On Wednesday, March 24, The Grady College of Journalism and Mass Communication welcomed five reporters of the celebrated Chauncey Bailey Project to the McGill Medal Round Table Discussion.
Talks on the UGA campus A production of Graybeal's JOUR3410 & JOUR3510 classes
On Wednesday, March 24, The Grady College of Journalism and Mass Communication welcomed five reporters of the celebrated Chauncey Bailey Project to the McGill Medal Round Table Discussion.

On Aug. 2, 2007, Chauncey Bailey was shot down while walking home from his job at the Oakland Post, in Oakland, California. A little over two years later, four of the reporters that finished the story he had been writing sat around the conference table describing their experiences with the Chauncey Bailey Project in the Drewry Reading Room of UGA’s Grady College of Journalism and Mass Communication. The Project received the McGill Medal for Journalist Courage on March 23 from the McGill Fellows. These journalists were selected because of their involvement with research that exposed the corruption in the Oakland Police Department and the Your Black Muslim Bakery, the organization connected with Bailey’s murder.
The project started a couple weeks after Bailey’s death with the help of about three-dozen volunteer reporters, editors and community members who’s goal it was to finish what Bailey started and to prove the project’s mantra, “You can’t kill a story by killing a Journalist”. The dozens of volunteers spent about two years in all, pouring through police reports, public documents and talking to sources. During this time, they wrote over a 100 stories about the murder, Bailey’s assassin and the police department’s failure to pursue the case. The four reporters, Thomas Peele, Josh Richman, Mary Fricker and Bob Butler, stressed that the key to their reporting was their use of public documents. Through these documents, they found mountains of evidence and verified information from sources. The documents, mostly untouched by local police detectives, revealed multiple types of fraud, the use of child labor and polygamy.
The four also emphasized that courage is necessary to reporting, not just for instances like the Chauncey Bailey Project, but for pursuing any difficult lead in a story. Mike Oliver, another project member, summed up their opinion. “A good journalist is one that won’t be intimidated, that won’t take no when they believe that the information should be made public.” They discussed how, without courage, they would not have been able to pursue leads with members of Your Black Muslim Bakery, and police department. This courage opened the doors for the Bakery and its members to be convicted of their crimes and the Oakland Police Department to reform their homicide department.
Although they never expected their work to last more than eight months, the journalists also never expected to discover the numerous stories they did. They took the years of dedication and the long hours the project required in stride and believe that it was the only way to honor Bailey’s life and work. “We simply did what we had to do after a friend and colleague was slain for his work. If a story dies along with the journalist, the journalist died in vain; letting that happen was never an option.” Richman said according to the Chauncey Bailey Project website. The journalists succeeded at just that, the memory of Bailey’s courage never died, it lives still today in the stories and hearts he impacted.
Josh Richman is a father of one from Queens, N.Y. As an active journalist of 18 years he currently works for the The Oakland Tribune/Bay Area News Group in California. Richman received his Bachelor of Arts in Journalism from University of Missouri while also studying a minor in political science. He began work for the Oakland Tribune in 1997. He has achieved many accomplishments throughout his journalistic career, but considers the Chauncey Bailey Project the biggest story he has covered. Richman’s most memorable work includes stories arising from terrorist attacks on September 11, 2001. He also recognizes a story he covered on Oakland Police Department’s reaction to antiwar protestors in 2003, which won awards.
Like Richman, Bob Butler also recognizes the Chauncey Bailey Project as the highlight of his career. Although the project has received The McGill Medal for Journalistic Courage, among other awards, Butler makes it clear that his satisfaction comes from the fact that criminals were indicted in the case. Butler has been in broadcast reporting for 31 years. As a native of Chelsea, Mass. Butler describes himself as a navy brat who finally settled in the Bay area of San Francisco when he landed a job with KCBS. He received his Bachelor of Arts in Journalism from San Francisco State and continues to work independently in the field.


The 300-person auditorium was nearly filled to capacity. Students, educators and professional biologists listened intently, so silent you could hear a pin drop. World-renowned Harvard professor Douglas Melton, Ph.D., emphasized the importance of research on cell development in order to use stem cells to create a pancreas and recreate human diabetes. “If you watch something develop, it’s very informative of what goes wrong,” he said in his lecture on Tuesday, March 23, part of the Hope Ritter lecture series offered by the UGA Department of Cellular Biology.
Melton, who established his own laboratory at Harvard and conducts research for the Howard Hughes Medical Institute, became motivated to find a cure for Type I diabetes after two of his children were diagnosed with the autoimmune disease. He has twice been listed as one of the 100 most influential people in the world by TIME magazine and for good reason. His research primarily focuses on ways to make insulin-producing cells, otherwise known as pancreatic beta (b) cells, which Type I diabetics do not have. He cited a statistic that made clear why his research is so important: 0.5 percent of newborns in the United States will be fully insulin-dependent by age 18.
The pancreatic beta cells that Melton’s research focuses on are located within the islets of Langerhans. He said that there are two main problems that need to be resolved. There is a loss of beta cells, so researchers must figure out how to make more of them. Researchers must also figure out how to stop the body’s immune system from attacking and killing its own beta cells.
How do scientists create more beta cells? “We should plan for success and try to do this in a way that is clinically relevant by using chemicals that tell cells what to do,” said Melton. The process of creating beta cells began by determining which genes were turned on or off during different stages of cell development. By manipulating these genes with chemicals in a lab, Melton has successfully differentiated cells to create definitive pancreatic cells.
What does this mean for diabetics? This is when Melton addressed the second problem – how to stop the immune system from attacking beta cells. The body can only make new beta cells by replication. All new beta cells must come from preexisting beta cells, so a Type I diabetic has lost all capability to create new beta cells. The entire audience laughed as Melton “quoted” what the body of a diabetic would say if simply injected with new beta cells. “Thanks! I recognize those cells. I’ve been killing them for a long time. I’m going to keep killing them!”
A major key, then, to cracking the code on Type I diabetes is figuring out why the immune system does not recognize the pancreas as “self” but rather treats it as an invader and tries to kill it. Melton next plans are to study the development of diabetes in mice. These mice are genetically modified so that the cells and tissues are actually human in nature. In this manner, Melton and his research team can find out which type of cell affects the onset of diabetes and how many different ways there are to develop the disease. “If that doesn’t work, I really don’t know what I’ll do,” he said.
Perhaps most relevant to diabetic patients today is finding out what triggers beta cells to divide, however. Melton cited an experiment in which a mouse cured itself of diabetes after having most of its beta cells killed in a laboratory setting. The residual beta cells boosted replication so that the mouse could cure itself.
“We’re very keen on finding signals for beta cell replication that could be useful in newly onset diabetes to boost replication and increase tolerance,” said Melton. Recently diagnosed diabetics often experience a “honeymoon period” in which the body still retains some capability to produce insulin before all of the beta cells have been killed. If scientists can keep the body from killing beta cells and induce replication before the cells are all gone, it is possible that the patient may regain the ability to produce insulin.
Douglas Melton began his lecture with the words, “I wasn’t certain I could do science.” He has clearly proven that not only can he do science, but he can also make a difference and inspire hope in the lives of millions of people.