SNL

I was exponentially more surprised when the same thing happened again, less than two minutes later. Yes, Seth was making multiple jokes about recent research, but the fact still stands — a lot more people know about those projects now than before the findings were worked into an SNL script.

Did you watch the November 12th episode of SNL? Do you remember which Weekend Update stories I’m talking about? No worries if you don’t — this post will refresh your memory, and take you beyond the one-liners.

With Emma Stone hosting and Coldplay performing, this past Saturday’s episode of SNL was already quite promising. However, when Seth Myers gave mention to not one, but two recent findings that I had come this close to posting on Try Nerdy…I was tickled.

Here’s a clip from Weekend Update that starts with the first nerdy reference (34:47) and ends with a second one (36:12):

The clip begins:

Researchers say that a new drug tested on monkeys has helped them lose weight with no dieting or exercise – it’s the easiest way to make the lean, sexy monkeys we’ve all been clamoring for.

Aside from being hilarious, this punchline makes a point — sometimes, research sounds ridiculous to the Average Joe. Whether it’s “fruit flies in France” or “sexy monkeys,” it’s not always immediately obvious how animal research relates to us as people. The common idea behind this type of research is that all living organisms — humans, monkeys, and, yes, fruit flies — are related on a big evolutionary tree, and that important biological mechanisms are probably conserved between us, or at least similar.

So about those monkeys. Monkeys are relatively quite close to humans on an evolutionary scale, so the discovery of a drug that makes obese monkeys lose weight effortlessly is kind of a big deal. Something that works in monkeys has a higher likelihood of working in humans, too. These monkeys, who became obese through overeating and under-activity, were given a drug that selectively destroyed the blood supply of fat tissues. Without a blood supply, the fat in these monkeys was broken down and reabsorbed.

Here’s fat in its normal state, thriving on a nutritious supply of blood:

Then this drug, called adipotide, kills the blood vessels supplying the fat, and the fat effectively melts away (the monkeys lost nearly 30% of their abdominal fat!):

If this drug gets approved for humans, it would be radically different from other weight loss drugs on the market, which typically try to suppress appetite or block absorption of dietary fats.

Near the end of Weekend Update, Seth surprised me again with another story that very nearly made it onto this site:

A new study suggests that people with high blood pressure suffer from emotional dampening and have trouble recognizing emotion in others – they’re called dads.

This got a laugh, but it basically summed up a study done at Clemson University in South Carolina. Researchers asked 106 participants to evaluate emotional expressions in faces and sentences, and individuals with higher resting blood pressures were significantly less accurate at the task. Imagine the irony: your job is super stressful, which drives your blood pressure up, which induces “emotional dampening,” which makes you interpret your boss’s constructive criticism as sarcastic prattle (which will probably lead to more stress down the line).

Oh, Mr. Steele, you're such a kidder.

The general idea at work here is that blood pressure can impact the central nervous system in complex ways; for example, hypertension is associated with decreased pain sensitivity. Perhaps a decrease in emotional sensitivity is part of the same phenomenon. Time (and more research) will tell, but until then, if someone misinterprets your words or fails to laugh at your joke, don’t get frustrated — maybe they’re just under a lot of stress…or eating a high-salt diet.

In any case, I’ll be paying closer attention to Weekend Update from now on, especially when I get blogger’s block.

Stay nerdy

 
Barnhart KF, Christianson DR, Hanley PW, Driessen WH, Bernacky BJ, Baze WB, Wen S, Tian M, Ma J, Kolonin MG, Saha PK, Do KA, Hulvat JF, Gelovani JG, Chan L, Arap W, & Pasqualini R (2011). A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys. Science translational medicine, 3 (108) PMID: 22072637

McCubbin JA, Merritt MM, Sollers JJ 3rd, Evans MK, Zonderman AB, Lane RD, & Thayer JF (2011). Cardiovascular-emotional dampening: the relationship between blood pressure and recognition of emotion. Psychosomatic medicine, 73 (9), 743-50 PMID: 22042880

The very recent publication of a draft of the Cannabis sativa genome has inspired me to briefly review why it’s so hard to do research on weed, and to highlight studies that have shown the benefits that can come from considering marijuana as more than just an abused substance.

Some would say our brains were made for marijuana, or vice versa, because of the abundant cannabinoid receptors that are directly activated by the primary psychoactive chemical in marijuana — a cannabinoid called delta-9-tetrahydrocannabinol (THC). The human body even produces its own endocannabinoids, which activate the same cannabinoid receptors. These receptors are known to have a role in everything from pain sensation to mood to appetite, and more, with some functions perhaps yet to be discovered.

 But about that medical research: much of what’s difficult in drug trials is establishing how toxic the test drug is and what its side effects are. Well, I think it’s generally accepted that there’s no documented human fatality from THC overdose, and as for side effects…well, just watch any one of the myriad “stoner movies” out there (e.g. 1, 2, 3, 4, 5, 6, 7, and 8). Many of the side effects are known quite well.

So what’s the big deal? Well, it all comes down to the fact that the Drug Enforcement Agency (DEA) classifies marijuana as a Schedule 1 drug, where it joins such baddies as heroin, LSD, and ecstasy. Schedule 1 drugs are defined as those that “have no currently accepted medical use in treatment in the United States.” The fact that marijuana is listed among these drugs can be perplexing, what with medical marijuana being legal in at least 16 states and our nation’s capitol.

"No medical use"? Let science decide.

So let’s say you’re a medical researcher, and you want to study the efficacy of marijuana in treating disease X; here are the three hurdles you have to jump: 1) applying for and receiving a license from the DEA, who fears Schedule 1 drugs getting into the wrong hands; 2) getting express approval from your research institution, who just might not want the stigma that comes with your research; and 3) securing funding, which, for Schedule 1 drugs, mostly comes from the National Institute on Drug Abuse (NIDA). NIDA has a government-sanctioned monopoly as the only legal source of marijuana for research in the U.S., and word on the street is that they don’t like to fund research that could conflict with their interest in, well, drug abuse.

To make a long story short, the debate over legalizing marijuana for medical research has a lot to it. Even if this legalization did occur, there would need to be firm oversight to make sure everyone and their mom didn’t run to sign up for studies just to get some reefer. But, in hopes of tilting the balance of this plant’s reputation, I am featuring a list of research studies in which THC, marijuana’s main active compound, appears to have done some good:

1. Cannabinoid Neuroimmune Modulation of SIV Disease. Monkeys with simian immunodeficiency virus (SIV, the monkey version of HIV) were given THC and experienced slowed disease progression, decreased amounts of virus, and milder tissue inflammation.

2. Chronic administration of THC prevents the behavioral effects of intermittent adolescent MDMA administration and attenuates MDMA-induced hyperthermia and neurotoxicity in rats. THC protected rats from ecstasy-induced hyperthermia and neurotoxicity, as well as prevented ecstasy’s behavioral effects.

3. Cannabinoids mediate opposing effects on inflammation-induced intestinal permeability. In inflammatory bowl diseases (IBD) like Crohn’s disease and ulcerative colitis, the intestines are inflamed; in this study, THC accelerated recovery from induced inflammation in human colorectal cells.

4. Neuroprotective effects of phytocannabinoid-based medicines in experimental models of Huntington’s disease. A THC-based treatment delayed the progression of Huntington’s Disease in rats.

5. Targeting cannabinoid receptors as a novel approach in the treatment of graft-versus-host disease: evidence from an experimental murine model. Mice with graft-versus-host disease were given THC and had increased numbers of immune cells, less tissue injury, less weight loss, and better overall survival.

6. Anti-tumoral action of cannabinoids on hepatocellular carcinoma: role of AMPK-dependent activation of autophagy. THC reduced the viability of human hepatocellular carcinoma (liver cancer) cells and of tumors grown from human cancer cells implanted in mice.

7. The cannabinoid receptor agonist THC attenuates weight loss in a rodent model of activity-based anorexia. THC caused anorexic rats to gain weight.

8. Pre- and post-conditioning treatment with an ultra-low dose of Δ9-tetrahydrocannabinol (THC) protects against pentylenetetrazole (PTZ)-induced cognitive damage. Mice given THC before or after induced epilepsy (a model of brain injury) were protected from long-lasting deficits in learning and memory.

9. A combined preclinical therapy of cannabinoids and temozolomide against glioma. THC had anti-tumor effects against gliomas (brain tumors) that were resistant to temozolomide, the standard treatment for gliomas; the gliomas in the studies were grown by implanting human glioma cells in mice.

10. Acute and chronic cannabinoid extracts administration affects motor function in a CREAE model of multiple sclerosis. In a mouse model of multiple sclerosis, injection with a THC-rich Cannabis sativa extract reduced neurological deficits.

…And that’s all just from this year.

van Bakel H, Stout JM, Cote AG, Tallon CM, Sharpe AG, Hughes TR, & Page JE (2011). The draft genome and transcriptome of Cannabis sativa. Genome biology, 12 (10) PMID: 22014239

…They’re venomous? They have how many sex chromosomes?? They might save the world?!? (Not joking about that last one…read on as I cover the basics, and the not-so-basics, of nature’s most beloved WTF moment.)

1. The mammalian egg-layer. Just because the platypus isn’t the only monotreme (it’s one of five), doesn’t make the fact any less perplexing. The platypus seems to represent an evolutionary fork in the road, like an animal that wanted the sweet perks of lactation without all the messiness of the live birth. Who can blame them, really? Oh, and about that lactation? The platypus female has no nipples, so the milk is just released straight through the pores of its skin. Talk about cutting out the middleman.

2. The duck bill. The electric field-sensing duck bill. Yes, we all know about that characteristically out-of-place-looking duck bill that appears to be glued on to the face of a more normal animal. It’s kind of humorous and it makes the platypus easily identifiable (and very amenable to cartoon depiction). As if a duck bill on a mammal wasn’t perplexing enough, nature equipped it with electrosensors. Incredibly, part of how a platypus tracks its prey is by detecting the electric fields generated by the prey’s muscle contractions. The platypus hunts not by sight, not by smell, but by electricity detection. Nice.

Platypus venom gland and duct

3. The excruciatingly painful venom. You see, I spent most of my life thinking of platypuses as cute, cuddly little guys. Recently, however, I’ve reneged on the “cuddly” part. Turns out, a male platypus can release an impressive venom from a spur on the hind foot; the venom doesn’t kill you, but you will feel a pain so intense that it may incapacitate you, and you might be extra pain-sensitive for as long as months. Coincidentally, venomous mammals are extremely rare — just like everything else about the platypus.

4. The absurd number of sex chromosomes. At this point, if you’re starting to feel a bit lacking compared to the platypus, don’t be too hard on yourself — they do have five times as many sex chromosomes as you do. A human female or male is XX or XY, respectively, but a platypus female or male is XXXXXXXXXX or XYXYXYXYXY. I won’t speculate as to why the platypus has so many of these, but because it overachieves in all other areas, I also won’t question it. As far as its other, non-sex chromosomes, the platypus genome has been found to include genes that have origins in birds, reptiles, amphibians, and fish. Is your brain hurting yet?

5. The ability to save us from superbacteria. Now let’s take things beyond the limits of what’s reasonable (if we hadn’t already). New research out of Australia has found that strong antimicrobial peptides are expressed in the platypus, and these peptides are effective against a broad range of bacteria. Because these antimicrobials are peptides, and not chemicals, they are promising candidates for natural treatments to fight multidrug resistant bacteria. Currently, there are very few options for defending against superbugs, and some may soon be resistant to all currently existing antibiotics.

So maybe now this shirt makes a little bit more sense:

The platypus: a little bit of LOL, a whole lot of WTF, and a definite TGP (Thank Goodness for Platypuses).

Stay nerdy!

Grützner F, Rens W, Tsend-Ayush E, El-Mogharbel N, O’Brien PC, Jones RC, Ferguson-Smith MA, & Marshall Graves JA (2004). In the platypus a meiotic chain of ten sex chromosomes shares genes with the bird Z and mammal X chromosomes. Nature, 432 (7019), 913-7 PMID: 15502814

Wang J, Wong ES, Whitley JC, Li J, Stringer JM, Short KR, Renfree MB, Belov K, & Cocks BG (2011). Ancient antimicrobial peptides kill antibiotic-resistant pathogens: Australian mammals provide new options. PloS one, 6 (8) PMID: 21912615

Yeah, you should check this out:

The authors started off by looking at the genes expressed in muscle biopsies from muscles undergoing atrophy, and they made note of which genes had high or low expression. Then, they screened 1300+ compounds for any that could (basically) decrease the high genes and increase the low genes, the idea being that any compound that could reverse the gene expression in muscle atrophy might be a good treatment. And they were right.

Ursolic acid

The screen identified ursolic acid, a compound found in large quantities in apple peels, as the only potential inhibitor of muscle atrophy. So the researchers injected ursolic acid into mice with atrophic muscles, which stopped muscle loss and increased muscle weight by 7%. Seven percent might not sound like a lot, but it is, considering that, again, this is the first compound shown to stop muscle loss at all. A 7% increase in muscle weight in a 180 lb man with typical muscle mass would mean a gain of over 5 pounds of muscle.

Ursolic acid diet shrinks fat cells

Things got even more interesting when normal mice were put on a diet with 0.27% ursolic acid: muscles got bigger and significantly stronger, blood levels of fat and cholesterol decreased, and fat cells shrank considerably, thus reducing fat weight significantly (see for yourself in a figure from the article, left). This is all in addition to the lowered blood sugar in fasting mice who received ursolic acid injections. To make things even better, the authors were able to identify genes that were increased or decreased by treatment, and that were probably responsible for these effects.

In my opinion, these scientists stumbled across something even greater than what they hoped to find. Their data on ursolic acid suggests its usefulness in treating everything from muscle atrophy to obesity to metabolic syndrome to type 2 diabetes. Not even mentioned in this paper is the work that has previously shown the ability of ursolic acid to inhibit cancer cells and Alzheimer’s proteins.

Okay, I’m impressed. What doesn’t ursolic acid do? Seems like it could be a future wonder drug! I’m very interested to see what scientists will try with this compound next…

Have a nerdy weekend!

Kunkel SD, Suneja M, Ebert SM, Bongers KS, Fox DK, Malmberg SE, Alipour F, Shields RK, & Adams CM (2011). mRNA expression signatures of human skeletal muscle atrophy identify a natural compound that increases muscle mass. Cell metabolism, 13 (6), 627-38 PMID: 21641545

Shishodia S, Majumdar S, Banerjee S, & Aggarwal BB (2003). Ursolic acid inhibits nuclear factor-kappaB activation induced by carcinogenic agents through suppression of IkappaBalpha kinase and p65 phosphorylation: correlation with down-regulation of cyclooxygenase 2, matrix metalloproteinase 9, and cyclin D1. Cancer research, 63 (15), 4375-83 PMID: 12907607

Pathak AK, Bhutani M, Nair AS, Ahn KS, Chakraborty A, Kadara H, Guha S, Sethi G, & Aggarwal BB (2007). Ursolic acid inhibits STAT3 activation pathway leading to suppression of proliferation and chemosensitization of human multiple myeloma cells. Molecular cancer research : MCR, 5 (9), 943-55 PMID: 17855663

Wilkinson K, Boyd JD, Glicksman M, Moore KJ, & El Khoury J (2011). A high-content drug screen identifies ursolic acid as an inhibitor of amyloid-{beta} interactions with its receptor CD36. The Journal of biological chemistry PMID: 21835916

Though this blog has already featured insects more than I would have imagined (i.e. at all), this post is about something I really feel the need to share. Because, every so often, I come across something for which the research is so overwhelmingly positive, I’m shocked that it’s not more well-known.

If you want to know what bees are up to now that could significantly impact human health, click on.

In short, bees are collecting this stuff called propolis. They collect it from plants and it’s sort of like sap, but apparently way more awesome. Bees use it to patch up the smaller holes in their hives, but researchers are using it on…everything.

1. Propolis and diabetes. In China, researchers gave propolis capsules to rats with type 2 diabetes. At the end of the experiment, rats who received propolis had significantly less sugar and fat in their blood, and more insulin, compared to diabetic mice who didn’t get propolis. Not bad for bee spackle. Given that almost 10% of the U.S. has diabetes, we need all the help we can get against this condition.

2. Propolis and ulcers. Stomach ulcers are no fun; they’re painful and can cause a lot of vomiting. Although 60% of stomach ulcers are caused by bacteria in the stomach, some cases occur after a person receives radiation, as with cancer treatment. So some compelling work in Egypt found that if mice were given propolis orally one hour before receiving radiation, they were largely protected against the formation of stomach ulcers. In fact, propolis-treated mice developed a whopping 75% fewer ulcers than untreated mice.

3. Propolis and burns. Anyone who has had a second-degree burn probably wouldn’t wish it on his worst enemy. Interestingly, researchers are still exploring what the best dressing is for these burns. A few weeks ago, a team in Brazil tried propolis. You’ve probably caught onto this pattern, but applying 5% propolis to second-degree burns on rats decreased inflammation and increased the rate of tissue repair. Look at this graph:

Pessolato et al. "Propolis and amnion reepithelialise second-degree burns in rats." Burns. July 6, 2011. Figure 6.

See those black bars that are way taller than the other bars? That’s showing the fact that burns treated with propolis produced a lot more collagen than untreated (gray bars) or tissue-grafted (white bars) burns after 1, 2, and 3 weeks into the experiment. Impressive stuff.

4. Propolis and atherosclerosis. I don’t think I need to give much preamble about atherosclerosis, but basically it’s when arteries become blocked because of fatty deposits, and it’s a serious risk factor for heart attacks. Lo and behold, when a different group from Brazil gave propolis to atherosclerotic mice, the condition of the animals improved. These mice were genetically predisposed to have high cholesterol and they were fed a high cholesterol diet to induce atherosclerosis. After 4 weeks of being given extracts from various types of propolis, the mice were sacrificed and mice who received propolis treatment had better ratios of good to bad cholesterol, and had smaller areas of atherosclerotic build-up.

Finally, if you still need more convincing…

5. Propolis and cancer. Glioblastoma is the most common and most detrimental type of brain tumor in humans. People with glioblastomas tend to only survive 1 or 2 years with treatment (3 months without). That’s why it’s pretty exciting that researchers in Brazil (Brazil is really on top of propolis) found that propolis slowed the growth of glioblastoma cells in their lab. Propolis was effective alone, and even more so in combination with a standard brain tumor drug.

What can’t propolis do? Glioblastoma isn’t the only form of cancer against which propolis has proven effective. These five scenarios I’ve described aren’t the only conditions in which propolis has been a successful treatment. I encourage you to do your research if you’re interested:

And/or consider picking up a bottle of the stuff:

If the research didn’t back it up, I wouldn’t advocate for it.

Li Y, Chen M, Xuan H, & Hu F (2012). Effects of encapsulated propolis on blood glycemic control, lipid metabolism, and insulin resistance in type 2 diabetes mellitus rats. Evidence-based complementary and alternative medicine : eCAM, 2012 PMID: 21716678

El-Ghazaly MA, Rashed RR, & Khayyal MT (2011). Anti-ulcerogenic effect of aqueous propolis extract and the influence of radiation exposure. International journal of radiation biology PMID: 21745002

Pessolato AG, Martins DD, Ambrósio CE, Mançanares CA, & de Carvalho AF (2011). Propolis and amnion reepithelialise second-degree burns in rats. Burns : journal of the International Society for Burn Injuries PMID: 21741176

Daleprane JB, da Silva Freitas V, Pacheco A, Rudnicki M, Faine LA, Dörr FA, Ikegaki M, Salazar LA, Ong TP, & Abdalla DS (2011). Anti-atherogenic and anti-angiogenic activities of polyphenols from propolis. The Journal of nutritional biochemistry PMID: 21764281

Borges KS, Brassesco MS, Scrideli CA, Soares AE, & Tone LG (2011). Antiproliferative effects of Tubi-bee propolis in glioblastoma cell lines. Genetics and molecular biology, 34 (2), 310-4 PMID: 21734835

I’ve watched enough episodes of House, M.D. (and it doesn’t take many) to know that when Dr. Gregory House and his medical team try to nail down each episode’s tricky medical condition, they often suggest a diagnosis of lupus along the way to the right answer.

I’m not unashamed to admit that until recently I couldn’t actually answer the question, “What is lupus?”…. Can you?

Don’t feel bad if you can’t; no one really knows what lupus is, because no one knows what causes lupus. In a nutshell, if you have lupus, it means your immune system has started attacking you — the very thing your immune system is meant to protect. It’s not known why the immune system starts doing this, but once it does, the condition is chronic and any part of your body can be targeted (kidneys, skin, hip joint, you name it).

Who gets lupus? Of the roughly 5 million people in the world with a form of lupus, most of them are women, and Blacks are more susceptible than Whites. You can’t catch lupus from anyone, and the best guess of how one ends up with lupus is through an inherited genetic predisposition (lupus sometimes occurs within families) that turns into full-blown disease after exposure to some environmental factor. A popular metaphor for this disease pattern is, “genes load the gun and environment pulls the trigger.”

Image Source: Color Atlas of Pediatric Dermatology Samuel Weinberg, Neil S. Prose, Leonard Kristal Copyright 2008, 1998, 1990, 1975, by the McGraw-Hill Companies, Inc. All rights reserved.

Because lupus can affect the entire body, symptoms of lupus are wide and varied. Rashes, such as the one at left, are common when the skin is attacked, and patients often experience hair loss, fever, joint pain, seizures, and many other complications as well. In fact, the most common cause of death in lupus patients is kidney failure, because kidneys under immune attack become too inflamed to function.

Being diagnosed with lupus simply requires checking off enough boxes of lupus symptoms for a long enough stretch of time to be classified as having the disease. Unfortunately for lupus sufferers, there is no cure for the disease, and attacking the problem — the immune system — would mean making the patient vulnerable to a whole host of opportunistic infections. Easing pain and preempting complications are currently the field standard.

However, new hope for lupus patients arrived in March of this year, when the FDA approved the first lupus drug to hit the market in 50 years. The drug, belimumab, is an antibody therapy that basically inhibits the factor responsible for B-cells (a type of immune cell) making so many antibodies against the patient. The drug is not perfect, it’s best as part of combination therapy and it has its own side effects, but it’s a definite step in the right direction for effective treatments. It means even scientists are getting better at asking themselves, “What is lupus?”

Espinosa G, & Cervera R (2010). Belimumab, a BLyS-specific inhibitor for the treatment of systemic lupus erythematosus. Drugs of today (Barcelona, Spain : 1998), 46 (12), 891-9 PMID: 21589946

For more on lupus, you can visit http://www.lupus.org and do your own research:

The research described in this article identifies a new potential way to target the ability of malaria parasites to hijack red blood cells for their own use.

Title: Malaria parasite clag3 genes determine channel-mediated nutrient uptake by infected red blood cells

Authors: Wang Nguitragool, Abdullah A.B. Bokhari, Ajay D. Pillai, Kempaiah Rayavara, Paresh Sharma, Brad Turpin, L. Aravind and Sanjay A. Desai

Date of publication: May 26, 2011

Direct link: http://www.cell.com/retrieve/pii/S0092867411005241

PMID: 21620134

Abstract: In order for malaria parasites to replicate inside of red blood cells, the parasites force the cells to take up increased amounts of nutrients. This is a conserved feature across diverse malaria parasite species and thus is an opportune drug target. It has been unclear exactly how the parasite forces the cell to take up more nutrients, although past studies have shown that the nutrients are taken in through some kind of channel — but is the channel already present in the red blood cells and waiting for activation, or did the parasites put them there? The best candidate for a channel made by parasites and inserted into red blood cells is a channel called the plasmodial surface anion channel (PSAC). These authors use genetic analysis to find a family of parasite genes that regulate PSAC, and this work also includes a screen for drugs that inhibit this channel — presumably, these drugs have the potential for stopping malaria parasites from taking advantage of red blood cells.

Methods: The researchers performed a chemical screen for drugs that would inhibit PSAC activity in cells infected with malaria parasites and two drugs, ISPA-28 and ISPA-43, are followed up. Genetic studies were done to identify and assess two related parasite genes, clag3.1 and clag3.2, that have a role in PSAC activity.

Results: This paper is perhaps more complex than the others I’ve featured, and I will try to only include the most salient points. The authors screened chemical compounds for any that would inhibit PSAC activity, and they tested this using cells infected with two different strains of malaria parasite. Conveniently, the compound ISPA-28 inhibited the channels for one strain significantly more than for the other, meaning that the two strains could be compared for genetic differences that might help explain how the channel works. It turned out that expression of one version of a gene versus another, clag3.1 versus clag3.2, determined whether the drug was effective at inhibiting PSAC. The authors even found another drug from their screen, ISPA-43, that had the opposite inhibition pattern of ISPA-28. This is to say that ISPA-28 inhibits the channels of parasites expressing clag3.1 and ISPA-43 inhibits the channels of parasites expressing clag3.2. More work needs to be done to fully explain how these genes interact with the PSAC channel to alter its susceptibility to these drugs, but the authors did find that the proteins encoded by these genes end up at the surface of red blood cells, where the channel is located.

Bottom line: These authors have found two versions of the same gene in some malaria parasites that can determine whether the parasite will be affected by a particular drug or not. Specifically, one of two drugs will inhibit the channel that lets nutrients into red blood cells during parasite infection, depending on which of two gene versions is present. Essentially, this work opens the door to a whole new world of ways to potentially treat malaria infections — by developing drugs and vaccines against the PSAC channel. Additionally, knowing which genes lend susceptibility to which drugs would mean that the parasites from infected persons could be screened to select the best treatment for the patient.

 
Nguitragool W, Bokhari AA, Pillai AD, Rayavara K, Sharma P, Turpin B, Aravind L, & Desai SA (2011). Malaria Parasite clag3 Genes Determine Channel-Mediated Nutrient Uptake by Infected Red Blood Cells. Cell, 145 (5), 665-77 PMID: 21620134

Photo credit: http://scienceblogs.com