This is the video of Harold Katcher’s presentation to the London Futurists. It was a great discussion, be sure to check it out.
#haroldkatcher #antiaging #rejuvenation #futurism
Circa 2012.
A bioengineer and geneticist at Harvard’s Wyss Institute have successfully stored 5.5 petabits of data — around 700 terabytes — in a single gram of DNA, smashing the previous DNA data density record by a thousand times.
The work, carried out by George Church and Sri Kosuri, basically treats DNA as just another digital storage device. Instead of binary data being encoded as magnetic regions on a hard drive platter, strands of DNA that store 96 bits are synthesized, with each of the bases (TGAC) representing a binary value (T and G = 1 A and C = 0).
Continue reading “Harvard cracks DNA storage, crams 700 terabytes of data into a single gram” »
“You may hit the tipping point when you’re 50; it may happen when you’re 80; it may never happen,” Schindler said. “But once you pass the tipping point, you’re going to accumulate high levels of amyloid that are likely to cause dementia. If we know how much amyloid someone has right now, we can calculate how long ago they hit the tipping point and estimate how much longer it will be until they are likely to develop symptoms.”
Summary: A new algorithm uses neuroimaging data of amyloid levels in the brain and takes into account a person’s age to determine when a person with genetic Alzheimer’s risk factors, and with no signs of cognitive decline, will develop the disease.
Source; WUSTL
Continue reading “Time Until Dementia Symptoms Appear Can Be Estimated via Brain Scan” »
Progress.
Replacing or editing disease-causing mutations holds great promise for treating many human diseases. Yet, delivering therapeutic genetic modifiers to specific cells in vivo has been challenging, particularly in large, anatomically distributed tissues such as skeletal muscle. Here, we establish an in vivo strategy to evolve and stringently select capsid variants of adeno-associated viruses (AAVs) that enable potent delivery to desired tissues. Using this method, we identify a class of RGD motif-containing capsids that transduces muscle with superior efficiency and selectivity after intravenous injection in mice and non-human primates. We demonstrate substantially enhanced potency and therapeutic efficacy of these engineered vectors compared to naturally occurring AAV capsids in two mouse models of genetic muscle disease. The top capsid variants from our selection approach show conserved potency for delivery across a variety of inbred mouse strains, and in cynomolgus macaques and human primary myotubes, with transduction dependent on target cell expressed integrin heterodimers.
The label on RecA together with fluorescent markers on the DNA allows the researchers to follow every step of the process accurately; for example, they conclude that the whole repair is finished in 15 minutes, on average, and that the template is located in about nine. Using microscopy, Elf and his team investigate the fate of the break site and its homologous copy in real-time. They also find that the cell responds by rearranging RecA to form thin filaments that span the length of the cell.
How the cell can mend broken 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).
Continue reading “Mending Broken DNA: Researchers Solve Puzzling Biological Search Problem” »
Watch the full documentary on Vimeo on demand: https://vimeo.com/ondemand/339083
The study of consciousness needs to be lifted out of the mysticism that has dominated it. Consciousness is not just a matter of philosophy or spirituality. It’s a matter of hard science. It’s a matter of understanding the brain and the mind — a pattern structure made out of information. It’s also a matter of engineering. If we can understand the functionality of the brain, its neural code, then we can build the same functionality into our computer systems. There’s no consensus on what produces consciousness, but everyone regardless of metaphysical views can agree what it is like to be conscious. Given that consciousness is subjectivity, what consciousness is like is what consciousness is.
That fossil wasn’t enough to confirm Africa as our homeland. Since that discovery, paleoanthropologists have amassed many thousands of fossils, and the evidence over and over again has pointed to Africa as our place of origin. Genetic studies reinforce that story. African apes are indeed our closest living relatives, with chimpanzees more closely related to us than to gorillas. In fact, many scientists now include great apes in the hominid family, using the narrower term “hominin” to refer to humans and our extinct cousins.
In a field with a reputation for bitter feuds and rivalries, the notion of humankind’s African origins unifies human evolution researchers. “I think everybody agrees and understands that Africa was very pivotal in the evolution of our species,” says Charles Musiba, a paleoanthropologist at the University of Colorado Denver.
Paleoanthropologists have sketched a rough timeline of how that evolution played out. Sometime between 9 million and 6 million years ago, the first hominins evolved. Walking upright on two legs distinguished our ancestors from other apes; our ancestors also had smaller canine teeth, perhaps a sign of less aggression and a change in social interactions. Between about 3.5 million and 3 million years ago, humankind’s forerunners ventured beyond wooded areas. Africa was growing drier, and grasslands spread across the continent. Hominins were also crafting stone tools by this time. The human genus, Homo, arrived between 2.5 million and 2 million years ago, maybe earlier, with larger brains than their predecessors. By at least 2 million years ago, Homo members started traveling from Africa to Eurasia. By about 300,000 years ago, Homo sapiens, our species, emerged.
Dementia has many faces, and because of the wide range of ways in which it can develop and affect patients, it can be very challenging to treat. Now, however, using supercomputer analysis of big data, researchers from Japan were able to predict that a single protein is a key factor in the damage caused by two very common forms of dementia.
In a study published this month in Communications Biology, researchers from Tokyo Medical and Dental University (TMDU) have revealed that the protein HMGB1 is a key player in both frontotemporal lobar degeneration and Alzheimer disease, two of the most common causes of dementia.
Frontotemporal lobar degeneration can be caused by mutation of a variety of genes, which means that no one treatment will be right for all patients. However, there are some similarities between frontotemporal lobar degeneration and Alzheimer disease, which led the researchers at Tokyo Medical and Dental University (TMDU) to explore whether these two conditions cause damage to the brain in the same way.
The discriminatory power of the UVB variable is somewhat limited in this study, because UVB radiation is low at this time of the year, particularly at the high northern latitude of UK—larger effects might be observed if variation in UVB is greater. We only used ambient UVB, and did not capture individual behavioural differences that would determine the actual level of vitamin D synthesis in the skin, such as duration and time of day spent outside, clothing, etc. It is important to note that time of year is the strongest predictor of vitD-UVB. To avoid bias control dates were assigned to follow the same distribution as case dates, which might have led to artificially diminished differences in vitD-UVB between cases and controls, however analysis relating to hospitalisation and death are not affected by this. We also conducted an analysis of the genetically-predicted vitamin D and a number of state-of-the-art MR analyses. However, the main limitation is the lack of power. Given the small number of COVID-19 patients and the relatively small percentage of variance (4.2%) explained by vitamin D-related genetic variants, this MR study was not adequately powered to detect small causal effect and negative results should be interpreted with caution. Additionally, MR studies only consider linear effects between 25-OHD levels and COVID-19 risk, which do not capture what happens at the extremes of vitamin D deficiency. Therefore, it cannot rule out the possibility that seriously ill patients (due to an underlying pathology) with extremely low vitamin D levels could be predisposed to COVID-19 infection and increased COVID-19 severity and mortality. Furthermore, 25-OHD levels are the used biomarker of vitamin D status in the study population, nevertheless, they correlate poorly with the active form of vitamin D (1,25-OH2D), which exerts the effects of vitamin D on a cellular level. Thus, this study cannot exclude effects of 1,25-OH2D on COVID-19 risk.
Another limitation of this cohort relates to the fact that not all participants have been tested for present (or past) COVID-19 infection; consequentially, taking participants who were not tested as controls could be a potential source of bias, given that misclassification of controls might be substantial due to the presence of asymptomatic infected individuals, further driving our findings to the null. This is evident from the 1:2 ratio between outpatient vs. inpatient cases. It should be acknowledged that the COVID-19 cases in UK biobank have a high rate of hospitalisation due to the very limited and targeted testing at this stage of the pandemic in the UK, so this study reflects mainly those with more severe COVID-19 and gives less information about true infection risk, or risk of milder disease. In addition, we excluded individuals with a negative COVID-19 testing result from the controls due to the risk of those being false negatives. Although there is a risk of introducing selection bias, we believe that the risk of introducing misclassification bias if we included them in the analysis could be higher22,23. Additionally, given the presence of asymptomatic infected individuals, taking participants who were not tested as controls could also be another potential source of bias. Our study assessed the effect of genetically predicted vitamin D levels on COVID-19 risk while taking into consideration of ambient UVB radiation during the pandemic. We show an indication of an inverse association between genetically predicted vitamin D levels and severe COVID-19. Findings from our study are consistent with a recent randomised controlled trial (RCT) that found protective effect of vitamin D supplementation among those hospitalised with COVID-1924. However, other clinical trials did not show an effect. For instance, a randomised trial of 240 patients showed that supplementation with a single very large dose of 200,000 IU of vitamin D3 that increased serum vitamin D levels (21–44 ng/ml) was nonetheless ineffective in decreasing the length of hospital stay or any other clinical outcomes among hospitalized patients with severe COVID-1925. It has been estimated that one SD change in standardized natural-log transformed 25-OHD levels corresponds to a change in 25-OHD levels of 29.2 nmol/l in vitamin D insufficient individuals (serum 25-OHD levels 50 nmol/l), which is comparable to the 21.2 nmol/l mean increase in 25-OHD levels conferred by taking daily 400 IU of cholecalciferol, the amount of vitamin D most often found in vitamin D supplements26. This estimation has clinical implication on the dose of vitamin D supplement for disease prevention. Given the lack of highly effective therapies against COVID-19, it is important to remain open-minded to emerging results from rigorously conducted studies of vitamin D.
In conclusion, we found no significant associations between COVID-19 risk and measured 25-OHD levels after adjusted for covariates, but this finding is limited by the fact that the vitamin D levels were measured on average 11 years before the pandemic. Ambient UVB was strongly and inversely associated with COVID-19 hospitalization and death. The main MR analysis did not show that genetically-predicted vitamin D levels were causally associated with COVID-19 risk, although MR sensitivity analyses indicated a potential causal effect. Overall, the effect of vitamin D levels on the risk or severity of COVID-19 remains controversial, further studies are needed to validate vitamin D supplementation as a means of protecting against worsened COVID-19.
A company formed by Harvard genetics professor George Church, known for his pioneering work in genome sequencing and gene splicing, hopes to genetically resurrect woolly mammoths.
