Apolipoprotein A-IV Concentrations and Clinical Outcomes In A Large CKD Cohort
ApoA-IV appears to be an independent risk marker for reduced all-cause mortality, cardiovascular events and heart failure in a large cohort of patients with CKD.
KEY FINDINGS: The data support a link between elevated apoA-IV concentrations and reduced inflammation in moderate CKD. ApoA-IV appears to be an independent risk marker for reduced all-cause mortality, cardiovascular events and heart failure in a large cohort of patients with CKD.
BACKGROUND: Chronic kidney disease (CKD) represents a chronic proinflammatory state and is associated with very high cardiovascular risk. Apolipoprotein A-IV (apoA-IV) has antiatherogenic, antioxidative, anti-inflammatory and antithrombotic properties and levels increase significantly during the course of CKD. Study aimed to investigate the association between apoA-IV and all-cause mortality and cardiovascular outcomes in the German Chronic Kidney Disease study.
DETAILS: This was a prospective cohort study including 5141 Caucasian patients with available apoA-IV measurements and CKD. The majority of the patients had an estimated glomerular filtration rate (eGFR) of 30-60 ml/min/1.73m2 or an eGFR >60 ml/min/1.73m2 in the presence of overt proteinuria. Median follow-up was 6.5 years. The association of apoA-IV with comorbidities at baseline and endpoints during follow-up was modelled adjusting for major confounders. Mean apoA-IV concentrations of the entire cohort were 28.9 ± 9.8 mg/dl. Patients in the highest apoA-IV quartile had the lowest high-sensitivity C-reactive protein values despite the highest prevalence of diabetes, albuminuria and the lowest eGFR. Each 10 mg/dl higher apoA-IV translated into lower odds of prevalent cardiovascular disease (1289 cases, odds ratio = 0.80, 95% confidence interval [CI] 0.72-0.86, p = 0.0000003). During follow-up, each 10 mg/dl higher apoA-IV was significantly associated with a lower risk for all-cause mortality (600 cases, hazard ratio [HR] = 0.81, 95% CI 0.73-0.89, p = 0.00004), incident major adverse cardiovascular events (506 cases, HR = 0.88, 95% CI 0.79-0.99, p = 0.03) and death or hospitalizations due to heart failure (346 cases, HR = 0.84, 95% CI 0.73-0.96, p = 0.01).
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Source: Schwaiger, J. P., Kollerits, B., Steinbrenner, I., et al. (2022). Apolipoprotein A-IV Concentrations And Clinical Outcomes In A Large Chronic Kidney Disease Cohort: Results from the GCKD Study. Journal of Internal Medicine. 2022; 291(5): 622-636. Published: May, 2022. DOI: 10.1111/joim.13437.
Long-Term Outcomes of Azacitidine, Venetoclax, and Gilteritinib in Newly Diagnosed FLT3-Mutated Acute Myeloid Leukemia
In a phase II study of 30 patients with newly diagnosed FLT3-mutated AML, azacitidine, venetoclax, and gilteritinib produced a 96% CR/CRi rate. At a median follow-up of 41.5 months, median RFS and OS were 23.4 and 29.7 months, with 3-year rates of 43% and 46%, respectively. Baseline RAS pathway mutations were associated with poorer outcomes, while 67% of evaluable relapses lacked detectable FLT3 mutations. The triplet produced durable remissions but frequently required treatment dose or duration reductions because of myelosuppression.
KEY FINDINGS: In this phase II study, azacitidine, venetoclax, and gilteritinib produced high remission rates and encouraging long-term survival in patients with newly diagnosed FLT3-mutated AML who were unfit for intensive chemotherapy. The 3-year RFS and OS rates were 43% and 46%, respectively, although outcomes were less favorable in patients with FLT3-ITD mutations and baseline RAS pathway mutations. Most evaluable relapses were FLT3-negative, suggesting that resistance may involve mechanisms beyond persistent FLT3-mutated disease. Dose or duration reductions were frequently required during consolidation, primarily reflecting the challenge of managing myelosuppression. Randomized studies are needed to establish the role of this triplet regimen relative to current standard approaches.
BACKGROUND: Relapse after frontline azacitidine and venetoclax remains a major challenge in patients with FLT3-mutated acute myeloid leukemia (AML), with relapse often associated with expansion of FLT3-mutated clones. This phase II study evaluated the long-term efficacy and safety of adding the FLT3 inhibitor gilteritinib to azacitidine and venetoclax in adults with newly diagnosed FLT3-mutated AML who were considered unfit for intensive chemotherapy.
DETAILS: Thirty patients with newly diagnosed FLT3-mutated AML were treated with the azacitidine, venetoclax, and gilteritinib triplet regimen. The median age was 71 years, and 22 (73%) patients had FLT3-ITD mutations. Fourteen patients (47%) proceeded to allogeneic hematopoietic stem cell transplantation in first remission. The median follow-up was 41.5 months.
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The complete remission or complete remission with incomplete hematologic recovery rate was 96%. Eleven patients (37%) subsequently relapsed, and among evaluable relapses, the FLT3 mutation was no longer detectable in 67%, indicating that relapse mechanisms were not necessarily driven by persistent FLT3-mutated disease.
The median relapse-free survival (RFS) was 23.4 months and median overall survival (OS) was 29.7 months. At 3 years, RFS was 43% and OS was 46%. Among patients with FLT3-ITD-mutated AML, median RFS and OS were 17.0 months and 21.8 months, respectively, with 3-year RFS and OS rates of 32% and 36%. Baseline RAS pathway mutations were associated with poorer outcomes.
Survival outcomes were similar regardless of whether patients underwent allogeneic hematopoietic stem cell transplantation in first remission. Among patients receiving at least one consolidation cycle, 68% required a reduction in the dose or duration of at least one study drug, highlighting the need to manage treatment-related myelosuppression during prolonged therapy.
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Source: Short, N. J., Kantarjian, H. M., Daver, N., et al. Long-Term Outcomes of Azacitidine, Venetoclax and Gilteritinib in Newly Diagnosed FLT3-Mutated AML. Blood Advances.. 2026; 10(17): 5743–5750. Published: May 27, 2026. DOI: 10.1182/bloodadvances.2026019841.
[Posted 2/Sep/2026]
AUDIENCE: Hematology, Oncology
KEY FINDINGS: In this phase II study, azacitidine, venetoclax, and gilteritinib produced high remission rates and encouraging long-term survival in patients with newly diagnosed FLT3-mutated AML who were unfit for intensive chemotherapy. The 3-year RFS and OS rates were 43% and 46%, respectively, although outcomes were less favorable in patients with FLT3-ITD mutations and baseline RAS pathway mutations. Most evaluable relapses were FLT3-negative, suggesting that resistance may involve mechanisms beyond persistent FLT3-mutated disease. Dose or duration reductions were frequently required during consolidation, primarily reflecting the challenge of managing myelosuppression. Randomized studies are needed to establish the role of this triplet regimen relative to current standard approaches.
BACKGROUND: Relapse after frontline azacitidine and venetoclax remains a major challenge in patients with FLT3-mutated acute myeloid leukemia (AML), with relapse often associated with expansion of FLT3-mutated clones. This phase II study evaluated the long-term efficacy and safety of adding the FLT3 inhibitor gilteritinib to azacitidine and venetoclax in adults with newly diagnosed FLT3-mutated AML who were considered unfit for intensive chemotherapy.
DETAILS: Thirty patients with newly diagnosed FLT3-mutated AML were treated with the azacitidine, venetoclax, and gilteritinib triplet regimen. The median age was 71 years, and 22 (73%) patients had FLT3-ITD mutations. Fourteen patients (47%) proceeded to allogeneic hematopoietic stem cell transplantation in first remission. The median follow-up was 41.5 months.
The complete remission or complete remission with incomplete hematologic recovery rate was 96%. Eleven patients (37%) subsequently relapsed, and among evaluable relapses, the FLT3 mutation was no longer detectable in 67%, indicating that relapse mechanisms were not necessarily driven by persistent FLT3-mutated disease.
The median relapse-free survival (RFS) was 23.4 months and median overall survival (OS) was 29.7 months. At 3 years, RFS was 43% and OS was 46%. Among patients with FLT3-ITD-mutated AML, median RFS and OS were 17.0 months and 21.8 months, respectively, with 3-year RFS and OS rates of 32% and 36%. Baseline RAS pathway mutations were associated with poorer outcomes.
Survival outcomes were similar regardless of whether patients underwent allogeneic hematopoietic stem cell transplantation in first remission. Among patients receiving at least one consolidation cycle, 68% required a reduction in the dose or duration of at least one study drug, highlighting the need to manage treatment-related myelosuppression during prolonged therapy.
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Source: Short, N. J., Kantarjian, H. M., Daver, N., et al. Long-Term Outcomes of Azacitidine, Venetoclax and Gilteritinib in Newly Diagnosed FLT3-Mutated AML. Blood Advances.. 2026; 10(17): 5743–5750. Published: May 27, 2026. DOI: 10.1182/bloodadvances.2026019841.
Somatic Diseases May Affect the Brain Primarily Through Vascular Injury and Neuronal Loss
A narrative review found that common age-related somatic diseases were consistently associated with brain atrophy, neuronal loss, and cerebrovascular lesions. Evidence linking these diseases to amyloid and tau pathology was limited and inconsistent. The findings suggest that systemic diseases may contribute to dementia primarily through non-Alzheimer's mechanisms, particularly vascular injury and neuronal loss. The review underscores the importance of recognizing mixed dementia and considering systemic health in the assessment of cognitive decline.
KEY FINDINGS: Common age-related somatic diseases appear to be more consistently associated with cerebrovascular injury, brain atrophy, and neuronal loss than with amyloid or tau pathology. These findings suggest that the relationship between systemic disease and dementia may involve multiple non-AD pathways rather than a direct effect on classical AD pathology. The review highlights the importance of recognizing mixed dementia and considering systemic health when evaluating brain aging and cognitive decline.
BACKGROUND: Several common age-related somatic diseases are associated with an increased risk of dementia, but the neuropathological pathways underlying these associations remain incompletely understood. This narrative review examined evidence linking heart disease, type 2 diabetes, kidney disease, liver disease, lung disease, and anemia with brain pathology, including Alzheimer's disease (AD)-related amyloid and tau pathology and non-AD changes such as neuronal loss, brain atrophy, cerebrovascular lesions, neuroinflammation, and non-AD proteinopathies.
DETAILS: The authors conducted a PubMed search for human studies investigating associations between somatic diseases and brain pathology using postmortem examinations, brain imaging, or cerebrospinal fluid biomarkers. The available evidence was qualitatively synthesized and graded according to its strength. The review specifically evaluated whether common systemic diseases were associated with AD-related pathology or with other forms of brain injury that may contribute to cognitive impairment and dementia.
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Across the conditions examined, the strongest and most consistent associations were between somatic diseases and global neuronal loss or brain atrophy, as well as cerebrovascular lesions. In contrast, associations between somatic diseases and amyloid or tau deposition were limited and inconsistent. The review found no systematic studies examining neuroinflammation or non-AD proteinopathies in relation to somatic diseases.
Overall, the available evidence suggests that systemic diseases may contribute to brain damage predominantly through non-AD mechanisms, particularly cerebrovascular injury and diffuse neuronal loss, rather than by directly driving the characteristic amyloid and tau pathology of AD. The authors emphasize that these processes may contribute to the complex combination of pathologies frequently underlying dementia in older adults.
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Source: Grande, G., Valletta, M., Gasparini, F., et al. Brain pathology in relation to somatic diseases: Exploring the body–brain crosstalk. Journal of Internal Medicine. 2026; 300(3): 223–237. Published: June 2, 2026. DOI: 10.1111/joim.70119.
Hypertension at 5 Months Postpartum in Women With Gestational Diabetes
Among 678 women with recent gestational diabetes mellitus, 26.4% developed hypertension by 5 months postpartum. Higher early-pregnancy weight and blood pressure, Black or mixed ethnicity, and gestational hypertension or pre-eclampsia were associated with increased risk. Postpartum hypertension was also associated with greater adiposity and dyslipidemia. The findings support structured postpartum screening for blood pressure and broader cardiometabolic risk after GDM.
KEY FINDINGS: Approximately one in four women with recent GDM developed hypertension by 5 months postpartum. Higher maternal weight and blood pressure early in pregnancy, as well as Black or mixed ethnicity, were associated with increased risk, while gestational hypertension or pre-eclampsia was also associated with postpartum hypertension. Women with postpartum hypertension had greater adiposity and more frequent dyslipidemia, highlighting the broader cardiometabolic abnormalities present after GDM. Because early-pregnancy characteristics provided only modest prediction, the findings support structured postpartum assessment that includes blood pressure and broader cardiometabolic risk evaluation rather than focusing solely on dysglycemia.
BACKGROUND: Gestational diabetes mellitus (GDM) is associated with an increased risk of later cardiometabolic disease, including hypertension. However, the occurrence and determinants of hypertension soon after pregnancy complicated by GDM have not been well defined. This prospective study evaluated the incidence and predictors of hypertension at 5 months postpartum and examined its relationship with other cardiometabolic abnormalities in women with recent GDM.
DETAILS: This single-center observational prospective cohort study was conducted at King's College Hospital, London, between September 2023 and January 2025. Women with GDM who received routine prenatal care at 12 weeks' gestation were invited for a postpartum assessment at approximately 5 months after delivery; women with chronic hypertension were excluded. The assessment included blood pressure, BMI, waist circumference, glucose status, lipid profile, and renal function. Hypertension was defined as systolic BP ≥ 130 mmHg, diastolic BP ≥ 80 mmHg, or receipt of antihypertensive treatment. Of 912 women with GDM invited for postpartum review, 696 (76.3%) attended. After excluding 18 women with chronic hypertension, 678 women constituted the study cohort. Follow-up occurred at a median of 5.1 (IQR, 4.4-6.7) months after birth.
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Among the 678 women with previous GDM, 179 (26.4%) developed hypertension at a median of 5.1 (IQR, 4.4-6.7) months postpartum. Women who subsequently developed hypertension had higher early-pregnancy weight and blood pressure. At 12 weeks' gestation, median weight was 79.3 kg versus 69.3 kg among women who remained normotensive, while median systolic BP was 121.8 versus 115.5 mmHg and median diastolic BP was 74.5 versus 70.3 mmHg, respectively. Obesity at this stage was also more frequent among women who later developed hypertension (50.3% vs 28.5%). Pregnancy hypertensive disorders were more common among women who developed postpartum hypertension. Gestational hypertension occurred in 8.4% versus 3.8%, and pre-eclampsia in 9.5% versus 1.8%, among women who developed postpartum hypertension compared with those who remained normotensive.
Multivariable analysis identified higher maternal age, Black or mixed ethnicity, higher weight, and higher systolic and diastolic BP at 12 weeks as predictors of postpartum hypertension. Black ethnicity was associated with an adjusted OR of 1.88 (95% CI, 1.19-3.00), mixed ethnicity with an adjusted OR of 2.75 (95% CI, 1.21-6.24), and weight ≥ 73 kg with an adjusted OR of 1.57 (95% CI, 1.04-2.38). Each 1-mmHg increase in systolic BP was associated with an adjusted OR of 1.04 (95% CI, 1.02-1.07), and each 1-mmHg increase in diastolic BP with an adjusted OR of 1.04 (95% CI, 1.00-1.07). Development of gestational hypertension or pre-eclampsia was associated with an adjusted OR of 3.00 (95% CI, 1.69-5.34).
At the postpartum assessment, women with hypertension had a median BMI of 30.1 (IQR, 26.7-36.8) kg/m² compared with 27.0 (IQR, 23.5-30.6) kg/m² among normotensive women. A waist-to-height ratio > 0.5 was present in 87.7% versus 69.1%, and dyslipidemia in 35.8% versus 24.4%, respectively. Dysglycemia and renal dysfunction did not differ significantly between the groups.
The prenatal prediction model had only modest discriminatory ability. The AUC was 0.723 (95% CI, 0.680-0.766) using characteristics available at 12 weeks and 0.739 (95% CI, 0.697-0.782) after adding gestational hypertension or pre-eclampsia. At a 20% false-positive rate, detection rates were 49.5% and 53.7%, respectively.
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Source: Gomez Fernández, C., Charakida, M., Moser, M., et al. Hypertension at 5 months postpartum in women with gestational diabetes. Ultrasound in Obstetrics & Gynecology. 2026; 68(2): 202-210. Published: July 17, 2026. DOI: 10.1002/uog.70291.
Psoriasis-Atopic Dermatitis Overlap Phenotype Shows Dual Type 2 and Type 3 Inflammation and Response to JAK1 Inhibition
Clinicians should consider Pso-Ec in adults with persistent lesions showing both psoriasis-like and eczema-like clinical and histopathologic features without a clearly dominant inflammatory pathway. The study found involvement of Th2/Tc2 and Th17/Tc17 pathways and JAK1-STAT2/6 signaling. Previous psoriasis- or atopic dermatitis-directed biologics were often inadequate, while JAK1 inhibitors achieved minimal disease activity in the patients studied. These findings suggest Pso-Ec may be a distinct phenotype for which JAK1 inhibition could be a targeted treatment option. However, the findings are limited by the small sample size and immunologic testing in only a subset of patients.
KEY FINDINGS: Clinicians should consider Pso-Ec when an adult patient has persistent lesions showing simultaneous psoriasiform and eczematous clinical and histopathologic characteristics, particularly when there is no clear dominant inflammatory pathway. In this study, the phenotype was associated with dual Th2/Tc2 and Th17/Tc17 activity and involvement of JAK1-STAT2/6 signaling. Prior Pso- or AD-directed biologics were often inadequate, whereas JAK1 inhibitors achieved minimal disease activity with BSA ≤2 and NRS ≤1 during a median 17-month follow-up. The findings support recognition of Pso-Ec as a distinct phenotype and suggest JAK1 inhibition as a mechanism-based therapeutic approach. The study's interpretation is limited by its small sample size and the fact that immunologic analyses were performed in a representative subset of patients.
BACKGROUND: Psoriasis (Pso) and atopic dermatitis (AD) are generally characterized by different dominant inflammatory pathways. However, some patients present with lesions containing both psoriasiform and eczematous features, creating diagnostic and therapeutic challenges. This prospective study characterized a distinct psoriasis–atopic dermatitis overlapping phenotype, termed Pso-Ec, with particular attention to its clinical, histopathologic, immunologic, and treatment characteristics.
DETAILS: The two-center prospective study enrolled 30 patients with Pso-Ec between January 2021 and December 2025. Reference cohorts consisted of 150 patients with typical Pso and 150 with AD. The Pso-Ec group included patients aged 13-72 years, with a mean age of 49.7 ± 17.7 years and a male-to-female ratio of 19:11. None had a previous history of Pso or AD. Notably, 63.3% had associated atopic diseases, compared with 2.7% of patients with typical Pso and 47.3% of those with AD (P < .001). Pso-Ec lesions were characterized clinically by ill-defined erythematous plaques, thin scales, excoriation, and prominent pruritus. Histopathologic examination demonstrated concurrent psoriatic and eczematous features within the same lesions. Immunologic assessment of lesional skin and peripheral blood identified simultaneous type 2 and type 3 inflammatory activity, represented by Th2/Tc2 and Th17/Tc17 populations. JAK1-STAT2/6 signaling was also implicated in the inflammatory profile.
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Treatment histories indicated that conventional pathway-directed biologic therapy was frequently inadequate in this phenotype. Among the Pso-Ec patients, 18 had previously received Pso-targeted biologics and 15 had received AD-targeted biologics, with responses described as often inadequate. In contrast, treatment with JAK1 inhibitors was associated with achievement of minimal disease activity, defined as body surface area (BSA) ≤2 and numerical rating scale (NRS) ≤1. This response was maintained during a median follow-up of 17 months. During follow-up, none of the patients progressed to a classic Pso or AD phenotype.
The investigators concluded that Pso-Ec represents a distinct, predominantly adult-onset inflammatory phenotype rather than simply a transitional presentation between psoriasis and atopic dermatitis. Its defining immunologic characteristic is the concurrent presence of type 2 and type 3 inflammation, which may explain the limited effectiveness of therapies directed primarily against either pathway. JAK1 inhibition emerged as an effective treatment option in this cohort.
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Source: Chen, M., Shen, C., Chen, C. B., et al. A Distinct Psoriasis–Atopic Dermatitis Overlapping Phenotype in Adults With Dual Type 2 and Type 3 Immune Features and Favorable Response to Janus Kinase 1 Inhibition. Journal of the American Academy of Dermatology. 2026; Published: September 22, 2026. DOI: 10.1016/j.jaad.2026.05.042.
Parental Responsibility May Drive Hesitation Toward AI Educational Services
This research is the first to uncover the impact of educational approaches on individuals' guilt and downstream behaviours in the AI-in-Education field, shedding light on attribution as its underlying mechanism and offering actionable strategies to enhance individuals' WOM. The findings offer novel insights to AI-human interaction psychological research and hold practical implications for AI-in-Education industry practitioners.
KEY FINDINGS: Across five experimental studies, AI educational services were associated with greater guilt, lower perceived value, and, in several conditions, less willingness to recommend the approach compared with direct parental engagement. The findings indicate that reluctance to use AI for children's education may be linked less to perceptions of AI capability and more to the belief that educating one's children is a parental responsibility. The study also suggests that framing AI use as necessary because of an individual's limitations, or demonstrating that other parents use AI services, may improve positive WOM toward these services.
BACKGROUND: Artificial intelligence (AI) educational services are increasingly positioned as tools that can assist children with learning and tutoring. However, the decision to use these services may be influenced by more than their perceived educational capability. This research examined how choosing AI educational services rather than direct parental involvement affects guilt, perceived value, and willingness to recommend the approach to others. Across five experimental studies, the investigators also examined whether perceived parental responsibility, intrinsic reasons for using AI, and conformity influence these responses.
DETAILS: The research used experimental designs comparing parental engagement with AI educational services across homework and writing-tutoring scenarios. Study 1a included 191 participants after exclusion of 9 cases; Study 1b included 200 participants; Study 2 included 200 participants; Study 3 included 390 participants; and Study 4 included 400 participants. Participants were recruited through the Credamo online platform.
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In Study 1a, participants who considered using AI educational services reported greater guilt and assigned a lower monetary valuation than those who personally tutored their children. Mean guilt scores were 2.74 (SD 1.81) with AI educational services versus 2.09 (SD 1.58) with parental engagement (t=2.67, p=.008). Mean valuation was 1219.31 (SD 1154.32) versus 2097.99 (SD 2217.96), respectively (t=3.41, p=.001).
Study 1b reproduced these findings without using pictures and after accounting for parental status. Guilt was higher with AI educational services than with parental engagement (5.23 [SD 2.94] vs 3.79 [SD 2.47]; F(1, 198)=14.07, p<.001, ηp2=.07). Valuation was lower with AI educational services (1219.62 [SD 1581.27] vs 2494.11 [SD 2530.90]; F(1, 198)=18.24, p=.001, ηp2=.08).
Study 2 extended the analysis to willingness to recommend the educational approach. Participants using AI educational services reported greater guilt, lower valuation, and lower word-of-mouth (WOM) intentions than participants engaging in education themselves. Among participants with children, guilt means were 3.09 (SD 2.35) for AI educational services and 2.32 (SD 2.31) for parental engagement (F=4.18, p=.043, ηp2=.03). Valuation was 477.83 (SD 547.20) versus 968.14 (SD 780.09), respectively (F=21.14, p<.001, ηp2=.12), while WOM was 7.83 (SD 1.65) versus 8.23 (SD 1.41) (F=4.77, p=.030, ηp2=.03).
Perceived responsibility for children's education emerged as an important explanatory mechanism. Attribution scores among participants with children were 6.27 (SD 2.50) in the AI condition and 8.79 (SD 0.86) in the parental-engagement condition (F=87.92, p<.001, ηp2=.36). Mediation analysis showed that attribution significantly mediated the relationship between educational approach and guilt, valuation, and WOM, with effects of 0.6116, -183.9280, and -0.8910, respectively.
Study 3 demonstrated that the reason for choosing AI could alter the pattern of WOM responses. When participants lacked the ability to tutor their children, those using AI educational services reported greater positive WOM than those personally tutoring their children: 7.60 (SD 1.47) versus 6.76 (SD 2.29), p=.006. In the control condition, the pattern was reversed, with WOM scores of 7.36 (SD 1.90) for AI educational services and 7.86 (SD 1.23) for parental engagement (p=.04).
Study 4 found that social conformity also influenced WOM. Overall, WOM was lower with AI educational services than with parental engagement: 7.59 (SD 2.19) versus 8.30 (SD 1.10) (F(1, 396)=17.23, p.001, ηp2=.04). When participants were given information that other parents were using AI educational services, the difference was no longer statistically significant (7.88 [SD 1.94] vs 8.24 [SD 1.23], p=.133). Without such conformity information, WOM was significantly lower for AI educational services (7.29 [SD 2.39] vs 8.36 [SD 0.94], p<.001).
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Source: Shao, A., Lu, Z., Liu, S. Q., et al. Demystifying the mist: Why do individuals hesitate to accept AI educational services?. British Journal of Psychology. 2026; 117(3): 932-956. Published: August, 2026. DOI: 10.1111/bjop.70040.
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