Happy birthday Madonna!Happy Madonna Day!
16 August 2010
Today is Madonna's birthday! It is a celebration that should happen around the world. Her music has taught me to be strong, passionate, playful, driven, myself, non-judgmental, proud of myself, not to be afraid of others judgments, and many other great and amazing things. Here's to the Queen of Pop! And no, I'm not referring to Lady Gaga. I'm referring to the one who did it all before her and who still reigns supreme!
Happy birthday Madonna!
Happy birthday Madonna!
Proposition 8
15 August 2010
Before I say anything serious about the subject, I wanted to say that it is hilarious how when the ruling was made that everybody in the west was freaking out, but nobody in the east cared. It seems like more than land distances the east from the west... Anyways, now back to what I wanted to say.
I don't believe I have ever said this on my blog before, but I supported the No on Prop. 8 campaign. The reasons for this are many, but I will name a few and possibly elaborate on them. First, I believe that God brought us here to make choices and determine what is the path of life we want to take. Isn't that what Jesus fought for in the pre-existence? Satan supported control and making everybody follow God's will to get back to heaven or Satan supported letting man do whatever he wanted with no consequences, thus gaining salvation no matter what (whichever you believe... I've heard both and I am more partial to the second). However, Christ fought for the ability to choose, and that is what God wanted. He gives us commandments to follow through prophets and personal revelation, BUT it is our choice whether we follow these or disregard them. That being said, it means that everybody should have the choice to do what they please and not have anyone else impose their beliefs on them. I'll give one caveat, I believe this in full unless it harms another person e.g. murder, stealing, rape, etc. I do not see same-sex marriages falling into this category. How are they harming other people? I see no harmful causes and if someone does have a harmful cause, please enlighten me and prove it with scientific evidence.
Second our country was built upon freedom, specifically many of the people who came to America were looking for religious freedom AKA freedom of beliefs. People wanted to believe what they wanted without persecution. That is the main reason they left Europe. Our Founding Fathers then said that all men (and women) are created equal and have certain unalienable rights, those of life, liberty, and the pursuit of happiness. If people are not allowed to enter into same-sex marriages (I consider marriage to be part of the unalienable right of the pursuit of happiness), they are not equal. However, our Founding Fathers stated that all men (and women) are CREATED EQUAL and have rights. This would make LGBT community second class citizens. Does this sound familiar? African-Americans were considered second class citizens for thousands of years. They did not obtain their full rights until 1968. Even though we have come a long way, some people still consider African Americans as second class citizens (then LGBT folks are lower to some... I guess that makes us third class citizens or pond scum). If we are all created equal, have certain unalienable rights, and are free, shouldn't we all have the EXACT same rights? I believe so.
Third, different morals does not mean the whole world is going to fall apart and end. People have had varying morals since the beginning of time. This goes back to the choice argument. We have the right to choose what to do and what is best for us. Just because you have different morals than someone else does not make you inherently better than them. They might be one of the most anthropic person in the world, but they might smoke and drink. Does that make you better than them? No. Also, the whole moral argument does not sit well with me. Why isn't there a bigger push to outlaw smoking, drinking alcohol and tea, having sex outside of marriage, having children out of wedlock, eating too much, etc.? All of those are considered morally wrong, but the prophet and the Church are not spending a lot of money fighting all of those evils. It doesn't entirely make sense to me. Where is the logical behind creating a law against one moral, but not another?
Finally, my opinion is completely summed up in this simple sentence written by a close friend. "It is ridiculous for someone to think their personal view of morality trumps someone else's freedom of choice and equality."
I have more I want to write, but I need to do other things. This is to be continued...
I don't believe I have ever said this on my blog before, but I supported the No on Prop. 8 campaign. The reasons for this are many, but I will name a few and possibly elaborate on them. First, I believe that God brought us here to make choices and determine what is the path of life we want to take. Isn't that what Jesus fought for in the pre-existence? Satan supported control and making everybody follow God's will to get back to heaven or Satan supported letting man do whatever he wanted with no consequences, thus gaining salvation no matter what (whichever you believe... I've heard both and I am more partial to the second). However, Christ fought for the ability to choose, and that is what God wanted. He gives us commandments to follow through prophets and personal revelation, BUT it is our choice whether we follow these or disregard them. That being said, it means that everybody should have the choice to do what they please and not have anyone else impose their beliefs on them. I'll give one caveat, I believe this in full unless it harms another person e.g. murder, stealing, rape, etc. I do not see same-sex marriages falling into this category. How are they harming other people? I see no harmful causes and if someone does have a harmful cause, please enlighten me and prove it with scientific evidence.
Second our country was built upon freedom, specifically many of the people who came to America were looking for religious freedom AKA freedom of beliefs. People wanted to believe what they wanted without persecution. That is the main reason they left Europe. Our Founding Fathers then said that all men (and women) are created equal and have certain unalienable rights, those of life, liberty, and the pursuit of happiness. If people are not allowed to enter into same-sex marriages (I consider marriage to be part of the unalienable right of the pursuit of happiness), they are not equal. However, our Founding Fathers stated that all men (and women) are CREATED EQUAL and have rights. This would make LGBT community second class citizens. Does this sound familiar? African-Americans were considered second class citizens for thousands of years. They did not obtain their full rights until 1968. Even though we have come a long way, some people still consider African Americans as second class citizens (then LGBT folks are lower to some... I guess that makes us third class citizens or pond scum). If we are all created equal, have certain unalienable rights, and are free, shouldn't we all have the EXACT same rights? I believe so.
Third, different morals does not mean the whole world is going to fall apart and end. People have had varying morals since the beginning of time. This goes back to the choice argument. We have the right to choose what to do and what is best for us. Just because you have different morals than someone else does not make you inherently better than them. They might be one of the most anthropic person in the world, but they might smoke and drink. Does that make you better than them? No. Also, the whole moral argument does not sit well with me. Why isn't there a bigger push to outlaw smoking, drinking alcohol and tea, having sex outside of marriage, having children out of wedlock, eating too much, etc.? All of those are considered morally wrong, but the prophet and the Church are not spending a lot of money fighting all of those evils. It doesn't entirely make sense to me. Where is the logical behind creating a law against one moral, but not another?
Finally, my opinion is completely summed up in this simple sentence written by a close friend. "It is ridiculous for someone to think their personal view of morality trumps someone else's freedom of choice and equality."
I have more I want to write, but I need to do other things. This is to be continued...
Prop. 8 In Brief
07 August 2010
I have some thoughts about the latest Prop. 8 news. I don't have the time to blog about it at the moment, but I will say that this hay-day, or gay-day if you will, probably won't last. You may see me as pessimistic, but I'm just being honest. If all of you think you are equal now just because of California, the truth is that we are not. That is all until I actually write the blog.
Recipes?
03 July 2010
Anyone have some fast recipes for dinner that they care to share with me? I realize that when I moved out here that I mainly know how to cook things that take too long to cook AKA over 30 minutes. If anyone cares to share their fast recipes, I'd greatly appreciate it!
PS I'll get to some hardcore blogging when I have more time. I'm still trying to get settled down here.
PS I'll get to some hardcore blogging when I have more time. I'm still trying to get settled down here.
Stubbornness pt. 1
16 June 2010
I am one of the most stubborn people you will meet. I am the most stubborn person in my family. I want to hear your thoughts on stubbornness. Is it good? Is it bad? Is it both? When is it good? When is it bad? Can stubbornness be changed?
I'd appreciate any thoughts you all have. After I read through yours, I'll post mine.
Thanks,
Sean
I'd appreciate any thoughts you all have. After I read through yours, I'll post mine.
Thanks,
Sean
This is What I Hope For...
15 June 2010
This is Dan Humphrey from Gossip Girl. I hope to find a friend like him while I'm working at the NIH.
Research Experience Statement
14 June 2010
This is the research that I have been doing for the past 2 years. Read it if you are interested or just skip it.
For nearly two years, I worked in Dr. Gregory Burton’s laboratory at Brigham Young University. His studies focus on understanding the molecular interactions between follicular dendritic cells (FDCs) and HIV. Specifically, we examined the contributions of two FDC receptors, CD32 (FcγR) and CD21 (CR2), that played significant roles in the trapping and long-term maintenance of HIV.
My first project was molecular cloning of HIV. We received samples of lymph nodes from HIV infected patients. I isolated the HIV virons and the RNA, and performed reverse transcription. After making cDNA, I PCR amplified the products, inserted the amplimers into vectors, and inserted them into bacteria. I then sequenced the inserts in the vectors and performed phylogenetic analysis of the HIV genome. This work showed that the HIV genome from one lymph node is not the same as another, and that the genome in the same lymph node is very similar. These findings were consistent with past research. This project was used to train me in basic laboratory techniques, and double-check the findings for a paper that is still in the process of being published.
My second project examined different pathways of FDC activation, and if FDCs up-regulate or down-regulate CD32 and CD21 through the different pathways. I isolated FDCs from human tonsillar tissue through positive selection using a FACS machine. To activate the cells, I incubated the FDCs with lipopolysaccharide (LPS), antibodies, complement, immune complexes, immune complexes+complement, neutralizing HIV antibody immune complexes, or neutralizing HIV antibody immune complexes+complement. After the incubation, I extracted the RNA from FDCs, performed reverse transcription, and then analyzed the cDNA with real time PCR. I found that each of these known immune system activators up-regulated CD32 and CD21 at differing degrees. During this project, I also incubated FDCs with alpha-1 antitrypsin. We found that alpha-1 antitrypsin deactivates FDCs, but we did not know why it deactivated these cells. These findings focused our group’s research on determining the intracellular pathways of activation through CD32 and CD21.
My third project focused on discovering the proteins associated with CD21 on FDCs. I hypothesized that CD21 on FDCs is associated with similar proteins as CD21 on B cells, meaning that the B cell co-receptor (CD21/CD19/CD81) is on FDCs. The B cell co-receptor could then activate FDCs in the same or a similar intracellular signaling pathway as B cells. The experimental protocol that I designed was to use fluorescently labeled antibodies to CD21, CD19, and CD81, and then use FRET analysis to determine if the proteins are associated with one another. If they were associated with one another, we would then perform protein cross-linkings and immunoprecipitations to determine the intracellular pathway of activation, and establish if it was the same or similar to the B cell co-receptor activation pathway. I grew hybridomas for CD21, CD19, and CD81, isolated the antibodies, and fluorescently labeled them. Then I isolated B cells from peripheral blood mononuclear cells (PBMCs) through positive selection using a MACS machine, and I isolated FDCs with the same methods as my second project. After separation of the cells, I incubated them with the fluorescently labeled antibodies, used a confocal microscope to perform FRET, and analyzed the results. When I left the laboratory, I had performed some preliminary trials without the α-CD81 antibody, because we were waiting for the α-CD81 antibody to be produced by another principle investigator. Despite missing the α-CD81 antibody, the preliminary results were promising.
My fourth project studied the role of FDCs in activating CD4+ T cells with a latent HIV infection. Studies have shown that FDCs and FDC supernatant can activate latent T cells, but the mechanism is not known. In efforts to determine the mechanism, I isolated CD4+ T cells from PBMCs through positive selection using a MACS machine. After activating the growth signal with IL-2 in the isolated cells, I would infect the cells with an HIV variant. The HIV variant has a faulty envelope gene that can be used to infect the cell, but its progeny can never bud off the cell. If the infection were not latent, the cell would die from viral overload. However, if the infection were latent, the CD4+ T cells would survive. After the latent infection was established, I induced viral protein formation with differing amounts of PHA+Ionomycin or IL-2+IL-7, measured p24 levels within the cells with α-p24 antibodies, and created dose curves comparing activator versus viral expression. These dose curves were then compared to induction of viral protein formation when the latent T cells were incubated with FDCs and FDC supernatant. When I left the lab, we were continuing to induce latent T cells with FDCs and PHA+Ionomycin or IL-2+IL-7, and we were performing mass spectrometry on the FDC supernatant to determine the protein that is causing latent T cells to form HIV particles.
Currently, I am working in Dr. Jeffery Gildersleeve’s laboratory at the National Institutes of Health, specifically in the National Cancer Institute for a year long post-baccalaureate. His research focuses on developing carbohydrate microarrays to assist in analyzing cellular markers, tumors, and vaccine efficacy. I am working on developing a microarray to test epitopes and specificity of antibodies formed by the HIV/AIDS vaccine. Developing this microarray would give researchers a rapid determination of the efficacy of the HIV/AIDS vaccine in the different stage trials of FDA approval.
For nearly two years, I worked in Dr. Gregory Burton’s laboratory at Brigham Young University. His studies focus on understanding the molecular interactions between follicular dendritic cells (FDCs) and HIV. Specifically, we examined the contributions of two FDC receptors, CD32 (FcγR) and CD21 (CR2), that played significant roles in the trapping and long-term maintenance of HIV.
My first project was molecular cloning of HIV. We received samples of lymph nodes from HIV infected patients. I isolated the HIV virons and the RNA, and performed reverse transcription. After making cDNA, I PCR amplified the products, inserted the amplimers into vectors, and inserted them into bacteria. I then sequenced the inserts in the vectors and performed phylogenetic analysis of the HIV genome. This work showed that the HIV genome from one lymph node is not the same as another, and that the genome in the same lymph node is very similar. These findings were consistent with past research. This project was used to train me in basic laboratory techniques, and double-check the findings for a paper that is still in the process of being published.
My second project examined different pathways of FDC activation, and if FDCs up-regulate or down-regulate CD32 and CD21 through the different pathways. I isolated FDCs from human tonsillar tissue through positive selection using a FACS machine. To activate the cells, I incubated the FDCs with lipopolysaccharide (LPS), antibodies, complement, immune complexes, immune complexes+complement, neutralizing HIV antibody immune complexes, or neutralizing HIV antibody immune complexes+complement. After the incubation, I extracted the RNA from FDCs, performed reverse transcription, and then analyzed the cDNA with real time PCR. I found that each of these known immune system activators up-regulated CD32 and CD21 at differing degrees. During this project, I also incubated FDCs with alpha-1 antitrypsin. We found that alpha-1 antitrypsin deactivates FDCs, but we did not know why it deactivated these cells. These findings focused our group’s research on determining the intracellular pathways of activation through CD32 and CD21.
My third project focused on discovering the proteins associated with CD21 on FDCs. I hypothesized that CD21 on FDCs is associated with similar proteins as CD21 on B cells, meaning that the B cell co-receptor (CD21/CD19/CD81) is on FDCs. The B cell co-receptor could then activate FDCs in the same or a similar intracellular signaling pathway as B cells. The experimental protocol that I designed was to use fluorescently labeled antibodies to CD21, CD19, and CD81, and then use FRET analysis to determine if the proteins are associated with one another. If they were associated with one another, we would then perform protein cross-linkings and immunoprecipitations to determine the intracellular pathway of activation, and establish if it was the same or similar to the B cell co-receptor activation pathway. I grew hybridomas for CD21, CD19, and CD81, isolated the antibodies, and fluorescently labeled them. Then I isolated B cells from peripheral blood mononuclear cells (PBMCs) through positive selection using a MACS machine, and I isolated FDCs with the same methods as my second project. After separation of the cells, I incubated them with the fluorescently labeled antibodies, used a confocal microscope to perform FRET, and analyzed the results. When I left the laboratory, I had performed some preliminary trials without the α-CD81 antibody, because we were waiting for the α-CD81 antibody to be produced by another principle investigator. Despite missing the α-CD81 antibody, the preliminary results were promising.
My fourth project studied the role of FDCs in activating CD4+ T cells with a latent HIV infection. Studies have shown that FDCs and FDC supernatant can activate latent T cells, but the mechanism is not known. In efforts to determine the mechanism, I isolated CD4+ T cells from PBMCs through positive selection using a MACS machine. After activating the growth signal with IL-2 in the isolated cells, I would infect the cells with an HIV variant. The HIV variant has a faulty envelope gene that can be used to infect the cell, but its progeny can never bud off the cell. If the infection were not latent, the cell would die from viral overload. However, if the infection were latent, the CD4+ T cells would survive. After the latent infection was established, I induced viral protein formation with differing amounts of PHA+Ionomycin or IL-2+IL-7, measured p24 levels within the cells with α-p24 antibodies, and created dose curves comparing activator versus viral expression. These dose curves were then compared to induction of viral protein formation when the latent T cells were incubated with FDCs and FDC supernatant. When I left the lab, we were continuing to induce latent T cells with FDCs and PHA+Ionomycin or IL-2+IL-7, and we were performing mass spectrometry on the FDC supernatant to determine the protein that is causing latent T cells to form HIV particles.
Currently, I am working in Dr. Jeffery Gildersleeve’s laboratory at the National Institutes of Health, specifically in the National Cancer Institute for a year long post-baccalaureate. His research focuses on developing carbohydrate microarrays to assist in analyzing cellular markers, tumors, and vaccine efficacy. I am working on developing a microarray to test epitopes and specificity of antibodies formed by the HIV/AIDS vaccine. Developing this microarray would give researchers a rapid determination of the efficacy of the HIV/AIDS vaccine in the different stage trials of FDA approval.
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