The Chemistry Behind Life

You can say that to me about a girl who doesn’t find me attractive, and fine. Whatever. No big deal.

But when you say that to me about my nurse, who won’t let me do any kind of patient care and defers to the male residents on the team even though I am the one who’s writing notes and orders for this patient… That pisses me off.

It’s ok if you’re not attracted to my gender. It’s not ok if you think I’m less of a physician because of it. It’s not ok if you think I’m less capable because of it. It’s not ok if you won’t let me be a functional part of the team because of it.

how well do you expect them to do after admission?

fortunately some guy named JH Ranson developed some criteria in 1974. (a quick google search turns up almost nothing about him, making this a rare occasion where the namesake didn’t get nearly enough fanfare. I don’t even know if it’s a him, but the 70s weren’t great on gender equality and clinical research was no exception.)

medicine is full of mnemonics and this is no exception. you’ll want to use “GA LAW and CHOBBS” here.

At admission / 0-hour:

Glucose (blood) >200 mg/dL

Age > 55 y/o

Lactate dehydrogenase (LDH) > 350 IU/L

Aspartate transaminase (AST) > 250 IU/L

WBC > 16000

At 48 hours:

Calcium (serum) < 8mg/dL

Hematocrit falls in excess of 10%

Oxygen (PaO2) < 60mmHg

BUN increase greater than 5 mg/dL (despite adequate hydration)

Base deficit > 4 mEq/L

Sequestration of fluid > 6L

Some societies alter the parameters above if the patient has gallstone pancreatitis–for our purposes (studying/entry-level clinical practice aka medical student) just stick with the criteria as written as I’m not sure the gallstone differentiation is universally accepted.

Anyway, now you have the criteria, how will they fare? What’s their prognosis?

Each criteria is worth one point.

< 2 points: 2% mortality

3-4 points: 16% mortality

5-6 points: 40% mortality

Current thesis status: This bar makes their own flavored alcohols. This is the pickle vodka. The jar has like five giant pickles floating in it. This tastes like pickle juice. Technically I’m not supposed to drink on my meds but I’ve been nursing this thing for hours and it’s not even halfway gone so I think I’m doing it right. It’s not like I can just chug pickle juice–it is a sweet precious nectar that must be savored.

Current thesis status: All of chapter two out of three (except the background and significance section) is done. I am beyond hallucinating. It’s hard to walk. I’m sure the bartenders think I’m drunk despite my last drink order being over four hours ago.

I reminded her THE SIGNED APPROVED COPY MUST BE SUBMITTED BY 3 PM ON AUGUST 12. You know, the version that incorporates her edits? She is not pulling her last minute bullshit on me again. Another professor has to read and approve the thesis, and I’m not getting her involved in my advisor’s trainwreck.

Anyway, after only 3.5 hours sleep I was planning to take a nap and work tonight, but after dinner and taking care of random house bs it’s bedtime anyway.

The Human Body 

Bacteria have been discovered in our guts that depend on one of our brain chemicals for survival. These bacteria consume GABA, a molecule crucial for calming the brain, and the fact that they gobble it up could help explain why the gut microbiome seems to affect mood.

Philip Strandwitz and his colleagues at Northeastern University in Boston discovered that they could only grow a species of recently discovered gut bacteria, called KLE1738, if they provide it with GABA molecules. “Nothing made it grow, except GABA,” Strandwitz said while announcing his findings at the annual meeting of the American Society for Microbiology in Boston last month.

GABA acts by inhibiting signals from nerve cells, calming down the activity of the brain, so it’s surprising to learn that a gut bacterium needs it to grow and reproduce. Having abnormally low levels of GABA is linked to depression and mood disorders, and this finding adds to growing evidence that our gut bacteria may affect our brains.

Cornell Chronicle

Physicians have been mystified by chronic fatigue syndrome, a condition where normal exertion leads to debilitating fatigue that isn’t alleviated by rest. There are no known triggers, and diagnosis requires lengthy tests administered by an expert.

Due to this lack of information, some people have even suggested the disease may be psychosomatic.

Now, for the first time, Cornell researchers report they have identified biological markers of the disease in gut bacteria and inflammatory microbial agents in the blood.

In a study published June 23 in the journal Microbiome, the team describes how they correctly diagnosed myalgic encephalomyeletis/chronic fatigue syndrome (ME/CFS) in 83 percent of patients through stool samples and blood work, offering a noninvasive diagnosis and a step toward understanding the cause of the disease.

“Our work demonstrates that the gut bacterial microbiome in ME/CFS patients isn’t normal, perhaps leading to gastrointestinal and inflammatory symptoms in victims of the disease,” saidMaureen Hanson, the Liberty Hyde Bailey Professor in the Department of Molecular Biology and Genetics and the paper’s senior author. “Furthermore, our detection of a biological abnormality provides further evidence against the ridiculous concept that the disease is psychological in origin.”

Ruth Ley, associate professor in the Departments of Molecular Biology and Genetics and Microbiology, is a co-author.

“In the future, we could see this technique as a complement to other noninvasive diagnoses, but if we have a better idea of what is going on with these gut microbes and patients, maybe clinicians could consider changing diets, using prebiotics such as dietary fibers or probiotics to help treat the disease,” said Ludovic Giloteaux, a postdoctoral researcher in both Hanson’s and Ley’s labs and first author of the study.

Researchers have evidence that an overactive immune system plays a role in chronic fatigue. Symptoms include fatigue even after sleep, muscle and joint pain, migraines and gastrointestinal distress. One hallmark of the condition is post-exertional malaise, meaning patients may take weeks to recover from minor exertion. To test for ME/CFS, clinicians may give patients a cardio-pulmonary exercise test where they ride a bike until they become fatigued. If the test is repeated the following day,  ME/CFS patients usually cannot reproduce their performance from the first day.

“That’s very typical and specific of people with ME/CFS, because healthy people, or even people who have heart disease, can reproduce the exercise on the second day, but these people cannot,” Giloteaux said.

In the study, Ithaca campus researchers collaborated with Dr. Susan Levine, an ME/CFS specialist in New York City, who recruited 48 people diagnosed with ME/CFS and 39 healthy controls to provide stool and blood samples.

The researchers sequenced regions of microbial DNA from the stool samples to identify different types of bacteria. Overall, the diversity of types of bacteria was greatly reduced and there were fewer bacterial species known to be anti-inflammatory in ME/CFS patients compared with healthy people, an observation also seen in people with Crohn’s disease and ulcerative colitis.

At the same time, the researchers discovered specific markers of inflammation in the blood, likely due to a leaky gut from intestinal problems that allow bacteria to enter the blood, Giloteaux said.

Bacteria in the blood will trigger an immune response, which could worsen symptoms.

The researchers have no evidence to distinguish whether the altered gut microbiome is a cause or a whether it is a consequence of disease, Giloteaux added.

In the future, the research team will look for evidence of viruses and fungi in the gut, to see whether one of these or an association of these along with bacteria may be causing or contributing to the illness.

Co-authors include Julia Goodrich, a doctoral student, and William Walters, a postdoctoral researcher, both in Ley’s lab.

The study was funded by the National Institutes of Health.

Can We Prevent Addiction Using Vaccines?

Ronald Crystal, chair of the Department of Genetic Medicine at Weill Cornell Medical College, replies 

Among them, addictive molecules are often too small to be spotted by the human immune system. Thus, they can circulate in the body undetected. Researchers have developed two basic strategies for overcoming this problem. One invokes so-called active immunity by tethering an addictive molecule to a larger molecule, such as the proteins that encase a common cold virus. This viral shell does not make people sick but does prompt the immune system to produce high levels of antibodies against it and whatever is attached to it. In our laboratory, we have tested this method in animal models and successfully blocked chemical forms of cocaine or nicotine from reaching the brain.

Another approach researchers are testing generates what is known as passive immunity against addictive molecules in the body. They have cultured monoclonal antibodies that can bind selectively to addictive molecules. The hurdle with this particular method is that monoclonal antibodies are expensive to produce and need to be administrated frequently to be effective.

We have tried to circumvent these issues by genetically modifying the liver of mice to produce and secrete sufficient quantities of antiaddictive monoclonal antibodies, but that work is still in its early stages. If successful, though, addiction vaccines would be a valuable aid to help addicts quit.

Image Credit: BRIAN STAUFFER

*get package that came packed in dry ice* 

adviser tells us a story of how when he was a post-doc they would take 2mL eppendorf tubes put some dry ice in them and toss them under other people bench’s and desks as tiny time bombs. 

“its hilarious when you scare someone so much they shove a pipet tip right through their work”

The long history of scientific innovation is filled with serendipitous discoveries, and we now have another one to add to the list: a drug that had previously been abandoned due to limited interest has now been shown to fight off two human viruses in laboratory conditions.

The drug in question, known as GSK983, was plucked from obscurity by chemist Chaitan Khosla from Stanford University, who showed it was effective in helping human cells fight off dengue fever and VEEV (Venezuelan equine encephalitis virus), which would normally kill the cells.

Using a screening process to identify the proteins produced by GSK983, Khosla and his team found that GSK983 was able to block the viruses from replicating by preventing the production of RNA (ribonucleic acid).