When did scientists first begin to talk about the replication crisis?
It is a term that has been bandied about since the 1970s.
Scientists have been grappling with the problem since then.
In the early 2000s, it was referred to as “the pandemic” by many, as the pandemic had spread across the globe and left millions without basic health care.
Today, it is called the “replication epidemic,” a term coined by a group of researchers led by University of California, San Diego, postdoctoral researcher Christopher W. Brown and his colleagues.
The term was first coined in the early 1990s by MIT’s Stephen T. Cohen, who was a fellow at Harvard University.
In an interview with NPR’s Rachel Martin in 2008, Cohen said, “It was the pandemics of the 1930s, 1940s and 1950s.
And then there was the flu pandemic in 1918.
So I think the replication issue was just the start of this pandemic.
So, I think that’s what people think.
We started to get a sense of it in the late 1970s, ’80s and early ’90s, and then we really got into a lot of the papers that were published.”
Cohen has since gone on to publish dozens of papers on the replication problem, including his landmark work on the origins of HIV.
In addition to his work on HIV, Cohen’s work has also found evidence that some of the world’s major genomic repositories are under threat from the panders.
The two papers cited above were co-authored by Cohen, with the help of researchers from the Center for Genomic Security, the University of Washington, the Broad Institute, and the National Center for Biotechnology Information.
The first paper, published in 2003, was co-written by the UC San Diego Center for Genetics, Genomics and Systems Biology, and published in Nature.
The second paper, co-led by UC San Francisco’s David Strominger, was published in 2008.
Both papers discussed how the problem of replication in scientific work is complex, but the key point in the first paper was that “the world has not yet caught up with the pace of progress in science.”
The second work, by Cohen and his collaborators, described the origins and nature of the replication pandemic, with their conclusion that “replications, not replicability, is the key problem of the pandemaker.
This is the issue that is getting so much attention.”
This was a big deal back in 2003 when Cohen and the UC Berkeley colleagues were first looking at the pandems origins.
Cohen was a young PhD student at UC Berkeley in the mid-1990s, working on an important project on how gene sequences were transferred from one species to another, including from a bacterium to a human.
His work involved finding a way to transfer DNA from one bacterium into another, and that led to the discovery of genes for the first human-to-human genetic transfer in 1994.
Cohen’s research was part of the National Institutes of Health’s (NIH) National Institute of Allergy and Infectious Diseases (NIAID), which was created by the National Science Foundation (NSF) in 1966.
He and his fellow researchers, including a colleague from UC Berkeley, Stephen Tappert, then used a computer to analyze the genome of a bacteria and found that the genome contained two new genes, one that was specific to a bacterioid and one that made use of the genes from another bacterium.
The new gene was named NSC1, and it was found to be the first new gene to be identified in human genomes in over 200 years.
Cohen and colleagues also showed that this gene was a member of a family of genes called “transposons.”
Transposons are genetic material that has altered their functions to make them compatible with other genes, and they are the major source of genetic diversity in genomes.
This gene was found in both the bacterioids genome and the human genome.
The team found that it was not a repeat of the original gene, and Cohen and others theorized that it might be a new genetic copy that was transferred from the bacterium that produced it.
Cohen also discovered that the new gene also had some of its function duplicated in the human, but he thought this was not enough to explain the phenomenon.
The authors of the second paper pointed out that the fact that the copy that transferred from bacterium NSC 1 was different from that that produced the original version would not necessarily imply that it had not been the original bacterium, or that it did not have a function that it copied from the original.
But, in their paper, the researchers also stated that there was “no evidence to suggest that the duplicated function of the gene is a consequence of a new, independent mutation, and no evidence that the original function of NSCs copy was not copied into NSC 2 and NSC 3 in a similar manner.” This means