<p>There seems to be a pattern to how to research/get published. I did about the same thing as you guys who mentioned what you did</p>
<p>Freshman Year: Reading biology textbooks and several medical journals/publications (in my area of interest)
Sophomore Year: Noticed a trend (or rather, noticed omissions) in a lot of the journals I was reading. At the same time I applied for a position in a lab, hoping not necessarily to conduct my own research but at least to learn. Got lucky and was allowed to do my own project.
Junior Year: Revision, revision, revision. Unfotunetely I didn't have any profs to look my stuff over, so I relied on looking at other people's published articles for formats, lengths, etc. Eventually submitted my research, and was notified months later of an acceptance.
Senior Year: Getting ready for college, thinking of what to do this summer....</p>
<p>Wow; I wasn't even thinking about research freshman year... but my sister did this Howard Hughes program so I thought I'd try for it too and it was great!</p>
<p>What really helps is doing clubs that get you intereted in research while also building one's base knowledge. Starting in Middle School I was in clubs relating to science and math, so that is why I was thinking about it freshman year.</p>
<p>You live in Montgomery County, MD, right? I'm in that program now.</p>
<p>I have two abstracts from it so far, only submitted one (my summer project):</p>
<p>"To protect themselves from the harmful foreign substances/organisms, most of the species, including humans have evolved an immune system, a system that is dedicated to the detection, removal, and future protection against foreign antigens. One of the most integral parts of the immune system is leukocytes, or white blood cells. These cells perform a variety of functions, such as phagocytosis, antibody production, and secreting cytotoxins to destroy antigens. Both inflammation and infection lead to the activation of the leukocyte followed by alterations in the cell phenotype that helps the cell to migrate to the site of inflammation.</p>
<p>Neutrophils are the most numerous of all white blood cells (around 70-80%) and are usually the first cells to arrive at a site of foreign antigen invasion. They are signaled by the release of a type of cytokine called a chemokine from injured or infected cells. These chemokines, such as SDF-1 (stromal cell-derived factor-1), chemoattract the neutrophils in the blood stream by inducing a chemokine gradient, that is, the concentration of SDF-1α is largest at the general site it is being released from and is diluted as it moves throughout the bloodstream. CXCR4, the chemokine receptor specific for SDF1 and present on the neutrophil surface, undergoes molecular changes and directs the cell towards the area in which the chemokine is most concentrated.</p>
<p>Our lab interest reigns in understanding the leukocyte activation and migration and studying the drugs that would influence the molecular mechanisms of cell activation So far, microscopy studies from our lab have shown that in the presence of SDF-1α signal, neutrophils, like lymphocytes, undergo molecular changes where the chemokine receptor CXCR4 moves to the leading edge and the adhesion molecule CD43 to the tail end of the cell. We have reproduced these results during the summer and used the IPlab imaging software to generate the statistics of the cells showing this phenomenon. The IPlab software program gives us the quantitative data on the molecular changes on the neutrophils isolated from mouse bone marrow. We were able to quantify the number of neutrophils where the chemokine receptor and adhesion molecules polarize to the opposite end on activation and also quantify the number of na</p>
<p>*** this is your abstract, dude, mine is just a paragraph, it doesnt describe everything in the process just what you do and what the result is. There is so muchexcess in that......</p>