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For the first time, researchers from Boston University School of Medicine (BUSM) have identified an ADP-ribosyltransferase enzyme that is active in the mitochondria (the organelle that generate most of the chemical energy needed to power biochemical reactions in cells) and characterized its activity. ADP-ribosyltransferases are enzymes that play a role in the modification of other proteins. The activity of this new mitochondrial enzyme, called NEURL4, is similar to that of PARP1, a nuclear enzyme well studied for its critical role in DNA damage repair and regulation of gene expression.
To characterize the enzymatic activity of NEURL4, the team led by first and co-corresponding author Maria Dafne Cardamone, PhD, former research assistant professor of biochemistry at BUSM, first performed in-vitro enzymatic assays. Then they generated a cell line in which NEURL4 was deleted using a gene editing system. From there they used mass spectrometry to compare the modifications on mitochondrial proteins in wild-type (“normal”) versus cells without NEURL4.
According to the researchers this approach led them to identify a number of mitochondrial proteins as targets of NEURL4, including mitochondrial LIG3, a protein involved in the repair of damaged mitochondrial DNA and confirmed that NEURL4 activity is required for the maintenance of mitochondrial DNA (mtDNA) integrity.
While this study does not have any direct implication for clinical treatments, the team says it represents an important step in understanding how cells maintain homeostasis and respond to oxidative stress. “While this will not directly improve people’s quality of life, we hope it will provide fertile grounds for new translational applications for the treatment of diseases with a mitochondrial component, such as cancer, diabetes, age-related neurodegenerative disorders and rare mitochondrial diseases” said co-corresponding author Valentina Perissi, PhD, associate professor of biochemistry and co-director of the Boston Nutrition Obesity Research Center at BUSM.
The researchers believe future studies investigating how NEURL4-mediated modifications of specific mitochondrial proteins affect mitochondrial functions could lead to the identification of novel regulatory strategies to target for therapeutic purposes. A better understanding of NEURL4 biology may also prove relevant for the treatment of male infertility. Mitochondrial DNA deletions are linked with reduced sperm mobility and infertility in both mice and humans and this research indicates that reduced NEURL4 expression in mice is associated with increased mtDNA deletions and markers of male infertility, such as reduced sperm count and increased sperm clumping.
Andrew Emili, PhD, and Julian Kwan, PhD, from the BU Center for Network Systems Biology (CNSB) collaborated on this research.
Funding for this study was provided by the National Institutes of Health (R01DK100422 and R01GM127625) to VP; Pilot and Feasibility Award to MDC from the Boston Nutrition and Obesity Center P30DK046200), and by the Grunebaum Cancer Foundation Fellowship to MDC.
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Blood levels of many commonly used antiepileptic drugs drop dramatically with the onset of pregnancy, report researchers from the University of Pittsburgh and the University of Minnesota today in JAMA Neurology.
The findings, collected as part of the multicenter study Maternal Outcomes and Neurodevelopmental Effects of Antiepileptic Drugs (MONEAD), explain why many people with epilepsy start experiencing breakthrough seizures after conception, reinforcing the need to proactively increase doses of certain antiseizure medications and closely monitor blood levels over the course of pregnancy.
When it comes to epilepsy, maintaining a fine-tuned medication regime is critical. Some people mistakenly believe that changes in the drugs’ blood concentration won’t occur until after 20 weeks of pregnancy, but our study shows how important it is to start monitoring and adjusting patients’ medication dosages early on,” said lead author Page Pennell, M.D., chair of neurology at Pitt and the principal investigator on the MONEAD trial. “Nearly half of all pregnancies in the United States are unplanned, so it is important to ensure that doctors have a clear picture of each patient’s baseline drug level even if they are not trying to conceive.”
Epilepsy is a life-altering neurological condition that affects children and adults alike, and two-thirds of cases do not have a known cause. In people with epilepsy, nerve cells in the brain are hyper-reactive, causing them to change the pattern of their electrical activity and become spontaneously active, millions of cells at a time. In people with epilepsy, that synchronous activation is manifested in seizures, which can make a person become disoriented, lose consciousness and, in some cases, experience limb movements or rigidity.
Clinical management of epilepsy has had a fraught medical history, compounded by myths and stigma over the centuries. Many people with epilepsy go undiagnosed or under-treated. Even though epileptic seizures can often be successfully controlled with medications, the first-generation drugs had a slew of dangerous side effects and were contraindicated for people who are trying to conceive.
Since then, safer medications have entered the U.S. market and become widely available, but clinicians started noticing a new problem — patients whose epilepsy was successfully managed with medications started having seizures soon after becoming pregnant.

Increased oxidative damage is linked to neurodegenerative disorders such as Alzheimer’s disease (AD). Even though the pathophysiology of AD has been widely investigated, the likely relationship between mitochondrial dysfunction and the disease remains largely unknown. A research team led by Prof. Koji Fukui from Japan’s Shibaura Institute of Technology has confirmed that AD progression is linked to oxidative brain damage, which impairs cognitive function in AD transgenic mice in an age-dependent manner.
The mitochondrial electron transport chain, which is required for generating energy during cellular processes, also produces reactive oxygen species (ROS) that attack tissue and cause oxidative damage. This damage can cause mitochondrial dysfunction and even lead to cell death. Since our brain uses more oxygen than other organs, it is more vulnerable to this ROS damage.
According to literature, ROS also causes the buildup of amyloid-β (Aβ), which marks the onset of Alzheimer’s disease (AD), a serious irreversible neurodegenerative disorder. Treatments for AD do not stop its progression, necessitating the development of new therapeutics.
In a prior study, a team of scientists found that oxidation levels were substantially higher in older rats with vitamin E deficiency than in younger rats. Furthermore, ROS production via mitochondrial oxidation could damage brain cells, implying a strong link between AD and mitochondrial dysfunction. To improve this understanding, the same group of scientists has now demonstrated that the progression of AD is closely associated with oxidative brain damage. The study, led by Prof. Koji Fukui, along with his colleagues Mr Naoki Yoshida, Mr. Yugo Kato, and Prof. Hirokatsu Takatsu, was recently published in Biomedicines. “We showed that oxidation negatively impacted the mitochondria which led to cognitive dysfunction,” explains Prof. Fukui, who is the corresponding author of the study.
The scientists used three groups of AD mice aged 3, 6, and 20 months, along with healthy controls. For testing their cognitive and coordination abilities, the mice were examined in two well-known experiments: the Morris water maze and the Rota-rod test. They discovered that the AD mice took longer to complete their maze goals but did not slow down. In the Rota-rod test, the 6- and 20-month-old AD mice stayed on the rod for a longer time, while the age-matched control mice fell quicker. Prof. Fukui explains, “The difference in fall time could be attributed to the weight difference between the two groups, as the control mice were heavier than the AD mice.” These results suggested that AD mice were cognitively impaired but did not have any coordination issues.
To identify which AD-related proteins were responsible for such cognitive impairment, the authors collected tissue samples from various parts of the brain from both groups of mice and assessed the levels of oxidative markers in the samples. First, they found that AD mice had higher levels of Aβ, with a gradual increase observed with age. To their surprise, the AD-related protein Aβ1-42 was significantly higher in the hippocampus than in other parts of the brain. However, they did not find any alterations in the levels of the tau protein, which is another marker that accumulates in AD pathology. Overall, it was confirmed that Aβ1-42 aggregation in the hippocampus caused cognitive impairment in AD mice.
The team also had speculations about ROS-induced mitochondrial damage being closely related to neuron survival. To validate their hypothesis, they determined the levels of some key mitochondrial oxidative enzymes, including nicotinamide-nucleotide adenylyltransferase (NMNAT)-3, which exhibits anti-ageing effects. While NMNAT-3 was found to be lowered, levels of 3-NT (3-nitrotyrosine), an indicator of higher oxidation, increased with age in AD mice. “With reduced levels of NMNAT-3 and higher levels of 3-NT, it is evident that oxidation causes mitochondrial dysfunction, and eventually leads to cognitive dysfunction,” comments Prof. Fukui.
The team is optimistic about the potential implications of their results, particularly in increasing the intake of antioxidant compounds that can help our bodies mitigate ROS. In fact, many natural antioxidants, such as vitamins E and C, can be obtained from dietary sources. Prof. Fukui concludes by surmising, “If mitochondria can be protected from ROS, mitochondrial function and cognitive function may be maintained. Future research should concentrate on developing diagnostic markers to detect early alterations in the brain, as well as exploring compounds with high antioxidant activity in mitochondria.”

A recent University of Toronto study, in collaboration with Parkdale Queen West Community Heath Centre and the Healthy Nail Salons Network, shows that nail technicians in discount salons are exposed to several chemicals widely used as plasticizers and flame retardants.
The study, to be published Feb. 14 in the journal Environmental Science and Technology, found that exposure to some hazardous chemicals was higher among nail technicians than among electronic waste workers.
“We were very surprised to find exposures for some chemicals up to 30 times higher among nail salon workers relative to exposures in homes, and up to 10 times higher than in e-waste handling facilities,” said Miriam Diamond, co-author and professor at the University of Toronto’s Department of Earth Sciences.
The study reported higher exposures of several phthalate plasticizers, which was expected given the use of these chemicals in personal care products. One phthalate plasticizer, DEHP, which is not allowed for use in cosmetics under the Canadian Environmental Protection Act, was found at low levels. “The finding of low exposure to the plasticizer DEHP is important — it shows the current regulations for this compound are working,” Diamond said.
However, what was unexpected was the finding of some high levels of flame retardants that are not known to be used in personal care products.
Several of the chemicals studied have some restrictions on their use (or restrictions are proposed) under the Canadian Environmental Protection Act. However, most of these chemicals are not explicitly regulated in Ontario workplaces. The specific source of these chemicals in nail salons was not determined in this study.

Human eggs often contain the wrong number of chromosomes, leading to miscarriages and infertility. A research team led by Melina Schuh at the Max Planck Institute (MPI) for Multidisciplinary Sciences has discovered that human eggs are missing an important protein, which acts as a molecular motor. This motor helps to stabilize the machinery that separates the chromosomes during cell division. The researchers’ findings open up new avenues for therapeutic approaches that could reduce chromosome segregation errors in human eggs.
A new life begins when an egg is fertilized by a sperm. In this fusion, the genetic information from each parent is combined. The sperm and egg both contribute a single copy of each of their 23 chromosomes. The newly developing embryo thus inherits a complete set of 46 chromosomes. However, the oocyte — the egg’s precursor cell — contains two copies of every chromosome and must therefore lose half of these before fertilization can take place. This happens in a specialized cell division called meiosis. A complex machinery — the spindle apparatus — ensures that a maturing oocyte retains the correct number of chromosomes. It consists of spindle fibers that attach to the chromosomes during meiosis. The fibers then pull one copy of each chromosome to opposite poles of the spindle, and the oocyte subsequently divides between them.
This process is highly error-prone in humans. If too many or too few chromosomes remain in the mature egg, there is a risk of miscarriage or diseases in the offspring such as Down syndrome. “We already know that human oocytes frequently assemble spindles with unstable poles. Such unstable spindles misarrange chromosomes during division,” says Melina Schuh, who heads the Department of Meiosis at the MPI for Multidisciplinary Sciences. These high error rates are much lower elsewhere in the animal kingdom. “The spindles of other mammalian oocytes were always stable in our experiments,” she reports.
Unstable spindles due to a missing motor protein
To find out what makes human spindles so unstable, the team compared the molecular inventory of proteins required for spindle stability, in different mammalian oocytes. For these experiments, the researchers used unfertilized human oocytes that were immature at the time of fertility treatment and donated by patients of the Bourn Hall Clinic (UK), Kinderwunschzentrum Göttingen (Germany) and Fertility Center Berlin (Germany) for research. For comparison with other mammalian species, they used oocytes from mice, pigs, and cattle.
The researchers discovered that human oocytes are deficient in the protein KIFC1. This motor protein forms bridges between spindle fibers, which help to align the fibers and prevent them from falling apart. “Compared to humans, oocytes from mice, pigs, and cattle contain significantly more KIFC1 protein,” explains Chun So, a postdoctoral fellow in Schuh’s department and the first author of the study. The scientists next investigated whether manipulation of the protein level affects spindle stability. They depleted KIFC1 protein in mouse and bovine oocytes using a new method co-developed in Schuh’s lab called Trim-Away. This technique rapidly degrades almost any target protein in any type of cell. “Without this motor protein, most mouse and bovine oocytes assembled unstable spindles like human oocytes and more chromosome segregation errors occurred. Thus, our results suggest that KIFC1 is critical in ensuring error-free distribution of chromosomes during meiosis,” the early career researcher adds.
A cornerstone for new therapeutic approaches
Could KIFC1 be a starting point for reducing chromosome separation errors in human eggs? “For us, the exciting question was: Do spindles become more stable if we introduce extra KIFC1 into human oocytes?” Schuh says. Indeed, under the microscope, oocytes supplemented with extra KIFC1 had significantly more stable spindles, resulting in fewer chromosome segregation errors. “Introducing KIFC1 into human oocytes could thus be a possible approach to reduce defective eggs. This might help to make fertility treatments more successful,” the Max Planck director hopes.
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Interferons are the host’s first line of defence against infections. Different subtypes of these messenger substances have different effects. A research team from Bochum and Essen showed which subtypes are most effective against SARS-CoV-2. The researchers not only elucidated the principles underlying the host’s defence mechanisms against the virus, but also presented potential alternative treatment options for high-risk patients in the early stages of an infection.
A team headed by Professor Stephanie Pfänder from the Department of Molecular and Medical Virology at Ruhr-Universität Bochum and Dr. Kathrin Sutter from the Institute of Virology at the University Hospital Essen published their findings in the Proceedings of the National Academy of Sciences on 22 February 2022 online first.
Clinical potential not yet fully explored
As messenger substances, interferons stimulate various responses of immune cells and play a key role in activating the immune system. They are proven active agents against various diseases, especially type I interferon alpha 2, which has been widely used against hepatitis C and B. “However, there are different subtypes of interferons whose clinical potential has not yet been fully explored,” points out Stephanie Pfänder.
The researchers comprehensively analysed the cellular response to these IFN subtypes. Using transcriptome analyses, it was possible to identify key IFN-stimulated genes which were differentially regulated after exposure to a specific interferon. Their information is translated into proteins. Proteome analyses showed how the protein expression in primary lung cells changes after the stimulation with different interferons. The researchers refer to the cellular reaction caused by the interferon subtypes as immune signature.
Certain subtypes elicit particularly effective immune response
“We showed that certain interferon-alpha subtypes are highly effective against SARS-CoV-2,” states Kathrin Sutter. “The antiviral activity of the different subtypes varies considerably.” For example, the alpha-5 subtype elicited a particularly effective immune signature against the virus. The antiviral effect that the researchers measured in cell culture increased even more significantly when combined with the antiviral drug remdesivir.
“Our study allows us to draw conclusions about which induced proteins and genes are particularly important in the fight against Sars-Cov-2,” stresses Stephanie Pfänder. In addition, the findings may offer an alternative in the treatment of Covid-19 patients through the early administration of specific interferon alpha subtypes with a strong antiviral effect.
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Materials provided by Ruhr-University Bochum. Original written by Meike Drießen; translated by Donata Zuber. Note: Content may be edited for style and length.

Researchers at the University of Toronto have identified hundreds of new proteins that could play a role in cystic fibrosis, and which may shed light on why some patients respond better than others to current therapies.
Many of these proteins — part of a group of druggable molecules called membrane proteins — interact with the CFTR protein, which when missing or faulty leads to the build-up of mucous in the lungs and other organs that is often fatal in cystic fibrosis.
“We identified more than 400 proteins associated with either healthy or mutant CFTR, and have shown that some of them could predict the variability seen in patient symptoms and treatment responses,” said Igor Stagljar, principal investigator on the study and a professor in the Donnelly Centre for Cellular and Biomolecular Research at U of T’s Temerty Faculty of Medicine.
“With a more comprehensive view of the CFTR protein interaction network, we can identify novel drug targets that should enable more patient-specific therapies,” Stagljar said.
The journal Molecular Systems Biology published the findings today, and featured them on the cover of its February issue.
To help identify protein-protein interactions involving CFTR, the researchers developed a new technology based on a platform they designed in 2014. The approach is a high-throughput version of their Mammalian Membrane Two-Hybrid system, and it allows for screening of many more membrane proteins that associate with a specific protein.

Atopic dermatitis, a common skin condition affecting both children and adults, is often thought of as an inflammatory disease that arises from a breakdown in the barrier function of the skin. Now a new study pinpoints a cascade of inflammatory signaling that precedes the appearance of skin ulcers, shedding light on the early stages of the condition and identifying potential novel molecular targets for therapeutic intervention.
The work, published in the journal Science Translational Medicine, was the result of a cross-school and cross-institutional collaboration among researchers at the University of Pennsylvania’s School of Dental Medicine and Perelman School of Medicine, Oak Ridge National Laboratory, and the University of Tennessee.
“You have researchers in the dental school noticing a skin condition, broadening their work to the medical school and experts on computational systems biology,” says Dana Graves, a co-corresponding author on the paper and a professor and vice dean for research and scholarship at Penn Dental Medicine. “Without this interdisciplinary collaboration, that initial finding would not have gone anywhere.”
John Seykora, a co-corresponding author and professor of dermatology at Penn Medicine, seconds that observation. “This shows one of the benefits of being part of a university with experts across fields,” he says. “Our dental school colleagues developed a mouse that manifested a particular skin phenotype, and the question was, What was this and did it resemble any disease we might know? And in the end it did, and it’s providing some novel insights into a very common skin condition in humans.”
The work began in Graves’ lab, with Kang Ko, then a student in the Doctor of Science in Dentistry program and now a Penn Dental Medicine assistant professor, leading an exploration of the role of inflammatory signaling in bone fracture healing in diabetes. A focus was on nuclear factor kappa-B (NF-kB), a master regulator of inflammatory responses. As part of that work, Ko, Graves, and colleagues developed a mouse model lacking an activator of NF-kB signaling, IKKB.
The researchers noticed that these animals developed skin lesions as they became young adults.

Embedded in abortion laws in Texas are disputed assertions about embryonic development and the procedure’s risks. Chief among them: whether the early embryo has a heart.The Texas law banning abortions after about six weeks of pregnancy is based on a singular premise disputed by many medical experts: that once an ultrasound detects electrical cardiac activity in an embryo, its heart is beating and a live birth is on the way.At this very early stage of a pregnancy, however, the embryo is the size of a pomegranate seed and has only a primitive tube of cardiac cells that emit electric pulses and pump blood.Language has long been a battleground in the political struggle over abortion, and the sparring now centers on a word with deep resonance: “heartbeat.”The Texas law, which makes no exceptions for cases of rape or incest, forbids abortion at the time a “heartbeat” can be heard, which usually occurs at six weeks of gestation. The appeal is emotional: Many parents-to-be are moved by sounds during an ultrasound scan. But what the law defines as the sound of a heartbeat is not considered by medical experts to be coming from a developed heart, which forms later in pregnancy.At least a dozen states have passed similar heartbeat laws that could be established if Roe v. Wade were overturned. At the moment, the Supreme Court appears to be leaning toward upholding a Mississippi law that bans abortion after 15 weeks of pregnancy, effectively ending the right to abortion established by the Roe decision in 1973.The potentially seismic shifts have brought renewed attention to both the scientific underpinnings of these laws and the medical claims made by educational materials that many states require to be given to women seeking abortions.Opponents of abortion say that women need to be better informed of its possible consequences, even unlikely ones.“We really desire for women to be empowered with information,” said Dr. Christina Francis, chair of the American Association of Pro-Life Obstetricians and Gynecologists, which opposes abortion. “Women are intelligent creatures and can make empowered choices when they have all the information they need.”A Houston woman held an ultrasound indicating that she was less than six weeks pregnant and therefore eligible for an abortion under state law.Evelyn Hockstein/ReutersBut many medical societies and experts say the laws and state-mandated educational materials rest on profound misconceptions about embryonic and fetal development and abortion risks. The Texas statute, for example, requires physicians to warn women that they may face a higher risk of breast cancer or infertility if they have an abortion, despite a lack of evidence.Women are told they could die from an abortion, though the procedure is generally considered safer than a tonsillectomy, and much safer than pregnancy and childbirth. The materials also warn that having an abortion may make women depressed or suicidal, though studies have not found that to be the case.According to an analysis by the Informed Consent Project at Rutgers University, nearly one-third of statements about abortion made in patient materials from more than two dozen states are medically inaccurate. Most of the inaccuracies pertain to descriptions of the first trimester. They generally misrepresent certain body systems as complete or present at earlier stages of development than they actually are.“Laws that are written by nonmedical people to regulate the practice of medicine, or dictate what clinicians have to say to their patients, are dangerous and affect our ability to care for patients,” said Dr. Nisha Verma, a fellow at the American College of Obstetricians and Gynecologists, which has objected to the idea that a fetus has a heart at six weeks.An ultrasound of a human embryo at six weeks.Mikael HäggströmIndeed, the most fraught contention, embedded in the Texas abortion law, is that the fetus at that stage has a heart and that its beating represents a “key medical predictor that an unborn child will reach live birth.”This sound, discernible on an ultrasound scan, has become a demarcation line in anti-abortion legislation in dozens of states, though most opponents of abortion rights argue that life begins at conception.While there is little disagreement about the basic developmental biology, there are sharp differences about the significance.The heart is one of the first organs to start developing, because the embryo’s growth and survival depend on the circulation of blood carrying oxygen and nutrients. The electric activity begins at around six weeks in a tube of cells that will become a heart, after multiple gyrations.It will bend and loop and twist itself into an S shape. Thick cushions of embryonic tissue will grow toward one another to create walls, and a ridge on the floor of the ventricle will rise to meet them to partition the heart.If all goes well, four chambers and valves will form by the ninth or 10th week of pregnancy, and the heart will continue developing throughout gestation. But a heartbeat’s familiar “lub-dub, lub-dub” sound is created by the closing of the heart’s valves, which do not exist in the six-week-old cardiac tube.To opponents of abortion, that is a distinction without a difference. “It is a heart tube, but it is still a heart,” Dr. Francis said. “The shape is different, but that doesn’t change the essence of what it is,” she added.Dr. Robin Pierucci, a neonatologist who is an associate scholar at the Charlotte Lozier Institute, which opposes abortion, said in an email: “Finding a fetal heartbeat is a sign of health.”A 2004 study found that when a moving heart tube could be detected at six to eight weeks of pregnancy, a live birth resulted 98 percent of the time, Dr. Pierucci said.But that study — which compared women who had lost earlier pregnancies with those who had not — also found that cardiac activity did not lead to a live birth among one in five women who had lost previous pregnancies.The consensus among most medical experts is that the electrical activity picked up on an ultrasound at six weeks is not the sound of a heart beating and does not guarantee a live birth. The sound expectant mothers hear during a scan is created by the machine itself, which translates the waves of electrical activity into something audible.Doctors are partly to blame for the confusion. Many physicians whose patients are excited about a desired pregnancy will use the word “heartbeat” to describe the cardiac activity heard on an early ultrasound. The word has even crept into the medical literature.Anti-abortion demonstrators outside the Supreme Court in November.Tom Brenner for The New York Times“What you see and hear on an early ultrasound is embryonic activity — electrical currents being sent through cells that will develop at a much later time into a heart,” said Dr. Gabriela Aguilar, an obstetrician-gynecologist and a former fellow with Physicians for Reproductive Health, which supports access to abortion.In September, representatives of the A.C.O.G., which supports the right to abortion, said in a Senate hearing that “while contemporary ultrasound can detect an electrically induced flickering of a portion of the embryonic tissue at about six weeks gestation, structurally and in function, a fetus’ heart develops over the entire course of pregnancy.”Heartbeat laws and other state measures intended to discourage abortion often require that women be warned of risks like infertility and cancer. Health providers are required to provide the materials to patients, even if they believe the information exaggerates the risks of abortion or is otherwise misleading.Texas’ current booklet offers two pages of warnings. Under the heading “Death,” the booklet informs women that the risk of dying of a legal abortion is 0.73 in 100,000, according to the Centers for Disease Control and Prevention.Understand the Texas Abortion LawCard 1 of 4The most restrictive in the country.

SharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesTeaching people about achieving sexual pleasure can help sell safe-sex messages, say researchers from the World Health Organization.Programmes using this approach improve condom use more than ones that focus only on the dangers of unprotected sex, their study has found.They say enjoyment – rather than fear – is a healthy motivator.Sex can be safe as well as enjoyable, according to one of the research project’s co-authors.Billions of dollars are spent around the world each year on sexual and reproductive health and rights services, yet many programs do not address one of the fundamental reasons many people have sex – to feel good. Anne Philpott, a public-health professional, set up The Pleasure Project – the group that worked with the WHO team – in 2004, as a result of the frustration of “endless Aids meetings where no one talked about people’s motivations for having sex”. She said: “Pleasure is arguably the most powerful motivating factor for having sex and yet has been absent from sex education or sexual-health interventions. “If you ask most people, ‘Did your sex education equip you for your relationships and sex lives?’ they will say, ‘No’.”Sex can be safe – and enjoyable. It’s about having open conversations and giving people confidence.”‘I didn’t know why we put a condom on a banana.”I wish I knew sex could be fun growing up’Globally, a million sexually transmitted infections are acquired every day, the majority without symptoms. Using a condom can protect against these, as well as prevent pregnancy. Anne said condoms should be marketed as pleasure tools – as a way to enhance feeling and reassurance. This video can not be playedTo play this video you need to enable JavaScript in your browser.The researchers trawled medical literature to find recent examples of different safe-sex programmes and measure their effects on behaviour change.They found 33 projects promoting pleasure along with the safe-sex message. And these tended to be more successful in terms of increasing condom usage than those that focused only on sexually transmitted infections and risk reduction. Teaching about pleasure, desire and joy alongside consent, wellbeing and safety are the objectives of a pleasure-based sex education programme. The WHO’s Dr Lianne Gonsalves, co-author of the research, published in Plos One journal, said: “This review provides a simple message: programmes which better reflect the reasons people have sex – including for pleasure – see better health outcomes. “The hope is that these results galvanise the sexual and reproductive health and rights community to promote services that educate and equip users to engage in sex that is safe, consensual, and pleasurable.”What to do if you think you may have an STIHow to use a condomBrookSexual and Reproductive Health and Research – WHOTerrence Higgins TrustThe Pleasure ProjectThe BBC is not responsible for the content of external sites.