Researchers at Johns Hopkins have found out how a protein crucial to learning works: by removing a biochemical “clamp” that prevents connections between nerve cells in the brain from growing stronger. The finding moves neuroscientists a step closer to figuring out how learning and memory work, and how problems with them can arise.
In a two-year longitudinal study involving 13 intensive care units in four U.S. hospitals, researchers found that better physical functioning — basic and complex activities considered essential for maintaining independence — is associated with remission of general anxiety and post-traumatic stress disorder (PTSD) symptoms.
By looking at the expression levels of downstream genes of the regulators in breast cancer, investigators have identified a gene signature in E2F4 that is predictive of estrogen receptor positive (ER+) breast cancer.
While many smokers may make quitting part of their New Year’s resolution – a new study may give some yet another reason to stop – the negative impact cigarette smoke has on chronic wounds. Despite the fact that chronic wounds cost up to $25 billion to treat annually, healthcare providers often don’t discuss smoking with their chronic wound patients. New research explores the connection between non-healing wounds and smoking – and the missed opportunities to help patients understand how their habit is hurting their ability to heal.
One of the mysteries in cancer biology is how one protein, TGF-beta, can both stop cancer from forming and encourage its aggressive growth. Now, researchers at the University of Michigan Comprehensive Cancer Center have uncovered a key gene that may explain this paradox and provide a potential target for treatment.
By developing cell lines that grow readily in culture, investigators have created a fast-track research tool that remains applicable to many scientists who use mouse melanoma as a model system.
An analysis of the genomes and epigenomes of lean and obese mice and humans has turned up a wealth of clues about how genes and the environment conspire to trigger diabetes, Johns Hopkins researchers say. Their findings reveal that obesity-induced changes to the epigenome — reversible chemical “tags” on DNA — are surprisingly similar in mice and humans, and might provide a new route to prevention and treatment of the disease, which affects hundreds of millions worldwide.
For a skin cell to do its job, it must turn on a completely different set of genes than a liver cell — and keep genes it doesn’t need switched off. One way of turning off large groups of genes at once is to send them to “time-out” at the edge of the nucleus. New research shows how DNA gets sent to the nucleus’ far edge, a process critical to controlling genes and determining cell fate.
Elderly patients admitted to ICUs are 35 percent more likely to die within five years of leaving the hospital if they develop an HAI. Preventing HAIs increases survival odds and cuts costs of care by more than $150,000.
A powerful “genome editing” technology known as CRISPR has been used by researchers since 2012 to trim, disrupt, replace or add to sequences of an organism’s DNA. Now, scientists at Johns Hopkins Medicine have shown that the system also precisely and efficiently alters human stem cells.
By adjusting the levels of a key signaling protein, researchers improved motor function and brain abnormalities in experimental animals with a form of Huntington’s disease, a severe neurodegenerative disorder.
Low alcohol consumption and a plant-based diet, both healthy habits aligning with current cancer prevention guidelines, are associated with reducing the risk of obesity-related cancers, a New York University study shows.
When University of Utah biologists fed mice sugar in doses proportional to what many people eat, the fructose-glucose mixture found in high-fructose corn syrup was more toxic than sucrose or table sugar, reducing both the reproduction and lifespan of female rodents.
Results from a study published on Jan. 2 in Science defy textbook science, showing for the first time that the building blocks of a protein, called amino acids, can be assembled without blueprints – DNA and an intermediate template called messenger RNA (mRNA). A team of researchers has observed a case in which another protein specifies which amino acids are added.
Scientists from the Johns Hopkins Kimmel Cancer Center have created a statistical model that measures the proportion of cancer incidence, across many tissue types, caused mainly by random mutations that occur when stem cells divide. By their measure, two-thirds of adult cancer incidence across tissues can be explained primarily by “bad luck,” when these random mutations occur in genes that can drive cancer growth, while the remaining third are due to environmental factors and inherited genes.
Case Western Reserve researchers have identified a two-pronged therapeutic approach that shows great potential for weakening and then defeating cancer cells. The team’s complex mix of genetic and biochemical experiments unearthed a way to increase the presence of a tumor-suppressing protein.
While an effective treatment is available for combating multidrug-resistant tuberculosis, it carries serious side effects for patients. New research conducted at the Center for Tuberculosis Research at the Johns Hopkins University School of Medicine shows that lower doses of the toxic drug bedaquiline — given together with verapamil, a medication that’s used to treat various heart conditions — can lead to the same antibacterial effects as higher toxic doses of bedaquiline.
University of Colorado Cancer Center study shows that pre-programmed stem cell demise allows cancer after radiation, and that NOTCH signaling can restore stem cell function.
Already known to cut proteins, the enzyme SPPL3 turns out to have additional talents, according to a new study from Johns Hopkins. In its newly discovered role, SPPL3 works without cutting proteins to activate T cells, the immune system’s foot soldiers. Because its structure is similar to that of presenilin enzymes, which have been implicated in Alzheimer’s disease, the researchers believe their findings could shed more light on presenilin functions, in addition to providing new insight into how the immune system is controlled.
Researchers at Johns Hopkins have discovered what keeps an enzyme from becoming overzealous in its clipping of DNA. Since controlled clipping is required for the production of specialized immune system proteins, an understanding of what keeps the enzyme in check should help explain why its mutant forms can lead to immunodeficiency and cancer.
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