Diseases such as Alzheimer’s and epilepsy will be easier to detect.
A 3D microchip made by a Swiss company will allow scientists to study the complexity of 3D cellular networks. This 3D chip will help to observe complex structures such as the human brain, according to a report published by Labiotech.eu.
Understanding how organs form and how their cells behave is essential to finding the causes and treatment for developmental disorders, as well as understanding certain diseases, said 3Brain.
A microchip that allows scientists to study the complexity of 3D cellular networks at unrivaled scale and precision has been added to 3Brain AG’s brain-on-chip portfolio.
In collaboration with Swiss precision manufacturing experts, CSEM, 3Brain AG made the announcement today (August 22).
The cell-electronic interface technology will also allow scientists to gain novel mechanistic insights into the inner workings of the most complex structure in the universe, the human brain.
“These results will have future implications in forensic medicine and genetic diagnosis.”
In 1999, François Brunelle, a Canadian artist, and photographer, began documenting look-alikes in a picture series “I’m not a look-alike!”
The project, undoubtedly, was a massive hit on social media and other parts of the internet, but it also drew the attention of scientists who study genetic relationships.
TABLE OF CONTENTS ————— 0:00–15:11 : Introduction. 15:11–36:12 CHAPTER 1: POSTHUMANISM a. Neurotechnology b. Neurophilosophy c. Teilhard de Chardin and the Noosphere.
36:12–54:39 CHAPTER 2 : TELEPATHY/ MIND-READING a. MRI b. fMRI c. EEG d. Cognitive Liberty e. Dream-recording, Dream-economies f. Social Credit Systems g. Libertism VS Determinism.
1:02:07–1:25:48 : CHAPTER 3 : MEMORY/ MIND-AUGMENTING a. Memory Erasure and Neuroplasticity b. Longterm Potentiation (LTP/LTD) c. Propanolol d. Optogenetics e. Neuromodulation f. Memory-hacking g. Postmodern Dystopias h. Total Recall, the Matrix, and Eternal Sunshine of the Spotless Mind i. Custom reality and identity.
Start listening with a 30-day Audible trial and your first audiobook plus two Audible Originals are free. Visit. http://www.audible.com/isaac or text “isaac” to 500–500. Cloning people is a staple of science fiction, and now something science can do, but what are the future social and legal consequences of cloning, and can we learn to make fully grown clones or even duplicate our memories?
All around smart guy Dr Goerge Church talking about genetic engineering technologies.
George Church, Ph.D. is a professor of genetics at Harvard Medical School and of health sciences and technology at both Harvard and the Massachusetts Institute of Technology. Dr. Church played an instrumental role in the Human Genome Project and is widely recognized as one of the premier scientists in the fields of gene editing technology and synthetic biology.
The technology is based on integrated circuits, which typically rely on silicon semiconductors in order to process information in a way that is similar to the role played by the brain in the human body.
The research team discovered that integrated circuits capable of performing computational tasks could be achieved using “nearly any material” around us.
“We have created the first example of an engineering material that can simultaneously sense, think and act upon mechanical stress, without requiring additional circuits to process such signals,” said Ryan Harne, an associate professor of mechanical engineering at Penn State.
Modulating Autophagy To Promote Healthspan — Dr. Ana Maria Cuervo, M.D., Ph.D., Albert Einstein College of Medicine.
Dr. Ana Maria Cuervo, M.D., Ph.D. (https://www.einsteinmed.edu/faculty/8784/ana-maria-cuervo/) is Co-Director of the Einstein Institute for Aging Research, and a member of the Einstein Liver Research Center and Cancer Center. She serves as a Professor in the Department of Developmental & Molecular Biology, and the Department of Medicine (Hepatology), and has the Robert and Renée Belfer Chair for the Study of Neurodegenerative Diseases.
Dr. Cuervo studied medicine and pursued a Ph.D. in biochemistry and molecular biology at the University of Valencia, as well as post-doctoral work at Tufts, and in 2001 she started her laboratory at Einstein, where she studies the role of protein-degradation in aging and age-related disorders, with emphasis in neurodegeneration and metabolic disorders.
Dr. Cuervo’s group is interested in understanding how altered proteins can be eliminated from cells and their components recycled. Her group has linked alterations in lysosomal protein degradation (autophagy) with different neurodegenerative diseases including Parkinson’s, Alzheimer’s and Huntington’s disease. They have also proven that restoration of normal lysosomal function prevents accumulation of damaged proteins with age, demonstrating this way that removal of these toxic products is possible. Her lab has also pioneered studies demonstrating a tight link between autophagy and cellular metabolism. They described how autophagy coordinates glucose and lipid metabolism and how failure of different autophagic pathways with age contribute to important metabolic disorders such as diabetes or obesity.
Dr. Cuervo is considered a leader in the field of protein degradation in relation to biology of aging and has been invited to present her work in numerous national and international institutions, including name lectures as the Robert R. Konh Memorial Lecture, the NIH Director’s, the Roy Walford, the Feodor Lynen, the Margaret Pittman, the IUBMB Award, the David H. Murdock, the Gerry Aurbach, the SEBBM L’Oreal-UNESCO for Women in Science, the C. Ronald Kahn Distinguished Lecture and the Harvey Society Lecture. She has organized and chaired international conferences on protein degradation and on aging, belongs to the editorial board of scientific journals in this topic, and is currently co-editor-in-chief of Aging Cell.
Aging is a complex and inevitable process that affects all organisms – and it is associated with tissue dysfunction, susceptibility to various diseases, and death [1]. The development of strategies like cellular reprogramming for increasing the duration of healthy life and promoting healthy aging is difficult since the mechanism of aging is not understood clearly. Aging is known to be associated with several hallmarks of aging – such as epigenetic alterations, genomic instability, cellular senescence, telomere shortening, mitochondrial dysfunction and altered intercellular communication.
Aging can be divided into two major phases: healthy aging and pathological aging. Healthy aging is the phase where the accumulation of minor alterations takes place, but pathological aging is the phase where clinical diseases and disabilities predominate along with the impairment of physiological functions [2].
Longevity. Technology: Notions regarding cells undergoing a unidirectional differentiation process during development existed previously [3]. However, in recent years cellular reprogramming using transcription factors has emerged as an important strategy for the rejuvenation of aging cells, erasing markers of cell damage and restoring epigenetic markers. These transcription factors also known as Yamanaka factors include Oct4, Sox2, Klf4, and c-Myc (OSKM). They can convert terminally differentiated somatic cells into pluripotent stem cells which are capable of dividing into any cell type of the body and thus can improve the health and longevity of individuals.
A test that can detect hundreds of thousands of different fragments of DNA sequences, proteins or antibodies could be built onto a tiny silicon chip. Researchers say the technology could lead to devices for medical diagnostics or environmental monitoring.
Scientists have long sought to untangle the mystery of how aging links to increased risk of heart disease, a predominant killer of our time. It’s a tough problem: many biological aspects, spanning nature to nurture, can subtly influence heart health. To untangle the mystery, some experiments have lasted over half a century and scaled to hundreds of thousands of people.
The good news? We’ve got clues. With age, heart cells drastically change their function, eventually struggling to contract and release. A new study published in Nature Aging looked deep into genetic code to unravel why this happens.
Starting with a dozen volunteers spanning 0 to 82 years old, the team sequenced the entire genome of 56 heart muscle cells, or cardiomyocytes. The result is the first landscape painting of genetic changes in the aging heart. As we age, the heart gets hit with a double whammy at the DNA level. Cells’ genetic code physically breaks down, while their ability to repair DNA erodes.
