Tips for Writing Your Research Proposal

1. Know yourself: Know your area of expertise, what are your strengths and what are your weaknesses. Play to your strengths, not to your weaknesses. If you want to get into a new area of research, learn something about the area before you write a proposal. Research previous work. Be a scholar.
2. Know the program from which you seek support: You are responsible for finding the appropriate program for support of your research. 
3. Read the program announcement: Programs and special activities have specific goals and specific requirements. If you don’t meet those goals and requirements, you have thrown out your chance of success. Read the announcement for what it says, not for what you want it to say. If your research does not fit easily within the scope of the topic areas outlined, your chance of success is nil.
4. Formulate an appropriate research objective: A research proposal is a proposal to conduct research, not to conduct development or design or some other activity. Research is a methodical process of building upon previous knowledge to derive or discover new knowledge, that is, something that isn’t known before the research is conducted. 
5. Develop a viable research plan: A viable research plan is a plan to accomplish your research objective that has a non-zero probability of success. The focus of the plan must be to accomplish the research objective.
6. State your research objective clearly in your proposal: A good research proposal includes a clear statement of the research objective. Early in the proposal is better than later in the proposal. The first sentence of the proposal is a good place. A good first sentence might be, “The research objective of this proposal is...” Do not use the word “develop” in the statement of your research objective. 
7. Frame your project around the work of others: Remember that research builds on the extant knowledge base, that is, upon the work of others. Be sure to frame your project appropriately, acknowledging the current limits of knowledge and making clear your contribution to the extension of these limits. Be sure that you include references to the extant work of others. 
8. Grammar and spelling count: Proposals are not graded on grammar. But if the grammar is not perfect, the result is ambiguities left to the reviewer to resolve. Ambiguities make the proposal difficult to read and often impossible to understand, and often result in low ratings. Be sure your grammar is perfect. 
9. Format and brevity are important: Do not feel that your proposal is rated based on its weight. Use 12-point fonts, use easily legible fonts, and use generous margins. Take pity on the reviewers. Make your proposal a pleasant reading experience that puts important concepts up front and makes them clear. Use figures appropriately to make and clarify points, but not as filler. 
10. Know the review process: Know how your proposal will be reviewed before you write it. Proposals that are reviewed by panels must be written to a broader audience than proposals that will be reviewed by mail. Mail review can seek out reviewers with very specific expertise in very narrow disciplines. 
11. Proof read your proposal before it is sent: Many proposals are sent out with idiotic mistakes, omissions, and errors of all sorts. Proposals have been submitted with the list of references omitted and with the references not referred to. Proposals have been submitted to the wrong program. Proposals have been submitted with misspellings in the title. These proposals were not successful. Stupid things like this kill a proposal. It is easy to catch them with a simple, but careful, proof reading. Don’t spend six or eight weeks writing a proposal just to kill it with stupid mistakes that are easily prevented.
12. Submit your proposal on time: Duh? Why work for two months on a proposal just to have it disqualified for being late? Remember, fairness dictates that proposal submission rules must apply to everyone. It is not up to the discretion of the program officer to grant you dispensation on deadlines. Get your proposal in two or three days before the deadline.

By: John Micheal

Bioluminescent Bacteria Could Light Up The Streets Of Paris

Paris has been known as "The City of Light" since the 19th century. Glowee

A French company is harnessing the power of bioluminescent bacteria to light up public areas.

Glowee, a Parisian start-up, plans to use bacteria found in squid to illuminate shop fronts, public spaces, and installations, with the hope of lighting up whole streets with these microbial lamps.

As the New Scientist reports, the lights consist of transparent cases filled with a gel containing the bioluminescent bacteria, alongside the sugars and oxygen they need to survive. The bacterium is both non-pathogenic and non-toxic.

There are obvious environmental benefits to using the bio-lights. Although the company has no intention of replacing all electric lighting with bioluminescence, it is a promising idea, with no need for electricity consumption and with considerably less carbon dioxide emissions than conventional means. On their website, the company says that "all the energy generated is used in the light production process. It is also less intense, allowing [Glowee] to limit the effect of light pollution.”

Presently, there are a few drawbacks to the lights. Their current design can only produce light for three days. Although the team hope to improve this lifespan, there is also the question of whether the cost and means of production could ever rival the efficiency of other light technology.

Although the cost and efficiency of Glowee remain unclear, there are some practical advantages. The lights are made of clear shells that can easily be trimmed and tailored to any shape and size. Additionally, the lights and casings appear transparent during the day.

Their inspiration came after a law was passed in July 2013 that forbids offices and retailers from keeping their shop fronts lit during the early hours of the morning in order to curb light pollution and energy consumption. Since Glowee emits a non-invasive soft light and won't eat into France's electricity network, it manages to bypass these laws.

After a crowdfunding campaign in May 2015, Glowee is now working on projects with event companies, urban furniture companies, and even Ben & Jerry’s (the ice cream guys).

But who knows, next time you’re taking a stroll through the “City of Light,” your path could be lit by some bioluminescent bacteria.

by Tom Hale

'Groundbreaking' cancer discovery holds promise for personalized therapy

Written by Honor Whiteman
Published: Friday 4 March, 2016

WE could be one step closer to personalized cancer vaccines; in what has been hailed a "groundbreaking" discovery, researchers suggest it could be possible to encourage the immune system to target and destroy cancer cells by identifying specific antigens on their surface.

In the journal Science, an international research team reveals how T cells - white blood cells that help the body fight infection - can recognize antigens that represent genetic faults, or mutations, in cancer cells.

Study coauthor Prof. Charles Swanton, of the University College London (UCL) Cancer Institute in the UK, and colleagues say the findings open the door to immunotherapies that could prime these T cells to identify the unique mutations and kill cancer cells.

Immunotherapy for the treatment of cancer - using a patient's own immune cells to fight the disease - has been increasingly investigated in recent years. Last year, for example, Medical News Today reported on two studies that hailed immunotherapy as highly effective against skin and lung cancers.

But there is one major barrier that is preventing the treatment from moving forward: the inability to guide immune cells toward the exact cancer cells they need to kill, while avoiding the destruction of healthy cells.

Identifying cancer targets for immune cells

This latest study may have uncovered much-needed targets on cancer cells, bringing researchers closer to a more precise, effective form of immunotherapy.

"For many years we have studied how the immune response to cancer is regulated without a clear understanding of what it is that immune cells recognize on cancerous cells," says study coauthor Dr. 

Sergio Quezada, head of the Immune Regulation and Cancer Immunotherapy Laboratory at the UCL Cancer Institute.

"Based on these new findings, we will be able to tell the immune system how to specifically recognize and attack tumors."

The researchers explain that as a tumor grows, a number of unique mutations arise in various parts of it. These mutations produce antigens on the surface of cancer cells within a tumor, which act as "flags" for T cells, prompting them to launch an attack.

While the T cells have the ability to eradicate all cancer cells within a tumor, they are not always able to reach their goal. The tumor can either launch a defense mechanism that deactivates the immune cells, or there are often simply too many mutations for the T cells to recognize and attack.

"Genetically diverse tumors are like a gang of hoodlums involved in different crimes - from robbery to smuggling. And the immune system struggles to keep on top of the cancer - just as it's difficult for police when there's so much going on," explains Dr. Quezada.

Uncovering the 'Achilles heel' of highly complex cancers

For their study, the researchers set out to pinpoint shared and unique antigens that may arise on the surface of cancer cells. To do so, they used The Cancer Genome Atlas (TCGA) to analyze the genetic data of more than 200 patients with one of two different forms of lung cancer - adenocarcinoma and squamous cell carcinoma.

From this data, the team identified certain antigens that represent early genetic mutations that were common across tumor cells.

Moving to the lab, the team isolated T cells from the tumors of two lung cancer patients. They found that their T cells were able to recognize these common antigens, suggesting that tumors contain immune cells that have the ability to identify cancer cells as harmful.

While the T cells were unable to kill the cancer cells due to the defenses the tumors put up, the researchers believe it may be possible to activate the T cells to target all the tumor cells in one go.

For example, a vaccine could be developed that switches on these T cells in a cancer patient, or it may be possible to harvest, grow or administer T cells back into a patient that can identify the common antigens present in each cancer cell.

"Our research shows that instead of aimlessly chasing crimes in different neighborhoods, we can give the police the information they need to get to the kingpin at the root of all organized crime - the weak spot in the patient's tumor - to wipe out the problem for good," says Dr. Quezada.

Prof. Swanton describes the teams findings as "exciting," adding:

While it may be a long time before such treatment is available in a clinical setting, the researchers say they hope to move to human trials within 2 years.

Meanwhile, another study reported by MNT sheds light on how tumors grow; researchers found that cancer cells influence nearby cells to increase production of a protein that triggers growth of blood vessels, which tumors need to survive.

Written by Honor Whiteman

Zika virus: Your questions answered

By Gretchen Vogel, Jon Cohen, Martin Enserink Jan. 29, 2016 , 3:30 PM

Where did the Zika virus come from?

First isolated in 1947 and first described in a paper in 1952, Zika has long been known to occur in Africa and Southeast Asia—but until a decade ago, fewer than 15 cases had been described in the scientific literature. In 2007, the virus caused a big outbreak on Yap, an island group in the Western Pacific that is part of the Federated States of Micronesia; since then, it went on a major tour of other Pacific Islands before it landed in Brazil, from where it started spreading rapidly to other parts of South America, Central America, Mexico, and the Caribbean.

Why has it exploded so suddenly?

There may have been big outbreaks in Africa and Asia in the past that went undetected; scientists weren't paying much attention. But the current massive epidemic was an event waiting to happen. Latin America has huge numbers of A. aegypti, also known as the yellow fever mosquito, an important vector for Zika. (The Asian tiger mosquito, A. albopictus, which is on the rise around the world, is believed to be a vector as well.) In addition, nobody in the Americas had immunity to the virus. Travel makes it worse. Aedes mosquitoes don't fly more than a few hundred meters during their lives; Zika travels from city to city and country to country when infected people get on cars, buses, trains, and planes.

These combined factors meant that the virus had the ability to spread far and fast once it had arrived.

Will Zika spread to the United States and Europe?

Both the United States and Europe have already seen "imported cases"—people who arrived from a Zika-affected country carrying the virus. This was widely expected given the size of the epidemic in Latin America. The key question is whether there will be local outbreaks—that is, mosquitoes spreading the virus from person to person. There's definitely a chance; A. albopictus occurs in several countries in southern Europe (and it may move north), while the southern and eastern United States have populations of both A. aegypti and A. albopictus.

If so, scientists expect outbreaks to be much smaller than elsewhere, based on past experience with mosquito-borne diseases. Recent dengue outbreaks in Florida, Texas, and Hawaii haven't sickened more than a few hundred people, for instance; an outbreak of a mosquito-borne disease called chikungunya in northern Italy in 2007—which started when a man infected with the virus arrived from India—ended after 197 cases. One reason that outbreaks in these countries tend to be smaller may be that people spend less time outside and live in houses that are more difficult for mosquitoes to enter; mosquito population sizes may play a role as well.

Do we know for sure that Zika is causing a rise in birth defects?

No. There is strong circumstantial evidence that areas in Brazil hit hard by Zika have experienced a sharp increase in the number of babies born with microcephaly, a condition in which the head is much smaller than normal because the brain fails to develop properly. But it will take at least several months before the results from the first case-control studies of pregnant women infected with Zika are available. Doctors in Brazil first noticed an increase in cases of microcephaly during ultrasounds of pregnant women in June and July, a few months after the sudden rise in Zika infections. Fetal medicine expert Manoel Sarno, who works at the Federal University of Bahia, says the pattern of brain damage he is seeing now looks distinct from microcephaly caused by other infections, such as cytomegalovirus (CMV) or rubella. He and his colleagues started a study in August that is following women infected with Zika during their pregnancy; the results could come out late summer. Similar studies are underway elsewhere in Brazil and in Columbia.

Are there other urgent questions that scientists are asking?

Plenty. Scientists have difficulty determining who has been infected and who hasn’t because diagnostic tests have limitations. The most accurate tests—which detect viral RNA in a patient’s blood—only work within a week of the first symptoms appearing. After that time, researchers can test for antibodies in blood. But current tests for Zika antibodies cross-react with antibodies to dengue, which is so widespread in Brazil—and much of the rest of Latin America—that almost all adults have antibodies to it. That makes it difficult to tell whether the mother of a baby born with microcephaly was infected with Zika earlier in her pregnancy.

Researchers would also like to know how often Zika is transmitted through sexual contact. One U.S. scientist who caught the virus in Africa passed it to his wife after he got home in 2008, and a second case of suspected sexual transmission happened in French Polynesia in 2013. But researchers have no idea what the risk is. (“If I was a man and I got Zika symptoms, I’d wait a couple of months before having unprotected sex,” virologist Scott Weaver of the University of Texas Medical Branch in Galveston recently told The New York Times.)

What drugs are available against Zika?

None. Until last year, Zika was so rare, and believed to be so mild, that nobody bothered to look for candidate drugs. Even now that the virus is surging, it's not obvious that there's a big market for an antiviral drug, because the vast majority of those infected have very few symptoms or none at all. And it's not clear that a drug could prevent birth defects when women contract Zika during pregnancy; by the time they become infected and develop symptoms, it may be too late to prevent such damage. A vaccine against Zika may offer more hope of preventing microcephaly.

And when can we expect a vaccine?

That will take years. Several groups have begun to make candidate Zika vaccines, a process that will take at least several months. Most of these vaccine approaches are piggybacking on existing vaccines. For example, many vaccines are made by stitching proteins from a pathogen’s surface into a harmless virus or vector; that is now being tried with Zika using those same vectors. Once a candidate vaccine is made, it will have to be tested in animals before humans.Human trials begin with small safety studies, then move on to larger studies that test whether the candidate product works. All of that usually takes 10 to 15 months. Given the urgency, the timeline could be compressed, but even so, Anthony Fauci, the director of the U.S. National Institute of Allergy and Infectious Diseases, told STAT that it may be at least 5 to 7 years before a Zika vaccine is commercially available.

Then what can we do to stop the spread of the virus?

Stop mosquitoes from biting people. Countries and communities can try to reduce mosquito populations by removing the small water reservoirs—such as flower pots, empty bottles, and discarded tires—in which Aedes mosquitoes like to breed. People can also reduce their personal exposure—especially important for women who are or might become pregnant—by putting screens on windows, covering their skin, and using insect repellant. However, history has shown that the impact of mosquito control on epidemics is modest at best, and they're difficult to sustain.

There must be better ways to control mosquitoes?

Not yet but they're in the works. A British biotech called Oxitec—which was recently purchased by Intrexon, a U.S. synthetic biology company—has developed A. aegyptimosquitoes containing a gene construct that will kill their offspring before they reach adulthood. When massive numbers of male individuals of this strain are released in the wild, they will mate with local females, producing offspring that are not viable, which has been shown to make a dent in the population.

In another line of research, scientists are infecting A. aegypti with a bacterium namedWolbachia, which reduces mosquitoes' ability to transmit diseases. The researchers developing these approaches were mostly thinking about dengue, but Zika's surge is giving their attempts a new sense of urgency. But again, it will take several years before these strategies are ready for prime time.

DOI: 10.1126/science.aae0291

Source: http://www.sciencemag.org/news/2016/01/zika-virus-your-questions-answered?utm_source=sciencemagazine&utm_medium=facebook-text&utm_campaign=zikaexplainer-2149

Zika virus is raising global alarm

Britain's Oxford University warned that a virus known as Zika, which is carried by mosquitoes and has caused a major outbreak in Brazil, has "the potential of rapid spread to new areas."

Zika was first detected in Africa in the 1940s and was unknown in the Americas until last year, but has now been confirmed in Brazil, Panama, Venezuela, El Salvador, Mexico, Suriname, the Dominican Republic, Colombia, Guatemala and Paraguay, according to public health officials. It is carried by the Aedes aegypti mosquito, which thrives in tropical climates and can also carry other diseases such as yellow fever, dengue fever and chikungunya.

Thousands of people in Brazil have been infected by Zika. While the virus is not thought to kill, health authorities there last year linked it to a surge in babies born with microcephaly, restricted head growth that seriously limits a child's mental and physical abilities.

Source: Medscape

Source: http://clinical-laboratory.blogspot.fi/2016/01/zika-virus-is-raising-global-alarm.html

7 Free Tools for Statistical Analysis

Which is the most important part of a research? Yes, it is ‘designing your experiments correctly’. Next comes ‘interpreting’ your results. Research in Biotechnology and other life sciences can produce a lot of quantitative data which needs to be analyzed for statistical significance. Many graduates know to use Word, Powerpoint and Excel to a certain level. However, many new emerging job opportunities in modern biology requires skill to deal with quantitative data.

Below, I’ve mentioned 7 free online tools to take care of statistical needs ranging from T-tests, multiple regressions to Cluster Analysis, Bootstrapping etc.

1. SISA (Simple Interactive Statistical Analysis)

Conduct your statistical analysis directly online, no need to download anything. Click SISA for more details. You can also study the given guides to determine the appropriate procedure for your research problem.

2. Open Epi

Open Epi is a free software program designed to cater for statistical needs in epidemiology. It can run from a web server or can also be downloaded and run without a web connection. You can also operate this program from your android or iphone.

3. Scistat Calc

This is actually a blog ( running on blogspot). It has online calculators for common probability functions and significance tests and also explanation of concepts and formulas behind each test. Please go through Scistat Calc, it’s a really useful blog.

4. Rice Virtual Lab in Statistics

It contains online statistics book, simulations, case studies and other resources for statistical analysis. You can access it here.

5. WINPEPI

This is a free software available only for Windows users. WINPEPI has many programs ranging from comparing any 2 independent samples to multiple poisson regression, for more details visit WINPEPI

6. Online Graph generators

Popular free online graph tools for producing neat scatter plots are Meta-calculator and Online Curve fitting. These are worth a try.

7. R ( Open Source Statistical software)

Most of the bachelors and masters students use MS Excel for their statistical needs. Excel can be used to calculate t-tests and other co-relations decently. But, when you are handling a lot of data and need to do something more, then Excel may not be the right choice.

R is more than a software. It is a language for statistical computing and graphics. It caters for a very wide variety of statistical analysis and the speciality of R language is that it produces quality graphs fit for publication (including mathematical symbols and formulae). It runs on Windows, Linux and also Mac. Moreover, it is free !!

Like any language it takes time to learn, but it has TONS of benefits. R language is widely used by statisticians and many commercial firms for data mining and analysis. To put it in very simple terms, it is comparable to MATLAB, but it is free. Download R language at https://www.r-project.org/

Details regarding Documentation can be found at R – documentation. Free online courses about how to use R can be found at Datacamp and Coursera (At coursera, the next session is from August 3 to August 30; 2015). R is actually one computer language which will always be useful for researchers and it is being constantly updated. Hence, it won’t be outdated soon. So why not invest your spare time to learn this useful language?

Flu Vaccine Becomes Universal

While many of us are spending the last half of the summer deciding where the nicest beaches are and who makes the best island cocktails, infectious disease scientists are looking ahead toward the next inevitable outbreak of the flu. Influenza hunters travel to hot zones that have long been the traditional breeding grounds and launching points for global seasonal pandemics. This is an important part of creating seasonal flu vaccines, which protect against only a few specific strains that researchers predict will be the most common for the upcoming year.

Anatomy of influenza virus. An array of subtypes for the surface coat protein hemagglutinin (blue) is what NIAID scientists used to create their universal vaccine. [CDC/Dan Higgins]

What if we could create a vaccine that could protect against most or all influenza strains? This has been the “grail quest” that numerous infectious disease researchers have strived toward for decades. Now, investigators from the National Institute of Allergy and Infectious Diseases (NIAID), a division of the National Institutes of Health, have developed a universal vaccine that may provide broad protection against numerous influenza strains, including ones that could cause future pandemics. 

"The reason researchers change the vaccine every year is that they want to specifically match the vaccine to the particular viruses that are circulating, such as H1N1. If the vaccine is just a little bit different to the target virus, it is not expected to offer much protection," explained senior author Jeffery Taubenberger, M.D., Ph.D., chief of the Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases at NIAID. "What we have done is design a strategy where you don't have to think about matching the vaccine antigen to the virus at all."

The findings from this study were published recently in mBio through an article entitled “An Intranasal Virus-Like Particle Vaccine Broadly Protects Mice from Multiple Subtypes of Influenza A Virus.”

Previous research into universal flu vaccines has focused on finding invariable regions of viral coat proteins that could be exploited to generate an immune response that provides significant protection. However, in this study the scientists took a different approach and engineered a virus-like particle (VLP) that expressed an array of hemagglutinin subtypes from the surface of the influenza virus, including H1, H3, H5, and H7.

"There are 16 different hemagglutinin subtypes that circulate in birds and are thought to be the basis for current and future influenza pandemics," stated Dr. Taubenberger. "The hypothesis was that the presentation of these different viral proteins would stimulate the development of cross-protective immunity that would provide broader protection against multiple subtypes."

The H1 and H3 subtypes were chosen as they have been linked to major influenza outbreaks since the 1918 Spanish flu pandemic, which has been estimated to have killed close to 100 million people. The investigators chose H5 and H7 subtypes, as they have been the cause of recent bird flu outbreaks and have a high potential to spread into humans.

The results from the study showed that 95% of mice vaccinated with the novel cocktail were protected against a lethal challenge from eight different influenza strains, while only 5% of unvaccinated mice survived. 

"Almost all of the animals that were vaccinated survived, including mice that were challenged with viruses that expressed hemagglutinin subtypes that were not in the vaccine at all, viruses that expressed H2, H6, H10, and H11," noted Dr. Taubenberger. "What that suggests is that this approach really gives us broad spectrum protection, and could serve as a basis for an effective pre-pandemic vaccine."

The NIAID team was also able to show that vaccine’s efficacy lasted for at least 6 months and that it worked well in older mice—an important point since current vaccines are less effective in the elderly.

"These initial findings are very positive and suggest a promising and practical strategy for developing a vaccine with amazing, broad protection," concluded Dr. Taubenberger.

Source: http://www.genengnews.com/gen-news-highlights/flu-vaccine-becomes-universal/81251534/

NASA finds ‘another Earth’ in Milky Way and it's called Earth 2.0

Earth 2.0 or Kepler 452b is so like Earth that Nasa believes it is possible that life once inhabited the planet. 

Nasa has found a twin Earth orbiting a star like the Sun in the Milky Way which scientists say ‘would feel a lot like home.’

Kepler 452b - which has been dubbed Earth 2.0 - is six billion years old, has a 385 day year and orbits its star at the same distance as us. It is 1,400 light-years away in the constellation Cygnus.


It is believed to be rocky, with active volcanoes and is so like Earth that Nasa believes it is possible that life once inhabited the planet.


Scientists said that the sunshine is so similar that plants could survive if taken to Kepler 452b.

But because it is 1.5 billion years older, scientists say it gives a ‘peek into a crystal ball showing a possible future for Earth’ as it reaches a point where it is no longer habitable.

“If Kepler 452b is indeed a rocky planet, its location could mean that it is just entering a runaway greenhouse phase of its climate history,” said Doug Caldwell, a SETI Institute scientist working on the Kepler mission.

“The increasing energy from its aging sun might be heating the surface and evaporating any oceans. The water vapour would be lost from the planet forever.

“Kepler 452b could be experiencing now what the Earth will undergo more than a billion years from now, as the Sun ages and grows brighter.”

The Kepler spacecraft has been looking for signs of new worlds outside the Solar System since May 2009, and has so far found more than 4,000 planets in the so-called ‘Goldilocks Zone’ – neither too hot, nor too cold to sustain life.

On Thursday Nasa announced they had found 500 new possible planets to add to the 4,175 already found by the telescope, and 12 were ‘Earth-like.’ But Kepler 452b is the first of the 12 to be confirmed as a planet and Nasa said it was the 'closest' to Earth that has ever been seen.

It is 60 percent larger in diameter than Earth and is considered a super-Earth-size planet.

“Today the Earth is a little less lonely because there is a new kid on the block,” said Jon Jenkins, Kepler data analysis lead at NASA's Ames Research Center in Moffett Field, California.

"If you travelled to this star with an arkful of plants...the plants would photosynthesise just perfectly fine. It would feel a lot like home from the standpoint of the sunshine.

“It is six billion years old. That is considerable opportunity for life to arise on its surface and its oceans should all the necessary conditions for life have appeared on this planet.

“This is the closest thing that we have to another planet like the Earth. And the Earth follows nearly in the footsteps of its older cousin and will be there in 1.5 billion years time.”



The area of the Milky Way in which Kepler is looking Credit: NASA

The discovery gives new hope that alien civilisations may exist beyond the Solar System. Earlier this week Professor Stephen Hawking and the Astronomer Royal Lord Martin Rees announced they were joining a $100 million project to seek out signs of extra-terrestrial intelligence in the Milky Way.

"We won't be going to this planet but our children's children's children might be," said Jeff Coughlin, Kepler research scientist at SETI Institute in Mountain View, California "It's a very long term goal but a very exciting one."

Kepler’s task is to look for rocky planets between half and twice the size of Earth where water could still exist on the surface.

Since liquid water is critical to life on Earth, many scientists believe the search for extra-terrestrial life should focus on planets where liquid water occurs.

The size of the planet also means it has enough gravity to pull in gases like hydrogen and helium to form an atmosphere.

The space observatory detects planets as their orbits cross in front of their star and cause a very tiny but periodic dimming of the star’s brightness.

Nasa is also trying to determine the fraction of the hundreds of billions of stars in our galaxy that might have such planets.

“We’re trying to answer fundamental questions, Where do we come from, where are we going? What’s the future of our Solar System,” John Grunsfeld, associate administrator for NASA's Science Mission Directorate .

“We’re going to take one small step in answering that question today.”

MicrobeWorld's After Hours - Antibiotic Resistant Bacteria

#Event

Titled: MicrobeWorld's After Hours - Antibiotic Resistant Bacteria

Difference between CV and Resume...........

With renovation in world, people become educated and smart but still there are few things people are unaware. Therefore today will talk about an important issue facing by beginners especially. You might be thinking that what it is. Yes there is an issue people are unaware that is difference between resume and CV. Now day’s even adults and working people do not know the exact difference. However, for understanding the difference, first of all everyone should know the definition of resume and CV.

CV Vs Resume

These two terms are entirely different from each other. People should know the difference between CV and resume.

What is CV? 

CV is basically called Curriculum Vitae.

• CV basically provides a complete summary of your educational background and extra achievements.
• It also contains your different experiences, researches, awards, honors, presentations and speeches.
• There is no word limit in CV.

CV used for what?

Normally fresh graduates and job seeker use CV. Moreover, purpose of CV is to apply for any internship, scholarship and job. It can also be called an application by a person who is applying for something.

What Resume means?

• Resume basically means complete information about your professional experiences.
• There is word or page limit in resume. Like you cannot extend from two pages.
• Precisely, resume is a way to show your capabilities in a proficient manner.

Resume used for what? 

It is used to apply for any industry, company, organization and governmental job. Through using resume anybody can show inner talent by offering good impression of personality. Main reason of resume is to get a reliable and good job.

Difference between CV and Resume: 

The major difference between CV and Resume is that person has to alter details for different position in Resume but in CV, it remains the similar. Moreover, in CV everything listed in a chain or we can say sequence but in Resume, you have to add your professional achievements and information in different manner without following any chronological order. Furthermore, CV has entire record of your educational career and your information. On the other hand, in Resume only target information is existed. No format is followed in Resume but in CV you have to follow certain format. CV can be prolonged but resume cannot be. In addition, Canada, America UK, South Africa, New Zealand, Ireland, is the countries where it is preferable to for CV instead of Resume. However, in India and Australia these two terms are transposable. People can also get differentiation information by taking help from internet as now people getting informed day by day.

So are you ready for a better life?

If you really want to achieve few goals in your life then make sure to know the dissimilarity between these two terms. Otherwise, you are unacquainted from a major distinction and for having a first-class job, cleverness and brain power both matter. So live a life with self-reliance and information by attaining your goals of life.

99 Facts about DNA. How many do you know?

Facts About DNA

1. DNA stands for deoxyribonucleic acid.
2. DNA is part of our definition of a living organism.
3. DNA is found in all living things.
4. DNA was first isolated in 1869 by Friedrich Miescher.
5. James Watson and Francis Crick figured out the structure of DNA.
6. DNA is a double helix.
7. The structure of DNA can be likened to a twisted ladder.
8. The rungs of the ladder are made up of “bases”
9. Adenine (A) is a base.
10. Thymine (T) is a base.
11. Cytosine (C) is a base
12. Guanine (G) is a base.
13. A always pairs with T in DNA.
14. C also pairs with G in DNA.
15. The amount of A is equal to the amoun tof T, same for C and G.
16. A+C = T+G
17. Hydrogen bonds hold the bases together.
18. The sides of the DNA ladder is made of sugars and phosphate atoms.
19. Bases attached to a sugar; this complex is called a nucleoside.
20. Sugar + phosphate + base = nucleotide.
21. The DNA ladder usually twists to the right.
22. There are many conformations of DNA: A-DNA, B-DNA, and Z-DNA are the only ones found in nature.
23. Almost all the cells in our body have DNA with the exception of red blood cells.
24. DNA is the “blueprint” of life.
25. Chromosomal or nuclear DNA is DNA found in the nucleus of cells.
26. Humans have 46 chromosomes.
27. Autosomal DNA is part of chromosomal DNA but does not include the two sex chromsomes – X and Y.
28. One chromosome can have as little as 50 million base pairs or as much as 250 million base pairs.
29. Mitochondrial DNA (mtDNA) is found in the mitochondria.
30. mtDNA is only passed from the mother to the child because only eggs have mitochondria, not sperm.
31. There’s a copy of our entire DNA sequence in every cell of our body with one exception.
32. Our entire DNA sequence is called a genome.
33. There’s an estimated 3 billion DNA bases in our genome.
34. One million bases (called a megabase and abbreviated Mb) of DNA sequence data is roughly equivalent to 1 megabyte of computer data storage space.
35. Our entire DNA sequence would fill 200 1,000-page New York City telephone directories.
36. A complete 3 billion base genome would take 3 gigabytes of storage space.
37. If unwound and tied together, the strands of DNA in one cell would stretch almost six feet but would be only 50 trillionths of an inch wide.
38. In humans, the DNA molecule in a non-sex cell would have a total length of 1.7 metres.
39. If you unwrap all the DNA you have in all your cells, you could reach the moon 6000 times!
40. Our sex cells–eggs and sperm–have only half of our total DNA.
41. Over 99% of our DNA sequence is the same as other humans’.
42. DNA can self-replicate using cellular machinery made of proteins.
43. Genes are made of DNA.
44. Genes are pieces of DNA passed from parent to offspring that contain hereditary information.
45. The average gene is 10,000 to 15,000 bases long.
46. The segment of DNA designated a gene is made up of exons and introns.
47. Exons have the code for making proteins.
48. Introns are intervening sequences sometimes called “junk DNA.”
49. Junk DNA’s function or lack thereof is a source of debate.
50. Part of “junk DNA” help to regulate the genomic activity.
51. There are an estimated 20,000 to 25,000 genes in our genome.
52. In 2000, a rough draft of the human genome (complete DNA sequence) was completed.
53. In 2003, the final draft of the human genome was completed.
54. The human genome sequence generated by the private genomics company Celera was based on DNA samples collected from five donors who identified themselves only by race and sex.
55. If all the DNA in your body was put end to end, it would reach to the sun and back over 600 times (100 trillion times six feet divided by 92 million miles).
56. It would take a person typing 60 words per minute, eight hours a day, around 50 years to type the human genome.
57. If all three billion letters in the human genome were stacked one millimeter apart, they would reach a height 7,000 times the height of the Empire State Building.
58. DNA is translated via cellular mechanisms into proteins.
59. DNA in sets of 3 bases, called a codon, code for amino acids, the building blocks of protein.
60. Changes in the DNA sequence are called mutations.
61. Many thing can cause mutations, including UV irradiation from the sun, chemicals like drugs, etc.
62. Mutations can be changes in just one DNA base.
63. Mutations can involve more than one DNA base.
64. Mutations can involve entire segments of chromosomes.
65. Single nucleotide polymorpshisms (SNPs) are single base changes in DNA.
66. Short tandem repeats (STRs) are short sequences of DNA repeated consecutively.
67. Some parts of the DNA sequence do not make proteins.
68. Genes make up only about 2-3% of our genome.
69. DNA is affected by the environment; environmental factors can turn genes on and off.
70. There are many ways you can analyze your DNA using commercially available tests.
71. Paternity tests compare segments of DNA between the potential father and child.
72. There are other types of relationship testing that compares DNA between siblings, grandparents and grandchild, etc.
73. DNA tests can help you understand your risk of disease.
74. A DNA mutation or variation may be associated with a higher risk of a number of diseases, including breast cancer.
75. DNA tests can help you understand your family history aka genetic genealogy.
76. DNA tests can help you understand your ethnic make-up.
77. DNA can be extracted from many different types of samples: blood, cheek cells, urine.
78. DNA can be stored either as cells on a cotton swab, buccal brush, or frozen blood or in extracted form.
79. In forensics, DNA analysis usually looks at 13 specific DNA markers (segments of DNA).
80. The odds that two individuals will have the same 13-loci DNA profile is about one in one billion.
81. A DNA fingerprint is a set of DNA markers that is unique for each individual except identical twins.
82. Identical twins share 100% of their genes.
83. Siblings share 50% of their genes.
84. A parent and child share 50% of their genes.
85. You can extract DNA at home from fruit and even your own cheek cells.
86. DNA is used to determine the pedigree for livestock or pets.
87. DNA is used in wildlife forensics to identify endangered species and people who hunt them (poachers).
88. DNA is used in identify victims of accidents or crime.
89. DNA is used to exonerate innocent people who’ve been wrongly convicted.
90. Many countries, including the US and UK, maintain a DNA database of convicted criminals.
91. The CODIS databank (COmbined DNA Index System) is maintained by the BI and has DNA profiles of convicted criminals.
92. Polymerase chain reaction (PCR) is used to amplify a sample of DNA so that there are more copies to analyze.
93. We eat DNA every day.
94. DNA testing is used to authenticate food like caviar and fine wine.
95. DNA is used to determine the purity of crops.
96. Genetically modified crops have DNA from another organism inserted to give the crops properties like pest resistance.
97. Dolly the cloned sheep had the same nuclear DNA as its donor mom but its mitochondrial DNA came from from the egg mom. (Does that make any sense?)
98. People like to talk about DNA even if it bears no relation to science or reality.
99. A group of bloggers who write regularly about DNA and genetics have banded to gether to form The DNA Network.

Phage Therapy - The Future of "Precision Treatment"

Published on: SCIENCE,19 June, 2015

Bacteriophage WINS !!!!

#Bacteriophage_Therapy     #Phage_Therapy    #E.coli_VS_Bacteriophage

#Phage_Therapy_in_Nepal

Extra DNA Base Discovered

By Jef Akst | June 23, 2015

An epigenetic variant of cytosine is stable in the genomes of living mice, suggesting a possible expansion of the DNA alphabet.

An epigenetic mark known as 5-formylcytosine (5fC) may be more than a transitory state that helps regulate gene expression. According to a study published yesterday (June 22) in Nature Chemical Biology, 5fC is stable in the mouse genome and may represent a fifth nucleotide in the DNA alphabet.

“It had been thought this modification was solely a short-lived intermediate, but the fact that we’ve demonstrated it can be stable in living tissue shows that it could regulate gene expression and potentially signal other events in cells,” coauthor Shankar Balasubramanian of the Cancer Research UK Cambridge Institute said in a press release.

While the function of the modified base—essentially a methylated cytosine with added oxygen—remains unclear, its position within the genome points to a role in gene expression. “This modification to DNA is found in very specific positions in the genome—the places which regulate genes,” lead author Martin Bachman, who conducted the research while at the University of Cambridge, said in the release. “In addition, it’s been found in every tissue in the body—albeit in very low levels.” High-resolution mass spectrometry revealed 5fC to be most common in the mouse brain, but even there it was present at only 10 parts per million or less.

But when the researchers enriched cultures of mouse cells or mice’s diets with stable isotopes of carbon and hydrogen, they found no uptake into 5fC bases, suggesting the modification is stable.

“If 5fC is present in the DNA of all tissues, it is probably there for a reason,” added Balasubramanian. “This will alter the thinking of people in the study of development and the role that these modifications may play in the development of certain diseases.”

Source: http://www.the-scientist.com/?articles.view/articleNo/43358/title/Extra-DNA-Base-Discovered/

Earth’s sixth mass extinction has begun, new study confirms !!!

Contributor

James Dyke

Lecturer in Complex Systems Simulation at University of Southampton

We are currently witnessing the start of a mass extinction event the likes of which have not been seen on Earth for at least 65 million years. This is the alarming finding of a new study published in the journal Science Advances.

The research was designed to determine how human actions over the past 500 years have affected the extinction rates of vertebrates: mammals, fish, birds, reptiles and amphibians. It found a clear signal of elevated species loss which has markedly accelerated over the past couple of hundred years, such that life on Earth is embarking on its sixth greatest extinction event in its 3.5 billion year history.

This latest research was conducted by an international team lead by Gerardo Ceballos of the National Autonomous University of Mexico. Measuring extinction rates is notoriously hard. Recently I reported on some of the fiendishly clever ways such rates have been estimated. These studies are producing profoundly worrying results.

However, there is always the risk that such work overestimates modern extinction rates because they need to make a number of assumptions given the very limited data available. Ceballos and his team wanted to put a floor on these numbers, to establish extinction rates for species that were very conservative, with the understanding that whatever the rate of species lost has actually been, it could not be any lower.

This makes their findings even more significant because even with such conservative estimates they find extinction rates are much, much higher than the background rate of extinction – the rate of species loss in the absence of any human impacts.

Here again, they err on the side of caution. A number of studies have attempted to estimate the background rate of extinction. These have produced upper values of about one out of every million species being lost each year. Using recent work by co-author Anthony Barnosky, they effectively double this background rate and so assume that two out of every million species will disappear through natural causes each year. This should mean that differences between the background and human driven extinction rates will be smaller. But they find that the magnitude of more recent extinctions is so great as to effectively swamp any natural processes.

Cumulative vertebrate species recorded as extinct or extinct in the wild by the IUCN (2012). Dashed black line represents background rate. This is the ‘highly conservative estimate’.

Click to enla

The “very conservative estimate” of species loss uses International Union of Conservation of Nature data. This contains documented examples of species becoming extinct. They use the same data source to produce the “conservative estimate” which includes known extinct species and those species believed to be extinct or extinct in the wild.

Farewell, broad-faced potoroo, we hardly knew yew....

The paper has been published in an open access journal and I would recommend reading it and the accompanying Supplementary Materials. This includes the list of vertebrate species known to have disappeared since the year 1500. The Latin names for these species would be familiar only to specialists, but even the common names are exotic and strange: the Cuban coney, red-bellied gracile, broad-faced potoroo and southern gastric brooding frog.

These particular outer branches of the great tree of life now stop. Some of their remains will be preserved, either as fossils in layers of rocks or glass eyed exhibits in museum cabinets. But the Earth will no longer see them scurry or soar, hear them croak or chirp.

You may wonder to what extent does this matter? Why should we worry if the natural process of extinction is amplified by humans and our expanding industrialised civilisation?

One response to this question essentially points out what the natural world does for us. Whether it’s pollinating our crops, purifying our water, providing fish to eat or fibres to weave, we are dependent on biodiveristy. Ecosystems can only continue to provide things for us if they continue to function in approximately the same way.

The relationship between species diversity and ecosystem function is very complex and not well understood. There may be gradual and reversible decreases in function with decreased biodiversity. There may be effectively no change until a tipping point occurs. The analogy here is popping out rivets from a plane’s wing. The aircraft will fly unimpaired if a few rivets are removed here or there, but to continue to remove rivets is to move the system closer to catastrophic failure.

This latest research tells us what we already knew. Humans have in the space of a few centuries swung a wrecking ball through the Earth’s biosphere. Liquidating biodiversity to produce products and services has an end point. Science is starting to sketch out what that end point could look like but it cannot tell us why to stop before we reach it.

If we regard the Earth as nothing more than a source of resources and a sink for our pollution, if we value other species only in terms of what they can provide to us, then we we will continue to unpick the fabric of life. Remove further rivets from spaceship earth. This not only increases the risk that it will cease to function in the ways that we and future generations will depend on, but can only reduce the complexity and beauty of our home in the cosmos.

Source: https://theconversation.com/earths-sixth-mass-extinction-has-begun-new-study-confirms-43432