Organs are in short supply. About 17 people die each day waiting for a transplant. New experimental methods of growing and tweaking organs could help.
Join us on Patreon!
https://www.patreon.com/MichaelLustgartenPhD
Quantify Discount Link (At-Home Blood Testing)
https://getquantify.io/mlustgarten.
Since the beginning of human storytelling, enhancing oneself to a “better version” was of vital interest to humans. A twenty-first century-philosophical movement called transhumanism dedicated itself to the topic of enhancement. It unites discussions from several disciplines, e.g. philosophy, social science, and neuroscience, and aims to form human beings in desirable ways with the help of science and technology (Bostrom, 2005; Loh, 2018; More, 2013). Enhancement is the employment of methods to enhance human cognition in healthy individuals (Colzato et al., 2021), thereby extending individual performance above already existing abilities. It should thus be distinguished from therapy, which is the application of methods to help individuals with illnesses or dysfunctions in restoring their abilities (Viertbauer & Kögerler, 2019). Although enhancement methods bear psychological implications, there is hardly any psychological research on them. However, as the use of enhancement methods has increased (Leon et al., 2019; McCabe et al., 2014), and with it the demand for official guidelines (Jwa, 2019), it is necessary to examine who would use these methods in the first place, especially because these technologies can easily be misused. Investigating personality traits and values of individuals who want to enhance themselves could not only support suppliers and manufacturers of enhancement technologies in creating guidelines for using enhancement, but also raise more general awareness on which individuals might be in favour of enhancement.
In previous studies investigating the intersection between enhancement and personality traits or values, vignettes were used to describe enhancement methods and to measure their acceptance among participants (e.g. Laakasuo et al., 2018, 2021). Thus, subjects were asked to read scenarios involving the use of a certain enhancement method and then—as a measure of acceptance—judge aspects (e.g. the morality) of the action undertaken in the corresponding scenario (e.g. Laakasuo et al., 2018, 2021). In the present study, we followed a similar vignette-based approach with a variety of different enhancement methods to investigate the link between the acceptance of enhancement (i.e., the willingness to use enhancement methods, hereinafter termed AoE), personality traits, and values. More specifically, we examined the acceptance of the most discussed cognitive enhancement methods: pharmacological enhancement, brain stimulation with transcranial electrical stimulation and deep brain stimulation, genetic enhancement, and mind upload (Bostrom, 2003; Dijkstra & Schuijff, 2016; Dresler et al., 2019; Gaspar et al., 2019; Loh, 2018).
Pharmacological enhancement has received much attention in the media and literature (Daubner et al., 2021; Schelle et al., 2014) and is defined as the application of prescription substances that are intended to ameliorate specific cognitive functions beyond medical indications (Schermer et al., 2009). The best-known drugs for cognitive enhancement are methylphenidate (Ritalin®), dextroamphetamine (Adderall®), and modafinil (Provigil®), which are usually prescribed for the treatment of clinical conditions (de Jongh et al., 2008; Mohamed, 2014; Schermer et al., 2009).
O.o! Circa 2021
False teeth could one day be a thing of the past, thanks to the discovery of an antibody that sparks the regeneration of lost teeth. By inhibiting the action of a gene called USAG-1, the antibody increases the availability of certain growth factors, and could eventually be used to help people grow a new set of pearly whites.
Publishing their work in the journal Science Advances, a team of researchers describes how they genetically modified mice to suffer from tooth agenesis, where some teeth fail to develop. Injecting pregnant mice from this line with the USAG-1 antibody, however, resulted in normal tooth development among their offspring. Moreover, a single administration of the antibody caused the growth of a whole new tooth in regular mice.
Continue reading “Researchers Have Found A Way To Regrow Teeth” »
A genetically modified version of the herpes virus has shown great potential in treating advanced cancers, according to a report by the Institute of Cancer Research in London published on Thursday.
A promising therapy
Although the treatment is still in early trials, researchers have found that RP2, a modified version of the herpes simplex virus, managed to kill cancer cells in a quarter of patients. The patients had cancers so advanced and complicated that they had run out of treatments to try.
Circa 2017 face_with_colon_three
LA JOLLA—Salk scientists have created a new version of the CRISPR/Cas9 genome editing technology that allows them to activate genes without creating breaks in the DNA, potentially circumventing a major hurdle to using gene editing technologies to treat human diseases.
According to recent research from Sweden’s Lund University, the most commonly used analytical method in population genetics is deeply flawed. This could have caused incorrect results and misconceptions regarding ethnicity and genetic relationships. The method has been used in hundreds of thousands of studies, influencing findings in medical genetics and even commercial ancestry tests. The findings were recently published in the journal Scientific Reports.
The pace at which scientific data can be gathered is increasing rapidly, resulting in huge and very complex databases, which has been nicknamed the “Big Data revolution.” Researchers employ statistical techniques to condense and simplify the data while maintaining the majority of the important information in order to make the data more manageable. PCA (principal component analysis) is perhaps the most widely used approach. Imagine PCA as an oven with flour, sugar, and eggs serving as the input data. The oven may always perform the same thing, but the ultimate result, a cake, is highly dependent on the ratios of the ingredients and how they are mixed.
“It is expected that this method will give correct results because it is so frequently used. But it is neither a guarantee of reliability nor produces statistically robust conclusions,” says Dr. Eran Elhaik, Associate Professor in molecular cell biology at Lund University.
Impaired reduction/oxidation (redox) metabolism is a key contributor to the etiology of many diseases, including primary mitochondrial disorders, cancer, neurodegeneration, and aging. However, mechanistic studies of redox imbalance remain challenging due to limited strategies which can perturb cellular redox metabolism and model pathology in various cellular, tissue, or organismal backgrounds without creating additional and potentially confounding metabolic perturbations. To date, most studies involving impaired redox metabolism have focused on oxidative stress and reactive oxygen species (ROS) production; consequently, less is known about the settings where there is an overabundance of reducing equivalents, termed reductive stress. NADH reductive stress has been modeled using pharmacologic inhibition of the electron transport chain (ETC) and ethanol supplementation. Still, both these methods have significant drawbacks. Here, we introduce a soluble transhydrogenase from E. coli (Ec STH) as a novel genetically encoded tool to promote NADH overproduction in living cells. When expressed in mammalian cells, Ec STH, and a mitochondrially-targeted version (mito Ec STH), can elevate the NADH/NAD+ ratio in a compartment-specific manner. Using this tool, we determine the metabolic and transcriptomic signatures of NADH reductive stress in mammalian cells. We also find that cellular responses to NADH reductive stress, including blunted proliferation, are dependent on cellular background and identify the metabolic reactions that sense changes in the cellular NADH/NAD+ balance. Collectively, our novel genetically encoded tool represents an orthogonal strategy to perturb redox metabolism and characterize the impact on normal physiology and disease states.
The authors have declared no competing interest.
Researchers at Mayo Clinic Comprehensive Cancer Center have identified a gene marker that may lead to a more effective, precision treatment for pancreatic ductal adenocarcinoma (PDAC). The researcher’s findings are published in Nature Cancer.
“Pancreatic ductal adenocarcinoma is one of the most lethal cancers,” says the paper’s senior author Zhenkun Lou, Ph.D. Dr. Lou says while Poly-ADP-ribose-polymerase inhibitors (PARPi) are now an FDA-approved option for standard maintenance therapy for patients with metastatic PDAC who harbor pathogenic germline BRCA1/2 mutations, only about 10 percent of patients with PDAC harbor pathogenic mutations of the homologous recombination (HR) genes. “This leaves most patients missing out on this encouraging treatment strategy,” says Dr. Lou.
In this study, Dr. Lou and his colleagues found that the protein METTL16 may be a new biomarker for PARPi treatment, and that PDAC with elevated expression of METTL16, may benefit from PARPi treatment.
Summary: In mice genetically more susceptible to PTSD following a stressful event, researchers found an increased expression of cortisol receptors on neurons in the CA1 region of the dorsal hippocampus. Those increased receptors enabled an elevated expression of the HCN1 protein and TRIP8b, reducing neural excitability.
Source: medical college of georgia at augusta university.
Social avoidance is a common symptom of PTSD, and scientists working to better understand why have laboratory evidence that while stress hormone levels consistently increase in the immediate aftermath of a traumatic event, there can be polar opposite consequences in parts of the brain down the line.
Impaired reduction/oxidation (redox) metabolism is a key contributor to the etiology of many diseases, including primary mitochondrial disorders, cancer, neurodegeneration, and aging. However, mechanistic studies of redox imbalance remain challenging due to limited strategies which can perturb cellular redox metabolism and model pathology in various cellular, tissue, or organismal backgrounds without creating additional and potentially confounding metabolic perturbations. To date, most studies involving impaired redox metabolism have focused on oxidative stress and reactive oxygen species (ROS) production; consequently, less is known about the settings where there is an overabundance of reducing equivalents, termed reductive stress. NADH reductive stress has been modeled using pharmacologic inhibition of the electron transport chain (ETC) and ethanol supplementation. Still, both these methods have significant drawbacks. Here, we introduce a soluble transhydrogenase from E. coli (Ec STH) as a novel genetically encoded tool to promote NADH overproduction in living cells. When expressed in mammalian cells, Ec STH, and a mitochondrially-targeted version (mito Ec STH), can elevate the NADH/NAD+ ratio in a compartment-specific manner. Using this tool, we determine the metabolic and transcriptomic signatures of NADH reductive stress in mammalian cells. We also find that cellular responses to NADH reductive stress, including blunted proliferation, are dependent on cellular background and identify the metabolic reactions that sense changes in the cellular NADH/NAD+ balance. Collectively, our novel genetically encoded tool represents an orthogonal strategy to perturb redox metabolism and characterize the impact on normal physiology and disease states.
