Of the various ways for a cell to die — necrosis, autophagy, etc. — apoptosis is probably the most orderly and contained. Also called programmed cell death (or, colloquially, “cellular suicide”), apoptosis is an effective way for diseased or damaged cells to remove themselves from a population before they can cause problems such as tumor formation.
Conventional wisdom holds that apoptosis is exclusive to multicellular organisms. Lieberman disagrees. She thinks that microbial cells — such as those of bacteria and parasites — can die in apoptotic fashion as well. In a recent Nature Medicine paper, she and her team make the case for the existence of what they’ve dubbed “microptosis.” And they think it could be harnessed to treat parasitic and other infections. …
Consider this scenario: A patient is home recovering from knee surgery to repair an ACL tear. Her pain medications are wearing off, and the surgical cuts are starting to throb. Reaching over to the table she picks up what’s essentially a souped-up laser pointer, points it at the surgical wound and turns it on. Within seconds, the pain starts to fade.
This picture isn’t as far-fetched as you might think. In a pair of simultaneous papers, Boston Children’s Hospital’s Daniel Kohane, MD, PhD, and his laboratory recently reported their efforts to create not one, but two methods for packaging long-lasting local anesthetics in microspheres that could be injected in advance by a surgeon or anesthesiologist and that would release the drugs when zapped with a laser. Both methods have one goal in common: to provide patients with durable, localized and personalized control of surgical, traumatic or chronic pain with minimal side effects. …
For some pediatric cancers, such as acute lymphoblastic leukemia, older forms of therapy — and older ways of defining who receives which therapy — have served well over the last few decades. But that approach is no longer sufficient. Revolutionary gains have been made in adult oncology using personalized genomic therapy — therapy based on matching treatments to the genetic makeup of a patient’s tumor. The time has come to take them to the pediatric space.
The global market for pain medications is huge — some estimates predict it will hit $41.6 billion by 2017. However, the costs of pain medicine development are huge, too; it takes roughly $900 million to bring a new analgesic compound to market. In part, this is because some 80 percent of compounds that look promising in preclinical animal studies (largely in rodents) fail in late-stage clinical trials.
The saying in the design world is that form follows function. But in biology, and protein biology in particular, it would be more correct to say that form begets function. Shape and structure are the foundation for most protein-based interactions in cells, and are why basic functions like receptor binding, antibody neutralization and gene transcription work.
Two enzymes in the immune system’s B cells, called RAG1 and RAG2, are a perfect example. Together, they form a complex that splices antibody-producing genes together in unique combinations through a process called V(D)J recombination. They do a similar job in T cells to build antigen-binding T-cell receptors (TCRs). In either case, the enzymes are essential to a robust immune response.
At the moment, it would appear the bacteria are winning. Antibiotic resistance is on the rise globally (in part because much of the public may not really understand how antibiotics work), threatening doctors’ ability to treat bacterial infections and potentially making surgery, chemotherapy and other medical procedures whose safety depends on antibiotic prophylaxis more risky.
Mapping antibiotic resistance — which bacteria are resistant to which drugs, and where — can help clinicians and public health officials decide how best to focus their control efforts. The challenge to date has been compiling resistance data in geographically useful ways.
“The data about antibiotic resistance are fragmented across laboratories and hospitals globally,” says Derek MacFadden, MD, a doctoral student at the Harvard T.H. Chan School of Public Health who is working with the HealthMap team in Boston Children’s Computational Health Informatics Program. “Most of the data that are available are very high level, so you can’t get an understanding of regional-level antibiotic resistance.”
This is where ResistanceOpen could come in handy. This new tool, launched by HealthMap team this week during the World Health Organization’s World Antibiotic Awareness Week, provides a window into regional and local antibiotic resistance patterns across the globe.
We’ve all heard the George Santayana quote, “Those who cannot remember the past are condemned to repeat it.” But there’s another way of thinking about the lessons that the past holds for the future: Those who do remember the past can recapture and harness earlier feelings of energy, urgency and possibility to overcome new problems, now and in the future.
In taking the audience on a tour through the last 60 years of advances in cancer biology, genomics and treatment, Mukherjee highlighted the central role pediatrics played as the starting point for the cancer successes we see today. How, he asked, did children come to play such a central role? What can we learn from the successes in the 1950s and ’60s, when pediatric cancer started to evolve from a death sentence to a treatable, even curable disease?
And how, he asked, can we recapture and harness the energy and urgency of that time today?
With SCNT, researchers take an egg cell and replace its nucleus with that of an adult cell (such as a skin cell) from another individual. The donated nucleus basically reboots an embryonic state, creating a clone of the original cell.
It’s a hot topic in both agriculture and regenerative medicine. SCNT-generated cells can be used to clone an animal (remember Dolly the sheep?) or produce embryonic stem (ES) cell lines for research. But it’s an inefficient process, producing very few animal clones or ES lines for the effort and material it takes.
Zhang’s team reported last year that they could boost SCNT’s efficiency significantly by removing an epigenetic roadblock that kept embryonic genes in the donated nucleus from activating in cloned cells. Now, in a new paper in Cell Stem Cell, Zhang and his collaborators report that they’ve extended their work to improve the efficiency of SCNT in human cells.
Part of the problem may be that, until now, the right tools haven’t been available to exploit GWAS data. But a few recent studies—including two out of Dana-Farber/Boston Children’s Cancer and Blood Disorders Center—have used GWAS data to identify therapeutically promising targets, and then manipulated those targets using the growing arsenal of gene editing methods.
“The main problems with measuring patient experience by survey are the small numbers of people who respond to surveys and the lag time,” says Jared Hawkins, MMSc, PhD, of Boston Children’s Hospital’s Computational Health Informatics Program (CHIP). “It can take up to two years before survey data are released to the public. Given that social media data are close to real time, we wanted to see if we could capture this discussion and if the content is useful.”
Hawkins, with Boston Children’s chief innovation officer, John Brownstein, PhD, and their colleagues collected more than 400,000 public tweets directed at the Twitter handles of nearly 2,400 U.S. hospitals between 2012 and 2013. Using machine learning, natural language processing and manual curation, they tagged 34,735 patient experience tweets directed at 1,726 hospital-owned Twitter accounts. …