molecular mechanism

Fieldwork, from plant fossils to robotics

“Thousands of US groundwater aquifers have been inadvertently contaminated with chlorinated solvents, such as perchloroethene (PCE) and trichloroethene (TCE). Chlorinated solvents are both toxic and persistent and classified as possible carcinogens by the U.S. Environmental Protection Agency. I am investigating the reaction of these chemicals with iron minerals commonly found in the soil. I synthesize iron and sulfur bearing minerals and monitor reactions in experiments with PCE or TCE. We hypothesize that these minerals are one natural pathway that transforms these contaminants to benign products.”

– Johnathan D. Culpepper, graduate research assistant, The University of Iowa

“The definitions of race and crime change. Criminology is a multidisciplinary field that combines my interest in human behavior and the diverse ways societies define deviance and race. I am generally interested in social institutions, racial ideology, inequality and social disorganization theory. For example, one of my current projects examines the link between African American-owned businesses and urban crime. Additionally, I am exploring how pre-hire psychological screenings impact adverse correctional employee behavior. As a former correctional officer, I am proud of scientifically addressing issues that may have implications on policy and practice by establishing research relationships with institutions.”

– TaLisa J. Carter, Ph.D. student, Department of Sociology and Criminal Justice, University of Delaware

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That’s a Wrap - September

Each month, the International Space Station focuses on an area of research. In September, the research focus was biology, encompassing cells, plants, animals, genetics, biochemistry, human physiology and more.

Benefits from this research are vast and include: combating diseases, reducing our environmental footprint, feeding the world’s population and developing cleaner energy.

Here’s a recap of some topics we studied this month:


Scientists studied T-cells in orbit to better understand how human immune systems change as they age. For an immune cell, the microgravity environment mimics the aging process. Because spaceflight-induced and aging-related immune suppression share key characteristics, researchers expect the results from this study will be relevant for the general population.

NASA to Napa

We raised a glass to the space station to toast how the study of plants in space led to air purification technology that keeps the air clean in wine cellars and is also used in homes and medical facilities to help prevent mold.

One-Year Mission

This month also marked the halfway point of the One-Year Mission. NASA Astronaut Scott Kelly and Roscosmos Cosmonaut Mikhail Kornienko reached the midpoint on Sept. 15. This mission will result in valuable data about human health and the effects of microgravity on the body.


Since microbes can threaten crew health and jeopardize equipment, scientists study them on astronauts’ skin and aboard the space station. Samples like saliva, blood, perspiration and swaps of equipment are collected to determine how microgravity, environment, diet and stress affect the microorganisms.

Model Organisms

Model organisms have characteristics that allow them to easily be maintained, reproduced and studied in a laboratory. Scientists investigate roundworms, medaka fish and rodents on the station because of this reason. They can also provide insight into the basic cellular and molecular mechanisms of the human body.

For more information about research on the International Space Station, go HERE.

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I hate this quote. So fucking much. She thinks she’s woke but really she’s showing her ignorance. As someone who actually works in a multi-million dollar cancer research facility, I can tell you that what we do is not some crazy Da-Vinci Code-esque plot to fool humanity. We’re not sitting there 9-5 with the cure in the fucking fridge playing monopoly, trying to fool you, watching loved ones die of different cancers. Cancer research groups are teams of extremely dedicated, intelligent and committed doctors who are doing their very fucking best to determine the molecular mechanisms underpinning one of the most elusive and multifaceted biological phenomenons in modern medicine. And here we have some uneducated, hippy conspiracy theorist who read this somewhere and decided to sticky tape it to her goddamn face. Like yes *clap clap* impactful.
This particular conspiracy theory is especially ludicrous because if you what to make a difference and “cure” cancer, don’t look for ways to undermine the research currently undergoing. Get a degree, like the rest of us, study for eight years, get yourself into a productive lab and do something. Don’t be this person, a sad, more than likely high school dropout who saw some fanatics YouTube rant and now thinks she knows how the real world works. Go home.
Also, who is “they?” Who is this “they” that is behind everything? Every country is spear handing their own branch of cancer research. All these labs collaborate and share their findings. This isn’t the damn matrix.

anonymous asked:

The cabbage repairs ACs right? I'm gonna start med school in the fall and my bf just graduated too but doesn't know what he wants to in life yet so he is working as an electrician with his dad. Everyone tells me that I should be with someone as "smart" as me and that one day I'll be making more money than him. It's not that I'm smarter I just studied harder and school wasn't his thing. Do people ever tell you the same thing about the cabbage?

Oh. My. Gosh.

First off, let me have a moment of righteous indignation on your behalf:

Ok, now that’s done with.

You are exactly right. And I have gotten the snob vibe a few times when my classmates or professors ask me what my betrothed does for a living. Luckily my family hasn’t given me any ilk of that sort.

There is this stupid snooty notion, especially among people who are very educated, that people who haven’t achieved as much schooling as they have aren’t as smart as they are. I don’t know about you, but I have met many highly educated people who are dumber than a box of rocks in every area of life except their little tiny window to expertise, which is silly.

Using myself and the Cabbage as an example: I am going to have an MD in two years, before that I went to college right out of high school, working two jobs and getting into mild amount of trouble that now just makes for funny stories. My partner made it to junior year of engineering school and decided he’d rather live in Colorado and snowboard, then he was in a bunch of bands and toured around and made legitimately poor life choices, and then he started working for an HVAC company and a year or so later he met me, and here we are almost 2 years later happy as can be.

I know a lot of things my partner does not: I’ve told him how cancer works, about why biostats can tell us that kale study he’s so excited about needs a bigger sample size, about why he should take ibuprofen instead of tylenol for his hangover, how sunscreen works, what sleep apnea is and why his mom needs to get that checked out, and occasionally some super nerdy art history stuff.

My partner knows a lot of things that I do not: how to fix the lawnmower when it would spontaneously die halfway through the front yard, how to change the lights in my car and change the oil, how to clean out air conditioner and heater to save us money on our bills, how to make a flawless steak, how to do a 360 flip on a snowboard, how to play a song on the guitar after hearing it once or twice, an exhaustive knowledge of 1990-2007 American rappers, how motors work, and what that weird sound the washing machine is making and how to fix it.

One pile of knowledge is not necessarily better than the other. Obviously he would be useless trying to take an H&P and figure out a differential, but I would be equally useless on a 98 degree day staring at a nonfunctional AC unit. It’s situational. To be 100% honest, sometimes I think that skilled labor knowledge is more useful in daily life than my cyclopedic knowledge of molecular cancer mechanisms- because if something breaks on me and I have no Cabbage or Padre to help, my options are replacing it or paying someone else to fix it.

Finally, it doesn’t matter who makes more money in the relationship. That someone even cares enough to point out that you, future lady physician, will make more money than your electrician male partner is a handy dandy little piece of bullshit brought to you by the patriarchy, or just a really greedy person. So what? As long as you are on the same page about how your money is to be used, as long as you always communicate openly and honestly about money even if it feels slimy, as long as you never put money above your partner you will be fine.

Personally, I think you are in a great spot. I think the Cabbage is so much smarter than me in many areas, and that makes our relationship fun because I get to learn from him all the time.

So tell those haters to piss off.


Science Becomes Art: Dance Your Ph.D. Thesis!

Modern dance isn’t typically known for exploring subjects like chemical signaling and defense in brown algal kelps. Avant-garde dancer and choreographer Merce Cunningham wasn’t known for developing statistical tools for biomedical research. 

But that doesn’t mean it can’t be done, and a crop of Ph.D. students and recent graduates is showing how. Just before the holiday last week, Science magazine announced the winners of its eighth annual Dance Your Ph.D. thesis competition. Contestants from the social, physical and life sciences interpreted highly complex concepts through movement, drawing on elements from tango, interpretive dance, hip-hop and other styles.

This year’s winner among 31 entries was Florence Metz, a Ph.D. student at the University of Bern in Switzerland, who took home $1,000 for a dance about her thesis on water policy. Her achievement represents the first time a social scientist has won the overall competition. See the other winners and videos of their dances below.

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New role of cholesterol in regulating brain proteins discovered

A study led by researchers at the Hospital del Mar Medical Research Institute (IMIM) and the Institute of Medical Physics and Biophysics at the Faculty of Medicine in Charité Hospital, Berlin, published in the journal Nature Communications, demonstrates that the cholesterol present in cell membranes can interfere with the function of an important brain membrane protein, through a previously unknown mode of interaction. Specifically, cholesterol is capable of regulating the activity of the adenosine receptor, by invading it and accessing the active site. This will allow new ways of interacting with these proteins to be devised that in the future could lead to drugs for treating diseases like Alzheimer’s.

The adenosine receptor belongs to the GPCR family (G Protein-Coupled Receptors), a large group of proteins located in cell membranes, which are key in the transmission of signals and communication between cells. GPCRs are therefore involved in the majority of important physiological processes, including the interpretation of sensory stimuli such as vision, smell, and taste, the regulation of the immune and inflammatory system, and behaviour modulation.

“Cholesterol is an essential component of neuronal membranes, where GPCRs reside along with other proteins. Interestingly, the levels of cholesterol in the membrane are altered in diseases such as Alzheimer’s, where GPCRs like the adenosine receptor play a key role”, explains Jana Selent, head of the GPCR Drug Discovery research group at the GRIB, a joint programme between Hospital del Mar Medical Research Institute (IMIM) and Universitat Pompeu Fabra (UPF). “This study has shown that cholesterol can exert direct action on this important family of proteins in neuronal membranes, the GPCRs, and establishes the basis for a hitherto unknown interaction pathway between the cell membrane and proteins”, adds the researcher.

Up to now, it was thought that membrane cholesterol could regulate the activity of these proteins through two mechanisms: either by altering the physical properties of the membrane, or by binding to the surface of the protein. In both cases, it was thought that cholesterol could only exercise its modulatory action from outside the protein.

However, by using latest-generation molecular simulations the researchers were able to detect the fact that cholesterol can leave the neuronal membrane and get within the adenosine receptor, in particular accessing the receptor’s active site. With this information, and in collaboration with Dr. Mairena Martin and Dr. José L. Albasanz from the University of Castilla-La Mancha, we designed an experimental protocol using cell assays to demonstrate that cholesterol is able to modulate the activity of this receptor by accessing its interior.

“Cholesterol levels in cell membranes could have a more direct effect than previously thought on the behaviour of key proteins in central nervous system diseases. In particular, high levels of membrane cholesterol like those present in Alzheimer’s patients probably block the adenosine receptor, which could in turn be related to certain symptoms observed in this disease”, explains Ramón Guixà González, a postdoctoral researcher at the Institute of Medical Physics and Biophysics at the Faculty of Medicine in Charité Hospital in Berlin and first author of the article. “Although other studies are needed to prove this relationship, this work provides key knowledge that could be used in the future in the development of new molecules that, like cholesterol, have the ability to get inside the receptor and modulate its activity”, says the researcher.

The results from this study represent a paradigm shift in the relationship between membrane cholesterol and GPCRs in the central nervous system, and open up new avenues of research in fields where the cholesterol-GPCR relationship is essential. It also appears that the cholesterol access pathway into the receptor is an evolutionary footprint. It is therefore necessary to discover whether the molecular mechanism described in this paper is present in other GPCRs and therefore potentially involved in a wide range of central nervous system diseases.

Two new studies uncover key players responsible for learning and memory formation

One of the most fascinating properties of the mammalian brain is its capacity to change throughout life. Experiences, whether studying for a test or experiencing a traumatic situation, alter our brains by modifying the activity and organization of specific neural circuitry, thereby modifying subsequent feelings, thoughts, and behavior. These changes take place in and among synapses, communication junctions between neurons. This experience-driven alteration of brain structure and function is called synaptic plasticity and it is considered the cellular basis for learning and memory.

Many research groups across the globe are dedicated to advancing our understanding of the fundamental principles of learning and memory formation. This understanding is dependent upon identifying the molecules involved in learning and memory and the roles they play in the process. Hundreds of molecules appear to be involved in the regulation of synaptic plasticity, and understanding the interactions among these molecules is crucial to fully understand how memory works.

There are several underlying mechanisms that work together to achieve synaptic plasticity, including changes in the amount of chemical signals released into a synapse and changes in how sensitive a cell’s response is to those signals. In particular, the protein BDNF, its receptor TrkB, and GTPase proteins are involved in some forms of synaptic plasticity, however, very little is known regarding when and where they are activated in the process.

By using sophisticated imaging techniques to monitor the spatiotemporal activation patterns of these molecules in single dendritic spines, the research group led by Dr. Ryohei Yasuda at Max Planck Florida Institute for Neuroscience and Dr. James McNamara at Duke University Medical Center have uncovered critical details of the interplay of these molecules during synaptic plasticity. These exciting findings were published online ahead of print in September 2016 as two independent publications in Nature (1, 2).

A surprising signaling system within the spine

In one of the publications (Harward and Hedrick et al.), the authors identified an autocrine signaling system – a system where molecules act on the same cells that produce them – within single dendritic spines. This autocrine signaling system is achieved by rapid release of the protein, BDNF, from a stimulated spine and subsequent activation of its receptor, TrkB, on the same spine, which further activates signaling inside the spine. This in turn leads to spine enlargement, the process essential for synaptic plasticity. In other words, signaling initiated inside the spine goes outside the spine and activates a receptor on the external surface of the spine, thereby evoking additional signals inside the spine. This finding of an autocrine signaling process within the dendritic spines surprised the scientists.

What are the consequences of the autocrine signaling within the spine?

The second publication (Hedrick and Harward et al.) reports that the autocrine signaling leads to activation of an additional set of signaling molecules called small GTPase proteins. The findings reveal a three-molecule model of structural plasticity, which implicates the localized, coincident activation of three GTPase proteins Rac1, Cdc42, and RhoA, as a causal feature of structural plasticity. It is known that these proteins regulate the shape of dendritic spines, however, how they work together to control spine structure has remained unclear. The researchers monitored the spatiotemporal activation patterns of these molecules in single dendritic spines during synaptic plasticity and found that all three proteins are activated simultaneously, but their activation patterns differed significantly. One of the differences is that RhoA and Rac1, when activated, spread beyond the stimulated spine to the surrounding dendrite, which facilitates plasticity of surrounding spines. Another difference is that Cdc42 activity was restricted to the stimulated spine, what seems to be necessary to produce spine-specific plasticity. Furthermore, the autocrine BDNF signaling is required for activation of Cdc42 and Rac1, but not for RhoA.

Unprecedented insights into the regulation of synaptic plasticity

These two studies provide unprecedented insights into the regulation of synaptic plasticity. One study revealed for the first time an autocrine signaling system and the second study presented a unique form of biochemical computation in dendrites involving the controlled complementation of three molecules. According to Dr. Yasuda, understanding the molecular mechanisms that are responsible for the regulation of synaptic strength is critical for understanding how neural circuits function, how they form, and how they are shaped by experience. Dr. McNamara noted that disorder of these signaling systems likely underlies dysfunction of synapses that cause epilepsy and a diversity of other diseases of the brain. Because hundreds of species of proteins are involved in the signal transduction that regulates synaptic plasticity, it is essential to investigate the dynamics of more proteins to better understand the signaling mechanisms in dendritic spines.

Future research in the Yasuda and McNamara Labs is expected to lead to significant advances in the understanding of intracellular signaling in neurons and will provide key insights into the mechanisms underlying synaptic plasticity and memory formation and brain diseases. These insights will hopefully lead to the development of drugs that could enhance memory and prevent or more effectively treat epilepsy and other brain disorders.

How Huntington’s Disease Protein Could Cause Death of Neurons

Scientists at the University of Pittsburgh School of Medicine have identified for the first time a key molecular mechanism by which the abnormal protein found in Huntington’s disease can cause brain cell death. The results of these studies, published today in Nature Neuroscience, could one day lead to ways to prevent the progressive neurological deterioration that characterizes the condition.

Huntington’s disease patients inherit from a parent a gene that contains too many repeats of a certain DNA sequence, which results in the production of an abnormal form of a protein called huntingtin (HTT), explained senior investigator Robert Friedlander, M.D., UPMC Professor of Neurosurgery and Neurobiology and chair, Department of Neurological Surgery, Pitt School of Medicine. But until now, studies have not suggested how HTT could cause disease.

“This study connects the dots for the first time and shows how huntingtin can cause problems for the mitochondria that lead to the death of neurons,” Dr. Friedlander said. “If we can disrupt the pathway, we may be able to identify new treatments for this devastating disease.”

Examination of brain tissue samples from both mice and human patients affected by Huntington’s disease showed that mutant HTT collects in the mitochondria, which are the energy suppliers of the cell. Using several biochemical approaches in follow-up mouse studies, the research team identified the mitochondrial proteins that bind to mutant HTT, noting its particular affinity for TIM23, a protein complex that transports other proteins from the rest of the cell into the mitochondria.

Further investigation revealed that mutant HTT inhibited TIM23’s ability to transport proteins across the mitochondrial membrane, slowing metabolic activity and ultimately triggering cell-suicide pathways. The team also found that mutant HTT-induced mitochondrial dysfunction occurred more often near the synapses, or junctions, of neurons, likely impairing the neuron’s ability to communicate or signal its neighbors.

To verify the findings, the researchers showed that producing more TIM23 could overcome the protein transport deficiency and prevent cell death.

“We learned also that these events occur very early in the disease process, not as the result of some other mutant HTT-induced changes,” Dr. Friedlander said. “This means that if we can find ways to intervene at this point, we may be able to prevent neurological damage.”

The team’s next steps include identifying exact binding sites and agents that can influence the interactions of HTT and TIM23.

The Brain’s Gardeners: Immune Cells ‘Prune’ Connections Between Neurons

A new study, published in the journal Nature Communications, shows that cells normally associated with protecting the brain from infection and injury also play an important role in rewiring the connections between nerve cells. While this discovery sheds new light on the mechanics of neuroplasticity, it could also help explain diseases like autism spectrum disorders, schizophrenia, and dementia, which may arise when this process breaks down and connections between brain cells are not formed or removed correctly.

(Image caption: Microglia (green) with purple representing the P2Y12 receptor which the study shows is a critical regulator in the process of pruning connections between nerve cells)

“We have long considered the reorganization of the brain’s network of connections as solely the domain of neurons,” said Ania Majewska, Ph.D., an associate professor in the Department of Neuroscience at the University of Rochester Medical Center (URMC) and senior author of the study. “These findings show that a precisely choreographed interaction between multiple cells types is necessary to carry out the formation and destruction of connections that allow proper signaling in the brain.”

The study is another example of a dramatic shift in scientists’ understanding of the role that the immune system, specifically cells called microglia, plays in maintaining brain function. Microglia have been long understood to be the sentinels of the central nervous system, patrolling the brain and spinal cord and springing into action to stamp out infections or gobble up dead cell tissue. However, scientists are now beginning to appreciate that, in addition to serving as the brain’s first line of defense, these cells also have a nurturing side, particularly as it relates to the connections between neurons.

The formation and removal of the physical connections between neurons is a critical part of maintaining a healthy brain and the process of creating new pathways and networks among brain cells enables us to absorb, learn, and memorize new information.  

“The brain’s network of connections is like a garden,” said Rebecca Lowery, a graduate student in Majewska’s lab and co-author of the study. “Not only does it require nourishment and a healthy environment, but every once in a while you need to prune dead branches and pull up weeds in order to allow new flowers to grow.”

While this constant reorganization of neural networks – called neuroplasticity – has been well understood for some time, the basic mechanisms by which connections between brain cells are made and broken has eluded scientists.

Performing experiments in mice, the researchers employed a well-established model of measuring neuroplasticity by observing how cells reorganize their connections when visual information received by the brain is reduced from two eyes to one.

The researchers found that in the mice’s brains microglia responded rapidly to changes in neuronal activity as the brain adapted to processing information from only one eye. They observed that the microglia targeted the synaptic cleft – the business end of the connection that transmits signals between neurons. The microglia “pulled up” the appropriate connections, physically disconnecting one neuron from another, while leaving other important connections intact.

This is similar to what occurs during an infection or injury, in which microglia are activated, quickly navigate towards the injured site, and remove dead or diseased tissue while leaving healthy tissue untouched.

The researchers also pinpointed one of the key molecular mechanisms in this process and observed that when a single receptor – called P2Y12 – was turned off the microglia ceased removing the connections between neurons.

These findings may provide new insight into disorders that are the characterized by sensory or cognitive dysfunction, such as autism spectrum disorders, schizophrenia, and dementia. It is possible that when the microglia’s synapse pruning function is interrupted or when the cells mistakenly remove the wrong connections – perhaps due to genetic factors or because the cells are too occupied elsewhere fighting an infection or injury – the result is impaired signaling between brain cells.

“These findings demonstrate that microglia are a dynamic and integral component of the complex machinery that allows neurons to reorganize their connections in the healthy mature brain,” said Grayson Sipe, a graduate student in Majewska’s lab and co-author of the study. “While more work needs to be done to fully understand this process, this study may help us understand how genetics or disruption of the immune system contributes to neurological disorders.”

Atomic-level view provides new insight into translation of touch into nerve signals

Whether stubbing a toe or stroking a cat, the sensation of touch starts out as a mechanical force that is then transformed into an electrical signal conveying pain or other sensations. Tiny channels in neurons act as translators by helping to formulate that signal to the brain. However, scientists know little about the fine details of how these channels work.

(Image caption: Molecular roadblock: The TRAAK channel (purple and orange) dampens sensations by letting potassium ions escape from a neuron. Researchers found the channel uses a never-before-seen system for blocking that flow of ions when it closes: A lipid (yellow) from the neuron membrane (gray) protrudes into the channel.)

New work at Rockefeller University has revealed that one such channel in humans responds to mechanical force using a never-before-seen mechanism. Researchers led by Roderick MacKinnon, John D. Rockefeller Jr. Professor and head of the Laboratory of Molecular Neurobiology and Biophysics examined the TRAAK channel, which is involved in painful touch sensation, at the molecular and atomic levels, finding that it works by reducing the flow of potassium ions that create an electrical signal. The researchers’ findings were released today (December 3) in Nature.

”It is fascinating to wonder how living cells evolved molecules capable of turning small mechanical forces, such as those associated with touch, into electrical signals in the nervous system. That question served as the impetus for this work,” MacKinnon says.

The channels that act as gates in the membranes that envelop neurons, including TRAAK, allow electrically charged atoms, called ions, to move in or out. It’s this movement that is the basis for an electrical signal that carries information. TRAAK channels are one of 78 types of channels in the human body that transport potassium ions; there are other devoted to other ion types. By allowing potassium to trickle out of the neuron, TRAAK normally quiets the neurons, balancing out other channels, which would otherwise create a strong electrical signal for pain.

“TRAAK acts kind of like the brakes on a painful touch sensation, while other channels act as the gas. If you take away the brakes, innocuous touch becomes painful,” says first author Stephen Brohawn, a postdoc in the lab.

Prior work in the lab has shown TRAAK responds to membrane tension – that is stretching caused by a physical force. However, it wasn’t clear how this force caused the channel to open. In fact, scientists had previously only explained the workings of two mechanical-force sensing channels, both of which are found in bacteria.

After purifying the protein that makes up TRAAK, the team crystallized it and determined its structure using X-ray diffraction analysis. Based on the pattern produced by X-rays bounced off the crystallized protein, scientists can infer the structure of the molecule. But because it is difficult to get high-quality crystals from TRAAK, the researchers used antibodies that targeted it to create a sort of scaffold to help guide the formation of crystals.

In the structural images revealed by this work, the researchers found a unique system is responsible for holding off the flow of ions. TRAAK’s central cavity, through which the ions must pass, is flanked by two spiral-shaped chains called helices. When both of these chains are kinked upward, the channel is open so potassium can leave the cell. But when one of these two chains relaxes downward, it uncovers a sort of side door into the center of the neuron membrane.

Neuron membranes, like all cell membranes, consist of two layers of molecules called lipids that have heads facing outward and greasy chains extending inward. When TRAAK’s side door is open, one of those greasy chains, called an acyl chain, pokes into TRAAK’s central cavity, blocking it so no potassium can pass. No known channel uses a mechanism like this.

“This is the first time anyone has seen, at a molecular level, how mechanical force can open a channel in animals, including humans,” Brohawn says. “When the membrane stretches, TRAAK widens, sort of like a dot on a balloon that expands as it is inflated. That wider conformation pulls the helices upward, preventing an acyl chain from blocking the channel, and so leaving it open for potassium ions.”

“The direct involvement of lipid molecules in the gating mechanism begins to explain another well-known property of TRAAK channels – that their gating is sensitive to general anesthetics and other molecules known to enter the lipid membrane where they insert themselves between its acyl chains. By doing so, it appears these anesthetics can shut down pain sensations by locking TRAAK in an open position,” MacKinnon says.

What’s On Board the Next SpaceX Cargo Launch?

Cargo and supplies are scheduled to launch to the International Space Station on Monday, July 18 at 12:45 a.m. EDT. The SpaceX Dragon cargo spacecraft will liftoff from our Kennedy Space Center in Florida.

Among the arriving cargo is the first of two international docking adapters, which will allow commercial spacecraft to dock to the station when transporting astronauts in the near future as part of our Commercial Crew Program.

This metallic ring, big enough for astronauts and cargo to fit through represents the first on-orbit element built to the docking measurements that are standardized for all the spacecraft builders across the world.

Its first users are expected to be the Boeing Starliner and SpaceX Crew Dragon spacecraft, which are both now in development.

What About the Science?!

Experiments launching to the station range from research into the effects of microgravity on the human body, to regulating temperature on spacecraft. Take a look at a few:

A Space-based DNA Sequencer

DNA testing aboard the space station typically requires collecting samples and sending them back to Earth to be analyzed. Our Biomolecule Sequencer Investigation will test a new device that will allow DNA sequencing in space for the first time! The samples in this first test will be DNA from a virus, a bacteria and a mouse.

How big is it? Picture your smartphone…then cut it in half. This miniature device has the potential to identify microbes, diagnose diseases and evaluate crew member health, and even help detect DNA-based life elsewhere in the solar system.


OsteoOmics is an experiment that will investigate the molecular mechanisms that dictate bone loss in microgravity. It does this by examining osteoblasts, which form bone; and osteoclasts, which dissolves bone. New ground-based studies are using magnetic levitation equipment to simulate gravity-related changes. This experiment hopes to validate whether this method accurately simulates the free-fall conditions of microgravity.

Results from this study could lead to better preventative care or therapeutic treatments for people suffering bone loss, both on Earth and in space!

Heart Cells Experiment

The goals of the Effects of Microgravity on Stem Cell-Derived Heart Cells (Heart Cells) investigation include increasing the understanding of the effects of microgravity on heart function, the improvement of heart disease modeling capabilities and the development of appropriate methods for cell therapy for people with heart disease on Earth.

Phase Change Material Heat Exchanger (PCM HX)

The goal of the Phase Change Material Heat Exchanger (PCM HX) project is to regulate internal spacecraft temperatures. Inside this device, we’re testing the freezing and thawing of material in an attempt to regulate temperature on a spacecraft. This phase-changing material (PCM) can be melted and solidified at certain high heat temperatures to store and release large amounts of energy.

Watch Launch!

Live coverage of the SpaceX launch will be available starting at 11:30 p.m. EDT on Sunday, July 17 via NASA Television

Make sure to follow us on Tumblr for your regular dose of space:

Update: The end is near! 

Dear followers,

I miss you all.  Months have passed since I last posted and the seasons have changed while I write my dissertation.  But, the end is near! I scheduled my defense for January 23, 2015.  I’m really excited to share my work with you!!! 

My PhD research is all about how to explain biological mechanisms, and I know how the tumblr science junkies can’t get enough of those.  But, how does a scientist explain a cellular mechanism and is it different from a learner’s explanation? My dissertation answers this and other questions in three manuscripts about how people learn to explain in biology.  As each manuscript is accepted into an open-access journal, I will blog about the major issues that my research addresses and the implication for explaining. In so doing, I hope to improve science communication on tumblr.

In other news, I am securing a post-doctoral research position and moving!  There are big changes ahead, so I hope to get back to blogging and spread the love of the molecular life sciences. 

Thank you loyal followers, love you all, and stay tuned!