Discover the fascinating world of nanotechnology and its impact on our lives. Learn about the science on a tiny scale and how it revolutionizes medicine, electronics, and everyday products.
Year 2023 Basically solar will last several billion years and make type 0 civilization resources obsolete by making trillions of dollars in profits with nearly zero emissions.
Between the Covid-19 pandemic, the Ukraine conflict, inflation, and the renewables transition, the 2020s have been a volatile decade for energy. The pandemic reduced demand for electricity and oil all over the world, causing prices to plummet. Then the Ukraine invasion brought sanctions on Russian oil and gas, pushing energy prices up and leaving European countries scrambling (particularly for natural gas). High energy prices have since contributed to inflation, and in many places utility costs are far surpassing inflation. All the while, worry over climate change has continued to mount, with calls to reduce our dependence on fossil fuels growing ever louder.
In short, the energy situation in the US and around the world is a mess. But the International Energy Agency released some good news in its recent World Energy Investment report. The report is compiled annually, and the 2023 version came out at the end of May. For the first time ever, it found that investment in renewables—specifically solar power—will overtake spending on oil.
Continue reading “Solar Power Investment Will Overtake Oil for the First Time Ever This Year” »
The role that Epstein-Barr virus (EBV) plays in the development of multiple sclerosis (MS) may be caused by a higher level of cross-reactivity, where the body’s immune system binds to the wrong target, than previously thought.
In a new study published in PLOS Pathogens, researchers looked at blood samples from people with MS, as well as healthy people infected with EBV and people recovering from glandular fever caused by recent EBV infection.
The study investigated how the immune system deals with EBV infection as part of worldwide efforts to understand how this common virus can lead to the development of multiple sclerosis, following 20 years of mounting evidence showing a link between the two.
Positive life experiences boost brain mitochondrial health, potentially providing protection against certain brain disorders and promoting longevity.
In @MedicalXpress: https://ow.ly/BNn750SrT3c.
In PNAS: https://ow.ly/wT1e50SrT3b.
Continue reading “Psychosocial experiences are associated with human brain mitochondrial biology” »
By 
Julia Robinson 2024–06-24T12:55:00
Researchers are on a quest to outsmart and overcome the sophisticated security system of the brain. Julia Robinson reports on some of the approaches being studied.
A remarkable discovery in the Siberian permafrost: a 44,000-year-old wolf with preserved stomach contents and organs.
This single-center longitudinal cohort study has followed known carriers of PRNP pathogenic variants at risk for prion disease, individuals with a close relative who died of genetic prion disease but who have not undergone predictive genetic testing, and controls. All participants were asymptomatic at first visit and returned roughly annually. We determined PRNP genotypes, measured NfL and GFAP in plasma, and RT-QuIC, total PrP, NfL, T-tau, and beta-synuclein in CSF.
Cirrus Therapeutics, the University of Bristol, and London’s Global University Institute of Ophthalmology have discovered a new treatment for age-related macular degeneration (AMD), the leading cause of vision loss among older adults.
Featured on the cover of the journal Science Translational Medicine, this research reveals that boosting a specific protein, IRAK-M, in retinal cells could offer a new and highly effective therapy for AMD.
AMD can severely impact a person’s vision. Patients suffering from AMD often start with blurred vision or seeing a black dot in their central vision, which can ultimately expand to the point where there is no useful central vision. Currently, AMD affects approximately 200 million people worldwide, a number projected to rise to 288 million by 2040 with graying populations. The exact cause of AMD is complex and thought to involve a combination of aging, environmental, and lifestyle factors.
The probe also achieved stable neural recordings in rat brains for up to two years, showing excellent biocompatibility and long-term recording stability, state news agency Xinhua reported.
Cheng Heping, with the Chinese Academy of Sciences and director of the National Centre for Biomedical Imaging Science at Peking University, told Xinhua that the achievement provided a powerful tool for high-throughput simultaneous monitoring of activity in multiple brain regions, and for exploring the relationships between neural activity and behaviour.
This study uncoversthe pivotal role of the enzyme METTL4 in promoting tumor metastasis through the mediation of nuclear N6-methyldeoxyadenosine (6mA) in mammalian cells. By utilizing cellular models, the study demonstrates how hypoxia induces METTL4 to mediate 6mA modifications. This process, in turn, activates genes essential for tumor metastasis, including the involvement of specific long noncoding RNA and a novel HIF-1α co-activator, ZMIZ1. These findings not only shed light on the epigenetic mechanisms driving tumor progression but also establish METTL4 as a prognostic marker for cancer and a potential target for therapeutic intervention. The promise of this discovery lies in its potential to inspire new strategies for combating hypoxia-induced tumor progression, opening avenues for further research and development in cancer treatment.
DNA N6-methyldeoxyadenosine (6mA) has been recognized in various organisms for its role in gene regulation. However, its function in mammalian cells, particularly in the context of cancer, has remained elusive. Previous studies have shown that 6mA modifications can influence gene expression and are present in several species, indicating a potential regulatory role in tumorigenesis. This research addresses a critical gap in understanding the nuclear role of 6mA and its enzymatic mediator METTL4, in mammalian tumor cells, particularly under hypoxia (a common condition in tumor microenvironments that promotes metastasis). The study posits that METTL4-mediated 6mA deposition is a key epigenetic modification that activates metastasis-inducing genes. This finding offers a new perspective on the mechanisms of tumor progression and identifying novel targets for therapeutic intervention.
Continue reading “The Enzyme Leading the Charge Against Tumor metastasis” »
