Chapter 21 Helpful Hints!

Alright pretty people, my last blog. So many memories! Well, enjoy!

Ok, so I liked this video because it related genomics and proteomics to cancer, and we know cancer pretty well from previous chapters. He used proper terminology and explained genomics and proteomics in a nice simple way. Some of the terms he used were new to me, but after looking them up I found that they were just diseases. He clearly distinguished between proteomics and genomics. Lastly, he predicted how much information we could learn from genomics and proteomics in the future which was astonishing to me! This is a nice quick video to watch to learn a few facts about genomics and proteomics.

So, this video talked about transposons. It had very dramatic music in the background which was interesting. Anyway, yeah the video talked about transposons and the different types of transposons we have. He also talked about DNA fingerprinting and how people in families would have more similar transposons, than two random people. From there, he explained how two different species who are closely related have more similar transposons than less related species. He also talked about Alu, and how scientists have used it for all kinds of research. This is another short video to watch and pick up some quick easy facts. Enjoy!

Gene Families and Male Infertility?

I know, I know reading my title peeked your interest. You are wondering how could gene families and male infertility possibly be related? Luckily for you, I shall explain how the two are related. You're welcome.

So as this article explains, researchers from the University of California at San Francisco have found the head of the family of genes that have been linked to some male infertility cases. The gene which was name BOULE was found in mice, fleas, and humans. BOULE has been found to be involved in creating sperm during meiosis. As I previously said, BOULE was found to be the head of the gene family. Two descendants of BOULE that scientists have already discovered are DAZ and DAZL. Both DAZ and DAZL have been linked to male infertility.

In fact, 13% of male infertility cases are because of mutations in DAZ, yet strangely, the gene does not does not appear to be essential for sperm development. The exact role of DAZL is not yet known in humans, but in frogs it is fundamental in the development of both male and female germ cells. New studies show that BOULE may actually be required for mature sperm development. If defects in BOULE are proven to be what caused the male infertility, then gene therapy might be attempted to try and solve the male infertility problem.

People's Plasma Proteome

There I go with my clever alliterations for titles once again... I know you are super impressed so I shall give you a second to contain yourself... Ready? Off we go!

So plasma is on of the main components of blood. Some people even sell theirs for money! As this article explains, the human plasma proteome has the potential to revolutionize disease diagnosis and therapeutic monitoring. Not only is plasma a great specimen, but it also has the largest and deepest version of the human proteome. Plasma obviously contains plasma proteins, but it also contains proteins from all other tissues, many distinct immunoglobin sequences, and extraordinary range of proteins.

At the moment, only 289 proteins have been reported in plasma, but there are so many more to be found! Right now, the only thing limiting scientists in getting all of these proteins is technology. Currently, we do not have the needed technological insight to get all of the proteins. Fortunately, recent advances in survey techniques will yield at least double the amount proteins we can find. Many of the proteins that we can and will find are indicative of human disease, so these proteins will definitely help us in understanding and combating many diseases. Even with all of these discoveries, only a few proteins are used in routine clinical diagnosis, and the rate the FDA allows these protein tests has declined over the past few years. Despite all of this, hopefully we can find and understand new proteins so we can fight off and combat disease.

Chapter 20 Helpful Hints!

This is a nice virtual lecture on gene cloning.  He explains all of the steps in gene cloning and also talks about organism cloning. After lecturing with just notes on the board, he brings out several diagrams to help pull all of the ideas together. The lecturer also cracks a joke every now and again, which is always nice! He uses all of the proper terminology and asks/presents those sorts of application problems that we all know Dr. Weber loves putting on exams. The video is a nice, quick watch.

Ok so the speaker speaks kind of slowly but alas, what can one do? So despite the speaker's slow voice, he gives quality information. Now when I say the video breaks down genomics, I mean it really breaks down genomics. It gives  information like DNA stores information and basics like that. However, it builds on these basics so that one understands genomics just like one understands what a gene is. This video is one of the ones that really help you understand core concepts, so that all other aspects can be understood better. Enjoy!

Crazy Canola!!

Again, with my clever alliterations. People ask me all the time how I come up with them and I just don't even know... Anyhoo, now that you have collected yourself from the excitement of my title, we shall begin!

So genetically modified organisms (GMOs) are organisms that have changes in their DNA due to genetic engineering technologies. So when one thinks of these organisms, a laboratory environment probably comes to mind. However, as this article explains, GMOs are popping up in some unexpected places. In Langdon, North Dakota a couple ecologists saw a yellow canola plant growing near a parking lot. They picked some of the plants and after conducting some tests discovered that the canola was genetically modified!

Surprisingly, this isn't a rare find. North Dakota grows loads of the canola both conventional and genetically modified. It is a weed and its seeds are used to make canola oil. The canola's scientific name is Brassica napus var oleifera. What may shock you even more is the fact that  almost everywhere the ecologists and their colleagues went, they found more of the GM canola! They even found the transgenic canola in fields in the middle of nowhere.
So what does this mean to you and me? This means that transgenic plants are probably cross-breeding in the wild and swapping introduced genes. Depending on your views on GM foods, this could very easily frighten/worry you, or not affect you at all. Now GM canola has been found everywhere from Canada to Japan. However, this is the first time the plants have been found to evolve in this way. Ecologist Cindy Sagers of the University of Arkansas, explained that there are new combinations of transgenic traits and the best explanation for this would be that the traits are stable outside of cultivation and that they are evolving.
Most of the transgenic plant populations die out quickly without continual replenishment, but the canola plant is not having this problem. It is able to hybridize with at least 2, and possibly 8, different wild weed species in North America.
As of now, there is no evidence to say whether herbicide resistance genes will either increase or decrease in fitness. Weed scientist Carol Mallory-Smith of Oregon State University, explained that the biggest concern is whether or not these traits will increase invasiveness or weediness and traits such as drought tolerance, salt tolerance, heat or cold tolerance. This canola plant is not the first escaped transgenic population, and due to advancements in technology, it probably won't be the last

Gotcha GMOs!

Wow. You are just awestricken by my title. Short, sweet, terse (you like that SAT vocab, I know), to the point, yet attention grabbing. I'll give you a few moments to collect your thoughts. You ready? Off we go!

So as you know since we did a major lab on them, GMOs are genetically modified organisms. That be as it may, a genetically modified organism, is an organism whose genetic material has been changed, altered, or modified using genetic engineering techniques. This article talks about how people are new trends in detecting genetically modified organisms.
Food is necessary for life, so everyone eats. (Wow, what a groundbreaking statement.) Anyway, since everyone eats, one cannot go mess around with food and sell it to people. This could lead to many people dying. Hence, just like with other aspects of food, genetically modifying food has to be authorized and regulated.

 

Now as time goes on, the production of genetically modified organisms has been increasing. There are so many new technologies that allow for the development of GMOs, but at the same token, advancing technology is also accounting for the many news ways of detecting GMO. Most of the methods involving GMO involve Polymerase Chain Reaction (PCR). After reading that little tidbit I felt all scientific and connected because we know what that is and we have done this! Anyhoo, as I was saying, PCR is the preferred method in detecting GMO because it can detect even minute amounts of the transgene material in the foods we eat.

It was also interesting to learn about the other methods used to detect GMO, as we already know about PCR. One method is based on quartz crystal microbalance piezoelectric biosensors, dry reagent dipstick-type sensors and surface plasmon resonance sensors. That was a mouthful... Another method involves using visible/near-infrared (vis/NIR) spectroscopy or mass spectrometry combined with chemometrics techniques. Yet again, another mouthful. So yes, to combat the increasing amount of unauthorized GMO products being produced, authorities are exploring various methods to detect the GMO products.

Chapter 18 Helpful Hints!

I love Khan Academy! So this is a nice lecture on viruses! In true Khan Academy style, he breaks down everything there is to know about viruses. The video goes into the main different types of viruses, and the steps the virus takes from entry to release. There were also many situational example presented in the video, which I always like because many questions on the exam are situational. Always a nice lecture to watch or just even listen to when you have like 20 minutes.

Ok, well I know this video doesn't exactly use proper terminology, but I really liked it! I actually found this video for fun on my own time... Yeah I need to find things to do with my time. So I found this video and really liked it! This video was made for the masses so they had to I guess put many of the terms in layman's terms... For example, they referred to ribosomes as "peanuty" things. I took the improper use of terminology almost like a challenge to see that I knew all of the proper names! So, i really liked the video because the speaking was so simple but also gave such amazing visuals! Enjoy!

Viruses WERE Odd Little Things...

Awww did my title make you feel all warm and gooey inside but also made you want to read more? I know, I know. It's ok, it's ok. I understand! You ready? Off we go with some blogging!

Ok so once again viruses  have come to mind-blow us all. As we know, there is a huge debate on whether or not viruses are alive because they only contain the necessary components to reproduce, and can only do cell by invading another cell. Now viruses are generally tiny little guys, that will multiply and mess some stuff up. Please note how I said they are little things. Most viruses are much smaller than their host cells and almost fully rely on processes in the host cell to reproduce. Along came these viruses, as explained by this article, and they just kind of threw all of this previous knowledge to the wind! These things are huge! They also come chock full of lots of DNA which encodes for a bunch of proteins. One great example would be Cafeteria roenbergensis. Oh my gosh perfect time to make a joke about it being cafeteria and eating a lot so that's why it's big... But I won't. Oooh! Even better I can reference Urma!! Yeah I like that better!

Look at that an artist's rendition! I'll even give you an actual picture! Lucky you!!

Those lovely pictures were pictures of Cafeteria roenbergensis. Scientists nicknamed them CroV. Based on their size I think it's obvious what I would nickname them... So CroV is the marine largest virus known to man at the moment! It is even bigger than some bacteria! CroV has a genome of 730,000 base pairs, about 544 predicted genes, and about 22 of these genes codes for tRNA's. CroV also does something special because it takes care of its DNA just like our cells do. Many smaller viruses do not take care of their DNA in the least bit, and often exploit the mutations which occur. CroV takes care of its DNA, just like we do! Its genome encodes for DNA repair enzymes, which actively repair the virus's DNA. Scientists believe that the large size is an advantage because amoebae eat the virus and then it gets to work!
CroV falls into a class of viruses called "mimiviruses" or "giant-viruses". French scientists gave the name mimivirus because they thought the viruses were mimicking microbes. As time has gone on, scientists are finding more and more of these mimviruses all around the world, and the ocean is filled with them!

Persistent Pesky Plasmids....

You are just luh-ving the alliteration. I know, I know. I'll give you some time to simmer down.... You ready? Off we go!

Ok so this article talks about plasmids! It's kind of funny how we always learn about stuff on the BioLeague tests after the tests. I remember staring at the test and being like, "What on Earth is a plasmid..." Woe is me... But I digress! So back to the article... Yeah it talks about plasmids!

So there was a study which done to help more clearly identify the link between farm-generated animal waste and the dissemination of antibiotic resistance in microbial soil communities, by mobile genetic elements. The study used electromagnetic induction (EMI) surveying of a soil sampling that was broiler chicken farm assisted from a chicken-waste-impacted site and a not-so affected site. The EMI showed that there were differences between the two samples in pH and tetracycline resistance (Tc(R)) level in the culturable soil bacteria. Also,  several tet and erm genes were sparsely or highly present in the soil.

 Alright so here comes the interesting part. I know you're thinking, "And where are the plasmids..." So, in all of the aspects I mentioned above there really wasn't a huge difference in the marginally affected site and sites in the pristine regional forest sites. However, when the farm was operating, tet(L), tet(M), tet(O), erm(A), erm(B), and erm(C) genes were detected in the soil affected by waste. Two years after all waste was removed from the farm, tet(L), tet(M), tet(O), and erm(C) genes were still detected. Woah! If we removed them, how on earth could they still be there? Those sneaky little plasmids is how they are still there!
Being as though scientists are just constantly asking more questions, they delve even deeper and found out more information. Species of Bhargavaea, Sporosarcina, and Bacillus were the plasmid's hosts. The plasmid's mobilization (mob) gene was quantified to so they could estimte how much of it was in the soil. The ratio of tet(L) to mob changed from 34:1 at the beginning of the two years to 1:1 at the end of the two years.

Chapter 16 Helpful Hints!

Once again, Khan Academy is here to make life easier! This is a nice lecture introducing you to heredity, which is basically what we learned this chapter. It starts at the beginning with the basics, like physical traits, and goes into homozygous and heterozygous as the video goes in. The video goes into dominant and recessive traits, and also touches on the different types of dominance there are, i.e. codominance. The video uses proper terminology like allele, homozygous, heterozygous, dominant, recessive, etc. The video also goes into Punnett Squares.

Ok so here's another nice video! Basically, the guy has a pedigree and is trying to figure out what type of disease is present in the family. He takes you step by step in eliminating choices and deducing what kind of disease is present in the family. Instead of looking at the pedigree as one big thing to figure out the disease, he goes step by step through the generations, which is different from what many people do. Being as though DWebs has asked questions using pedigrees, it would make sense for us to see this on the exam, so this would be a great help! Wait, you're probably gonna read this after the exam... Oh well...

Good Golly Guys Got the Gene!

I just love alliterations... Don't you? I know my amazing title just blew your mind so I'll give you some time to settle down... You alright now? Let's go!

Alright so you may be wondering exactly what gene is this girl talking about. Well, get ready for this...  As this article explains, scientists have finally identified the gene the Gregor Mendel used to manipulate in his pea plants experiments! As you should recall, these are the experiments that Mendel used to establish the basic laws of genetics!

Scientists have specifically pinpointed the gene he used to control the pea plants color. This gene is common to many plant species, and the plants use it to break down a green pigment molecule. This is now the third of seven genes Mendel manipulated that researches have identified! Before, researchers were never able to identify the gene for seed color because the pea genome was so huge. Luckily, plant geneticist Ian Armstead of the Institute of Grassland and Environmental Research in Aberystwyth, Wales, and the lead author of a report on the findings was able to stumble upon the gene.
Armstead and his colleagues were working to locate the sequence of a gene called staygreen (sgr) in the meadow grass Festuca pratensis. Some variants of this gene cause the plant to remain green even in unfavorable conditions like drought, because they cannot break down a green pigment. Festuca is genetically similar to rice, which has already had its genome sequenced. Armstead and his group compared genetic markers on the sgr region of the grass's chromosome to the respective region in the rice genome. They found 30 potential genes, including one similar to other pigment-metabolizing proteins. They then tested and confirmed that this was the equivalent to the sgr gene. To then find out if the equivalent sgr pea gene was one of the genes Mendel manipulated in his experiments, the researchers picked out the location of its sequence from pea plants that had different seed colors. Lo and behold, it was found on the same part of the chromosome as the gene that Mendel used!

Japanese Flounder Sex Determination

Perhaps you'll get a clever title next time...

SO in humans, the sex of an individual basically is determined by whether or not they have XX or XY. Females are XX and males XY. This is not the case in all animals, as we saw in this chapter. As this article explains, Japanese Flounder also use the XX/XY system to determine the sex of their species. However, unlike humans the fish can be induced to become phenotypic males or females. This is done by gender rearing them in either 18 or 27 degrees Celsius.

 

Because of this, Japanese flounder are great to use to study the molecular mechanisms that cause temperature-dependent sex determination. Researchers previously showed that cortisol causes female-to-male sex reversal by directly suppressing mRNA expression of ovary-type aromatase (cyp19a1).  cyp19a1 is a steroidogenic enzyme that converts androgens to estrogens in the gonads.

 An inhibitor of cortisol prevented XX flounder from becoming masculine at 27 degrees. This suggests that masculinization by high temperature is because of the suppression of cyp19a1 mRNA expression caused by elevated cortisol levels during differentiation in the gonads. In this current study, researchers found that exposure to high temperatures during gonadal sex differentiation upregulates mRNA expression of retinoid-degrading enzyme (cyp26b1). This happens concurrently with the masculinization of XX gonads and also delays meiotic initiation of germ cells. Cortisol induces cyp26b1 mRNA expression thereby suppressing specific meiotic marker synaptonemal complex protein 3 (sycp3) mRNA expressions in gonads during the sexual differentiation.
This suggests that exposure to high temperature causes cyp26b1 mRNA expression and delays meiotic initiation of germ cells. It does do by elevating cortisol levels during gonadal sex differentiation in Japanese flounder.

Chapter 15 Helpful Hints!

Once again Khan Academy comes to the rescue. Even though we've been learning about meiosis for years now, I am always confused when it comes to diploid and haploid and that "n" thingy. So this video was super helpful because it help explain in nice terms as Khan Academy tend s to do.  The video is a nice lecture that one could watch before an exam for a nice refresher. Of course it uses all of the terms we know and explains meiosis 1 and meiosis 2. It also compares and contrasts meiosis to mitosis every now and again, which I think is very helpful because I have a feeling there's going to be a question or two about comparing and contrasting the two processes on an exam.

This is a nice quick video on the cell cycle. Although it is brief, it has a decent amount of details and information packed into it. For example, structures like centromeres and kinetochores are identified and labeled when they are in action during the cell cycle. The video also explains the G1, S, and G2 phases during interphase which many people and many videos tend to forget is part of the cell cycle.

Silly Cilia!

Awww you're taken aback by my super cute title?? How sweet, how sweet. Give yourself some time to calm down. You ready? Off we go!

As I am hoping you already know, mitosis is the process of cell division that produces two identical daughter cells. So this article talks about the role of cilia proteins during mitosis. Researchers at the University of Massachusetts Medical School have discovered a role for the cilia proteins IFT88, that was previously unknown. Oh hey look, since most of us are aiming to go to medical school, if you go there you can tell them you already know things about them! Lucky you. You're welcome. Anyway, so yes, they discovered a previous unknown role for IFT88. This newly discovered roles suggests that this could be a possible alternative or contributory cause for cilia-related diseases like primary ciliary dyskinesia, and polycystic kidney disease. Here's a nice picture of some actual cilia.

IFT88 is part of a family of transport proteins and cellular machinery that is in charge of moving materials from the cell body to the cilia. It is a slender protrusion responsible for motility and sensory input known for its ability to build cilia. If IFT88 is not present, cilia are either not able to form or defective. Scientists have linked cilia dysfunction to a number of  ciliopathies. IFT88 absence has been linked to polycistic kidney disease (PKD), which is characterized by the presence of multiple cysts in the kidneys. PKD is also believed to be caused by cilia dysfunction in kidney cells.
Stephen J. Doxsey, PhD, professor of molecular medicine and biochemistry & molecular pharmacology and cell biology and lead author of the study, and his colleagues observed that the IFT88 protein is present at the poles of the mitotic spindle. They knew 1FT88 and other proteins were present at the spindle poles, but their functions were unknown. Benedicte Delaval, PhD, found that IFT88 plays a part in transporting materials required for building the spindle poles during cell division. Ergo, the loss of IFT88 protein during mitosis causes there to be a delay in mitotic division and misalignment of the direction and plane of cell division. This of course is not good.
Both cilia and spindle fibers arise from centrosomes, leading Doxsey to hypothesize that there is a deeper, underlying connection between the two. Until more research and test and studies are conducted... the world may never know...

Super Amazingly Cool Spindle Assembly Checkpoint (SAC SAC!!)

Hey pretty person! If you are a boy then... take that as you will. I know you're in awe from my fetch title I'll give you a second to calm down. Are you good? Ok, let us begin!

So this article talks about the Spindle Assembly Checkpoint (SAC) and its importance in the cell. So as I'm sure you know meiosis is the process used by germ cells to produce gametes. If you didn't know that then... woe is you. Anyhoo, meiosis consists of meiosis 1 and meiosis 2. Meiosis 1 separates homologous chromosomes and meiosis 2 separates sister chromatids. Here's a picture, as they always make things better.

Now to separate or pull the chromosomes into daughter cells, the cell produces spindle fibers. If the spindle fibers connect to the centromeres of the chromosomes they are called kinetochore spindle fibers, and they are called non-kinetochore spindle fibers if they do not connect to the spindle fibers. If chromosomes are not separated properly, it leads to daughter cells being anupleoid, which will lead to the cell being killed once fertilization has occurred or birth defects in the offspring. Here's a picture showing spindle fibers although I'm hoping you already know what they look like...

In mitosis, SAC exists to ensure that proper chromosome segregation has occurred. In the last decade, most notably in the past several years, researchers have found a checkpoint similar to SAC in meiosis! There is evidence that points to the existence of SAC functions in meiosis. This evidence is provided by studies on many components of SAC. This includes but is not limited to SAC proteins mitotic-arrest deficient-1 (Mad1), Mad2, budding uninhibited by benzimidazole-1 (Bub1), Bub3, BubR1 and Mps1. I was going to be lazy and not list all of them but alas, I shall list them all as it's probably the right thing to do. More componenets include microtubule-kinetochore attachment regulators Ndc80 complex, chromosomal passenger complex, mitotic centromere-associated kinesin (MCAK), kinetochore null 1 (KNL1) and Mis12 complex and spindle stability regulators. So in conclusion, SAC does exist in meiosis but in order to fully understand it and all of its components, more research needs to be done.

Chapter 14 Helpful Hints!

Okey dokey here we go!

This video was great! It explains point mutations, insertions, and deletions in a clear and informative manner. It also seems like it would help before a Dr. Weber exam because it explains the effects of mutations on organisms as well, and we all know how DWebs likes to ask questions like that.. The video explains the difference between mutations that occur during mitosis along with meiosis.  I also really liked this video because along with explaining the mutations, it showed videos of how the mutations occur and also how the body tries to fix the mutations. Enjoy!

Ok so this is a pretty cool video. Rather than explaining the cell cycle which we have honestly studied to death and then some... this video focuses on and explains the Cell Cycle Checkpoints. For example, in class we learned about cyclin and CDK, but the video goes into more detail about how those molecules work. It also talks about p53 and it's functions like stimulating the production of proteins that bind and inactivate CDK molecules, activating enzymes required to repair DNA, and apoptosis. Again, I like this video because it goes into what happens when some of these molecules lose their functions because we all know how a certain Bio teacher enjoys putting questions like these on the exams... Well, enjoy!

Mutation Makes Mirror Movements

Alright heroes/cool kids, this article talks about a specific mutation and the effect it has on the body. There is a mutation that messes with your immune system causing you to always do mirror movements. Meaning if you raise your right hand, the left one is going up with it. In more formal terms, one side of the body always involuntarily mirrors movements done voluntarily on the other side of the body.
Now you may be thinking that this must be such an annoying disease to live with but people like Andree Marion live with it every hour of every day. Marion is a 47-year-old accountant from St. Sauveur, Quebec and it turns out her 19-year-old son also has mirror movements. In fact if you trace Marion's family back four generations, of her 23 blood relatives, about half of them have mirror movements. These rare mirror movements are caused by a gene defect.

A neurologist and geneticist at the University of Montreal named Guy Roleau was the senior author of a study that uncovered the mutation found in Marion and her relatives. The wires of the nervous system cross. Axons from motor neurons in the brain sweep over the middle of the body before connecting to other motor neurons in the spinal cord. These motor neurons then connect to the muscles. Roleau comments on how scientists still don't know why or how this happens in humans.

Mirror movements are quite rare and are normally found only in people with disorders of nervous system crossings. No one in Marion's family had any such disorder so Roleau and colleagues were given a great opportunity to see just how wiring went wrong. What they found was the in Marion and relatives, the right side of the brain controlled the right hand... but also the left hand. Some axons crossed over, but some did not. The axons that didn't cross over would just go on the exact same spinal motor neuron, just on the opposite side of the spinal cord.
Since Marion and many relatives had mirror movements, Roleau and his team knew it was hereditary. While it took them one and half year to collect the DNA from all of the relatives it only took them 3 months to find the faulty gene. the faulty gene was deleted in colorectal cancer (DCC). This mutation interferes with DCC's interaction with netrin, which is a diffusible extracellular protein that helps guide axons across the body's midline while the body is developing. DCC is expressed in the midline of the nervous system. Once axons sense the protein they begin to move towards it. However, this mutation cuts the level of functionality of the protein in Marion and relatives. In essence, they don't have enough of the protein to get all of the nerves to cross over.
Marion explained that she always noticed the mirror movements since she was a child, but they were never a big concern because she was able to do what she wanted. Marion can type and drive without any difficulty. She joked the only thing she has a problem with is playing pool. What a jokester Ms. Marion is... She also said she has to be careful when cutting and cooking food. Marion also noted that her mirror movements are more pronounced than her sons. For her son, the mirror movements are more in his hands, while hers are also in the biceps and toes.

Anthracycline and Cancer

So this article talks about anthracyclines and the role they play in treating many childhood cancers. Anthracyclines are a class of drugs used in cancer chemotherapy derived from Streptomyces bacteria. Although anthracyclinescan help to get rid of the cancer, they are quite harmful to the heart. The effects on the heart can be seen while treatment is going on or even many years after treatment has ended. Before deciding to use anthracyclinesone, one should be familiar with its antitumor effects and cardiotoxic effects.

 

To see what would be better, scientists conducted a series of tests in order to be able to compare antitumour efficacy of treatment including or not including anthracyclines in children with several different childhood cancers. Researchers discovered that at the moment evidence is not strong enough to say that anthracyclines have an increased antitumour effect in acute lymphoblastic leukaemia (ALL) as compared to treatment without anthracyclines. However, there's some suggestion saying that anthracyclins do have an increased antitumor effect. In order to make a definite conclusion on anthracyclin effect on ALL, more research and tests need to be done. Researchers only found limited data on Wilms' tumour, habdomyosarcoma/undifferentiated sarcoma, Ewing's sarcoma, non‐Hodgkin lymphoma, and heptoblastoma, so they could not draw any conclusions. This is a relatively new concept, so at the moment there is no data for other childhood cancers. Although a general link between anthracyclins and childhood cancers has been shown, more high quality research needs to be done before definite conclusions can be drawn.

Helpful Hints!!

This video is so helpful! It's a nice lecture about gene regulation. To understand the much more complex Eukaryotic gene regulation, he starts out explaining Prokaryotic gene regulation. He includes lots of pictures and diagrams that follow along with what he's saying. He manages to speak in a very easy to understand way, while still using all of the names and terms we've learned.

I really liked this video! It explains what microRNAs do and how they impact the cell. The video also talks about what could happen if microRNAs do not work. As many of us intend to go into medicine, I also liked the video because it explained how microRNAs are now being looked at to figure out more medicines and diseases. The display is simple and engaging. It reminded me a bit of part of the lecture we watched on telomeres!

You Are What You Eat!

This article talks about how microRNA from rice and other vegetables were found in the blood of 21 volunteers. Chen-Yu Zhang of Nanjing University in China conducted a study about plant-animal microRNA transfers. Blood was collected from 21 volunteers, and their bloodstreams contained about 30 different microRNAs from commonly eaten plants. MicroRNAs are short sequences of nucleotides and although they do not code for proteins, they prevent specific genes from producing the proteins the encode for.

 Although the microRNAs do not code for proteins, they can apparently cell function. A specific rice microRNA was shown to bind to and inhibit the activity of receptors controlling the removal of LDL ("bad" cholesterol) from the bloodstream. MicroRNAs are now being compared to vitamins and minerals as perhaps another functional molecule obtained from food. Zhang comments that these findings may also illuminate our understanding of co-evolution. Co-evolution is the process by which genetic changes in one species trigger genetic changes in another species. For example, human ability to digest lactose in milk after infancy arose only after we began to domesticate cattle. This suggests that perhaps the plants we cultivate and eat have altered us in some way.

And It Begins Again...

Break's over and our blogs begin once again!

So this article talked about transcriptional  regulation of gene expression during osmotic stress. Now even though stress can suppress growth and proliferation, cells can induce adaptive responses allowing them to maintain growth and proliferation functions under stress. There have been numerous studies on the inhibitory effects of stress on cells, but not much is known about how growth-promoting pathways influence stress response. To find out more information, researchers decided to analyze the effect of mammalian target of rapamycin (mTOR), a central growth controller, on the osmotic stress response.

 This picture demonstrates mTOR's role in the process of 

the cell sustaining cell size and proliferative capacity.

Researchers found that mammalian cells that were exposed to moderate hypertonicity maintained active mTOR. mTOR was required to sustain their cell size and proliferative capacity. mTOR regulated the induction of diverse osmostress response genes. These genes included targets of the tonicity-responsive transcription factor NFAT5 and NFAT5-independent genes. Genes that were sensitive to mTOR-included regulators of stress responses, growth and proliferation. Among these genes, researchers identified REDD1 and REDD2, which had been previously characterized as mTOR inhibitors in other stress contexts. mTOR facilitated transcription-permissive conditions for several osmoresponsive genes by enhancing histone H4 acetylation and RNA polymerase II being present at the scene.