Publisher Health

It has been long been known that cannabis users develop psychosis more often than non-users, but what is still not fully clear is whether cannabis actually causes psychosis and, if so, who is most at risk. A new study published in Translational Psychiatry by researchers at the Centre for Addiction and Mental Health (CAMH) and King’s College London helps shed light on both questions. The research shows that while cannabis users had higher rates of psychotic experiences than non-users across the board, the difference was especially pronounced among those with high genetic predisposition to schizophrenia.
“These results are significant because they’re the first evidence we’ve seen that people genetically prone to psychosis might be disproportionately affected by cannabis,” said lead author Dr. Michael Wainberg, Scientist the Krembil Centre for Neuroinformatics at CAMH. “And because genetic risk scoring is still in its early days, the true influence of genetics on the cannabis-psychosis relationship may be even greater than what we found here.”
Using data from the UK Biobank, a large-scale biomedical database containing participants’ in-depth genetic and health information, the authors analyzed the relationship between genetics, cannabis use and psychotic experiences across more than 100,000 people. Each person reported their frequency of past cannabis use, and whether they had ever had various types of psychotic experiences, such as auditory or visual hallucinations. The researchers also scored each person’s genetic risk for schizophrenia, by looking at which of their DNA mutations were more common among schizophrenia patients than among the general population.
Overall, people who had used cannabis were 50 per cent more likely to report psychotic experiences than people who had not. However, this increase was not uniform across the study group: among the fifth of participants with the highest genetic risk scores for schizophrenia, it was 60 per cent, and among the fifth with the lowest scores, it was only 40 per cent. In other words, people genetically predisposed to schizophrenia were at disproportionately higher risk for psychotic experiences if they also had a history of cannabis use.
Notably, because much less is known about the genetics of schizophrenia in non-white populations, the study’s analysis was limited to self-reported white participants. “This study, while limited in scope, is an important step forward in understanding how cannabis use and genetics may interact to influence psychosis risk,” added senior author Dr. Shreejoy Tripathy, Independent Scientist at the Krembil Centre for Neuroinformatics, who supervised the study. “The more we know about the connection between cannabis and psychosis, the more we can inform the public about the potential risks of using this substance. This research offers a window into a future where genetics can help empower individuals to make more informed decisions about drug use.”
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A recent case study from North Carolina State University and the University of North Carolina at Chapel Hill demonstrates that, with training, neural control of a powered prosthetic ankle can restore a wide range of abilities, including standing on very challenging surfaces and squatting. The researchers are currently working with a larger group of study participants to see how broadly applicable the findings may be.
“This case study shows that it is possible to use these neural control technologies, in which devices respond to electrical signals from a patient’s muscles, to help patients using robotic prosthetic ankles move more naturally and intuitively,” says Helen Huang, corresponding author of the study. Huang is the Jackson Family Distinguished Professor in the Joint Department of Biomedical Engineering at NC State and UNC.
“This work demonstrates that these technologies can give patients the ability to do more than we previously thought possible,” says Aaron Fleming, first author of the study and a Ph.D. candidate in the joint biomedical engineering department.
Most of the existing research on robotic prosthetic ankles has focused solely on walking using autonomous control. Autonomous control, in this context, means that while the person wearing the prosthesis decides whether to walk or stand still, the fine movements involved in those movements happen automatically — rather than because of anything the wearer is doing.
Huang, Fleming and their collaborators wanted to know what would happen if an amputee, working with a physical therapist, trained with a neurally controlled powered prosthetic ankle on activities that are challenging with typical prostheses. Would it be possible for amputees to regain a fuller range of control in the many daily motions that people make with their ankles in addition to walking?
The powered prosthesis in this study reads electrical signals from two residual calf muscles. Those calf muscles are responsible for controlling ankle motion. The prosthetic technology uses a control paradigm developed by the researchers to convert electrical signals from those muscles into commands that control the movement of the prosthesis.

The smells that newborn mice are exposed to (or “imprint” on to use the academic term) affect many social behaviors later in life, but how this happens is still a mystery. Scientists from Japan have now discovered the molecules necessary for imprinting. Their new study sheds light on the decision-making process and neurodevelopmental disorders such as autism spectrum disorders. It also proposes more effective use of oxytocin therapy for such disorders at an early age.
Imprinting is a popularly known phenomenon, wherein certain animals and birds become fixated on sights and smells they see immediately after being born. In ducklings, this can be the first moving object, usually the mother duck. In migrating fish like salmon and trout, it is the smells they knew as neonates that guides them back to their home river as adults. How does this happen?
Exposure to environmental input during a critical period early in life is important for forming sensory maps and neural circuits in the brain. In mammals, early exposure to environmental inputs, as in the case of imprinting, is known to affect perception and social behavior later in life. Visual imprinting has been widely studied, but the neurological workings of smell-based or “olfactory” imprinting remain a mystery.
To find out more, scientists from Japan, including Drs. Nobuko Inoue, Hirofumi Nishizumi, and Hitoshi Sakano at University of Fukui and Drs. Kazutaka Mogi and Takefumi Kikusui at Azabu University, worked on understanding the mechanism of olfactory imprinting during the critical period in mice. Their study, published in eLife, offers fascinating results. “We discovered three molecules involved in this process,” reports Dr. Nishizumi, “Semaphorin 7A (Sema7A), a signaling molecule produced in olfactory sensory neurons, Plexin C1 (PlxnC1), a receptor for Sema7A expressed in the dendrites of mitral/tufted cells, and oxytocin, a brain peptide known as love hormone.”
During the critical period, when a newborn mouse pup is exposed to an odor, the signaling molecule Sema7A initiates the imprinting response to the odor by interacting with the receptor PlxnC1. As this receptor is only localized in the dendrites in the first week after birth, it sets the narrow time limitation of the critical period. The hormone oxytocin released in the nursed infants imposes the positive quality of the odor memory.
It is previously known that male mice normally show strong curiosity toward unfamiliar mouse scents of both genders. “Blocking” Sema7A signaling during the critical period results in the mice not responding in their usual manner; they display avoidance response to the stranger mice.
An interesting result of this study is the conflicting response to aversive odors. Let’s say, a pup is exposed to an innately aversive odor during the critical period; this imprinted odor will now induce a positive response against the innate natural response towards the odor. Here, the hard-wired innate circuit and the imprinted memory circuit are in competition, and the imprinting circuit takes over. To solve this dilemma and reach a conclusion, the brain must have detailed a mechanism of a crosstalk between the positive and negative responses, which opens a variety of research questions in the human context.
So, what do these results say about the human brain?
First, the results of the study open many research questions for the functioning of the human brain and behavior. Like the critical period in the mouse olfactory system, can we find such a period in humans, possibly in other sensory systems? The way the mouse brain chooses imprinted memory over innate response, do we humans also follow similar decision-making processes?
Secondly, this study also suggests that improper sensory inputs may cause neuro-developmental disorders, such as autism spectrum disorders (ASD) and attachment disorders (AD). Oxytocin is widely used for treating ASD symptoms in adults. However, Dr. Nishizumi says, “our study indicates that oxytocin treatment in early neonates is more effective than after the critical period in improving the impairment of social behavior. Thus, oxytocin treatment of infants will be helpful in preventing the ASD and AD, which may open a new therapeutic procedure for neurodevelopmental disorders.”
This study adds valuable new insights to our understanding of decision making and mind struggle in humans and reveals new research paths in the neuroscience of all types of imprinting.
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Materials provided by University of Fukui. Note: Content may be edited for style and length.

New research led by a professor at NUI Galway is set to change how doctors treat some patients with high blood pressure — a condition that affects more than one in four men and one in five women.
The study by researchers at NUI Galway, Johns Hopkins University and Harvard Medical School found no evidence that diastolic blood pressure — the bottom reading on a blood pressure test — can be harmful to patients when reduced to levels that were previously considered to be too low.
Lead researcher Bill McEvoy, Professor of Preventive Cardiology at NUI Galway and a Consultant Cardiologist at University Hospital Galway, said the findings have the potential to immediately influence the clinical care of patients.
Professor McEvoy said: “We now have detailed research based on genetics that provides doctors with much-needed clarity on how to treat patients who have a pattern of high systolic values — the top reading for blood pressure — but low values for the diastolic, or bottom, reading.
“This type of blood pressure pattern is often seen in older adults. Old studies using less reliable research methods suggested that the risk for a heart attack began to increase when diastolic blood pressure was below 70 or above 90. Therefore, it was presumed there was a sweet-spot for the diastolic reading.”
High blood pressure is a major cause of premature death worldwide, with more than 1 billion people having the condition. It is linked with brain, kidney and other diseases, but it is best known as a risk factor for heart attack. More recently, high blood pressure has emerged as one of the major underlying conditions that increase the risk of poor outcomes for people who become infected with Covid-19.
Professor McEvoy and the international research team analysed genetic and survival data from more than 47,000 patients worldwide. The study, published in the medical journal Circulation, showed: There appears to be no lower limit of normal for diastolic blood pressure and no evidence in this genetic analysis that diastolic blood pressure can be too low. There was no genetic evidence of increased risk of heart disease when a patient’s diastolic blood pressure reading is as low as 50. The authors also confirmed that values of the top, systolic, blood pressure reading above 120 increased the risk of heart disease and stroke.Blood pressure medications reduce both systolic and diastolic values.
Professor McEvoy added: “Because doctors often focus on keeping the bottom blood pressure reading in the 70-90 range, they may have been undertreating some adults with persistently high systolic blood pressure.
“The findings of this study free up doctors to treat the systolic value when it is elevated and to not worry about the diastolic blood pressure falling too low.
“My advice now to GPs is to treat their patients with high blood pressure to a systolic level of between 100-130mmHg, where possible and without side effects, and to not worry about the diastolic blood pressure value.” Dr Joe Gallagher, Irish College of General Practioners’ Lead, National Heart Programme, said: “This data helps remove uncertainty about how to treat people who have an elevated systolic blood pressure but low diastolic blood pressure. This is a common clinical problem which causes much debate. It will help impact clinical practice internationally and shows the importance of Irish researchers in clinical research.”
The research team used new technologies to take into account genetic information that is unbiased, which was not the case with prior observational studies. They assessed data from 47,407 patients in five groups with a median age of 60.
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Studies show wearing masks and social distancing can contain the spread of the COVID-19 virus, but their combined effectiveness is not precisely known.
In Chaos, by AIP Publishing, researchers at New York University and Politecnico di Torino in Italy developed a network model to study the effects of these two measures on the spread of airborne diseases like COVID-19. The model shows viral outbreaks can be prevented if at least 60% of a population complies with both measures.
“Neither social distancing nor mask wearing alone are likely sufficient to halt the spread of COVID-19, unless almost the entire population adheres to the single measure,” author Maurizio Porfiri said. “But if a significant fraction of the population adheres to both measures, viral spreading can be prevented without mass vaccination.”
A network model encompasses nodes, or data points, and edges, or links between nodes. Such models are used in applications ranging from marketing to tracking bird migration. In the researchers’ model, based on a susceptible, exposed, infected, or removed (recovered or has died) framework, each node represents a person’s health status. The edges represent potential contacts between pairs of individuals.
The model accounts for activity variability, meaning a few highly active nodes are responsible for much of the network’s contacts. This mirrors the validated assumption that most people have few interactions and only a few interact with many others. Scenarios involving social distancing without mask wearing and vice versa were also tested by setting up the measures as separate variables.
The model drew on cellphone mobility data and Facebook surveys obtained from the Institute for Health Metrics and Evaluation at the University of Washington. The data showed people who wear masks are also those who tend to reduce their mobility. Based on this premise, nodes were split into individuals who regularly wear masks and socially distance and those whose behavior remains largely unchanged by an epidemic or pandemic.
Using data collected by The New York Times to gauge the model’s effectiveness, the researchers analyzed the cumulative cases per capita in all 50 states and the District of Columbia between July 14, 2020, when the Centers for Disease Control and Prevention officially recommended mask wearing, through Dec. 10.
In addition to showing the effects of combining mask wearing and social distancing, the model shows the critical need for widespread adherence to public health measures.
“U.S. states suffering the most from the largest number of infections last fall were also those where people complied less with public health guidelines, thereby falling well above the epidemic threshold predicted by our model,” Porfiri said.
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Materials provided by American Institute of Physics. Note: Content may be edited for style and length.

Evolutionary anthropologists from the University of Vienna and colleagues now present evidence for a different explanation, published in PNAS. A larger bony pelvic canal is disadvantageous for the pelvic floor’s ability to support the fetus and the inner organs and predisposes one to incontinence.
The human pelvis is simultaneously subject to obstetric selection, favoring a more spacious birth canal, and an opposing selective force that favors a smaller pelvic canal. Previous work of scientists from the University of Vienna has already led to a relatively good understanding of this evolutionary “trade-off” and how it results in the high rates of obstructed labor in modern humans. However, it has remained unclear what the advantage of a narrow birth canal is, given its disadvantage for childbirth. It has long been thought that a smaller birth canal is advantageous for bipedal locomotor performance. A different, less prominent explanation is that it enhances pelvic floor functionality. The muscles of the human pelvic floor play a vital role in supporting our inner organs and a heavy fetus, and in maintaining continence. A larger pelvic canal would increase the downward deformation of the pelvic floor, increasing the risk of pelvic floor disorders, such as pelvic organ prolapse and incontinence. However, this “pelvic floor hypothesis” has been challenging to prove.
A team of evolutionary anthropologists and engineers from the University of Vienna, the Konrad Lorenz Institute for Evolution and Cognition Research, and the University of Texas at Austin (USA) used a new approach to test this hypothesis. The researchers, led by Katya Stansfield and Nicole Grunstra from the Department of Evolutionary Biology, simulated a Finite Element model of a human pelvic floor across a range of different surface areas and thicknesses and investigated the deformation in response to pressure. “Finite Element analysis allowed us to isolate the effect of pelvic floor geometry by controlling for other risk factors, such as age, number of births, and tissue weakness,” says Stansfield. This approach also enabled the team to model pelvic floor size across a broader range of variation than can be observed in the human population, “because natural selection may prevent the occurrence of such ‘extreme’ sizes precisely because of the disadvantages for pelvic floor functionality,” explains Grunstra.
As predicted by the pelvic floor hypothesis, larger pelvic floors deformed disproportionately more than smaller pelvic floors. “Our results support the notion that smaller pelvic floors — and thus smaller birth canals — are biomechanically advantageous for organ and fetal support despite their disadvantage for childbirth,” says Stansfield.
The researchers also found that thicker pelvic floors were more resistant to bending and stretching, which partly compensated for the increase in pelvic floor deformation as a result of increased surface area. So why did natural selection not result in a larger birth canal that eases childbirth, along with a disproportionately thicker pelvic floor that compensates for the extra deformation? “We found that thicker pelvic floors require quite a bit higher intra-abdominal pressures in order to undergo stretching, which is actually necessary during childbirth,” says Grunstra. The pressures generated by women in labor are among the highest recorded intra-abdominal pressures and they may be difficult to increase further. “Being unable to push the baby through a resistant pelvic floor would equally complicate childbirth, and so we think we have identified a second evolutionary trade-off, this time in the thickness of the pelvic floor,” concludes Grunstra. “Both the size of the birth canal and the thickness of the pelvic floor appear to be evolutionary ‘compromises’ enforced by multiple opposing selective pressures,” says co-author Philipp Mitteroecker.
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Altering a mosquito’s gut genes to make them spread antimalarial genes to the next generation of their species shows promise as an approach to curb malaria, suggests a preliminary study published today in eLife.
The study is the latest in a series of steps toward using CRISPR-Cas9 gene-editing technology to make changes in mosquito genes that could reduce their ability to spread malaria. If further studies support this approach, it could provide a new way to reduce illnesses and deaths caused by malaria.
Growing mosquito resistance to pesticides, as well as malaria parasite resistance to antimalarial drugs, has created an urgent need for new ways to fight the disease. Gene drives are being tested as a new approach. They work by creating genetically modified mosquitoes that, when released into the environment, would spread genes that either reduce mosquito populations or make the insects less likely to spread the malaria parasite. But scientists must prove that this approach is safe and effective before releasing genetically modified mosquitoes into the wild.
“Gene drives are promising tools for malaria control,” says first author Astrid Hoermann, Research Associate at Imperial College London, UK. “But we wanted a clear pathway for safely testing such tools in countries where the disease most commonly occurs.”
In the study, Hoermann and colleagues genetically modified the malaria-transmitting mosquito Anopheles gambiae. They used the CRISPR-Cas9 technology to insert a gene that encodes an antimalarial protein amidst genes that are turned on after the mosquito eats a blood meal. The team did this in a manner that allowed the whole section of DNA to also function as a gene drive that could be passed on to most of the mosquitoes’ offspring. They initially inserted the gene along with a fluorescent marker to help them track it in three different spots in the DNA, and then later removed the marker, leaving only a minor genetic modification behind.
Next, the team bred the mosquitoes to see if they were able to successfully reproduce and remain healthy. They also tested how well the malaria parasite developed in the mosquitoes’ guts. Their experiments provide preliminary evidence that this approach to genetic modifications could create successful gene drives.
“These genetic modifications are passive, and could be tested in the field and undergo a stringent regulatory process to ensure they are safe and effective in blocking the parasite without raising concerns of accidental spread in the environment,” explains senior author Nikolai Windbichler, Senior Lecturer at the Department of Life Sciences, Imperial College London. “However, once we combine them with other mosquitoes with an active gene drive, they turn into gene drives themselves without the need for any further changes. Our approach thus brings gene drives one step closer to being tested in the field as a malaria elimination strategy.”
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Materials provided by eLife. Note: Content may be edited for style and length.

SARS-CoV-2 is the virus responsible for the COVID-19 pandemic. We know that mutations in the genome of SARS-CoV-2 have occurred and spread, but what effect do those mutations have? Current methods for studying mutations in the SARS-CoV-2 genome are very complicated and time-consuming because coronaviruses have large genomes, but now a team from Osaka University and Hokkaido University have developed a quick, PCR-based reverse genetics system for analyzing SARS-CoV-2 mutations.
This system uses the polymerase chain reaction (PCR) and a circular polymerase extension reaction (CPER) to reconstruct the full-length cDNA of viral genome. This process does not involve the use of bacteria, which can introduce further unwanted mutations, and takes only two weeks using simple steps to generate infectious virus particles. Previous methods took a couple of months and were very complicated procedures.
“This method allows us to quickly examine the biological features of mutations in the SARS-CoV-2,” says lead author of the study Shiho Torii. “We can use the CPER technique to create recombinant viruses with each mutation and examine their biological features in comparison with the parental virus.” The large circular genome of SARS-CoV-2 can be constructed from smaller DNA fragments that can then be made into a viable viral genome with CPER, and used to infect suitable host cells. A large amount of infectious virus particles can be recovered nine days later.
“We believe that our CPER method will contribute to the understanding of the mechanisms underlying propagation and pathogenesis of SARS-CoV-2, as well as help determine the biological significance of emerging mutations,” explains corresponding author Yoshiharu Matsuura. “This could accelerate the development of novel therapeutics and preventative measures for COVID-19.” The team also suggest that the use of the CPER method will allow researchers to insert “reporter genes” into the SARS-CoV-2 genome to “tag” genes or proteins of interest. This will enable a greater understanding of how SARS-CoV-2 infects cells and causes COVID-19, assisting with the development of therapies. The CPER method could even allow a recombinant virus that is unable to cause disease to be generated, which could be used as a safe and effective vaccine for SARS-CoV-2.
Mutations are arising in the SARS-CoV-2 population all the time, as well as questions as to what those mutations do and whether they could affect the efficacy of vaccines. “Our simple and rapid method allows scientists around the globe to characterize the mutants, which is a vital step forward in our fight against the SARS-CoV-2,” says Takasuke Fukuhara of the research group.
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Asthma afflicts more than 300 million people worldwide. The most severe manifestation, known as non-Th2, or non-atopic childhood asthma, represents the majority of the cases, greater than 85%, particularly in low-income countries, according to Hyunok Choi, an associate professor at the Lehigh University College of Health. Yet, whether non-Th2 is a distinct disease (or endotype) or simply a unique set of symptoms (or phenotype) remains unknown.
“Non-Th2 asthma is associated with very poor prognosis in children and great, life-long suffering due to the absence of effective therapies,” says Choi. “There is an urgent need to better understand its mechanistic origin to enable early diagnosis and to stop the progression of the disease before it becomes severe.”
Studies show that nearly 50% of the children whose asthma is poorly controlled are expected to emerge as severe adult cases. Yet, a one-size-fits-all treatment approach, currently the norm for asthma, is ineffective and, says Choi, and partially responsible for asthma’s growing economic burden.
“The primary reason for lack of therapeutic and preventive measures is that no etiologic, or causal, driver has ever been identified for the non-Th2 asthma,” says Choi.
Now, for the first time, an epidemiological study, led by Choi, has shown that not only is non-Th2 a distinct disease, its likely inducer is early childhood exposure to airborne Benzo[a]pyrene, a byproduct of fossil fuel combustion. Choi and her colleagues are the first to demonstrate air pollution as a driver of the most challenging type of asthma, the severe subtype which is non-responsive to current therapies.
The team describes their results in an article recently published online in Environmental Health Journal called “Airborne Benzo[a]Pyrene May Contribute to Divergent Pheno-Endotypes in Children.”
What is termed asthma is an umbrella word for multiple diseases with common symptoms. Asthma has been broadly classified as two major sets of symptoms: T helper cell high (Th2-high) and T helper cell low (non-Th2). Th2-high is associated with early-childhood allergies to common pollutants such as pet dander, tree pollens, or mold. In contrast, non-TH2 is not related to an allergic response. The non-Th2 type, marked explicitly by being non-allergy-related, is far less understood than the TH-2 type and could transform into severe or difficult to treat type.
“The identification of non-Th2 asthma as a distinct disease, with early exposure to Benzo[a]pyrene as a driver, has the potential to impact tens of millions of sufferers, since this would make it possible to intervene before the onset of irreversible respiratory injuries,” says Choi.
The team tested two comparable groups of children from an industrial city, Ostrava, and the surrounding semi-rural area of Southern Bohemia, in the Czech Republic: 194 children with asthma and a control group consisting of 191 children. According to the study, Ostrava is an industrial city with a high level of coal mining activities, coal processing, and metallurgical refinement. The district-level ambient mean for Benzo[a]pyrene at the time of their investigation November 2008) was 11-times higher than the recommended outdoor and indoor air quality standard.
Not only was elevated exposure to Benzo[a]pyrene associated with correspondingly elevated odds of non-Th2 asthma, it was also associated with depressed systemic oxidant levels.
“Contrary to the current body of evidence supporting adult onset of non-atopic asthma, our data suggest for the first time that the lung function deficit and suppressed oxidative stress levels during early childhood are critical sentinel events preceding non-atopic asthma,” says Choi.
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Materials provided by Lehigh University. Original written by Lori Friedman. Note: Content may be edited for style and length.