The biggest concern with anti-bacterial soaps and the like is essentially the fast-forward nature of Darwinism in single-cell organisms. You kill all the bacteria that are susceptible to Anti-Bac A and the ones that are left get a wide-open ecosystem with none of their weaker brethren to hinder their reproduction. Before long, none of the bacteria that used to be weakened by Anti-Bac A are around, leaving you to find Anti-Bac B in a hurry. Because the new bacteria are wiping people out.
But researchers at the University of Rochester are aiming at another, more effective way to deal with bacteria. One that doesn’t allow them to evolve around the latest defense, because it goes to the core of how cells – any cells, really – operate. The new theory is that we may someday be able to interrupt the processing of two key proteins used in ribosomes. Ribosomes are the protein-creating organelle in the cell. Without properly-functioning ribosomes, no cell can live. Interrupt these two key proteins and you kill the cell:
They discovered that two proteins already present in E. coli cells—RbfA and KsgA—need to be in balance with each other in order for ribosomes to function. If those proteins are present in the wrong concentrations, the ribosomes will not mature properly and will be unable to produce proteins, leading to the death of the cells. Their findings are being published this week in the journal Molecular Microbiology.
Researching, cataloging and analyzing proteins is one of the major biological research competencies of the Rochester area. Another research project at RIT discovered the protein required to allow photosynthesis in algae. Once again, finding a path to disrupt the use of this particular protein would create an organism-specific means to control an undesirable population.
In this case, researchers are again focusing on a specific species – E. Coli – but identifying similar proteins in other species would work as well.
If you’re like me (god help you), hours of your week are spent trawling through press releases from colleges and universities in the area, looking for the next big breakthrough in science news. But if you’re like me, you’re probably not reading this blog. You’re writing your own.
And if you came across the article I just read from the University of Buffalo news, you’d find yourself scratching your head, wondering how you can get some grant money. It can’t be hard. Because the latest technology news from the UB Medical School is that the AMA has granted an unspecified amount of money to the school to create “cloud-based patient simulations” that third-year medical school students can use to test out their skills:
The i-Human Patients platform is a cloud-based service for medical students that simulates a patient visit. Students use the software to interview and examine animations of patients, order and review diagnostic tests, develop diagnostic hypotheses and create a treatment plan. Online guidance and comprehensive feedback occurs at every step of the process.
Ok. So, basically CBT’s for medical students. Really?
I’m sure I’m missing… something. But this strikes me as quite possibly the least-effective possible use of money for medical research. Perhaps the article doesn’t get specific enough with what they’re building, but it seems to me that a Twistaplot book for med students would work just as well. Because you put it “In the Cloud” does not make it newer or better.
I’d love to hear from anyone with more information on this subject. Seriously: tell me I’m wrong.
Schizophrenia is a cypher to science. It is an inherited disease, yet it does not go strictly from one generation to the next. It may skip a few. There are even arguments that schizophrenia may be caused by environmental instead of genetic factors. But one thing most schizophrenics have in common:
They smoke. A lot.
Researchers at the University of Buffalo believe that schizophrenics smoke because nicotine is a form of self-medication, and that by working with smoking cessation drugs (nicotinic agonists, they call that), doctors may be able to help repair cognitive functions of the sufferers.
How is this possible? They believe they have discovered a single genetic pathway, or series of DNA segments that work together, that controls as many as 160 different traits, all associated with the disease:
“How is it possible to have 100 patients with schizophrenia and each one has a different genetic mutation that causes the disorder?” asks Stachowiak. “It’s possible because INFS integrates diverse neurological signals that control the development of embryonic stem cell and neural progenitor cells, and links pathways involving schizophrenia-linked genes.
“INFS functions like the conductor of an orchestra,” explains Stachowiak. “It doesn’t matter which musician is playing the wrong note, it brings down the conductor and the whole orchestra. With INFS, we propose that when there is an alteration or mutation in a single schizophrenia-linked gene, the INFS system that controls development of the whole brain becomes untuned. That’s how schizophrenia develops.”
The link between smoking and schizophrenia is well-established. Because there is such a strong, common link between smoking and this otherwise disparately symptomatic disease, researchers believe that nicotine and nicotinic agonists may be affecting this pathway.
News out of the University of Rochester ( @urmcdiscoveries ) this week suggests that the key to understanding dementia and other cognitive degeneration over the age of 60 may be understanding trauma to the brain so slight as to be imperceptible when it happens. These events are known as “mini-strokes” (microinfarcts to their friends) and have previously been missed by traditional MRI, which is not sensitive enough to detect their passage. However:
Microinfarcts are far more common than previously understood; it is believed that about 50 percent of individuals over the age of 60 have experienced at least one mini-stroke. Studies have also correlated the presence of mini-strokes with the symptoms of dementia. An estimated 55 percent of individuals with mild dementia and upwards of 70 percent of individuals with more severe symptoms show evidence of past mini-strokes. This association has led researchers to believe that these mini-strokes may be key contributors to age-related cognitive decline and dementia.
When people think of “a stroke,” the thing they envision is anything but a subtle or imperceptible. And it is true that stroke events we’re more familiar with are sudden and life-altering events. But according to the article, any damage done to brain tissue as a result of a disruption of blood flow is considered a stroke. And these events can happen very slowly and very subtly. Up to several weeks, according to the research.
So now that you know this, just try not to think about it every time you get a headache, ok? Ok.
Scientists are often fond of saying “correlation does not prove causality.” That meaning: just because two things happen at the same time or in sequence in no way implies that one caused the other. They may simply have coincidentally happened in an order tantalizing us to make hasty assumptions.
I cannot say for certain that the study the University of Rochester released today does or does not display that false sense of causality. But my sense is that much more research is probably necessary. This study followed about 5,000 respondents to a questionnaire about pain after treatment for back issues. The results pretty conclusively correlated less back pain with those who either quit smoking years ago or never smoked, compared to those who currently smoked. However:
Of the 5,333 people, those who had never smoked or had quit some time ago reported less pain than smokers or those who had just quit. By the end of the follow-up period, the people who had recently quit or who quit during treatment showed significant improvements in pain. People who continued to smoke during treatment had no improvement in pain on all scales.
Behrend noted that younger people tended to comprise the group of current smokers and those who only decided to quit during treatment; this is consistent with other studies showing that smoking is associated with degenerative spine disease at a younger age. Older patients tended to comprise the group who had never smoked or quit long ago.
The trouble here is that we’re dealing with two hugely divergent groups of people. To simply say that the fact that they smoke or don’t smoke is one correlated item is to completely under cut all the other vastly significant differences between these two groups. For example: those who continue to smoke into old age are probably also making a great deal many more decisions which are not beneficial to their health. And those who quit smoking while still young are probably eager to move on.
When I quit smoking six years or so ago, I swore I’d never be what I always referred to as a “Born Again Non-Smoker.” It is easy, when smoking is such a great scapegoat and straw man, to blame the habit for all the ills of any individual and claim the Holy Grail of health benefits every time something seems to prove a socially agreed-upon conclusion. But this report leaves a whole lot to be desired in the facts department.