Potentially Safe Additive to Wine that Prevents Bad Taste

Apathy killed the cat

Whenever I am at my parents' house, I always partake in nightly wine tasting with them. That feeling of warmth going down my throat, that fine crisp taste when swishing it around in my mouth, it's perfect. My parents have a wine rack, and each time I visit I try a different bottle. I like to believe I am pretty indifferent to wines, as I don't usually notice big differences that could set me off of the particular brand, but sometimes wine just loses it's taste, and it's scent, making it undrinkable. This is caused by oxidation. Oxygen can enter even through a corked bottle, binding to metals such as iron to create a foul taste and/or smell. Luckily, scientists recently found a possible additive to wine that will slow the oxidation process. Two oxidation states are found in wine: iron(II)oxide and iron(III)oxide. Since both are iron, chelating agents (molecules that bind metal ions) for both states were looked at. These agents included Ferrozine, bipyridine, EDTA, and phytic acid. All chelating agents inhibited oxidation. To arrive at the conclusion that these molecules were in fact working chelators, the scientists had to measure the concentration of iron in white pinot gris wine, and then measure the oxidation that occurred when chelating agents were put in. Previous methods to get rid of the metals in the wine that caused oxidation to occur were too expensive to be the solution to the problem. However, phytic acid seems to be the best choice of chelating agent, as it is safe for consumption. My question to you is this: Why should scientists focus on this particular problem in wines? Do you think money would be better spent on human cures rather than wine cures?

For more information, click here.

Familial Alzheimer's: How Stem Cells Could Help Identify Its Origins

Alzheimer's isn't something to joke about. Never forget that!

Alzheimer's disease is a common 'forgetting' disease among older people. One type of AD, familial AD, is passed down from family members. Through the use of pluripotent stem cells, a team of scientists were able to understand more clearly the origins of familial AD by studying the protein presenilin 1 (PS1). PS1 is an enzymatic protein that regulates gamma secretase, which cleaves amyloid precursor proteins (APPs). The functions of APP are not entirely known, but it is believed that the cleaved products of APP, amyloid betas, can cause plaques to form that can kill neurons in the brain if cleaved wrong, most likely causing AD. The scientists discovered that mutant forms of PS1 caused twice the amount of APP that were cut wrong. Here is where the pluripotent stem cells came in. Neurons that were derived from Craig Ventor's own stem cells were created, each with different alleles of the PSEN1 mutant gene. This helped them figure out what effects different mutations had on the neurological level. My question to you is this: Pluripotent stem cells are stem cells that have the potential to form any other type of cell it needs to in the body, and because it has the potential, it is still in its infancy at the time and usually is taken from human embryos. However, because the stem cells used here were derived from an adult, and not from a human embryo, do you believe stem cells are now significant in scientific experimentation?

For more information, click here.

Blog 10.2 Mitotic Chromosome 3-Dimensional Structure Mapping

5-year-old's rendition of the human chromosome

Well I couldn't wait to write about this one, so I am doing another blog for this week! Finally, after approximately one and a half centuries of debate, the scientists at MIT pinpointed a universal method in all types of cells of condensed mitotic chromosome organization. Before this, scientists had no way of knowing the exact method of how DNA was condensed in the chromosome, as microscopes were not technically advanced enough to observe the process, which led to different suggested methods. It was already known that DNA had to be tightly condensed in order for successful transportation to daughter cells, but how it actually folded was debatable. The most common textbook explanation of how DNA was condensed was via multifold coiling, where coils form coils form coils (supercoils). However, there was another explanation of how DNA was condensed, stating that a series of loops were formed, attaching to a linear axial structure, ultimately becoming the chromosomal backbone. To solve this dilemma, scientists used chromosomal conformation capture to find exact contact points on different chromosomes during the metaphase part of mitosis, creating 3D models from contact point spatial arrangement. After comparing this model to the two previously suggested models, we can now throw the multifold coiling method out the window. In actuality, the chromosome was compacted in two phases: first to form loops with a circumference of approximately 100,000 base pairs, and second to tightly compress these loops like a slinky. What's strange about this is that condensed DNA is not as highly organized as we had originally thought it to be. Loops formed pretty much randomly, meaning that condensing is variable. My question to you is this: What things can scientists experiment on once the entire mitotic chromosome or
ganization process is understood?

For more information, click here.

Blog 10.1 Gastric Cancer is Lacto(ferricin) Intolerant

A cow goes, "Moooooolecular Biology"

Scientists have recently found a way to kill human stomach cancer cells using an enzyme found in cow milk called lactoferricin B25, which is a known antimicrobial and anticancer agent. Previously, like other cancers, gastric cancers have usually only been treated at an early stage via chemotherapy. Using lactoferricin B peptide fragments, the B25 fragment was the only peptide found to effectively kill human gastric adenocarcinoma cells. Scientists saw that the cells lost their ability to adhere to walls of the cell plates when lactoferricin B25 was present. A bit later, the cells started to die by, first, both apoptosis (cell suicide) and autophagy, then solely by apoptosis. It was also found that a cleaved key protein called Beclin-1 increased gradually in the presence of the lactoferricin B25. This is a good thing, as Beclin-1 is linked to tumor inhibition, which causes the anticancer effects of lactoferricin to increase. My question to you is this: How do you think scientists will/should go about experimenting with this potential cancer curing peptide (for example: testing on monkeys, testing on mice, or even straight to testing on humans)? If you can, explain why you think they will/should do this.

To read more about this, click here.

Stopping The Superbugs For Good

It's a bird, it's a plane, no... it's superbug!

Every year, new flu shots are being created to take out the new and improved influenza viruses that descended from the resistant few who survived the year before. This example of resistance increase in viruses is one of the milder cases. You could see where being resistant to everything could be a problem. Well now there is hope. Scientists recently suggested a possible solution to the problem would be to use antimicrobial peptides (AMPs) in order to poke holes in the cell membrane, holes that expand until the cell bursts. In order to observe such a small and quick action, however, the scientists had to generate and program their own AMP and get it to bind to a supported lipid bilayer (SLB) so that they could facilitate when the AMP would bind, therefore allowing the expansion of nanometer-sized pores to be seen and tested. After studying the process of pore expansion in enough detail, it was suggested that when the first AMP binds to the membrane, it triggers a response to other AMPs to start binding to the membrane, causing multiple pore expansions. My question to you is this: What makes AMP so special? Why wouldn't viral resistance come into play again and render AMP useless? This question has a specific answer, but I'd like to see some of your opinions as well.

For more information, click here.

You Are What You Eat?

Awww..... can you say, "KSR2"?

It's not uncommon to see an obese individual walking about anymore, what with all the fast food and door-to-door pizza deliveries. Well sometimes it really  isn't that person's fault. In fact, scientists recently discovered the gene (KSR2) that affects appetite and metabolism when mutations occur.  These mutations can cause metabolism to slow, and on top of that increase the desire to eat: A DOUBLE WHAMMY!!! What first led scientists to this conclusion was that when taking the KSR2 gene out of mice completely, obesity occurred. KSR2 was then studied in humans, which showed the gene worked similarly to the mice (Don't worry, I'm sure they DID NOT take the entire gene out, that would just be unethical). KSR2 was continuously observed, with mutations causing defects such as lower heart rate and severe resistance to insulin. Scientists began testing mutation-correcting (NOT gene-altering) drugs until one drug in particular, metformin, solved the problem of low fatty acid oxidation levels. My question to you is this: It seems like every week mutations in genes are being corrected for by seemingly simple methods. Could science REALLY be evolving that fast, or are there some factors being overlooked by the optimistic bloggers writing about these research stories?

For more information, click here for the research article.

Inflammatory Bowel Disease: Road to the Cure

Many of us have heard of Inflammatory Bowel Disease, right? Well, a team of scientists recently discovered a new variety of stem cells in the gut of a mouse embryo, cells not like those previously described in the gut. They knew they were able to grow the cells at just the right conditions for them to form mature intestinal tissue, and with this knowledge they transplanted these cells into adult mice with Inflammatory Bowel Disease. It took just 3 hours for the cells to repair infected areas of the gut. Scientists took human stem cells similar to the mice stem cells and are setting up another experiment to see whether the same method works for humans. Let's stay hopeful. My question to you is this: Do you think treatment could really have been this easy all along? Why hasn't this been done before now?

The Research paper can be found here.