Ben Alleva ’13: Black Fellow in Bioscience

As this was my final week working in the lab at Baylor College of Medicine, I did my best to get as much done on each project; especially since I had to present my research to the entire lab on Wednesday. Although I thought I would be done with the microsatellite project once I had sifted through the information I had received last week, I was quite mistaken. Once I had sifted through the information and presented it to Claudia through a PowerPoint presentation, I was given 17 more DNA samples from the mothers of patients within the cohort. Microsatellite genotyping of these DNA samples would give us further proof that the mechanism behind the duplication of the MECP2 loci is in fact inter-chromosomal. Unfortunately, I did not finish the analysis of this data before my presentation Wednesday. After the presentation, I was told I would be given co-authorship on the paper Claudia is currently working. I am very excited about this and can’t wait to see the finished manuscript. By the end of the week I had finished my portion of the research on this project.

My second project, the Moebius Project, was a bit disappointing in terms of results, but this project has been going on for over a year so I did not expect too much. Of the five possible de novo mutations I had found, I was only able to test three. This was due to the DNA sequencing of two of the parents (of two different patients) was of poor quality. Of the three that I was able to test, I found only one of the mutations sites to be de novo. More likely than not, this is just a point mutation rather than it being the cause of the syndrome. After I got these results, my part in this project was complete.

For my final project, the fusion gene project, I received the primers I designed for the five patients as well as the twins with Rett Syndrome early in the week. I worked as quickly as I could so that I could present as much of my findings as possible to the lab. Sadly, only one of the primer sets for the five patients actually worked, but we also saw bands on the agarose gel for the twins with Rett Syndrome. We then sent positive results for sequencing. Once we received the results, we found that the one patient that actually had the band (the amplified product) only part of the fusion gene was amplified. We were only able to successfully amplify the exon of one of the genes involved in the fusion, but we only amplified a small portion of the exon from the other gene involved in the fusion. Unfortunately, my time in the lab ran out before I was able to design another set of primers and test them to see if we could amplify both genes involved in the fusion. With the twins with Rett Syndrome, our first PCR amplification gave us bands, showing we had successfully amplified the MECP2 gene. When we repeated these results, the bands appeared in different places, and in some cases the bands didn’t appear at all. After seeing these results, we decided that the bands were artifactual due to the primers not binding correctly. After we received these results, my work on this project was finished.

The end of this week was very bittersweet. I thoroughly enjoyed working in Dr. Lupski’s lab this summer. I learned a great amount about genetics and experimental science. I also discovered where I would like my future to head and I was given the knowledge of how to get there. I am very grateful for all the people who made this fantastic opportunity for me possible.

The pictures below are of my mentor, Dr. Claudia Fonseca, and I and the other is of me working in the lab.

Ben Alleva ’13: Black Fellow in Bioscience

This week was a bit stressful because I tried to get as many results as possible before I presented to others involved in the SMART Program on Wednesday. For the microsatellite project, we received the forward primer I re-designed last week and ran PCR then an agarose gel. Although bands appeared on the gel, the brighter band (the more highly amplified ban), was not at the location we were expecting; basically this means we did not amplify the microsatellite region. This may have been caused by secondary structure of the primers which caused the PCR was not to proceed properly. Due to these results we have decided to put aside this primer set/microsatellite region (as well as the ones that proved not to be polymorphic) and concentrated on the polymorphic microsatellite region. For this, we took a cohort of patients and amplified the microsatellite sequence with the fourth primer set. This sample size was approximately 40 different patients, and we sent the amplified sequence for each patient for microsatellite genotyping. By the end of the week we received the data from the genotyping and have begun to sift through it to find out whether the mechanism behind the genomic rearrangement is an inter or intra-chromosomal mechanism. One of the more interesting comparisons we can make from the data is between mothers and their sons (there are three cases of this within the cohort). From this comparison, we can see the microsatellite inheritance from the mother which will also provide us clues of whether there was an exchange of microsatellite region between two chromosomes during the duplication. If there was, then the mechanism would be inter-chromosomal; if not, then the mechanism would be intra-chromosomal. Once I am able to figure this out, with the data from the microsatellite genotyping of the polymorphic microsatellite region, I will be done working on this project for the summer.

On the fusion genes project, I was given five more patients to design primers for amplifying the fusion gene region. By the end of the week I had designed primers for all five patients and expect to receive them early next week. I was also given two patients, twin girls, diagnosed with Rett Syndrome. Rett Syndrome is caused by a loss of the MECP2 gene on the X chromosome. What is interesting about this case is that the twins have a duplication of the MECP2 gene, but they still have a clinical diagnosis for Rett Syndrome. Our hypothesis is that due to the mechanism and where the duplicated segment is located, in respect to the original MECP2 gene, a deactivation occurred. We are trying to figure out how this occurred through the use of sequencing.

The last project, the Moebius project, I made no progress this week. This weekend I hope to amplify, in the parental DNA of the Moebius Syndrome patients, the exons that contain possible De Novo mutations in the patients (I currently have 5 possible De Novo mutations I must test). I’m hoping on Monday I can send these amplifications to Lone Star Sequencing, then by Wednesday (when I present in front of the lab) I have the portion of the Moebius Project I took on completed.

The presentation I gave on Wednesday went pretty well. A PI within the Molecular and Human Genetics Department ran the presentation session, there were five of us that presented. It was interesting to see what others worked on over the summer. They also gave me a few suggestions for what I should work on before I present in front of the lab next Wednesday. All in all, it was a good presentation day.

The end of this week was a sad one. Almost all the people in the SMART Program have left, technically the SMART Program is now over, and there is only a handful of us left (the ones who arrived late). Below is a picture of my suite mates and I.

Ben Alleva ’13: Black Fellow in Bioscience

This past week I have made some great progress on all of my projects. We received the reverse primer that I redesigned last week for the microsatellite project. We used the new reverse primer with the forward primer of the set that previously did not work to see if we could amplify the microsatellite sequence with this new primer. Unfortunately, no amplified bands appeared on the agarose gel. We ran a Gradient PCR, and no amplified bands appeared on this gel either. After looking at the data, we realized that the forward primer could very well be the problem. We decided to design a new forward primer (with fluorescence). While we waited for this new primer to be delivered, we sent the amplified products with the four successful primer sets for microsatellite genotyping. The company we use (Lonestar Sequencing) has a machine that allows for detection of microsatellite regions within an amplified product. By the end of the week, we received the data from the microsatellite genotyping and were able to analyze the data. One microsatellite region we amplified proved to be polymorphic; meaning the copy number of the repeated sequence differs between individuals. The other three we sent were not polymorphic, although when we compared them to the reference genome they differed in copy number. This suggests that they are polymorphic and there may be a bias within our patient DNA samples. Our next step would be to expand our pool of patient DNA samples, PCR, and send the amplified products for microsatellite genotyping.

Early this week, we received the primers I had designed for the fusion genes project. Before we were able to run PCR, we had to synthesize cDNA (complementary DNA). This is done by first extracting messenger RNA from each patient’s blood sample. Using this messenger RNA as a template, cDNA is synthesized and is ready for PCR. We were only able to create cDNA for three of the patients, and so we performed PCR on these three patients hoping to amplify the fusion genes. Only two of the three patients showed expression of fusion genes in the agarose gel, if no amplification bands appeared there was no expression of the fusion gene. We then ran a Gradient PCR with the patient that showed no expression of the fusion gene. The results of the Gradient PCR confirmed that no fusion gene was expressed in this patient. The other two patients that showed expression of the fusion gene were sent for sequencing. We expect to receive the sequencing data early next week. Once we receive this data, we will begin putting together figures to show how the genes are fused. Although it would be interesting to confirm if these fusion genes create new proteins and have some sort of phenotypic expression, that is not part of this project; by the end of the project, we will only be able to hypothesize whether these fusion genes would create new proteins and phenotypic expression or not.

This week I was finally able to push further on the Moebius Syndrome project. I was finally able to analyze the data sent back from the sequencing company. I found six possible loci among three different genes that may be linked to Moebius Syndrome (in this case, the likelihood of these loci being linked to Moebius Syndrome is quite low). I put together a PowerPoint presentation illustrating the loci. I then sent this PowerPoint to Claudia, who is gone for the next couple weeks. Once I get them back, I will be comparing the parental DNA to the patients to be sure these mutations are De Novo. The reason being there is no inheritance of Moebius Syndrome from the parents, this disease is most likely caused by a De Novo mutation.

Outside of the lab, it has been a relaxing week. Most of my time has been spent finishing up the presentations I have to give in the next two weeks. Last Friday, a group of us from the SMART program went to a place called Wild West. I learned how to two-step, a few line dances, and how to wobble. It was a ton of fun; sadly it was the last big event we would all do together before everyone heads out at the end of next week. Although there are no pictures of me dancing, here is one I took of a few of my friends.

Ben Alleva ’13: Black Fellow in Bioscience

This last week I spent almost the entirety of my time in the lab working on the fusion gene and microsatellite projects. On the microsatellite project, we were very fortunate that the primers I designed last week (we were told they would be delivered in two weeks) actually arrived in half a week’s time. With these newly arrived primer sets, I have been running PCR. The first agarose gel I ran was very disappointing. I got results from only the first primer set, but the problem was there were no results when I used the first primer set with control DNA. This made us very wary of the results from the gel, so I ran another PCR and agarose gel in hopes for better results. This one was not as disappointing, but very inconsistent. There were results from four of the five designed primer sets, but none, except the first primer set, had all DNA samples amplified. Although, once again, there was a problem with the results of the first primer set; not only did the first primer set amplify all the DNA samples, but it also had an amplification band in the Blank (no DNA). This means that contamination must have occurred during the setup of the PCR. Luckily, the contamination only occurred in the first set of primers; I was able to aliquot a new concentration of the first primer set, and when I ran a third gel for this set, the results came out great (all DNA samples were amplified and the Blank had no bands). Although we were getting results for four of the primer sets, the second primer set was still not producing results. To see if the melting temperature was the problem, I ran a Gradient PCR over the weekend. Basically, a Gradient PCR is the same exact reaction in eight different tubes. The only difference is that a range of melting temperatures (50ºC to 60ºC) was used for the eight samples. The results came back with two different amplified bands in each temperature, except around 57º-60ºC there were no amplification bands. At 50ºC, only the amplified band length that we were looking for appeared. This is odd because at that low melting temperature the primers should not be working. From these results we concluded that the primers, in this set (or at least one of them), must not be working in the reaction. We then decided to re-design the reverse primer because it is not fluorescently labeled and thus cheaper to re-order. Also, when we looked at the reverse primer’s sequence we realized it was too G-C rich, which can cause problems during the reaction. That is where we left the project until next week.

At the beginning of the week, I was introduced to the fusion gene project. Just as a reminder, the idea of this project is that the mechanisms causing genomic rearrangements (such as duplications or triplications of genomic sequences) may also cause some patients to have two genes (or portions of genes) that were once far from each other become fused. The question then is if these newly fused genes actually code for proteins. If so, this may cause problems or may even be partially accountable for clinical expression of genomic disorders. To start the project, I was given six patients with possible fusion genes. By the end of the week, we cut out two candidates because the directions of transcription for the fused genes were in opposite directions or the genes were not fused (basically this means that it is not possible for any protein to be coded for and transcribed to messenger RNA). I was given Array-comparative genomic hybridization analyses of each of the patients, and from these figures I had to design primers for the fused gene junctions. Some of the patients were tough to design primers for because in some cases the different exons (the part of genes that codes for proteins) were inverted causing the primer to be reversed. I also had to figure out which exon of one gene actually fused with the exon of another gene, if the transcription directions were in the same direction, and if primers were even possible due to SNPs, LINEs, and SINEs. The entire week I worked on designing these primers, and was finally able to order them on Friday. We should be receiving them early next week.

This week I also started working on presentations I will have to give to members of the SMART Program as well as to members of the Lupski lab. At Cornell College, I have given many presentations and am not nervous about having to present the research I have accomplished thus far. If I have learned one thing from giving presentations at Cornell, it is that I should prepare early. Preparing the night before a presentation is not only stressful but reflects poorly during the presentation. Preparing early will allow me to get more comfortable with the material and allow for the presentations to go smoothly. I hope it goes to plan!

Ben Alleva ’13: Black Fellow in Bioscience

This week, I started off by working on the MECP2 gene related project that Claudia had alluded to the previous week. Claudia explained to me that I was to put this project at the very top of my to-do list, as it was of the utmost importance to complete quickly. After coming back from her weeks of conferences, she realized that more support is needed for her paper before it can be sent for publishing. To provide this extra support, I would have to find microsatellites (tandem repeats in DNA) in the Xq28 band on chromosome X. Monday and most of Tuesday I spent my time going through a website with a large list of microsatellites near the MECP2 gene on the X chromosome. Then I went through through multiple literature sites to find previously studied microsatellites in the Xq28 band; I also went through the human reference genome to find other microsatellites that have not previously been mentioned in the literature. This was a long, tiring task, but at Cornell College I have spent countless hours working with literature as well as with microsatellites. That experience made this part of the project infinitely easier. The toughest part of doing this was finding microsatellites that were not contained within LINEs (long interspersed nuclear elements), SINEs (short interspersed nuclear elements), containing SNPs (single nucleotide polymorphisms), or having LINEs/SINEs surrounding these microsatellites (this occurs A LOT). The reason we don’t want any of these is because it would make it almost impossible (if not entirely impossible) to create primers that would bind and amplify the specific microsatellite without amplifying other segments in the genome (SINEs and LINEs are long sequence repeats in the human genome and comprise approximately 15% of the entire human genome). Once I found 5 good microsatellites (yes, I was only able to find 5 good microsatellites of the many I looked at, which was easily over 100), I had to design primers to amplify these microsatellite segments. I worked on this Tuesday and finished them late Thursday. I ended up using previously designed primers, for exons, near the locations of the microsatellites. Although, in some cases I had to modify them so that SNPs were not in the segment of DNA that the primers would bind to. The presence of SNPs in these genomic segments would cause the likelihood of the primers to bind to decrease, definitely not what we want to happen. Once I was able to finish designing these primers and we double-checked that, in theory, they would work correctly, we sent the data for them to be created and have a special fluorescence label be put on them. We were told these primers would not be delivered to us for two weeks (cutting it close to the end of my Fellowship). Claudia then decided that next week we will start working on the fusion gene project she had originally planned for us to work on, at least until the specially made primers are delivered.

Friday I went back to the Moebius Syndrome project and ran PCR on 11 different samples to, hopefully, find more possibilities of gene-linkage. At the beginning of next week, I will clean the PCR products and send them off to be sequenced. In the meantime, I have received chromatograms of the previous PCR products we sent for sequencing and will begin analyzing them.

On the fourth of July, a group of us in the SMART Program put together an afternoon long volleyball tournament. We then headed over to Hermann Park to listen to the Houston Symphony Orchestra (they had 18 cannons go off during the 1812 Overture) and watch fireworks.

Below is a picture of one of the BCM buildings in the skyline.

Ben Alleva ’13: Black Fellow in Bioscience

Success! At the beginning of this week Pengfei and I found that decreasing the ramp speed gave us distinct bands on our agarose gel, meaning the PCR amplifications were successful. We then cleaned the successful PCR products and sent them off to be sequenced. Sometime next week we will receive the sequencing results and hopefully find that the amplified sequences were the desired segements of DNA rather than error. Soon after we got these results, Pengfei had to leave for a conference and left me to attempt to repeat the success we had on Monday. I was able to run the breakpoint junction PCR twice, but both times no results appeared. This makes us a bit suspicious of the results we obtained on Monday, but we will only be able to truly tell if they were the amplified segments we were looking for once we analyze the sequencing next week.

I was also able to make some progress on the Moebius Syndrome project this week. I received two primers, designed by Claudia, and ran PCR with them. All of the samples showed positive results, so I cleaned the PCR products and sent them off for sequencing to see if these sequences provide us with any hints to linking Moebius Syndrome to a gene or set of genes. I then designed nine more sets of primers that I will receive next week so I can run more tests to see if I can find any further possible gene-linkages.

On Thursday, my mentor, Dr. Claudia Carvahlo Fonseca, returned from her three week conference trip to Germany and Brazil. I will be working next week with her on the MECP2 gene project (dealing with fusion genes). Although when she told me we would be working on the project starting next week, she made it sound like we may be diverging from the original plan and doing something else closely related to this project. It would be more based on a paper she is currently working on to be published. I’m excited to find out what it will be!

On another note, my parents came out to visit the last weekend. I showed them around the medical district in Houston as well as the Rice University campus (it really is a beautiful campus). We also went out to Kemah to walk along the boardwalk and do a little shopping. It was a lot of fun and it was great to have them out to visit. Here are a few pictures we had taken while they were in Houston.

Ben Alleva ’13: Black Fellow in Bioscience

This week started off a bit disappointing. No results appeared on the agarose gel from the breakpoint junction PCR. This is slightly frustrating because Pangfei was able to get results last time he performed this type of PCR, but I am no stranger to not producing results. At Cornell College, I have had many unsuccessful PCR results, but I’ve learned to get past the fact that it failed and come up with possible reasons as to why it was unsuccessful; from there, I can run different controls or try new reagents to figure out what was causing the problem. The oddest part of not getting results was that not even the first PCR, of the two, actually worked. We decided to repeat the breakpoint junction PCR but with different reagents. Once again, this provided us with no results. We then ran a control, using different primers that we knew would provide us with clear results, which came out positive. This meant that our DNA samples were not degraded. This made things even more confusing. We decided that we would each run the two protocols separately to see if the problem was contamination of the PCR products or reagents during the setup of the PCR. Neither of us produced any results showing that contamination was not the problem; by this time we were utterly confused as to what the problem could possibly be. Next week we will perform the two protocols again, with the same control, on a machine that cuts the ramp speed in half. We are hoping this change in ramp speed will allow more time for the primers and nucleotides to bind and create the amplified strands. The downside is that with a decrease in ramp speed, there is a greater likelihood that error will occur. With this in mind, we hope that next week this change will finally give us the results we are looking for so that we may continue with this project and sequence the amplified segments.

This week, Claudia and I were able to do a bit more with the Moebius Syndrome project. I was given a list of possible genes and given free rein on developing primers to amplify these gene sequences. This is a lot tougher process than I thought it would be. First, I struggled to get the program for developing primers to download. Either I would have to pay for the program or download a bunch of viruses/advertisements/free trials (nothing is truly free these days). I finally decided to suck it up and use the computers shared in the lab. The process of developing primers is a lot of referring to a reference genome, then comparing the possible primer options on the Primer3 program; this is to make sure they have less chance of binding to each other as well as having similar Tm (melting temperature) so that the primers will work simultaneously. I regret not having taken any computer courses at Cornell College thus far. I have discovered that understanding computers and programs specific to genetic analysis is very important for this type of research. Another important lesson I learned is that proper and detailed note taking is very important. For the past couple weeks, I have seen multiple researchers in the lab struggle with their experiments because they are unable to reproduce protocols and results that others have been able to perform. It’s a very frustrating situation; professors at Cornell College constantly remind us that keeping good notebooks is important. Now I truly understand why they say such things.

Ben Alleva ’13: Black Fellow in Bioscience

The beginning of this week was a bit less exciting than the previous week’s. I had to make up lab training courses that I had missed (because I was a week late arriving to the program). Basically, it was listening to a lecture for a few hours, taking a short quiz, and then taking a quick blood borne pathogens course online. Nothing too exciting there; although once the training was over, I was able to get back to lab and began working with Pangfei Liu who just recently started his post-doc work. Pangfei and I worked on a lab technique called array-comparative genomic hybridization, aCGH for short. Using this technique, we have the ability to analyze copy number variation and breakpoint junctions of genomic disorder rearrangements. This allows us a comprehensive view of the human genome that can be viewed at a level of resolution of only a few kilobases (keep in mind the entire human genome is billions of nucleotide base pairs). This is especially important to see where duplications and triplications of the genome are located. It also shows us the locations of breakpoint junctions, this especially sought after in Dr. Lupski’s lab because these points in the genome can tell us what sort of mechanism caused the duplications and triplications.

After we performed the aCGH and analyzed the results, we began a breakpoint junction PCR. Basically, it is two PCR protocols performed back-to-back on the same DNA sample. The purpose of the first PCR protocol is to amplify the duplicated and/or triplicated segments of DNA. This is done with primers that are not completely compatible (meaning the sequence of the primer is not completely matched with the desired attachment point for the primers) with the desired genomic sequence for amplification. The reason for this is because sequences near the desired segments (not the desired genomic sequences for amplification) will be similarly compatible with these primers. Theoretically, the designed primers will have a slight affinity to the desired duplicated and triplicated segments and will amplify these segments rather than the undesired similar genomic segments. This is where the second PCR protocol comes in. The primers used in this protocol are much more specific and allow us to amplify the breakpoint junction (that caused the duplication and triplication to occur). We only just started the breakpoint junction PCR on Friday and expect to get results Monday of next week. Once we are able to see these results and analyze them, we will send the DNA samples for sequencing. This will give us the last bit of information we need to figure out the exact mechanism behind this occurrence of duplication/triplication.

With the Moebius Syndrome project, we were unable to make any headway. Claudia is working on about 20 other projects and had little time to put any effort into this project. Hopefully, next week we will begin designing primers to test other genes for a possible linkage to Moebius Syndrome. I am very excited for this because I have not designed primers before and it will be another technique I can add to my repertoire.

Other than working in the lab, I was able to get out a little over the weekend and went to the Houston Galleria. It is a large shopping mall with a lot of really nice stores, some of which were way out of my price range. It was really nice to get away from the dorms and the lab to get better acquainted with the other participants in the SMART Program.

Below are two photos of the building where Dr. Lupski’s lab is located (don’t worry; I don’t dress like this when I go to lab).

Ben Alleva ’13: Black Fellow in Bioscience

Due to the fact that I arrived late to the beginning of the SMART program, I skipped all of the orientation seminars that the other 85 students involved in the program had to attend. Instead, I went straight to Dr. James Lupski’s lab and met everyone I would be working with for the entirety of the Fellowship.  It was a bit overwhelming since there are at least 13 other researchers working in this lab (ranging from under-grad to post-doc work). Most of this first week was spent learning about the main project I would be helping Dr. Claudia Carvalho Fonseca research. Up until now, Claudia has been working with duplications and triplications of the MECP2 gene located on the X chromosome.  If the MECP2 gene is not found on one of the X chromosomes in females, they have what is called Rett Syndrome.  Rett Syndrome is a neurodevelopment disorder that leads to development reversals especially in language and hand-usage. If the MECP2 gene is duplicated on the X chromosome in males, this usually does not matter in females because they have two X chromosomes and the inactivation pattern minimizes the effect, they have what is called Lubs syndrome which leads to developmental delay, mental retardation, and seizures.  The main reason for looking at this is that the entire lab (of Dr. James Lupski) is focused on the mechanisms behind duplications of genomic sequence.  The research project I will work on is closely related to the MECP2 gene duplication/triplication work already done in the lab.  I will be working with fusion genes.  Fusion genes are genes that are not close to each other on a reference genome, but due to the mechanism of duplication or triplication, a gene is next to, or fused with, one of the duplicate or triplicates.  Fusion genes are a side-effect of the mechanism and has had little research performed on it.

A major goal, before I’m able to begin work on the research project, is to learn and gain experience with lab techniques that are able to detect copy number variation in genomic DNA. Copy number variation are DNA segments that may be present at a variable number of copies in comparison to a reference genome which has a variable copy number of N = 2 (Zhang et al. 2009).  These techniques will be extremely useful with the research on fusion genes.  For the second half of the week, I worked with Claudia Gonzaga-Jauregui, a graduate student at Baylor College of Medicine.  She is looking at Moebius Syndrome which is a disorder present at birth that affects the 6th and 7th cranial nerves.  This causes the loss of ability to move the face, especially a hindrance in facial expressions, as well as the inability to move the eyes laterally. There may also be problems with the hands and feet, respiratory problems, speech and swallowing disorders, other visual impairments, sensory integration dysfunction, sleep disorders, and body strength problems. The problem is that there is no known gene linked to this disorder. Through the use of PCR, DNA sequencing, and designing primers, Claudia is attempting to find polymorphisms in genes that may be linked to this disorder.

Starting with this project, Moebius Syndrome research, I count myself as fortunate.  So far, I have mostly performed PCR and run agarose gels, which I have done countless times with Craig Tepper over last summer and through the Biology courses  I have taken over the past few years. Something new I have been working with is using computer programs to analyze DNA sequences.  I have started to become familiar with a program called BioEdit which allows me to visualize the DNA sequence with a chromatogram.  Then, I’m able to compare this sequence to an online database to find any unknown polymorphisms.  I’ve realized, after a week of being in lab, that all the researchers here (whether graduate student or post-doc) are proficient with computers, especially with programs related to their research.  By the end of the Fellowship, I hope to become proficient with computer programs related to my main research project.

Not only am I enjoying the lab work and working with others in the lab, I’ve also been enjoying the sites and events outside of the lab. Here are just a couple pictures of the Houston skyline from the Wiess College Dormitory at Rice University.