Fragile X syndrome is a genetic disorder caused by a mutation in a gene that lies at the tip of the X chromosome. It is linked to autism spectrum disorders.
People with fragile X experience a range of symptoms that include cognitive impairment, developmental and speech delays and hyperactivity. They may also have some physical features such as large ears and foreheads, flabby muscles and poor coordination.
For many people, depression turns out to be one of the most disabling illnesses that we have in society. Despite the treatments that we have available, many people are not responding that well. It’s a disorder that can be very disabling in society. It’s also a disorder that has medical consequences. By understand the neurobiology of depression we hope to be able more to find the right treatment for the patient suffering from this disease. The current standard of care for the treatment of depression is based on what we call the monoamine deficiency hypothesis. Essentially, presuming that one of three neurotransmitters in the brain is deficient or underactive. But the reality is, there are more than 100 neurotransmitters in the brain. And billions of connections between neurons. So we know that that’s a limited hypothesis. Neurotransmitters can be thought of as the chemical messengers within the brain, it’s what helps one cell in the brain communicate with another, to pass that message along from one brain region to another. For decades, we thought that the primary pathology, the primary cause of depression was some abnormality in these neurotransmitters, specifically serotonin or norepinephrine. However, norepinephrine and serotonin did not seem to be able to account for this cause, or to cause the symptoms of depression in people who had major depression. Instead, the chemical messengers between the nerve cells in the higher centers of the brain, which include glutamate and GABA, were possibilities as alternative causes for the symptoms of depression. When you’re exposed to severe and chronic stress like people experience when they have depression, you lose some of the connections between the nerve cells. The communication in these circuits becomes inefficient and noisy, we think that the loss of these synaptic connections contributes to the biology of depression. There are clear differences between a healthy brain and a depressed brain. And the exciting thing is, when you treat that depression effectively, the brain goes back to looking like a healthy brain, both at the cellular level and at a global scale. It’s critical to understand the neurobiology of depression and how the brain plays a role in that for two main reasons. One, it helps us understand how the disease develops and progresses, and we can start to target treatments based on that. We are in a new era of psychiatry. This is a paradigm shift, away from a model of monoaminergic deficiency to a fuller understanding of the brain as a complex neurochemical organ. All of the research is driven by the imperative to alleviate human suffering. Depression is one of the most substantial contributors to human suffering. The opportunity to make even a tiny dent in that is an incredible opportunity.
Can the fountain of youth come in the form a pill?
Imagine this: a cocktail of specialized chemicals that rejuvenates your whole body, from your eyes and brain to your kidneys and muscles—bringing you back to a more youthful version of yourself.
Powders of samples were weighed into precleaned Savillex beakers and dissolved with mixtures of 22 M HF and 14 M HNO3 acids in a 2:1 volume ratio. The modern OIBs and four reference materials (that is, BHVO-2, BCR-2, AGV-2 and BIR-1) were digested on a hot plate at 120 °C for four days. Note that all chondrite and Archaean ultramafic/mafic rock samples were digested in Parr bomb vessels at 220 °C for three days to ensure full dissolution of refractory phases. Dissolution of the dried samples in 5–10 ml 6 M HCl at 120 °C and evaporation was carried out several times to decompose the fluorides formed from HF digestion until clear solutions were obtained. An aliquot of each sample was taken and spiked with a prepared 47 Ti–49 Ti double spike to determine in advance the Ti concentration using an iCAP RQ inductively coupled plasma mass spectrometer at the Centre for Star and Planet Formation (StarPlan) at the University of Copenhagen. Afterwards, aliquots containing 6 µg Ti were taken and mixed with a 47 Ti–49 Ti double spike as described previously in ref. 34. The dried mixtures were dissolved with 6 M HCl at 120 °C overnight to ensure sample–spike equilibration.
Titanium was separated from matrix elements following a three-step purification protocol using AG1x8 (200–400 meshes) and DGA resins34,68, that is, first to separate Fe with 6 M HCl elution on AG1x8 columns, second to remove most of the major and trace elements through 12 M HNO3 elution and to collect Ti with Milli-Q H2O on DGA columns and third to purify Ti from the remaining matrix elements with 4 M HF cleaning on AG1x8 columns. An extra DGA pass can be carried out to remove trace amounts of Ca and Cr in the final Ti cuts. To destroy the resin particles and organics from column chemistry, the Ti cuts were treated with 14 M HNO3 at 120 °C before storage in 0.5 M HNO3 + 0.01 M HF acids.
Titanium isotopic compositions of the purified samples were measured using the ThermoFisher Scientific Neoma Multicollector ICP-MS. Sample solutions with 500–800 ppb Ti dissolved in 0.5 M HNO3 + 0.01 M HF were introduced into the multicollector inductively coupled plasma source mass spectrometer by means of an APEX HF desolvating nebulizer from Elemental Scientific and a sapphire injector was used instead of the quartz-made injector to reduce the production of silicon fluorides from the use of HF solvent. An actively cooled membrane desolvation component was attached after the APEX to suppress oxide formation and to stabilize the signals, and N2 gas at a flow rate of a few ml min−1 was added to improve the sensitivity. Such a setting typically provides an intensity of around 15 V on 48 Ti+ at an uptake rate of about 50 μl min−1 for a 600-ppb Ti solution under a medium mass-resolution mode.
A team of researchers has recently claimed to have discovered six chemical cocktails that could help reverse biological aging. Yet these preliminary laboratory results are a long way away from being applied to humans.
Chemical propulsion has long been the standard for spaceflight, but for humans to reach Mars, we’ll need a much more powerful and efficient propulsion. Nuclear thermal propulsion (NTP) engines offer thrust as high as conventional chemical propulsion with much higher efficiency.
A new approach to developing semiconductor materials at tiny scales could help boost applications that rely on converting light to energy. A Los Alamos-led research team incorporated magnetic dopants into specially engineered colloidal quantum dots—nanoscale-size semiconductor crystals—and was able to achieve effects that may power solar cell technology, photo detectors and applications that depend on light to drive chemical reactions.
“In quantum dots comprising a lead-selenide core and a cadmium-selenide shell, manganese ions act as tiny magnets whose magnetic spins strongly interact with both the core and the shell of the quantum dot,” said Victor Klimov, leader of the Los Alamos nanotechnology team and the project’s principal investigator. “In the course of these interactions, energy can be transferred to and from the manganese ion by flipping its spin—a process commonly termed spin exchange.”
In spin-exchange carrier multiplication, a single absorbed photon generates not one but two electron-hole pairs, also known as excitons, which occur as a result of spin-flip relaxation of an excited manganese ion.
The term molybdenum disulfide may sound familiar to some car drivers and mechanics. No wonder: the substance, discovered by U.S. chemist Alfred Sonntag in the 1940s, is still used today as a high-performance lubricant in engines and turbines, but also for bolts and screws.
This is due to the special chemical structure of this solid, whose individual material layers are easily displaceable relative to one another. However, molybdenum disulfide (chemically MoS2) not only lubricates well, but it is also possible to exfoliate a single atomic layer of this material or to grow it synthetically on a wafer scale.
The controlled isolation of a MoS2 monolayer was achieved only a few years ago, but is already considered a materials science breakthrough with enormous technological potential. The Empa team now wants to work with precisely this class of materials.
DNA can do more than pass genetic code from one generation to the next. For nearly 20 years, scientists have known of the molecule’s ability to stabilize nanometer-sized clusters of silver atoms. Some of these structures glow visibly in red and green, making them useful in a variety of chemical and biosensing applications.
Stacy Copp, UCI assistant professor of materials science and engineering, wanted to see if the capabilities of these tiny fluorescent markers could be stretched even further—into the near-infrared range of the electromagnetic spectrum—to give bioscience researchers the power to see through living cells and even centimeters of biological tissue, opening doors to enhanced methods of disease detection and treatment.
“There is untapped potential to extend fluorescence by DNA-stabilized silver nanoclusters into the near-infrared region,” she says. “The reason that’s so interesting is because our biological tissues and fluids are much more transparent to near-infrared light than to visible light.”
This is a good use of AI. Definitely regular it but I can see it’s contributing to medical research.
Summary: Researchers have utilized artificial intelligence to uncover the promising potential of extra virgin olive oil (EVOO) in combating Alzheimer’s disease (AD).
By integrating AI, chemistry, and omics research, the study identified specific bioactive compounds in EVOO that could contribute to the treatment and prevention of AD. Ten phytochemicals within EVOO, such as quercetin, genistein, luteolin, and kaempferol, were found to exhibit potential impacts on AD protein networks.
