Large language models (LLMs) are increasingly used to write and edit scientific manuscripts; however, their fluency can obscure mismatches between linguistic claim strength and evidential support. This tutorial examines such mismatches through the lens of epistemic integrity, defined as accurate alignment of scientific statements with the quality, strength, and scope of the underlying evidence. It presents sentence-level epistemic markers that require careful human judgment, including reporting verbs, hedges, tense choices, evaluative adjectives and adverbs, and local scope markers. Inappropriate modification of these features can overstate or understate certainty, strengthen or weaken a claim beyond what the evidence warrants, or distort an author’s intended emphasis. The tutorial also addresses discourse-level issues, including the need to clearly distinguish between results and interpretation, shifts in certainty across manuscript sections, consistency in scope limitations, and cumulative changes in evaluative tone. Because LLMs cannot independently assess study design, methodological limitations, disciplinary conventions, or evidential sufficiency, polished revisions may introduce epistemic miscalibration even when they are grammatically correct. Editors should therefore evaluate not only local wording but also the consistency of claims across the manuscript. Human editorial expertise remains essential for preserving rhetorical coherence, evidential accuracy, and scientific integrity in artificial intelligence–assisted academic writing, alongside attention to grammar, style, clarity, and readability.
Purpose The psoas–lumbar vertebral index (PLVI), a marker of central sarcopenia measured using computed tomography (CT) or magnetic resonance imaging (MRI), has been linked to the development of postherpetic neuralgia (PHN). Whether PLVI predicts short-term pain relief after pulsed radiofrequency (pRF) treatment of the dorsal root ganglion (DRG) in established PHN remains unknown. This pilot study examined the association between PLVI and the reduction in numeric rating scale (NRS) pain scores 1 month after pRF. Methods Patients with PHN who underwent DRG pRF and had CT or MRI scans available for PLVI measurement were retrospectively reviewed. Correlations of the NRS reduction rate with PLVI and other variables were assessed, with 95% confidence intervals (CIs). Patients were divided into low- and high-PLVI groups using sex-specific medians and compared; multivariable regression was adjusted for sex. A supplementary responder analysis used thresholds of ≥30% and ≥50% reduction. Results In 19 patients, NRS scores decreased from 4.8±1.7 to 3.2±1.7, with a reduction rate of 29.3%±34.0%. PLVI was not significantly correlated with the reduction rate (r=−0.17; 95% CI, −0.58 to 0.31; P=0.49); neither the reduction rate (P=0.71) nor responder rates differed between the low- and high-PLVI groups. Male sex was associated with a smaller reduction (adjusted B=−47.2 percentage points; 95% CI, −90.9 to −3.5; P=0.036), although the unadjusted group comparison was not significant (Welch P=0.051) and 15 variables were tested without correction for multiple comparisons. Conclusion This pilot cohort showed no detectable association between PLVI and short-term pain relief after pRF; its small size precludes establishing the absence of an association. The exploratory sex difference warrants investigation in larger prospective studies with comprehensive sarcopenia assessment.
Purpose Healthcare planning and resource allocation require accurate estimates of the burden of motor neuron diseases (MNDs). This study evaluated the global impact of MNDs from 1990 to 2021 as part of the Global Burden of Disease (GBD) Study 2021. Methods GBD 2021 data were used to assess the global burden of MNDs from 1990 to 2021 in terms of prevalence, incidence, disability-adjusted life years (DALYs), and deaths. The relationship between MND burden and the Socio-demographic Index (SDI) was also examined. Results Globally, MNDs accounted for 272,732 prevalent cases (95% uncertainty interval [UI], 236,195–313,676), 64,178 incident cases (95% UI, 58,506–70,270), 1,040,566 DALYs (95% UI, 963,064–1,123,956), and 39,082 deaths (95% UI, 35,757–42,433) in 2021. The corresponding age-standardized rates per 100,000 people were 3.31 (95% UI, 2.86–3.80) for prevalence, 0.46 (95% UI, 0.42–0.49) for mortality, and 12.17 (95% UI, 11.24–13.15) for DALYs. From 1990 to 2021, the numbers of prevalent and incident cases increased, but their age-standardized rates decreased by 1.36% and 4.69%, respectively. By contrast, the age-standardized mortality rate increased by 19.84%. MND burden was generally higher in regions with a high SDI, although rates in high-income Asia Pacific were relatively low compared with those in regions with similar SDI values. Conclusion From 1990 to 2021, the absolute burden of MNDs increased, age-standardized prevalence and incidence rates declined slightly, and mortality-related burden increased. These trends underscore the need for evidence-based national and global healthcare planning. Geographic variation in MND burden may reflect regional differences in the roles of sociodemographic and genetic factors.
Irritant contact dermatitis (ICD) is the most common form of contact dermatitis and a leading cause of occupational skin disease, but remains underrecognized relative to allergic contact dermatitis (ACD). Direct chemical or physical injury to the epidermal barrier causes ICD, which can develop in anyone when exposure intensity or duration exceeds the skin’s repair capacity. ICD is increasingly understood to involve more than barrier disruption: it is an innate immune-mediated inflammatory disorder involving keratinocyte-derived cytokines, neutrophil recruitment, C-C motif chemokine ligand 2–C-C motif chemokine receptor 2–interleukin-1β signaling, Toll-like receptor 3, and inflammasome activation. Host factors, particularly atopic dermatitis and filaggrin loss-of-function variants, further influence susceptibility. Clinical phenotypes range from acute irritant reactions to chronic cumulative dermatitis, and occupational wet work is a major preventable exposure. Distinguishing ICD from ACD is difficult because their clinical and histopathological features overlap, they may coexist, and ICD-related barrier damage may facilitate subsequent allergic sensitization. Diagnosis therefore requires assessment of exposure history, lesion distribution, symptom quality, and temporal course, with patch testing when ACD is suspected. Molecular biomarker panels and noninvasive imaging or barrier-assessment techniques may improve diagnostic precision, but remain investigational. Management should prioritize identifying and removing irritants, reducing exposure, implementing appropriate protective measures, and restoring the epidermal barrier. Recognizing ICD as a distinct clinical entity, rather than simply a diagnosis of exclusion, is essential for accurate diagnosis and effective management of contact dermatitis in clinical practice.
