Amazing Science
675.5K views | +706 today
Amazing Science
Amazing science facts - 3D_printing • aging • AI • anthropology • art • astronomy • bigdata • bioinformatics • biology • biotech • chemistry • computers • cosmology • education • environment • evolution • future • genetics • genomics • geosciences • green_energy • history • language • map • material_science • math • med • medicine • microscopy • nanotech • neuroscience • paleontology • photography • photonics • physics • postings • robotics • science • technology • video
Your new post is loading...
Scooped by Dr. Stefan Gruenwald!

Zika anniversary: What has been learned?

Zika anniversary: What has been learned? | Amazing Science |

One year ago, Brazil reported the first laboratory-confirmed cases of Zika. The virus had cropped up elsewhere in a few earlier outbreaks, too, but it didn’t seem all that threatening at the time. Zika symptoms were generally pretty mild — or even nonexistent, the Pan American Health Organization and the World Health Organization reported in an epidemiological alert May 7, 2015. The alert made no mention of pregnant women, babies or microcephaly. In fact, it noted: “Complications (neurological, autoimmune) are rare.”


What a difference a year makes. Now scientists have convincingly tied Zika infection to birth defects, and suspect it’s behind an uptick in neurological disorders in adults, too. But researchers are still figuring out how the virus acts, and how to stop it. A vaccine is in the works, but could take years.


So Zika-fighting tactics have gotten creative. A new billboard in Brazil lures mosquitoes in with spritzes of humanlike scent, and then traps them inside a chamber to die. (It kills hundreds of mosquitoes a day, the billboard’s makers tout, but scientists have yet to weigh in.) Researchers have recently explored other methods to rein in Zika.


This and more from recent research:

  • The best weapon against Zika may be a mosquito-infecting bacteria. Mosquitoes harboringWolbachia pipientis resisted infection from two strains of Zika virus circulating in Brazil, researchers report May 4 in Cell Host & Microbe. And if Wolbachia-carrying mosquitoes do get infected, they’re less likely to transmit the virus. Releasing these mosquitoes in the wild could help halt Zika’s spread
  • An antimalarial drug called chloroquine could also work against Zika. When added to human brain cells and mouse minibrains in the lab, the drug helped prevent Zika infection. It also kept minibrains looking somewhat healthy, researchers report May 2 at Chloroquine is a promising candidate for clinical trials, the authors write, because it’s safe for use in pregnant women.
  • Zika kills brain cells by cranking up production of a protein that triggers cellular self-destruction, researchers report May 6 in Cell Stem Cell. Scientists knew that infection with the virus could kill cells, shrinking minibrains grown in the lab, but until now, they didn’t understand how. The protein, an immune molecule called TLR3, could act as a target for therapies.
  • A new paper-based Zika test could offer doctors a quick and easy way to detect the virus. The test senses Zika RNA and can differentiate between African and American strains, scientists report May 6 in Cell. Though still in the proof-of-concept stage, the test was able to confirm Zika’s presence in samples from an infected macaque. The news comes on the heels of the FDA’s recent approval of a commercial test for Zika.
No comment yet.
Scooped by Dr. Stefan Gruenwald!

Why are carrots orange? Genome sequencing gives clues

Why are carrots orange? Genome sequencing gives clues | Amazing Science |
The humble supermarket carrot owes its deep orange colour to a newly-found gene, according to an analysis of the full carrot genome.


Carrots are members of the Apiaceae family of plants, which include celery, parsley, fennel, coriander, dill and parsnip. They are related to crops in the sunflower, artichoke and lettuce — the latter which it split from about 72 million years ago. Historically, carrots had small white roots with a woody interior. They most likely came from areas of Iran and Afghanistan, where they still grow today.


Initially they were grown for their aromatic leaves, but over hundreds of years farmers turned a naturally occurring subspecies of the carrot into a larger, less woody root. Domesticated yellow and purple carrots were found in Central Asia around 1,000 years ago, and an orange version emerged in late 16th century Holland, most probably from crossing yellow carrots with purple ones.


By using NGS technologies, researchers sequenced the genomes of 35 different carrot specimens and subspecies, both wild and cultivated, in an attempt to understand how carrots evolved into those we find in our fridge. They found a gene responsible for the high concentration of beta-carotene in the orange carrot taproot. They also identified more than 32,000 genes in a typical orange carrot.


The genome could help breed carrots that have high levels of beta-carotene and are pest resistant.

No comment yet.
Scooped by Dr. Stefan Gruenwald!

The octopus genome and the evolution of cephalopod neural and morphological novelties

The octopus genome and the evolution of cephalopod neural and morphological novelties | Amazing Science |

Coleoid cephalopods (octopus, squid and cuttlefish) are active, resourceful predators with a rich behavioural repertoire. They have the largest nervous systems among the invertebrates and present other striking morphological innovations including camera-like eyes, prehensile arms, a highly derived early embryogenesis and a remarkably sophisticated adaptive colouration system. To investigate the molecular bases of cephalopod brain and body innovations, a group of scientists now sequenced the genome and multiple transcriptomes of the California two-spot octopus, Octopus bimaculoides. They found no evidence for hypothesized whole-genome duplications in the octopus lineage. The core developmental and neuronal gene repertoire of the octopus is broadly similar to that found across invertebrate bilaterians, except for massive expansions in two gene families previously thought to be uniquely enlarged in vertebrates: the protocadherins, which regulate neuronal development, and the C2H2 superfamily of zinc-finger transcription factors.


Extensive messenger RNA editing generates transcript and protein diversity in genes involved in neural excitability, as previously described, as well as in genes participating in a broad range of other cellular functions. The researchers identified hundreds of cephalopod-specific genes, many of which showed elevated expression levels in such specialized structures as the skin, the suckers and the nervous system. They also found evidence for large-scale genomic rearrangements that are closely associated with transposable element expansions.


In summary, the present analysis suggests that substantial expansion of a handful of gene families, along with extensive remodelling of genome linkage and repetitive content, played a critical role in the evolution of cephalopod morphological innovations, including their large and complex nervous systems.

No comment yet.
Scooped by Dr. Stefan Gruenwald!

Astrobiologists Make List of Biosignature Gases to Guide Search for Extraterrestrial Life

Astrobiologists Make List of Biosignature Gases to Guide Search for Extraterrestrial Life | Amazing Science |

“Thousands of exoplanets are known to orbit nearby stars. Plans for the next generation of space-based and ground-based telescopes are fueling the anticipation that a precious few habitable planets can be identified in the coming decade,” Prof. Seager and her colleagues explained.


“Even more highly anticipated is the chance to find signs of life on these habitable planets by way of biosignature gases.”

The team proposes that all stable and potential volatile molecules should be considered as possible biosignature gases.


In their paper published online in the journal Astrobiology, Prof. Seager and co-authors laid the groundwork for identifying such gases by conducting a massive search for molecules with six or fewer non-hydrogen atoms. “To maximize our chances of recognizing biosignature gases, we promote the concept that all stable and potentially volatile molecules should initially be considered as viable biosignature gases,” they said. “We present a new approach to the subject of biosignature gases by systematically constructing lists of volatile molecules in different categories.”


“An exhaustive list up to six non-H atoms is presented, totaling about 14,000 molecules. About 2,500 of these are CNOPSH (C – carbon, N – nitrogen, O – oxygen, P – phosphorus, S – sulfur, and H – hydrogen) compounds.”


The team also describes how this list can help enhance our understanding of the limits of biochemistry on Earth. “This work reminds me of Darwin’s voyage aboard The Beagle, exploring the vast diversity of life by sailing around the world,” said Dr. Nancy Kiang, Senior Editor of the journal Astrobiology and a scientist at NASA’s Goddard Institute for Space Studies.

No comment yet.
Rescooped by Dr. Stefan Gruenwald from Gaia Diary!

This Deep Sea Jellyfish Looks Like It Came From Outer Space

This Deep Sea Jellyfish Looks Like It Came From Outer Space | Amazing Science |

Researchers working near the Mariana Trench have captured footage of a jellyfish that boggles the imagination.


Researchers working on the NOAA’s ship Okeanos Explorerdispatched their remotely operated vehicle Deep Discoverer to the Enigma Seamount, a ridge located just west of the Mariana Trench. At a depth of 2.3 miles (3.7 km), it managed to capture video of this rather remarkable jellyfish.

Via Mariaschnee
No comment yet.
Rescooped by Dr. Stefan Gruenwald from Fragments of Science!

Immune cells glue broken blood vessels back together

Immune cells glue broken blood vessels back together | Amazing Science |

"As we age, tiny blood vessels in the brain stiffen and sometimes rupture, causing "microbleeds." This damage has been associated with neurodegenerative diseases and cognitive decline, but whether the brain can naturally repair itself beyond growing new blood-vessel tissue has been unknown.  


A zebrafish study published on May 3 in Immunity describes for the first time how white blood cells called macrophages can grab the broken ends of a blood vessel and stick them back together. "

Via Mariaschnee
ANDREAS SOFRONIOU's curator insight, May 5, 1:02 AM
Watch immune cells 'glue' broken blood vessels back together
Scooped by Dr. Stefan Gruenwald!

Modular proteins can be used to track or manipulate RNA inside living cells

Modular proteins can be used to track or manipulate RNA inside living cells | Amazing Science |

MIT researchers have devised a new set of proteins that can be customized to bind arbitrary RNA sequences, making it possible to image RNA inside living cells, monitor what a particular RNA strand is doing, and even control RNA activity. The new strategy is based on human RNA-binding proteins that normally help guide embryonic development. The research team adapted the proteins so that they can be easily targeted to desired RNA sequences. “You could use these proteins to do measurements of RNA generation, for example, or of the translation of RNA to proteins,” says Edward Boyden, an associate professor of biological engineering and brain and cognitive sciences at the MIT Media Lab. “This could have broad utility throughout biology and bioengineering.”


Unlike previous efforts to control RNA with proteins, the new MIT system consists of modular components, which the researchers believe will make it easier to perform a wide variety of RNA manipulations. “Modularity is one of the core design principles of engineering. If you can make things out of repeatable parts, you don’t have to agonize over the design. You simply build things out of predictable, linkable units,” says Boyden, who is also a member of MIT’s McGovern Institute for Brain Research.


Boyden is the senior author of a paper describing the new system in the Proceedings of the National Academy of Sciences. The paper’s lead authors are postdoc Katarzyna Adamala and grad student Daniel Martin-Alarcon.


Living cells contain many types of RNA that perform different roles. One of the best known varieties is messenger RNA (mRNA), which is copied from DNA and carries protein-coding information to cell structures called ribosomes, where mRNA directs protein assembly in a process called translation. Monitoring mRNA could tell scientists a great deal about which genes are being expressed in a cell, and tweaking the translation of mRNA would allow them to alter gene expression without having to modify the cell’s DNA.


To achieve this, the MIT team set out to adapt naturally occurring proteins called Pumilio homology domains. These RNA-binding proteins include sequences of amino acids that bind to one of the ribonucleotide bases that make up RNA. In recent years, scientists have been working on developing these proteins for experimental use, but until now it was more of a trial-and-error process to create proteins that would bind to a particular RNA sequence.


“It was not a truly modular code,” Boyden says, referring to the protein’s amino acid sequences. “You still had to tweak it on a case-by-case basis. Whereas now, given an RNA sequence, you can specify on paper a protein to target it.”


To create their code, the researchers tested out many amino acid combinations and found a particular set of amino acids that will bind each of the four bases at any position in the target sequence. Using this system, which they call Pumby (for Pumilio-based assembly), the researchers effectively targeted RNA sequences varying in length from six to 18 bases.


“I think it’s a breakthrough technology that they’ve developed here,” says Robert Singer, a professor of anatomy and structural biology, cell biology, and neuroscience at Albert Einstein College of Medicine, who was not involved in the research. “Everything that’s been done to target RNA so far requires modifying the RNA you want to target by attaching a sequence that binds to a specific protein. With this technique you just design the protein alone, so there’s no need to modify the RNA, which means you could target any RNA in any cell.”

No comment yet.
Scooped by Dr. Stefan Gruenwald!

Virus trading cards

Virus trading cards | Amazing Science |

Viruses are surprisingly symmetrical, and each trading card shows the structure of the viral capsid - the protein shell protecting the genetic material inside a virus. To make the 3D animations I used UCSF Chimera, a free molecular modeling program. When scientists discover a new protein structure they upload it to the worldwide Protein Data Bank. Each entry is assigned a unique ID number, which you can use to call up the structure in programs like Chimera or PyMol.

Use Tom Goddard’s tutorial to learn how to display viral capsids, and it’s actually a fairly simple process. You can even 3D print structures straight from Chimera.


Molecular Modeling: Molecular graphics and analyses were performed with the UCSF Chimera package. Chimera is developed by the Resource for Biocomputing, Visualization, and Informatics at the University of California, San Francisco (supported by NIGMS P41-GM103311).

No comment yet.
Scooped by Dr. Stefan Gruenwald!

How EVE Online's Project Discovery is remapping human biology

How EVE Online's Project Discovery is remapping human biology | Amazing Science |

EVE Online isn't just a game about internet spaceships and sci-fi politics. Since March, developer CCP Games has been running Project Discovery – an initiative to help improve scientific understanding of the human body at the tiniest levels. Run in conjunction with the Human Protein Atlas and Massively Multiplayer Online Science, the project taps into EVE Online's greatest resource – its player base – to help categorise millions of proteins.


"We show them an image, and they can change the colour of it, putting green or red dyes on it to help them analyse it a little bit better," Linzi Campbell, game designer on Project Discovery, tells WIRED. "Then we also show them examples – cytoplasm is their favourite one! We show them what each of the different images should look like, and just get them to pick a few that they identify within the image. The identifications are scrambled each time, so it's not as simple as going 'ok, every time I just pick the one on the right' – they have to really think about it."


The analysis project is worked into EVE Online as a minigame, and works within the context of the game's lore. "We have this NPC organisation called the Drifters – they're like a mysterious entity in New Eden [EVE's interplanetary setting]," Campbell explains. "The players don't know an awful lot about the Drifters at the minute, so we disguised it within the universe as Drifter DNA that they were analysing. I think it just fit perfectly. We branded this as [research being done by] the Sisters of Eve, and they're analysing this Drifter DNA." 


The response has been tremendous. "We've had an amazing number of classifications, way over our greatest expectations," says Emma Lundberg, associate professor at the Human Protein Atlas. "Right now, after six weeks, we've had almost eight million classifications, and the players spent 16.2 million minutes playing the minigame. When we did the math, that translated – in Swedish measures – to 163 working years. It's crazy."


"We had a little guess, internally. We said if we get 40,000+ classifications a day, we're happy. If we get 100,000 per day, then we're amazed," Lundberg adds. "But when it peaked in the beginning, we had 900,000 classifications in one day. Now it's stabilised, but we're still getting around 200,000 a day, so everyone is mind-blown. We never expected it."

No comment yet.
Scooped by Dr. Stefan Gruenwald!

Exosomes - History and Promise

Exosomes - History and Promise | Amazing Science |
It was discovered some time ago that eukaryotic cells regularly secrete such structures as microvesicles, macromolecular complexes, and small molecules into their ambient environment. Exosomes are one of the types of natural nanoparticles (or nanovesicles) that have shown promise in many areas of research, diagnostics and therapy. They are small lipid membrane vesicles (30-120 nm) generated by fusion of cytoplasmic endosomal multivesicular bodies within the cell surface. Exosomes are found throughout the body in such fluids as blood, saliva, urine, and breast milk. Furthermore, all types of cells secrete them in in vitro culture. It is believed that they have many natural functions, including acting as transporters of nucleic acids (mostly RNA), cytosolic proteins and metabolites to many cells, tissues or organs throughout the body. Much remains to be understood regarding how they are formed, as well as of their targeting and ultimate physiological activity. But many don’t realize that some activities have been rather thoroughly demonstrated─ such as their function in some sort of either local or more systemic intercellular communication.
Exosomes as ToolsGeneral interest in exosomes is now growing for many reasons. One is because of the observation of their natural activity with antigen-presenting cells and in immune responses in the body. Their potential as very powerful biomedical tools of both diagnostic and therapeutic value is now being more widely reported. Applications described include using them as immunotherapeutic reagents, vectors of engineered genetic constructs, and vaccine particles. They’ve also been described as tools in the diagnosis or prognosis of a wide variety of disorders, such as cancer and neurodegenerative diseases. Also, their potential in tissue-level microcommunication is driving interest in such therapeutic activities as cardiac repair following heart attacks. Their potential as biomarkers is being explored because their content has been described as a “fingerprint” of differentiation or signaling or regulation status of the cell generating them. For example, by monitoring the exosomes secreted by transplanted cells, one may be able to predict the status or potentially even the outcome of cell therapy procedures. Clinical trials are in progress for exosomes in many therapeutic functions, for many indications. One example is using dendritic cell-derived exosomes to initiate immune response to cancers.Exosome Manufacturing
Exosome product manufacturing involves many distinct areas of study. First of all, we are interested in their efficient and robust generation at a sufficient scale. Also, because they are found in such raw materials as animal serum, avoiding process-related contaminants is a concern. Finally, a variety of means of separating them from other types of extracellular vesicles and cell debris is under study. As exosomes are being examined in so many applications, their production involves many distinct platforms and concerns. First of all, an appropriate and effective culture mode is required for any cell line that is specifically required by the application. Also, one must consider the quality systems and regulatory status of the materials and manufacturing environment for the particular product addressed. Finally, a robust process must be described for the scale and duration of production demanded. As things exist now, their production can be described as 1) the at-scale expansion and culture of the parent cell-line, 2) the collection or harvest of the culture media containing the secreted exosomes, and 3) the isolation or purification of the desired exosomes from not only other macrovesicles, macromolecular complexes, and small molecules, but from such other process contaminants as cellular debris and culture media components.
No comment yet.
Rescooped by Dr. Stefan Gruenwald from Sustainable Complex Coevolutionary Systems Engineering!

Dynamic models of the complex microbial metapopulation of lake mendota

Dynamic models of the complex microbial metapopulation of lake mendota | Amazing Science |
Population modelling: Understanding lake microbes A lake microbe population model developed by US researchers reveals how environmental factors affect community dyamics.


Like many other environments, Lake Mendota, WI, USA, is populated by many thousand microbial species. Only about 1,000 of these constitute between 80 and 99% of the total microbial community, depending on the season, whereas the remaining species are rare. The functioning and resilience of the lake ecosystem depend on these microorganisms, and it is therefore important to understand their dynamics throughout the year.


Via Dr Alejandro Martinez-Garcia
No comment yet.
Scooped by Dr. Stefan Gruenwald!

Intelligent? Brainless slime can 'learn' without a nervous system

Intelligent? Brainless slime can 'learn' without a nervous system | Amazing Science |
What is intelligence? The definitions vary, but all infer the use of grey matter, whether in a cat or a human, to learn from experience.


A slime made up of independent, single cells, they found, can "learn" to avoid irritants despite having no central nervous system. "Tantalizing results suggest that the hallmarks for learning can occur at the level of single cells," the team wrote in a paper published in the journal Proceedings of the Royal Society B.


For the study, researchers from Belgium and France sought to demonstrate "habituation learning" in a brainless organism. Habituation learning is when original behaviour changes in response to repeated stimulus—think of a human losing their fear of needles after being repeatedly exposed to them in phobia therapy.


The team wanted to see whether an organism without a nervous system could similarly "learn" from experience and change its behavior accordingly.

No comment yet.
Scooped by Dr. Stefan Gruenwald!

Do 'genetic superheroes' exist? Or did media overhype Resilience Project?

Do 'genetic superheroes' exist? Or did media overhype Resilience Project? | Amazing Science |
Genetic Superheroes. Hitting the genetic lottery. 13 Incredibly lucky people. Bulletproof genomes.


That’s just a few of the ways people have described the results from a recent analysis of the genomes of over half a million people which found that 13 lucky people have disease causing mutations, but don’t exhibit any symptoms.


The study is the largest effort, to date, to identify so called ‘resilient’ individuals. These are healthy people who possess a mutation in their genome that is known to be disease causing. Many believe the DNA of these resilient people hold the key to treating genetic diseases, like cystic fibrosis, that today are incurable.


The existence of these 13 genetic Herculeses has created much excitement in the media:

  • STAT: Genetic ‘unicorns’ defy their own DNA — and hint at treatments
  • NPR: How Do ‘Genetic Superheroes’ Overcome Their Bad DNA?
  • BBC‘Superhero DNA’ Keeps Diseases at Bay


But did the study really identify a few lucky winners of the genome lottery? What’s the real story here? The study published in the journal Nature Biotechnology by a team of international scientists led by researchers at Icahn School of Medicine at Mount Sinai in New York City searched the genomes of 589,306 people—all over the age of 30—for 874 genes that are linked to 584 genetic diseases. All of these diseases begin to affect a person during childhood, like cystic fibrosis, Tay-sachs and Pfeiffer syndrome.


The team obtained these sequences from a variety of previous studies, but most of the data—nearly 400,000 samples—came from the at-home, personal genetics test 23andMe. (On the 23andMe consent forms, customers can select a box to allow their DNA to be used in such research.) Pooling all of this data, the scientists identified 15,597 potentially resilient individuals, but after a rigorous screen of these candidates, they eliminated almost all of them, settling on just 13, they believed were resilient.


The study is considered, by the Resilience Project leaders to be a ‘proof of concept’ study which means they modestly set out to prove their methods could identify resilient individuals. The study’s leader, Stephen Friend, says the idea to look for resilient people came out of frustration from the lack of success he had in looking at the problem from the other way. He and other biotech researchers usually search for genetic variants common in a number of sick individuals and then look for ways to fix the defect, but Friend admits they have been largely unsuccessful using this approach. He hopes that by looking for resilient people instead, he will discover why they are resilient and then use that knowledge to treat those who do exhibit symptoms.


But some have begun to question the validity of the resilience of these candidates, which could blow a hole in the conclusions. The study was a retrospective analysis, meaning the authors looked over data from other studies to establish connections, but they did not personally examine any of the participants. More importantly, for many they never can. In several of the studies they borrowed data from, recontact was not even considered when asking for participant consent. For participant’s samples from 23andMe, the consent for recontact falls into a gray area because the company does not specifically ask for permission to recontact on its consent form.


Nature Biotechnology published an independent commentary from Daniel MacArthur, a geneticist who teaches at Harvard University and conducts research at Massachusetts General Hospital. MacArthur explains why this data collection flaw hurts the study’s validity: "Perhaps most unfortunately, the researchers could not recontact the majority of resilient individuals for further study because of a lack of necessary consent forms. This means that some of their resilient cases may be mirages (the result of undisclosed disease cases, sample swaps, or somatic mosaicism), and this lack of consent precluded the collection of further clinical and genetic data to explore possible resilience mechanisms."

No comment yet.
Scooped by Dr. Stefan Gruenwald!

History of road-tripping shaped dromedar's DNA

History of road-tripping shaped dromedar's DNA | Amazing Science |
Centuries of caravan domestication and travel left some metaphorical tire marks on Arabian camel genes, researchers find.


Arabian camels (Camelus dromedarius) have trekked across ancient caravan routes in Asia and Africa for 3,000 years. But it’s unclear how camels’ domestication has affected their genetic blueprints.


To find out, Faisal Almathen of King Faisal University in Saudi Arabia and his colleagues combed through the DNA of 1,083 modern camels and ancient remains of wild and domesticated camels found at archaeological sites going back to 5000 B.C.


Camels run high on genetic diversity thanks to periodic restocking from now-extinct wild populations in the centuries after their domestication, the team reports May 9 in the Proceedings of the National Academy of Sciences. Travel on human caravan routes also created a steady flow of genes between different domesticated populations, except in a geographically isolated group in East Africa. That diversity may give some camel populations a leg up in adapting to future changes in climate, the authors suggest. 

No comment yet.
Scooped by Dr. Stefan Gruenwald!

Scientists hope to save near-extinct rhinos with stem cells

Scientists hope to save near-extinct rhinos with stem cells | Amazing Science |

The northern white rhinoceros is in far worse straits than most rhinos. There are just three members of the species left, and they can't breed normally -- if nothing happens, extinction is guaranteed. And that's leading researchers to try a dramatic technological solution to keep the northern white rhino around. They're planning to transform both frozen and living rhino cells into stem cells that could grow into eggs and sperm for the in vitro fertilization of a surrogate southern white rhino. This would not only resurrect the species, but create enough diversity that the new population should survive in the wild.


Of course, planning a revival and achieving it aren't one and the same. The technique might require growing the cells alongside tissue from other animals, and there's no guarantee that you'd get a healthy rhino on the other end. Also, zoos don't always have the many millions of dollars needed to make this project happen. If everything comes together, though, it could prove that science has what it takes to bring a species back from the brink.

No comment yet.
Scooped by Dr. Stefan Gruenwald!

Intestinal worms boost immune system in a surprising way

Intestinal worms boost immune system in a surprising way | Amazing Science |

In order to fight invading pathogens, the immune system uses “outposts” throughout the body, called lymph nodes. These are small, centimeter-long organs that filter fluids, get rid of waste materials, and trap pathogens, e.g. bacteria or viruses. Lymph nodes are packed with immune cells, and are known to grow in size, or ‘swell’, when they detect invading pathogens. But now, EPFL scientists have unexpectedly discovered that lymph nodes also produce more immune cells when the host is infected with a more complex invader: an intestinal worm.


The discovery is published in Cell Reports, and has significant implications for our understanding of how the immune system responds to infections. The discovery was made by the lab of Nicola Harris at EPFL. Her postdoc and first author Lalit Kumar Dubey noticed that the lymph nodes of mice that had been infected with the intestinal worm Heligmosomoides polygyrus bakeri had massively grown in size. This worm is an excellent tool for studying how the worm interacts with its host, and is therefore used as a standard throughout labs working in the field.

Lymph nodes have microscopic compartments called “follicles”, where they store a specific type of immune cells, the B-cells. Stored in the follicles, B-cells pump out antibodies into the bloodstream to attack invading pathogens.


The researchers found that the mouse lymph nodes were actually producing more follicles, suggesting they were producing more B-cells in response to the worm infection. Of course, this is not a simple event. Like many biological processes, it involves an entire sequence of molecular signals that result in the formation of new cells and tissue.


The EPFL scientists were able to reconstruct the molecular sequence, which is fairly complex: when the mouse is infected with the intestinal worm, a “cytokine” molecule is produced. This cytokine then stimulates B-cells in the lymph nodes to produce a molecule called a lymphotoxin. The lymphotoxin then interacts with the cells that form the foundation of the actual lymph node – the so-called “stromal cells”. The stromal cells then produce another cytokine, which stimulates the production of new follicles in the lymph node.

No comment yet.
Scooped by Dr. Stefan Gruenwald!

99.999 percent of microbe species remain undiscovered, researchers claim

99.999 percent of microbe species remain undiscovered, researchers claim | Amazing Science |
Microbes make up the vast majority of species on Earth, but when it comes to identifying them, humans seems clueless.


Earth could harbor 1 trillion microbial species, but humans only know about 0.001 percent of them, two biologists from Indiana University suggest in a paper published Monday in Proceedings of the National Academy of Sciences.  


"We've done a pretty good job of cataloguing macrobes. Maybe every few years you'll hear about a new worm at the bottom of the ocean, but the rate we are exploring new plants and animals is slowing down," Jay Lennon, a microbial biology researcher at Indiana University Bloomington (IU) and co-author of the new study. "But it's only in the last 20 to 30 years that people have figured out how to identify microbes; we are still in an area of discovery. Before this study, it was hard to know where we were. These are the most abundant life on Earth, so from a scientific perspective, we've missed a huge group," he says. 

No comment yet.
Scooped by Dr. Stefan Gruenwald!

Natural antibodies could combat Tasmanian devil cancer

Natural antibodies could combat Tasmanian devil cancer | Amazing Science |
Deakin University scientists may have found a way to stop the cancer that has been killing Tasmanian devils for the past 20 years.


Dr Beata Ujvari, from Deakin's Centre for Integrative Ecology within the School of Life and Environmental Sciences, investigated differences in molecules found in the devils' immune systems, comparing those that had the cancer, known as the Tasmanian Devil Facial Tumour Disease, and those that didn't.


We know from human and animal studies that certain natural antibodies are able to recognise and kill cancerous cells, so we wanted to see whether the presence of these molecules would also determine tumor development in Tasmanian devils," Dr Ujvari said.


"We found that devils that have a higher ratio of these natural antibodies were less likely to have cancer. "We can deduce then that devils with higher natural antibody ratio are therefore less susceptible to the contagious cancer."


Dr Ujvari said the results could potentially halt the spread of disease that has devastated the Tasmanian devil population since its first sighting in 1996, hopefully enabling new vaccine and treatment options.


The research, "Immunoglubolin dynamics and cancer prevalence in Tasmanian devils (Sarcophilus harrisii)" is published in the latest edition of Nature Scientific Reports. "Anti-tumor vaccines that enhance the production of these natural antibodies, or direct treatment of the cancer with natural antibodies, could become a solution to help halt this disease," Dr Ujvari said.


"This process known as 'active immunotherapy', is becoming more and more accepted in treating human cancers, and we think it could be the magic bullet in saving the Tasmanian devils from extinction."


The facial cancer is spread from devil to devil via biting during social interactions, and has caused massive population declines of Tasmanian devils since its first sighting in 1996, in Tasmania. Dr Ujvari said that because the cancer was transmitted from devil to devil, their immune system should recognise the cells as foreign objects, like a pathogen, and work to eliminate them from the victim's system.


"However, this disease's cells are able to avoid recognition by the devils' immune systems and develop into large ulcerating tumors that ultimately kills the animals," she said.

No comment yet.
Scooped by Dr. Stefan Gruenwald!

The Shrinking Mitochondrion Phenomenom

The Shrinking Mitochondrion Phenomenom | Amazing Science |
Scanning the mitochondrial genomes of thousands of species is beginning to shed light on why some genes were lost while others were retained.


Billions of years ago, one cell—the ancestral cell of modern eukaryotes—engulfed another, a microbe that gave rise to today’s mitochondria. Over evolutionary history, the relationship between our cells and these squatters has become a close one; mitochondria provide us with energy and enjoy protection from the outside environment in return. As a result of this interdependence, our mitochondria, which once possessed their own complete genome, have lost most of their genes: while the microbe that was engulfed so many years ago is estimated to have contained thousands of genes, humans have just 13 remaining genes in their mitochondrial DNA (mtDNA).


Some mitochondrial genes have disappeared completely; others have been transferred to our cells’ nuclei for safekeeping, away from the chemically harsh environment of the mitochondrion. This is akin to storing books in a nice, dry, central library, instead of a leaky shed where they could get damaged. In humans, damage to mitochondrial genes can result in devastating genetic diseases, so why keep any books at all in the leaky shed?


Researchers have proposed diverse hypotheses to explain mitochondrial gene retention. Perhaps the products of some genes are hard to introduce into the mitochondrion once they’ve been made elsewhere. (Mitochondria have their own ribosomes and are capable of translating their retained genes in-house.) Or perhaps keeping some mitochondrial genes allows the cell to control each organelle individually. Historically, it has been hard to gather quantitative support for any of these ideas, but in the world of big (and growing) biological data we now have the power to shed light on this question. The mtDNA sequences of thousands of organisms as diverse as plants, worms, yeasts, protists, and humans have now been sequenced, yielding information on the patterns of gene loss and on the gene properties that may have governed this loss.

No comment yet.
Scooped by Dr. Stefan Gruenwald!

The next step in DNA computing: GPS mapping?

The next step in DNA computing: GPS mapping? | Amazing Science |

Conventional silicon-based computing, which has advanced by leaps and bounds in recent decades, is pushing against its practical limits. DNA computing could help take the digital era to the next level. Scientists are now reporting progress toward that goal with the development of a novel DNA-based GPS. They describe their advance in ACS' The Journal of Physical Chemistry B.


Jian-Jun Shu and colleagues note that Moore's law, which marked its 50thanniversary in April, posited that the number of transistors on a computer chip would double every year. This doubling has enabled smartphone and tablet technology that has revolutionized computing, but continuing the pattern will come with high costs. In search of a more affordable way forward, scientists are exploring the use of DNA for its programmability, fast processing speeds and tiny size. So far, they have been able to store and process information with the genetic material and perform basic computing tasks. Shu's team set out to take the next step.


The researchers built a programmable DNA-based processor that performs two computing tasks at the same time. On a map of six locations and multiple possible paths, it calculated the shortest routes between two different starting points and two destinations. The researchers say that in addition to cost- and time-savings over other DNA-based computers, their system could help scientists understand how the brain's "internal GPS" works.

No comment yet.
Scooped by Dr. Stefan Gruenwald!

Tracking Zika Virus' Evolution

Tracking Zika Virus' Evolution | Amazing Science |

Sequence analysis of 41 viral strains reveals more than a half-century of change.


Comparing the sequences of 30 strains of Zika virus isolated from humans, 10 from mosquitoes, and one from monkeys has revealed significant evolutionary change over the past 70 years, according to a study published today (April 15) in Cell Host & Microbe. Specifically, the sequences of the viral strains showed notable divergence between the Asian and African lineages and suggest that modern Zika virus strains derived from the Asian lineage, as they are more similar to the Malaysian/1966 strain than the Nigerian/1968 strain. Additionally, the gene for the pre-membrane precursor protein has very high variability among the Zika strains examined, which modeling work suggests may affect the protein’s structure.


“We believe these changes may, at least partially, explain why the virus has demonstrated the capacity to spread exponentially in the human population in the Americas,” study coauthor Genhong Cheng of the University of California, Los Angeles, said in a press release. “These changes could enable the virus to replicate more efficiently, invade new tissues that provide protective niches for viral propagation, or evade the immune system, leading to viral persistence.”


But it is not possible to directly test whether these mutations affect the virus’s spread in humans, virologist Vincent Racaniello noted on his blog. “It’s easy to blame mutations in the viral genome for novel patterns of transmission or pathogenesis,” he wrote. “There is no reason to assume that such changes influence virulence, disease patterns, or transmission in humans.”

No comment yet.
Scooped by Dr. Stefan Gruenwald!

Signals that make early stem cells identified

Signals that make early stem cells identified | Amazing Science |

Stem cells work throughout our lives as a sort of handyman, repairing damaged tissues and renewing some normal ones, like the skin we shed. Scientists have come to understand much about how stem cells function when we are adults, but less is known about where these stem cells come from to begin with, as an embryo is developing.


Now, researchers at The Rockefeller University have identified a new mechanism by which cells are instructed during development to become stem cells. The results, published in Cell on January 14, help explain how communication between cells mediates this process, and may have implications for skin cancer treatments. The researchers traced the cell divisions that occur as hair follicles form in mice to determine where stem cells first emerge. Above, developing hair follicles are shown at various stages.


“While adult stem cells are increasingly well-characterized, we know little about their origins. Here, we show that in the skin, stem cell progenitors of the hair follicle are specified as soon as the cells within the single-layered embryonic epidermis begin to divide downward to form an embryonic hair bud,” explains Elaine Fuchs, Rebecca C. Lancefield Professor and head of the Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Development. “This timing was much earlier than previously thought, and gives us new insights into the establishment of these very special cells.”


Clusters of stem cells receive signals from other nearby cells that instruct them to either stay a stem cell or differentiate into a specific cell type. These instructive groups of cells, called the “niche,” are known to maintain adult stem cell populations. Less well understood is how the niche forms, or when and where stem cells first appear during embryonic development.


“Adult stem cells are dependent on the niche for instructions on both how to become a stem cell, and how to control stem cell population size,” says first author Tamara Ouspenskaia. “The question was, does the niche appear first and call other cells over to become stem cells? Or is it the other way around? Stem cells could be appearing elsewhere first and then recruiting the niche.”


Working in the mouse hair follicle, a region that contains active stem cells, Fuchs and colleagues investigated the cell divisions that occur as a hair follicle is first forming. The hair follicle begins as a small bud called a placode, and develops into a tissue of multiple layers, comprised of different cell types. By labeling cells within the placode and tracing their progeny, the researchers determined that from each division, one daughter cell stayed put, while the other escaped to a different layer.

No comment yet.
Scooped by Dr. Stefan Gruenwald!

MicroRNA Pathway Could Lead to New Avenues for Leukemia Treatment

MicroRNA Pathway Could Lead to New Avenues for Leukemia Treatment | Amazing Science |

Cancer researchers at the University of Cincinnati have found a particular signaling route in microRNA (miR-22) that could lead to targets for acute myeloid leukemia, the most common type of fast-growing cancer of the blood and bone marrow. These findings are being published in the April 26 issue of the online journal Nature Communications.  

Acute myeloid leukemia (AML) is the most common type of acute leukemia and occurs when the bone marrow begins to make blasts, cells that have not yet completely matured. These blasts normally develop into white blood cells. However, in AML, these cells do not develop and are unable to ward off infections.
Jianjun Chen, PhD, associate professor in the Department of Cancer Biology at the UC College of Medicine, member of the UC Cancer Institute and lead author on the study, says that microRNAs are sophistically controlled and play key roles in the development of cancer.
"MicroRNAs make up a class of small, non-coding internal RNAs that control a gene’s job, or expression, by directing their target messaging RNAs, or mRNAs, to inhibit or stop. Cellular organisms use mRNA to convey genetic information,” he says. "Previous research has shown that microRNA miR-22 is linked to breast cancer and other blood disorders which sometimes turn into AML, but we found in this study that it could be an essential anti-tumor gate keeper in AML when it is down-regulated, meaning its function is minimized.
"When we forced miR-22 expression, we saw difficulty in leukemia cells developing, growing and thriving. miR-22 targets multiple cancer causing genes (CRTC1, FLT3 and MYCBP) and blocks certain pathways (CREB and MYC). The down-regulation, or decreased output, of miR-22 in AML is caused by the loss of the number of DNA being copied and/or stopping their expression through a pathway called TET1/GFI1/EZH2/SIN3A. Also, nanoparticles carrying miR-22 DNA oligonucleotides (short nucleic acid molecules) prevented leukemia advancement.”
Chen, who conducted the study using bone marrow transplant samples and animal models, says that the ten-eleven translocation proteins (TET1/2/3) in mammals help to control genetic expression in normal developmental processes in contrast to mutations that cause function loss and tumor-slowing with TET2, which is observed in blood and stem cell cancers. 
"We recently reported that TET1 plays an essential cancer generating role in certain AML where it activates expression of homeobox genes, which are a large family of similar genes that direct the formation of many body structures during early embryonic development,” he says. "However, it is unknown whether TET1 can also function as a repressor for cellular function in cancer, and its role in microRNA expression has rarely been studied.”
Chen says these findings are important in targeting a cancer that is both common and fatal. "The majority of patients with ALM usually don’t survive longer than five years, even with chemotherapy, which is why the development of new effective therapies based on the underlying mechanisms of the disease is so important,” he says, adding that this pathogenesis as well as drug response to AML is unclear. "Our study uncovers a previously unappreciated signaling pathway (TET1/GFI1/EZH2/SIN3A⊣miR-22⊣CREB-MYC) and provides new insights into genetic mechanisms causing and progressing AML and also highlights the clinical potential of miR-22-based AML therapy. More research on this pathway and ways to target it are necessary.”
No comment yet.
Scooped by Dr. Stefan Gruenwald!

Secret Flexibility Found in Protein-Protein Interactions

Secret Flexibility Found in Protein-Protein Interactions | Amazing Science |
Proteins transact much of a cell’s daily business. Messages are sent from one part of the cell to another, for instance, by a protein bucket brigade — one attaches to another, which then switches on another, which then modifies another, and so on, culminating in a string of alterations that delivers the message. A protein’s particular shape helps determine what it can attach to and therefore what it can do. Finding out which proteins another protein will stick to is often the first step in understanding its role in the cell.

Marc Vidal, a biologist at Dana-Farber, has a long history of tracing such protein partnerships on a grand scale. His lab looks to see how large numbers of proteins interact with one another and how those interactions might change in someone with a disease. But it can be frustrating to do this when you aren’t sure whether you should assume that proteins from the same gene do the same thing. Even if we perfectly understand a particular genome sequence, “we still don’t have a perfect knowledge of the components that are encoded by the genome,” Vidal said. “And the reason is that the good old rules don’t hold.”

To see just how often the old rules might be broken, the Vidal lab and their collaborators gathered a set of proteins made from about 1,500 genes — about 8 percent of our total complement. They sorted out which proteins came from the same genes, finding that about 500 of the genes made at least two. Then they ran multiple tests in which each of the proteins was given the chance to attach to more than 15,000 other proteins often found in the cell. Finally, they compared each protein’s results to those of its sibling proteins — all those proteins made by the same gene. How often did sibling proteins attach to the same partners? How often did they not?

The answer was rather unexpected. “It was so striking,” said David Hill, a scientist at Dana-Farber, that he thought, “This can’t be right; we’ve got to figure out what we did wrong.” But the results held up to prodding. They found that 61 percent of sibling protein pairs share some but not all of their interactions. Moreover, nearly one in five of all sibling protein pairs had nothing in common. Comparing the proteins in their data set with proteins made by separate genes, the team found that in many cases the sibling proteins’ interactions were as different as if they’d had totally unrelated origins.
No comment yet.
Scooped by Dr. Stefan Gruenwald!

Skeletal stem cells form the blueprint of the face structure

Skeletal stem cells form the blueprint of the face structure | Amazing Science |

Timing is everything when it comes to the development of the vertebrate face. In a new study published in PLoS Genetics, USC Stem Cell researcher Lindsey Barske from the laboratory of Gage Crump and her colleagues identify the roles of key molecular signals that control this critical timing.


Previous work from the Crump and other labs demonstrated that two types of molecular signals, called Jagged-Notch and Endothelin1 (Edn1), are critical for shaping the face. Loss of these signals results in facial deformities in both zebrafish and humans, revealing these as essential for patterning the faces of all vertebrates.


Using sophisticated genetic, genomic and imaging tools to study zebrafish, the researchers discovered that Jagged-Notch and Edn1 work in tandem to control where and when stem cells turn into facial cartilage. In the lower face, Edn1 signals accelerate cartilage formation early in development. In the upper face, Jagged-Notch signals prevent stem cells from making cartilage until later in development. The authors found that these differences in the timing of stem cells turning into cartilage play a major role in making the upper and lower regions of the face distinct from one another.


"We've shown that the earliest blueprint of the facial skeleton is set up by spatially intersecting signals that control when stem cells turn into cartilage or bone. Logically, therefore, small shifts in the levels of these signals throughout evolution could account for much of the diversity of shapes we see within the skulls of different animals, as well as the wonderful array of facial shapes seen in humans," said Barske, lead author and A.P. Giannini postdoctoral research fellow.

No comment yet.