A standard chemistry laboratory is one having all the essential equipments, apparatuses and instruments like glassware, thermometers, sterilizers, distillation equipment, and so on. For any laboratory owner, it is very essential to find the right supplier of chemistry laboratory equipments. All chemistry lab products need to be handled with great care and hence should be of good quality so that they last for long time and handle harsh situations. That is why it is very essential to get the stuff from established chemistry lab equipment suppliers, who offer both new and refurbished products from leading manufacturers, along with warranties, service contracts, discounts and other benefits.
 

Chemistry Lab Equipment of High Quality: As already mentioned, for a scientist or researcher or any person working in a chemistry lab, high quality chemistry laboratory equipment is needed. These equipments are both durable and safe to use. For instance, the glass bottles used in a chemistry lab, which store chemical solvents and solutes, must be able to store the contents for a long period of time and at the same time should be able to retain their chemical properties. The flammable chemistry laboratory equipment must also be safe to use when exposed to flames. Educational institutes, factories, research centers, in which there is a chemistry lab, these factors are taken into consideration when purchasing chemistry lab equipments. In other words, the lab equipment must be manufactured from quality material. The user should source the product from a lab equipment manufacturer or a supplier who would ensure the the lab equipment offers durability, resilience and ability to withstand chemical reactions and temperature and pressure fluctuations.

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Model organisms are used to study basic mechanisms common to many forms of life and to experiment with biological processes that may be difficult or unethical to study in humans. Model organisms are usually chosen for some combination of ease of study (for example, the transparent bodies of the nematode Caenorhabditis elegans or the zebrafish Brachydanio rerio ), ability to grow and reproduce quickly in a small space ( Arabidopsis thaliana, a four-inch plant with a life cycle of four to six weeks), prominent cell structure.

Scanning electron micrograph of the head of a fruit fly ( Drosophila melanogaster ). of interest (the giant chromosomes of the fruit fly Drosophila melanogaster ), or ability to closely model some aspect of human biology (the mammalian genome and complex brain of the mouse). Most model organisms combine many if not all of these characteristics.

Escherichia coli bacteria provide an especially important model for studies of gene regulation. Yeast ( Saccharomyces cerevisiae ) are used for a wide variety of studies in eukaryotic chromosome structure and gene regulation, as well as virtually every aspect of cell function, including the control of the cell cycle and signal transduction . The slime mold Dictyostelium discoideum is used to study cell motility and other aspects of cell function, especially those with applications to cancer. C. elegans has provided a window on the fate of individual cells during development, as each cell can be followed as it is formed, takes its place, and begins to function.

Drosophila is central in the study of chromosomes and molecular aspects of development, especially development of the nervous system. Zebrafish and the frog Xenopus laevis are used most often to study vertebrate development. Arabidopsis is the major model of plant cell biology and genetics. Finally, cultures of human cells are often used to examine response to drugs, effects of genetic mutations, and other aspects of health and disease.

The genomes of each of these organisms are either fully sequenced or soon will be, allowing further investigation of the links between gene expression and cell function. This will make these models even more valuable, and also allow investigation of fundamental questions about the similarities and differences among all types of organisms.

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An analysis of the metabolic profile of a rat model of chronic pain has identified novel dysregulated metabolites that may underlie the condition, according to a study published today (January 22) in Nature Chemical Biology. If the results hold up in humans, one of these metabolites, which has not previously been associated with neuropathic pain, could potentially serve as both a molecular indicator of and therapeutic target for the condition, for which few treatment options exist.

The findings are “a great example of how metabolomics is leading to novel insights into, in this case pain, and how that’s mediated,” said Lloyd Sumner, a metabolomics researcher at the Samuel Roberts Noble Foundation who was not involved in the research.

In the United States, more than 30 percent of adults suffer from chronic pain of one form or another. Neuropathic pain is a form of chronic pain induced by previous nerve damage, like the phantom pain felt by those who have lost limbs. “Neuropathic pain is the worst,” because it’s the hardest to treat, said Gary Patti, an assistant professor at Washington University in St. Louis and lead author of the study. “It is a disease with an unmet medical need.”

While a research associate at the Scripps Research Institute in La Jolla, California, Patti and his then-research advisor, Gary Siuzdak, senior director of the Center for Metabolomics and Mass Spectrometry and professor of Chemistry and Molecular Biology at Scripps, used an animal model of the condition, in which rats are subjected to tibial nerve transection (TNT)—that is, the tibial nerve in one leg is severed and allowed to heal. Three weeks later, these animals apparently continue to experience pain, though the wound itself has healed.

Rather than studying the genes involved, or the proteins they encode, the researchers identified instead potential metabolic players in this response. Metabolites, after all, are the ultimate molecular arbiters of biological function, the molecules upon which proteins often act.

The team used an approach called untargeted metabolomics to profile the metabolites at the site of injury, the neural cell body of the damaged nerve, the dorsal horn (where the damaged nerve connects to the spinal cord), , and in the blood. It was essentially a molecular fishing expedition—collecting boatloads of data that can point to molecules that may be involved.

“We are seeing many more metabolites than can be accounted for by the canonical pathways in biochemistry textbooks,” Patti said. “The untargeted approach allows us to explore that space.”

In total, the team observed some 733 mass spectrometric peaks whose levels varied at least 2-fold between control and TNT animals. The vast majority of them were localized not at the site of injury, but at the dorsal horn of the spinal cord. In particular, the researchers noticed differential expression of several members of the sphingomyelin-ceramide pathway, a lipid metabolic pathway linked to, among other things, myelin formation and programmed cell death. “That screamed at us that this pathway was important,” Siuzdak said.

The team then tested these different molecules directly to see whether they could induce a pain response on their own. Indeed, one such metabolite, called N,N-dimethylsphingosine (DMS),  induced symptoms akin to neuropathic pain when injected directly into the animals at comparable concentrations to those found in TNT rats a few weeks after injury. The authors also determined that DMS may function by activating astrocytes, inducing them to release cytokines such as IL-1beta and MCP-1, both of which are associated with inflammation and pain.

If validated in humans, DMS could potentially serve as a biomarker of for neuropathic pain, Sumner said. Furthermore, “by defining specific molecules involved in the pain response, [the finding] also provides a pathway for mediating the pain management,” he added. “If they can mediate how those molecules are made and modify that with inhibitors or other medications, then the opportunity for pain management is substantial.”

Indeed, Siuzdak calls his approach “therapeutic metabolomics.” “You survey the pathways, find molecules that are dysregulated, and then find enzymes that produce those molecules. We are currently trying to figure out explicitly what enzyme produces DMS, because that’s a much more specific target.”

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More than 500 million years ago, single-celled organisms on Earth's surface began forming multi-cellular clusters that ultimately became plants and animals. Just how that happened is a question that has eluded evolutionary biologists.
 
Now scientists have replicated that key step in the laboratory using common Brewer's yeast, a single-celled organism.  The yeast "evolved" into multi-cellular clusters that work together cooperatively, reproduce and adapt to their environment - in essence, they became precursors to life on Earth as it is today.  The results are published in this week's issue of the journal Proceedings of the National Academy of Sciences (PNAS).
 
"The finding that the division-of-labour evolves so quickly and repeatedly in these 'snowflake' clusters is a big surprise," says George Gilchrist, acting deputy division director of the National Science Foundation's (NSF) Division of Environmental Biology, which funded the research.
 
"The first step toward multi-cellular complexity seems to be less of an evolutionary hurdle than theory would suggest," says Gilchrist. "This will stimulate a lot of important research questions."
 
It all started two years ago with a casual comment over coffee that bridging the famous multi-cellularity gap would be "just about the coolest thing we could do," recalled Will Ratcliff and Michael Travisano, scientists at the University of Minnesota (UMN) and authors of the PNAS paper.
 
Other authors of the paper are Ford Denison and Mark Borrello of UMN.  Then came the big surprise: it wasn't that difficult.  Using yeast cells, culture media and a centrifuge, it only took the biologists one experiment conducted over about 60 days.
 
"I don't think anyone had ever tried it before," says Ratcliff. "There aren't many scientists doing experimental evolution, and they're trying to answer questions about evolution, not recreate it."
 
The results have earned praise from evolutionary biologists around the world.  "To understand why the world is full of plants and animals, including humans, we need to know how one-celled organisms made the switch to living as a group, as multi-celled organisms," says Sam Scheiner, program director in NSF's Division of Environmental Biology.
 
"This study is the first to experimentally observe that transition," says Scheiner, "providing a look at an event that took place hundreds of millions of years ago."
 
In essence, here's how the experiments worked:
 
The scientists chose Brewer's yeast, or Saccharomyces cerevisiae, a species of yeast used since ancient times to make bread and beer because it is abundant in nature and grows easily.
 
They added it to nutrient-rich culture media and allowed the cells to grow for a day in test tubes.
 
Then they used a centrifuge to stratify the contents by weight.
 
As the mixture settled, cell clusters landed on the bottom of the tubes faster because they are heavier. The biologists removed the clusters, transferred them to fresh media, and agitated them again.
 
Sixty cycles later, the clusters - now hundreds of cells - looked like spherical snowflakes.
 
Analysis showed that the clusters were not just groups of random cells that adhered to each other, but related cells that remained attached following cell division.
 
That was significant because it meant that they were genetically similar, which promotes cooperation. When the clusters reached a critical size, some cells died off in a process known as apoptosis to allow offspring to separate.
 
The offspring reproduced only after they attained the size of their parents.
 
"A cluster alone isn't multi-cellular," Ratcliff says. "But when cells in a cluster cooperate, make sacrifices for the common good, and adapt to change, that's an evolutionary transition to multi-cellularity."
 
In order for multi-cellular organisms to form, most cells need to sacrifice their ability to reproduce, an altruistic action that favors the whole but not the individual, Ratcliff says.
 
For example, all cells in the human body are essentially a support system that allows sperm and eggs to pass DNA along to the next generation.
 
Thus multi-cellularity is by its nature very cooperative.  "Some of the best competitors in nature are those that engage in cooperation, and our experiment bears that out," says Travisano.  Evolutionary biologists have estimated that multi-cellularity evolved independently in about 25 groups.  Travisano and Ratcliff wonder why it didn't evolve more often since it's not that difficult to recreate in a lab.
 
Considering that trillions of one-celled organisms lived on Earth for millions of years, it seems like it should have, Ratcliff says.  That may be a question the biologists will answer in the future using the fossil record for thousands of generations of multi-cellular clusters, which are stored in a freezer in Travisano's lab.
 
Since the frozen samples contain multiple cell lines that independently became multi-cellular, the researchers can compare them to learn whether similar or different mechanisms and genes were responsible in each case, Travisano says.
 
The next steps will be to look at the role of multi-cellularity in cancer, aging and other critical areas of biology.  "Multi-cellular yeast is a valuable resource for investigating a wide variety of medically and biologically important topics," Travisano says.
 
"Cancer was recently described as a fossil from the origin of multi-cellularity, which can be directly investigated with the yeast system.  "Similarly the origins of aging, development and the evolution of complex morphologies are open to direct experimental investigation that would otherwise be difficult or impossible."

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The origin of multicellular life is one of the most important milestones in earth's history. And despite it happening independently nearly two dozen times in the past, very little is known about the way the initial evolution from unicellular to multicellular life had taken place. This is because these transitions occurred some 200 million years ago.

Short time
Contrary to the general perception that this important transition was challenging, and took a long time to happen, scientists have experimentally proved the ease with which this can take place. They achieved the transition in a yeast species in very short span of time — 60 days.

The multicellular yeast showed many key characteristics of a truly many-celled organism. “The first crucial steps in the transition [can take place] remarkably quickly under an appropriate selective condition,” the scientists write in their paper published recently in the Proceedings of the National Academy of Sciences.

Organisms, both unicellular and multicellular, have to adapt to changing conditions like temperature, pressure, nutrient supply, oxygen content etc to survive. For instance, failure to adapt to changing climatic conditions resulted in the extinction of dinosaurs.

Selection pressure
In this case, the scientists used gravity as a selection pressure as it was easy to observe, study and replicate in a lab using test tubes. Such a selection pressure is however not seen in nature. They used gravity to select for primitive multicellularity by allowing clusters of unicellular yeast to settle at the bottom. Clustering yeast settles faster than single cells, and bigger clusters settle faster than smaller clusters.

At the end of the day, those clusters that had settled at the bottom were separated and transferred to a new test tube. After repeating the cycle for two weeks, the researchers could see yeast forming into snowflake-like clusters.

Clusters do tend to form in nature by adhesion of cells. While cells in such clusters are genetically distinct, the clusters formed in the lab were found to be genetically identical. Genetically identical cells in a cluster could have formed only by division of mother cells into daughter cells.

Proof of division
The proof that the clusters were formed by the division of individual cells came through 16 hours of microscopic examination for growth. Cells taken from the clusters proved their hallmark characteristic — each cell giving “rise to a new snowflake-like cluster [cell].”

Cells did not divide at random. While cells in the juvenile stage grew rapidly to multiple cells, and hence helped in increasing the size of the cluster, the fully-grown adult stage was marked by division of the matured cells into daughter cells. The presence of both juvenile and adult stages is a mark of true multicellularity.

The fact that single-celled yeast “sacrifices” its ability to reproduce for the good of a collection of cells makes the transition very challenging. It goes against the grain of Darwinian principles.

The scientists also investigated the most vital and crucial question that has been dogging science — transition from unicellular to multicellular life. The most important difference between unicellular and multicellular life lies in the size of the daughter cells. While unicellular yeast divides into two daughter cells of similar size as the parent cell, the daughter cells of multicellular yeast “were consistently half the size of their parental clusters [cells].”

Division of labour
Division of labour between individual cells — another important characteristic of higher order organisms — was seen in the yeast snowflakes. Such is the importance of this characteristic that higher-order organisms have clearly demarcated functions carried out by a specific set of cells. In fact, as the authors write, “cellular differentiation is a hallmark of complex multicellularity.”

Apoptosis
Similarly, apoptosis or programmed cell death (where old cells die after a point of time) was witnessed. Though apoptosis is seen even in single-celled yeast and other species, the end purpose of apoptosis witnessed in snowflakes was quite different.

It was in response to selective pressure — apoptotic cells breaking off from the snowflakes and allowing the rest of the flake to produce greater number of cells within a given time. Bigger clusters settle faster at the bottom and hence become eligible for repeated studies.

For instance, apoptosis had evolved so quickly between selection 14 and 60 that the snowflakes at selection 60 were much bigger than that of at 14. This kind of apoptosis has never before been seen in unicellular yeast.

All these characteristics seen in the snowflakes “demonstrate that multicellular traits readily evolve as a consequence of among-group selection [selective pressure],” the researchers write.

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In as little as 100 generations, yeast selected to settle more quickly through a test tube evolved into multicellular, snowflake-like clusters, according to a paper published today (January 16) in Proceedings of the National Academy of Sciences. Over the course of the experiment, the clusters evolved to be larger, produce multicellular progeny, and even show differentiation of the cells within the cluster—all key characteristics of multicellular organisms.

“It’s very cool to demonstrate that [multicellularity] can happen so quickly,” said evolutionary biologist Mansi Srivastava of the Whitehead Institute for Biomedical Research in Massachusetts, who was not involved in the research. “Looking at the fossil record, we learned it took a very long time whenever these different transitions to multicellularity happened. Here they show it can happen very quickly.”

“[The study] was provocative,” agreed biochemist Todd Miller of Stony Brook University in New York, who did not participate in the work. “It’s a different way of attacking the problem [of how multicellularity evolved]—coming from a simple system that doesn’t normally do this and seeing what it takes to make it do it.”

The evolution of multicellular life has long intrigued evolutionary biologists. Cells coming together and cooperating for the good of the group goes against basic Darwinian principles. Yet multicellularity has evolved some two dozen times independently in nature, and has shaped the world as we know it.

But because most transitions to multicellularity happened more than 200 million years ago, many questions remain about how it happened. What were the ecological conditions that drove the transitions? And how did organisms overcome the conflicts of interest that accompany any sort of cooperative effort?

To gain a better understanding of the initial leap from singularity, University of Minnesota evolutionary biologist Michael Travisano, his postdoc Will Ratcliff, and their colleagues decided to see if they could recreate such a transition in the lab. Their strategy was simple: grow yeast in test tubes, shake up those test tubes every 24 hours, and select those organisms that fell to the bottom quickest to transfer to new media and propagate the population. After 2 weeks and about 100 generations, the researchers began to see the yeast forming snowflake-like clusters that dropped to the bottom of the test tubes 34 percent faster than single cells.

“We went to the microscope and were blown away,” Ratcliff said. “They form these clusters, and these clusters have these emergent properties of multicellular life.”

The clusters continued to evolve over the course of the experiment, growing larger and asexually producing multicellular progeny. The yeast showed signs of having juvenile and adult life stages—only producing progeny once the cluster reached a certain size. They even evolved a kind of division of labor among the cells of the cluster, with certain yeast cells more readily undergoing apoptosis. Those apoptotic cells sacrificed their own reproductive output, but seemed to aid the reproduction of the entire cluster by allowing smaller cluster progeny to break off from the parent.

These results indicate that the clusters, not the individual cells, were the unit of selection—“the key evolutionary step in how you get multicellularity evolving,” Ratcliff said.

But this is just one experiment under admittedly contrived conditions. “What remains to be seen for me is how relevant is it to actual transitions to multicellularity,” said Srivastava.

Indeed, the authors of the PNAS study admit that selecting for yeast cells or clusters that settled most quickly isn’t exactly a “natural” selection pressure. But there could be some important lessons here, Ratcliff insisted. “If we really understand the way that multicellularity can evolve, then that gives us a lot of insight to how this could have occurred in the past,” he said.

The clusters, for example, were all the result of incomplete cell division—daughter cells sticking to their parent cells. A similar result was recently found in choanoflagellates, the closest single-celled relatives of animals, suggesting that post-division adhesion may be an important mechanism for the initial leap to multicellularity. In contrast to aggregation—mechanisms of multicellular formation in slime molds and biofilms—cells that adhere following division are all highly related, which may help reduce within-cluster conflict.

The question now is what molecules and genes underlie such changes. “Were there any changes in expression of signaling genes after they selected the snowflakes?” Miller asked. Additionally, “it would be really cool to look at what the underlying genetic changes were that led to these [multicellular phenotypes],” added Srivastava.

Indeed, Ratcliff and his colleagues have already sequenced the common ancestor of their snowflake yeast populations, as well as several independently evolved cluster lines, and are working to analyze and publish that data.

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NEW YORK — Scientists say they've identified the first genetic mutation with a major effect on the risk of prostate cancer that runs in families and strikes men early, by age 55. The mutation accounts for only about 1 per cent of all prostate cancers. But studying it might help scientists understand the disease in general and find better treatments.

More than 240,000 men are expected to be diagnosed with prostate cancer in the United States this year. Most cases are sporadic rather than inherited, and on average they are diagnosed around age 70. The work is reported in Thursday's issue of the New England Journal of Medicine. The researchers said inheriting the mutation raises the risk of prostate cancer by 10 times or more.

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Massachusetts General Hospital (MGH) investigators have developed a novel strategy to protect the liver from drug-induced injury and improve associated drug safety. In their report receiving advance online publication in the journal Nature Biotechnology, the team reports that inhibition of a type of cell-to-cell communication can protect against the damage caused by liver-toxic drugs such as acetaminophen.

"Our findings suggest that this therapy could be a clinically viable strategy for treating patients with drug-induced liver injury," says Suraj Patel, PhD, of the MGH Department of Surgery, the paper's lead author. "This work also has the potential to change the way drugs are developed and formulated, which could improve drug safety by providing medications with reduced risk of liver toxicity."

Developing, approving and prescribing a drug requires that the therapeutic benefits be weighed against any potential toxicities. Liver toxicity limits the development of many therapeutic compounds and presents major challenges to both clinical medicine and to the pharmaceutical industry. Drug-induced liver injury is the most common cause of acute liver failure in the U.S. and is also the most frequent reason for abandoning drugs early in development or withdrawing them from the market. Since no pharmaceutical strategies currently exist for preventing drug-induced liver injury, treatment options are limited to discontinuing the offending drug, supportive care and transplantation for end-stage liver failure.

Gap junctions are hollow channels that connect neighboring cells and allow direct intercellular communication between coupled cells. In the heart, gap junctions are known to propagate the electrical activity required for contraction, but their role in the liver is poorly defined. Recent work by the MGH team and others has shown that assemblies of intercellular gap junctions spread immune signals from injured liver cells to surrounding undamaged cells, amplifying overall inflammation and injury. The current study was designed to discover the potential of targeting liver-specific gap junctions to limit drug-induced liver injury.

The researchers first used a strain of genetically mutated mice that lack a particular liver-specific gap junction. The mice were administered various liver-toxic drugs, such as the commonly used medicine acetaminophen. Overdoses of acetaminophen, which is best known under the brand name Tylenol, are the most frequent cause of drug-induced liver injury. Compared to normal mice, those lacking liver gap junctions were protected against liver damage, inflammation and death caused by administration of liver-toxic drugs.

The team then identified a small-molecule inhibitor of liver gap junctions that, when given with or even after the toxic drugs, protected the livers of normal mice against any injury and prevented their death. Additionally, cell culture experiments indicated that blocking gap junctions limited the spread through liver cells of damaging free radicals and oxidative stress, suggesting a possible mechanism for the observed protection.

"This finding is very exciting and potentially very powerful from a number of basic science and clinical application standpoints, which we are continuing to explore," says Martin Yarmush, MD, PhD, director of the MGH Center for Engineering in Medicine and senior author of the study. "However, before we can think about applying this approach to patients, we need to know more about any off-target effects of these gap junction inhibitors and better understand the long-term ramifications of temporarily blocking liver-specific gap junction channels."

A patent related to the work has been filed by Partners Healthcare, and an early stage biotechnology company, Heprotech Inc., was recently established to develop this new technology further. "The findings from this work suggest a novel drug development strategy in which therapeutically effective but potentially liver-toxic compounds could be co-formulated with selective gap junction inhibitors to improve their safety," explains Patel, a co-founder of Heprotech along with Yarmush. "We look forward to helping commercialize this new technology, with the ultimate goal of developing liver-safe pharmaceuticals and better treatments for drug-induced liver injury."

Patel is a research fellow in the MGH Department of Surgery and Yarmush is a faculty member in the Harvard-MIT Division of Health Science. Additional co-authors of the study are Jack Milwid, PhD, Kevin King, MD, PhD, Stefan Bohr, MD, PhD, Arvin Iracheta-Vellve, Matthew Li, Antonia Vitalo, Biju Parekkadan, PhD, and Rohit Jindal, PhD, all with the MGH Center for Engineering in Medicine. The work was supported by grants from the National Institutes of Health and Shriners Hospitals for Children.

Massachusetts General Hospital (www.massgeneral.org), founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $750 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.

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Investigators in the Massachusetts General Hospital (MGH) Center for Systems Biology have discovered a previously unknown type of immune cell, a B cell that can produce the important growth factor GM-CSF, which stimulates many other immune cells. They also found that these novel cells may help protect against the overwhelming, life-threatening immune reaction known as sepsis.

"B cells are a family of white blood cells that secrete antibodies, and GM-CSF induces the production or activation of granulocytes and macrophages, other white blood cells that have specific roles in the immune system," says Filip Swirski, PhD, of the MGH Center for Systems Biology, senior author of the report that is to be published in the journal Science and is receiving advance release on the Science Express website. "Our findings are surprising not only because B cells were not previously known to produce GM-CSF in vivo but also because they indicate these novel cells initiate an important immune response."

As part of a separate investigation, Swirski and his team analyzed production of GM-CSF (granulocyte macrophage colony-stimulating factor) in tissue from several important organs. They were surprised to find that application of a bacterial molecule known to produce a powerful immune response induced GM-CSF production by what turned out to be a previously unknown family of B cells in the spleen. Because GM-CSF is known to activate white blood cells as part of the innate immune response – the body's first line defence against pathogens – the novel cells were named innate response activator (IRA) B cells.

The researchers went on to identify distinguishing characteristics of IRA-B cells, including gene expression patterns not seen in other B cells. They also determined that IRA-B cells derive from B cells known as B1a B cells. These IRA-B cell precursors originally reside in the peritoneal cavity but, after detecting the presence of invading bacteria, travel to the spleen or bone marrow where they differentiate into IRA-B cells that can either produce antibodies or release GM-CSF.

"While the IRA-B cell shares many attributes with other B cells, it is unique in its involvement with GM-CSF production," explains Clinton Robbins, PhD, co-lead author of the Science article. "Instead of the classic way that B cells recognize antigens, B1a B cells produce IRA-B cells after recognizing bacteria via a type of receptor known to be involved in the first steps of inflammation. The IRA-B cell, therefore, appears to be an early orchestrator of the immune system."

To test the potential role of IRA-B cells in sepsis, the researchers developed a mouse model in which B cells were totally unable to produce GM-CSF, preventing the generation of IRA-B cells. Those mice were unable to mount a defense against induced sepsis and died much earlier and in greater numbers than did control animals. Inflammatory markers in the infected mice lacking IRA-B cells suggested a defect in the ability to clear bacteria.

"We think that IRA-B cells sound a distress call when they deliver GM-CSF to the spleen, an organ where cells known to be important to the recognition and clearance of bacteria reside," explains Swirski, an immunologist who is an assistant professor of Radiology at Harvard Medical School. "Sepsis is an immunological conundrum. On the one hand it results from failure of the immune system to control infection. On the other hand, immune cells that do respond inflict damage and contribute to complications such as leakage of blood vessel walls and septic shock. Striking a balance between controlling infection and controlling inflammation is a major therapeutic goal, and we believe the IRA-B cell is a critical, previously unrecognized component in that balance."

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"A Universe From Nothing: Why There Is Something Rather Than Nothing" (Free Press), by Lawrence M. Krauss: In fall 2009, the theoretical physicist Lawrence M. Krauss gave a talk about recent discoveries in cosmology that he engagingly titled, "A Universe From Nothing: Why There Is Something Rather Than Nothing."

The popularity of the video, viewed nearly a million times on YouTube, prompted Krauss to develop the ideas in the talk into this short, elegant account of the origins of our universe and its likely demise trillions of years from now.

The best-selling author of "The Physics of Star Trek," Krauss possesses a rare talent for making the hardest ideas in astrophysics accessible to the layman, due in part to his sly humor. In another universe, Krauss could have been a stand-up comedian.

Indeed, the evolutionary biologist Richard Dawkins, who contributes an afterword to the book, dubs his friend the "Woody Allen of cosmology." One favorite joke involves Edwin Hubble, whose life story, Krauss deadpans, bolsters his faith in humanity "because he started out as a lawyer and then became an astronomer."

In just under 200 pages, Krauss walks us through a hundred years of mind-bending breakthroughs in astrophysics, which have led scientists to the inescapable conclusion that our universe sprang out of nothing — "without design, intent or purpose" — and is destined to return to that bleak, cold, dark space.

A professor at Arizona State University, Krauss clearly relishes his iconoclastic role, gleefully demolishing all theories of creation that require a creator — that is, most religions. In the early 2000s, when he was teaching physics at Case Western Reserve University, he very publicly took on creationists in a fight over the science curriculum in Ohio public schools.

But one has to hope that this book won't appeal only to the partisans of the culture wars — it's just too good and interesting for that. Krauss is genuinely in awe of the "wondrously strange" nature of our physical world, and his enthusiasm is infectious.

Here he is explaining how every atom in our bodies was forged billions of years ago in the nuclear furnaces of exploding stars: "We are all, literally, star children, and our bodies made of stardust." The book bursts with such poetic conceits.

For Krauss, the prospect of a godless universe is "invigorating," not scary. "It motivates us to draw meaning from our own actions," he writes, "and to make the most of our brief existence in the sun."

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