Whether you are a student, a professional, or simply a science enthusiast, this article will provide you an engaging and informative insights and updates. Plus, as a compliment, you will get a peep into pretty quirky AI generated images by me related to those particular topics.
In today's blog, you will read about the following science events of the week:
- Researchers studying Chernobyl Dogs to understand effects of radiation
- Astrobiologists training AI to help find life on Mars
- The mice with two dads and technically no mom
- Research shows neurons in throat detect infection early on and notify brain.
- Lab-leak hypothesis comes back to haunt China
- New COVID pill shortens symptoms of infection
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| Researchers studying Chernobyl dogs, Training AI to find life on Mars, The mice with two dads but no mom and other science news of the Week; Mufawad |
Researchers studying Chernobyl Dogs to understand effects of radiation
On 26 April 1986, two explosions rocked the nuclear power plant near the Ukrainian city of Chernobyl, leading to death and destruction and the evacuation of thousands of people, properties and pets.
In the days after the accident, response crews sought out abandoned and stray dogs, but some seem to have survived. DNA collected from feral dogs living near the power plant today reveals that they are the descendants of dogs that were either present at the time of the accident or settled in the area shortly afterwards.
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| Pic generated by Mufawad using AI |
The immediate impacts of the accident at Chernobyl were obvious, with around 30 people who worked at the power plant and firefighters who attended after the disaster dying of radiation poisoning within a few months of the catastrophe.
However, the health effects of low-levels of radiation are still hotly debated. According to Science Advances, “Timothy Mousseau”, an evolutionary ecologist at the University of South Carolina in Columbia, joined a volunteer mission to provide veterinary care to the hundreds of stray dogs living in the exclusion zone around the Chernobyl power plant.
Over the course of three years, Mousseau and his colleagues collected blood samples from around 300 dogs living at the power plant and around the mostly deserted city of Chernobyl after volunteers had sedated the animals with tranquilizer darts.
DNA analysis of the canines revealed that they were not newcomers to the area, and that they have been isolated from other dog populations for decades. The researchers studied the DNA samples of dogs living near the Chernobyl nuclear power plant after the 1986 accident.
They found that those living closest to the power plant are genetically distinct from their kin living just a few kilometres away. The dogs' continued presence in the area shows that they have been able to survive and breed, even while living near the reactor, "which of course is remarkable".
The 1986 accident deposited the deadly radioactive isotope caesium-137 at levels 10-400 times higher near the power plant than in the city of Chernobyl, just 15 kilometres away.
These DNA samples of these feral dogs are valuable because these animals tend to share many of the same spaces and diets as humans, but teasing out which genetic changes in the dogs are caused by radiation and which are caused by other factors — such as inbreeding or non-radioactive pollutants — won't be easy.
The team acknowledges these challenges, but argues that their detailed knowledge of these dogs' ancestry, as well as knowledge of the levels of radiation different dogs were historically exposed to, provides an ideal focus group for future studies.
Although the ongoing war in Ukraine hasn't stopped the group's research, but with fewer tourists visiting and leaving food scraps, Chernobyl's dogs are struggling to get by according to Science Advances.
However, an NGO is providing food to the strays, safeguarding the survival of the dogs and their radioactive legacy.
Astrobiologists training AI to help find life on Mars
The Artificial intelligence (AI) and machine learning does have the potential to revolutionize the search for life on other planets. But before these tools can tackle distant locales such as Mars, they need to be tested here on Earth.
In this regard, A team of researchers have successfully trained an AI to map biosignatures i.e; any feature which provides evidence of past or present life, in a three-square-kilometre area of Chile's Atacama Desert.
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| Pic generated by Mufawad using AI |
According to Nature Astronomy, Kimberley Warren-Rhodes, a senior research scientist at the SETI Institute in Mountain View, California, and lead author on the paper, has been chasing the biosignatures since the early 2000s, when she realized how few tools existed to study the biology of other planets.
She wanted to combine her background in statistical ecology with emerging technologies such as AI to help mission scientists, who ‘ according to her’ are under a lot of pressure to find biosignatures, but tightly constrained in how they do so.
Normally Rovers that are controlled remotely from Earth, for example, can travel only limited distances and collect relatively few specimens, placing a premium on sampling locations that are the most likely to yield life. This is where such AI can help.
Warren-Rhodes and her groups search for life Beginning in 2016, when they travelled to the high, parched plateau of the Atacama Desert that is considered as a Mars analogue and stays at an elevation of around 3,500 metres in the Chilean Andes. They searched for rock-dwelling, photosynthetic organisms called endoliths.
To fully characterize the environment of Atacama desert, the researchers collected everything from drone footage to geochemical analyses to DNA sequences. The idea was to mimic the modes and means of information collection on Mars
Then, the team fed its data into an AI-based convolutional neural network (CNN) and a machine-learning algorithm that in turn predicted where life was most likely to be found in the Atacama. By targeting their sample collection on the basis of AI feedback, the researchers were surprisingly able to reduce their search area by up to 97% and increase their likelihood of finding life by up to 88%. "
Specifically, the team found that endoliths in the Atacama were most often found in a mineral called alabaster, which is porous and retains water and tended to aggregate in transitional areas between various microhabitats, such as where sand and alabaster crystals abut one another. "
The mice with two dads and technically no mom
Researchers have made eggs from the cells of male mice and showed that, once fertilized and implanted into female mice, the eggs can develop into seemingly healthy, fertile offspring.
The approach, announced in second week of March at the Third International Summit on Human Genome Editing in London, which has not yet been published and is a long way from being used in humans.
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| Pic generated by Mufawad using AI |
However, it is an early proof-of-concept for a technique that raises the possibility of a way to treat some causes of infertility or even allow for single-parent embryos.
Researchers have been working towards this feat for years, and in 2018, one team reported using embryonic stem cells made from sperm or eggs to generate pups with either two fathers or two mothers.
In 2020, a team led by developmental biologist Katsuhiko Hayashi described the genetic changes necessary for cells to mature into eggs in a lab dish, and in 2021, the same researchers demonstrated that they could reconstruct the environment of mouse ovaries to grow eggs that produce healthy offspring.
Hayashi and his colleagues embarked on a project to create eggs using cells taken from an adult male mouse, reprogrammed these to create stem-cell-like induced pluripotent stem cells. They then treated the cells with a compound called reversine, which can promote errors in how chromosomes are distributed during cell division, and looked for cells that were chromosomally female, with two copies of the X chromosome.
They then fertilized the eggs using mouse sperm and transferred the resulting embryos into the uterus of a female mouse. The survival rate was low, with only 7 developing into pups, but the pups grew normally and were fertile as adults.
The technique is a long way from any kind of medical application, as there are big differences between a mouse and a human. To translate discoveries in reproductive and stem-cell biology from mice to the clinic, Hayashi's team will need to carefully characterize the pups from the experiment and look at whether the 'epigenetic' chemical modifications to DNA that can influence gene activity are preserved properly in the eggs derived from male cells.
Additionally, performing the same technique with human cells might require researchers to grow the egg cells in the laboratory for longer than was necessary with mouse cells, which could lead to both genetic and epigenetic abnormalities.
Hayashi's chromosomal-engineering approach could one day provide a treatment for some forms of infertility caused by sex-chromosomal conditions such as Turner's syndrome. It could also take human reproduction into new territory, allowing male couples to have biological children together with the aid of surrogate mothers.
However, such applications will require more than technical refinement of a biological method, but also a broader societal discussion about the ethics and implications of implementing them.
Scientists have identified neurons in mice that notify the brain of a flu infection, triggering decreases in movement, hunger and thirst and kickstart the sickness-behaviour program. This study flips previous thinking on its head, that suggested that prostaglandins are key to triggering sickness behaviours.
We all know Aspirin and ibuprofen were intaken to block prostaglandin production and suppress sickness behaviours. However, this research is paradigm-shifting in terms of how we think about sickness behaviour.
The authors showed that actually a specific prostaglandin receptor, called EP3, is responsible for generating sickness behaviours which is present on neurons and brain. To test its function, they deleted the brain's EP3 receptors in mice and infected them with flu virus. However, the mice still changed their behaviour, thus indicating that the brain is not getting infection “dispatches” from blood-borne prostaglandins.
The researchers found that the key agents are a specific EP3-containing population of neurons located in the mouse's neck. These neurons have branches that stretch from the mouse equivalent of the tonsils to the brainstem, and the results tell a narrative of illness: flu viruses enter the airway and infect throat cells.
The infection alert then travels along the neurons' branches on a dedicated highway to the brain, giving the brain information about exactly where the infection is occurring. The researchers suggest that further dedicated pathways could potentially exist for detecting gut infections, triggering nausea, and reducing the spread of pathogens.
The study also revealed a paradox: when the team blocked certain behaviours, such as food avoidance, mice were less likely to die of the flu. It was speculated that this behaviour-modifying system might have evolved because it is beneficial in most cases of infection, even if it isn't in all.
However according to Nature, these new results don't tell the full story. The infection-sensing tonsil neurons are responsible for sickness behaviour only during a flu infection's first stage, which affects the upper airway and lasts roughly a week. As the virus moves into the lower respiratory tract over the course of the illness, another nerve pathway takes over the job of driving sickness behaviours. If we could find a way to block that second pathway, it could have tremendous clinical impact.
In an interesting development, The US House of Representatives held the first in a series of public hearings on 8th of March aimed at exploring how the COVID-19 pandemic began. The Republicans who control the House, invited three of the witnesses: Jamie Metzl, a senior fellow at the Atlantic Council, Robert Redfield, former director of the Centers for Disease Control and Prevention, and Nicholas Wade, a former science editor for the New York Times to the house for questioning.
Democrats invited one witness, Paul Auwaerter, clinical director of the Division of Infectious Diseases at Johns Hopkins School of Medicine in Baltimore, Maryland. The hearing itself offered a heavy dose of political theatre, with Republican committee members suggesting that Anthony Fauci had steered the scientific community to dismiss a lab leak early in the pandemic.
Researchers have been working towards this feat for years, and in 2018, one team reported using embryonic stem cells made from sperm or eggs to generate pups with either two fathers or two mothers.
In 2020, a team led by developmental biologist Katsuhiko Hayashi described the genetic changes necessary for cells to mature into eggs in a lab dish, and in 2021, the same researchers demonstrated that they could reconstruct the environment of mouse ovaries to grow eggs that produce healthy offspring.
Hayashi and his colleagues embarked on a project to create eggs using cells taken from an adult male mouse, reprogrammed these to create stem-cell-like induced pluripotent stem cells. They then treated the cells with a compound called reversine, which can promote errors in how chromosomes are distributed during cell division, and looked for cells that were chromosomally female, with two copies of the X chromosome.
They then fertilized the eggs using mouse sperm and transferred the resulting embryos into the uterus of a female mouse. The survival rate was low, with only 7 developing into pups, but the pups grew normally and were fertile as adults.
The technique is a long way from any kind of medical application, as there are big differences between a mouse and a human. To translate discoveries in reproductive and stem-cell biology from mice to the clinic, Hayashi's team will need to carefully characterize the pups from the experiment and look at whether the 'epigenetic' chemical modifications to DNA that can influence gene activity are preserved properly in the eggs derived from male cells.
Additionally, performing the same technique with human cells might require researchers to grow the egg cells in the laboratory for longer than was necessary with mouse cells, which could lead to both genetic and epigenetic abnormalities.
Hayashi's chromosomal-engineering approach could one day provide a treatment for some forms of infertility caused by sex-chromosomal conditions such as Turner's syndrome. It could also take human reproduction into new territory, allowing male couples to have biological children together with the aid of surrogate mothers.
However, such applications will require more than technical refinement of a biological method, but also a broader societal discussion about the ethics and implications of implementing them.
Research shows neurons in throat detect infection early on and notify brain.
Scientists have identified neurons in mice that notify the brain of a flu infection, triggering decreases in movement, hunger and thirst and kickstart the sickness-behaviour program. This study flips previous thinking on its head, that suggested that prostaglandins are key to triggering sickness behaviours.
We all know Aspirin and ibuprofen were intaken to block prostaglandin production and suppress sickness behaviours. However, this research is paradigm-shifting in terms of how we think about sickness behaviour.
The authors showed that actually a specific prostaglandin receptor, called EP3, is responsible for generating sickness behaviours which is present on neurons and brain. To test its function, they deleted the brain's EP3 receptors in mice and infected them with flu virus. However, the mice still changed their behaviour, thus indicating that the brain is not getting infection “dispatches” from blood-borne prostaglandins.
 |
| Pic generated by Mufawad using AI |
The infection alert then travels along the neurons' branches on a dedicated highway to the brain, giving the brain information about exactly where the infection is occurring. The researchers suggest that further dedicated pathways could potentially exist for detecting gut infections, triggering nausea, and reducing the spread of pathogens.
The study also revealed a paradox: when the team blocked certain behaviours, such as food avoidance, mice were less likely to die of the flu. It was speculated that this behaviour-modifying system might have evolved because it is beneficial in most cases of infection, even if it isn't in all.
However according to Nature, these new results don't tell the full story. The infection-sensing tonsil neurons are responsible for sickness behaviour only during a flu infection's first stage, which affects the upper airway and lasts roughly a week. As the virus moves into the lower respiratory tract over the course of the illness, another nerve pathway takes over the job of driving sickness behaviours. If we could find a way to block that second pathway, it could have tremendous clinical impact.
Lab-leak hypothesis comes back to haunt China
In an interesting development, The US House of Representatives held the first in a series of public hearings on 8th of March aimed at exploring how the COVID-19 pandemic began. The Republicans who control the House, invited three of the witnesses: Jamie Metzl, a senior fellow at the Atlantic Council, Robert Redfield, former director of the Centers for Disease Control and Prevention, and Nicholas Wade, a former science editor for the New York Times to the house for questioning.
Democrats invited one witness, Paul Auwaerter, clinical director of the Division of Infectious Diseases at Johns Hopkins School of Medicine in Baltimore, Maryland. The hearing itself offered a heavy dose of political theatre, with Republican committee members suggesting that Anthony Fauci had steered the scientific community to dismiss a lab leak early in the pandemic.
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| Pic generated by Mufawad using AI |
The most important details in this text are that the US Department of Energy (DOE) had given a classified intelligence report to the White House in which it updated its stance on COVID-19's origins. The National Intelligence Council and four other agencies support the idea that the pandemic had a natural origin, with "low confidence".
The FBI director Christopher Wray, according to CNN, confirmed that his agency has for some time believed that SARS-CoV-2 escaped accidentally from a lab in China, but he did not reveal any evidence informing the agency's views. According to Nature, Michael Worobey, an evolutionary biologist at the University of Arizona, Tucson, found the proceedings "shockingly unscientific" and that they do not bode well for the overall investigation.
The Chinese has been slow to release data on the pandemic, and Zeng Yixin, vice-minister of China's National Health Commission, recently rejected a plan by the WHO to further investigate the possibility that "China's breach of laboratory protocols caused the virus to leak". This 8th March hearing has made it clear that the political debate isn't going away and Michael Worobey is disappointed that the witnesses and committee members didn't engage with the scientific evidence, which points to a natural origin.
The committee is yet to schedule its next hearing.
The drug is manufactured by Shionogi in Osaka, Japan, which believes the data also show the potential to prevent long COVID, but scientists are sceptical about that claim and critical of the design of the clinical trial.
The research was presented at the Conference on Retroviruses and Opportunistic Infections (CROI) in Seattle, Washington, on 21 February, and has not yet been peer reviewed according to NYT Science.
The FBI director Christopher Wray, according to CNN, confirmed that his agency has for some time believed that SARS-CoV-2 escaped accidentally from a lab in China, but he did not reveal any evidence informing the agency's views. According to Nature, Michael Worobey, an evolutionary biologist at the University of Arizona, Tucson, found the proceedings "shockingly unscientific" and that they do not bode well for the overall investigation.
The Chinese has been slow to release data on the pandemic, and Zeng Yixin, vice-minister of China's National Health Commission, recently rejected a plan by the WHO to further investigate the possibility that "China's breach of laboratory protocols caused the virus to leak". This 8th March hearing has made it clear that the political debate isn't going away and Michael Worobey is disappointed that the witnesses and committee members didn't engage with the scientific evidence, which points to a natural origin.
The committee is yet to schedule its next hearing.
New COVID pill shortens symptoms of infection
In another development related to Covid 19, an antiviral discovered called “Ensitrelvir” shortens symptoms of mild to moderate COVID-19 to about a day, and is the first drug to make a statistically significant cut to the number of days people test positive for SARS-CoV-2.The drug is manufactured by Shionogi in Osaka, Japan, which believes the data also show the potential to prevent long COVID, but scientists are sceptical about that claim and critical of the design of the clinical trial.
The research was presented at the Conference on Retroviruses and Opportunistic Infections (CROI) in Seattle, Washington, on 21 February, and has not yet been peer reviewed according to NYT Science.
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| Pic generated by Mufawad using AI |
Two oral antivirals, Paxlovid and Molnupiravir, are already widely used to treat COVID. The study conducted in this regard, investigated roughly 1,200 people, with the main goal of determining whether the drug could accelerate recovery. The results showed that participants who took the 125-milligram dose recovered from five specific symptoms about 24 hours earlier than those in the control group.
The study was the first to show a statistically significant reduction in the time to a negative test result. Participants who had developed long COVID were defined as having developed two or more of the same symptoms at least twice in a row over this period.
The “Shionogi” concluded that participants who received “Ensitrelvir” had a reduced risk of developing long COVID, but scientists who were not involved with the study point out that the trial was not specifically intended to investigate the risk of long COVID.
Simon Portsmouth, head of clinical development at Shionogi in Florham Park, New Jersey, says that the company could not specify the plan for analysing long COVID data ahead of time because long COVID was less clearly defined in the past than now. (As reported in NYT Science)
However, the data that Shionogi has made public support the idea that antivirals protect against long COVID at least when residual virus is involved in causing prolonged symptoms. However, there's no consensus that persistent virus causes long COVID and the optimal study to investigate whether antivirals prevent long COVID is not yet available.
The study was the first to show a statistically significant reduction in the time to a negative test result. Participants who had developed long COVID were defined as having developed two or more of the same symptoms at least twice in a row over this period.
The “Shionogi” concluded that participants who received “Ensitrelvir” had a reduced risk of developing long COVID, but scientists who were not involved with the study point out that the trial was not specifically intended to investigate the risk of long COVID.
Simon Portsmouth, head of clinical development at Shionogi in Florham Park, New Jersey, says that the company could not specify the plan for analysing long COVID data ahead of time because long COVID was less clearly defined in the past than now. (As reported in NYT Science)
However, the data that Shionogi has made public support the idea that antivirals protect against long COVID at least when residual virus is involved in causing prolonged symptoms. However, there's no consensus that persistent virus causes long COVID and the optimal study to investigate whether antivirals prevent long COVID is not yet available.
