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Silent treatment represents a subtle yet harmful form of ostracism, often accompanied by emotional distress and ambiguity regarding the reasons for exclusion. This research investigated the emotional responses of individuals exposed to silent treatment, with a particular focus on the role of guilt. Study 1 involved participants recalling episodes of silent treatment and neglect, allowing for a comparison of the emotions elicited in these relational contexts. Results indicated that guilt, sadness, and fear were more pronounced during silent treatment, while the source was perceived as expressing greater anger and disgust. Study 2 employed an experimental design to explore the specific nature of guilt, distinguishing between altruistic and deontological guilt. Findings revealed that silent treatment is associated with heightened deontological guilt, which is linked to violations of moral norms and uncertainty. These studies provide a contribution to the understanding of silent treatment and its implications for relational and emotional well-being.

Type 2 diabetes mellitus (T2DM) is associated with a substantially increased risk of cardiovascular complications, many of which remain silent until advanced stages. Silent myocardial ischemia (SMI), characterized by objective evidence of ischemia without anginal symptoms, is prevalent in diabetic populations due to autonomic neuropathy. Early identification of asymptomatic individuals harboring subclinical coronary artery disease (CAD) is crucial for timely intervention. This study aimed to determine the prevalence of coronary risk factors and SMI in asymptomatic patients with T2DM and to identify clinical and biochemical predictors associated with positive stress test findings. This cross-sectional observational study enrolled 71 patients with T2DM (American Diabetes Association 2023 criteria) without known CAD at a tertiary care center in North India. All participants underwent treadmill stress testing (TMT) using the Bruce protocol. Demographic, lifestyle, clinical, and biochemical parameters were compared between TMT-positive (silent ischemia) and TMT-negative groups using chi-squared tests, Student's t-test, and Mann-Whitney U test as appropriate. SMI was detected in 18.31% (13/71) of participants. TMT-positive individuals demonstrated significantly higher prevalence of sedentary lifestyle (84.6% vs. 50%; p=0.011), diabetes duration >5 years (84.6% vs. 44.8%; p=0.004), hypertension (46.2% vs. 25.9%; p<0.001), smoking (76.9% vs. 44.8%; p=0.018), and family history of hypertension (69.2% vs. 31%; p=0.005). Biochemically, the TMT-positive group showed elevated serum urea (p=0.003), creatinine (p<0.001), triglycerides (p<0.001), low-density lipoprotein (LDL) (p=0.034), total cholesterol (p=0.002), and urinary albumin-to-creatinine ratio (UACR) (p<0.001) and lower high-density lipoprotein (HDL) (p<0.001). A significant proportion of asymptomatic T2DM patients harbor SMI. Longer diabetes duration, sedentary lifestyle, hypertension, dyslipidemia, and microalbuminuria are key predictors. Routine cardiovascular screening using non-invasive modalities should be considered in high-risk diabetic individuals even without overt symptoms.

Aphasiacs with impaired vocal organs suffer profound communication barriers, making silent speech decoding essential. Although audible speech is absent, subtle multi-muscle activities are retained. This provides a physiological basis for the sensing modality that reliably decodes silent speech. Yet conventional microphone and piezoelectric films remain susceptible to dispersion-fidelity conflict, external disturbance in the complex environments, and are further constrained by sensing-communication separation. Here, we report an in-sensor communication scarf interface that imperceptibly captures multi-muscle activities and ultrarobustly decodes silent speech. By fusing spoof surface plasmon-driven in-sensor electromagnetic physiological communication with metamaterial topological embroidery, the system establishes exquisite reconciliation between dispersion-regulated spatial selectivity and ultrahigh fidelity (7&#x2009;fs&#xb2;), enabling phase-resolved differentiation and precise capture of multi-muscle activities. This minimalist yet informative rich component design radically transcends limitations of sensing-communication separation, microphone, and piezoelectric films, and greatly delivers anti-motion artifact by 24,300%, anti-electromagnetic interference by 46.4&#x2009;dB, and anti-noise by 33.44&#x2009;dB in the complex environments. Combining with machine learning, the interface achieves 98.7% recognition and supports assistive interaction and sleep apnea monitoring. The interface bridges metamaterial electromagnetics and human electrophysiology, establishing a transformative in-sensor physiological decoding paradigm for electromagnetic physiological communication and adaptive myogenic interfacing.

The emergence of plasmid-mediated colistin resistance genes (mcr genes) poses a major threat to public health. Among these, the mcr-9 gene is frequently detected without conferring phenotypic resistance. An mcr-9-positive Enterobacter hormaechei isolated from a canine urinary tract infection in Portugal was characterized by whole-genome sequencing, revealing a multidrug-resistant IncHI2 plasmid carrying the mcr-9 gene. This plasmid showed structural similarity to other publicly available plasmid sequences from human and animal sources worldwide. The strain harbored a conserved genetic region composed of the nickel/copper-associated operon rcnR-rcnA-pcoE-ISSgsp1-pcoS-IS903-mcr-9-wbuC, which is involved in metal homeostasis and copper tolerance under anaerobic conditions. Antimicrobial susceptibility testing revealed colistin susceptibility. Notably, the regulatory genes qseC and qseB, which have been implicated in the activation of mcr-9 expression, were absent, potentially explaining this phenotype. These findings highlight the silent dissemination potential of mcr-9 in companion animals and reinforce the importance of genomic surveillance under a One Health framework.

Acute silent ischemic lesions (ASILs) usually present as diffusion weighted imaging hyperintensity with corresponding apparent diffusion coefficient hypointensity, indicating a possibly unstable ischemic pattern in severe intracranial stenosis. However, there is still no conclusive evidence that preprocedural ASILs are associated with inhospital stroke after percutaneous transluminal angioplasty and stenting (PTAS). A single center retrospective cohort study was conducted among patients with severe symptomatic intracranial atherosclerotic stenosis (severe sICAS) who underwent PTAS at a tertiary care center between January 2019 and October 2024. Among 1727 initially screened patients, 1427 eligible patients were included according to preprocedural ASIL status. The primary endpoint was prespecified as stroke or death during the index hospitalization. Multivariable logistic regression was used to evaluate the association between ASILs and the primary endpoint. Sensitivity analyses included propensity score matching, inverse probability of treatment weighting using winsorized stabilized weights, doubly robust weighted modeling using the same winsorized stabilized weights, Firth penalized logistic regression, early period exclusion analyses, and parsimonious models addressing events-per-variable concerns. Apparent within cohort discrimination and reclassification were assessed by the area under the receiver operating characteristic curve, DeLong test, continuous net reclassification improvement, and integrated discrimination improvement. Of the 1427 participants, 60 (4.2%) had the primary endpoint, all of which were inhospital stroke events; no inhospital deaths occurred. Preprocedural ASILs were associated with inhospital stroke in univariable analysis (OR 4.62, 95%&#x2009;CI 2.68 to 7.98; P<0.001) and remained independently associated with inhospital stroke in the prespecified multivariable model (OR 5.00, 95%&#x2009;CI 2.70 to 9.26; P<0.001). The association remained consistent in propensity score matching (OR 4.20, 95%&#x2009;CI 1.58 to 11.14; P=0.004), inverse probability of treatment weighting using winsorized stabilized weights (OR 3.94, 95%&#x2009;CI 2.16 to 7.18; P<0.001), doubly robust weighted modeling using the same winsorized stabilized weights (OR 4.12, 95%&#x2009;CI 2.26 to 7.52; P<0.001), and Firth penalized logistic regression (OR 4.72, 95%&#x2009;CI 2.57 to 8.56; P<0.001). Adding ASIL status to the prespecified clinical model increased the apparent AUC from 0.705 to 0.763 (DeLong P=0.010) and improved reclassification. Preprocedural ASILs were independently associated with inhospital stroke after PTAS in patients with severe sICAS. Incorporation of ASIL status into a prespecified clinical model was associated with improved apparent within cohort discrimination and reclassification, but external validation is required before clinical application.

Health information technology (HIT) is now integral to healthcare delivery, supporting clinical documentation, prescribing, diagnostics, and care coordination. Although these technologies offer substantial benefits, they have also introduced new patient safety risks that are often difficult to anticipate, detect, or manage. Many HIT-related safety problems arise not from isolated technical failures or individual mistakes, but from complex interactions between digital systems, clinical work practices, organisational structures, and governance arrangements. Traditional patient safety models that focus on discrete errors or linear causality are therefore insufficient for explaining how digital risks emerge and persist in practice. This article develops a sociotechnical theory of HIT-related risk grounded in patient safety science and sociotechnical systems theory. The theory is informed by empirical insights from incident-based research on HIT-related safety problems and synthesises evidence from real-world incident narratives. It adopts a conceptual, theory-building approach informed by purposive, iterative engagement with the relevant literature on health IT safety, sociotechnical systems, and resilience-oriented patient safety frameworks. Rather than analysing a single dataset, the paper identifies recurring mechanisms through which digital risks arise, remain hidden, propagate across contexts, and become recoverable or not. The proposed theory conceptualises HIT-related risk as a dynamic process involving four interrelated mechanisms: risk emergence, risk concealment, risk propagation, and recoverability. Risks emerge through misalignments between system design, configuration, and clinical workflows; they are concealed by automation, information fragmentation, and adaptive workarounds; they propagate through tightly coupled digital infrastructures and shared dependencies; and their recoverability depends on organisational capacity for detection, escalation, and learning. Together, these mechanisms explain why HIT-related incidents may affect multiple patients or services, why attribution to individual error is misleading, and why safety problems may persist despite corrective efforts. By reframing HIT-related incidents as manifestations of system-level vulnerabilities rather than isolated failures, this sociotechnical theory provides a coherent explanatory framework for understanding digital patient safety. It highlights how risks can evolve silently within routine practice, vary in visibility and scale, and emphasises the importance of organisational learning, governance, and resilience in managing digital safety risks.

In ADHD, a heterogeneous neurodevelopmental condition, behavioral and motor manifestations may reflect multiple inefficient or perturbed inhibitory systems. To evaluate Transcranial Magnetic Stimulation (TMS) evoked cortical silent period (CSP) duration, an indicator of GABA B receptor-mediated inhibition in motor cortex, as a potential biomarker of Attention-Deficit/Hyperactivity Disorder (ADHD) in children. We retrospectively analyzed TMS data, obtained using both round and figure-of-8 coils, from three cross-sectional studies conducted in 8- to 12-year-old children with ADHD (n=79; 10.7 +/- 1.5 years old) and age-and-sex-matched typically-developing controls (n=96; 10.5 +/- 1.4 years old). Median CSP was 32% shorter in ADHD (p=0.02). Regression analysis demonstrated a relationship between shorter CSP and both lower active motor thresholds (p < 0.0001) and more severe hyperactivity symptom rating (p = 0.026). Test-retest CSP measures in 83 children showed moderate reliability (intraclass correlation 0.77 [ADHD], 0.75 [controls]). TMS-evoked CSP may be a useful biomarker in future investigations of ADHD subtypes, domains of impaired function, or treatment outcomes.

The ipsilateral silent period (iSP) is used to study interhemispheric control of voluntary motor output. It involves a brief suppression of electromyographic (EMG) activity in a muscle during isometric contraction, triggered by Transcranial Magnetic Stimulation (TMS) over the ipsilateral primary motor cortex (M1). The aim of this study was to investigate cortical activity associated with iSP. The study involved 28 healthy right-handed volunteers who performed maximal contractions of the left hand (unimanual) or both hands (bimanual) across conditions with and without TMS. We combined TMS to left M1 with functional Near-Infrared Spectroscopy (fNIRS) over the right hemisphere. EMG was recorded from the hand muscles to quantify the iSP. A significantly greater normalized iSP area was found in the TMS bimanual condition compared to the unimanual one, with a strong correlation between the two. fNIRS revealed higher oxyhemoglobin (HbO) concentration changes in the No TMS condition than in the TMS conditions. Specifically, TMS induced HbO decreases in motor, prefrontal, premotor, parietal, and temporal areas. Reductions in premotor and parietal areas correlated with M1 activity decrease only in unimanual condition. In TMS conditions, a positive correlation was found between fNIRS HbO values in associative parietal cortex and the normalized iSP area: the higher the HbO concentration changes, the greater the inhibition. These findings show reduced M1 activity and demonstrate that a broader frontoparietal network is influenced by the transcallosal motor output. These findings contribute to a better understanding of interhemispheric inhibition and may have implications for the study of neurological disorders.

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Paint-derived particles are increasingly recognised as a major contributor to marine microplastic pollution, yet emissions from active vessels under routine operational conditions remain poorly characterised. We tested the hypothesis that exposed deck coatings on operational ships continuously generate and accumulate paint-derived micro- and meso-particles in the absence of maintenance activities. Samples were collected from accumulation zones adjacent to drainage points on three vessel types: an offshore support vessel, a container ship, and a liquefied natural gas carrier. Size-fractionated material was analysed using microscopy, FTIR/NIR spectroscopy, and multispectral imaging. Across vessels, more than 90% of classified particles were paint-derived fragments or iron oxide-rich corrosion products, while a minor fraction consisted of synthetic polymer fibres and fragments. Although the study design does not allow calculation of emission rates per unit area, the consistent presence and dominance of coating-derived debris across vessel types provide field-based evidence that routine weathering of deck coatings represents an ongoing and currently unregulated source of micro-sized particulate pollution. These findings identify exposed ship superstructures as a previously undercharacterised emission pathway and support the inclusion of coating degradation in ship-borne microplastic inventories and maritime sustainability frameworks.

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Cryoglobulinemia is an immune complex-mediated disorder that can be associated with autoimmune diseases, lymphoproliferative disorders, and chronic infections. Renal involvement can be a prominent manifestation and may occasionally be the initial clue to an underlying systemic condition. Here, we describe a 33-year-old woman who presented with pedal edema, intermittent arthralgia, hematuria, and impaired renal function. Kidney biopsy demonstrated characteristic intraluminal pseudothrombi with dominant immunoglobulin M deposition, consistent with cryoglobulinemic glomerulonephritis. Subsequently, serologic testing confirmed mixed cryoglobulinemia. Further evaluation revealed strong positivity for anti-Sj&#xf6;gren syndrome-related antigen-A and anti-Sj&#xf6;gren syndrome-related antigen-B antibodies, and a labial salivary gland biopsy fulfilled the 2016 American College of Rheumatology European Alliance of Associations for Rheumatology criteria for Sj&#xf6;gren syndrome, despite the absence of sicca symptoms. Treatment with corticosteroids and rituximab led to significant improvement in renal function. The clinical course was complicated by secondary thrombotic microangiopathy, which responded to plasma exchange. This report highlights the diagnostic value of kidney biopsy in uncovering occult systemic autoimmune disease and emphasizes that Sj&#xf6;gren syndrome may initially present with isolated renal manifestations. Early recognition is essential for the timely initiation of appropriate immunomodulatory therapy.

Amniotic fluid embolism is a serious complication of pregnancy where fetal cells, amniotic fluid, and debris enter the maternal circulation, leading to cardiovascular collapse, respiratory issues, and disseminated intravascular coagulation, which can cause acute hemorrhage. Although the exact cause of this embolization is unknown, it frequently occurs in healthy women during pregnancy, after obstetric procedures, or within 48 hours after delivery. Early symptoms of amniotic fluid embolism are often nonspecific, potentially leading to misdiagnosis and increased maternal mortality and morbidity. The goal of this review is to synthesize the current literature on early diagnosis methods, increase awareness and understanding of AFE, and ultimately improve outcomes for mothers and their babies. The importance of early recognition and intervention is also highlighted, as well as the potential for long-term complications such as cognitive disabilities in affected infants. We conducted a literature review and highlighted articles that pertained to the historical perspectives of the disease, its pathophysiology, diagnosis, and management. Sources, including PubMed, were used as search engines, and applicable articles were cited as references. AFE is one of the leading causes of maternal mortality and morbidity, as misdiagnosis is prevalent due to a lack of definitive diagnostic protocols for AFE. While new diagnostic methods are available, further study is needed to ensure that disease sensitivity is accurate. Further research is needed to understand the mechanism and presentation of AFE, as prompt intervention is associated with positive maternal and fetal outcomes.

The main unmet need of Parkinson's disease (PD) is the lack of a therapy able to slow progression. The field is shifting from syndromic diagnosis toward biologically anchored definitions and staging, enabling PD identification before motor onset. In this context, imaging biomarkers provide in vivo measures to identify subtypes, enrich cohorts, and track changes in disease-modifying trials. This review focuses on the role of monoaminergic imaging for preclinical intervention. Monoaminergic imaging captures both the core substrate of motor phenoconversion and extranigral mechanisms underlying early non-motor symptoms. Presynaptic dopaminergic imaging remains the most robust marker of conversion risk in prodromal cohorts, while noradrenergic and serotonergic imaging delineate early brainstem and limbic involvement. Peripheral autonomic imaging further extends biomarker coverage, with cardiac sympathetic imaging detecting early extracerebral denervation in prodromal stages. Together, harmonised monoaminergic imaging provides a unifying framework for staging and clinical trial readiness.

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