– Keeping saliva secretion up after radiotherapy, or how finding where stem cells crucial to salivary gland regeneration reside may help prevent irreversible tissue damage and loss of saliva production after head-and-neck cancer radiotherapy
– Getting cold in type 2 diabetes, or how a protocol involving sitting in a cold room for several hours can improve insulin sensitivity in patients with type 2 diabetes
– Another big, big, big virus, or how a new giant virus was recently discovered in a 30,000-year-old permafrost sample from Siberia
- Keeping saliva secretion up after radiotherapy
During radiotherapy, irradiation of healthy tissue close to the tumor is unavoidable. In the case of head and neck cancer, radiotherapy results in relatively high survival rates but may severely compromise the quality of life of surviving patients by irreversibly damaging the salivary glands. Destruction of salivary gland tissue leads to a drastic decrease in saliva production and, as a result, to increased susceptibility to oral infections as well as impaired swallowing, food mastication, taste, and speech.
A research group in the Netherlands has now pinpointed where stem and progenitor cells reside in the parotid glands, which are the largest of the salivary glands. They show that irradiation of this region in rats prevents the salivary tissue from regenerating and leads to long-term gland dysfunction and hyposalivation. Similarly, they find that, in head and neck cancer patients, the amount of radiation to these structures predicts how well or how poorly the salivary glands function one year after radiotherapy.
The researchers propose that, now that the areas containing the cells necessary to the regeneration of salivary gland tissue are known, it should be possible to spare them and thus reduce the risk of post-radiotherapy xerostomia (dry mouth syndrome). New radiation treatment technologies should make such a high-precision targeting of the radiation field possible.
(van Luijk et al. Science Translational Medicine 16 September 2015. doi: 10.1126/scitranslmed.aac4441)
- Getting cold in type 2 diabetes
In individuals with type 2 diabetes, sensitivity to insulin is severely decreased, meaning that the cells of the body stop responding or respond very little to insulin. As a consequence, normal glucose metabolism is impaired, and blood glucose levels rise higher than normal. Brown adipose tissue (BAT), a particular type of fat, has garnered a lot of interest (and media attention) in the past few years, as it was reported to be more efficient than white adipose tissue (WAT) at using (by oxidating) triglycerides and glucose to produce energy and then consume this energy to produce heat. (WAT, typically, is the subcutaneous and visceral fat, the “bad fat”.) Recently, exposure to cold (cold acclimation) has been linked to an increase in BAT quantity and activity.
In a small trial, researchers therefore asked whether cold acclimation could activate BAT and help improve glucose homeostasis in eight individuals with type 2 diabetes. The patients, dressed in shorts and T-shirt, started by spending 2h in a room at a temperature of 14-15°C on the first day of the trial, then 4h the next day, and finally 6h each day from day 3 to 10. At the end of the 10-day cold acclimation period, the researchers assessed the patients’ BAT activity and compared it to what it was before cold acclimation. They found that BAT activity was now higher than before the trial, but still very low compared to that usually found in young, healthy individuals. There were no signs of WAT “beiging”, that is, no indication that a 10-day cold acclimation period induced conversion of WAT to a more BAT-like type of fat. Nevertheless, the researchers found that insulin sensitivity was markedly increased in patients after cold acclimation.
Although the mechanisms by which cold exposure augmented insulin sensitivity in these individuals remain unclear, the researchers suggest that cold acclimation might be another strategy worth considering to improve type 2 diabetes patients’ metabolic health.
(Hanssen et al. Nature Medicine 6 July 2015. doi: 10.1038/nm.3891)
- Another big, big, big virus
Two years ago, I mentioned in an “In brief” post the discovery of two giant viruses, dubbed Pandoraviruses by the team of French researchers that had unearthed them (more details here). Viruses had always been considered tiny particles containing only a few genes, but the discovery of Mimiviruses in 2003, followed by Megavirus chilensis in 2011 and Pandoraviruses in 2013, extended the realm occupied by viruses in Earth’s microbial diversity. About a year ago, the same team of researchers described yet another giant virus, called Pithovirus sibericum. Now, they are back with a fifth one: Mollivirus sibericum.
All those giant viruses have in common to infect amoebae (single-cell eukaryotic organisms commonly found in soil), to nearly rival bacteria in cell and genome size, and to carry a large number of DNA sequences that do not resemble anything known so far. However, they also differ from one another in their virion structure (icosahedral, amphora-shaped, or spherical), genome size and sequence (not only are most of these DNA sequences not similar to anything known, but they are also different from one giant virus to the next), and replication cycle. The two Pandoraviruses from 2013 had been discovered in a marine sediment layer off the coast of Chile and in mud from a freshwater pond in Australia. The two more recent ones, Pithovirus and Mollivirus, have been recovered from a 30,000-year old permafrost layer sample from Siberia.
(Legendre et al. PNAS 22 September 2015. doi: 10.1073/pnas.1510795112)