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ScienceDaily (June 18, 2012) ? UC Santa Barbara scientists turned to the simple sponge to find clues about the evolution of the complex nervous system and found that, but for a mechanism that coordinates the expression of genes that lead to the formation of neural synapses, sponges and the rest of the animal world may not be so distant after all. Their findings, titled “Functionalization of a protosynaptic gene expression network,” are published in the Proceedings of the National Academy of Sciences.
“If you’re interested in finding the truly ancient origins of the nervous system itself, we know where to look,” said Kenneth Kosik, Harriman Professor of Neuroscience Research in the Department of Molecular, Cellular & Developmental Biology, and co-director of UCSB’s Neuroscience Research Institute.
That place, said Kosik, is the evolutionary period of time when virtually the rest of the animal kingdom branched off from a common ancestor it shared with sponges, the oldest known animal group with living representatives. Something must have happened to spur the evolution of the nervous system, a characteristic shared by creatures as simple as jellyfish and hydra to complex humans, according to Kosik.
A previous sequencing of the genome of the Amphimedon queenslandica — a sponge that lives in Australia’s Great Barrier Reef — showed that it contained the same genes that lead to the formation of synapses, the highly specialized characteristic component of the nervous system that sends chemical and electrical signals between cells. Synapses are like microprocessors, said Kosik explaining that they carry out many sophisticated functions: They send and receive signals, and they also change behaviors with interaction — a property called “plasticity.”
“Specifically, we were hoping to understand why the marine sponge, despite having almost all the genes necessary to build a neuronal synapse, does not have any neurons at all,” said the paper’s first author, UCSB postdoctoral researcher Cecilia Conaco, from the UCSB Department of Molecular, Cellular, and Developmental Biology (MCDB) and Neuroscience Research Institute (NRI). “In the bigger scheme of things, we were hoping to gain an understanding of the various factors that contribute to the evolution of these complex cellular machines.”
This time the scientists, including Danielle Bassett, from the Department of Physics and the Sage Center for the Study of the Mind, and Hongjun Zhou and Mary Luz Arcila, from NRI and MCDB, examined the sponge’s RNA (ribonucleic acid), a macromolecule that controls gene expression. They followed the activity of the genes that encode for the proteins in a synapse throughout the different stages of the sponge’s development.
“We found a lot of them turning on and off, as if they were doing something,” said Kosik. However, compared to the same genes in other animals, which are expressed in unison, suggesting a coordinated effort to make a synapse, the ones in sponges were not coordinated.
“It was as if the synapse gene network was not wired together yet,” said Kosik. The critical step in the evolution of the nervous system as we know it, he said, was not the invention of a gene that created the synapse, but the regulation of preexisting genes that were somehow coordinated to express simultaneously, a mechanism that took hold in the rest of the animal kingdom.
The work isn’t over, said Kosik. Plans for future research include a deeper look at some of the steps that lead to the formation of the synapse; and a study of the changes in nervous systems after they began to evolve.
“Is the human brain just a lot more of the same stuff, or has it changed in a qualitative way?” he asked.
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The above story is reprinted from materials provided by University of California – Santa Barbara.
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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
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§ February 15th, 2012 § Filed under hail § Tagged system § No Comments
ScienceDaily (Feb. 13, 2012) ? At the most basic level, the immune system must distinguish self from non-self, that is, it must discriminate between the molecular signatures of invading pathogens (non-self antigens) and cellular constituents that usually pose no risk to health (self-antigens).
The system is far from foolproof. Cancer cells can undergo unchecked proliferation, producing self-antigens that are tolerated by the immune system, rather than being targeted for destruction. At the opposite extreme, a range of so-called autoimmune disorders can result when healthy cells in the body are misidentified as hazards. The immune system has developed a further line of protection against such autoimmune responses in order to limit the pathology that can result. Essentially, the immune system is programmed to ‘turn itself off’ after prolonged recognition of an antigen.
In a new study appearing in the current issue of the journal Science, Dr. Joseph Blattman, a researcher at Arizona State University’s Biodesign Institute examines how CD8 T cells — critical weapons in the body’s defensive arsenal — are regulated when they transition from this tolerant state to an activated state and back.”We have previously shown that prolonged stimulation of T cells in disseminated cancers or chronic viral infections results in a tolerant state to the tumor or pathogen. It was never clear if this ‘immune exhaustion’ was a reversible fate or if ‘resting’ the T cells by removing them from the cancer or infection environment could restore their function” said Dr. Blattman. “These results show that even if you can temporarily rescue a tolerant T cell, it is hard-wired to become tolerant again.”
Lymphocytes or white blood cells are central players in the immune systems of all vertebrates, and come in various types. Large granular lymphocytes include natural killer cells (NK cells), while small lymphocytes consist of T cells and B cells. Cytotoxic T cells (also called CD8 T cells) take their name from their place of maturation in the thymus gland and the CD8 glycoprotein adorning their surfaces. These cells help the immune system identify infected or malignant cells and are the main cells responsible for eliminating them.
In the thymus, T cells undergo both positive and negative selection. In this process, T cells that bind too weakly or too strongly to self-antigens are weeded out, undergoing cell death. The first group would result in a deficient immune response to foreign invasion while the latter would tend to overreact to self proteins, leading to autoimmunity. Only about 2 percent of these developing T cells or thymocytes will survive. This dual process of selection generally produces cells capable of recognizing foreign threats while maintaining a tolerance for self-antigens.
However, some self-reactive CD8 T cells do make it out of the thymus and are exposed to self-antigen. In order to avoid causing autoimmune disease, the stimulation by self cells results in T cell tolerance. This could be for a number of reasons including lack of costimulation, the presence of regulatory T cells that inhibit CD8 T cell responses, or continuous stimulation by self antigens. This essential safeguard however can become an Achilles’ heel, causing unresponsiveness in CD8 T cells to certain cancer antigens, many of which are self-antigens. One of the central challenges in tumor immunology is to somehow short-circuit T cell tolerance to tumor/self-antigens, without provoking autoimmunity.
Dr. Blattman and his group sought to illuminate the underlying molecular mechanisms of self-tolerance and the regulatory programs that maintain or break it. Contrary to prevailing theory, the group demonstrated in a mouse model that T cells return to the tolerant state even in the absence of self-antigen. Further, such cells could be induced to proliferate and become functional if the lymphocyte cell numbers fell to appropriately low levels — a condition known as lymphopenia — and that this effect is observed even when self-antigen is present.
Because T cells are known to proliferate in lymphopenic environments, such as after chemotherapy and/or irradiation in cancer patients, the researchers used this to ‘trick’ T cells into proliferating in order to reset their function. This strategy did restore their function temporarily, but within a month afterwards, the T cells once again became tolerant even if they did not continue to encounter the tumor antigen.
The current research overturns a central paradigm regarding T-cell tolerance to self-antigens and may provoke a fundamental rethinking of the underlying mechanisms that govern the immune response. The results will help identify the molecular events that lead to T cell tolerance to tumor antigens, which should aid in development of strategies to permanently restore the function of T cells. This, in turn, should suggest new approaches for the treatment of cancer and chronic viral infections that employ adoptive transfer of modified cancer-specific T cells that make these cells resistant to becoming tolerant.
“Adoptive immunotherapy with T cells is an exciting strategy for combating cancer because the transferred T cells don’t kill all dividing cells, but instead only target the cells expressing the cancer antigen. The problem has been that the transferred T cells usually become tolerant to the cancer” said Dr. Blattman. “By knowing the rules governing T cell tolerance, we will be able to identify what regulates this process and design ways of overcoming it in order to provide more effective cancer therapies.”
The rescue of CT8 T cell functionality was indeed transient, in the mouse studies undertaken. When lymphocyte numbers in mice rebounded (having been reduced through irradiation), CD8 T cell tolerance snapped back into place, and the genetic master plan for these cells was reestablished. This fact implies that while a genetic blueprint oversees T cell tolerance, this characteristic is not entirely fixed, but may be subject to epigenetic regulation, that is, non-genetically encoded regulation that is transferred to each dividing cell.
Using techniques of genome-wide mRNA and microRNA profiling, Dr. Blattman and his colleagues uncovered a tolerance-specific gene profile for CD8 T cells, further demonstrating that this gene-based regulatory system could be overridden under lymphopenic conditions.
The rescue of CD8 T cells through this method has been dubbed homeostasis-driven proliferation. The mechanism operates even in the absence of a cognate antigen, but apparently shuts down once T cell homeostasis has been reestablished. Rescued T cells showed a reduction or down-regulation of tolerance-specific genes as well as an up-regulation of some 475 “rescue-associated” genes.
Evidentially, T cells are able to recall the tolerance program initially established after their first encounter with self-antigen, returning to it as a default, following repletion of lymphocyte numbers. While the precise mechanisms that account for this tolerant memory remain unclear, various forms of epigenetic gene regulation, not reliant on DNA sequence, are implied.
Future research will attempt to identify the signaling pathways associated with the interruption and reacquisition of T cell tolerance, which appears to operate independently of surface T cell receptors. Further, use of lymphopenia-mediated rescue of CD8 T cells for cancer therapy will require that tolerance-specific epigenetic memory somehow be erased.
Finally, lymphopenia-based T cell proliferation and activation also provides a model to describe heightened autoimmunity following organ transplantation, particularly cases of graft-host rejection. Such autoimmunity is often of a transient nature, again suggesting that T cell tolerance is reset once lymphocyte populations rebound following surgery.
“These results clearly suggest that epigenetic mechanisms are in place to maintain tolerance in T cells specific for self antigens. Uncovering precisely which key molecules and genes are important in this process should help us to improve T cell based approaches to the treatment of cancer, as well as to induce tolerance in T cells causing autoimmunity,” said Dr. Blattman.
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The above story is reprinted from materials provided by Arizona State University. The original article was written by Richard Harth, science writer, The Biodesign Institute.
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
Journal Reference:
- A. Schietinger, J. J. Delrow, R. S. Basom, J. N. Blattman, P. D. Greenberg. Rescued Tolerant CD8 T Cells Are Preprogrammed to Reestablish the Tolerant State. Science, 2012; 335 (6069): 723 DOI: 10.1126/science.1214277
Note: If no author is given, the source is cited instead.
Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
Source: http://www.sciencedaily.com/releases/2012/02/120213185643.htm
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BRUSSELS ? Europe’s main weapon in the battle against climate change is now fighting for its own survival.
In early January, investors in the continent’s cap-and-trade system still had to pay some euro14 ($18.30) for the right to emit one ton of carbon dioxide into the air. By last week, the price of one emission allowance had tumbled to a meager euro6.41 ? making it much cheaper to pollute and slashing the financial incentives for companies to invest in low-carbon technologies.
Analysts warn that the prospect of another recession in the debt-ridden continent, and the accompanying decline in emissions, could push prices below euro2 by the end of next month.
The troubles in the carbon market, a system being watched closely from California to China, is linked to the struggles of Europe’ other ambitious project, the euro. And just as financial investors have looked to the European Central Bank to save the currency through massive intervention in the bond markets, analysts say the emissions market may need similar centralized help.
Last week, 19 companies, including oil giant Royal Dutch Shell PLC, Philips Electronics NV and supermarket chain Tesco PLC, sent a letter to the European Commission urging it to reduce the number of emission allowances in the system and figure out how to protect the market from future economic shocks. The commission and national governments jointly manage the cap-and-trade system.
“The lower price is really undermining the development of technologies that will be needed in the decades to come,” said David Hone, Shell’s climate change adviser.
Shell, which is mostly known for selling oil and gas, has been one of the pioneers of carbon capture and storage, projects in which CO2 emissions are stored underground so they don’t get released into the atmosphere and contribute to global warming. But investing in new technologies like carbon capture and storage only becomes commercially viable at a carbon price of between euro25 and euro30, Hone said.
“Over the last few months, we have seen some of these projects disappear,” he added.
In October, the U.K. government shut down the carbon capture project in Longannet in eastern Scotland in which Shell was one of the partners.
While the prospect of another recession is the main reason for the recent drop in carbon prices, experts say that ? just like with the euro ? serious flaws in the system are exacerbating the problems and could lead to its failure if they can’t be fixed.
The economic crisis has lowered emissions and thus hit the price of carbon allowances. But the drop has been so dramatic because there were too many allowances in the system to begin with.
To get industry and skeptical governments on board, the Commission set a very high cap for emissions when it launched the carbon market in 2005.
Since then, most allowances have been given out for free to the 11,000 power stations and factories covered by the system based on their historical emissions. Companies that emit less carbon dioxide than they are allowed can sell their spare permits to firms that exceed their limit. As of next year, airlines will also be included in the system.
But the big test for Europe’s carbon market ? and whether it can provide the financial incentives for cutting emissions ? will come in 2013, when governments start selling a growing number of allowances at auctions.
It is before then that the Commission has to intervene, say the companies that wrote last week’s letters.
There are signs that their calls are being heard.
On Tuesday, the environment committee of the European Parliament voted to withdraw some 1.4 billion allowances, about 15 percent of the total, from the carbon market between 2013 and 2020. At the same time, the committee said, the annual cap should be cut by 2.25 percent per year, rather than the 1.74 percent currently planned.
While the committee vote is the first step in a long process of changing the system and few industry watchers expect the figures to survive negotiations among EU states trying to protect their national industries, it caused carbon prices to jump more than 18 percent.
“It opens up a much deeper discussion about what does the intervention look like and when is it going to happen,” says Sanjeev Kumar, an expert on carbon trading at environmental watchdog E3G in Brussels.
“Without intervention,” warned Kumar, “not only the ETS is over, but Europe’s climate policy is over. It will put Europe back into the dark ages.”
Apart from failing to encourage the necessary cuts in emissions and technological innovation, the collapse in the carbon price could also worsen Europe’s debt crisis.
Between 2013 and 2020, when companies have to pay for more and more of their allowances, the cap-and-tade system could raise as much as euro190 billion for government across the EU if prices recover.
“This is a pretty important revenue stream for most member states,” says Rob Elsworth, of climate campaign group Sandbag in London. “And they are watching revenues just disappear.”
Experts like Kumar and Elsworth are hopeful that states will garner the political will to save the carbon trading system, which has pioneered the market-based approach to saving the environment.
“If you take away this green-economy narrative,” asked Elsworth, “what’s really left of Europe?”
Source: http://us.rd.yahoo.com/dailynews/rss/europe/*http%3A//news.yahoo.com/s/ap/20111220/ap_on_bi_ge/eu_carbon_trading
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Constructions ERP refers to a software solution with integrated data system that meets all areas of an organization. Constructions ERP consists of modules, such as Property Management System (REMS), Financial Accounting System (AF), Human Resource Management, Payroll System (HRPMS) and leasing of real estate and maintenance management. Property Management A well-established (REMS) has properties that each must meet a construction company, from its pre-construction by the construction. You must maintain the ability to prompt and accurate processing of data and can effectively manage project data, clients, brokers, etc. The real estate leasing and maintenance management for the rental of the office of a construction project, after completion.
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These modules can be used by a construction company, in whole or separated. Each module is equipped with robust features and functionality that work effectively and independently. The use of constructions ERP allows a company?s attention due to its primary business type, are out of the office and property management functions are completely handled by the ERP software. Function construction leader in ERP software market, characterized by its security, scalability and customization. A secure system is that it can be accessed only by authorized users. Scalability refers to the system?s ability to develop the growing needs of the organization and a customizable system is one whose properties can be tailored to the needs of the organization. Constructions ERP is a software system that can be used by a construction company to reap the benefits of increased turnover and higher profits.
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