Sunday, June 24, 2018

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Friday, September 9, 2016

From nostrils to crocodile blood – ten surprising places to look for antibiotics

Amazing things lurk up there… Shutterstock

One in ten people's noses contain bacteria that could be the source of a powerful new antibiotic, German scientists say. Even resistant superbugs, such as MRSA and vancomycin-resistant enterococci, died when exposed to this new compound, lugdunin.

Antimicrobial resistance is a major global threat, with Europe facing "Antimicrobial Armageddon" by 2025. Leading scientists predict a million deaths from untreatable infections if more new antibiotics aren't found.

So academics hunting for new drugs in unusual places such as human "snot" are on the right track. Here are ten more surprising places scientists are looking for antibiotics, from ants and cow stomachs to medieval libraries and snake blood.

1. Ants

The microbes living in and on tropical ants are studied for antibacterial and antifungal drugs by scientists across the world. Matt Hutchings from the University of East Anglia leads a major British study, prospecting bioactive compounds from fungus-farming attine and arboreal ants.

Attine (leaf cutter) ants from the Americas rely on antibiotics produced by actinomycete bacteria carried on their cuticles to protect their fungal garden from infestations. Tree-living, sap-drinking African slender ants and American Allomerus ants are thought to protect their host trees by cultivating mostly Gram-negative bacteria. These produce antibiotics and other compounds, which affect plant pathogens and deter herbivores from destroying their host plants. Hutchings said:

It's very exciting that ants not only evolved agriculture before humans but also combination therapy with natural antibiotics. Humans are just starting to realise that this is one way to slow down the rise of drug resistant bacteria – the so called superbugs.

2. Crocodile blood

Crocodiles not only have the strongest bite, their immune system is also very potent. It allows them to recover quickly from injuries that would kill other animals. Scientists from Cardiff Metropolitan University gave an update at a recent international symposium on the blood of Thai crocodiles as an antibacterial source. Crocodile blood haemoglobin could kill highly-resistant superbugs, such asKlebsiella pneumoniae and Pseudomonas aeruginosa. These can cause urinary tract infections and pneumonia in already sick patients or those with cystic fibrosis.

Test us … if you dare. Shutterstock

3. Cow stomachs

If you thought that cows just turn grass into milk, beef and manure, then think again. The stomachs of the cow harbour billions of microbes that help digest the grass, while competing with each other for their own food. Sharon Huws' team from Aberystwyth University has identified over 100 novel antimicrobial candidates from rumenmicroorganisms. The most promising compounds from pre-clinical tests are currently undergoing further trials.

4. Dirt, deserts and 10 Downing Street

Around two-thirds of currently prescribed antibiotics come from soil bacteria. Swansea University Medical School is leading studies digging for antibiotics directly from dirt and very dry habitats. I reported on a dirt studyand we are now working with industry to engineer a commercially viable route to novel antibiotics from dirt.

Paul Dyson's team at Swansea is isolating microbes from extreme environments such as the Gobi and Arabian deserts and high-altitude Tibetan soils that hardly sustain life. These microbes are now producing antibiotic leads in the laboratory.

Source of a cure? Shutterstock

And anyone can help. The garden of 10 Downing Street was dug up recently as part of a project to crowdsource samples for the Small World Initiative. SWI's Nicole Broderick said of the progress made by thousands of students across the globe: "The grand goal is to find new antibiotics, while getting young people interested in science."

5. Frog skin and foam

Frogs have been known to make deadly compounds for centuries – the skin of poison dart frogs contains alkaloid toxins that can kill humans quickly. Recently, many other species of frogs have been tested for antimicrobialsand antibiotic-delivery systems. The tiny Caribbean Tungaran frog produces a foamwith its hindlegs that protects its eggs from infection and predation. This foam slowly releases antimicrobials, which scientists at the University of Strathclyde are now testing as novel drug delivery systems for wound care. Paul Hoskisson said: "I'd say we are about half way there to making a stable foam. Once we do that, we would then need to test it in patients, but that will take a few years yet."

6. Honey

Honey is not only spread on toast, it's been used to treat patients' wounds for centuries. Honey made from the nectar of the Mānuka tree is particularly potent for wound infections. Microbiologists from Cardiff Metropolitan University have discovered that combinations of Mānuka honey and regular antibiotics can make MRSA more sensitive. Rose Cooper, professor of microbiology, said:

This indicates that existing antibiotics may be more effective against drug-resistant infections if used in combination with Mānuka honey.

7. Maggots and cockroaches

Other creepy crawlies are also a proven success. Maggot secretions, cockroach brains, and the humid brood cells of beewolf wasps all contain antimicrobials. Patients suffering from chronic open wounds, or resistant superbug infections, are often reluctant to undergo maggot therapy, but Yamni Nigam from Swansea University has launched the innovative #loveamaggot campaign. Nigam claims that "maggot therapy is a quick and highly effective way to treat infected and festering wounds. Limbs, and even lives, of chronically ill patients have been saved".

8. Medieval libraries

The interdisciplinary AncientBiotics consortium is hunting for recipes to treat infections in ancient books. One of the recipes found in Bald's Leechbook, an Anglo-Saxon manuscript held in the British Library, proved particularly powerful against superbugs. Consortium founding member Freya Harrison said the team thought the eye salve might show a "small amount of antibiotic activity … But we were absolutely blown away by just how effective the combination of ingredients was".

Old books could contain new drugs. Shutterstock

9. Sharks

The immune system of sharks is naturally powerful to protect them against bacterial and viral infections. This led investigators from the Georgetown University Medical Center to search for shark compounds with therapeutical potential. They discovered that the steroid compound squalamine from dogfish sharks is effective against human pathogenic bacteria – for example Pseudomonas aeruginosa – and human viruses such as dengue and hepatitis.

10. Snakes

Scientists from the Aga Khan University in Pakistan tested whether animals eating germ-infested rodents harboured powerful antimicrobials. They discovered that the blood and other organs such as lungs and gallbladder from black cobra snakes showed activity against human pathogenic bacteria, fungi and amoeba.

Our current range of antibiotics is under severe threat by superbugs with fast evolving resistance. Scientists must keep looking for new antibiotics, even in unusual places such as the human nose. It's a search that could save millions of lives.

Friday, July 15, 2016

A cancer patient needs your help!!!

Esther is a 30 year old NCE holder who has been battling cancer for over 6 months. She has been unable to pay for all the treatments and medications. Her aged parent have spent all they had to get they little treatment they can afford. Great Minders International have moved her from her home to Ekiti State Teaching Hospital, Ado Ekiti. She is set to undergo more treatments at an extremely high cost. Her life may very well, depend on this course of treatment. The only thing standing in her way is the means to pay for it.

Great Minders International is calling for donations from individuals and organizations to help save Esther's life. Please join us in helping Esther win this life threatening battle.

Donate to:

ACCOUNT NUMBER: 2018388785
ACCOUNT NAME: MR J.O MAKANJUOLA
BANK: UBA

Contact:

08060426538
07031851545
08035628710

#TeamGreatMinders
#LetsSaveEsther

Sunday, May 15, 2016

Chloroquine Protects Against Zika In Vitro

The antimalarial drug reduces the number of infected Vero and human brain microvascular endothelial cells—among other cell types—in culture, researchers report in a preprint.
WIKIMEDIA, 

Chloroquine, a 4-aminoquinoline, is a weak base with anti-inflammatory proprieties already usedto prevent and treat malaria. The drug has protective effects against dengue infection in monkeys and inhibits replication of the virus in infected Vero cells. According to researchers in Brazil, chloroquine appears to also protect against Zika virus infection in various cell types in vitro. The team published its results last week (May 2) in a bioRxiv preprint.

Amilcar Tanuri at the Federal University of Rio de Janeiro and colleagues tested the effects of chloroquine in different Zika virus–infected cell types, observing each culture for five days. Flow cytometry and immunofluorescence staining revealed that chloroquine at 25 and 50 μM reduced the number of Zika-infected Vero cells by 65 percent and 95 percent, respectively. When tested in human brain microvascular endothelial cells (hBMEC), which are often used to model the blood-brain barrier, chloroquine protected 80 percent of the cells examined from Zika-induced death, the researchers reported.

"Chloroquine . . . is not an antiviral drug as it acts on the cell and not on the virus," Tanuri told The Scientist.

Zika is known to target neurospheres and brain organoids; viral infection is associated withmicrocephaly and other abnormalities of the central nervous system in mice and humans. In the present study, Tanuri's team found that chloroquine treatment of Zika-infected mouse neurospheres enabled these cells to differentiate as usual, suggesting that the drug can rescue the neurite extension phenotype.  

Although chloroquine-mediated inhibition of viral infection can occur in both early and late stages of the viral replication cycle, the team observed that adding chloroquine at 30 minutes to 12 hours after infection reduced release of Zika virus (nine to 20 times compared with untreated cells). The drug did not reduce viral production when administered 24 hours after infection. This indicated that chloroquine is most effective in the early phase of Zika infection, when the virus enters the cell, the researchers noted.

David O'Connor, a professor of pathology and laboratory medicine at the University of Wisconsin–Madison who was not involved with the study, noted that regulatory agenices have already deemed chloroquine safe for use in pregnant women. "There will be a lot of enthusiasm for evaluating different interventions for use in pregnancy, but determining their safety and effectiveness will be time-consuming and could expose pregnant women to risk," he wrote in an email. "If chloroquine is even partially effective at reducing the risk or severity of Zika virus infection during pregnancy, its proven safety could make it extremely valuable."

Dosing remains a hurdle, however. The half maximal effective concentration of chloroquine that protected 50 percent of cells from Zika-induced death was between 9.82 and 14.2 μM, depending on the cell type, the Federal University team showed. (Chloroquine is sometimes administered in high concentrations—250 and 500 mg—to pregnant women who have lupus or rheumatoid arthritis.)

"At this point we are not suggesting to use chloroquine against Zika virus infection in pregnant women as the dose required to reach the same 14.2 uM of chloroquine, here used to protect hBEMEC, could be too high. Only a clinical trial will tell what is the right dose and real benefit of chloroquine," Tanuri said, adding that he hopes chloroquine derivatives might show similar—or enhanced—effects against Zika virus infection.

It is not yet known to what extent reduction of the virus in cells might impact the development of microcephaly. Paolo Zanotto of the University of São Paulo, who works on dengue and zika but was not involved in the study, wrote in a Facebook message that preclinical studies using animal models of Zika virus infection will be required to test the effects of chloroquine in vivo.

"Considering that the antiviral drugs so far tested against Zika infection are all toxic for the fetus, the finding that chloroquine has an effect against Zika infection is very promising," said Zanotto.

R. Delvecchio et al., "Chloroquine inhibits Zika virus infection in different cellular models,"bioRxiv, doi:10.1101/051268, 2016.

Tuesday, April 12, 2016

Antibiotics don't promote swapping of resistance genes

Antibiotics can lead to increased populations of resistant bacteria through changes in death-rates rather than an increase in the swapping of resistant genes.

Credit: Duke University

Researchers have shown that, outside of a few specific examples, antibiotics do not promote the spread of bacterial antibiotic resistance through genetic swapping, as previously assumed.

While the overuse of antibiotics is undeniably at the heart of the growing global crisis, new research published online April 11 inNature Microbiology suggests differential birth and death rates and not DNA donation are to blame. The results have implications for designing antibiotic protocols to avoid the spread of antibacterial resistance.

"The entire field knows there's a huge problem of overusing antibiotics," said Lingchong You, the Paul Ruffin Scarborough Associate Professor of Engineering at Duke University and lead author on the paper. "It is incredibly tempting to assume that antibiotics are promoting the spread of resistance by increasing the rate at which bacteria share resistant genes with each other, but our research shows they often aren't."

It's long been known that bacteria can swap DNA through a process called conjugation, which allows helpful genes to spread quickly between individuals and even between species.

Because the number of resistant bacteria rises when antibiotics fail to kill them, researchers assumed that the drugs increased the amount of genetic swapping taking place. But You thought maybe the drugs were killing off the two "parent" lineages and allowing a newly resistant strain to thrive instead.

"Previous studies haven't been able to tease these two ideas apart, but our work decoupled them," said Allison Lopatkin, a doctoral student in You's laboratory and the lead author of the study. "We showed at the single-cell level that the exchange of resistant genes is not influenced by antibiotics at all, which is in contrast to the literature."

In her experiments, Lopatkin put bacterial cells under a sort of suspended animation where they could neither die nor reproduce but they could still swap genes. With the birth and death rates no longer a variable, the researchers could see how the rate of gene exchanges responded to antibiotics.

They tested nine clinical pathogens commonly associated with the rapid spread of resistance and exposed them to ten common drugs representing each major class of antibiotics. The rates of gene exchange in each test remained flat and, in a few cases, actually decreased slightly as the concentration of antibiotics grew.

"It would seem that when antibiotics are applied, the DNA swapping has already occurred and continues to do so," You said. "Depending on their doses, the drugs can let the newly resistant bacteria emerge as the winners. When this occurs, the new strain is much more prevalent than before if tests are run after some growth of the new strain."

You points out that there are a few proven examples of antibiotics directly inducing the expression of the genes responsible for donating resistance, but they are very specific. For example, the antibiotic tetracycline induces the expression of genes that only transfer tetracycline resistance.

The new study shows that despite these outliers, antibiotics don't promote resistance spread by inducing global changes at the cellular level. The researchers hope further research will soon help clinicians design better antibacterial protocols.

"This has direct implications in terms of how we design doses and protocols," said You. "Some antibacterial combinations can drastically promote the overall transfer dynamics. Other combinations, on the other hand, can suppress the pathogens equally well without promoting genetic transfers. These are the issues we're hoping to address in follow-up research. We're trying to learn how to design the antibiotic treatment protocols in such a way that they will be effective but won't promote the spread of antibiotic resistance."

Story Source:

The above post is reprinted from materials provided by Duke UniversityNote: Materials may be edited for content and length.

Wednesday, March 23, 2016

This might be "Bye Bye to condoms" as scientists finds a cure for HIV/AIDS

Researchers at Philadelphia's Temple University have made a thrilling breakthrough on the path to cure HIV/AIDS . In a recent experiment, they managed to remove HIV-1 DNA out of the human genome. And when they reintroduced HIV to the edited genomes, the cells were no longer infected with the virus .‎

It's a huge leap towards the goal of curing the disease that has killed over 25 million people since the 1980's. Treatment has come a long way in the last few years, yet the scientists said antiretroviral drugs, which can regulate the disease, are not a permanent solution. As soon as a person stops receiving the treatment, their cells are once again open to the infection, and the virus usually progresses into AIDS. At this point, doctors are able to keep the virus at bay, but not cure it.

The Temple University scientists may have brought us one step closer to a cure. They employed CRISPR/Cas9 gene editing technology, first developed in 2012 , to cut HIV-1 out of the genome, after which the human DNA healed itself.‎

Dr. Kamel Khalili, director of the Comprehensive NeuroAIDS Center at Temple University claims that they are ready to put his new gene therapy into a new drug that will cure HIV in patients even after they stop taking the drugs.

In an interview, Dr Khalili said:
"The findings are important on multiple levels. They demonstrate the effectiveness of our gene editing system in eliminating HIV from the DNA of CD4 T-cells and, by introducing mutations into the viral genome, permanently inactivating its replication. Further, they show that the system can protect cells from reinfection and that the technology is safe for the cells, with no toxic effects," 

Monday, February 29, 2016