Fight against malaria gets two new weapons

(Credit: Getty Images)

Two new strategies show promise in battling malaria, a disease that kills more than 400,000 people each year, mostly children ages five and under in sub-Saharan Africa.

Both new strategies involve making Anopheles mosquitoes more resistant to malaria parasites, which live in the insects and infect humans when female mosquitoes feed on human blood.

Building mosquito resistance to the parasite would reduce the need for repeated, continuous use of other malaria control measures, such as insecticides and bed nets.

One team of researchers from the Johns Hopkins Bloomberg School of Public Health’s Malaria Research Institute discovered a strain of bacteria that can spread rapidly and persist long-term among malaria-carrying mosquitoes. They genetically modified the bacterial strain in a way that strongly suppresses development of malaria parasites, making mosquitoes much less likely to transmit parasites to humans.

A second team of researchers used a genetic modification to boost the immune system of malaria-carrying mosquitoes. The genetic change not only suppresses malaria parasites in the insects but also spreads quickly in a test population by changing mosquitoes’ mating preferences.

If the teams’ initial promising results continue to pan out, altered bacteria and mosquitoes eventually could be released into populations of wild mosquitoes. There, they would spread the genetic changes and eventually reduce malaria transmission to humans.

Odd microbes

In the first study, the discovery of the new mosquito-infecting bacterial strain was a chance event.

“We were working with a different bacterium when a researcher on the project happened to find evidence of a bacterial colony in our mosquitoes’ ovaries,” says senior author Marcelo Jacobs-Lorena, a professor of molecular microbiology and immunology. “That was unusual—normally we find bacteria only in the mosquito gut.”

His team soon characterized these odd microbes as a strain of Serratia bacteria, and dubbed them Serratia AS1.

Researchers have been developing genetically engineered bacteria that can infect mosquito populations and kill the malaria parasites the mosquitoes harbor, without harming the mosquitoes themselves. Getting such bacteria to spread efficiently has been a key challenge, but experiments revealed Serratia AS1 is almost perfect for the task. Unlike other mosquito-infecting bacteria, Serratia AS1 turned out to be easily transmitted from males to females during mating and from female mosquitoes to their offspring.

‘Coloring’ parasite genes shows malaria’s weak spot

The scientists modified Serratia AS1 by adding genes for five potent antimalarial proteins. Powered by the proteins, the bacteria strongly inhibited parasite development in colonized mosquitoes, reducing levels of an early stage of the parasite by more than 90 percent. Experiments also showed that the modified Serratia AS1 bacteria do not have a significant effect on lifespan or fertility of the mosquitoes themselves.

“So far all indications are that these anti-malarial proteins are universally effective against malaria parasites, and the Serratia AS1 bacteria that carry them can go into any malaria-carrying mosquito species,” Jacobs-Lorena says.

Changing mosquito mating preference

In the second study, a team led by George Dimopoulos, also a professor of molecular microbiology and immunology, made small modifications to the DNA of malaria-transmitting Anopheles mosquitoes to boost the activity of their immune genes. The enhanced immunity made the mosquitoes more resistant to infection by malaria parasites, and thus less likely to transmit the parasites to humans.

That result was expected. What was not expected was the unusually high efficiency with which the modified mosquitoes spread their genetic modification to later generations in a mixed population of modified and unmodified, wild-type mosquitoes.

Investigating this surprising result, Dimopoulos and colleagues found that boosting the mosquitoes’ immune genes also altered the mix of bacterial species in the mosquito intestine and reproductive organs. This change in the insect “microbiota” in turn led to a change in mating preferences: Modified male mosquitoes began to prefer unmodified, wild-type females, while wild-type males began to prefer modified females.

New drug could be back-up in fight against malaria

“We believe that, by changing the microbiota, we’re changing the scent of modified mosquitoes—which in turn alters mating preference,” Dimopoulos says. “It’s the perfect change in mating preference in this case, because it maximizes the chances of producing genetically modified offspring when mosquitoes compete for mates.”

Dimopoulos’s modified mosquito population has now been living in a colony in his laboratory for more than seven years, and has retained its high level of resistance to malaria for all that time without any apparent adverse side effects.

The two research groups describe their findings in the journal Science.

The National Institute of Allergy and Infectious Diseases and Bloomberg Philanthropies provided funding for both studies. The Chinese Academy of Sciences and the National Nature Science Foundation of China also funded the Jacobs-Lorena research.

Source: Johns Hopkins University


Malaria parasite packs bags to travel from host to host

(Credit: jev55/Flickr)

The parasite that causes malaria has not one, but two, specialized proteins that protect its messenger RNA—genetic material that encodes for proteins—until the parasite takes up residence in a new mosquito or a human host, researchers report.

A new study describes the two proteins and reveals an additional role that one may play to facilitate RNA-based interactions between the parasite, its mosquito vector, and its human host.

“Understanding the malaria parasite and how it interacts with its host may provide insights that could help prevent the spread of this often-fatal disease,” says Scott Lindner, an assistant professor of biochemistry and molecular biology at Penn State and senior author of the study, which appears in the journal mSphere.

Always ready to move

“The malaria parasite has a complex life cycle that includes phases in the mosquito vector, the human liver, and in human blood. Moreover, the parasite has no idea when it’s going to be transmitted from a mosquito to a human host and back, so it always needs to be ready to be transmitted,” Lindner says.

“It prepares for this by making and packaging up the mRNAs that it will eventually need for making proteins inside its new host or a new mosquito,” he explains.

During this process, called translational repression, special proteins bind to mRNAs and prevent them from being translated into protein. One protein binds to the mRNA’s poly(A) tail—a repeated string of As or adenosine molecules added to the end of most mRNA strands. This helps to form a silenced complex of proteins and RNA that is poised for action after the parasite is transmitted to the host.

Most single-celled organisms have one type of this poly(A)-binding protein, while multi-cellular organisms have two. In this study, the researchers characterize two types of poly(A)-binding proteins in the single-celled Plasmodium parasite, both of which contribute to translational regulation.

“We knew from our lab’s previous work that Plasmodium had a type of poly(A)-binding protein that functions outside of the nucleus of the cell,” says Allen Minns, research technician at Penn State and first author of the paper.

“This protein binds and protects the poly(A) tail at one end of an mRNA strand. In this study, we used biochemical approaches to further characterize this protein, and found that it also has a specialized job receiving mRNAs. It forms chains without the presence of RNA, which potentially allows large assemblies of the protein to quickly protect the entire length of the poly(A) tail.”

The researchers also identified and characterized a second type of poly(A)-binding protein that functions inside the nucleus of the parasite during the blood stages of its life cycle.

In multi-cellular organisms, this second poly(A)-binding protein usually performs a quality control check before mRNA exits the nucleus, confirming that the mRNA is constructed properly. These quality control proteins then pass on the mRNA strand to other proteins outside of the nucleus, which direct translational repression to translate or package the mRNA for later use.

Inside vs. outside

In addition to an important role in translational regulation inside of the cell, the researchers also discovered that the non-nuclear poly(A)-binding protein may play a surprising role outside of the cell.

Fight against malaria gets two new weapons

“When the parasite takes the form of a sporozoite in the mosquito, we actually don’t see the vast majority of the non-nuclear poly(A)-binding protein inside the cell where we expected it to be—where it would interact with mRNAs produced by the parasite,” says Lindner.

“Instead, the protein accumulates at the surface of the sporozoite and is shed when the parasite moves,” he says. “We don’t see this happening in other life stages of the parasite, and this is now the third RNA-binding protein found to be on the surface of the sporozoite. The parasite is putting these RNA-binding proteins out there on its surface for a reason; the new and exciting question is why.”

The researchers speculate that the poly(A)-binding proteins on the sporozoite surface allow the parasite to interact with RNA from sources outside of the parasite and could thus provide an opportunity for the parasite to interact with the mosquito or the host through their RNA.

“This study suggests that the parasite’s interaction with outside RNA is probably much more pervasive than we thought it was,” says Lindner. “It is possible that this kind of interaction could eventually provide a new target for intervention strategies, but the first step is understanding why the malaria parasite has these poly(A)-binding proteins on the sporozoite surface.”

Enzyme discovery could offer new malaria drugs

In addition to Lindner and Minns, the research team includes Penn State graduate students Kevin Hart and Suriyasri Subramanian, and Susan Hafenstein, associate professor of biochemistry and molecular biology at Penn State University Park and associate professor medicine and of microbiology and immunology at the Penn State College of Medicine.

The National Institutes of Health and the Huck Institutes of the Life Sciences supported the work.

Source: Penn State

Malaria can be deadly because of these proteins

Khmer families get their temperature taken during an intense malaria screening which is part of a World Health Organization (WHO) on a Malaria Containment project along the Thai-Cambodian border in Andong Thma village in Pailin province. (Credit: Getty Images)

The most severe strains of malaria infection are associated with a small group of proteins, according to a new study.

The finding could be a step toward a vaccine against the deadliest forms of the disease.

“The great burden of mortality for malaria is in children under five.”

Not all cases of malaria are the same. There are thousands of different strains—some parasites cause only mild symptoms, while other more severe forms can cause disease and death.

And not all people are the same. Some infected people show no obvious symptoms, while others succumb to a severe and, ultimately, fatal disease. This second group often includes young children who have not yet had a chance to develop a strong immune response to the parasite.

“The great burden of mortality for malaria is in children under five,” says Michael Duffy, a malaria researcher with the School of BioSciences and the Bio21 Institute at the University of Melbourne.

Why are children high risk?

The World Health Organization reported 429,000 malaria deaths in 2015, of which 70 percent were children under the age of 5. Why are children at such high risk of death? And why do some die while others survive?

“We asked ourselves—is it something about the humans or the parasites that results in this difference?” Duffy says. “We think it’s an interplay of both.

“What we think is that the immunologically naïve—that is, people who have never previously been exposed—get infected with these parasites and those parasites that cause severe disease dominate in these early infections. Either you become immune or you die.”

Duffy believes the key to combating the public health challenge is to focus on those people who are most susceptible to severe strains—young children—and focus on those malaria strains that are most likely to cause death.

But how can you tell a deadly strain from a more benign one?

Different malaria strains

Researchers developed a fingerprinting technique to uniquely identify different strains of malaria in a population based on the genes (called var genes) that code for the surface protein PfEMP1. This protein plays a key role in the parasite’s ability to evade our immune systems.

Each parasite contains around 60 versions of the var gene and when in the bloodstream of a host, these genes are expressed one at a time, each time building a new surface protein.

“We won’t eradicate malaria, but we may be able to protect children when they are most vulnerable to death or serious morbidity…”

“So you develop immunity to one protein and you start to kill off the parasites expressing it,” Duffy says. “And then it spontaneously switches to another protein to which you have no immunity.”

A few years ago, researchers discovered there is probably a particular set of PfEMP1 proteins that cause severe disease.

“Once you are immune to them, you are immune to severe disease, but you can still be infected with uncomplicated malaria, or be asymptomatic,” Duffy says.

To test this, researchers used new sequencing and fingerprinting technologies to sample parasites isolated from the blood of 44 adults in a location where malaria is endemic in the state of Papua in Indonesia. Twenty-three people had severe malaria.

Researchers then assembled 4,662 pieces of var genes that were being expressed in these parasites and compared the genes expressed in severe cases against those expressed in mild cases.

They used advanced statistical processing to show that a tiny subset of the thousands of var genes that were present were being expressed at a higher rate in patients with severe malaria than in those with uncomplicated strains.

Other groups have tested patients in India and Africa for known var genes and have found similarly found an association between the expression of certain genes and severe malaria.

However, this test on the Papuan community was the first time the association could be made with all the genes that were present, not just those that were already known about.

“This is the first time anyone has taken the genes that are expressed, sequenced everything that’s there and tried to assemble them, to work out what’s present and what’s different between severe and uncomplicated cases,” Duffy says.

Malaria parasite packs bags to travel from host to host

Incredibly, all the proteins associated with severe malaria in India and Africa were also upregulated (had a heightened response) in the severe cases in Papua, suggesting that this small group of deadly proteins is highly conserved around the world.

Looking forward

With their comprehensive screening technology, the research team also found many severe-malaria-associated proteins that hadn’t been identified elsewhere.

Researchers are now looking to test children in malaria-endemic regions of Africa—the group by far the most at risk from death—to see if the new deadly proteins they found in Papua are also present there.

“We also want to look for serological responses—whether people have antibodies to these proteins in their blood,” Duffy says.

“Are kids with severe infections missing antibodies to these proteins? Do those who don’t get severe infections have them?” A positive result could lead to a solution to the malaria vaccine puzzle.

A broadly effective vaccine remains elusive largely because malaria is so diverse and each parasite is constantly changing its attack strategy, finding a valid target for a vaccine is hard.

“But now we are starting to understand that, of the thousands of versions of the PfEMP1 protein that are out there, only a handful, maybe 20 or 30, are causing the most severe cases of malaria. And so, we might be able to target vaccines to just these severe versions.

“We won’t eradicate malaria, but we may be able to protect children when they are most vulnerable to death or serious morbidity from malaria, and thus greatly reduce the burden of the disease.”

Fight against malaria gets two new weapons

The findings appear in PLOS Biology. Other researchers are from the University of Melbourne; Oxford University; the Walter and Eliza Hall Institute of Medical Research; the Eijkman Institute for Molecular Biology in Jakarta, Indonesia; the Timika Malaria Research Program; Papuan Health and Community Development Foundation, Indonesia; the Peter McCallum Cancer Centre; and Charles Darwin University.

Source: University of Melbourne

What if we’re not Earth’s first big civilization?

(Credit: Getty Images)

How do we really know that there weren’t civilizations on Earth before ours? A new paper addresses this question.

Imagine if, many millions of years ago, dinosaurs drove cars through cities of mile-high buildings. A preposterous idea, right? Over the course of tens of millions of years, however, all of the direct evidence of a civilization—its artifacts and remains—gets ground to dust. How do we know there weren’t previous industrial civilizations on Earth that rose and fell long before human beings appeared?

It’s a compelling thought experiment, and one that Adam Frank, a professor of physics and astronomy at the University of Rochester, and Gavin Schmidt, the director of the NASA Goddard Institute for Space Studies, take up in the International Journal of Astrobiology. Frank also considers the evidence in The Atlantic.

The history of the world

“Gavin and I have not seen any evidence of another industrial civilization,” Frank explains. But by looking at the deep past in the right way, a new set of questions about civilizations and the planet appears: What geological footprints do civilizations leave? Is it possible to detect an industrial civilization in the geological record once it disappears from the face of its host planet?

“These questions make us think about the future and the past in a much different way, including how any planetary-scale civilization might rise and fall.”

In what they deem the “Silurian Hypothesis,” Frank and Schmidt define a civilization by its energy use.

Human beings are just entering a new geological era that many researchers refer to as the Anthropocene, the period in which human activity strongly influences the climate and environment. In the Anthropocene, fossil fuels have become central to the geological footprint humans will leave behind on Earth.

By looking at the Anthropocene’s imprint, Schmidt and Frank examine what kinds of clues future scientists might detect to determine that human beings existed. In doing so, they also lay out evidence of what might be left behind if industrial civilizations like ours existed millions of years in the past.

Human beings began burning fossil fuels more than 300 years ago, marking the beginnings of industrialization. The researchers note that the emission of fossil fuels into the atmosphere has already changed the carbon cycle in a way that is recorded in carbon isotope records.

Other ways human beings might leave behind a geological footprint include:

  • Global warming, from the release of carbon dioxide and perturbations to the nitrogen cycle from fertilizers
  • Agriculture, through greatly increased erosion and sedimentation rates
  • Plastics, synthetic pollutants, and even things such as steroids, which will be geochemically detectable for millions, and perhaps even billions, of years
  • Nuclear war, if it happened, which would leave behind unusual radioactive isotopes

“As an industrial civilization, we’re driving changes in the isotopic abundances because we’re burning carbon,” Frank says. “But burning fossil fuels may actually shut us down as a civilization. What imprints would this or other kinds of industrial activity from a long dead civilization leave over tens of millions of years?”

A new perspective on climate change

The questions that Frank and Schmidt raise are part of a broader effort to address climate change from an astrobiological perspective, and a new way of thinking about life and civilizations across the universe. Looking at the rise and fall of civilizations in terms of their planetary impacts can also affect how researchers approach future explorations of other planets.

“We know early Mars and, perhaps, early Venus were more habitable than they are now, and conceivably we will one day drill through the geological sediments there, too,” Schmidt says. “This helps us think about what we should be looking for.”

Schmidt points to an irony, however: if a civilization is able to find a more sustainable way to produce energy without harming its host planet, it will leave behind less evidence that it was there.

“You want to have a nice, large-scale civilization that does wonderful things but that doesn’t push the planet into domains that are dangerous for itself, the civilization,” Frank says. “We need to figure out a way of producing and using energy that doesn’t put us at risk.”

That said, the earth will be just fine, Frank says. It’s more a question of whether humans will be.

Can we create a version of civilization that doesn’t push the earth into a domain that’s dangerous for us as a species?

“The point is not to ‘save the earth,’” says Frank. “No matter what we do to the planet, we’re just creating niches for the next cycle of evolution. But, if we continue on this trajectory of using fossil fuels and ignoring the climate change it drives, we human beings may not be part of Earth’s ongoing evolution.”

Inspiration from Doctor Who

Frank and Schmidt call their study the Silurian Hypothesis after a race of intelligent, bipedal reptiles—known as the Silurians—introduced in a 1970 episode of the British science fiction series Doctor Who.

The Silurians supposedly evolved on Earth during the eponymous era, a geological time period lasting from 443 million to 416 million years ago. To avoid any kind of catastrophe, the reptiles went into hibernation for millions of years before secret nuclear experiments in a Welsh mine awakened them.

“When we were writing this paper,” Schmidt says, “I tried to find examples of terrestrial, non-human civilizations in the science-fiction literature, but I wasn’t able to find anything earlier than the 1970s. Despite it being exceedingly unlikely that there were any civilizations in the Silurian period—this was before the land plants and animals had really established themselves—it seemed fitting to name our idea after the first example that people thought about, even if this is fiction.”

Source: University of Rochester

Scientist debunks 5 food allergy myths

(Credit: Getty Images)

A surge in childhood food allergies across the United States has turned classrooms into homemade-treat-free zones and parents into experts at scanning labels. But what’s fact and what’s fiction?

Ruchi Gupta has been at the forefront of food allergy research, applying her findings both in her clinical practice and in her home. After Gupta began her career, her daughter was diagnosed with peanut, tree nut, and egg allergies. The impact of that diagnosis, and the struggle to separate fact from fiction, cemented Gupta’s drive to understand more about allergies, help families cope, and empower food allergy sufferers to lead full, fearless lives.

Part of that work, she explains, means debunking some of the myths and misconceptions about food allergies. Gupta, a professor of pediatrics at Northwestern University, acknowledges that while there is still much more to learn—and she’s leading some of that path-breaking research—there are things we do know.

food allergy chart
Prevalence of specific allergies among food-allergic children. (Credit: Northwestern)

Below, Gupta explains some of the most common misconceptions about food allergy prevalence, impact, and prognosis for patients.

1. Food allergies are rare and aren’t often serious

Eight percent of children in the US—or 6 million kids—have at least one food allergy. That means 1 in 13 children—two kids in every classroom—must avoid certain foods.

And those allergies can be fatal. In fact, 40 percent of children with food allergies have suffered a life-threatening reaction, Gupta says.

Nine items account for the vast majority of food allergies: peanuts, eggs, milk, soy, wheat, tree nuts, fin fish, shellfish, and sesame, all foods that can be hard to avoid in grocery stores and restaurants.

2. Food labels make it easy to know what’s safe for people with food allergies

Food labels can be a minefield. Manufacturers are required to identify the presence of the top allergens in their products, but “precautionary” allergen labeling is voluntary and unregulated.

“Precautionary labeling includes ‘may contain’ and ‘manufactured on equipment that processes…,’” Gupta says. “A lot of companies are adding these, and that’s tough for families who have no way of knowing if products with these labels are safe.”

Avoiding foods with any allergen labeling is only an option for families who can afford to buy specially marked, allergen-free products. “Often, many families take chances because almost everything has one of those precautionary allergen labels on it,” Gupta says.

3. Eating a little bit of a food won’t hurt

Giving a food-allergic person a small amount of the food they’re allergic to will not necessarily reduce the allergy and can be extremely dangerous, even deadly.

But, Gupta says, feeding peanut products early to all infants around 6 months can help reduce the odds of developing a peanut allergy. Gupta coauthored new guidelines, endorsed by the American Academy of Pediatrics, recommending this careful dosing of peanut products to infants as a means of reducing peanut allergies.

This practice requires risk assessment by a pediatrician, Gupta says. If a child has severe eczema or egg allergy, both of which place them at high risk for peanut allergy, parents should first introduce peanuts to their child in an allergist’s office.

4. Food allergies mostly impact high-income, white families

Research shows food allergies affect families across all income levels and racial and ethnic backgrounds.

“In our prevalence study, we found that African-American and Asian-American children actually had higher rates of food allergy but lower rates of being diagnosed,” Gupta says. “Interestingly, we also found low-income kids had lower rates of food allergy and lower rates of being diagnosed.”

“It’s often hard to understand how food, which we need to live, could hurt you.”

Additionally, low-income families are more dependent on costly emergency care, spending 2.5 times more on hospitalizations and trips to the emergency department. Low-income families often lack access to specialty care and allergen-free foods that could prevent dangerous allergic reactions.

Gupta is now looking into the lower diagnosis rates. It could be that low-income parents simply avoid feeding their children foods they’ve reacted to in the past, without seeing a doctor to test for allergies.

“We’re looking at the Medicaid database to see what happens to kids—how they’re getting diagnosed with food allergies, and then how many of them are getting follow-up care from an allergist,” she says. “We want to know what prescriptions they’re getting and what kind of tests are being done.”

5. Beyond avoiding certain foods, there’s not much that can be done to help kids with food allergies

There are several proactive steps families can take in addition to getting rid of unsafe foods.

For example, families should explain the allergy to everyone who helps care for their child. It’s important, to make sure everyone understands what to do in case of an emergency, the signs of an allergic reaction, and how to use an epinephrine auto-injector.

Are baby wipes and dust key ‘ingredients’ for food allergies?

“Beyond that, one of the biggest things parents can do is connect with others,” Gupta says. Parent groups also help kids with food allergy connect with kids like them. Children can feel anxious or isolated as a result of their food allergies: Some are bullied for their food restriction, while others don’t know how to explain their allergies to friends.

“It’s often hard to understand how food, which we need to live, could hurt you,” Gupta says. “It’s critical that we help friends and family members understand how real food allergies are.”

Source: Northwestern University

3 cups of tea, coffee per day good for heart: Study

Cup of coffee
Cup of coffee

Drinking up to three cups of tea or coffee per day could protect people from developing irregular heartbeats or arrhythmia, a new study revealed on Tuesday.

Coffee is one of the most popular drinks in the world and the most common form of cognitive enhancement.

However, more than 80 per cent of clinicians in the United States recommend patients with palpitations or arrhythmia to abstain or reduce caffeine.

But the new study which involved researchers in the University of Melbourne’s Baker Heart and Diabetes Institute along with partners in the United States consistently demonstrated a reduction in atrial fibrillation (irregular heartbeats) with increasing levels of caffeine ingestion.

The research analysed multiple population-based studies which involved 228,465 participants to find the frequency of atrial fibrillation decreased by 6 per cent in regular coffee drinkers, while a further analysis of 115,993 patients showed a risk reduction of 13 per cent.

“There is a public perception, often based on anecdotal experience, that caffeine is a common acute trigger for heart rhythm problems,’’ lead author Peter Kistler from the Baker Heart and Diabetes Institute said.

“Our extensive review of the medical literature suggests this is not the case.’’

“Caffeinated beverages such as coffee and tea may have long term anti-arrhythmic properties mediated by antioxidant effects and antagonism of adenosine,’’ Kistler concluded.

“In numerous population-based studies, patients who regularly consume coffee and tea at moderate levels have a lower lifetime risk of developing heart rhythm problems and possibly improved survival.’’

However, due to significantly higher concentrations of caffeine, researchers advised that energy drinks should be avoided for people with pre-existing structural heart disease. (Xinhua/NAN)

Breaking: NANS factions sheathe swords, fix May 3rd for unity convention

From left: Aruna Kadiri and Chinonso Obasi

The two factions of the National Association of Nigerian Students (NANS), have agreed to put their differences aside and hold a unity  convention in the interest of Nigerian students.

The two factions led by Mr Chinonso Obasi, and Mr Aruna kadiri, after a conciliatory meeting on Tuesday in Abuja, fixed May 3 to May 5, for the NANS 2018 convention, at a yet to be announced venue.

A resolution signed by Obasi and Kadiri, and made available to the News Agency of Nigeria (NAN), said the parties agreed to set up convention planning committee.

The resolution said that the duo would henceforth be addressed as co-presidents, pending the emergence of new NANS leadership.

“We resolved to constitute a 60-man Convention Planning Committee (CPC), with the existing Kadiri’s list with an amended Obasi’s list, bringing in a co-chairman and co-secretary.

“Henceforth, the supporters of Kadiri, and Obasi, must abide by the resolutions and abstain from using foul language on one another,’’ the resolution stated.

Obasi was elected NANS President on July 19, 2016, at a convention held at Patani Stadium, Gombe, while Kadiri emerged President at a parallel convention, held on Sept. 4,  2016 at Old Parade Ground, Abuja.