A new report from the government has found there is “no clinical benefit” to having a blood test for Pfas after the so-called “forever chemical” was found in local water supplies in the Blue Mountains.
The NSW Health Expert Advisory Panel on per- and polyfluoroalkyl substances (Pfas), convened by the state’s chief health officer, Dr Kerry Chant, to provide advice on the evidence and guidance related to the potential health effects, published its findings in a final report on Tuesday. All recommendations have been accepted by NSW Health.
The panel included science and health experts in cancer, hormone and heart health, epidemiology, pathology, primary care, public health and risk communication.
They found, based on the substantial research related to Pfas already undertaken, “the health effects of Pfas appear to be small”.
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Pfas are a class of manufactured chemicals used to make products that resist heat, stains, grease and water – sometimes called “forever chemicals” as they are difficult to destroy and can remain in soil, groundwater and travel long distances.
The report acknowledged that studies have reported an association with some health effects, but noted the findings are inconsistent across different studies with “limited evidence of a dose-response relationship”.
The report also found that “while clinical testing for Pfas is commercially available, the current scientific evidence indicates that there is there is no clinical benefit for an individual to have a blood test for Pfas”.
The authors stated Pfas blood tests were unlikely to guide medical care “because Pfas will be detected in most people, there are many different Pfas types and blood levels do not predict any current or future health outcomes”.
They also warned that Pfas blood test results can cause unnecessary concern and subsequent interventions may cause harms.
The report recommended that “should a health care provider order a blood test for Pfas for a patient, the health care provider should provide clear contextual information about the test and its limitations to the patient, to manage expectations and avoid misinterpretation”.
The authors also suggest doctors can support patients concerned with their serum PFAS levels by engaging in usual preventative health interventions, “as many of the health conditions potentially associated with PFAS are common in the community and are associated with well-established risk factors”.
The panel acknowledged their recommendation differs from the National Academies of Science Engineering and Medicine (NASEM), an independent institution in the United States, whose guidance documents recommended individual blood testing and the use of blood levels to inform clinical care.
They also noted the Agency for Toxic Substances and Disease Registry, overseen by the US Centers for Disease Control and Prevention, gives advice to clinicians on managing and evaluating Pfas exposure and has not adopted NASEM’s recommendations on individual blood testing and health-based screening based on Pfas blood levels.
Jon Dee, the convener of the Stop Pfas community group in the Blue Mountains, said 25 people in the area had paid $500 out of pocket to have the blood test for Pfas.
Dee said they wanted to see how their blood test compared with the areas of Williamtown, Oakey and Katherine, which were contaminated with Pfas due to firefighting activities on nearby defence force bases.
“If you look at the average blood test level of people in the Blue Mountains, we are two to three times higher than the average Pfas levels in those defence communities that have been compensated by the federal government,” Dee said.
Dee said what concerned the community was how many of them with high Pfas levels in their blood have also had health issues that have been known to be associated with Pfas, including cancer.
“It’s been totally ignored by NSW Health … We’ve demanded free blood tests for everyone else.”
Dee said the group was taking a class action against the New South Wales government and Sydney Water.
“The findings of this report clearly are more to do with reducing the legal liability of Sydney Water than actually looking after the health of people in the Blue Mountains,” Dee said.
The panel acknowledged genuine concern in communities about Pfas exposure.
“There is considerable concern, particularly in the Blue Mountains community, about exposure to Pfas through drinking water, and NSW Health takes these concerns very seriously,” Chant said.
“NSW Health will continue to support local clinicians with information for GPs who may be managing patients with concerns about Pfas exposure including evidence about potential adverse health effects, counselling patients, the utility of blood tests for Pfas and the role of further investigations.”
Transcranial magnetic stimulation (TMS) may augment standard language therapy to help slow the progression of primary progressive aphasia (PPA), a neurodegenerative disorder that erodes communication.
In a randomized sham-controlled clinical trial, 6 months of active intermittent theta-burst TMS
plus language therapy improved or mitigated decline in regional brain metabolism, trained language abilities, functional impairment, and neuropsychiatric symptoms in adults with PPA.
The study was published online on August 11 in JAMA Network Open.
PPA is a heterogeneous clinical syndrome marked by progressive speech and/or language impairment. Most cases stem from frontotemporal degeneration or Alzheimer’s disease. There are currently no effective drug treatments, although speech-language therapy has proven to be helpful.
TMS can induce changes in cortical excitability, potentially promoting the reorganization of language networks, and has shown promise as adjunctive treatment for post-stroke aphasia.
Previous studies examining the short-term effects of TMS on PPA reported “encouraging” results, but the longer-term effects, beyond more than a few weeks of intervention, have not been examined, until now.
For the study, the researchers led by Jordi Matias-Guiu, MD, PhD, with the Department of Neurology, Hospital Clínico San Carlos, Madrid, Spain, recruited 63 adults with early-stage PPA (42 women; mean age, 72 years).
Participants were randomized (2:1) to either active intermittent theta-burst TMS or sham TMS for 6 months, immediately followed by evidence-based language therapy for PPA.
The trial consisted of a 24-week treatment that included a 2-week intensive course, in which active TMS or sham TMS combined with language therapy was applied daily, followed by a maintenance phase in which the same stimulation was applied weekly for 22 weeks. Participants were assessed at baseline, 3 months after the start of the treatment, and at the end of the treatment (6 months following baseline).
The main outcome was the standardized uptake value ratio (SUVR) on FDG PET imaging in the left hemisphere, assessed at baseline and at 6 months (immediately following the intervention).
The primary outcome was positive with higher adjusted mean SUVR in the active group than in the sham TMS group (0.78 vs 0.77; P = .046).
Active TMS was also associated with significant improvement on all secondary language outcomes at 6 months, including the mini linguistic state examination, with an adjusted mean difference at 6 months of 7.71 (P = .002). Patients in the sham group worsened on this measure compared with those in the active group.
Active TMS also led to improvement in confrontation naming of trained words, which improved by a mean 23.8 points in active recipients compared with sham TMS recipients.
Functional independence also benefited, with daily-living scores falling (indicating better performance) by 5.4 points in the active group compared with the sham TMS group. Neuropsychiatric symptoms eased as well, with a 4-point advantage on the neuropsychiatric inventory scale.
There were no significant differences in the number of adverse events. Adherence to treatment protocol was high (92%).
“Overall, these findings suggest that the combination of TMS and language therapy is a feasible and effective treatment option for PPA,” the researchers concluded.
They said future studies should investigate the potential for TMS paired with an evidence-based speech-language intervention to sustain or extend these benefits beyond 6 months.
This study had no commercial funding. The authors declared no relevant conflicts of interest.
New research, published in The Journal of Immunology, discovered that a parasitic worm suppresses neurons in the skin to evade detection. The researchers suggest that the worm likely evolved this mechanism to enhance its own survival, and that the discovery of the molecules responsible for the suppression could aid in the development of new painkillers.
Schistosomiasis is a parasitic infection caused by helminths, a type of worm. Infection occurs during contact with infested water through activities like swimming, washing clothes, and fishing, when larvae penetrate the skin. Surprisingly, the worm often evades detection by the immune system, unlike other bacteria or parasites that typically cause pain, itching, or rashes.
In this new study, researchers from Tulane School of Medicine aimed to find out why the parasitic worm Schistosoma mansoni doesn’t cause pain or itching when it penetrates the skin. Their findings show that S. mansoni causes a reduction in the activity of TRPV1+, a protein that sends signals the brain interprets as heat, pain, or itching. As part of pain-sensing in sensory neurons, TRPV1+ regulates immune responses in many scenarios such as infection, allergy, cancer, autoimmunity, and even hair growth.
The researchers found that S. mansoni produces molecules that suppress TRPV1+ to block signals from being sent to the brain, allowing S. mansoni to infect the skin largely undetected. It is likely S. mansoni evolved the molecules that block TRPV1+ to enhance its survival.
“If we identify and isolate the molecules used by helminths to block TRPV1+ activation, it may present a novel alternative to current opioid-based treatments for reducing pain,” said Dr. De’Broski R. Herbert, Professor of Immunology at Tulane School of Medicine, who led the study. “The molecules that block TRPV1+ could also be developed into therapeutics that reduce disease severity for individuals suffering from painful inflammatory conditions.”
The study also found that TRPV1+ is necessary for initiating host protection against S. mansoni. TRPV1+ activation leads to the rapid mobilization of immune cells, including gd T cells, monocytes, and neutrophils, that induce inflammation. This inflammation plays a crucial role in host resistance to the larval entry into the skin. These findings highlight the importance of neurons that sense pain and itching in successful immune responses
“Identifying the molecules in S. mansoni that block TRPV1+ could inform preventive treatments for schistosomiasis. We envision a topical agent which activates TRPV1+ to prevent infection from contaminated water for individuals at risk of acquiring S. mansoni,” said Dr. Herbert.
In this study, mice were infected with S. mansoi and evaluated for their sensitivity to pain as well as the role of TRPV1+ in preventing infection. Researchers next plan to identify the nature of the secreted or surface-associated helminth molecules that are responsible for blocking TRPV1+ activity and specific gd T cell subsets that are responsible for immune responses. The researchers also seek to further understand the neurons that helminths have evolved to suppress.
Experts at the University of Edinburgh carried out a post-mortem brain examination on 25 cats which exhibited symptoms of dementia in life, including confusion, sleep disruption and an increase in vocalisation, in a bid explore new treatments for humans.
Previously, researchers have studied genetically modified rodents, although the species does not naturally suffer from dementia.
In feline dementia brains, a build-up was found of amyloid-beta, a toxic protein and one of the defining features of Alzheimer’s disease, leading to hopes of a “wonderful” breakthrough due to increased accuracy.
The breakthrough was hailed as a “perfect natural model for Alzheimer’s” by scientists who worked on it.
Microscopy images revealed a build-up of amyloid-beta within synapses of older cats and feline dementia, and scientists hope the findings offer a clearer idea of how amyloid-beta may lead to feline cognitive dysfunction and memory loss, offering a valuable model for studying dementia in people.
Synapses allow the flow of messages between brain cells, and losing these causes reduced memory and thinking abilities in humans with Alzheimer’s.
Researchers found evidence that brain support cells, astrocytes and microglia, engulfed the affected synapses, known as synaptic pruning, an important process during brain development but which contributes to dementia.
Experts believe the findings could contribute to the development of new treatments for Alzheimer’s disease, as well as help to understand and manage feline dementia.
Previously, scientists studying Alzheimer’s relied on genetically modified rodent models. However, studying feline dementia has the potential to help develop human treatments, due to increased accuracy, it is hoped.
The study, funded by Wellcome and the UK Dementia Research Institute, is published in the European Journal of Neuroscience, and included scientists from the Universities of Edinburgh and California, UK Dementia Research Institute and Scottish Brain Sciences.
Dr Robert McGeachan, study lead from the University of Edinburgh’s Royal (Dick) School of Veterinary Studies, said: “Dementia is a devastating disease – whether it affects humans, cats, or dogs. Our findings highlight the striking similarities between feline dementia and Alzheimer’s disease in people.
“This opens the door to exploring whether promising new treatments for human Alzheimer’s disease could also help our ageing pets.
“Because cats naturally develop these brain changes, they may also offer a more accurate model of the disease than traditional laboratory animals, ultimately benefiting both species and their caregivers.”
Professor Danielle Gunn-Moore, personal chair of Feline Medicine at the Royal (Dick) School of Veterinary Studies, said: “Feline dementia is so distressing for the cat and for its person.
“It is by undertaking studies like this that we will understand how best to treat them. This will be wonderful for the cats, their owners, people with Alzheimer’s and their loved ones.
“Feline dementia is the perfect natural model for Alzheimer’s – everyone benefits.”
We conducted a retrospective cohort study that included 5,128 incident Chinese CAPD patients from seven PD centers in China between January 1, 2005, and May 31, 2023. Patients aged < 18 years or those with a follow-up time of < 3 months were excluded. Patients with malignant tumors or severe liver disease were excluded. Patients with missing data or abnormal values were excluded from this study.
We constructed the CUS scores to evaluate the prognosis of patients with CAPD. Each condition was assigned a score of 1, 2, 3, or 4 depending on the Charlson Comorbidity Index (CCI)14. Based on our previous studies7,8,9,15,16,17,18,19, the CUS scores comprised nine conditions with relative mortality risks ≥ 1.2 or greater, and these conditions were also weighted based on their relative risks. Clinical conditions (common comorbidities and complications in patients with CAPD) and associated scores were as follows (1 point each): cerebrovascular disease, cardiovascular disease (myocardial infarction or congestive heart failure), peripheral vascular disease, diabetes mellitus, hypertension, hyperlipidemia, malnutrition (serum albumin < 3.8 g/dL), and anemia (hemoglobin < 11.0 g/dL). Patients aged 50 years or older received additional points: 18–49 years, + 0; 50–59 years old, + 1 point; 60–69 years old, + 2 points; 70–79 years old, + 3 points; and 80 years or older, + 4 points (Figure S1). The scores were summed to obtain the total score (CUS score), which was used to assess mortality in patients with CAPD.
Two well-trained nurses collected demographic data, comorbidities, and laboratory data one week (5.4 ± 1.1 days) before the start of PD in each facility, including age at study entry, sex, body mass index (BMI), current smoker, current alcohol use, comorbidities (DM, hypertension, a history of cerebrovascular disease, cardiovascular disease, or peripheral vascular disease, and hyperlipidemia), medication use (calcium channel blockers [CCB], β-blockers, angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers [ACEI/ARBs]), and laboratory measurements (serum albumin and hemoglobin). Weight was measured in the absence of peritoneal dialysis.
The primary outcome was all-cause mortality. Cerebrovascular and cardiovascular (CVD) deaths due to cerebrovascular disease, myocardial infarction, congestive heart failure, and peripheral vascular disease were recorded. The details of the CAPD follow-up have been previously described20. The follow-up period was from the start of PD to the date of death, transfer to hemodialysis, renal transplantation, transfer to another dialysis center, loss to follow-up, or May 31, 2023. Patients who were lost to follow-up were censored on the date of the last examination.
This study was conducted in accordance with the Declaration of Helsinki and received approval from the ethical and scientific review boards of Zhejiang Provincial People’s Hospital, approval number [QT2023233]. The ethical and scientific review boards of Zhejiang Provincial People’s Hospital have granted an exemption from requiring written informed consent.
Continuous variables are presented as means with standard deviations (SDs) for normally distributed data or medians with interquartile ranges (IQR) for skewed data. The normality of the parameters was examined using the Shapiro-Wilk test. Categorical variables are expressed as the number of patients. We first used restricted cubic spline plots to explore the nonlinearity assumptions between the CUS scores and the risk of all-cause mortality, fitting a restricted cubic spline function with four knots (at the 25th, 50th, 75th, and 95th percentiles)21. All patients were categorized based on the threshold value of the CUS scores (hazard ratio [HR] = 1.0) using restricted cubic spline plots for the primary analysis.
Survival was calculated using the Kaplan-Meier method, and differences in survival distributions were assessed using a log-rank test. We primarily used cause-specific hazard models to explore the association between the CUS scores and mortality risk. Patients who experienced events such as transfer to hemodialysis, renal transplantation, transfer to other centers, or loss to follow-up were censored, which impeded the occurrence of death. Thus, Transfer to hemodialysis, renal transplantation, transfer to other centers, and loss to follow-up before death were considered competing risks. We constructed subdistribution hazard models to confirm the associations observed in the primary analysis. The main difference between the two hazard models is that subjects experiencing a competing risk event remain in the risk set in the sub-distribution hazard model but are removed from the cause-specific hazard model22,23. These models were constructed after adjusting for sex, BMI, current smoking status, current alcohol use, medication use, and centers. The results from the multivariable hazard models were presented as HRs and 95% confidence intervals (95% CIs). Stratified analyses were performed to assess the potential effects of sex modification.
To minimize the potential for reverse causation, we conducted analyses that excluded deaths in the first two years of follow-up. In addition, for patients with a short-term follow-up period, interesting outcomes may only be partially observed, with underreporting of mortality incidence. We further analyzed the association in patients with at least 24 months of follow-up to fully observe the outcomes. All analyses were performed using Stata version 15.1. (StataCorp, College Station, TX, USA).
Cats develop dementia similarly to humans, a study has shown.
Scientists at the University of Edinburgh examined the brains of 25 cats which exhibited symptoms of dementia – like confusion, sleep disruption and an increase in vocalisation – after their death, in a bid to find both treatments for both felines and humans.
A buildup of amyloid-beta, a toxic protein and one of the defining features of Alzheimer’s disease, was found in the examined brains, leading researchers to call the breakthrough a “perfect natural model for Alzheimer’s”.
Microscopy images revealed the amyloid-beta buildup within synapses of older cats. Synapses allow the flow of messages between brain cells, and losing these causes reduced memory and cognitive abilities in humans with Alzheimer’s disease.
Scientists are hoping the findings of the study provide a clearer idea of how amyloid-beta could lead to memory loss and feline cognitive dysfunction, as well as offer a model for studying dementia in people.
They previously relied on models studying genetically modified rodents, even though the species doesn’t naturally suffer from dementia.
The findings could contribute to developing new treatments for Alzheimer’s disease and help to manage feline dementia, experts said.
Read more from Sky News:
Blood test for dementia is highly accurate
Dementia: Sleep problems could ‘double risk’
Dr Robert McGeachan, study lead from the University of Edinburgh’s Royal (Dick) School of Veterinary Studies, said: “This opens the door to exploring whether promising new treatments for human Alzheimer’s disease could also help our ageing pets.
“Because cats naturally develop these brain changes, they may also offer a more accurate model of the disease than traditional laboratory animals, ultimately benefiting both species and their caregivers.”
The study, which included scientists from the universities of Edinburgh and California, the UK Dementia Research Institute and Scottish Brain Sciences, was funded by Wellcome and the UK Dementia Research Institute.
Dementia is becoming a growing concern in the US, and it’s not just something that affects “old age.” With an aging population and longer life spans, the number of people living with dementia is climbing fast. Alzheimer’s disease is the most common type, but there are other forms too, all impacting memory, thinking, and daily life. Experts say lifestyle factors like poor diet, inactivity, and even constant stress can raise your risk. The scary part? There’s still no cure. That’s why brain health tips, from staying active to learning new skills, are more important now than ever.A few months before, a neurologist trained at Mayo Clinic and University of Minnesota (as per his Instagram profile), shared an interesting information for all on social media. In a short video, the expert listed three habits that can help one reduce the risk of dementia and improve brain health and one among them was turning off GPS.“GPS makes our lives too convenient. Relying too much on GPS can weaken your brain’s spatial memory,” he said. Multiple studies have found that people who habitually use GPS navigation tend to have poorer spatial memory. When navigating without GPS, these individuals struggle more to remember routes, recognize landmarks, and form mental “maps” of their environment. The hippocampus, a brain region critical for memory and navigation, is less active when we follow turn-by-turn GPS instructions compared to navigating independently. Over time, relying on GPS means this area of the brain gets less “exercise”.Some research, including studies on London taxi drivers (who learn city layouts by memory), suggests that exercising navigation skills can actually increase the size and function of the hippocampus. In contrast, people who heavily use GPS may experience a lack of growth or even shrinkage in these regions as they age.“It’s interesting what you said about GPS. I have observed recently that UBER drivers in my city do not know their way around. Some can’t even follow the instructions on their GPS. I remember taxi drivers, in my younger days, really knew their way around the city,” writes one user. “When I was kid I could visualize exactly where I was and where I was going. I always new what direction I was facing (north,south etc) but these days I only know the sky is up cause it’s blue,” writes another.
GPS reduces spatial memory and mental mapping abilities with heavy, long-term use. This is due to less engagement and exercise of the hippocampus.There is no evidence that GPS alone causes dementia. However, it may contribute to reduced cognitive reserve in the hippocampus, which could make the symptoms of dementia more apparent or severe if the disease develops.Maintaining navigation skills is important for brain health. Try occasionally navigating without GPS, paying attention to landmarks, or practicing new routes to challenge your brain.
Excessive intake of energy drinks, and sleeping with lights on are the two lesser known triggers of dementia he said. Energy drinks are loaded with caffeine and sugar, which might give you a quick buzz, but constant overconsumption can mess with your heart, blood vessels, and even brain chemistry. Over the years, that stress on your body could contribute to memory and cognitive decline. Then there’s the light-at-night problem — your brain needs darkness to produce melatonin, the hormone that helps you sleep and repair. If you’re snoozing with the TV glowing or the lights on, your sleep quality tanks, and your brain misses out on the deep rest it needs to stay sharp. Both habits might seem harmless now, but your future self could thank you for cutting back on the energy drinks and hitting the lights at bedtime.
Cesarean section between June 2024 and October 2024 in the Department of Perinatology, Health Sciences University, Etlik City Hospital, Ankara, Türkiye were prospectively included in the study.
The surgical teams consisted of an experienced specialist in obstetrics and gynecology (more than four years after graduation), a senior resident and a surgical nurse with at least four years of experience in assisting with cesarean sections. All surgical operations performed by the specialist. Operating room staff and surgeons were informed and trained on the collection procedures. Plastic baskets were placed in each operating room and the team members placed the used gloves in these baskets after the each operation. All used surgical gloves from the scrubbed surgical team were collected. Collected gloves were inspected visually for macro perforation just after placing in the basket. Patients were excluded from the study if any glove used by the scrubbed surgical team showed a macro-perforation either noticed intraoperatively or identified during immediate visual inspection after the surgery. The remaining gloves, which appeared visually intact, were examined using a water-fill test, right after the each surgery, in the concurrent operation room, during the operation room cleaning, according to the American Society for Testing and Materials [6]. Under standard operation room temperature, a 38 cm long plastic tube was used for the test. The gloves were attached to the distal end of the tube and 1000 ml of tap water was poured through the tube into the gloves. The perforation was recognized as water leakage or water jet from the glove surface or as droplet formation at the toe tip. The observation time was two minutes. Gloves with a positive water filling test were defined as the study group and negative gloves as the control group (Figs. 1 and 2).
Water Fill Test Method for Detecting Glove Perforations
Glove Perforation Demonstrated by Water Fill Test in a Clinical Setting
Elective cesarean deliveries were defined as planned procedures performed before the onset of labor in clinically stable patients, whereas emergency cesarean deliveries included all other cases, including those with labor or clinical indications such as prolonged rupture of membranes, maternal fever, or fetal distress. Patients who were categorized as class 1 or 2 according to the American Society of Anesthesiologists (ASA) physical status classification were included in the study. The surgical site was cleaned by senior resident, with alcohol and combined with 4% chlorhexidine and waited some minutes for air-dried. The urinary catheter was placed preoperatively in the operating room. After skin antisepsis and urinary catheterization, the surgical area was draped using sterile, disposable surgical drape sets. Draping was performed by the senior resident in accordance with standard sterile technique protocols. Pfannenstiel skin incision, incision in the lower segment of the uterus, detachment of the placenta by fundal massage, exteriorization of the uterus for repair, single-layer uterine closure, suture closure of the subcutaneous layer if the subcutaneous tissue was thicker than 2 cm, subcutaneous closure with a Prolene suture, and the use of a blunt needle tip were established as standard surgical procedures in the study. Antibiotic prophylaxis (2 g cephazolin) was administered intravenously before skin incision. Single layer latex gloves were used for all procedures and double-gloved surgeries did not included to study. Early removal of the urinary catheter was performed routinely. Patients were physically examined daily during hospitalization and again in person on postoperative days 10 and 30 by the attending obstetrician.
The diagnosis of surgical site infection, diagnosed by specialist in obstetrics and gynecology, was based on the definition of the National Healthcare Safety Network of the United States Centers for Disease Control and Prevention [7]. Superficial surgical site infections were analyzed for the study. Deep incisions or organ/space infections did not occur in the study groups.
Subjects were excluded if they: (1) did not provide informed consent, (2) had a history of inflammatory disease or clinical chorioamnionitis, (3) had multiple pregnancies, (4) were classified as ASA class III or higher, (5) underwent midline skin incision, (6) had known allergies to chlorhexidine, antibiotics, or latex, or (7) were lost to follow-up.
All patients gave their informed consent to participate in this project. The study was approved by the institution’s ethics committee and was conducted in accordance with the Declaration of Helsinki.
A priori sample size calculation was performed using G*Power version 3.1.9.7. In the absence of previous studies to estimate the effect size, a medium effect size (w = 0.3) was assumed. With α = 0.05 and power = 0.80, the required sample size for a chi-square test with 1 degree of freedom was calculated as 88 participants (44 per group). However, due to the naturally occurring frequency of glove perforation during the study period, only 32 patients could be included in the perforation group. The control group included 505 patients, reflecting the actual surgical population.
To evaluate the adequacy of this sample, a post-hoc power analysis was also conducted based on the observed effect size (w = 1.545). With α = 0.05 and a total sample size of 537 (n₁ = 505, n₂ = 32), the calculated power (1 − β) exceeded 99.9%, indicating sufficient statistical sensitivity to detect differences between groups.
All statistical analyses were performed using Jamovi version 2.6.26 (The Jamovi Project, Sydney, Australia). The variables were examined using visual (histogram, probability plots) and analytical methods (Kolmogrov-Simirnov/Shapiro-Wilk test) to determine whether they were normally distributed or not. The Levene test was used to assess the homogeneity of variance. Descriptive analyzes using medians and interquartile ranges (IQR) (Q1-Q3) were performed for the non-normally distributed numerical data. Mann-Whitney U-tests were performed to compare these parameters between the groups. For the categorical variables, descriptive analyzes were performed using frequencies and percentages. The relationships between the categorical variables were analyzed using the chi-square test or Fisher’s exact test. A p-value of less than 0.05 was considered a statistically significant.
Additionally, a multivariable logistic regression analysis was performed to evaluate the independent association between glove micro-perforation and surgical site infection (SSI). Known confounding variables including emergency cesarean section, diabetes mellitus, obesity, surgical duration, and intraoperative blood loss were included in the model to adjust for potential effects.
Oxytocin promotes social behaviors and helps maintain relationships. But clinical trials in patients with autism show variability in how consistently oxytocin improves these behaviors. Steve Chang, from Yale University, led a study to explore how oxytocin influences brain activity to shape social behavior in rhesus monkeys and why its effects are so variable. This work is featured in JNeurosci‘s Central Questions for Social Neuroscience Research Special Collection.
The researchers focused on the basolateral amygdala (BLA) and the anterior cingulate cortex (ACC) because these brain areas process reward and integrate information during social decision-making. Delivering oxytocin directly into the BLA had state-dependent effects; when monkeys were socially motivated prior to oxytocin exposure, the hormone maintained socially beneficial decisions and social task behavior over a longer time period, but oxytocin didn’t influence the same monkeys when they were less motivated. Brain activity supported these results showing that oxytocin increased BLA and ACC activity only when monkeys were socially motivated. Activity in the BLA and ACC was also more coordinated during prolonged social states, suggesting that oxytocin may stabilize communication in this pathway to sustain social behavior.
Says Chang, “We previously found that communication between these brain areas is important for social reward and behavior. So, the link between enhancement of this signal and prolonged social behavior was interesting to see.” Elaborating on clinical implications, Chang adds, “We have to be more careful and not just use a standardized approach. Even within individuals, there are variations in the effectiveness of oxytocin treatment! It may be important to individually tailor treatments.”
Source:
Journal reference:
Meisner, O. C., et al. Oxytocin in the amygdala sustains prosocial behavior via state-dependent amygdala-prefrontal modulation. JNeurosci. doi.org/10.1523/JNEUROSCI.2416-24.2025.