Publisher Health

New study from Brigham researchers highlights a correlation between symptoms of insomnia and hypertension in women.
Getting enough sleep has never been more difficult in today’s fast-paced environment. Yet new research from investigators in the Channing Division of Network Medicine of Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system, highlights why getting a good night’s sleep is critical to staying healthy. Their research unveils that women who struggled with getting enough sleep were at greater risk of developing hypertension, or high blood pressure. Results are published in the journal Hypertension.
“These findings suggest that individuals who struggle with symptoms of insomnia may be at risk of hypertension and could benefit from preemptive screening,” explained Shahab Haghayegh, Ph.D., a research fellow at the Brigham and Harvard Medical School. “Hypertension is associated with many other physical and mental health complications. The sooner we can identify individuals with high blood pressure and treat them for it, the better we can mitigate future health issues.”
Both hypertension and sleep disorders are becoming increasingly prevalent among adults in the United States. In fact, more than 35% of US adults do not get enough sleep at night, according to the Centers for Disease Control and Prevention. The American Academy of Sleep Medicine suggests that 30% of Americans experience symptoms of insomnia. Strikingly, 45% of U.S. adults live with high blood pressure.
Haghayegh and colleagues followed 66,122 participants between 25 and 42 years of age in the Nurses’ Health Study II (NHS2) cohort, all without hypertension at the study’s onset, over sixteen years (from 2001 until 2017). Investigators collected information on participants’ age, race, body mass index (BMI), diet, lifestyle, physical activity, history of sleep apnea, and family history of hypertension and assessed the incidence of hypertension among the group every two years. They first began measuring sleep duration in 2001, then did so again in 2009, recording the average number of hours slept over a 24-hour period. They also tracked sleeping difficulties, such as having trouble falling or staying asleep or waking up early in the morning, collecting responses at several time points throughout the study.
Data analyses revealed that women with sleeping difficulties had higher BMIs, lower physical activity, and poorer diets, on average. Researcher also found that those who struggled with sleep were more likely to smoke and drink alcohol and have previously gone through menopause.
Among the 25,987 cases of hypertension documented over the follow-up, women who slept less than seven to eight hours a night had a significantly higher risk of developing hypertension, according to the data collected. Similarly, women who had trouble falling asleep and staying asleep were also more likely to develop hypertension. Waking up early in the morning was not associated with this increased risk. Notably, these associations, remained significant after controlling for participant shift work schedules (night versus day shifts) and chronotype (morningness versus eveningness).

The new research has identified a genetic scar left in the genomes of bacteria as they become resistant to antibiotic treatment.
This significant breakthrough in understanding how antibiotic resistance occurs will allow scientists to better predict which strains of pneumonia will become highly resistant in the future, giving them time to put control measures in place to help save patients’ lives.
Pneumonia is a very serious infection and the third leading cause of death in the UK population. Often these infections are caused by a bacterium called Streptococcus pneumoniae (S.pneumoniae). Antibiotics are given to patients to kill the bacteria, however the bacteria are finding ways to become resistant and this resistance threatens patient treatment in the long-term.
The Sheffield team discovered mutations called pde1 act as an evolutionary gateway through which the S.pneumoniae cells start to become resistant to antibiotics.
Lead author, Dr Andrew Fenton from the School of Biosciences at the University of Sheffield, said: “Pneumonia is a dangerous and deadly infection and effective treatment with antibiotics is essential for patient care. However, the effectiveness of antibiotics is increasingly under threat as the bacteria which cause pneumonia become resistant to antibiotic treatment over time.
“This research has identified a genetic scar left in the genomes of bacteria as they become resistant to antibiotic treatment. This is a major step forward in understanding how resistance occurs and how we might be able to predict it.
“If we understand the emergence of antibiotic resistance then we can predict what groups of bacterial strains are becoming more dangerous. Giving us time to put control measures in place to stop their spread, saving patients’ lives.”
Over the last 10 years there have been many large-scale genome association and genetic studies focused on S.pneumoniae antibiotic resistance but these have, so far, not led to effective mitigations.
This study, published in the journal PNAS, is a significant step forward in the molecular understanding of resistance and adds pde1 to the select few mutations known to promote antibiotic resistance in S. pneumoniae.

Researchers at the University of California, Davis, have developed a proof-of-concept sensor that may usher in a new era for millimeter wave radars. In fact, they call its design a “mission impossible” made possible.
Millimeter wave radars send fast-moving electromagnetic waves to targets to analyze their movement, position and speed from the waves bounced back. The benefits of millimeter waves are their natural sensitivity to small-scale movements and their ability to focus on and sense data from microscopic objects.
The new sensor uses an innovative millimeter wave radar design to detect vibrations a thousand times smaller, and changes in a target’s position one hundred times smaller, than a strand of human hair, making it better or on par with the world’s most accurate sensors. Yet unlike its peers, this one is the size of a sesame seed, is cheap to produce and features a long battery life.
Professor Omeed Momeni and his lab in the Department of Electrical and Computer Engineering led the effort. It is part of an ongoing project funded by the Foundation for Food & Agriculture Research, or FFAR, to develop a low-cost sensor capable of tracking the water status of individual plants. This new radar is the necessary steppingstone that proves it is possible. The work is published in the September 2023 issue of IEEE Journal of Solid-State Circuits.
Challenge of millimeter waves
Millimeter wave is the electromagnetic frequency between microwaves and infrared, ranging from 30 to 300 gigahertz. It enables fast communication networks, such as 5G, and is desirable for its short-range sensing capabilities. But it can be tough to work with due to high power consumption and limited performance of semiconductors at these frequencies.
The primary issue the team faced throughout its first year working on the sensor was homing in on the desired source. There was so much noise that, when the researchers attempted to pick up the delicate signal of a small leaf thinning, their sensors were drowned out.

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Parents, teachers, coaches and other adults shouting at denigrating or verbally threatening children can be as damaging to their development as sexual or physical abuse, a new study finds.

The study, published in the journal Child Abuse & Neglect, reviewed 166 earlier studies to produce a detailed analysis of the existing literature on the topic.

The authors called for childhood verbal abuse to be ascribed its own category of maltreatment to facilitate prevention.

Child maltreatment is currently classified into four categories — physical abuse, sexual abuse, emotional abuse, of which verbal abuse is a part, and neglect — and this study can inform strategies for prevention and treatment.

Unlike other forms of emotional abuse, including indifference, silent treatment and witnessing domestic violence, researchers categorized verbal abuse as more “overt” and said it “warrants special attention.”

Commissioned by Words Matter — a British charity that aims to improve children’s health by ending verbal abuse — the study was carried out by researchers at Wingate University in North Carolina and University College London.

“Childhood verbal abuse desperately needs to be acknowledged as an abuse subtype because of the lifelong negative consequences,” said professor Shanta Dube, the study’s lead author and director of Wingate University’s Master of Public Health Program, in a statement.

The study, which studied the impact of shouting by adults such as parents, teachers and coaches, cited several papers that suggested the lasting effects of childhood verbal abuse can manifest as mental distress, such as depression and anger; externalizing symptoms, such as committing crimes, substance use or perpetrating abuse; and physical health outcomes, such as developing obesity or lung disease.

Jessica Bondy, the founder of Words Matter, stressed the importance of grasping “the true scale and impact of childhood verbal abuse.”

“All adults get overloaded sometimes and say things unintentionally,” she said in a statement. “We have to work collectively to devise ways to recognize these actions and end childhood verbal abuse by adults so children can flourish.”

This latest study found that a potentially significant “shift in childhood abuse may be occurring,” as the prevalence of childhood emotional abuse has increased while physical and sexual abuse have declined, according to the World Health Organization in 2014 and four other papers cited in the new study.

Researchers also called for a “need for consistency” in defining childhood verbal abuse so that its “prevalence and impact can be appropriately measured, and interventions developed.

Resources available on the Words Matter website encourage adults to avoid shouting, insults, putdowns or name calling when talking to children, as well as thinking before speaking and taking time to repair a relationship with the child after something hurtful has been said.

Similarly, the first rule of yelling is to refrain from critique while doing it, Elizabeth Gershoff, a professor of human development and family sciences at the University of Texas at Austin and researcher on parental discipline, told CNN in 2019.

Considering the audience is important too, she added. Toddlers are likely to only absorb the frustration and not the substance of the yell, while some children respond differently to being yelled at.

Correction: A previous version of this story misidentified the journal name.

Allowing eyewitnesses to dynamically explore digital faces using a new interactive procedure can significantly improve identification accuracy compared to the video lineup and photo array procedures used by police worldwide, a new study reveals.
Interactive lineups present digital 3D faces that witnesses can rotate and view from different angles using a computer mouse — enabling witnesses to actively explore and match faces to their recollection.
Publishing their findings today (2 Oct) in Proceedings of the National Academy of Sciences, psychologists found that the interactive procedure enhanced people’s ability to correctly identify perpetrators and avoid misidentifications.
Lead author and PhD student Marlene Meyer from the School of Psychology at the University of Birmingham said: “Witnesses were much better at telling innocent from guilty suspects using the interactive lineups. This technology creates retrieval conditions that boost memory performance.”
Researchers recruited 550 volunteer ‘witnesses’ to test ability to make a correct identification of previously seen individuals. To test their memories, witnesses were shown images of the perpetrator, alongside filler images of similar faces. The researchers found that presenting the images via interactive lineups improved accuracy by 27-35% over photo arrays and 35-75% over video lineups.
Professor Heather Flowe from the School of Psychology at the University of Birmingham and senior author of the paper commented: “By integrating this technology, we may observe a dramatic reduction in identification errors, which will pave the way towards more just outcomes in criminal investigations and proceedings around the world. This tech update to police procedures warrants further testing and adoption to prevent wrongful convictions.”
The study is the first to experimentally compare interactive lineups against police video lineups and photo arrays. The results, showing interactive lineups’ superiority over the two most widely used identification procedures used by law enforcement, could potentially revolutionise how law enforcement agencies conduct eyewitness identification.
“This study highlights the exciting potential of interactive lineups,” said Matt Whitwam, Director of Promaps, a software company that supplies police forces with lineup technology. “We look forward to working with law enforcement to test interactive systems that harness technological advances for more accurate investigations.”

Researchers from Karolinska Institutet have published a study in Alzheimer’s Research & Therapy that addresses possible associations between chronic stress, mild cognitive impairment and Alzheimer’s disease. The study shows how people aged between 18 and 65 with a previous diagnosis of chronic stress and depression were more likely than other people to be diagnosed with mild cognitive impairment or Alzheimer’s disease.
Some 160,000 people have some form of dementia in Sweden, Alzheimer’s disease being the most common, a figure that is rising with our life expectancy. At the same time, many new diagnostic methods and early-intervention therapies have been developed in recent years, which foregrounds the need to identify more risk factors for the disease.
Previous studies have demonstrated a possible association between chronic stress, depression and dementia. This present study now shows that people who have been diagnosed with chronic stress or depression are more likely to be diagnosed with Alzheimer’s disease.
The study shows that the risk of Alzheimer’s disease was more than twice as high in patients with chronic stress and in patients with depression as it was in patients without either condition; in patients with both chronic stress and depression it was up to four times as high.
The risk of developing cognitive impairment was elevated about as much. A patient is deemed to be suffering chronic stress when he or she has been under stress with no opportunity for recuperation for at least six months.
“The risk is still very small and the causality is unknown,” says the study’s last author Axel C. Carlsson, docent at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet. “That said, the finding is important in that it enables us to improve preventative efforts and understand links with the other risk factors for dementia.”
The study was conducted using Region Stockholm’s administrative healthcare database, which contains all healthcare contacts compensated by the region. The researchers focused on patients between the ages of 18 and 65 and between 2012 and 2013. They identified 44,447 people with a diagnosis of chronic stress and/or depression and followed them for eight years to see how many of them were later diagnosed with mild cognitive impairment or Alzheimer’s disease.

Circadian rhythms, the internal biological clocks that regulate our daily activities, are essential for maintaining health and well-being. While the role of transcription in these rhythms is well-established, a new study sheds light on the critical importance of post-transcriptional processes. The research, titled “Circadian ribosome profiling reveals a role for the Period2 upstream open reading frame in sleep,” to be published in PNAS, redefines our understanding of how translation and post-transcriptional processes influence the body’s internal clock and its impact on sleep patterns.
Timing Is Everything
By using ribosome profiling, the research team examined the timing of ribosome binding in relation to peak protein and RNA levels. They discovered significant differences in the timing of these processes, suggesting a complex post-translational control of circadian protein production. “We built upon our previous work to precisely quantify the level of circadian proteins in mice held in constant darkness over a 24-hour period, which controls for the confounding effects of light,” says corresponding author Hiroki Ueda. “Using ribosome profiling, I wanted to see how the binding of ribosomes to RNA related to the timing of when those proteins actually got made. And by trying to answer this basic timing question, we found that ribosomes bind an upstream open reading frame in Period2 which altered the amplitude of circadian rhythms and disrupted sleep in mice,” adds lead author Arthur Millius.
uORFs: Silent Regulators Speak Out
The researchers found many upstream open reading frames (uORFs) in the 5′ untranslated region of circadian mRNAs, which is the part of RNA before the so-called “coding sequence” that gets translated by ribosomes into protein. These uORFs were associated with reduced ribosome binding in the main coding sequence and reduced reporter expression in a variety of circadian assays tested by the researchers suggesting a role for uORFs in shaping circadian protein expression. “About half of genes in mice and humans have at least one uORF,” explains Dimitri Perrin, the team’s bioinformatician, “but it’s particularly interesting that about 75% of genes associated with circadian rhythms have an uORF, which means that circadian rhythms are particularly susceptible to this type of post-transcriptional regulation.”
Per2 uORF Mutation and Sleep
Mutating the uORF in the core clock gene Period2 (Per2) yielded intriguing results. It boosted Per2 mRNA expression while significantly reducing total sleep duration in mice, particularly during transitions between light and dark. “Our sleep data suggests that disrupting uORFs can have physiological impacts on mice behavior, which shows that you don’t have to mutate the protein to have an effect,” explains Rikuhiro Yamada who analyzed the phenotype of the mice using the lab’s snappy sleep stager system. “We performed ribosome profiling on the Per2 uORF mutant mice, and although ribosome binding was enhanced in the mutant mice, it was the increase in Per2 mRNA levels that was the most surprising,” continues Arthur Millius. “We thought uORFs would primarily affect mRNA translation, but it turns out they might also trigger an RNA degradation response similar to nonsense mediated decay.”
PER2 protein is at the center of the inhibitory feedback loop that underlies the molecular mechanisms that control circadian rhythms, but its importance goes beyond just regulating sleep. Per2 expression is deregulated in breast cancer, downregulated in patients with acute myeloid leukemia, and disruption of Per2 results in tumorgenesis in mice. Therefore, understanding the post-transcriptional processes that shape Per2 expression has wide-ranging implications for the various fields, including circadian rhythms and medicine, and could provide new insights into how cancer hijacks a cell’s normal circadian program or help improve drugs with time-dependent therapeutic efficacy.

The research teams of Professor René Ketting at the Institute of Molecular Biology (IMB) in Mainz, Germany, and Dr. Sebastian Falk at the Max Perutz Labs in Vienna, Austria, have identified a new enzyme called PUCH, which plays a key role in preventing the spread of parasitic DNA in our genomes. These findings may reveal new insights into how our bodies detect and fight bacteria and viruses to prevent infections.
Our cells are under constant attack from millions of foreign intruders, such as viruses and bacteria. To keep us from getting sick, our bodies have an immune system — a whole army of cells that specializes in detecting and destroying these invaders. However, our cells face threats not only from external enemies but also from within.
Genomic parasites populate a large part of the genome
An amazing 45 percent of our genome is comprised of thousands of genomic parasites, i.e., repetitive DNA sequences called transposable elements (TEs). TEs are found in all organisms but have no specific function. They can, however, be dangerous. TEs are also called “jumping genes” because they can copy and paste themselves into new locations in our DNA. This is a major problem because it can lead to mutations that cause ouer cells to stop working normally or to become cancerous. As such, almost half of our genome is engaged in a constant guerrilla war with the other half as TEs seek to multiply, while our cells try to prevent them from spreading.
How do our cells combat these internal enemies? Fortunately, our cells have evolved a genomic defense system of specialized proteins whose job it is to hunt down TEs and prevent them from replicating. In a new paper published in Nature, René Ketting and Sebastian Falk together with their research teams report their discovery of PUCH — a completely new, previously unknown type of enzyme, which is key to this genomic defense system. They found that PUCH plays a crucial role in producing small molecules called piRNAs, which detect TEs when they attempt to “jump.” They then activate the genomic defense system to stop TEs before they paste themselves into new locations in our DNA.
The researchers discovered PUCH in the cells of the roundworm C. elegans, a simple invertebrate often used in biological research. However, the findings may also shed light on how our own immune system works. PUCH is characterized by unique molecular structures called Schlafen folds. Enzymes with Schlafen folds are also found in mice and humans, where they appear to play a role in innate immunity, the body’s first line of defense against viruses and bacteria. For example, some Schlafen proteins interfere with the replication of viruses in humans. On the other hand, some viruses such as monkeypox viruses, for example, may also use Schlafen proteins to attack the cell’s defense system. René Ketting suspects that Schlafen proteins may have a wider, conserved role in immunity in many species, including humans.
“Schlafen proteins may represent a previously unknown molecular link between immune responses in mammals and deeply conserved RNA-based mechanisms that control TEs,” said Ketting, who is also a Professor of Biology at Johannes Gutenberg University Mainz (JGU). If so, Schlafen proteins may represent a common defense mechanism against both external enemies like viruses and bacteria as well as internal ones such as TEs. “It’s conceivable that Schlafen proteins have been repurposed into enzymes that protect cells from infectious DNA sequences, such as TEs,” added Sebastian Falk. “This discovery may profoundly impact our understanding of innate immune biology.”

A team of researchers at the Medical University of Vienna has discovered that dormant tumor cells surviving chemotherapy can be targeted through the inhibition of a specific protein called P-glycoprotein (P-gp). This discovery opens up new possibilities for delaying relapse and is particularly relevant for aggressive triple-negative breast cancer (TNBC), for which there are currently few effective treatments. The findings, published in the journal Drug Resistance Updates, could represent a step forward in the treatment of this type of cancer.
So-called “triple-negative breast cancer” is a particularly dangerous form of breast cancer. It is characterised by an early relapse and a poor survival rate. Until now, there have only been limited treatment options, and chemotherapy protocols are often not sufficiently effective. Therapy resistance, where cancer cells do not respond to conventional treatments, has long been a major problem. A research team at MedUni Vienna’s Center for Cancer Research has now discovered why this happens and how it can be prevented.
Certain cancer cells evade chemotherapy by entering a dormant cell state. Such cancer cells can persist undetected for several months or even years before they start to proliferate again to give rise to tumor relapse. Although cytotoxic agents are less effective against nondividing cells, drug tolerant persister cells must come up with additional protective measures to cope with the toxic effects of chemotherapy. Researchers led by Gergely Szakács at MedUni Vienna’s Center for Cancer Research found that this partially happens through the activation of a protein called P-glycoprotein (P-gp), which helps to clean cells from secondary damage inflicted by chemotherapy.
“P-gp has been well-known as a protein that can export chemotherapeutic drugs from the cells, but its role in protecting dormant cancer cells has not been proven. The discovery that P-gp contributes to the removal of toxic lipids from rare surviving cancer cells represents a vulnerability that can be exploited to prevent relapse. The good thing is that there are already drugs that can block this protein, so we were able to test our hypothesis.” explains Gergely Szakács, the lead author of the study.
In a mouse model of triple-negative breast cancer, prolonged inhibition of P-gp prior to the onset of resistance with a drug called tariquidar significantly prolonged the survival of mice, indicating that the critical population of drug-tolerant cancer cells can be targeted by blocking P-glycoprotein. These results could mean that patients with triple-negative breast cancer have a better chance of being cured in the future. Researchers are now working to translate these findings into clinical practice to better treat patients.

Until recently, our understanding of Parkinson’s disease has been quite limited, which has been apparent in the limited treatment options and management of this debilitating condition.
Our recent understanding has primarily revolved around the genetic factors responsible for familial cases, while the causative factors in the vast majority of patients remained unknown.
However, in a new study, researchers from the University of Copenhagen have unveiled new insights into the workings of the brain in Parkinson’s patients. Leading the groundbreaking discovery is Professor Shohreh Issazadeh-Navikas.
“For the first time, we can show that mitochondria, the vital energy producers within brain cells, particularly neurons, undergo damage, leading to disruptions in mitochondrial DNA[LP1] . This initiates and spreads the disease like a wildfire through the brain,” says Shohreh Issazadeh-Navikas and adds:
“Our findings establish that the spread of the damaged genetic material, the mitochondrial DNA, causes the symptoms reminiscent of Parkinson’s disease and its progression to dementia.”
Parkinson’s disease is a chronic condition that affects the central nervous system, leading to symptoms such as difficulty walking, tremors, cognitive challenges, and, eventually, dementia.
The disease afflicts over 10 million people worldwide. While there is currently no cure, certain medical treatments can offer relief from its symptoms.