of ourselves. To rephrase: building a mirror-image version of biology means rewriting the fundamental operating system of life.
Sound a bit too sci-fi? Let me explain. Similar to how our left hand can’t wear a right-hand glove, the building blocks of life—DNA, RNA, and proteins—are etched into specific 3D structures. Flip them around, as if reflected by a mirror, and they can no longer function inside the body. Scientists aren’t yet sure why nature picked just one shape out of two potential mirror images. But they’re ready to test it out.
A new study in Science made strides by reworking parts of the body’s protein-making machine into its mirror image. At the center is a structure called the ribosome, which intakes genetic code and translates it into amino acids—the Lego blocks for all proteins. The ribosome is an iconic cellular architecture, fused from two main molecular components: RNA and proteins.
Summary: Mutations of the PTEN gene cause neurons to grow to twice the size and form four times the number of synaptic connections to other neurons as a normal neuron. Removing the RAPTOR gene, an essential gene in the mTORC1 signaling pathway, prevents the neuronal and synaptic overgrowth associated with PTEN mutations. Using Rapamycin to inhibit mTORC1 rescues all the changes in neuronal overgrowth.
Source: the geisel school of medicine at dartmouth.
Findings from a new study published in Cell Reports, involving a collaborative effort between researchers at the Luikart Laboratory at Dartmouth’s Geisel School of Medicine and the Weston Laboratory at the University of Vermont, are providing further insight into the neurobiological basis of autism spectrum disorders (ASD) and pointing to possible treatments.
