Background: Breast clip marker movement after ultrasound-guided biopsy can negatively affect lesion re-localisation rates and surgical outcomes, underscoring the need for improved understanding of the factors influencing clip displacement. Thus, this study aimed to compare four different breast clip markers and identify risk factors for clip migration and dislocation after ultrasound-guided placement. Methods: This retrospective study included 350 patients who underwent ultrasound-guided biopsy of a newly diagnosed breast lesion with placement of one of four types of breast clips (UltraClip Dual Trigger Biodur 108 Coil Marker [UC], TUMARK Professional [TP], TUMARK Vision [TV] and HydroMARK Breast Biopsy Site Marker [HM]). Clip migration and dislocation were assessed immediately after placement and during follow-up imaging for at least 3 months. A binary logistic regression analysis was performed to identify predictors of clip dislocation including lesional, perilesional and procedural parameters. Results: Clip migration rates were 26.0%, 18.0%, 10.0% and 25.0% and clip dislocation rates were 14.0%, 20.0%, 9.0% and 38.0% for UC, TP, TV and HM, respectively. Features significantly associated with clip dislocation included predominantly fatty surrounding tissue (p = 0.046) with low perilesional shear wave velocities (p = 0.054), smooth lesion contours (p = 0.041), soft lesion strain elastography (p =0.001), low clip-to-lesion-surface distance (p = 0.002) and the use of an HM breast clip (p = 0.032). Conclusions: The type of breast clip-marker, as well as perilesional and lesional characteristics, influence the likelihood of clip dislocation. Notably, the hydrogel-coated clip (HM) exhibited the highest rate of dislocation.

ABSTRACT Background Evidence suggests psychological factors including personality traits can have impact on the development and course of irritable bowel syndrome (IBS) and associated health‐related quality of life (HrQoL), with large individual heterogeneity. Main aim of this study was to examine between‐persons associations and within‐sample concurrent associations of the personality traits neuroticism, extraversion, conscientiousness, openness and agreeableness with gastrointestinal (GI) symptoms, psychological factors and HrQoL in IBS‐patients. Methods Cross‐sectional data from an observational IBS‐study (n = 194, mean age 51.36 years, 74.4% female) was used. Patients completed the Big Five Inventory (BFI)‐44 questionnaire regarding personality traits, and questionnaires on symptom severity (GSRS‐IBS), general anxiety (HADS‐A, GAD‐7), GI‐specific anxiety (VSI), and HrQoL (36‐SF). A multivariable regression model and a network correlation analysis were performed. Key Results Neuroticism showed the most relevant between‐persons associations, confirmed by within‐sample concurrent associations: associated with increased GI‐specific anxiety (B 7.234, p = 0.040), general anxiety (B 0.954, p = 0.040), and decreased mental HrQoL (B—3.576, p = 0.007). Extraversion showed an opposing pattern including increased mental HrQoL (B = 4.266, p = 0.001), with strong association to neuroticism. While no significant between‐person associations emerged between abdominal pain and personality traits, significantly associated to higher general anxiety (B = 6.304, p < 0.001) and GI‐specific anxiety (B = 0.034, p < 0.001) were shown. Conclusion This study reinforces the association between personality traits and IBS, highlighting the integral connection to not only other psychological factors but also GI‐symptoms. These findings support a multifactorial, personalized approach to IBS, advocating for the integration of personality assessment—particularly neuroticism and extraversion—into the biopsychosocial model.

SARS-CoV-2 infection is driven by extensive interactions between viral proteins and host cellular factors, yet the structural properties of host proteins within these interaction networks remain incompletely understood. Intrinsically disordered proteins and regions are key contributors to protein-protein interaction networks due to their conformational flexibility and associated with it multifunctionality, binding promiscuity, and regulatory versatility. In this study, we performed a systematic, proteome-wide analysis of intrinsic disorder in human proteins interacting with SARS-CoV-2 by integrating five experimentally validated interaction datasets comprising 2055 unique host proteins. Using disorder prediction, structural confidence assessment, functional and domain annotation, protein-protein interaction network analysis, phase-separation propensity estimation, and independent validation with the D2P2 platform on a selected set of proteins, we characterized the structural organization of the SARS-CoV-2 human interactome. Our results reveal a balanced distribution of ordered and disordered host proteins, distinct functional and domain signatures across disorder classes, consistent inverse relationships between disorder and structural confidence, and increased network connectivity and phase-separation propensity among highly disordered interactors. These findings indicate that SARS-CoV-2 exploits structural diversity within the host proteome rather than preferentially targeting a single disorder class and highlight intrinsic disorder as a key contributor to interaction plasticity and network organization at the systems level.

BACKGROUND Enteric infectious diseases claim more than 1 million lives annually and are among the top ten causes of death in children younger than 5 years. Remarkable global investment has been dedicated to enteric infectious disease prevention and control; however, the shifting global health landscape is testing the continuance of progress. To evaluate the current status and guide future interventions, we present the latest epidemiological estimates of enteric infectious diseases from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2023 and assess progress towards the Global Action Plan for the Prevention and Control of Pneumonia and Diarrhoea (GAPPD) mortality target of fewer than 20 deaths per 100 000 children younger than 5 years by 2025. METHODS We quantified the incidence, mortality, and disability-adjusted life-years (DALYs) of enteric infectious diseases by age, sex, and year across 204 countries and territories from 1990 to 2023. In GBD 2023, the following were considered under the category of enteric infectious diseases: diarrhoeal diseases, enteric fever (typhoid and paratyphoid), invasive non-typhoidal Salmonella spp (iNTS) infections, and other intestinal infectious diseases. We also examined 15 aetiologies contributing to diarrhoeal diseases. Incidence and prevalence were estimated with DisMod-MR (version 2.1), a Bayesian meta-regression tool, drawing on data from systematic reviews, population-based surveys, claims data, and hospital sources. Cause-specific mortality was modelled with Cause of Death Ensemble Modelling based on data from sources including vital registration, mortality surveillance, verbal autopsy, and minimally invasive tissue sampling. Years of life lost and years lived with disability were computed and combined to derive DALYs. For aetiology-specific estimation, population-attributable fractions (PAFs) for 15 pathogens were derived with a counterfactual framework. Point estimates and 95% uncertainty intervals (UIs) were generated from 250 draws from the posterior distribution. FINDINGS In 2023, enteric infectious diseases resulted in an estimated 1·27 million (95% UI 0·963-1·68) deaths globally, declining from 3·69 million (3·04-4·56) in 1990. The global age-standardised mortality rate (ASMR) decreased from 74·1 (62·0-92·9) per 100 000 population to 16·4 (12·6-21·3) per 100 000 population during the same period. Diarrhoeal diseases accounted for most deaths in 2023 (1·11 million [0·811-1·54]), followed by enteric fever and iNTS. South Asia and sub-Saharan Africa remained the most affected regions in 2023, with 599 000 (441 000-882 000) and 501 000 (373 000-648 000) deaths due to enteric infectious diseases, respectively, predominantly from diarrhoeal disease. Rotavirus was the leading cause of all-age diarrhoeal disease deaths (PAF 16·3% [12·0-21·5]), followed by norovirus (10·2% [2·4-17·0]) and Shigella spp (9·3% [5·4-15·2]). Among children younger than 5 years, PAFs of deaths due to diarrhoeal diseases were 40·2% (32·5-48·5) for rotavirus, 24·0% (15·1-36·7) for Shigella spp, and 23·4% (13·7-34·3) for adenovirus. Across 204 countries and territories, 141 met the GAPPD mortality target in 2023. The driving aetiologies among countries that did not meet the target in 2023 varied slightly by GBD super-region, but the highest or second-highest number of deaths in children younger than 5 years were consistently attributed to rotavirus. Astrovirus and sapovirus, newly included in GBD 2023, were responsible for 24 600 (6290-49 000) and 18 800 (4650-44 400) deaths, respectively, in 2023, mainly in children younger than 5 years. INTERPRETATION Our findings show that mortality and ASMRs of enteric infectious diseases declined substantially between 1990 and 2023. This decline is consistent with the expansion of public health measures and broader socioeconomic development. However, the burden in 2023 remains considerably high, with the highest mortality concentrated in sub-Saharan Africa and south Asia. Considering that more than a quarter of all countries had yet to meet the GAPPD mortality target in 2023, sustained efforts are needed to address the persistent burden in affected countries and to adapt to the changing global health landscape. FUNDING Gates Foundation.

Background: Hofbauer cells (HBCs) are the only immunocompetent cells within the stroma of chorionic villi and play a key role in immune regulation and placental development throughout gestation. Their phenotype, abundance, and proliferative activity change in accordance with the needs of the fetoplacental unit. Methods: Thirty healthy human placentas across all three trimesters were analyzed. Samples were processed using standard histological protocols and immunohistochemically stained with CD45, CD68, CD86, and Ki-67 markers. Morphometric analysis was performed to determine the following parameters: percentage of HBCs, numerical areal density, and proliferative index. Results: HBCs were immunoreactive for CD45 and CD68, while CD86 immunoreactivity was not observed in any trimester. The proportion of HBCs was highest in the second trimester and lowest in the third. Numerical areal density was highest in the second trimester (22.21 ± 3.86) and lowest in the first (8.27 ± 4.18). The proliferative index was highest in the first trimester (82.45 ± 10.19%), decreased significantly in the second, and was completely absent in the third trimester. Conclusions: During physiological placental development, Hofbauer cells maintain a predominantly non-M1 macrophage phenotype, accompanied by a gradual reduction in proliferative activity.

Diabetic nephropathy (DN) is a major microvascular complication of diabetes mellitus and the leading cause of end‐stage renal disease. Oxidative stress and inflammation are central drivers of DN progression, yet no effective therapies exist to prevent or delay renal injury. This study investigated the renoprotective effects of glycine (GLY), N‐acetylcysteine (NAC), and their combination administered at early versus late stages of streptozotocin induced diabetes. Forty‐eight male Wistar rats (n = 48) were allocated into five groups: healthy controls (Group 1, n = 6), untreated diabetic rats (Group 2, n = 6), and three treatment groups (Groups 3–5, each n = 12). Diabetes was induced by a single intraperitoneal streptozotocin injection (55 mg/kg). Group 3 received NAC (100 mg/kg), Group 4 received GLY (250 mg/kg), and Group 5 received NAC + GLY. Each treatment group was subdivided into early (6 week, n = 6) and late (12 week, n = 6) intervention subgroups. Treatments were administered orally. Renal tissue was evaluated using classic histology, geometric morphometric analysis, and biochemical assays of superoxide dismutase (SOD) and myeloperoxidase (MPO). Statistical analyzes were performed using ANOVA with appropriate post hoc tests (p < 0.05). Untreated diabetic rats (Group 2) showed significantly decreased SOD activity, increased MPO levels, marked mesangial matrix expansion, glomerular hypercellularity, tubular epithelial degeneration, and interstitial inflammation with fibrosis. NAC (Group 3) and GLY (Group 4) each improved oxidative stress markers and partially restored glomerular and tubular morphology, with early treatment subgroups exhibiting more substantial benefit than late subgroups. The combined NAC + GLY therapy (Group 5) demonstrated the strongest renoprotective effect, preserving renal structure and biochemical parameters closest to healthy controls. To conclude, early combined administration of glycine and N‐acetylcysteine yields superior protection against diabetes‐induced renal injury compared with individual treatments. These findings support the therapeutic potential of antioxidant‐amino acid combinations in preventing or delaying diabetic nephropathy.