First Hospital of Qinhuangdao

Standardized clinical photography is crucial for diagnosis, documentation, and research. However, existing protocols often rely on expensive equipment or operator skill, limiting adoption in resource-limited settings. We developed a laser-level-assisted protocol for standardized facial photography using a smartphone. A total of 100 patients were photographed using both conventional and laser-level-assisted methods by two attending physicians. Three standard views were captured. Subjective image quality was evaluated using a modified 5-point Likert scale, and objective assessment was performed using ImageJ-based measurements. Statistical comparisons were conducted using linear mixed-effects models to account for within-subject clustering across methods, operators, and views. Mixed-effects models showed that laser-level-assisted photography required less acquisition time than conventional photography (estimated mean difference = -4.06 s, 95% CI -4.71 to -3.44; P < 0.001) and achieved higher subjective scores (estimated mean difference = +0.64 points, 95% CI +0.60 to +0.68; P < 0.001) and objective scores (estimated mean difference = +1.52 points, 95% CI +1.25 to +1.79; P < 0.001). Inter-rater reliability for subjective scoring was excellent (ICC = 0.93). The laser-level-assisted workflow also showed minimal operator-related variation compared with conventional acquisition. Laser-level-assisted smartphone photography provides a reproducible, cost-effective, and operator-independent approach for standardized facial medical imaging. This scalable method may facilitate clinical documentation, training, and mobile healthcare, particularly in resource-constrained settings. This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Introduction: Current guidelines lack consensus on fibrinogen replacement thresholds in critical hemorrhage. This study aims to establish evidence-based supplementation thresholds and optimal targets for ICU patients with major bleeding, providing a framework for individualized coagulation management. Methods: This prospective multicenter cohort study enrolled 197 patients with severe hemorrhage and coagulopathy from 12 tertiary ICUs in China. Standardized systems collected demographics, laboratory parameters, and interventions. Analysis comprised two phases: (1) Restricted cubic spline (RCS) models evaluated nonlinear associations between baseline fibrinogen and outcomes (hemostasis, ICU mortality), identifying a critical threshold at 1.54 g/L; (2) Post-treatment fibrinogen peaks (within 72h) were stratified into subgroups based on prior MIMIC-IV validation: < 1.54 g/L (low-risk), 1.54–2.0 g/L (intermediate), 2.0–2.5 g/L (target), ≥2.5 g/L (high-level). Statistical analyses included Cochran-Armitage test (dose-response), Firth’s regression (small-sample bias correction), and Kruskal-Wallis tests with Benjamini-Hochberg FDR correction (FDR< 0.05; transfusion heterogeneity). Results: We enrolled 197 patients with massive hemorrhage (treatment: n=98; control: n=99). Baseline data showed the treatment group had significantly greater blood loss (1735vs.967 mL, P=0.013), lower fibrinogen (1.49vs.2.04 g/L, P=0.001), and higher APACHE II scores (19.5vs.16.7, P=0.047). Pretreatment fibrinogen showed nonlinear associations with hemostasis and ICU mortality (both Pnon-linear< 0.001), identifying a critical threshold at 1.54 g/L. Post-treatment fibrinogen levels of 2.0-2.5 g/L achieved a hemostasis rate of 75%-80%; higher levels (2.5-3.5 g/L) showed slightly reduced efficacy. Mortality was 35% for levels < 1.5 g/L, significantly decreasing to 15% at 2.0-2.5 g/L, and approaching zero at 2.5-3.5 g/L. Post-treatment levels also showed nonlinear associations with outcomes (both Pnon-linear< 0.001), with a critical threshold at 2.5 g/L. Conclusions: Fibrinogen levels predict outcomes in critically ill patients with massive hemorrhage. Initiation of fibrinogen supplementation is recommended when levels fall below 1.5g/L, targeting 2.0–2.5g/L as the optimal therapeutic window to improve prognosis.

Background Surgical management of chronic ear diseases, particularly middle ear cholesteatoma and chronic otitis media, often results in significant skin defects in the external auditory canal (EAC) and auricular region. Objectives To evaluate the clinical efficacy and safety of xenogeneic acellular dermal matrix (xeno-ADM) in repairing ear skin defects following surgical resection of middle ear pathologies. Material and methods A prospective cohort study was conducted from March 2024 to April 2025 at a single tertiary care center. One hundred and twelve consecutive patients with ear skin defects underwent reconstruction using xeno-ADM. Primary outcomes included epithelialization time, functional recovery (ear canal patency, hearing improvement), and postoperative complications. Secondary outcomes included surgical difficulty, patient satisfaction, and physician evaluation. Air conduction threshold changes were measured pre- and postoperatively. Pain was assessed using Visual Analog Scale. Results Mean epithelialization time was 36.0 days. All patients achieved complete epithelialization with 100% ear canal patency. Hearing improved significantly with mean air conduction threshold reduction of −13.32 ± 14.67 dB, with 94% of patients showing improvement or stability. Postoperative pain was minimal. Complications were rare: mild exudate in 75.0%, local infection in 0.9%, partial membrane loss in 13.4% (successfully managed with reapplication). No rejection reactions occurred. Patient satisfaction was 100% for both appearance and function. Conclusions and significance Xeno-ADM demonstrates excellent efficacy and safety for ear skin defect repair, offering rapid epithelialization, significant hearing improvement, minimal pain, and high patient satisfaction during the mean follow-up of 6 months. However, the absence of a control group limits the strength of these conclusions, and long-term outcomes remain unknown due to the limited follow-up duration.

This study compared the incidence of adverse events in patients with unresectable intrahepatic cholangiocarcinoma (ICC) receiving drug-eluting bead transarterial chemoembolization (DEB-TACE) either alone or in combination with immune checkpoint inhibitors (ICIs). A retrospective analysis was conducted on patients with unresectable ICC who received either DEB-TACE alone or in combination with ICIs treatment from February 2019 to April 2024. Of the enrolled 247 ICC patients, 178 received DEB-TACE combined with ICIs treatment, while 69 patients received DEB-TACE alone. Adverse events were recorded and compared between the two groups. Binary logistic regression analysis was used to determine the significant risk factors of adverse events. The overall incidence of adverse events was 19.1% (34/178) in the DEB-TACE+ICIs group and 13.0% (9/69) in the DEB-TACE group. The DEB-TACE+ICIs group exhibited a statistically significantly higher incidence of liver abscesses than the DEB-TACE group (13.5% vs. 2.9%, P = 0.015). Binary logistic regression analysis showed that combined ICIs treatment (P = 0.027, odds ratio = 5.583, 95% confidence interval: 1.212-25.725) and grade 1 artery occlusion (P = 0.001, odds ratio = 31.380, 95% confidence interval: 4.098-240.263) were independently associated with an increased risk of developing liver abscess. Combined ICIs treatment and grade 1 arterial occlusion were independently associated with an increased risk of liver abscesses. Clinicians should closely monitor for liver abscess formation when administering DEB-TACE in combination with ICIs, particularly in patients with grade 1 arterial occlusions.

To establish a new diagnostic model to predict the split renal function impairment in patients with obstructive hydronephrosis. A set of retrospective data was analyzed, including enhanced CT of 382 kidney data from 191 patients with obstructive hydronephrosis collected from 2017 to 2024. These kidneys were divided into renal dysfunction and non-renal dysfunction group. Risk factors for renal dysfunction were identified using logistic regression analysis, and a new diagnostic model was established and then the ROC curve was used to evaluate the effect of the diagnostic model to diagnose in diagnosing renal function impairment. In the training set, renal cortex volume, venous phase renal medulla CT values (VP-HuRM), and hydronephrosis were identified as independent risk factors for renal function impairment with odds ratios of 0.959 (0.946–0.972), 0.987 (0.977–0.996), and 4.625 (2.110–10.138), respectively. The diagnostic accuracy of the model (AUC) for detecting renal function impairment was 0.896 (0.858–0.934), with the Cut-off value of-0.124. The AUC for distinguishing between the non-renal dysfunction group and mild renal dysfunction group, and between severe renal dysfunction group and mild renal dysfunction group were: 0.852 (0.801–0.903), 0.848 (0.780–0.916), respectively. The AUCs in the validation set were: 0.928 (0.882–0.973), 0.885 (0.815–0.954), 0.886 (0.797–0.975), respectively. The diagnostic model based on CT with enhancement has certain clinical value in predicting the degree of split renal function impairment, aiding in the clinical accurate diagnosis of split glomerular filtration rate (sGFR) in patients with obstructive hydronephrosis and holding significant clinical value.

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CDK2 is a principal mediator of CDK4/6 resistance. Concurrent CDK2/4/6 blockade may be effective in treating HR-positive, HER2-negative advanced breast cancer (ABC). This randomized, double-blind, parallel-controlled, phase 3 trial (ClinicalTrials.gov, NCT05375461) assessed the efficacy of culmerciclib, a CDK2/4/6 inhibitor, plus fulvestrant in ABC. Patients with HR-positive, HER2-negative, locally recurrent or metastatic breast cancer were randomized (2:1) to receive culmerciclib plus fulvestrant or matching placebo plus fulvestrant. Between March 18, 2022 and March 3, 2023, 293 pretreated patients (median age 53.0 years; pre- or perimenopausal 42.3%; bone metastasis 65.2%) were randomized to assigned treatments. At this prespecified interim analysis, culmerciclib plus fulvestrant extended the median investigator-assessed progression-free survival (PFS) significantly, the primary endpoint, as compared with placebo plus fulvestrant (16.6 months, 95% CI 13.8 to not evaluable versus 7.5 months, 95% CI 5.3 to 11.0; hazard ratio 0.36, 95% CI 0.26–0.51; stratified log rank test P < 0.001). Consistent effects were observed across diverse subgroups of patients. At a median follow-up duration of 13.8 months, overall survival was immature. The investigators-assessed objective response rate was 40.2% (95% CI, 33.3–47.5) for culmerciclib compared to 12.1% (95% CI 6.4–20.2) for placebo (stratified Mantel-Haenszel χ2 test P < 0.001). Diarrhea (87.1%) and neutropenia (80.4%) were the most common toxicities with culmerciclib plus fulvestrant. In conclusion, this randomized clinical trial met its primary outcome. Culmerciclib plus fulvestrant is well tolerated and leads to a significant gain in PFS of pretreated HR-positive HER2-negative ABC patients.

Abstract Background Oral carcinoma is a prevalent malignancy with limited therapeutic options, highlighting the need to elucidate molecular mechanisms driving tumor progression. Aim This study explores the interplay between LKB1 and STAT3 signaling pathways in Oral carcinoma pathogenesis. Methods Two Oral carcinoma cell lines including HSC-3 and KB were used. Results We demonstrate that honokiol, an LKB1 activator, unexpectedly enhances the growth of oral carcinoma cells, while genetic knockdown of LKB1 further promotes cell proliferation, suggesting a context-dependent tumor-suppressive role for LKB1 in Oral carcinoma. Mechanistically, honokiol inhibits phosphorylation of STAT3 (p-STAT3), a key oncogenic driver, in oral carcinoma cells. Consistent with this, pharmacological inhibition of p-STAT3 using Stattic suppresses Oral carcinoma cell growth, whereas activation of STAT3 with Colivelin promotes proliferation, underscoring the critical role of STAT3 signaling in Oral carcinoma progression. Importantly, Colivelin rescues honokiol-mediated growth inhibition, indicating that honokiol exerts its antitumor effects, at least in part, through suppression of STAT3 activity. These findings reveal a novel crosstalk between LKB1 and STAT3 pathways in oral carcinoma and suggest that targeting STAT3 signaling may represent a promising therapeutic strategy for oral cancer. Conclusion This study provides new insights into the molecular mechanisms underlying oral carcinoma progression and identifies potential targets for therapeutic intervention.