Post-traumatic stress disorder (PTSD) is a mental health condition caused by the dysregulation or overgeneralization of memories related to traumatic events. Investigating the interplay between explicit narrative and implicit emotional memory contributes to a better understanding of the mechanisms underlying PTSD.

This case–control study focused on two groups: unmedicated patients with PTSD and a trauma-exposed control (TEC) group who did not develop PTSD. Experiments included real-time measurements of blood oxygenation changes using functional near-infrared spectroscopy during trauma narration and processing of emotional and linguistic data through natural language processing (NLP).

Real-time fNIRS monitoring showed that PTSD patients (mean [SD] Oxy-Hb activation, 0.153 [0.084], 95% CI 0.124 to 0.182) had significantly higher brain activity in the left anterior medial prefrontal cortex (L-amPFC) within 10 s after expressing negative emotional words compared with the control group (0.047 [0.026], 95% CI 0.038 to 0.056; p < 0.001). In the control group, there was a significant time-series correlation between the use of negative emotional memory words and activation of the L-amPFC (latency 3.82 s, slope = 0.0067, peak value = 0.184, difference = 0.273; Spearman’s r = 0.727, p < 0.001). In contrast, the left anterior cingulate prefrontal cortex of PTSD patients remained in a state of high activation (peak value = 0.153, difference = 0.084) with no apparent latency period.

PTSD patients display overactivity in pathways associated with rapid emotional responses and diminished regulation in cognitive processing areas. Interventions targeting these pathways may alleviate symptoms of PTSD.

Caring for children with solid tumors (STs) can impact caregiver’s physical and mental health. Caregiver mastery, which influences psychological well-being, is vital in improving outcomes for both caregivers and children. The study aimed to investigate the relationship between caregiver mastery, anxiety, depression, fear of disease progression (FoP), caregiver burden, and the quality of life (QOL) of children with ST.

This cross-sectional study was conducted from June 2022 to April 2023 at a Grade A tertiary hospital in Shandong. Family caregivers of children with ST completed several validated measures, including the Pediatric Quality of Life Inventory (PedsQL) 3.0 Cancer Module, the Fear of Progression Questionnaire-parent version (FoP-Q-SF/PR), the Zarit Burden Interview Scale (ZBI), the hospital anxiety and depression scale (HADS), and the Caregiver Mastery Scale. Multiple linear regression analyses assessed the relationships between FoP, caregiver burden, anxiety, depression, caregiver mastery, and children’s QOL. Results were expressed as β and 95% confidence intervals (CIs).

A total of 454 caregivers participated. Caregiver mastery was positively correlated with children’s QOL (β = 0.80, 95% CI: 0.20 to 1.39). Depression (β = −0.64, 95% CI: −0.83 to −0.45), anxiety (β = −0.67, 95% CI: −0.85 to −0.49), caregiver burden (β = −1.20, 95% CI: −1.60 to −0.80), and FoP (β = −0.04, 95% CI: −0.05 to −0.03) were negatively related to children’s QOL. Caregiver mastery moderated the associations between depression, caregiver burden, FoP, and children’s QOL, while also improving the effect of mild anxiety on QOL.

The study underscores the importance of fostering caregiver mastery to mitigate the negative impact of caregiver distress on children’s QOL and improve outcomes for both caregivers and children with solid tumors.

Caregiver mastery moderates the effects of anxiety, depression, FoP, and caregiver burdenon children’s QOL. Supporting caregiver mastery can alleviate caregiver burden and enhance both caregiver and child well-being.

Anhedonia characterizes major depressive episodes in bipolar depression and is associated with more severe illness/poor prognosis. These post hoc analyses assess effect of cariprazine 1.5 and 3 mg/d on anhedonia symptoms in patients with bipolar I depression.

Data were pooled from 3 randomized, double-blind, placebo-controlled bipolar I depression trials in cariprazine. Cariprazine 1.5 and 3 mg/d versus placebo were evaluated in patient subgroups stratified by median baseline MADRS anhedonia score (higher anhedonia=score ≥19; lower anhedonia=score <19). Outcomes included mean change from baseline to week 6 in MADRS total and anhedonia factor score (sum of apparent sadness, reported sadness, concentration, lassitude, and inability to feel items). The proportion of patients with week 6 anhedonia factor response (≥50% improvement from baseline) was also determined. Changes from baseline were analyzed using a mixed-effect model for repeated measures.

There were 760 patients in the higher anhedonia subgroup (placebo=249, cariprazine: 1.5 mg/d=261; 3 mg/d=250) and 623 patients in the lower anhedonia subgroup (placebo=211, cariprazine: 1.5 mg/d=200; 3 mg/d=212). Mean baseline MADRS total score was higher in the higher anhedonia subgroup (total=33.6) than in the lower anhedonia subgroup (total=27.6). Change from baseline to week 6 in MADRS total score was greater for both cariprazine doses versus placebo in the higher anhedonia subgroup (least squares mean difference [LSMD] and 95% confidence interval [CI]: 1.5 mg/d=-3.01 [-4.84, -1.19], P=.0012; 3 mg/d: -3.26 [-5.12, -1.40], P=.0006); in the lower anhedonia subgroup, cariprazine 1.5 mg/d was statistically significant versus placebo (-2.61 [-4.28, -0.93], P=.0024). In the higher anhedonia subgroup at week 6, change from baseline in anhedonia factor score was significant versus placebo for both cariprazine doses (1.5 mg/d=-1.97 [-3.13, -0.81], P=.0009; 3 mg/d=-2.07 [-3.26, -0.89], P=.0006); in the lower subgroup, the difference was significant versus placebo for cariprazine 1.5 mg/d (-1.70 [-2.77, -0.62], P=.0021). After adjusting for changes in other depressive symptoms, LSMDs versus placebo in the anhedonia factor score remained significant for cariprazine 1.5 mg/d (-1.21 [-2.05, -0.36], P=.0052) and 3 mg/d (-1.00 [-1.86, -0.14], P=.0233) in the higher anhedonia subgroup, and for 1.5 mg/d (-1.06 [-1.92, -0.19], P=.0164) in the lower subgroup. In the higher anhedonia subgroup, rates of anhedonia factor response were greater versus placebo (31.7%) for cariprazine 1.5 mg/d (44.8%, P=.0028) and 3 mg/d (45.6%, P=.0019); in the lower subgroup, response rates were 39.3% for placebo, 48.0% for 1.5 mg/d, and 46.7% for 3 mg/d. Adverse events in ≥5% cariprazine and twice placebo were nausea, akathisia, restlessness, and EPS.

Those with bipolar depression and anhedonia cariprazine demonstrated a potent antidepressant and antianhedonic effect in higher/lower anhedonia subgroups.

AbbVie

This data was previously presented at the European College of Neuropsychopharmacology (ECNP) Congress; Barcelona, Spain; October 7 – 10, 2023.

Assess effect of predominant polarity on efficacy of cariprazine in patients with bipolar I (BP-I) disorder. Predominant polarity may be an important clinical consideration in BP-I disorder, with predominant depressive episodes associated with delayed diagnosis and higher rates of suicidality, while predominant manic episodes are associated with younger onset, manic/psychotic first episode, and more substance abuse [1].

Data were pooled from 3 randomized, double-blind, cariprazine trials in BP-I depression and 3 trials in BP-I mania. Post hoc analyses were performed in subgroups from the bipolar depression studies with/without predominant depression (≥2:1 ratio of prior lifetime depressive to manic episodes), and in subgroups from the bipolar mania studies with and without predominant mania (≥2:1 ratio of prior lifetime manic to depressive episodes). Change from baseline to week 6 in Montgomery-Åsberg Depression Rating Scale (MADRS) total score was evaluated for cariprazine 1.5 and 3 mg/d versus placebo (bipolar depression studies); change from baseline to week 3 in Young Mania Rating Scale total score was evaluated for cariprazine 3-12 mg/d versus placebo (bipolar mania studies). Change from baseline analyzed using mixed-effect model for repeated measures in pooled intent-to-treat population from each indication.

In bipolar depression studies, there were 624 patients (45% of total study population) in the predominantly depressive subgroup (placebo=197, cariprazine: 1.5 mg/d=217; 3 mg/d=210) and 750 patients (55%) in the subgroup without predominant depression (placebo=258, cariprazine: 1.5 mg/d=241; 3 mg/d=251). In the predominant depressive subgroup, LSMDs for MADRS total score change from baseline were significant versus placebo for cariprazine 1.5 mg/d (-2.49 [-4.30, -.68], P=.0071) and 3 mg/d (-2.48 [-4.31, -.65], P=.0079); in the subgroup without predominant depression, LSMDs were also significant versus placebo for both doses (1.5 mg/d=-3.30 [-5.06, -1.54], P=.0002; 3 mg/d=-2.53 [-4.29, -.77], P=.0049). In bipolar mania studies, there were 721 patients (73% of total study population) in the predominantly manic episode subgroup (placebo=307, cariprazine 3-12 mg/d =414) and 267 patients (27%) in the subgroup without predominant manic episodes (placebo=102, cariprazine 3-12 mg/d=165). In predominant mania subgroup, LSMD in YMRS total score change from baseline was significant for cariprazine 3-12 mg/d versus placebo (-4.65 [-6.29, -3.02], P<.0001); in subgroup without predominant mania, the LSMD for cariprazine versus placebo was also significant (-7.56 [-10.30, -4.82], P<.0001).

Cariprazine was efficacious in treating BP-I mood episodes regardless of predominant polarity for the presenting mood episode. Cariprazine was effective against symptoms of depression in patients with BP-I depression with/without predominant depressive episodes, and against symptoms of mania in patients with BP-I mania with/ without predominant manic episodes.

AbbVie

This data was previously presented at the Annual ECNP Congress; Barcelona, Spain; October 7-10, 2023.

The exploration of molecular characteristics has emerged as a prominent trend to advance precision medicine. The utilization of genetic testing to guide therapy is integral to precision medicine. This study aims to investigate the potential patient populations for the reimbursement of next-generation sequencing (NGS) and assess the budget impact from the perspective of Taiwan’s single insurer, the National Health Insurance Administration.

To comprehend the scope for medicines with companion diagnostics (CDx) involved, we analyze the U.S. Food and Drug Administration-approved/cleared diagnostic tests, conduct a literature review to identify medicines approved by the European Medicines Agency that require a CDx, and identify the medicines with CDx involved covered by the National Health Insurance (NHI) in Taiwan. Subsequently, we explore the potential reimbursement indications for NGS testing and conduct a budget impact analysis to evaluate the expected financial impact for the NHI over a five-year period. Furthermore, sensitivity analyses are conducted to deal with uncertainty.

We have compiled 13 cancer types for which NGS can serve as a companion diagnostic. These encompass non-small-cell lung cancer, colorectal cancer, breast cancer, ovarian cancer, biliary tract cancer, acute myeloid leukemia, acute lymphoblastic leukemia, melanoma, cholangiocarcinoma, prostate cancer, pancreatic cancer, gastrointestinal stromal tumor, and thyroid cancer/medullary thyroid cancer. The implementation of NGS reimbursement in NHI will benefit 25,000 to 30,000 patients undergoing targeted therapies. The projected incremental budget impact ranges from TWD570 million to TWD650 million (USD19 million to USD22 million) over five years.

This study focuses on evaluating the financial impact of incorporating NGS testing into NHI reimbursement for relevant cancer drug indications. The findings can serve as references for the planning of reimbursement policies. However, with the advancement of precision medicine, it is foreseeable that there will be a broader range of applications for NGS, and its cost will gradually decrease.

The microRNA-200 family plays a key role in inflammatory and vascular processes, making it a relevant target for Kawasaki disease, a vasculitis with coronary complications. This study aimed to evaluate the diagnostic potential of urinary exosomal microRNA-200 family members in Kawasaki disease patients.

Urine samples from 15 Kawasaki disease patients and 15 healthy controls underwent total exosome isolation and high-throughput sequencing. Differential expression of microRNA-200 family members was validated using quantitative real-time polymerase chain reaction. Diagnostic potential was assessed via receiver operating characteristic analysis, and correlations with clinical parameters were evaluated using Spearman correlation.

High-throughput sequencing identified upregulation of microRNA-429, microRNA-200b-3p/5p, microRNA-141-3p, microRNA-200a-3p/5p, and microRNA-200c-3p in Kawasaki disease patients. We confirmed significant upregulation of microRNA-200a-3p/5p, microRNA-200b-3p/5p, and microRNA-429, with receiver operating characteristic analysis showing high diagnostic potential for these microRNAs (area under the curves of 0.844, 0.791, 0.942, 0.842, and 0.898, respectively) and a combined analysis yielding a perfect area under the curve of 1.000. MicroRNA-141 and microRNA-200c-3p/5p, however, showed no significant diagnostic value. MicroRNA-200a-3p and microRNA-200a-5p were positively correlated with white blood cells, platelet counts, and C-reactive protein, while microRNA-200b-3p and microRNA-429 were positively correlated with white blood cells, platelet counts, erythrocyte sedimentation rate, and C-reactive protein. microRNA-200b-5p showed moderate correlations with platelet counts and erythrocyte sedimentation rate.

Urinary exosomal microRNA-200 family members, especially microRNA-200a-3p/5p, microRNA-200b-3p/5p, and microRNA-429, demonstrate strong diagnostic potential for Kawasaki disease, correlating with key inflammatory markers. MicroRNA-141 and microRNA-200c did not demonstrate significant diagnostic utility.

Various studies have highlighted the increased incidence and symptoms of depression and anxiety in paediatric cancer survivors (PCS). Yet no meta-analysis has focused on post-traumatic stress disorder (PTSD) or post-traumatic stress symptoms (PTSS) in PCS and their family nucleus.

To evaluate the overall risk of PTSD and severity of PTSS in PCS and their family nucleus. Secondary objectives include identifying potential risk factors of PTSD and high PTSS.

We systematically searched PubMed, Embase and PsycINFO for studies comparing the risk of PTSD and PTSS severity among PCS, their family nucleus and non-cancer controls. PRISMA reporting guidelines were followed. Random effects meta-analyses and meta-regressions were conducted.

From 1089 records, we included 21 studies. PCS have an increased risk of PTSD (risk ratio 2.36, 95% CI 1.37–4.06) and decreased PTSS severity (standardised mean difference −0.29, 95% CI −0.50 to −0.08). Subgroup analyses of other categorical study-level characteristics revealed that female PCS who were older at diagnosis and data collection had a significantly higher risk of PTSD. Meta-regression were insignificant. Family nucleus did not show a significantly increased risk of PTSD (risk ratio 1.13, 95% CI 0.59–5.00) and PTSS severity (standardised mean difference 0.53, 95% CI −0.00 to 1.06). Systematically reviewing studies on the family nucleus found that the majority reported a significantly increased risk of psychological trauma compared with the comparator. Lower education, income and social status were also risk factors.

Timely identification and interventions are imperative for policy makers and healthcare providers to prevent trauma from worsening in this population group.