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“When the outbreak first started in March and we heard about this deadly virus, Ebola, I was in Kakata,” says Austin S. Jallah, a student nurse at Kakata University, in Margibi County, Liberia. “People really doubted the fact that Ebola was real, until we heard about the first case in the hospital. I wasn’t one of those who doubted though. Because I am a student nurse, I had read about the Ebola virus before, how it was first discovered back in 1976.” Jallah adds, “I am grateful that my Ebola experience can impact the knowledge of our health workers and help to eradicate this disease from Liberia.”

One of the reasons cancer is so deadly is that it can evade attack from the body's immune system, which allows tumors to flourish and spread. Scientists can try to induce the immune system, known as immunotherapy, to go into attack mode to fight cancer and to build long lasting immune resistance to cancer cells. Now, researchers at the Wyss Institute for Biologically Inspired Engineering at Harvard University and Harvard's School of Engineering and Applied Sciences (SEAS) show a non–surgical injection of programmable biomaterial that spontaneously assembles in vivo into a 3D structure could fight and even help prevent cancer and also infectious disease such as HIV. Their findings are reported in Nature Biotechnology.

Sexual behavior of teenage girls does not appear to be impacted by the human papilloma virus (HPV) vaccine, according to Queen’s researchers Drs. Leah Smith and Linda Lévesque.

Ebola virus disease presents a unique occupational health challenge to healthcare institutions, and Ebola readiness and response can drain al-ready-scarce infection prevention resources. This is reflected in a recent survey of infection preventionists at U.S. hospitals conducted by the Association for Professionals in Infection Control and Epidemiology (APIC) in which only 6 percent of healthcare institutions are well-prepared to receive a patient with the Ebola virus. Infection preventionists everywhere are hoping that the Ebola crisis can shed new light on the importance of a properly funded and resourced department.

The Centers for Disease Control and Prevention (CDC) statistics are well known - 1 in every 20 hospital patients acquires an infection while receiving medical care in hospitals. The CDC’s most recent estimates blame these healthcare-associated infections (HAIs) for nearly 100,000 deaths annually. 

An international research collaborative has determined that a promising anti-malarial compound tricks the immune system to rapidly destroy red blood cells infected with the malaria parasite but leave healthy cells unharmed. St. Jude Children's Research Hospital scientists led the study, which appears in the current online early edition of the Proceedings of the National Academy of Sciences (PNAS).

Penicillin, the wonder drug discovered in 1928, works in ways that are still mysterious almost a century later. One of the oldest and most widely used antibiotics, it attacks enzymes that build the bacterial cell wall, a mesh that surrounds the bacterial membrane and gives the cells their integrity and shape. Once that wall is breached, bacteria die - allowing us to recover from infection. That would be the end of the story, if resistance to penicillin and other antibiotics hadn’t emerged over recent decades as a serious threat to human health. While scientists continue to search for new antibiotics, they still don’t understand very much about how the old ones work. Now Thomas Bernhardt, associate professor of microbiology and immunobiology at Harvard Medical School, and his colleagues have added another chapter to the story. Their findings, published Dec. 4 in Cell, reveal how penicillin deals bacteria a devastating blow - which may lead to new ways to thwart drug resistance.

The bacterium Salmonella Typhi causes typhoid fever in humans, but leaves other mammals unaffected. Researchers at University of California, San Diego and Yale University Schools of Medicine now offer one explanation - CMAH, an enzyme that humans lack. Without this enzyme, a toxin deployed by the bacteria is much better able to bind and enter human cells, making us sick. The study is published in the Dec. 4 issue of the journal Cell.