Has human evolution come to a standstill? Advances in technology and medicine have radically changed the way we live, but could they be changing the course of our genetic future? The surprising truth behind how modern progress may be changing our biology — and what it means for our survival.
Junk DNA may not be so ‘junky’ after all – these regions may hide genetic material coding for tiny proteins involved in disease processes like cancer and immunology.
Our records of the human genome may still be missing tens of thousands of ‘dark’ genes. These hard-to-detect sequences of genetic material can code for tiny proteins, some involved in disease processes like cancer and immunology, a global consortium of researchers has confirmed.
They may explain why past estimates of our genome’s size were way larger than what the Human Genome Project discovered 20 years ago.
The new international study, still awaiting peer review, shows our library of human genes very much continues to be a work in progress, as more subtle genetic features are picked up with advances in technology, and as continued exploration uncovers gaps and errors in the record.
Chaperones are molecular machines that help proteins in the cell fold into their proper shape. Among them, UNC45 plays a critical role in muscle health by ensuring the proper function of myosin, a key protein essential for muscle movement. UNC45 manages this by directing damaged myosin to degradation pathways while guiding correctly folded myosin toward assembly. Researchers from Tim Clausen’s lab at the IMP have uncovered the mechanisms behind this process, providing new insights into how disruptions in myosin quality control can lead to serious muscle disorders. Their findings have been published in Nature Communications.
Muscle movement relies on the interaction between two key proteins: actin and myosin. These proteins slide past each other to generate the force needed for movement. For this process to work efficiently, actin and myosin must be precisely organized within the sarcomere, the basic structural and functional unit of muscle cells. This arrangement is crucial for maintaining muscle health, particularly during exercise, periods of stress, and as the body ages.
To ensure proteins achieve their correct shape, cells use specialized molecular assistants called chaperones. These chaperones act as caretakers, helping proteins fold and assemble correctly. For myosin, which makes up about 16% of the total protein in muscle cells, proper structure is especially important. One critical chaperone for this task is UNC45, found in all eukaryotic organisms. Identified through genetic studies, UNC45 plays a vital role in shaping myosin and preserving the integrity of the sarcomere. The importance of UNC45 is evident in severe muscle disorders, known as myopathies, which can result from mutations in the UNC45 gene.
As we explore space outside our solar system, genetic engineering offers hope for overcoming challenges like radiation exposure and the effects of microgravity. By understanding and modifying our genes, we could make astronauts more resilient and improve their health in space. However, these advancements raise important ethical questions about safety, fairness, and long-term impacts, which must be carefully considered as we develop new space travel technologies.
We are on the edge of exploring space outside our solar system. This is not just a major advancement in technology, but a transformation for all of mankind. As we aim for the stars, we also try to understand more about ourselves. Our exploration into space will determine the future of our history. However, this thrilling adventure comes with many challenges. We need to build faster spacecraft, develop ways to live sustainably in space and deal with the physical and mental difficulties of long space missions. Genetics may help us solve some of these problems. As we travel further into space, it will be important to understand how genetics affects our ability to adapt to the space environment. This knowledge will be crucial for the success of space missions and the well-being of astronauts.
Genetics offers a hopeful path to overcoming many challenges in space exploration. As we venture further into space, it becomes essential to understand how our genes affect the way we adapt to the space environment. Genetics affects many aspects of an astronaut’s ability to survive and do well in space. It influences how the body handles exposure to radiation, deals with microgravity, and copes with isolation. Some genetic differences, like changes in the Methylene-TetraHydrofolate-Reductase (MTHR) gene, can make certain people more vulnerable to the harmful effects of radiation in space. With tools like genetic testing and personalized medicine, space agencies can now choose the best-suited astronauts and develop health strategies to improve their safety and performance in harsh space conditions.
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From the article:
Scientists in Boston, Massachusetts have made reprogrammed stem cells from the blood of centenarians.
Centenarians offer an opportunity to study longevity. People who’ve lived to 100 have an amazing ability to bounce back from insult and injury, says George Murphy, a stem-cell biologist at the Boston University Chobanian & Avedisian School of Medicine. One centenarian he knows recovered from the 1912 Spanish flu and COVID-19, twice. One theory that explains centenarians’ robust age is that they possess a genetic makeup that protects them from diseases.
But testing that idea is a challenge. People of that age are rare, which makes blood and skin samples from them a precious resource for research. That gave Murphy and his colleagues the idea to create a bank of centenarian cells that could be shared among scientists.
Colorectal cancer (CRC) remains one of the most clinically challenging malignancies facing our public health system. CRC accounts for the second and third most common cancer in males and females, respectively. In addition, CRC represents one of the most deadly cancers, expected to result in over 50,000 mortalities in 2024.
Hereditary colorectal cancer (HCRC) occurs when a parent passes a cancer gene to a child. Unfortunately, we have not identified a single gene that causes the disease. Hereditary CRC syndromes, such as hereditary non-polyposis colorectal cancer (HNPCC; also known as Lynch syndrome) and familial adenomatous polyposis (FAP), describe a group of genetic diseases that confer a high risk of developing CRC. As our knowledge has expanded, we have learned about a growing number of genetic variants in the genes that predispose carriers to CRC. However, the precise role of some variants in the development of CRC cancer remains unclear. Uncovering more information about these variants, called variants of uncertain significance.
As our knowledge has expanded, we have learned about a growing number of genetic variants in the genes which predispose carriers to CRC. However, the precise role of some variants in the development of CRC cancer remains unclear. Uncovering more information about these variants, called variants of uncertain significance (VUS), can aid in optimizing screening and surveillance programs.
Viviana Gradinaru, an assistant professor of biology at Caltech, discovered her passion for neuroscience as an undergraduate at Caltech, her alma mater. Viviana did her Ph.D. work with Karl Deisseroth at Stanford University where she played an instrumental role in the early development and applications of optogenetics, a research area concerned with the perturbation of neuronal activity via light-controlled ion channels and pumps. More information on her own lab at Caltech can be found at glab.caltech.edu. Viviana is also interested in entrepreneurship for better human health and has co-founded a company, Circuit Therapeutics, based on optogenetics.
In the spirit of ideas worth spreading, TEDx is a program of local, self-organized events that bring people together to share a TED-like experience. At a TEDx event, TEDTalks video and live speakers combine to spark deep discussion and connection in a small group. These local, self-organized events are branded TEDx, where x = independently organized TED event. The TED Conference provides general guidance for the TEDx program, but individual TEDx events are self-organized.* (*Subject to certain rules and regulations)\ \ .
On January 18, 2013, Caltech hosted TEDxCaltech: The Brain, a forward-looking celebration of humankind’s quest to understand the brain, by exploring the past, present and future of neuroscience. Visit TEDxCaltech.com for more details.
We present a DNA self-assembly based molecular data writing strategy to enable parallel movable-type printing for scalable DNA storage.
Memorial Sloan Kettering Cancer Center-led researchers have identified a small molecule called gliocidin that kills glioblastoma cells without damaging healthy cells, potentially offering a new therapeutic avenue for this aggressive brain tumor.
Glioblastoma remains one of the most lethal primary brain tumors, with current therapies failing to significantly improve patient survival rates. Glioblastoma is difficult to treat for several reasons. The tumor consists of many different types of cells, making it difficult for treatments to target them all effectively.
There are few genetic changes in the cancer for drugs to target, and the tumor creates an environment that weakens the body’s immune response against it. Even getting medications near targets in the brain is challenging because the protective blood-brain barrier blocks entry for most potential drug treatments.
