Super-gonorrhoea spread causes ‘deep concern’

Two women pick up the hard-to-treat infection, and a European party destination is one line of inquiry.

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Cheap common drugs may help mental illness

Drugs may already exist that could help patients with bipolar, schizophrenia and severe mental illness.

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Health24.com | Woman accidentally given erectile dysfunction cream for dry eyes

We often leave our doctor’s rooms with a script, and head over to the chemist who magically translates the often messy scrawl and issues us with the medication we need.

But what happens when the chemist gets it wrong and cannot actually read what your doctor has written? Or mistakenly dispenses the wrong medication?

For a woman in Glasgow it meant a trip to the emergency room after she suffered from chemical injuries to her eye. The BBC reports that her doctor had prescribed an eye lubricant called VitA-POS that is used to treat severe dry eyes and corneal erosions. However, the chemist misread this and dispensed Vitaros, an erectile dysfunction cream, instead.

After she used the erectile dysfunction cream, she suffered from eye pain, blurred vision, redness and a swollen eyelid. Fortunately the mild chemical injury was treated in hospital with topical antibiotics, steroids and lubricants. The injury cleared up after a few days and she didn’t lose her sight.

Prescribing errors

According to Dr Magdalena Edington, from Glasgow’s Tennent Institute of Ophthalmology, “Prescribing errors are common, and medications with similar names and packaging increase risk. However, it is unusual in this case that no individual, including the patient, general practitioner or dispensing pharmacist, questioned erectile dysfunction cream being prescribed to a female patient, with ocular application instructions.”

Dr Edington wants to raise awareness that medications with similar spellings exist, and she encourages prescribers “to ensure that handwritten prescriptions are printed in block capital letters (including the hyphen with VitA-POS) to avoid similar scenarios in the future”.

What you can do

According to the Center for Advancing Health, you as the patient must understand your prescription medication. Before you leave your doctor’s office, make sure you know the following:

  • The name of the medication you’ve been prescribed
  • Why you need to take it
  • When and how you need to take it
  • How long it will take before you see results from the medication
  • What to do if you notice any problems or side effects

Dr Brent Ridge admits there have been times when he has been less than thorough in his explanations. “On these occasions, my patients called my office afterward, as they should have.”

He says when you pick up your prescription, make sure the label matches what you thought you were getting. “If you notice a discrepancy, tell the pharmacist. If you’re familiar with the prescription you’re picking up, such as a refill, you might notice changes. The shape and colour of some pills, as well as the engravings that appear on some tablets, can change from one refill to the next, especially if the pills are generic. But if you have any doubts, ask the pharmacist.” 

Image credit: iStock 

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Health24.com | Prostate cancer – The silent killer few South African men are prepared to talk about

It all began with what I had expected to be a routine telephone call from Dr Grant, my medical doctor, following my annual check-up in September 2018. He calls me every year after conducting the extensive medical check-up during which, among other tests, blood samples are drawn and taken to the laboratory for analysis. Over the years, Dr Grant would simply call to assure me that all was well; but not in 2018.

“Your PSA (Prostate Specific Antigen) is rather elevated”, he told me in a calm, yet concerned, voice, “I need you to arrange to see a urologist for a prostate exam and biopsy, just to be sure that there is nothing to be worried about”. He gave me the name of the suggested specialist whose offices I promptly called to make an appointment.

The two weeks that I had to wait for the appointment seemed the longest I’d ever had to wait. When the time came, Dr Moolman turned out to be a relatively young, affable man who was reassuring in his manner. To be sure, I had also done a bit of reading about him and what he does before I went to see him.

Moolman conducted the dreaded and notorious “finger test” that many men loath, for its invasiveness and promptly suggested a biopsy. Fortunately, the finger test lasted just a few quick seconds and was done before I realised it. The biopsy is done under general anaesthetic during which random samples are taken from the prostate gland and taken to the laboratory for testing.

Of the sixteen that were taken from mine, ten returned with positive indications of the presence of prostate cancer. The highest Gleason Score – which indicates the level of aggressiveness of the cancer – was eight. Ten is the highest score. I consider myself lucky to have gone for regular tests and had the cancer diagnosed before it could spread to other parts of the body.

Some good news

So, the bad news was confirmed; but there was also what I’ll describe as some good news under the circumstances. The good news was that all indications at that time pointed to the cancer being concentrated in the prostate gland and none of it having metastasised into the neighbouring tissue and bone.

Further blood tests, a bone scan and MRI scan, were done over the next few weeks to ascertain these facts. Dr Moolman also took the time to explain available treatment options to me. 

Essentially, I could go the traditional Brachytherapy route, which consists of the implantation of radioactive seeds into the prostate gland to attack and kill the cancer. But this method offers no immediate guarantees, as I’d have to wait for some nine months to be fully assured if the cancer has been treated.

And anything could happen in the intervening period, including the resurgence of the cancer. Were the latter to happen, the radioactive seeds could not be injected for the second time, as this can only be done once. Treatment would mean possible chemotherapy and a lifelong regular observation.          

The alternative treatment option was to undergo a Da Vinci X robotics surgery, also called the “Robotic assisted laparoscopic prostatectomy”. It is the latest, higher definition, version of the first generation Da Vinci SI Surgery. “This minimally invasive procedure”, Moolman explained, “is performed with the use of a robotic surgical system that is designed to complete procedures with an extremely high level of precision. Six tiny incisions are made to enable the insertion of small surgical instruments and a drainage pipe into the abdomen.

The surgical tools, together with a high-definition camera, are mounted onto the machine’s robotic arms so that the cameras allow the surgeon to see the inside of the body in detail. The flexible instruments can bend and rotate much more than the human hand can, allowing for complete accuracy”.

The procedure enables the surgeon to remove the prostate gland from the urethra, around which it is normally wrapped. This procedure is recommended in cases like mine, where there is cancer inside the prostate gland that hasn’t spread to the surrounding organs and tissue.

For better cure results, Dr Moolman routinely removes the seminal vesicles with the prostate gland. In cases where the MRI scan shows the cancer to have spread outside the prostate, a wider resection margin is performed to make sure that no cancer is left behind after surgery.

If a patient is a good candidate – with very localised cancer like mine – a bilateral nerve sparing prostatectomy will be performed to ensure the return of erectile function after the surgery.

This unexpected personal journey with prostate cancer – no one in my family, including my father who died at the age of 92, is known to have had the cancer – as well as further information from Dr Moolman – opened my eyes to broader, pertinent, societal issues in South Africa:

• Most men either do not know they have to be tested annually (from the age of 40 for African men and 50 for Caucasian men), they’re too scared to go for tests, or they simply underestimate the potential danger of this silent killer of men;

• Most men are not comfortable discussing personal medical issues, especially prostate cancer; possibly because of the stigma associated with it (potential sexual dysfunction or incontinence); 

• Because of the absence of symptoms in the earlier stages of the cancer, most men think they’re fine and do not need to be tested. In reality, when symptoms begin to show – e.g. blood in the urine, difficulty passing urine, pain or a burning sensation when passing urine, or unusually frequent urination, especially at night – chances are that the cancer is already in an advanced stage. This is often the case with those (mostly) African men who live in rural areas and, in many cases, either lack the means, e.g. medical insurance, to get regularly screened for prostate cancer, or simply lack the awareness for it;  

• It’s important to note that 50-60% of African men in state hospitals are diagnosed with metastatic prostate cancer. This means they get diagnosed too late after the onset of prostate cancer and can therefore not be cured with therapy. More awareness is needed to prevent this; 

• Studies have also shown that African men have a bigger risk of being diagnosed with more aggressive prostate cancer than Caucasian men;

• Treatment costs are prohibitive. The Da Vinci Surgery is currently only available in private hospitals and not in the government sector, which only offers open surgery or radiation therapy;• There are currently only six Da Vinci systems in SA, with each machine costing in excess of $1000,000;

Since I’m on a Coastal Core Plan with Discovery Health – also called the Hospital Plan – which paid for the core surgery and hospital stay, I had to find another source to complement the many excess medical costs associated with this treatment. For this, I accessed additional funds through my Life Cover with Old Mutual, which also came to the party when I needed it.    

Thanks to Dr Moolman’s expertise, I was discharged from hospital two days after surgery and a bilateral nerve sparing prostatectomy to ensure a return of erectile function. 70% of his patients leave the hospital after a night following surgery.  None of this is possible with the open and traditional laparoscopic surgery. Once discharged from hospital, patient, loving, support by family and friends makes a huge difference.

Given the vast income disparities in SA, as well as difficult access to medical insurance for the majority of our citizens, there is an opportunity for government and the private sector to form some kind of Private-Public-Partnership in order to bring costs for the more modern Da Vinci X Surgery down and to make it available in the public health sector.

But until this becomes reality, African men need to take their health more seriously and get checked on a regular basis after the age of 40. Only early diagnosis can improve survival and cure rates.  

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Health24.com | Acne advice for returning students

As if the start of a new school year isn’t stressful enough, many teens may find their acne worsening when classes start, a skin doctor says.

During summer holidays, acne often eases because teens have less stress and more sun exposure, but it could flare up now that they’re back in school, explained Dr David Shupp. He’s a dermatologist at Penn State Health Medical Group.

Girls more susceptible

“A teen often feels alone in suffering from embarrassing pimples,” Shupp said in a Penn State news release.

“Because acne is caused primarily by hormone levels, the condition often begins at puberty and clears up by the late 20s,” he added. “Girls are more susceptible than boys to hormone-related acne.”

For teens with mild acne, the first step is to try over-the-counter creams, gels or lotions applied directly to affected areas. Teens with other skin conditions – such as eczema or psoriasis – should consult their doctor before using over-the-counter acne medications, Shupp advised.

The most common over-the-counter acne medications contain:

  • Benzoyl peroxide, which kills bacteria, helps remove excess oil from the skin and reduces inflammation.
  • Salicylic acid, which dries excess oils and works best for blackheads and whiteheads.
  • Adapalene, which prevents plugging of hair follicles and is available over-the-counter in 0.1% strength.

“If over-the-counter medications don’t provide enough relief from acne, it’s time to discuss prescription medications with a dermatologist or family physician,” Shupp suggested.

Prescription acne treatments include:

  • Stronger retinoids, such as Retin-A. These are among the most effective topical medications but can be more drying than over-the-counter options.
  • Antibiotics, which can be administered orally or via a topical gel or cream to kill excess bacteria. Topical antibiotics are often combined with benzoyl peroxide to maximize effectiveness while lowering the risk of antibiotic resistance.
  • Hormonal treatments, which impact the balance of hormones that cause acne and are usually prescribed to supplement topical medications or antibiotics in young women.
  • Isotretinoin (Accutane) is a powerful vitamin A derivative used to treat severe acne that does not respond to other medications. Potential side effects include birth defects, so teenage and adult women taking this oral medication must undergo monthly pregnancy tests.

Don’t use acne medications prescribed for someone else, Shupp said.

Along with treatment, there are a number of things teens can do to reduce acne, he added.

Permanent scarring

Gently clean affected skin twice a day. Avoid scrubbing, which can damage the skin and aggravate an acne problem. Do not use abrasive products.

Use oil-free cosmetics, sunscreen, moisturizer and hair products. They’re labelled “noncomedogenic”.

Keep hands and hair away from the face to reduce the transfer of oil. Don’t squeeze pimples. This can cause permanent scarring.

The most common skin condition in the United States, acne strikes close to 85% of people between the ages of 12 and 24, according to the American Academy of Dermatology.

Image credit: iStock

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Health24.com | Men, don’t ignore those pelvic floor exercises

Pelvic floor exercises are commonly targeted at women. But for men, as they age in particular, the exercises can be of massive benefit – especially for a condition such as incontinence.

While pelvic muscles can weaken due to age, there are other factors that can contribute to their deterioration, such as an injury or surgery.

Surgeries like the removal of the prostate (radical prostatectomy), as well as conditions like diabetes can affect the pelvic floor muscles.

Watch for more on pelvic floor exercises.

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Brain plasticity restored in adult mice through targeting specific nerve cell connections

Neuroscientists at Tufts University School of Medicine, in collaboration with colleagues at Yale University School of Medicine, have discovered a new molecular mechanism that is essential for maturation of brain function and may be used to restore plasticity in aged brains. Unlike previous research that broadly manipulated brain plasticity using approaches that affected the entire brain, this study targets for the first time a specific molecule acting on a single type of neuronal connection to modulate brain function. This restores the brain’s ability to rewire itself.

The research in mice could advance understanding and treatment of human diseases such as autism spectrum disorders and stroke. It is published in Cell Reports on January 8, 2019.

The human brain is very plastic during childhood, and all young mammals have a “critical period” when different areas of their brains can remodel neural connections in response to external stimuli. Disruption of this precise developmental sequence results in serious damage; conditions such as autism potentially involve disrupted critical periods.

“It’s been known for a while that maturation of inhibitory nerve cells in the brain controls the onset of critical period plasticity, but how this plasticity wanes as the brain matures is not understood,” said Adema Ribic, Ph.D., research scientist at Tufts School of Medicine and first author of the new study. “We’ve had some evidence that a set of molecules called SynCAMs may be involved in this process, so we decided to dig deeper into those specific molecules.”

The study focused on the visual cortex, the part of the brain responsible for processing visual scenes, in which plasticity has been examined in many species. Using advanced viral tools and electrophysiological techniques, the researchers were able to measure activity of nerve cells (neurons) in awake mice freely responding to visual stimuli. They found that removal of the SynCAM 1 molecule from the brain increased plasticity in the visual cortex of both young and adult mice. Further research found that SynCAM 1 controls a very specific type of neuronal connection termed synapses: the long-distance synapses between the visual thalamus, located beneath the cerebral cortex, and inhibitory neurons in the cortex. SynCAM 1 was found to be necessary for the formation of synapses between thalamus and inhibitory neurons, which in turn helps inhibitory neurons to mature and actively restrict critical period plasticity.

Ribic likens inhibitory neurons to a dial controlling when brain plasticity can occur. Plasticity is needed during early development, as the function of different brain areas matures. Mature function is then ‘cemented’ into place by molecules like SynCAM 1.

“Our study identified a fundamental mechanism that controls brain plasticity, and perhaps most exciting, we can show that a process in the adult brain actively suppresses plasticity,” said study senior author Thomas Biederer, Ph.D., associate professor of neuroscience at Tufts School of Medicine and a member of the neuroscience program faculty at the Sackler School of Graduate Biomedical Sciences at Tufts. “Therefore, the limited ability of the mature brain to change is not simply a consequence of age but is directly enforced by the SynCAM 1 mechanism. This allows us to target the mechanism to re-open plasticity in the mature brain, which could be relevant for treating disorders like autism.”

Focusing on a single molecule and synapse type to induce the heightened plasticity should support development of treatments with reduced potential for side effects. “For example, antidepressants may restore plasticity but will also have a lot of other effects,” said Ribic, who noted that more plasticity isn’t always better. “Our study found a way to increase plasticity in a very controlled way, both spatially and temporally. Combined with the latest approaches in genetic manipulation, this may prove to be a new path to tackle both childhood disorders and brain injury in adults.”

The researchers still need to determine if this plasticity mechanism will work in humans as well as mice and can be activated repeatedly. While there are obviously major differences between rodents and humans, studies in multiple species suggest that the general mechanisms of plasticity are similar.

The study is the latest work from the Biederer group at Tufts University School of Medicine, which focuses on mechanisms of synapse formation and plasticity in the context of normal development and neurodevelopmental disorders.

Story Source:

Materials provided by Tufts University, Health Sciences Campus. Note: Content may be edited for style and length.

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Bee mite arrival in Hawaii causes pathogen changes in honeybee predators

The reddish-brown varroa mite, a parasite of honeybees and accidentally introduced in the Big Island of Hawaii in 2007-08, is about the size of a pinhead. Yet, its effects there are concerning to entomologists because the mite is found nearly everywhere honeybees are present.

A team led by entomologists at the University of California, Riverside, performed a study on the Big Island and found viruses associated with the mite have spilled over into the western yellowjacket, a honeybee predator and honey raider. The result is a hidden, yet remarkable, change in the genetic diversity of viruses associated with the larger pathogen community of the mite and wasp, with repercussions yet to be understood.

“Already, we are seeing that the arrival of the varroa mite in honeybee populations in Hawaii has favored a few virulent strains,” said Erin E. Wilson Rankin, an assistant professor of entomology and lead investigator of the study published Jan. 9 in the Proceedings of the Royal Society B. “We do not know what the effects of these strains will be. What we know is that the effects of the varroa mite have cascaded through entire communities in Hawaii and probably around the world.”

In particular, the researchers saw a loss in the diversity of deformed wing virus, or DWV, variants, resulting in new strains whose impact is hard to predict. DWV, widespread in honeybee populations globally and made up of several variants, is thought to be partly responsible for global die-off of honeybee colonies. DWV infects bumblebees and has been detected in other insects. The yellowjacket wasps can acquire this virus directly or indirectly from honeybees.

By a stroke of luck, the researchers had the benefit of studying the honeybee and yellowjacket populations on the Big Island both before and after the varroa mite was introduced there. They saw more association of honeybees with pathogens after the appearance of the mite. Indeed, some pathogens were detected in the honeybee and wasp populations only after the mite was introduced to the island.

“This is one of the first descriptions of pathogens in the western yellowjacket,” Wilson Rankin said. “Evidently, pathogens known to be associated with varroa have spread into non-bee species, despite the mite itself being a bee specialist. We suspect the spread in yellowjackets is partly due to the wasp’s propensity to prey upon bees, which is one way the wasps may be exposed to the pathogens.”

Wilson Rankin noted the pathogens are often incorrectly called “bee pathogens” because they were first found in bees. The pathogens, however, are found in a wide variety of insects.

“We are seeing entirely different predators being affected,” she said. “The mite is not vectoring viruses to the wasps. The viral spread is happening through predation and through flowers. Predators may be passing on pathogens to other species. The yellowjacket, for example, preys on both honeybees and native bees, and may explain why both bee populations are showing the same viruses.”

Wilson Rankin explained wasps have been overlooked by researchers because these arthropods do not have “warm, fuzzy, and furry connotations.”

“They look scary,” she added. “People also get stung by them. People are more afraid of wasps than bees. But our work shows we can examine the health of the arthropod community by using species other than bees. We show for the first time that a predator is being affected by a parasite that does not even infect it.”

The researchers sampled 25-45 bees and wasps for one part of the study, and then about 100 individuals, analyzed in groups, for each of the species during the period before and after the mite was introduced to the Big Island. The researchers did not study native bees, focusing instead on honeybees and yellowjacket wasps, neither of which is native to Hawaii.

“Our findings suggest that pathogen transmission from domesticated bees, such as honeybees, may be important even for non-bee insects like the wasps we studied,” said Kevin J. Loope, the research paper’s first author, who worked as a postdoctoral scholar in the Wilson Rankin lab during the study. “The impacts may be more subtle than previously observed: we found changes in the genetic variation of viruses found in the wasps, but not changes in the amount of virus. These findings suggest we should look more broadly and in greater detail to figure out how moving domesticated bees for agriculture may influence wild populations of insects.

Loope, now a research assistant professor in the Department of Biology at Georgia Southern University, explained that finding overlap in the pathogens of yellowjacket wasps and domesticated bees also means that using pathogens to control undesirable wasp populations is risky.

“Any biological control efforts using pathogens should be carefully evaluated to prevent inadvertent harm to beneficial bees,” he said.

He added that the research team was surprised to find a dramatic difference in the viral genetic diversity between the wasp samples from the two periods — before and after the varroa mite was detected on the Big Island.

“We had predicted we would observe a decline in wasp viral diversity matching the decline described in honeybees in Hawaii, but we were still surprised to see this borne out in the data,” he said. “It’s not so often that you see what you’ve predicted in biology.”

Wilson Rankin and Loope were joined in the research by Philip J. Lester of Victoria University of Wellington, New Zealand; and James W. Baty of Malaghan Institute of Medical Research, New Zealand. Genetic analyses on the bee and wasp samples were performed at UCR and in New Zealand.

Wilson Rankin was supported by grants from the National Science Foundation and the Hellman Fellows Fund. Loope was supported by a postdoctoral fellowship from the National Institute of Food and Agriculture of the U.S. Department of Agriculture.

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Finding an elusive mutation that turns altruism into selfish behavior among honeybees

Among the social insects, bees have developed a strong and rich social network, where busy worker bees tend to the queen, who in turn, controls reproduction for the benefit of the hive.

But the South African Cape honey bee (Apis mellifera capensis) can flaunt these rules. In a process of genetic trickery called thelytoky syndrome, worker bee females ignore the queen’s orders and begin to reproduce on their own.

Scientists, in their own altruistic effort to protect the Cape honey bees from a recent devastating blight, transferred the Cape honey bees to a northeastern region — only to see the Cape bees wreak havoc among colonies of the neighboring honey bee subspecies A. m. scutellata.

The A. capensis bees turned from altruistic workers to the guests who would not leave — becoming social parasites that forage on their own into foreign colonies, reproducing an army of loyal workers, stealing all the honey, and eventually, dethroning the queen and taking over the host colony.

This type of behavior, despite making for bad neighbors, makes a lot of evolutionary sense. If the queen is lost, then the thelytoky syndrome at one point must have first kicked in as a life raft to save the colony. But if this is the case, why hasn’t it become a more widespread phenomenon for other bee species?

Recently, scientists have combed through bee genomes to narrow down the genetics behind thelytoky, and linked these to candidate genes in the past few years — but to date, the master genetic switch has not been found.

Now, for the first time, a group led by Denise Aumer and Eckart Stolle, working in the lab of Robin Moritz at the Martin-Luther-Universität Halle-Wittenberg’s Institute of Biology, have finally found the root cause responsible for thelytoky. The findings were published in the advanced online edition of Molecular Biology and Evolution.

“Uncovering the genetic architecture underlying thelytoky is a big step towards understanding this mode of reproduction, not only in the Cape honeybee, but also in other insect species in general (e.g. many invasive ants reproduce in a very similar fashion),” said Stolle. “After having worked on the topic for so many years with so much efforts by our colleagues and us to add pieces to the puzzle and also with the one or other dead end, it is a huge accomplishment for us to have come to this point.”

By comparing the genomes of Cape honeybees which produce diploid female offspring (thelytoky) with those producing haploid male offspring (arrhenotoky, i.e. the expected mode of reproduction), they identified a candidate gene located on chromosome one, LOC409096, and proposed to call it Thelytoky (Th), as the major regulator of the selfish worker bee reproduction. Thelytoky encodes a receptor protein with a transmembrane helix and a signal peptide at the extracellular N-terminus, indicating that it is linked to a secretory pathway.

Specifically, a single mutational substitution in exon 7 of Thelytoky causes a change from the polar amino acid threonine to the non-polar amino acid isoleucine in the protein sequence, leading to substantial structural modifications and likely functional consequences. In addition, they confirmed their genetic data by showing that RNA levels of Thelytoky were elevated only in the selfish bees. They also performed DNA sequencing of another honey bee population and found the same exact mutation amongst the socially parasitic lineage of the Cape honey bee, but not among workers of other honey bee subspecies.

From the study of the genetics, they determined that Cape bee selfishness exhibits a dominant inheritance pattern, which means that only one mutation that needs to be passed down to perform the selfish genetic switch.

But the genetics are a bit more complicated because it turns out that the selfish gene still needs its altruistic partner (known as the social, or arrhenotoky form of the gene).

“The genetic control of the thelytoky syndrome is regulated by a more complex genetic mechanism than previously assumed,” said Aumer. “The thelytoky allele (Th) is not recessive, i.e., needing two copies of the mutated gene, but rather a dominant allele. This dominant mutation expresses the phenotype (thelytoky) when one copy of the gene is the mutated variant, and the other copy is the one variant typical for the Cape honey bee.”

“But at the same time, it appears that having two copies of the mutated variant is detrimental, perhaps even lethal, while having two copies of the “regular” Cape bee variant of this genes makes them reproduce normally. Any other combination of the mutated variant with another subspecies’ variant would be non-matching alleles and would result in either non-functional or fertile normally reproducing (arrhenotokous) phenotypes. Therefore, the Cape bee typical Th variant seems to complement the mutated Th variant in a way that the offspring is fertile and expresses the unique set of phenotypes referred to as thelytoky syndrome.”

Because only one gene can get passed on during reproduction, the genetics not only explain why breeders, for the past 150 years, have been mostly unsuccessful with producing thelytokous workers from mating the Cape bees with others, but also why the thelytoky behavior hasn’t spread into other bee populations.

Genetically, it turns out you still need a little altruism to be truly selfish. When only one is passed on from interbreeding, the effect is lost without its partner gene.

“On a broader level, the identified genetic architecture of thelytoky in honey bees may serve as a model for other eusocial species with similar thelytokous reproduction, in particular for novel ant model systems, such as Platythyrea punctata and the clonal raider ant Ooceraea biroi,” wrote the authors in the Molecular Biology and Evolution publication.

And just like the striking case of malaria and hemoglobin genes in humans, the study shows how just a single change in the DNA can have such a dramatic effect on a species, or in this case, changing the behavior of a bee from a helper to a mercenary.

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Woman given impotence cream for eye problem

Its name was similar to one for dry eye and was given by mistake to a woman, who was injured as a result.

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