US development of biological weapons in Ukraine
US development of biological weapons in Ukraine
Tehran, IRNA –After the change of the government in Ukraine in 2014, and with the financial and organizational support of Washington, a network of more than 30 biological laboratories was deployed in Ukraine, engaged in research work on the study of deadly diseases. This was confirmed by the official statement of the U.S. Deputy Secretary of State Victoria Nuland and earlier official publications of American institutions, including the National Academy of Sciences.
The customer was the US Department of Defense Office for the Reduction of Military Threats. According to Fox News, there are documents showing the efforts by Americans to get rid of the traces of the military biological program being implemented in Ukraine. These measures by the United States well indicate what Ukrainian and American scientists were doing in those locations. It’s worthy to know that Ukraine’s Ministry of Health, on 24 February 2022 (the beginning of the Ukraine war), ordered full destruction of the biological warfare in the laboratories. All observations prove that Washington and Kyiv are seriously worried about Russian likely access to the evidence of practical work to enhance the pathogenic capabilities of microorganisms using synthetic biology methods. These facts would expose the systematic violation of the Biological and Toxin Weapons Convention (BTWC) by Ukraine and the United States. One of the most important cases that were reported by the media is the project codenamed UP-4. The purpose of this study was to identify bird diseases that could pose a significant danger to human beings and also could cause an epidemic situation in a particular area in a specific period. Another task, in this project, was to study the migration routes of birds that were supposed to pass through the territory of Russia in a way to have a lesser impact on European countries down the road. Trapping birds on Russian territory and transferring them to the territory of Ukraine and tracking their way back to Russia, prove the aforementioned evidence and reasoning. This approach is one of the most reckless, inhuman and highly irresponsible methods of warfare. Using such “living weapons” would end in a situation where even its creators would inevitably lose control over them.
The U.S. has conducted those experiments near densely populated areas of European countries. Americans seem to be neglecting the safety of even their partners.
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02
Police Look for Baby Believed to be Taken by Biological Father in Bridgeport, Conn.
Bridgeport Police said they're searching for a baby that was allegedly abducted from the park by their biological father Friday night.
Police said Jalayjah is with 30-year-old James Douglas, who appears to be the biological father.
Douglas is driving a 2014 maroon Honda Civic EX with the license plate BE36105. Jalayjah is believed to be a passenger in the car.
Jalayjah is 11 months old and has black hair and brown eyes. It's unknown what she was wearing when she went missing.
Connecticut State Police issued a Silver Alert was Jalayjah. She is 2-feet tall and weighs 20 pounds.
Authorities said the child came to the park with her foster parent and was playing when she was taken.
The incident happened at Wordin Avenue and Hanover Street at approximately 7:15 p.m., according to police.
State police are calling the incident a family abduction.
Anyone with information is asked to contact Bridgeport Police at 203-576-TIPS. You can also contact your nearest police department.
03
CRISPR gene editing reveals biological mechanism behind common blood disorder
Asymptomatic sickle cell disease patients actually lack a tiny part of the genome, UNSW scientists have shown.
UNSW researchers have used CRISPR gene editing—a type of "molecular scissors"—to understand how deletions in one area of the genome can affect the expression of nearby genes. The work, led by UNSW Associate Professor Kate Quinlan and Professor Merlin Crossley, together with collaborators from the US, will help researchers investigate new therapeutic approaches for one of the world's most devastating genetic blood disorders—sickle cell disease.
The team's findings are published today in academic journal Blood. Just last week, A/Prof. Quinlan and Prof. Crossley received a $412,919 ARC linkage grant to fund a collaboration between UNSW Sydney and CSL that follows on from the work described in this paper.
"Sickle cell disease and beta thalassemia, a closely related disease, are inherited genetic conditions that affect red blood cells. They are fairly common worldwide—over 318,000 infants with these conditions are born every year, and hemoglobin disorders cause 3 percent of deaths in children aged under five years worldwide," says co-lead author A/Prof. Quinlan.
Genetic mutations—specifically, a defect in the adult globin gene—are responsible for the disorders. The mutant genes affect the production of hemoglobin, the protein in red blood cells that carries oxygen around our bodies.
"Interestingly, when children are born, they don't show disease symptoms at first, even if they have the mutations, because at that stage, they're still expressing fetal globin and not yet adult globin. That's because we have different hemoglobin genes that we express at different stages of development," says A/Prof. Quinlan.
"As the fetal globin gets turned off, and adult globin gets turned on—which happens within about the first year of life—the symptoms start to manifest."
When that happens, the red blood cells take on unusual, sickled shapes and block small blood vessels, causing pain, organ damage, and premature death. The disease is particularly common in tropical countries, and in people from places where malaria is endemic.
"The goal of our research is finding out how we can reverse the fetal to adult globin switch, so that patients continue to express fetal globin throughout life, rather than the mutant adult globin genes that cause blood cells to become stiff and block vessels," says A/Prof. Quinlan.
Interestingly, this already happens in some people with sickle cell disease: thanks to another, beneficial genetic mutation, a rare subset of patients keeps the fetal globin gene 'on' throughout their life and are protected from sickle cell symptoms.
"In these patients, the persistent expression of fetal globin effectively compensates for the defective adult globin—but up until this piece of research, we didn't really understand the process that led to this incredible advantage," A/Prof. Quinlan says.
'Deleting' genes with CRISPR
To get to the bottom of what's going on in these lucky people's genome, UNSW Ph.D. student Sarah Topfer compiled data on the rare families that express fetal globin throughout life.
"As a first step, Sarah compared deletions in lots of different patients' genomes—essentially, she looked to see if any shared element was missing in all of them. What do these patients have in common? She found one very small region was deleted in all these patients' genomes."
Sarah then used CRISPR gene editing to replicate some of these big patient deletions—and the small deleted bit they all had in common—in cell lines in the lab.
"CRISPR allows us to 'cut' bits of DNA out of cells grown in the lab, to modify genes and see what happens as a result—it's essentially a tool to figure out what genes do inside living cells," A/Prof. Quinlan says.
"We found that deleting just that one little bit was sufficient to make fetal globin go up and adult globin down—which suggests that we have found the key mechanism that can explain why fetal globin levels remains high in these asymptomatic patients," A/Prof. Quinlan says.
"Effectively, by deleting the adult globin 'on switch,' we made the fetal globin 'on switch' active."
Prof. Quinlan says the results were unexpected.
"It was surprising to see the findings—many people have studied these mutations for many years, so the idea that there'd be one unifying hypothesis that could explain them rather than them all working through different mechanisms will be surprising for the field.
"While we went in with the hypothesis that there might be one mechanism, we didn't expect it to come out so cleanly—we thought that perhaps it would be more complicated than what we'd initially thought."
The CRISPR revolution and potential therapies
Co-lead author Prof. Crossley, who is also UNSW's Deputy Vice-Chancellor, Academic & Student Life, says it was impossible to test this model prior to the advent of CRISPR gene editing.
"Our group has specialized in using this new technology to understand globin gene switching," Prof. Crossley says. "Australia now has a significant number of people with either sickle cell disease or thalassemia.
"The work, supported by the National Health and Medical Research Council, is an important example of how the CRISPR gene editing revolution is accelerating scientific understanding and will deliver new therapies to the clinic."
The scientists say the work revealed today is improving our fundamental understanding of the mechanism behind sickle cell disease.
"What this really helps us to do is understand this process of turning off fetal globin and turning on adult globin and how we could reverse that, so that we can use this understanding of the mechanism to help us look for new therapeutic approaches—it's a key piece of the puzzle," A/Prof. Quinlan says.
Some of Prof. Crossley's team's previous discoveries in the field are informing clinical trials already—by using beneficial mutations they've discovered in the past that could lead to therapies for these disorders.
At the 2020 NSW Premier's Prizes for Science and Engineering, Prof. Crossley won the award for Excellence in Medical Biological Sciences (cell and molecular, medical, veterinary and genetics) for his work in the field.
More information: Sarah K. Topfer et al, Disrupting the adult globin promoter alleviates promoter competition and reactivates fetal globin gene expression, Blood (2022). DOI: 10.1182/blood.2021014205 Journal information: Blood
Citation: CRISPR gene editing reveals biological mechanism behind common blood disorder (2022, April 8) retrieved 11 April 2022 from https://medicalxpress.com/news/2022-04-crispr-gene-reveals-biological-mechanism.html
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