New Stem Cell Guidelines

The National Institutes of Health (NIH) is about to change its definition of human embryonic stem cells (hESCs) in light of recent trends in stem cell research.

In March of 2009 President Barack Obama signed an executive order once again permitting the use of hESCs in research. According to the executive order, the NIH is charged with ensuring that NIH-funded research in which hESCs are used is ethically responsible, scientifically worthy, and conducted in accordance with applicable law. NIH does that by setting strict guidelines for what types of cells may be used and how they must be derived.

According to the current NIH guidelines, part of the definition of hESCs is that they are cells “derived from the inner cell mass of blastocyst stage human embryos”1. But the definition apparently had the unintended consequence of excluding some cell lines that were derived from even earlier, morula-stage cells (Review Figure 21.5 in Johnson’s Human Biology). The revised language will read, “derived from early stage human embryos, up to and including the blastocyst stage”, so that these more recent cell lines may be used in federally funded research projects.

The new guidelines do not change the rigorous ethical standards for deriving human cell lines. They just make more stem cell lines available to researchers.

1 Federal Register vol. 75, no. 35, Tuesday, Feb. 23, 2010, p. 8085-8086.

Bacterial Resistance to Antibiotics

The prevailing thought has always been that bacterial resistance to antibiotics comes about by a process of natural selection. When antibiotics kill most but not all of a bacterial population, the bacteria that survive are those that were most resistant to the antibiotic. These resistant bacteria then flourish, passing their resistance genes on to other bacteria and outcompeting their more vulnerable kin. The more times an antibiotic is used, then, the more likely it becomes that the surviving bacteria will be resistant to it.

But now researchers have found another mechanism for bacterial resistance to antibiotics. It turns out that antibiotics induce the formation of toxic molecules within bacteria called reactive oxygen species, or free radicals, that help kill the bacteria. But if the concentration of antibiotic is below the threshold for killing the bacteria outright, the free radicals cause mutations in the bacteria, some of which by random chance may confer drug resistance. In other words, antibiotics speed up the process of bacterial evolution in the surviving bacteria.

The finding opens a new avenue for research – finding molecules that prevent this bacterial mutagenesis, thus perhaps delaying the development of antibiotic resistance.

Platelet-Rich Plasma Therapy Revisited

About a year ago I described PRP (platelet-rich plasma) therapy as an exciting and potentially effective new treatment for injuries to tendons and ligaments (see "PRP Therapy for Connective Tissue Injuries"). Apparently athletes and other patients were asking for the treatment, even though insurance companies were reluctant to pay for it. I asked, “Does it work?” and mentioned that several clinical trials were currently underway to find out.

The results of several of the clinical trials are now in, and the results are not encouraging. In one study of patients with Achilles tendon injuries, PRP therapy was no more effective than an injection of saline (the control). In another study of tennis elbow, PRP therapy appeared to be slightly more effective than injections of steroids (the standard treatment these days). However, some scientists have criticized the tennis elbow study for not having a control group. Steroid injections are known to reduce pain in the short-term but to slow healing in the long-term. So the jury is still out on whether PRP therapy for tennis elbow is actually better than no treatment at all.

No doubt, studies with other tendon/ligament injuries using different study protocols will be done in the future. In the meantime, enthusiasm for PRP therapy has cooled just a little.

Carbon Dioxide and Forest Growth

Plants require carbon dioxide (CO2) for growth. How are they affected by the rise in atmospheric CO2 that occurred over the last century, as a result of human activities such as the burning of fossil fuels? Do plants use more CO2 (i.e, grow faster) when more CO2 is available?

There is some evidence that they may. A study of 55 forest plots in the Eastern United States reveals that the tree biomass is increasing at a faster rate now than in several decades past. After factoring out other known factors, the most likely causes appear to be increases in atmospheric CO2 and in temperature. This may be good news, for it means that as the atmospheric CO2 rises, some of the excess CO2 may naturally be stored in Earth's forest biomass. This could be slowing the rate of rise of CO2 (and global warming) that would otherwise occur.

Smoking and Breast Sagging

A couple of years ago a plastic surgeon and his colleagues did a study in which they interviewed 132 women who had requested breast lift surgery or breast augmentation. The goal of the interviews was to try to determine whether there was any truth to the commonly held belief that breast-feeding causes breast sagging later in life.

The results showed no difference in the degree of breast ptosis (sagging) between women who had breastfed and those who had not. However, factors that did correlate with breast sagging included the woman’s age, how many pregnancies she had had, and whether she had smoked.

Yes, you read that right - smoking. It is well known that smoking damages elastin, the protein fibers in skin responsible for skin’s youthful appearance and elasticity. That’s why chronic smokers are much more likely to have wrinkled skin than non-smokers. It would not be much of a stretch (no pun intended) to hypothesize that healthy elastin supports breast tissue and helps maintain breast shape.

One more reason not to smoke?