I just like making my post titles really outrageous!
According to Science Daily, light can actually trigger cancer cells to die, known as a death switch. This switch is turned on by exposing a peptide the researches created to "external light pulses [that will] convert it into a cell death signal".
From what I took out of the article, it seems as if they will be able to alter the interactions in B-cell lymphoma cancer cells thus controlling rapid division and slowing the growth process down if not totally stopping the spread.
They propose the idea that through this method of transient photoactivation, they will be able to identify the cells that are "normally resistant to chemotherapy", thus aid in the development of treatments for cancer patients that will be more effective.
My question to you all is, how does this differ from radiation? Isn't radiation killing cancer cells by light in the form of lasers?
The link to the article is below:
Light Triggers Death Switch in Cancer Cells
Wednesday, October 16, 2013
Tuesday, October 8, 2013
Blog 6b: Feces in a Pill...Yummy!
SO! For this blog I found an article that talks about having feces in a pill! Isn't that just appealing?!
Well for those who suffer from Clostridum difficile, " a bacterial infection that causes diarrhea and fever" and responsible for 14,000 US citizen deaths, would much rather take a pill filled with feces rather than the current techniques in killing the bacteria.
As of now, the bacteria is killed with fecal transplants of donor feces by "enemas, colonoscopies, or nasal tubes that run directly to the gut" (OUCH!). The donor feces have healthy microbes that gets rid of C. difficile and promotes growth of good bacteria.
So, TECHNICALLY these patients are not literally digesting a pill with feces, but the microbes extracting for a feces donor are put into the pill. The next step is to stop asking healthy individuals for fecal samples (LOL). Therefore, the idea of make a pill that uses bacteria grown in a laboratory is not far fetched; only issue is how much it would cost to get a laboratory up and running with all the work that goes behind this research.
"As Tom Moore, a physician and infectious-disease specialist in Wichita, Kansas, puts it: 'It'll be difficult to compete with the ready availability and very cheap costs of human poop.' "
What do you all think about this method of delivering healthy microbes to the human gut? Would it just be better to stick with what we have been doing?
Click the link to read more about it
http://www.scientificamerican.com/article.cfm?id=feces-filled-pill-stops-gut-infection
Well for those who suffer from Clostridum difficile, " a bacterial infection that causes diarrhea and fever" and responsible for 14,000 US citizen deaths, would much rather take a pill filled with feces rather than the current techniques in killing the bacteria.
As of now, the bacteria is killed with fecal transplants of donor feces by "enemas, colonoscopies, or nasal tubes that run directly to the gut" (OUCH!). The donor feces have healthy microbes that gets rid of C. difficile and promotes growth of good bacteria.
So, TECHNICALLY these patients are not literally digesting a pill with feces, but the microbes extracting for a feces donor are put into the pill. The next step is to stop asking healthy individuals for fecal samples (LOL). Therefore, the idea of make a pill that uses bacteria grown in a laboratory is not far fetched; only issue is how much it would cost to get a laboratory up and running with all the work that goes behind this research.
"As Tom Moore, a physician and infectious-disease specialist in Wichita, Kansas, puts it: 'It'll be difficult to compete with the ready availability and very cheap costs of human poop.' "
What do you all think about this method of delivering healthy microbes to the human gut? Would it just be better to stick with what we have been doing?
Click the link to read more about it
http://www.scientificamerican.com/article.cfm?id=feces-filled-pill-stops-gut-infection
Blog 6a: Smoking Pregnant Mothers and their Allergenic Children
Smoking while pregnant has always been a strong factor in the way newborn children develop abnormally, but the exact reason or processes behind developmental issues were never clear. This research article attempts to show a connection between microRNA and the child's probability to develop allergies at a young age.
The group of scientist focus on microRNA-223, microRNA-155 and regulatory T cells, because to their best knowledge, these microRNAs are responsible for immune response and the T cells aid in preventing overactive immune systems. If there is damage to the T cells that interrupts its function, this will cause "the self-regulatory function of the immune system [to] be reduced, [thus], possibly resulting in allergies".
Collected blood samples from pregnant women and the birth cord of those children who were just born, were analyzed to estimate concentrations of microRNAs and number of regulatory T cells. When specifically examining microRNA-233, it was said that a high concentration for this microRNA and high value of T cells would prove that children exposed to tobacco smoke are most likely to develop allergies before the age of three. This assumption was made by connecting high values of microRNA-233 to low regulatory T-cell numbers, thus the immune system is not as strong as a healthy child's would be. Also, it was stated that the chance of developing eczema are higher when the child has high microRNA-223 concentrations.
I thought the theory behind this article was very interesting. My only question is, how does having allergies actually explain the reason for developmental issues such as "respiratory diseases, diabetes type II, or asthma"? These were all examples given in the article as things a child are prone to developing because of having a mother who smoke during pregnancy. Maybe I am just missing something, but that link is a little confusing.
What do y'all think?!
Here is the link so you can read it for yourself
http://www.sciencedaily.com/releases/2013/10/131007094324.htm
The group of scientist focus on microRNA-223, microRNA-155 and regulatory T cells, because to their best knowledge, these microRNAs are responsible for immune response and the T cells aid in preventing overactive immune systems. If there is damage to the T cells that interrupts its function, this will cause "the self-regulatory function of the immune system [to] be reduced, [thus], possibly resulting in allergies".
Collected blood samples from pregnant women and the birth cord of those children who were just born, were analyzed to estimate concentrations of microRNAs and number of regulatory T cells. When specifically examining microRNA-233, it was said that a high concentration for this microRNA and high value of T cells would prove that children exposed to tobacco smoke are most likely to develop allergies before the age of three. This assumption was made by connecting high values of microRNA-233 to low regulatory T-cell numbers, thus the immune system is not as strong as a healthy child's would be. Also, it was stated that the chance of developing eczema are higher when the child has high microRNA-223 concentrations.
I thought the theory behind this article was very interesting. My only question is, how does having allergies actually explain the reason for developmental issues such as "respiratory diseases, diabetes type II, or asthma"? These were all examples given in the article as things a child are prone to developing because of having a mother who smoke during pregnancy. Maybe I am just missing something, but that link is a little confusing.
What do y'all think?!
Here is the link so you can read it for yourself
http://www.sciencedaily.com/releases/2013/10/131007094324.htm
Sunday, September 29, 2013
Depression = Diabetes?
In a recent article, it has been stated that those who take anti-depressant pills usually also have type 2 diabetes. According to the article a link between the two seems to be there, but there is not strong proof the actually show that one causes the other.
The authors did raise the issue that it may be, those who take these pills naturally put on weight, thus increasing their changes of diabetes. In addition to this, they also mentioned the possibility that the "drugs themselves could interfere with blood sugar control."
Either way, it is interesting to think that there may be a link between the two. I wonder if the same goes for birth control pills. I've been told many females gain weight when taking these pills. Interesting I'd say!
What do you all think about it? Is it possible that anti-depressants can cause type 2 diabetes?
Link to article:
http://www.bbc.co.uk/news/health-24217982
The authors did raise the issue that it may be, those who take these pills naturally put on weight, thus increasing their changes of diabetes. In addition to this, they also mentioned the possibility that the "drugs themselves could interfere with blood sugar control."
Either way, it is interesting to think that there may be a link between the two. I wonder if the same goes for birth control pills. I've been told many females gain weight when taking these pills. Interesting I'd say!
What do you all think about it? Is it possible that anti-depressants can cause type 2 diabetes?
Link to article:
http://www.bbc.co.uk/news/health-24217982
Friday, September 20, 2013
Stopping the Spread of a Tumor
In recent news, it has been published that there is a molecular pathway that aids in the "ability of malignant glimoa cells in a brain tumor to spread" and damage healthy brain tissues. The malignant gliomas cells are something hard to fight. This is due to their resistance to both chemotherapy and radiation therapy coupled with its' ability to invade surrounding areas of the brain, thus, ultimately leading to death.
One method that is currently in use to shrink tumors, is to cut off provided oxygen (from low-oxygen environments) via blood supply; this is done by taking anti-angiogenesis drugs. Angiogenesis is a process of forming new blood vessels. Stopping angeiogenesis will, in a sense, starve the tumor and not allow it to spread.
The researches at University of Alabama at Birmingham have identified two proteins that link the increased motility of these cells with areas of low-oxygen or hypoxia. One of these proteins are responsible for signaling when hypoxia is activated (Src). The other protein is regulated by Src, neural Wiskott-Aldrich syndrome, or N-WASP for short. When the researches used protein inhibitors to shut off Src and N-WASP, hypoxia "lost its ability to augment cell movement". This means, spreading came to a stop.
In the end, the idea of creating anti-motility drugs are in close reach.
I think the vary idea would be awesome! To be able to stop the spread of tumor, thus possibly saving ones' life if caught early. My only question is, with this research being specific to the malignant gliomas cells, how can this be applied to other tumorous cells?
Just tell me what do y'all think about it, I'm excited to hear y'alls feedback!
Link to article:
Proteins Identified That May Help Brain Tumors Spread
Link to article:
Proteins Identified That May Help Brain Tumors Spread
Tuesday, September 17, 2013
No Use in Dieting Anymore...
In a fairly recent article, it states that dieting may not help to keep the weight off. The reason why you ask? Well, apparently there are nerves in the stomach that tells us when we're full, and a hormone, leptin, to encourage one to stop food intake; when continuous high-fat food consumption takes place, these nerves and hormones are desensitized. This means, those who are considered obese, even after losing weight, are 95% likely that they will gain the weight back within two years. Since this article only discusses obese people, it leaves out people are simply overweight. What does this mean for those persons? Good question.
One question I have is what if it is not desensitized nerves and hormones making people gain their weight back? Yes, this aids in people not being able to tell if they are full or not, but what about the saying "my eyes were bigger than my stomach"? People, who are trying to diet, should not depend on their body to say "I'm full," but notice their proportions and come to the conclusion that, what they are eating is enough to satisfy their hunger, not aim to get full.
But maybe that's just me. What do you all think about it?
Link to Article:
Monday, September 9, 2013
Change Your Diet, Change Your Taste
In the article I found from Science Daily, "Diet Experience Can Alter Taste Preferences" they propose the idea that if fed a long-term diet of a certain food or substance, you'll eventually learn to like something you probably did not before (aversive). The authors of this article based this study on the phenomenon that happens with humans.
They used the fruit fly Drosophila melanogaster as the animal model and focused on camphor, a safe food additive that is considered aversive. Over time the fruit fly showed signs of accepting foods containing camphor; this was identified by degradation of the Transient Receptor Potential-Like protein. Plus and minus some other signs, the authors then reversed the entire experiment by putting the flies on a camphor-free diet. The levels of TRPL still decreased, proving that even when provided with food that was once aversive, the flies continued to chose it as a preference.
In my opinion, forcing defenseless flies to eat something they wouldn't normally eat is a response to their survival mechanism. Wouldn't humans do the same?! If my sole food source was eating something I liked, topped with something I didn't, I too would find the good in it for the sake of survival.
I am not sure if the way the authors went about the method of proving how our diets can change our taste preference was truly accurate, but it is intriguing. What do you all think?
http://www.sciencedaily.com/releases/2013/09/130909093159.htm
They used the fruit fly Drosophila melanogaster as the animal model and focused on camphor, a safe food additive that is considered aversive. Over time the fruit fly showed signs of accepting foods containing camphor; this was identified by degradation of the Transient Receptor Potential-Like protein. Plus and minus some other signs, the authors then reversed the entire experiment by putting the flies on a camphor-free diet. The levels of TRPL still decreased, proving that even when provided with food that was once aversive, the flies continued to chose it as a preference.
In my opinion, forcing defenseless flies to eat something they wouldn't normally eat is a response to their survival mechanism. Wouldn't humans do the same?! If my sole food source was eating something I liked, topped with something I didn't, I too would find the good in it for the sake of survival.
I am not sure if the way the authors went about the method of proving how our diets can change our taste preference was truly accurate, but it is intriguing. What do you all think?
http://www.sciencedaily.com/releases/2013/09/130909093159.htm
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