Sony MUST fix the PS3

I have decided to write this in the time it takes to update Little Big Planet to version 1.04. Since its release, I have been debating buying Little Big Planet due to several concerns I have about its network infrastructure and level moderation, so I decided to rent it first. It finally arrived today, and following inserting this highly anticipated game into my PS3, I was forced to update to the latest version of the game. I am cool with this, it happens ALL the time with Xbox 360 games and requires a brief moment of my time to allow a brief quick download followed by a quick installation. Updating the PS3 however, is another story. It has been some time since I have even turned on my PS3 mainly because of the pain in the ass it is to update the system firmware (a process that routinely take 10+ minutes). Thus, because it has been so long since I have played my PS3, I of course have to update the system firmware before I can begin playing LBP (in the biz, we call that a vicious cycle). After sucking it up and updating my system to Firmware ver. 2.53, I finally click on LBP with great anticipation...only to discover I have to apply not one, but three patches before I can actually play. While this process is now 88% complete, it has already soured my experience and makes me realize why I prefer my XBOX 360. Sony, YOU MUST FIX THIS. Take a page from the Xbox playbook, make this process FAST! Make this process PAINLESS! And in the words of my good friend Oscar Rogers, JUST FIX IT!

UPDATE: At least Little Big Planet was worth it, wow.

Michael Crichton Reaches 'The End'

As a kid, my mother read to my sisters and I constantly, anything from Little Women to Theodore Taylor's The Kay. When I reached the age where I could read to myself at a high enough level, I was excited to finally have the autonomy to choose what fantastical worlds I was going to immerse myself in. Including the requisite Stephen King and John Grisham novels, I began to read the works of Michael Crichton. The Great Train Robbery, The Terminal Man, and The Andromeda Strain all captured my young imagination and held it long enough for me to actually want to learn more about each elegantly incorporated topic that Crichton always managed to weave into his narratives. While his books always managed to land on my library reserve card, I would have considered many other authors to be more influential in terms of my own real world interests. However, that changed in 1990 when Crichton published a novel called Jurassic Park, which I read cover to cover in less 3 days, quite an accomplishment for any eleven year old. That novel and its sequel, The Lost World, introduced me to a topic that was previously unknown to me, molecular genetics, a field in which I eventually earned a Ph.D. and am currently working in. Since then, I have anxiously awaited every one of his many releases, some with more fanfare (Timeline) than others (Next), but always finding a way to captivate my imagination and transport me back to a time when I believed anything was possible. So yesterday, upon hearing the news of Mr. Crichton's death at the fairly young age of 66, I was quite saddened but even more so I was reminded of my origins, the inspirations that have shaped the direction my life has taken and the avenues that I persued in part because of him and his works. While some have described his books as fun summer reading with no more impact than a romance novel, I am proof of a life well spent inspiring youthful imaginations.

The Way it Should Be

The fantastic open world racing/crashing game Burnout Paradise has been on store shelves for almost a year now, and in my own collection for almost as long. Burnout allows you to race around the fictional city of Paradise, a fantastical world filled with almost as many street racers as it has ramps decorating its city streets. For the last ten months I have continued to sporadically pop Burnout Paradise into my Xbox 360 and play for large chunks of time. This differs from most of my game collection, which typically sits on the shelf after I have either completed the game or grown tired of its multiplayer modes. The reason I continually go back to Burnout Paradise is because its developer, Criterion Games, has figured out how to make games that to stay relevant beyond its release window. Criterion actually supports its game, continuously adding new modes, challenges, and content FOR FREE (a phrase I hate to use in this situation because many developers forget that we did actually pay 60 bucks for the game). The most recent updates added new cars, a whole new class of vehicles in motorcycles, weather effects, and day/night cycles. These features completely changed the game for me, creating new challenges and renewing my enthusiasm for it. While many multiplayer FPSs have followed this model by adding in new maps for players to compete against one another, these updates are typically pay-to-play and rarely enhance the single player experience. While I am all about the video game industry getting paid (lord knows I do my part to support it), I sincerely appreciate the recognition by Criterion that their consumers will continue to support their game if THEY do. So cheers to you Criterion Games and congratulations on your success, keep up the good work (and clearly they intend to as they have already announced an additional 4 future updates for Burnout). Here's hoping the rest of the industry sees your success and follows in your footsteps.

The Greatest PrObama Tee Ever

Here is my latest creation, which if you are a Star Wars fan, should make your mouth water. I am currently printing it up on a tee for myself.

McCain for Galactic Emperor

While I myself could not think of one valuable asset McCain could bring to the Presidency of the United States, there are other positions for which he is perhaps better suited.

The Role of Racism in Evolution

With the U.S. presidential election in sight, the racial divide is more prevalent than ever across the U.S. and the world. A relatively large number of individuals have made it clear that they will or will not vote for Barack Obama simply because of his skin color. This fascinating behavior is steeped in deep rooted historical and cultural connections, but what if its due to something deeper? Something so intrinsic that it is simply instinctual to associate with those of a like appearance.

This week in Nature, a trans-national team of zoologists published an article demonstrating what we all knew in the first place...everyone's a racist. The group examined the mating habits of similar yet visually distinct populations of cichlids that inhabit African lakes. The scientists observed that red and blue varieties of the fish species did not interbreed with each other, despite being biologically capable. However, those same cichlid species will mate regardless of thier partners color if the lakes in which they lived were polluted to the point where thier vision was impaired. The researchers concluded that the blue fish and red fish don't mate with one another simply by discriminating against fish of a different color. This supports the notion that species can evolve separately from one another using a theoretical evolutionary strategy called sensory drive, which defines that organisms use their senses rather than instinct to discern appropriate mating partners. These studies demonstrated that each variety of fish maintained their 'racial purity' if you will, by discriminating based on skin color.

Maybe Dave Chappelle was on to something...

Exciting New Developments in anti-MRSA Drugs

Ever since the deployment of commercially produced Penicillin in 1942, researchers and pharmaceutical companies have been racing to develop more effective, diverse, and broader spectrum antibiotics to treat a variety of bacterial infections. However, interest in antibiotic discovery and development has waned in recent years, in part due to a paradigm shift in pharmaceutical development from curing diseases to treating 'lifestyle' conditions (i.e. Restless Leg Syndrome). While this has been a financially sound decision for shareholders, it has left the human population in danger of encountering microorganisms that have evolved a resistance to most if not all commercially produced antibiotics. A perfect example of this is the prolific MRSA (methicillin resistant Staphylococcus aureus) or MDRSA (Multi-Drug Resistant Staphylococcus aureus), which is the causitive agent of Staph infections and has become a worldwide pandemic. Staph infections result in painful skin wounds that do not heal without treatment and can lead to a lethal septicemia in which the bacteria enter the blood stream and systemically proliferate. MRSA infections have become so dangerous and prolific, the CDC reports that more Americans die of MRSA infections than AIDS each year.

Fortunately, an article published this week in Science, has reported the discovery of a novel antibiotic effective against MRSA ad MDRSA. This new antibiotic, called PC190723, was identified by what the authors describe as 'a fragment based approach' to a process called synthetic chemistry. This involves taking a known molecule that exhibits some modest antibacterial activity and synthetically adding to its structure a variety of chemical moieties. The authors began with a chemical known as 3-Methoxybenzamine (3-MBA), a chemical known to disrupt cell division in the bacterium Bacillus subtilis, and synthetically added two moieties called 'benzamide' and 'thiazolopyridine'. The resulting molecule, known as PC190723, exhibited an antibacterial activity of over 2000 times that of it predacessor, 3-MBA. In fact, PC190723 is capable of inhibiting growth of both MRSA and MDRSA at concentrations as low as 1 microgram per mL (for reference, vancomycin, a commonly used antibiotic for MRSA treatment inhibits bacterial growth at concentrations of 2 micrograms per mL). The authors demonstrate that PC190723 inhibits MRSA (and other bacterial species) cell division by interfering with a protein known as FtsZ, which is required for the bacterium to identify its own cellular midpoint. Without functioning FtsZ, the cellular machinery necessary to drive cell division cannot localize the cell midpoint, effectively preventing the bacteria from dividing (inset photo depicts a MRSA cell dividing at its midpoint).

The most exciting result described in this publication, is that PC190723 offered complete protection to mice infected with a normally lethal dose of Staphylococcus aureus. The authors also demonstrated that PC190723 has no effect on the growth of cultured human cells, further suggesting its potential as a safe and effective anti-bacterial therapy. This molecule is currently in the early stages of clinical trials and hopefully will be available sooner than later to help combat the MRSA pandemic.