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Comment by Dr. Krishna Kumari Challa on August 21, 2023 at 12:08pm

In a new study, researchers focused on how parasites influence populations of tiny crustaceans commonly called "water fleas," from the genus Daphnia.
Daphnia grow up to 5 millimeters long, inhabiting various freshwater habitats where they feed on single-celled algae, bacteria, and protists. In turn, they serve as a food source for other larger aquatic species, like fish, tadpoles, and insects.

Using two Daphnia species with differing levels of parasite resistance, the researchers tested how the presence of parasites affected an ecological phenomenon known as the competitive exclusion principle, or Gause's law, among the water fleas.

Biodiversity is a key feature of healthy ecosystems, Orlansky and Ben-Ami note, and related species can share space if their relationships with predators and natural resources are different enough.

According to Gause's law, however, two species with identical niches in the same habitat can't coexist indefinitely at constant levels. If they're too similar, even a small advantage can help one species dominate, leaving others to eventually die out or seek a different niche.
The Daphnia species in this study are adapted to small rock pools – relatively enclosed habitats where many aquatic lifeforms can't migrate or come and go on their own.
Part 2

Comment by Dr. Krishna Kumari Challa on August 21, 2023 at 12:06pm

Parasites Are Actually Vital For Some Species' Survival, Study Shows

Parasites are understandably unpopular. Some cause horrible illnesses in their hosts, and even the less dangerous ones are often creepy or gross.

While they can be monsters, parasites aren't all bad. Many organisms benefit from species that survive by sucking the very life from others. Even their hosts might get a kickback or two.
Now a new study suggests some species can only survive in certain habitats if parasites are there, too.

Parasites come in many shapes and sizes, from viruses and amoebae to plants like mistletoe and animals like nematodes or mosquitoes. They all use a host for resources, which they typically harm but don't kill. As the late entomologist E.O. Wilson put it, parasites are "predators that eat prey in units of less than one."

Similar to the way predators can help regulate their overall ecosystem, parasites often provide overlooked ecological services that are only obvious in their absence.
the horrors of individual parasitic infections belie the surprising value these creatures offer for their broader community.

"Parasites and pathogens are an integral part of any ecosystem. Despite their bad reputation, parasites play a key role in shaping population dynamics, community structure, and biodiversity, thanks to their influence on the balance between the species in that ecosystem
Part 1

Comment by Dr. Krishna Kumari Challa on August 20, 2023 at 12:50pm

Why Does It Take a While For a Tan to Show Up? Scientists Have Finally Worked It Out

Your skin's response to Sun exposure may seem delayed, but there's a good reason for it, scientists have found.

Through experiments on both human and mouse skin, researchers  have discovered that the development of a tan only occurs after the skin has taken care of emergency DNA repair.

We have two mechanisms designed to protect the skin from exposure to dangerous UV radiation. 

The first mechanism repairs the DNA in the skin cells damaged by the radiation, while the second mechanism involves increased production of melanin, which darkens the skin in order to protect it from future exposure to radiation.

The delay in tanning is a result of resource prioritization. Basically, all of the cell's resources mobilize to repair radiation damage as quickly as possible. It's only once that task is complete that the cell can allocate resources to the production of melanin.

To test this hypothesis, the researchers first exposed human skin, obtained from consenting surgery patients and cultured in petri dishes, to UVB radiation. This was so that they could study the activity in the cell in response to radiation damage. They confirmed that a protein kinase called ATM, activated by DNA damage and critical to cell repair, springs into action shortly after exposure to UVB radiation. That's interesting, but the team needed more information. So, the follow-up step was to trigger the activation of ATM in the absence of UVB exposure and observe the results. This phase of the experiment was conducted on mouse models, and more human skin samples in petri dishes. In both mouse and human skin, a tan developed after an interval, even in the absence of harmful radiation. A close inspection of the cellular processes involved showed that the activation of ATM blocks the activation of the MITF protein responsible for increasing melanin production, so that DNA repair can take precedence.

The genetic information must be protected from mutations, so this repair mechanism takes precedence inside the cell during exposure to ultraviolet radiation from the sun.

The team suspects that DNA repair may even harness some of the components of the pigmentation mechanism in order to maximize the chances of cell survival, and minimize the chances of mutation. The discovery, the team says, could be used to help study, understand, prevent, and treat the effects of skin radiation damage.

https://www.sciencedirect.com/science/article/abs/pii/S0022202X2302...

Comment by Dr. Krishna Kumari Challa on August 20, 2023 at 12:30pm

Scientists find way to wipe a cell's memory to better reprogram it as a stem cell

In a study published in Nature,  scientists have resolved a long-standing problem in regenerative medicine. They developed a new method to reprogram human cells to better mimic embryonic stem cells, with significant implications for biomedical and therapeutic uses.

In a revolutionary advance in the mid-2000s, it was discovered that the non-reproductive adult cells of the body, called somatic cells, could be artificially reprogrammed into a state that resembles embryonic stem (ES) cells which have the capacity to then generate any cell of the body.

The ability to artificially reprogram human somatic cells, such as skin cells, into these so-called induced pluripotent stem (iPS) cells provided a way to make an essentially unlimited supply of ES-like cells, with widespread applications in disease modeling, drug screening and cell-based therapies.

However, a persistent problem with the conventional reprograming process is that iPS cells can retain an epigenetic memory of their original somatic state, as well as other epigenetic abnormalities. This can create functional differences between the iPS cells and the ES cells they're supposed to imitate, and specialized cells subsequently derived from them, which limits their use.

Researchers have now developed a new method, called transient-naïve-treatment (TNT) reprogramming, that mimics the reset of a cell's epigenome that happens in very early embryonic development. This significantly reduces the differences between iPS cells and ES cells and maximizes the effectiveness of how human iPS cells can be applied. 

By studying how the somatic cell epigenome changed throughout the reprogramming process, they pinpointed when epigenetic aberrations emerged, and introduced a new epigenome reset step to avoid them and erase the memory.

TNT reprogramming will establish a new benchmark for cell therapies and biomedical research, and substantially advance their progress.

https://www.nature.com/articles/s41586-023-06424-7?utm_medium=affil...

Comment by Dr. Krishna Kumari Challa on August 20, 2023 at 12:24pm

Using magnetic rust nanoparticles to clean water

Comment by Dr. Krishna Kumari Challa on August 19, 2023 at 12:26pm

WHO’s first traditional-medicine summit
Yesterday kicked off the first-ever World Health Organization (WHO) summit dedicated to traditional medicine, including disciplines as wide-ranging as Ayurveda, yoga, homeopathy and complementary therapies. Billions of people use traditional healing systems, so some researchers have called for more rigorous science, such as randomized control trials or systematic reviews, to understand these practices and to ensure the safety of products such as herbal medicines. But some scientists worry that the summit will be insufficiently critical, resulting in “the often-before voiced platitudes and wishful thinking”, according to complementary-medicine researcher Edzard Ernst.

https://www.nature.com/articles/d41586-023-02636-z?utm_source=Natur...

Comment by Dr. Krishna Kumari Challa on August 19, 2023 at 12:23pm

This has fueled the excessive consumption and pollution that a portion of the current world population is now responsible for, which is set to increase as financial security and population sizes increase, Rees argues. A changing climate is evidence of the strain the planet is already under but it's only a tiny fraction of the overall problem of overshoot, Rees argues. As Rees points out, as we continue to use an abundance of fossil fuels we're simultaneously ignoring the other symptoms of overshoot too. From our consumption of biomass to the disruption of planetary nutrient cycles, these interlinked problems are all propelling Earth's sixth mass extinction and risking a chaotic break-down of our planet's essential life-support systems.

What's more, our proposed solutions, such as switching to renewables don't actually address the problem of exponential population growth and in fact further contribute to the excess consumption that goes along with it. The question is whether improvements in technology – in everything from combating climate change to increasing food production – are capable of keeping pace with the growing demands our consumption places on the planet. If innovation can't provide solutions, food shortages, habitat instability, war, and disease may well start to make an impact in population numbers, this study predicts. "While no major symptom of overshoot can be adequately addressed in isolation from the others, addressing overshoot directly would reduce all important symptoms simultaneously," Rees explains. Another point that Rees makes – and he's not the first to do so – is that we need to be much more aware of the peril that we're in, and should be working out ways to get a better balance between our give-and-take relationship with the planet. "In the best of all possible worlds, the whole transition might actually be managed in ways that prevent unnecessary suffering of millions (billions?) of people, but this is not happening – and cannot happen – in a world blind to its own predicament," writes Rees.

https://www.mdpi.com/2673-4060/4/3/32

Part 2

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Comment by Dr. Krishna Kumari Challa on August 19, 2023 at 12:22pm

Major 'Population Correction' Coming For Humanity, Scientist thinks

A little over two centuries ago, in the year 1800, roughly a billion people called Earth home.

Just a century later, it had grown by another 600 million.

Today, there are around 8 billion people on the planet.

That sort of growth is unsustainable for our ecosphere, risking a 'population correction' that according to a new study could occur before the century is out. The prediction is the work of population ecologist William Rees from the University of British Columbia in Canada. He argues that we're using up Earth's resources at an unsustainable rate, and that our natural tendencies as humans make it difficult for us to correct this "advanced ecological overshoot".

The result could be some kind of civilizational collapse that 'corrects' the world's population, Rees says – one that could happen before the end of the century in a worst case scenario. Only the richest and most resilient societies would be left.

"Homo sapiens has evolved to reproduce exponentially, expand geographically, and consume all available resources," Rees writes in his published paper.
For most of humanity's evolutionary history, such expansionist tendencies have been countered by negative feedback. However, the scientific revolution and the use of fossil fuels reduced many forms of negative feedback, enabling us to realize our full potential for exponential growth."

Rees points out our dominance over the planet has made us forget that we are still governed by natural selection. What's more, our natural inclination towards short-term thinking, which served us exceedingly well in our evolutionary past, continues to compel us to take as much as we can possibly get when it's available.
Part 1

Comment by Dr. Krishna Kumari Challa on August 19, 2023 at 12:17pm

Why killer bacteria affect some people more severely

Why are certain people more severely affected than others by invasive streptococcal infections? According to a new study the answer lies in our genome. Carriers of a certain variant of the STING gene are at greater risk, particularly if they encounter the bacterial strains that have increased in the western world since the 1980s. The findings, published in Nature Communications, could pave the way for better treatments in cases where disease development is often rapid and fatal.

Group A streptococci are fairly common bacteria that can cause, among other things, strep throat or impetigo. However, if the bacteria become invasive, the situation can become very dangerous. In this case, the name sometimes changes to murder bacteria or flesh-eating bacteria and can give rise to life-threatening conditions such as blood poisoning and septic shock, or soft tissue infections that may make an amputation necessary.

Invasive streptococcal infections have increased in recent decades. The reason for this is not fully understood.

The outcome of infections can vary considerably, and it is still unknown why certain infected individuals develop life-threatening conditions while others don’t.

It depends on an interplay between the genes in people and bacteria.

The researchers’ hypothesis proved to be correct – the genes are different and that affects the risk of developing serious conditions.

The results, published in Nature Communications, provide a molecular explanation of how group A streptococci give rise to tissue-degrading and life-threatening inflammation.

The study also shows how the severity of an infection depends on the interplay between one gene – STING – in our immune system and a bacterial enzyme found in the bacteria that have become more prevalent in the western world since the 1980s. This explains why some people are more severely affected than others.

A person with the ”bad” gene variant of STING has a 20 per cent risk of having a limb amputated in the event of an invasive infection by the worst bacteria. For people with the ”good” gene variant, the risk is only three per cent. The percentage of patients suffering from septic shock also differs depending on the interplay between our STING variants and the bacteria’s enzyme activity.

“The difference is due to a unique combination of genetic material from the host and pathogen. This is partly due to that fact that the immune system of people with a certain variant of the STING gene triggers a misguided and dangerous inflammatory response. The other factor is that the outcome also depends on whether we are infected by the bacteria that are more aggressive because they have a very active variant of the NADase enzyme. Conversely, normal activation of the immune system due to another STING variant and lower bacterial enzyme activity is associated with protection.

The researchers also studied the evolution of the different STING variants in humans. The results show that the risk variant of STING appeared in humans around 35,000 years ago and that it spread to varying degrees around the world in connection with the first agricultural revolution 10,000 years ago. The consequence today is that the risk variant of STING is more common in some parts of the world than others.

https://www.nature.com/articles/s41467-023-39771-0

Comment by Dr. Krishna Kumari Challa on August 19, 2023 at 12:00pm

Researchers discover how stem cells choose their identity

Researchers discovered that stem cells first specialize into a functional cell and then move to their proper location—rather than the other way around. They revealed a new model to show how stem cells specialize into functional cells. They found that their position in the organ is not as important as current models claim. Rather, stem cells choose their identity first and only then move to their appropriate position.

These discoveries were made using intestinal organoids and the new TypeTracker technique, which can now be used to understand other organs at the cellular level and the effects of mutations and medications.

Our intestines contain different types of cells, each of which has a specific task. Just like in many other places in our body, the cells in the intestines are constantly renewed: stem cells develop into specialized cells that perform a function, for example, to secrete substances that protect the intestine or to absorb nutrients from food.

From previous research we know that stem cells reside in the valleys of the intestinal wall (the 'crypts'), while most specialized and functional cells are located at the top of the mountains (the 'villi').

The cells in the intestinal wall are renewed about every week, using the stem cells in the crypts that grow, divide and migrate to the villi. We used to think that by moving upwards to the villus, the stem cells are instructed to become a functional cell. This has been a very appealing model, as it naturally explains how these functional cells are positioned at the right location. However, our data shows a different picture.

This data was obtained using organoids: mini-organs that mimic the original organ so realistically that scientists can use them to unravel its functioning or to test medicines.

The identity of the cells is determined by certain proteins. Stem cells adopted their functional identity much earlier than previously thought. They did so when still deep inside the crypt, before migrating towards the villus region that was thought to provide the trigger to start the specialization process.

Xuan Zheng et al, Organoid cell fate dynamics in space and time, Science Advances (2023). DOI: 10.1126/sciadv.add6480. www.science.org/doi/10.1126/sciadv.add6480

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