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Comment by Dr. Krishna Kumari Challa on June 16, 2023 at 11:01am

Seeing Dead Flies Makes Other Flies Die Faster

There might be a weird benefit to leaving dead flies where they fall .

Research has shown that when fruit flies of the species Drosophila melanogaster are exposed to the carcasses of their dead friends, their lifespan shrinks in a significant and measurable way.

They start acting withdrawn, lose body fat, and their aging accelerates to the point that they die sooner than fruit flies that don't see their dead buddies just lying where they fall like some macabre fruit fly graveyard.

And now scientists have a better idea about why this happens. Two neuron types receptive to the neurotransmitter serotonin become activated when fruit flies perceive dead comrades, and this increased activity accelerates the flies' aging process.

Scientists have seen similar effects in other animals: necrophoresis, or the removal of dead conspecifics, in eusocial insects; vocalization and corpse inspection in elephants; or an increase in levels of regulatory hormones called glucocorticoids in nonhuman primates.

https://journals.plos.org/plosbiology/article?id=10.1371/journal.pb...

Comment by Dr. Krishna Kumari Challa on June 16, 2023 at 9:00am

To form the vesicles and to get the nanostructures inside these vesicles, the team used an established method, placing the nanostructures in a solution of water and sugar (sucrose) and adding this to a layer of oil and lipids and another layer of glucose.

Spinning (centrifuging) this combination of substances resulted in droplets of oil with a membrane composed of a double layer of lipids, mimicking the membrane that separates cells from the outside world, with the nanostructures migrating inside these droplets.

Nishkantha Arulkumaran et al, Creating complex protocells and prototissues using simple DNA building blocks, Nature Communications (2023). DOI: 10.1038/s41467-023-36875-5

Part 2

Comment by Dr. Krishna Kumari Challa on June 16, 2023 at 9:00am

Researchers  artificially re-creates cell 'skeletons' using strands of DNA

 

 The tiny tubes and thread-like structures that give cells their shape and help determine their function have been artificially re-created using strands of DNA in a study by researchers.

The research, published in Nature Communications, represents a key step toward synthetic "smart cells" that could be used to sense diseases, deliver drugs or repair damaged cells inside the body.

Cells, about a thousandth of a millimeter in size, are the fundamental units of all life. They contain "skeletons" made of proteins that fulfill a number of functions, such as providing structural support, helping the cell move around, and transporting materials within the cell.

Re-creating these tubes and threads using proteins is challenging, so the researchers used strands of DNA as building blocks, and were able to precisely customize the structures' dimensions (from about 20 to 400 nanometers thick) and stiffness (from flexible to ultra-rigid).

These tubes and threads were integrated inside cell-like sacs as well as coated on to the sacs' exterior—functioning as a cytoskeleton (inside the cell) or exoskeleton (outside the cell). Most bacteria have what can be described as an exoskeleton, whereas plants, animals and other multicellular organisms have a cytoskeleton.

The tubes and threads were found to stabilize the sacs (vesicles), reducing the chance of them rupturing, in a similar way to how these skeletal structures work in real cells.

The research team was also able to control the exact location of the tubes and fibers in real-time while they were inside the vesicles by attaching magnetic nanoparticles to the structures using an external magnet.

 This work can help to unlock future smart cells able to sense diseases, repair damaged cells by fusing with them, and deliver drugs in a more targeted way—for instance, by carrying a drug or antibiotic and releasing it exactly where it is needed in the body.

This initial study gave promising signs that these protocells may have limited toxicity for humans and the next step is to move from the laboratory to animals to investigate further how these protocells interact with living tissue.

Researchers need to ensure they are stable in the body and able to circulate the blood stream—then we can adapt them to target cancers or pathogenic bacteria.

In addition, the researchers showed how their protocells could combine to form something analogous to living tissue. They placed the protocells in a solution of water and sugar. The cells sank (as they were heavier than the solution) and the evaporation of the water induced a swirling current that pushed the cells together. The team were able to bind these cells more tightly together by placing nanotubes or fibers on the exterior of the cells (giving the cells a "hairy" appearance). This caused the cells to lose their spherical shape and form a honeycomb pattern.

 

The researchers created the tubes and threads by placing strands of DNA in a solution of magnesium chloride, which is heated and then cooled at a fixed rate of half a degree a minute. This triggered the DNA to self-assemble into an ordered structure. By varying the magnesium concentration of the solution, the researchers were able to determine the dimensions and stiffness of the structure.

Part 1

Comment by Dr. Krishna Kumari Challa on June 14, 2023 at 11:38am

How cells kill themselves

Comment by Dr. Krishna Kumari Challa on June 14, 2023 at 10:25am

 How microplastics stick around in human airways

Research shows humans might inhale about 16.2 bits of microplastic every hour, which is equivalent to a credit card over an entire week. And these microplastics—tiny debris in the environment generated from the degradation of plastic products—usually contain toxic pollutants and chemicals.

Inhaled microplastics can pose serious health risks, so understanding how they travel in the respiratory system is essential for prevention and treatment of respiratory diseases.

Researchers  explored the movement of microplastics with different shapes (spherical, tetrahedral, and cylindrical) and sizes (1.6, 2.56, and 5.56 microns) and under slow and fast breathing conditions.

Microplastics tended to collect in hot spots in the nasal cavity and oropharynx, or back of the throat.

The complicated and highly asymmetric anatomical shape of the airway and complex flow behavior in the nasal cavity and oropharynx causes the microplastics to deviate from the flow pathline and deposit in those areas.

The flow speed, particle inertia, and asymmetric anatomy influence the overall deposition and increase the deposition concentration in nasal cavities and the oropharynx area.

Breathing conditions and microplastic size influenced the overall microplastic deposition rate in airways. An increased flow rate led to less deposition, and the largest (5.56 micron) microplastics were deposited in the airways more often than their smaller counterparts.

This study emphasizes the need for greater awareness of the presence and potential health impacts of microplastics in the air we breathe.

How microplastics are transported and deposited in realistic upper airways, Physics of Fluids (2023). DOI: 10.1063/5.0150703

Comment by Dr. Krishna Kumari Challa on June 14, 2023 at 9:49am

One consistent finding throughout the populations studied was that age was not the single determinant factor in a person's response to inflammatory stress. Some younger persons with poor immune resilience had the same signatures and immune health grades commonly seen in older persons. This finding suggests that the ability to restore and maintain immunocompetence at younger ages may be linked to life span. Another factor noted across the populations and species was that higher levels of optimal immune resilience were observed more often in females than males.

These assessments have utility for understanding who might be at greater risk for developing diseases that affect the immune system, how individuals are responding to treatment, and whether, as well as to what extent, they will recover.

Sunil Ahuja, Immune resilience despite inflammatory stress promotes longevity and favorable health outcomes including resistance to infection, Nature Communications (2023). DOI: 10.1038/s41467-023-38238-6. www.nature.com/articles/s41467-023-38238-6

Part 2

Comment by Dr. Krishna Kumari Challa on June 14, 2023 at 9:47am

People who preserve 'immune resilience' live longer and resist infections, study finds

Researchers have revealed that the capacity to resist or recover from infections and other sources of inflammatory stress—called "immune resilience"—differs widely among individuals. The researchers developed a unique set of metrics to quantify the level of immune resilience. This will aid in decisions for health care and help researchers understand differences in life span and health outcomes in persons of similar ages. 

Although age plays an important role in the body's response to infectious and other inflammatory stressors, some persons preserve and/or restore optimal immune resilience regardless of age.

Immune resilience is the capacity to maintain good immune function, called immunocompetence, and minimize inflammation while experiencing inflammatory stressors. 

Researchers found that during aging and when experiencing inflammatory stress, some persons resist degradation of immune resilience.

individuals with optimal levels of immune resilience were more likely to:

• Live longer.
• Resist HIV and influenza infections.
• Resist AIDS.
• Resist recurrence of skin cancer after kidney transplant.
• Survive COVID-19 infection.
• Survive sepsis.

Part 1

Comment by Dr. Krishna Kumari Challa on June 13, 2023 at 12:13pm

Using Nanoparticles to Combat Antibiotic Resistance Bacteria

Comment by Dr. Krishna Kumari Challa on June 13, 2023 at 12:11pm

New study reveals how blood triggers brain disease

 In patients with neurological diseases like Alzheimer's disease and multiple sclerosis, immune cells in the brain known as microglia that normally fulfill beneficial functions become harmful to neurons, leading to cognitive dysfunction and motor impairment. These harmful immune cells may also contribute to age-related cognitive decline in people without dementia.

For some time, scientists have been trying to better understand the triggers responsible for turning good microglia bad, and their exact contribution during disease. If they could identify what makes microglia toxic, they could find new ways to treat neurological diseases.

Now, researchers  showed that exposure to blood leaking into the brain turns on harmful genes in microglia, transforming them into toxic cells that can destroy neurons.

The scientists discovered that a blood protein called fibrin—which normally aids blood clotting—is responsible for turning on the detrimental genes in microglia, both in Alzheimer's disease and multiple sclerosis. The findings, published in the journal Nature Immunology, suggest that counteracting the blood toxicity caused by fibrin can protect the brain from harmful inflammation and loss of neurons in neurological diseases.

Individuals with neurological diseases like Alzheimer's disease and multiple sclerosis have abnormalities within the vast network of blood vessels in their brain, which allow blood proteins to seep into brain areas responsible for cognitive and motor functions. Blood leaks in the brain occur early and correlate with worse prognosis in many of these diseases.

In the new study, the researchers found that different blood proteins activate distinct molecular processes in microglia. What's more, they identified that fibrin is responsible for driving unique gene and protein activities that make microglia toxic to neurons. The other blood proteins tested were not mainly responsible for these toxic effects.

https://www.nature.com/articles/s41590-023-01522-0

Comment by Dr. Krishna Kumari Challa on June 13, 2023 at 10:33am

One unproven theory is that day length might have stalled at a constant value in Earth's distant past. In addition to tides in the ocean related to the pull of the moon, Earth also has solar tides related to the atmosphere heating up during daytime.

Solar atmospheric tides are not as strong as lunar oceanic tides, but this would not always have been the case. When Earth was rotating faster in the past, the tug of the moon would have been much weaker. Unlike the pull of the moon, the sun's tide instead pushes Earth. So while the moon slows Earth's rotation down, the sun speeds it up.

Because of this, if in the past these two opposite forces were to have become been equal to each other, such a tidal resonance would have caused Earth's day length to stop changing and to have remained constant for some time.

And that's exactly what the new data compilation showed.

Earth's day length appears to have stopped its long-term increase and flatlined at about 19 hours roughly between two to one billion years ago.

The timing of the stalling intriguingly lies between the two largest rises in oxygen.

The new study thus supports the idea that Earth's rise to modern oxygen levels had to wait for longer days for photosynthetic bacteria to generate more oxygen each day.

Mitchell, R.N. et al, Mid-Proterozoic day length stalled by tidal resonance, Nature Geoscience (2023). DOI: 10.1038/s41561-023-01202-6. www.nature.com/articles/s41561-023-01202-6

part 2

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