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Scientists decode opium poppy genome

Scientists have determined the DNA code of the opium poppy genome, uncovering key steps in how the plant evolved to produce the pharmaceutical compounds used to make vital medicines.

The discovery may pave the way for scientists to improve yields and the disease resistance of the medicinal plant, securing a reliable and cheap supply of the most effective drugs for pain relief and palliative care.

The breakthrough, by researchers at the University of York in partnership with the Wellcome Sanger Institute, UK, and international colleagues, reveals the origins of the genetic pathway leading to the production of the cough suppressant noscapine and painkiller drugs morphine and codeine.

Co-corresponding author, Professor Ian Graham, from the Centre for Novel Agricultural Products, Department of Biology at the University of York, said: “Biochemists have been curious for decades about how plants have evolved to become one of the richest sources of chemical diversity on earth. Using high quality genome assembly, our study has deciphered how this has happened in opium poppy.

“At the same time this research will provide the foundation for the development of molecular plant breeding tools that can be used to ensure there is a reliable and cheap supply of the most effective painkillers available for pain relief and palliative care for societies in not just developed but also developing world countries.”

Synthetic biology based approaches to manufacturing compounds such as noscapine, codeine and morphine are now being developed whereby genes from the plant are engineered into microbial systems such as yeast to enable production in industrial fermenters. However, opium poppy remains the cheapest and sole commercial source of these pharmaceutical compounds by some distance.

The scientists from the University of York and Wellcome Sanger Institute in the United Kingdom together with colleagues from Xi’an Jiaotong University and Shanghai Ocean University in China and Sun Pharmaceutical Industries (Australia) Pty Ltd, produced a high quality assembly of the 2.7 GigaBase genome sequence distributed across 11 chromosomes.

This enabled the researchers to identify a large cluster of 15 genes that encode enzymes involved in two distinct biosynthetic pathways involved in the production of both noscapine and the compounds leading to codeine and morphine.

Plants have the capacity to duplicate their genomes and when this happens there is freedom for the duplicated genes to evolve to do other things. This has allowed plants to develop new machinery to make a diverse array of chemical compounds that are used to defend against attack from harmful microbes and herbivores and to attract beneficial species such as bees to assist in pollination.

The genome assembly allowed the researchers to identify the ancestral genes that came together to produce the STORR gene fusion that is responsible for the first major step on the pathway to morphine and codeine. This fusion event happened before a relatively recent whole genome duplication event in the opium poppy genome 7.8 million years ago.

Co-corresponding author Professor Kai Ye from Xi’an Jiaotong University said “A highly repetitive plant genome and the intermingled evolutionary events in the past 100 million years complicated our analysis. We utilized complementary cutting-edge genome sequencing technologies with sophisticated mathematical models and analysis methods to investigate the evolutionary history of the opium poppy genome.

“It is intriguing that two biosynthetic pathways came to the same genomic region due to a series of duplication, shuffling and fusion structural events, enabling concerted production of novel metabolic compounds.”

Joint first author Professor Zemin Ning from the Wellcome Trust Sanger Institute said “Combining various sequencing technologies is the key for producing a high quality assembly for opium poppy genome. With a genome size similar to humans, the main challenge for this project was to handle repeat elements which make up 70.9% of the genome.”

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Researchers are turning to deadly venoms in their quests for life-saving therapies

Venomous reptiles, bugs and marine life have notorious reputations as dangerous, sometimes life-threatening creatures. But in a paper in the current issue of Science, first author Mandë Holford, an associate professor of chemistry and biochemistry at The Graduate Center of The City University of New York (GC/CUNY) and Hunter College, details how technology and a growing understanding of the evolution of venoms are pointing the way toward entirely new classes of drugs capable of treating diabetes, autoimmune diseases, chronic pain, and other conditions.

According to Holford and her colleagues, venomous species account for more than 15 percent of the Earth’s documented biodiversity, and they can be found in virtually all marine and terrestrial habitats. Still, researchers have studied very few venoms because until recently they lacked the appropriate technology for analyzing the tiny amounts of venom that can be extracted from these mostly small species. But innovations in omics (technologies that map the roles, relationships, and actions of an organism’s molecular structure) are allowing researchers to uncover evolutionary changes and diversification among specific venomous species that could prove useful in developing new drugs capable of precisely targeting and binding to molecules that are active in certain human diseases.

“Knowing more about the evolutionary history of venomous species can help us make more targeted decisions about the potential use of venom compounds in treating illnesses,” said Holford. “New environments, the development of venom resistance in its prey, and other factors can cause a species to evolve in order to survive. These changes can produce novel compounds — some of which may prove extremely useful in drug development.”

To date, only six Food and Drug Administration-approved, venom-derived drugs have been developed as a result of modern-day research, but Holford and her colleagues believe greater investment in venom research could yield therapies for currently untreatable diseases as well as improved therapeutic options.

Potential drug advances include therapeutic peptides derived from the venomous sea anemone, which researchers believe could treat autoimmune diseases; therapeutic neurotoxins derived from the Conus magus, which scientists think could provide non-addictive treatment of chronic pain; chlorotoxin from the deathstalker scorpion, which could be the basis for a surgical tumor-imaging technique; and spider toxins, which could yield ecofriendly insecticides.

Holford and her follow authors conclude that an evolution-informed perspective will help focus venom research so that it can leverage the extraordinary biochemical warfare created by nature to yield transformative therapeutics and bio-insecticides.

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Lenovo ThinkPad X1 Extreme adds graphics chops to its top biz laptop – CNET

Lori Grunin/CNET

The ThinkPad X1 Extreme isn’t the first Lenovo with discrete graphics or even the first mainstream ThinkPad with it: the 15-inch Yoga 720 launched with an Nvidia GTX 1050 option and the T series has had an option for Nvidia’s mobile graphics solution, the MX150, for a little while. But the X1 Extreme is the first of its top-end ThinkPad X1 line of business laptops with the option to combine a GTX 1050 Ti Max-Q with the bright, wide-gamut 4K screen that debuted earlier this year.

That makes it a potentially high performer for creatives who don’t need, or want to spend the money on, Lenovo’s sibling lightweight mobile workstation the ThinkPad P1. Though the entry prices for both are close — that laptop starts at about $1,900, while the X1 Extreme starts at $1,860  — it isn’t nearly as svelte-looking and doesn’t offer the better, Dolby Vision HDR-supporting display.

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Of course, the first thing people think of for discrete GPUs is gaming, and this will probably deliver decent performance for those days when you need to kill a few hours in an airport or hotel room. However, the ThinkPad’s keyboard feels a little mushy to me for gaming if you’re not using a controller.

Heat’s a big problem with the Max-Q designs, since their fans are supposed hit a lower sound volume than their high-test alternatives. Lenovo’s addressed that by adding a heat-dissipating aluminum alloy bottom cover to its veteran X1 carbon-fiber body. Otherwise, it’s the standard X1 clamshell design.

Other specs include:

  • Up to 8th-generation Intel Core i7 with vPro (Core i9 starting in November)
  • Windows 10 Pro 
  • Nvidia GeForce GTX 1050 Ti (Max-Q with 4GB GDDR5) 
  • Display: 15.6-inch IPS 300nits, 4K IPS touchscreen 400nits 
  • Up to 64GB DDR4 RAM 2,666MHz 
  • Storage: up to 2TB SSD, SD card slot 
  • Battery life: up to 15 hours 
  • Two USB 3.1 Type-A ports, two USB-C/Thunderbolt ports and one HDMI 2.0 
  • Weight: 3.8 to 4 pounds/1.7 to 1.8 kg depending upon display
  • Microsoft Cortana and Amazon Alexa support

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Presynapses come in a packet

Synapses are the interfaces for information exchange between neurons. Teams of scientists working with Professor Dr. Volker Haucke, Director at the Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP) and Professor at the Freie Universitaet Berlin, and Professor Dr. Stephan Sigrist at the Freie Universität Berlin discovered the materials, which form new presynapses for the release of transmitters. The findings may help to design better nerve-regenerating therapies in the future.

To date, we have a fairly good understanding how nerve cells (neurons) communicate with each other. Central in this information transfer is the release of neurotransmitters at chemical synapses. At synapses, signal-transmitting presynapses face postsynapses, which recognize the chemical signals and relay them. “By contrast, we still know relatively little as to how synapses are formed,” points out Professor Volker Haucke.

The release of neurotransmitter at presynapses requires their storage synaptic vesicles (bubble-like structures). Furthermore, scaffold proteins have to be present at the right time and location to ensure proper transmitter release. Until now, it was unclear how synaptic vesicle components and scaffold proteins get to synaptic cell junctions. Moreover, it was unclear from which cellular building blocks scaffold proteins and vesicles are made. The teams of Professor Dr. Volker Haucke and Professor Dr. Stephan Sigrist studied neurons from mouse brain and Drosophila larvae to learn more about the processes forming presynapses. The results of their work have just been published in the journal Neuron on August 30, 2018.

The scientists found answers to both questions: They discovered that for the most part, vesicle and scaffold proteins are co-transported to the presynapse in a packet. Hence, vesicle and scaffold proteins arrive at the nascent synapse as a preformed functional unit, so neurotransmitter release may start instantaneously. The scientists could also show that this mechanism is evolutionary conserved from flies to mice and probably humans. The team also revealed that scaffold and vesicle proteins are transported in organelles that share characteristics with so-called lysosomes. Professor Haucke explains: “This is extremely surprising as scientists used to believe that lysosomes are mostly responsible for the degradation of cell components. However, in the context of the developing nervous system, these lysosome-related vesicles appear to have a distinct assembly function as they are involved in forming the presynapses where transmitters are released.”

These discoveries made by the scientists at the Leibniz-Forschungsinstitut für Molekulare Pharmakologie and the Freie Universitaet Berlin are of significance beyond basic research: For example, during learning processes synapses need to be remodelled to amplify signals. Professor Dr. Stephan Sigrist comments: “We were able to establish such a signal amplification in Drosophila larvae. When we programmed the neurons to deliver additional scaffold proteins and transport packets, they fired with more intensity than before.” This correlation may prove useful in the treatment of congenital degenerative neuronal diseases or for the regeneration of neurons after major accidents for example. To enable injured people to walk again, nerve paths must regenerate and new synapses must form or be re-established. The described findings may allow to accelerate this process in a targeted fashion.

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The Lenovo Yoga Book gets a second chapter – CNET

The dual-screen laptop is an idea that comes around every few years, but never quite manages to catch on. Learning from its previous attempt, the new Lenovo Yoga Book C930 changes up the formula in a way that is at least highly novel.

We’ve seen the idea of a laptop with a second screen in place of a keyboard a few times before. There was the Acer Iconia back in 2011, the original dual-LCD Yoga Book (in both Windows and Android versions) in 2016 and earlier this year, a sneak peek at an Asus prototype called Project Precog. This overall design might even be the future of mobile phones, once foldable screens become common.

Lori Grunin/CNET

The biggest issue with previous dual-screen laptops, including the first Yoga Book, is that typing on an onscreen keyboard just doesn’t work very well for most people, especially on a large, slick glass surface with little to no tactile feedback. Even iPad onscreen typing is still considered kludgey.

For the second-gen Yoga Book, now Windows-only, Lenovo is replacing the bottom display with a touch-enabled e-ink keyboard. That means you get a more specialized input device, better finger traction on the matte screen, faster response than the previous full-color touchscreen and potentially much better battery life.

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It does mean, though, that you can’t use the bottom screen as a secondary or extended Windows display, and you lose out on some flexibility in tools and widgets that can replace the keyboard. The keyboard adds multiple language and layout support, as well as a touch pad that can pop up only when needed.


Lori Grunin/CNET

Think ink 

In my brief hands-on time with a prototype of the new Yoga Book, I thought the E Ink keyboard was more responsive and easier to use than the original Yoga Book, but superfast typists may find it has trouble keeping up (this may improve in the final version). The haptic response was decent, but it’s not the same as having per-key feedback.

Of course, you can use the E Ink display as a reader, but for now it only supports PDF files, not proprietary formats like Amazon’s Kindle e-books. That feels like it’ll be a make-or-break feature to add if at all possible.

A few other tricks the new Yoga Book has up its sleeve:

  • A Wacom active pen with a magnetic attachment to the body
  • A knock-to-open hinge that pops the lid pen with a tap
  • Dolby Atmos support
  • A larger, higher-res 2,560×1,600 primary display

The new Yoga Book C930 will be offered in both Intel Core m5 and Core i5 versions, starting in October for $999 and up. International price and release details were not yet available. 

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Children's bone cancers could remain hidden for years before diagnosis

Scientists have discovered that some childhood bone cancers start growing years before they are currently diagnosed. Researchers at the Wellcome Sanger Institute and Hospital for Sick Children (SickKids), Canada discovered large-scale genetic rearrangements in Ewing Sarcomas and other children’s cancers, and showed these can take years to form in bone or soft tissue. This study will help unravel the causes of childhood cancers and raises the possibility of finding ways to diagnose and treat these cancers earlier in the future.

Reported in the journal Science today (31st August 2018), the research also showed that cancers with the complex genetic rearrangements were more aggressive and could benefit from more intense treatment than other cancers. This will help doctors decide on the best treatment for each patient.

Ewing sarcoma is a rare cancer found mainly in bone or soft tissue of young teenagers as they grow, and is the second most commonly diagnosed bone cancer in children and young people. Treatment involves chemotherapy, surgery to remove the affected part of the bone if possible and radiotherapy. However, this harsh regime has hardly changed for the last 40 years and fails about one third of patients.

Cancer is a genetic disease and in Ewing sarcoma, two specific genes, EWSR1 and ETS, are fused together. To understand the genetic events leading to this, researchers sequenced and analysed the genomes of 124 tumours. They discovered that in nearly half of the cases, the main gene fusion occurred when the DNA completely rearranged itself, forming complex loops of DNA.

Dr Adam Shlien, one of the lead authors on the paper, Associate Director of Translational Genetics and Scientist in Genetics & Genome Biology, and co-Director of the SickKids Cancer Sequencing (KiCS) program at SickKids, said: “Many childhood sarcomas are driven by gene fusions, however until now we have not known how or when these key events occur, or whether these processes change at relapse. We found dramatic early chromosomal shattering in 42 per cent of Ewing sarcomas, not only fusing two critical genes together, but also disrupting a number of important areas.”

The earlier a cancer is diagnosed, the easier it is to treat, but until now it was thought that Ewing sarcoma was very fast growing. Surprisingly, the researchers found that the complex DNA rearrangements that cause Ewing sarcoma had occurred years before the tumour was diagnosed. This offers possibilities of finding ways to screen for these cancers to treat them earlier.

Dr Sam Behjati one of the lead authors on the paper from Wellcome Sanger Institute and University of Cambridge Department of Pediatrics, said: “In principle this study provides evidence that Ewing sarcoma could be detectable earlier, possibly even before it reveals itself as disease. If we could detect these childhood cancers sooner, when tumours are smaller, they would be much easier to treat. Further research is needed, but this possibility of finding a way to diagnose Ewing sarcomas earlier could help patients in the future.”

The researchers discovered that Ewing Sarcomas with these complex genetic rearrangements were more aggressive than those with simple gene-fusions, and that any relapses needed different treatments. Understanding this could help clinicians offer the best treatment options for each patient.

Dr. David Malkin, co-lead author, Staff Oncologist, Scientist and co-Director of the SickKids Cancer Sequencing (KiCS) program, said: “As an increasing and diverse number of tumour genome sequences become available, we may be able to define further rearrangement processes that underlie fusion genes and thus unravel the causes of fusion-driven human cancers. Our goal is to better understand these cancers in an attempt to improve treatment and outcomes.”

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Predicting how splicing errors impact disease risk

No one knows how many times in a day, or even an hour, the trillions of cells in our body need to make proteins. But we do know that it’s going on all the time, on a massive scale. We also know that every time this happens, an editing process takes place in the cell nucleus. Called RNA splicing, it makes sure that the RNA “instructions” sent to cellular protein factories correspond precisely with the blueprint encoded in our genes.

Researchers led by Adrian Krainer, a Cold Spring Harbor Laboratory (CSHL) Professor, and Assistant Professor Justin Kinney, are teasing out the rules that guide how cells process these RNA messages, enabling better predictions about the impact of specific genetic mutations that affect this process. This in turn will help assess how certain mutations affect a person’s risk for disease.

Splicing removes interrupting segments called introns from the raw, unedited RNA copy of a gene, leaving only the exons, or protein-coding regions. There are over 200,000 introns in the human genome, and if they are spliced out imprecisely, cells will generate faulty proteins. The results can be life-threatening: about 14% of the single-letter mutations that have been linked to human diseases are thought to occur within the DNA sequences that flag intron positions in the genome.

The cell’s splicing machinery seeks “splice sites” to correctly remove introns from a raw RNA message. Splice sites throughout the genome are similar but not identical, and small changes don’t always impair splicing efficiency. For the splice site at the beginning of an intron — known as its 5′ [“five-prime”] splice site, Krainer says, “we know that at the first and second [DNA-letter] position, mutations have a very strong impact. Mutations elsewhere in the intron can have dramatic effects or no effect, or something in between.”

That’s made it hard to predict how mutations at splice sites within disease-linked genes will impact patients. For example, mutations in the genes BRCA1 or BRCA2 can increase a woman’s risk of breast and ovarian cancer, but not every mutation is harmful.

In experiments led by first author Mandy Wong, a Krainer lab postdoc, the team created 5′ splice sites with every possible combination of DNA letters, then measured how well the associated introns were removed from a larger piece of RNA. For their experiments, they used introns from three disease-associated genes — BRCA2 and two genes in which mutations cause neurodegenerative diseases, IKBKAP and SMN1.

In one intron of each of the three genes, the team tested over 32,000 5′ splice sites. They found that specific DNA sequences corresponded with similar splicing efficiency or inefficiency in different introns. This is a step toward making general predictions. But they also found that other features of each gene — the larger context — tended to modify the impact in each specific case. In other words: how a mutation within a given 5′ splice site will affect splicing is somewhat predictable, but is also influenced by context beyond the splice site itself.

Krainer says this knowledge will better help predict the impact of splice-site mutations — but a deeper investigation is needed.

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Drug-resistance of gonorrhea in the EU: Persistent but stable

Neisseria gonorrhoea continues to show high levels of resistance to azithromycin across the European Union and European Economic Area, according to the 2016 results of the European Gonococcal Antimicrobial Surveillance Programme (Euro-GASP). This threatens the effectiveness of the currently recommended dual therapy regimen for gonorrhoea. Overall, the rates of resistance to cefixime, ceftriaxone and azithromycin have remained stable when compared to recent years.

The main antibiotics currently recommended for gonorrhoea treatment in Europe, so-called third generation cephalosporins, are the last remaining options for effective first-line antimicrobial single therapy. As susceptibility of Neisseria gonorrhoea to these antimicrobials had decreased in the past, the European treatment guidelines suggest the addition of azithromycin to the basic course of the cephalosporins ceftriaxone or cefixime.

In order to monitor the continued effectiveness of this treatment regimen, countries of the European Union and European Economic Area (EU/EEA) participate in Euro-GASP sentinel surveillance programme. Each year they submit isolates to test susceptibility of Neisseria gonorrhoeae to the antibiotics commonly used to treat gonorrhoea.

In 2016, 25 EU/EEA countries collected and tested 2 660 gonococcal isolates showing stable rates of resistance against cefixime (2.1%), ciprofloxacin and azithromycin (7.5%) compared with 2015. No isolates with resistance to ceftriaxone were detected compared with one in 2015, five in 2014 and seven in 2013.

While the absence of ceftriaxone resistance among the tested isolates in 2016 is encouraging, the persistent level of resistance to azithromycin is of concern as it threatens to reduce the effectiveness of the recommended dual therapy with ceftriaxone and azithromycin.

Among those patients for whom information on their treatment course was reported in 2016, 86% were administered ceftriaxone and more than half received combined treatment with azithromycin. The use of two antimicrobials for gonorrhoea treatment has likely contributed to increased susceptibility to ceftriaxone. However, Euro-GASP data completeness for the variable ‘treatment used’ has still some way to go overall with just 37% in 2016.

Minimising the threat of untreatable gonorrhoea

With more than 75,000 reported cases in 2016, gonorrhoea is the second most commonly notified sexually transmitted infection (STI) in the EU/EEA countries. Apart from these reports, many more asymptomatic infections are know to occur.

Successful gonorrhoea treatment with antibiotics not only reduces the risk of complications such as pelvic inflammatory disease, ectopic pregnancies, infertility or increased HIV transmission in some settings. Combined with regular testing to diagnose and treat infections at an early stage, it also serves as one of the main public health strategies in order to reduce further transmission.

In light of limited alternatives to the current combination therapy introduced in 2012, ECDC launched a regional response plan to control multidrug-resistant gonorrhoea to minimise the threat of drug-resistant gonorrhoea in Europe. ECDC is currently revising the plan, also following recent reports of extensively drug resistant gonorrhoea strains that reached Europe.

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Pushing big data to rapidly advance patient care

The breakneck pace of biomedical discovery is outstripping clinicians’ ability to incorporate this new knowledge into practice.

Charles Friedman, Ph.D. and his colleagues recently wrote an article in the Journal of General Internal Medicine about a possible way to approach this problem, one that will accelerate the movement of newly-generated evidence about the management of health and disease into practice that improves the health of patients.

Traditionally, it has taken many years, and even decades, for the knowledge produced from studies to change medical practice. For example, the authors note in the article, the use of clot-busting drugs for the treatment of heart attacks was delayed by as much as 20 years because of this inability to quickly incorporate new evidence.

“There are lots of reasons why new knowledge isn’t being rapidly incorporated into practice,” says Friedman. “If you have to read it in a journal, understand it, figure out what to do based on it, and fit that process into your busy day and complicated work flow, for a lot of practitioners, there’s just not enough room for this.”

Informing medical practice

Much of the generation of new evidence is done by groups like the federal Agency for Healthcare Quality and Research and the Cochrane Collaboration, a UK-based non-profit group designed to organize medical research into systematic reviews and meta analyses. These reviews synthesize all of the available medical research about a given topic with the hope of informing medical practice. However, that movement of this accumulated knowledge to medical practice can happen incredibly slowly, if at all.

The new article focuses on the need to harness the power of technology to enable health systems to analyze the data they generate during the process of taking care of patients to generate new “local” evidence and use this in combination with published reviewed evidence to improve health outcomes.

The key to using both types of evidence, they argue, is transforming human readable knowledge — the words, tables and figures in a typical journal article — into computable forms of that same knowledge.

“A lot of scientific studies result in some kind of model: an equation, a guideline, a statistical relationship, or an algorithm. All of these kinds of models can be expressed as computer code that can automatically generate advice about a specific patient,” Friedman explains. When both “local” models and published models are available in computable forms, it is suddenly possible to generate advice that reflects both kinds of sources.

Computable forms are key

He notes that while Michigan Medicine, along with most other health systems that use electronic health records, is using its data to continuously improve quality of care, putting this knowledge in computable forms creates many new ways to apply that knowledge to improve care.

The University of Michigan Medical School’s Department of Learning Health Sciences is taking the lead in transforming biomedical knowledge into computable forms that are open and accessible to anyone. They’ve created a computer platform called the Knowledge Grid, that stores computable knowledge in digital libraries and then uses that knowledge to generate patient-specific advice.

“The value of Big Data is to generate Big Knowledge,” says Friedman. “The power of Big Data is to provide better models. If all those models do is sit in journal articles, no one’s going to be any healthier.”

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Missing men, missing infertility: New research flags up problem

Men are missing from fertility debates and crucial support services because they are often not included in studies and, when they are, it is usually only married, heterosexual men who are asked for data.

New research, ‘Missing men, missing infertility: The enactment of sex/gender in surveys in low and middle-income countries’ has been completed by a team at Lancaster University in the UK.

Dr Jasmine Fledderjohann and Professor Celia Roberts from the Department of Sociology say it is vital to explore the gender issue in in/fertility research as men are often missing.

Their study focused on the Demographic and Health Surveys (DHS), which have been widely-used in low and middle income countries over the past several decades to understand demographic processes and family building.

The study finds these important data engage in unintentional yet highly consequential practices of designing the surveys differently for men versus women, producing gender inequalities.

“First, we wanted to know, across time and place, were men included in the surveys at all? Then, if men were included, which men were included?” explained Dr Fledderjohann, a lecturer in Sociology and Social Work.

“And how did choices about which men to include line up to choices about which women to include? Finally, where men were included, what kinds of questions were they asked and how did the kinds of questions asked shape what kinds of conclusions we could draw from the data?”

The research identified two processes through which surveys had the potential to render male infertility invisible: identifying who to survey in an exclusionary way and asking survey questions in a way that selects out some groups/issues.

Compiling information about survey samples in the DHS, and combining this with a qualitative examination of survey design, they identified areas of men’s invisibility across time and place.

While inclusion of men in DHS samples had increased over time, some men (e.g. single, divorced and transgender) remained missing in many survey settings.

This, said the authors, was problematic from a reproductive justice perspective. Survey results, which both reflect and contribute to men’s invisibility, are widely used as an evidence-base for family and population policies. Men’s invisibility from data and research therefore has the potential to make them invisible in policy discussions about family building, too.

Reproductive health services are typically only made available to those whose reproductive health needs are recognised. Men’s exclusion from the reproductive debate, the authors argue, contributes to gender inequalities in who is supported in (and held accountable for) family building within families and societies.

“The good news is, the availability of data for men has increased over time, although men in some regions are comparatively neglected,” adds Dr Fledderjohann. “For example, relative to the availability of surveys for women, there is less data available for men in Latin America, North Africa, and parts of South Asia than for sub-Saharan Africa.

“Even where men were surveyed, however, often not all men were surveyed and, where they were surveyed, the way questions were asked limited our ability to understand some family building processes — for example, infertility in the context of polygyny.

“There are some negative consequences to being left out of data for men. For example, support for difficulties conceiving is available only to those whose needs are recognized.

“However, there can also be some benefits to invisibility. Where reproduction is not seen as men’s domain (a view reinforced by their absence from data) the blame for reproductive failure tends to fall on women’s shoulders.

“In short, this is an issue that impacts men and women alike. It both reflects and creates a specific notion of who should take responsibility for family building and there’s great potential for both men and women to be disadvantaged in this process.”