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Living Antibiotics: The New Last Line of Defense?

Posted on Aug 15, 2017 in Blog

When Alexander Fleming discovered penicillin in 1928, it started a new era in medicine: the era of antibiotics. Once penicillin could be efficiently purified in bulk in the 1940’s, it gave doctors access to an incredibly powerful tool to cure previously deadly diseases such as pneumonia and gonorrhea. However, antibiotics did not quite turn out to be a class of miracle drugs. Over time, many bacteria have been able to able to adapt to antibiotic treatment and develop resistance to the drugs. This has created an arms race between pharmaceutical companies and bacteria; as bacteria strains become resistant to antibiotics, drug companies must work to develop new medicines to fight them. In some cases, the bacteria seem to be winning. According to the CDC, more than 2 million people are infected by antibiotic-resistant bacteria in the US annually and 23,000 people die from drug-resistant infections every year. Most of these bacteria are only resistant to certain classes of antibiotics, although there have been almost 10 cases of totally-resistant bacteria in the US so far.

While the number of cases of bacteria that are completely resistant to all known antibiotic drugs is low, this is a nightmare scenario for health care. To develop a new last line of defense against antibiotic-resistant strains, researchers are looking to fight bacteria with…other bacteria. The plan is to harness bacteria that naturally prey on other bacteria, and use these predators to attack infections within the human body. Scientists are studying a strain of bacteria called Bdellovibrio bacteriovorus to this end. B. bacteriovorus attacks “gram-negative” bacteria, i.e. bacteria that have both an inner cell membrane and an outer cell wall. Many of the most dangerous antibiotic-resistant bacterial strains are gram-negative, such as the Enterobacteriaceae family (which includes pathogens such as Salmonella and E. coli) including Shigella spp (which causes dysentery).

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Serotonin, Nerve Cell Wiring, and Depression

Posted on Jun 29, 2017 in Blog

serotonin

Model of a Serotonin Molecule

Depression, or major depressive disorder (MDD) as it is known clinically, is one of the most common debilitative disorders on the planet. In 2015, it’s estimated that 216 million people (about 3% of the world population) suffered from depression. In the United States, depression is the leading cause of disability for people between the ages of 15 and 44. According to the Anxiety and Depression Association of America, MDD affects more than 15 million Americans annually – 6.7% of the adult population. Depression is believed to be caused by some combination of genetic, environmental, and psychological factors. However, the specific cause of the condition remains unknown.

In the past, the brain’s serotonin-delivery (serotonergic) system has been suspected to be involved with many psychiatric conditions, including depression. Serotonin is a chemical produced primarily in the gastrointestinal tract, but also plays a role in the function of the nervous system. It is thought to play a part in feelings of happiness, well-being, etc. Serotonin that gets used by the nervous system is predominantly managed in a part of the brain called the Raphe nuclei, which is in the brainstem. There aren’t many serotonergic cells in this area (only about 300,000), but they can deliver serotonin to the rest of the brain through a complex system of axons. Most studies of the causes of depression have focused on how serotonin is created and processed chemically in the brain when looking for causal links. However, a new study looks at how the axons that deliver the chemical spread out through the brain and what genes effect their development.

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Modifying Mosquitoes for Genetic Sterility

Posted on Jun 2, 2017 in Blog

Aedes aegypti mosquitoDengue fever is one of the most pressing threats to global health. The World Health Organization considers it the most critical mosquito-borne virus. The symptoms include sudden-onset fever, headache (usually located behind the eyes), muscle and joint pains (thus the moniker “breakbone fever”), and a rash. The virus is spreading rapidly, with infection rates increasing by a factor of thirty over the last fifty years. More than 2.5 billion people in over 100 countries are at risk. While a vaccine for dengue fever was introduced in 2016, it is not 100% effective and researchers are still looking at novel ways to prevent infection.

One of the new approaches to prevent infection involves releasing bacterially-infected mosquitoes into the wild to crash the local population. This approach has been tested before, which we briefly mentioned in our blog about Zika last year. The method uses Wolbachia bacteria to control the population. Wolbachia is one of the most common parasitic microbes on the planet. They infect arthropods, including a high proportion of insects such as mosquitoes.

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The Need for Climate-Friendly Refrigerants & Technologies

Posted on Apr 28, 2017 in Blog

1,1,1,2-tetrafluoroethane/R-134aEver since the development of vapor-compression refrigeration in the early 20th century, chemists have constantly been tinkering to find more efficient and cost-effective refrigerants. Until the late 1980’s, the most common refrigerants were chlorofluorocarbons, or CFCs. CFCs are organic compounds made up of carbon, chlorine, and fluorine (derived from methane, ethane, and propane), and are best known by their DuPont brand name: Freon. However, CFCs were found to be contributing to the depletion of the ozone layer, and in 1987 the multi-national Montreal Protocol on Substances that Deplete the Ozone Layer was agreed upon, which involved phasing out CFCs as refrigerants.

As CFCs were phased out throughout the 1990s, their primary replacements as refrigerant were hydrofluorocarbons, or HFCs. HFCs contain hydrogen atoms instead of the chlorine atoms found in CFCs. One of the most prolific HFCs, 1,1,1,2-tetrafluoroethane (known more commonly as R-134a), is used by Powers Scientific in all our refrigerated chambers. HFCs are an upgrade over CFCs in that they are much less destructive to the ozone layer. However, they are not a perfect solution. As concerns about climate change continue to grow, HFCs have come under scrutiny for their global warming potential (GWP). As the levels of HFCs in the atmosphere continue to increase, so does the climate risk. To keep this emergent environmental danger in check, world leaders met in Rwanda last October to make a deal to lower HFC usage. They agreed to lower the worldwide usage of HFCs by 80-85% by 2047.

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Minimizing Water Loss in Plants Through Genetics

Posted on Mar 30, 2017 in Blog

cactusPhotosynthesis, the driver for all plant life on earth, requires three things: water, carbon dioxide and sunlight. Carbon dioxide and sunlight are in plentiful supply across the earth, but water can be much more difficult to come by in certain areas. Of course, a scarce water supply does not mean that plants can’t survive – many plant species can do just fine in very dry climates. One of the key principles for plants to grow in these areas is to conserve as much water as possible. Most plants bring carbon dioxide into their system by opening their stomata (pores, usually in the of leaves or stems, that control oxygen and carbon dioxide exchange) during the day to fuel photosynthesis. However, opening the stomata during the day is grossly water inefficient. Evaporation from the heat of the sun’s rays leads to massive amounts of water loss.

To combat the evaporative losses, the best thing to do would be to keep the stomata closed during the day and and then open them for carbon dioxide intake at night when the temperate is lower. However, the main hurdle to this approach is that the entire point of bringing carbon dioxide into the plant is so that it can be used in photosynthesis. Since photosynthesis requires light, bringing in carbon dioxide at night would be useless for most plants. However, some plants have figured out a way around this problem. The process is referred to as crassulacean acid metabolism, or CAM, which is named for the family of plants in which it was first studied, i.e., the Crassulaceae plant family. (note that CAM stands for how Crassulaceae metabolize acid, NOT how “crassulacean acid” is metabolized.)

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Trying to Turn Back the Aging Clock

Posted on Mar 2, 2017 in Blog

Epigenetic nucleosome structureDNA is fundamental for carrying genetic instructions for the growth and development of all known living organisms. However, DNA is not the sole tool for implementing genetic instructions. Epigenetic marks are cellular features that are made up of various amino acid and protein groups that can modify proteins within a cell. These epigenetic marks are not governed by the genetic code, but are nevertheless capable of influencing the way genes are expressed. The buildup of these epigenetic marks in our cells has been suspected as a driving factor of the aging process.

What if there was a way to strip these epigenetic marks from cells? Would that allow us to effectively reset the aging clock? A recent article in Science News talks about how researchers are working on answering that question through experiments on genetically engineered mice. The research took mice that had been genetically engineered to express two important characteristics. The first trait necessary was to show the same premature aging patterns as mice used as models to study Hutchinson Gilford Progeria Syndrome. The second required trait was the ability for the mice to produce four specific proteins when given an externally-controllable trigger. These proteins – Oct4, Sox2, Klf4, and c-Myc – or OSKM for short, are also known as “Yamanaka factors” after the Nobel prize-winning Shinya Yamanaka, who discovered that these proteins could turn adult cells into induced pluripotent stem cells (iPS cells).

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