University Medical Center Freiburg

CT perfusion (CTP) is widely used to assess infarct core in acute stroke, yet real-world data on its reproducibility and temporal dynamics are limited. We retrospectively identified patients with repeated CTP scans. Core and hypoperfusion volumes were quantified using standard thresholds (CBF <30 %, Tmax >6 s). Clinical and imaging data were reviewed to identify cases with disruptive events. We analyzed scan-to-scan differences in core volume, hypoperfusion volume, ASPECTS, and intensity metrics, including median Tmax (in hypoperfusion), CBF, and NCCT HU (in core), using Bland-Altman analysis and assessed their association with time between scans. Among 32 patients with repeated CTP (26 with repeated NCCT), three were excluded due to disruptive events. In the remaining 29 cases, mean scan-to-scan differences for infarct core volume (4.8 ± 19.6 mL), hypoperfusion volume (3.86 ± 39.1 mL), and ASPECTS (-0.4 ± 1.6) indicated minimal systematic bias at the group level but substantial variability. Correlation coefficients were high (r = 0.90, 0.93, and 0.70, respectively; all p < 0.0001), and no statistically significant paired differences or association with scan interval were observed. Intensity-based metrics likewise showed minimal bias with lower variability (Tmax -0.3 ± 1.07 s; CBF -3.11 ± 7.3 %; NCCT HU -3.0 ± 4.9 %), high correlations (Tmax r = 0.87, CBF r = 0.91, NCCT HU r = 0.69; all p < 0.02), and no association with time between scans. Repeated CTP showed no systematic group-level scan-to-scan bias suggestive of infarct growth, while a substantial degree of variability was observed, with intensity-based metrics demonstrating lower variability than volume estimates. These findings support temporal consistency of perfusion-derived metrics at the group level and question the applicability of linear infarct growth rate (IGR) concepts to perfusion imaging, which primarily reflects a hemodynamic state rather than time-dependent tissue progression.

Stress significantly influences eating behavior, yet individual responses vary. Binge eating - a core feature of Binge Eating Disorder and Bulimia Nervosa - is frequently triggered by acute stress. One proposed mechanism is that stress increases the motivational salience of food cues, which could promote craving and food intake. To test this idea experimentally, this study examined how stress affects attentional bias toward food, and how such changes relate to food craving and food intake in individuals with binge eating behaviors compared with individuals without binge eating. Using a mixed experimental design, 130 participants (68 with binge eating, 62 without binge eating) completed sessions with and without stress induction via a video-conference Trier Social Stress Test. Attentional bias was assessed via the Dot Probe Paradigm and eye tracking, food craving was measured via self-reports, and food intake was measured behaviorally. Stress did not significantly change attentional bias toward food, nor did it affect food intake. Stress did increase craving in the group with binge eating, indicating that stress enhanced the motivational value of food. The absence of corresponding changes in attentional bias suggests that heightened craving under stress does not necessarily translate into measurable shifts in attentional allocation toward food cues, or that stress may influence motivational processes without altering overt attentional patterns. Another possibility is that methodological restraints specific to our study design limited the detection of stress-related changes in attentional processes. Further research is needed to clarify the role of attentional processes in stress-related eating, especially regarding binge eating.

Atrial fibrillation (AF) is a well-known risk factor for ischaemic stroke. Emerging evidence suggests that atrial cardiomyopathy (AtCM), independent of AF, may be a key contributor to stroke risk. We aimed to evaluate whether non-invasive AtCM markers assessed by electrocardiography (ECG), transthoracic echocardiography (TTE), and blood-based biomarkers provide incremental diagnostic value beyond established clinical risk factors for identifying cerebral stroke lesions on magnetic resonance imaging (MRI). We analysed 1794 Hamburg City Health Study participants who underwent cerebral MRI with available baseline 12-lead ECG and TTE in sinus rhythm. Logistic regression analyses were performed to identify associations between non-invasive AtCM markers and stroke lesions. The incremental discriminatory performance of these markers beyond clinical risk factors was assessed. Stroke lesions were present in 152 participants (8.5%). Male sex, history of prior AF, and higher CHA2DS2-VA score were significantly associated with stroke lesions. Among AtCM markers, amplified P-wave duration (APWD), P-wave area in lead II, PR interval, left atrial volume index, left atrial ejection fraction, and NT-proBNP were also significant. Combining both clinical and AtCM markers, only CHA2DS2-VA score (OR: 1.95 per point, 95% CI: 1.49-2.55, P < 0.001) and P-wave area in lead II (OR: 0.99 per 100 µV·ms, 95% CI: 0.98-1.00, P = 0.031) remained independent predictors. However, this resulted in only marginal improvement in discrimination (ΔAUC: 0.03, 95% CI: 0.0001-0.0594) compared with the clinical risk factor model alone. The incremental diagnostic value of AtCM markers beyond clinical risk factors for MRI-defined cerebral lesions is limited, likely reflecting the heterogeneous aetiology of stroke lesions in a general population cohort.

Transactive response DNA binding protein 43 kDa (TDP-43) pathology, is a central molecular hallmark of amyotrophic lateral sclerosis (ALS). However, the underlying triggers are incompletely understood. Here, we show that infection with herpes simplex virus (HSV) induces molecular hallmarks of ALS in various in vitro and in vivo models and is associated with an increased risk of ALS in human population data. German healthcare provider data (n = 238,440) and herpesvirus serology of an ALS patient and control cohort (n = 1,100) showed that HSV infection elevated the ALS risk by 210% and odds by ~65%, respectively. On a molecular level, HSV infection promoted TDP-43 pathology in neuronal cell models, human iPSC-derived motoneurons and cerebral organoids, mice, and human tissue sections. This effect was triggered by HSV-1 or 2, but not by several other related herpesviruses. Mechanistically, the infected cell protein 0 (ICP0) of HSV-1/2 drives TDP-43 pathology by disturbance of promyelocytic leukemia nuclear bodies (PML-NBs), thereby abrogating TDP-43 SUMO2/3ylation. Taken together, we reveal a previously unrecognized association between HSV infection and ALS and clarify the underlying molecular mechanism that drives TDP-43 pathology. Our data may guide future studies into therapeutic and prophylactic interventions against ALS.

Guttae are a hallmark of Fuchs endothelial corneal dystrophy (FECD) and the disease’s progression. A posterior fibrillar layer (PFL) that covers central guttae has been previously described, but its formation and progression remain unclear. This study aims to further investigate the characteristics of guttae and the PFL in FECD. In a well-characterized prospective FECD patient cohort, a total of 43 DMEK (Descemet membrane endothelial keratoplasty) specimens were immunostained for ZO1 or COL1, flat-mounted, and analyzed using differential interference contrast (DIC), autofluorescence (excited at 480 nm), and polarized light microscopy. Guttae and PFL were quantified and correlated with clinical data. Guttae were visualized by DIC and autofluorescence imaging and classified into two types with gradual transition: peripheral, knob-like guttae and central, flat guttae. Guttae with low autofluorescence often were covered by corneal endothelial cells (CEnC). Central guttae were found to be covered by a PFL that contained COL1 and was visualized using polarized light microscopy. The PFL displayed a fibrous structure that blurred guttae in DIC illumination. Its presence correlated with clinical parameters, such as anterior scatter and post-operative corneal edema resolution providing insight into the relation of PFL and FECD severity. The combination of DIC, autofluorescence, and polarized light microscopy provides a robust method for investigating guttae and the PFL. This could facilitate preoperative assessment of corneal donor tissue and enhance postoperative clinical diagnostics by detailed detection of guttae and PFL in patients.

To compare two dispersive ophthalmic viscosurgical devices (OVD), Z-HYALCOAT (investigational) and HEALON EndoCoat (control), with a 3-month postoperative follow-up. Multicenter study conducted in 11 sites across Europe. Prospective, randomized, masked, multicenter post market study. Adult subjects having clear intraocular media excluding the presence of cataract and scheduled for uncomplicated age-related cataract removal by phacoemulsification and IOL implantation in the capsular bag with sole administration of either investigational or control device as per randomization scheme were included in this study. Primary endpoint was the incidence of IOP ≥ 30 mmHg. Other endpoints included slit lamp observations, corneal endothelial cell density (ECD), surgeon-reported device functionality, and rate of adverse events (AEs) and device deficiencies (DDs). In total, 242 subjects were treated in this study (123 with the investigational OVD and 119 with the control OVD). In per-protocol population, 13 eyes (11.2%) from the investigational group and 19 (17.0%) from the control group reached an IOP equal to or higher than 30 mmHg at 8 hours following device use. Slit lamp examinations performed up to 3 months did not reveal any relevant differences between the groups. ECD loss was also similar between the groups. Surgeon-reported OVD functionality was generally favorable and comparable for both devices. This investigation proved the non-inferiority of Z-HYALCOAT to HEALON EndoCoat in terms of IOP spikes and showed the two devices to be highly similar in all evaluated aspects.

The S2K guideline, organized by the German Respiratory Society, is aimed at physicians in Germany, Switzerland, and Austria who perform outpatient or inpatient diagnostic flexible bronchoscopy in adult patients. Its goal is to standardize the procedure, minimize complications, and improve diagnostic safety. The guideline specifically addresses specialists in pulmonology, thoracic surgery, and hospital hygiene, as well as nursing and technical staff. It provides evidence- and consensus-based recommendations on indications, preparation, execution, hygiene measures, and aftercare. Additionally, it serves as an information resource for physicians from other specialties, payers, professional societies, and can support quality management. It applies to medical care in Germany, Austria, and Switzerland and incorporates the latest scientific findings up to the date of publication.