Rubidium Frequency Standard Explained

You’ve probably heard of rubidium frequency standards, which are used where you need an extremely accurate time or frequency reference. [IMSAI] guy has a good explainer video about what’s actually going on inside one of these standards. Much of the basic idea also applies to cesium standards.

The explainer starts with the periodic table. Rubidium and cesium are both alkali metals, with a single electron in their outermost electron shell. Rubidium has 37 electrons, with the outermost one relatively loosely bound. Naturally occurring rubidium consists mainly of two isotopes, rubidium-85 and rubidium-87, which have the same number of protons and electrons but different numbers of neutrons.

A rubidium standard typically has three gas cells that have a bit of rubidium in them. An RF-excited rubidium-87 discharge lamp produces light at very specific wavelengths. The RF energy excites rubidium atoms into higher electronic states, and when their electrons fall back to lower-energy states, the atoms emit photons.

That light passes through a filter cell containing rubidium-85. The filter preferentially absorbs part of the lamp’s spectrum, leaving light that optically pumps the rubidium-87 atoms in the second resonance cell into one of two closely spaced hyperfine states of the atom’s ground state.

Those two states differ because of the interaction between the magnetic moment of the outer electron and that of the rubidium-87 nucleus. Their energy separation corresponds to a microwave frequency of about 6.835 GHz.

The resonance cell is illuminated by the filtered light while also being exposed to microwave energy from a local oscillator. When the microwave frequency is exactly equal to the rubidium-87 hyperfine transition frequency, it transfers atoms between the two ground-state hyperfine levels. That changes how strongly the cell absorbs the optical pumping light, producing a detectable dip in the light reaching a photodetector.

Electronics then servo the microwave oscillator onto the center of that absorption dip, using a feedback technique somewhat analogous to a phase-locked loop. Once locked, the oscillator is effectively referenced to an atomic transition rather than to the dimensions or mechanical properties of a crystal, giving you an extremely stable frequency standard.

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Sketching Temporary Circuits With A Light-Triggered Floquet Topological Insulator

In semiconductor technology, a base material like silicon is permanently modified to induce certain electrical behavior. In comparison a topological insulator material could be used to create temporary circuits using something like light exposure. An example of this is the Floquet topological state, which has long been theorized, but is now claimed to have been demonstrated in SnTe semiconductor material, per a paper by [F. Chassot] et al. in Nature Physics.

The concept of topological insulators was first proposed in 1985, but proving their existence was hard. Recently photonic Floquet topological insulators (PFTIs) have gained interest, with experiments by [Qian Ma] et al. in 2025 as well as other teams confirming aspects of the theory.

This recent publication by [Chassot] et al. would thus confirm that optical control of topological insulators is thus possible. At the core of this effect is the band inversion that results from the light pulses, with the change in conduction being very brief, essentially for as long as the femtosecond pulses were maintained.

Although still very much in the fundamental research phase, the research on these electronic topological insulators offers an interesting look at potential new technologies, much like the field of photonic topological insulators does for photonics.

How The Vagus Nerve Promotes Healthy Cognition Via Acetylcholine Signaling

It’s been said for centuries that you cannot think on an empty stomach, and that love goes through the stomach. Although these may seem like merely cute jabs at the simplicity of human nature, recent research in rat models by [Logan Tierno Lauer] et al. indicates that the gut may be more influential in something as fundamental as memory formation and cognitive function than previously assumed.

Key to the gut-brain connection is the vagus nerve, an essential part of the autonomic nervous system that wires the brain into the body’s organs, including the gastrointestinal (GI) tract. It provides both sensory and motor fibers, so that the brain can literally sense the state of said GI tract, with various triggers as result. One of these is – as demonstrated in the paper – the release of acetylcholine (aCh) an important neurotransmitters in the CNS for cognitive functions including attention, memory and motivation.

Using in vivo fiber photometry it was found that during eating medial septum neurons released aCh, with various ways to impair this mechanism along the vagus nerve leading to this response disappearing. This also confirms earlier research that points the finger at a so-called early life Western Diet (WD) causing impaired memory and overall cognitive function, likely due this high fat and high sugar diet causing dysfunction in this aCh regulation mechanism.

Beyond once again reinforcing the need to eat healthily, this research also provides further insights in condition with declining cognitive function, such as Alzheimer’s and dementia.

De-Aging Human Tissue Using Special Enzyme To Remove AGEs

With human bodies being bags of mostly salty water and countless messy biochemical processes, it’s little wonder that over time some residues tend to collect in these systems. Although evolution has seen fit to also evolve a range of mechanisms to clean up many of those messes, some of these waste products are left to gather, such as advanced glycation end-products (AGEs). Implicated in everything from diabetes to chronic kidney disease and general aging-related conditions, recently researchers have developed a way to break down one type of these AGEs.

Called N(6)-Carboxymethyllysine (CML), there is evidence to suggest that the presence of AGEs like it in the extracellular matrix (ECM) has damaging effects on the ECM’s functioning, as observed in e.g. the inhibiting of collagen crosslinking and the resulting ‘aging’ of skin among other tissues. Essentially these waste product jam up the normal biochemical machinery, while also triggering pro-inflammatory factors.

Beyond aging-related conditions, this can result in a whole range of other diseases that may be resolved if these waste products could be cleaned out. To this end [Narisa Trabosh] et al. of the San Francisco-based Revel Pharmaceuticals laboratory created CMLase, an enzyme that breaks down CML.

Arterial tissue treated with the CMLase enzyme shows a clear difference. (Credit: Trabosh et al., Nature communications, 2026)
Arterial tissue treated with the CMLase enzyme shows a clear difference. (Credit: Trabosh et al., Nature communications, 2026)

The challenge here was to design this enzyme, which used a genetic selection approach in modified E. coli to narrow down suitable enzymes, optimized for dealing with free CML. Once they were fairly confident that they had a working enzyme, they had to test it and observe the results.

This testing was performed in model proteins in vitro, as well as in tissue samples from elderly donors. These latter included lens, skin and arterial tissue, all of which are long-lived tissues that have plenty of time to collect CML. After treatment with CMLase the presence of CML in these tissues was reduced by 55% for skin and 75% for arterial tissue.

Of course, as also noted in the article these are ex vivo experiments that do not yet directly translate to living patients. An initial human trial would need to show safety above all, even if the amount of waste produced by the clean-up of CML won’t be that significant.

Subsequent trials would need to demonstrate that such removal of CML leads to healthier tissues, which if confirmed would open the path for other pathogenic AGEs to get their own matching enzyme.

Filling High Pressure CO2 Tanks From Sugar Fermentation Gas

After previously using the fermenting of sugar to obtain ethanol fuel, [Hyperspace Pirate] figured that it’d be a waste to just blast the other half of the yeast production in the form of carbon dioxide into the air. This poses the slight problem that gaseous CO2 is fairly bulky, while compressing it into a liquid isn’t exactly for the faint of heart. This of course means that it’s a fun challenge, involving a beach ball, vapor-compression and various compressors.

Although at room temperature compressing CO2 into a liquid requires quite extreme pressures, if you lower it to freezing temperatures it becomes quite feasible to use more typical off-the-shell compressors.

In the video both oil-less and regular compressors are used, mostly because ultimately you want to get pure CO2 into the bottle, without oil or water. Here a few methods are explored, including a pre-cooler with the oil-less compressor as it cannot quite hit the same pressures. With a typical compressor linked to an oil-separator you can directly fill the tank, which is pretty nice, though even with this removal of water turned out to be a chore.

Desiccating the gas that comes out of the fermentation vat, is attempted using a converted water filter that’s filled with desiccant beads, but as the later tests show, this isn’t quite good enough to prevent moisture to make it into the bottle and clogging its nozzle. Of course, moisture here is more acceptable than oil for most applications, so with some more work this could be quite a feasible method to fill bottles with liquid CO2 for various nefarious applications like paintball guns and more.

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Fast Volumetric Imaging Of Seizures With Adaptive Optics Light Sheet Microscopy

Seizure in zebrafish larva imaged using AO setup. (Credit: Bingxi Liu et al., Biomedical Optics Express, 2026)
Seizure in zebrafish larva imaged using AO setup. (Credit: Bingxi Liu et al., Biomedical Optics Express, 2026)

Key to understanding something like epilepsy is to be able to record highly transient events in biological tissues. Generally this is done using light sheet microscopy, which provides effectively a 2D ‘slice’ of the tissue in question, but to observe a brief event in a larger biological system you need to be able to rapidly change the layer and focus between the virtual layers. This is what [Bingxi Liu] et al. al did using adaptive optics with an electrically tunable lens (ETL) in order to capture seizures in the brain of zebrafishes.

Their system can capture a volume of 499 × 499 × 150 μm3 at 4 volumes per second, which is large enough to fit optically transparent zebrafish larva into. The optical setup is shown in the above image, with the design based on the OpenSPIM platform for selective plane illumination microscopy.

Here the 488 nm laser provides the illumination (excitation) of the layer, while the 543 nm laser is for calibration purposes. The ETL is thus in the imaging path that allows for capturing by a digital camera, while a beam splitter directs part of the captured data to a Shack-Hartmann wave front sensor (SHWFS), which is part of the adaptive optics system.

After a seizure was induced in the zebrafish larva using the drug pentylenetetrazol the results were recorded using this system. It showed the seizure’s origin in the posterior brain, with subsequent propagation to the anterior before subsiding gradually over tens of seconds.

This system should be quite useful even outside of seizure research, as there are a lot of 3D systems in biology where having a relatively high-speed microscopic capture can be very revealing.

Targeting Allele-Specific Faulty MRNA In SCNA2 Mutation Patients

When an individual is born with genetic defects, there are a few ways to deal with the impact of the faulty genes. The most extreme solution is direct DNA editing to repair the mutation, while the treatment of symptoms with medication is the least invasive, though this comes with its own set of disadvantages. Antisense therapy keeps a middle ground here, by targeting the messenger RNA (mRNA) that forms the bridge between DNA and the translation into a functional protein by the ribosome.

In a recent study by [Olivia Kim-McManus] et al. antisense therapy with an allele-specific feature was demonstrated in two individuals with SCN2A mutations. These mutations had resulted in severe epilepsy and developmental disorders, due to how instrumental this gene is for normal functioning of the human central nervous system (CNS) where it regulates the initiation of action potentials.

Although SCN2A mutations are rarely inherited, for the approximately 1 in 80,000 affected the consequences can be quite dramatic. The two major types of mutations are classified as gain-of-function (GoF) and loss-of-function (LoF) with respectively hyper- and hyposensitivity of the resulting NAv1.2 sodium channels.

This translates especially in the case of GoF mutations into various symptoms, ranging from mild to severe (daily) epileptic attacks starting as an infant, stalled neurodevelopment and various types of autism (ASD). Often sodium channel blockers are prescribed for the GoF cases to limit epileptic attacks.

Usually with the responsible mutations only a single copy of the gene is affected, so while regular antisense therapy could be used, this would risk also modifying the healthy SCN2A mRNA copy. To get around this, an individualized treatment was developed, targeting the allele with the mutated gene for the two patients in the study: 9- and 14-year old boys with severe developmental and epileptic encephalopathies (DEE) that had left them with daily seizures and despite sodium-channel blockers and other typical medications.

Study outcome of the 14-year old boy with DEE after ASO therapy. (Credit: Kim-McManus et al., Nature Medicine, 2026)
Study outcome of the 14-year old boy with DEE after ASO therapy. (Credit: Kim-McManus et al., Nature Medicine, 2026)

During the trial, the 9-year old boy received 12 doses over 24 months of antisense oligonucleotides (ASOs) adapted to his affected allele, allowing for the cessation of the anti-seizure medication phenytoin, with an overall reduction in seizures. In the case of the 14-year old boy 8 doses were administered over 16 months, resulting in an average of two seizures a day being reduced to zero.

Although the focus of the study was on treating these seizures, by addressing the underlying cause of faulty mRNA transcriptions, changes in the neurodevelopmental state could also be observed. In particular language and motor skills improved, with erratic and irritable behavior reducing. The by then 15-year year old boy was able to walk unassisted, showing clear progression from the previous infantile state.

The advantage of ASOs over typical anti-seizure medication is of course that it directly addresses the faulty mRNA and thus the resulting faulty sodium channels. Since ASOs tend to hang around in a cell for a considerable amount of time, they could be quite a viable alternative treatment even for less severe cases. Whether early application of individualized ASOs in affected infants could lead to a more or less normal neurodevelopment would also be an interesting study question.

Naturally, directly addressing the faulty gene or upregulating the healthy gene would be the ideal and permanent solution, with research here also underway in mice models with the use of CRISPR-based tools.