Arm fractures followed soon by death

Photo provided by Andre van Schalkwyk of Antilogic

Broken arm? No problem! One trip to the hospital, and you’re ready to continue your long healthy life. Maybe not. University of Helsikinki’s very own have reported a strong link between upper limb fracture and increased rate of death.

Just shy of 6,000 people of Finland who sustained bone fractures to their upper extremities were followed for an average of six years between 2002 and 2012. Researchers wanted to find out if those with shoulder, arm, wrist, etc. fractures had an increased risk of death similar to those with hip fractures.

Previous studies have documented that people with one or more hip fractures have nearly a three times higher rate of dying than people of the same age without a hip fracture. The standardized mortality ratio (SMR) was 2.18 for women and 3.17 for men. The SMR is the amount of deaths of a studied population as compared to the general population. An SMR of 1 would mean an equal rate of death in both populations, while an SMR of 2 would mean 100% more cases of death in the studied population.

This study found that 12% of the studied population had died five years after their upper extremity fracture. For individuals between 16 and 59 years old, there were nearly 200% more cases of death for individuals with a bone fracture as compared to those without (SMR: 2.2 for women, 3.0 for men). Individuals 60 years of age and older had an average of 40% more cases of death (SMR: 1.2 for women, 1.6 for men). If the fracture was in the individual’s humerus, the arm bone that extends from shoulder to elbow, mortality was much higher for both sexes of all ages.

Leading causes of death for individuals sustaining upper limb fractures were cardiovascular disease, accidents, and violence. No, this does not mean a broken arm increases risk of heart attack (except in the mother of the son who broke his arm playing street hockey), but concern should be raised after sustaining fracture.

People who break an arm, or sustain similar upper extremity fractures, may be more frail than others, leading a risky lifestyle, or just unlucky. Whatever the reason, this study says be careful in the future and stay healthy!

Reference:
Axel Somersaloa, Juha Palonevab, Hannu Kautiainencd, Eija Lönnroose, Mikko Heinänenf, Ilkka Kivirantaf. Increased mortality after upper extremity fracture requiring inpatient care. Acta Orthopaedica, 2015.
http://dx.doi.org/10.3109/17453674.2015.1043833

Herpes don’t hurt me!

Courtesy of Emneth Design

“Don’t look at me, I’m a monster!” The herpes simplex virus (HSV) plagues many people worldwide putting them at social and more importantly physical danger as the virus can lead to mortal complications. Researchers of the University of Washington and Hutchinson Cancer Research Center found that Nelfavir can trap herpes within cells and turn it from a danger to an annoyance.

This study looked into the ways in which Nelfinavir (NFV), an anti-cancer drug, could be used to combat the virus causing herpes, specifically HSV-1. HSV is a non-living, infectious agent that looks like a durian fruit. The DNA of the virus is inside while the outside “skin” is made of protein and “spikes” are made of glycoproteins (sugar-proteins). The glycoproteins are what allow the virus to enter human cells and infect. HSV infection causes the cell to waste its resources to make new viruses that can infect other cells. With HSV comes elevated risk of aquiring HIV and Kaposi sarcoma, a cancer.

Imagine a factory that makes cars and all the machinery inside is blue. The factory can be equated to a cell. If a virus infects, this would be akin to someone adding instructions and an extra machine or two to the factory that now allows bombs to be made in the car factory. Imagine the extra machine is yellow. It is easy to spot and get rid of the extra machinery that is making bombs if it does not look like the original factory machinery. This is how most drugs target and destroy viruses. The virus machinery is often easy to differentiate from cell machinery. What if the virus machinery were also blue? This is when a virus becomes drug resistant. The virus has changed, so the drug can no longer target and destroy it. Instead of targeting the virus itself, another method of stopping viruses is by changing the cell machinery so that it will rarely make a fully functioning bomb (virus). This is how NFV acts on HSV-1.

The researchers infected human connective tissue cells, fibroblasts, with HSV-1 and treated with NFV to measure its effectiveness in blocking virus production in vitro. It was found that NFV blocked viral protein maturation, glycoprotein development, and viral packaging.

Virus retention inside the cell was 79:14, NFV treated:untreated
Virus particles found outside the cell was 3:51, NFV treated:untreated
Virus completion inside the cell was 0:9, NFV treated:untreated

This meant that although HSV-1 was getting into the cells, new viruses were created broken and could not leave or infect other cells. It was also found that HSV-1 was not becoming resistant to the drug even after subjected to drug pressure. This is because NFV affects the cell rather than virus.

This newfound use for Nelfinavir shows promise for longterm control of herpes. This ubiquitous and malignant virus may soon be just a small bother.

Reference:
Soren Gantt, Eliora Gachelet, Jacquelyn Carlsson, Serge Barcy, Corey Casper, Michael Lagunoff. Nelfinavir Impairs Glycosylation of Herpes Simplex Virus 1 Envelope Proteins and Blocks Virus Maturation. Advances in Virology, 2015
http://dx.doi.org/10.1155/2015/687162