Communicating translational research
Young investigators master the art of writing about science
Whether it’s cells talking to other cells, physicians speaking with patients or scientists garnering public support for research, communication plays a vital role in science and human health.
For doctoral students enrolled at The University of Texas Health Science Center at Houston (UTHealth) Graduate School of Biomedical Sciences, writing ability is especially critical. In fact, it will continue to be important throughout their careers as they prepare the grants, reports and papers on which the success of their professional work and their funding depend.
To encourage students to hone their writing skills, UTHealth Graduate School of Biomedical Sciences dean George Stancel, Ph.D., launched a competition – with prizes ranging from $250 to $1,000 – to see who among UTHealth graduate students wrote best about their work. So that contestants could get some help with their writing before they composed their entries, he also sponsored a workshop, presented by Karen K. Kaplan, director of communications, and Cynthia J. Johnson, Ph.D., communications manager.
Contest judges were Eric Berger, science reporter and blogger for the Houston Chronicle; Rob Cahill, senior media relations specialist, Office of Institutional Advancement; Jade Boyd, associate director, News and Media Relations at Rice University; Barbara Hyde, director of communications, American Society for Microbiology; Ruth SoRelle, chief science editor, Baylor College of Medicine and editor of From the Laboratories; and Toni Greene, who did her doctoral work at UTHealth Graduate School of Biomedical Sciences and UTHealth Medical School.
The two categories for submission were: Fundamental Basic Research and Clinical and Translational Research. Here are the winners and their winning entries.
Fundamental Basic Research
Quality control on a small scale – in your body
How do manufacturers make sure that a product is fully functional before it leaves the factory? Quality control! A quick look at the items we use in our daily lives reveals the essential role that quality control plays in our well-being. Everything from the food we eat, to the clothes we wear, to the cell phone in your pocket was subjected to quality control to ensure that it lacked defects.
Not surprisingly, the manufacturers and food inspectors of the world aren’t the only ones interested in quality control – so are the cells in our bodies. There are many quality control mechanisms working constantly within us to check for normal processes gone awry. These mechanisms are so important for life that our cells cannot survive without them.
Graduate student Angela Bhalla studies one such quality control mechanism that checks a substance in our cells, called RNA, for errors. RNA is a nucleic acid similar to DNA, the carrier of our genetic material. The relationship between RNA and DNA is similar to that of a sewing pattern and the cloth cut following the pattern: DNA is used as a template to make RNA. However, just as the cut cloth is not a garment ready to wear, RNA itself is not the final, functional product in a cell. It serves as a template for making protein, and it is proteins that perform the functions essential for a cell to live.
Angela’s research focuses on faulty RNAs containing a signal that causes them to be too short. The consequence of a too-short RNA in a cell is similar to when only enough cloth is cut to make half of a garment – it is incomplete. When a faulty RNA is used as a template to make protein, the resulting proteins are also incomplete, and may be toxic to a cell. Faulty RNAs of this nature are detected by a quality control mechanism called nonsense-mediated decay (NMD).
Recently, Angela’s project led to the identification of an additional RNA quality control mechanism for faulty RNAs. It takes place on the outer surface of a unique part of the cell called the nucleus. In addition to housing the cell’s DNA, the nucleus is also the site at which RNAs are made. This newly identified quality control mechanism, called the nonsense-codon induced partitioning shift, or NIPS for short, traps faulty RNAs on the outer surface of the nucleus, making it more difficult for them to be used as templates to make proteins.
The findings from Angela’s research help us understand how our body’s quality control mechanisms work under normal circumstances. Faulty RNAs that are too short are responsible for one-third of all inherited human diseases such as cystic fibrosis, beta thalassemia and even cancer. A greater understanding of the inner workings of these pathways will help researchers develop techniques to combat not only diseases caused by faulty RNA, but also those caused when quality control itself goes awry in the future.
Clinical and Translational Science
Research on actin mutations may provide new insights into cardiovascular disease
Researchers have recently made an exciting discovery: mistakes in a single gene cause not just one, but three major cardiovascular diseases. Cardiovascular diseases are the number one killer in the United States, and much research is currently being done to understand and prevent these diseases. New studies of one gene mutation that causes multiple cardiovascular diseases may provide valuable insight into how these diseases progress. Genes contain all of the information needed for the body to function normally. Copies of genes, known as RNA, are made by the cell and used as templates to generate proteins, which then carry out essential functions within the cell. A mistake in a gene is called a mutation, and causes the cell to make defective protein, triggering a series of events within the cell that lead to the development of disease.
Mutations in one gene, actin, cause aneurysms, which are abnormal enlargements of a blood vessel. Currently, the only treatment is surgical repair once the aneurysm grows too large or too rapidly. In addition to aneurysms, individuals with a mutation in their actin gene are much more likely to have heart attacks and strokes at an abnormally young age. All of these conditions can lead to premature death if not recognized and treated early on. This presents an intriguing paradox: how can a mistake in a single gene cause enlargement of blood vessels, as seen in aneurysms, and blockage of other blood vessels, as seen in heart attack and stroke? The answer may lie within the protein that is made by the defective gene. Actin is absolutely essential for the specialized muscle cells in blood vessels to function properly. With each heartbeat, blood is pumped through the vessels, and the vessels are stretched. The actin in these specialized muscle cells enables the vessels to return to their proper shape and size. Interestingly, the specialized muscle cells that contain defective actin grow more rapidly in number than their counterparts with normal actin. This abnormal cell growth may contribute both to the expansion of some blood vessels and the blockage of others.
A second major change that occurs is in the way that actin is arranged in diseased cells. Normally, actin forms long strands or filaments within the cell; however, this does not happen properly in the diseased cells. The same processes that cause actin to form filaments in the cells can also control the rate of cell growth under certain conditions. Research is underway to determine whether these processes are happening more rapidly in the cells containing defective actin, thus causing the cells to increase in number more rapidly.
Once we understand how actin mutations lead to disease in the blood vessels, drugs can be developed to block the processes that cause these diseases. Alternatively, existing drugs that prevent cells from growing too rapidly in other diseases, such as cancer drugs, may also be utilized. These drugs may slow the progression of disease in individuals with actin mutations, and prevent premature deaths.