Max Planck Institute for the Study of Religious and Ethnic Diversity

Efficient detection of breathing impairment is critical for treatment and prognosis in neuromuscular disorders. However, standard pulmonary function tests often yield ambiguous results. This prospective study evaluates whether advanced real-time MRI (RT-MRI) combined with deep learning-based image segmentation provides sensitive outcome measures for respiratory dysfunction in late-onset Pompe disease (LOPD), a model disease for diaphragmatic weakness. Eleven Pompe patients (mean age 52.2 years; 55% female) and 11 controls (mean age 50.9 years; 55% female) were included. RT-MRI with a temporal resolution of 50 ms, combined with U-Net-supported lung segmentation, revealed significantly reduced diaphragmatic motion in Pompe patients compared to controls and unmasked paradoxical diaphragmatic motion in Pompe patients (7 of 11). Reduced diaphragmatic sniff velocity and pathological diaphragmatic/thoracic synchronicity were detected in Pompe patients with still normal results in standard pulmonary function tests. Fatty involution of the diaphragm as quantified by fast T1 mapping correlated significantly with functional parameters from RT-MRI and pulmonary function tests. RT-MRI combined with deep learning-based lung segmentation offers novel biomarkers for early detection of respiratory muscle weakness. This new technique provides useful outcome measures for clinical care as well as treatment studies in patients with neuromuscular breathing impairment. The technique can also be used to characterize physiologic breathing patterns in healthy individuals.

ABSTRACTThe determination of the relative and absolute configuration of natural compounds is a very challenging task. Among other anisotropic NMR parameters, residual chemical shift anisotropy (RCSA) induced by anisotropic media is an invaluable tool to determine relative configurations of natural and synthetic organic molecules in solution. This review introduces various RCSA‐based methodologies for the structural elucidation of natural products. The current availability of alignment media in organic solvents for RCSA measurements is also discussed as are applications of RCSAs for structural analysis of various natural products.

Abstract This article explores the theory of racial whitening’s role in the political attempt to reshape the national collective in the First Brazilian Republic (1889-1930) to explain the theory’s origins and characteristics and suggest its international relevance. It is argued that this theory—which proposed that Brazil could modernize through interracial marriage and mass European immigration—was not a Brazilian or Latin American peculiarity but was aligned with a transformist strand of previous scientific racialism. The main novelty came from wide political resonance, not intellectual newness. In addition, the article demonstrates that racial whitening oriented the First Republic to construct ambiguous, yet effective, structures of discrimination, aimed at molding the national collective. These structures seem to have anticipated the transformation of racial relations elsewhere, preceding the global shift in the justification of institutional racism from biological to cultural bases after 1945. The article then underscores the importance of understanding historical dependencies and subtle mechanisms through which racism can be perpetuated, especially in societies that claim to be racially progressive.

Protein–lipid crosstalk is fundamental to homeostasis in the endoplasmic reticulum (ER). The ER-associated degradation (ERAD) pathway, a branch of the ubiquitin–proteasome system, maintains ER membrane properties by degrading lipid metabolic enzymes. However, the ERAD components that sense membrane properties and their mechanisms remain poorly defined. Using reconstituted systems with purified ERAD factors, we show that membrane composition modulates the ubiquitination cascade at multiple levels. The membrane-anchored E2 UBE2J2 acts as a sensor for lipid packing: in loosely packed membranes, UBE2J2 becomes inactive due to membrane association that impedes ubiquitin loading, while tighter packing promotes its active conformation and interaction with E1. UBE2J2 activity directs ubiquitin transfer by the E3 ligases RNF145, MARCHF6, and RNF139, targeting both themselves and the substrate squalene monooxygenase. Additionally, RNF145 senses cholesterol, altering its oligomerization and activity. These findings reveal that ERAD integrates multiple lipid signals, with UBE2J2 relaying and extending the effect of lipid signals through its cooperation with multiple E3 ligases.

Cotranslational protein folding follows a distinct pathway shaped by the vectorial emergence of the peptide and spatial constraints of the ribosome exit tunnel. Variations in translation rhythm can cause misfolding linked to disease; however, predicting cotranslational folding pathways remains challenging. Here, we computationally predict and experimentally validate a vectorial hierarchy of folding resolved at the atomistic level, where early intermediates are stabilized through non-native hydrophobic interactions before rearranging into the native-like fold. Disrupting these interactions destabilizes intermediates and impairs folding. The chaperone trigger factor alters the cotranslational folding pathway by keeping the nascent peptide dynamic until the full domain emerges. Our results highlight an unexpected role of surface-exposed residues in protein folding on the ribosome and provide tools to improve folding prediction and protein design.

ABSTRACTReversible self‐assembly of nanoparticles remains challenging due to limited molecular mobility. Moreover, reported successful examples typically rely on inorganic‐core nanoparticles that require surface pre‐functionalization with specific stimuli‐responsive ligands. Here, we demonstrate reversible self‐assembly of organic nanoparticles through the selective self‐modulation of aliphatic chains, without the need for prior modification with external stimuli‐responsive ligands. D‐glucose 11‐octadecylthioundecanoate (D‐Glc‐C11S18E) self‐assembles into microspheres (3–6 µm) comprising nanospheres (100–300 nm). Within these nanospheres, octadecylthioundecanoyl (C29) groups form interior crystalline domains (C29 lamella) while octadecyl (C18) chains organize at nanosphere interfaces (C18 lamella). Thermal triggering enables selective reversibility: at 50°C, the C18 lamella dissociates into disordered structures while the C29 lamella remains intact; cooling to 20°C regenerates the C18 lamella. In methanol, this process drives reversible microsphere‐nanosphere morphological transitions (validated by scanning electron microscopy/dynamic light scattering), accompanied by a reversible fluorescence modulation. Both structural and optical modulations exhibit no apparent fatigue over 10 consecutive cycles. Energy decomposition analysis reveals stronger C29 binding energy (ΔEint = –29.80 kcal/mol vs. C18's –19.90 kcal/mol), explaining selective reversibility. Density functional theory calculations confirm the distinct highest occupied molecular orbital‐lowest unoccupied molecular orbital gaps correlating with emission wavelengths. Leveraging the temperature/wavelength‐dependent fluorescence, we constructed a multi‐input logic gate. This work establishes a new insight for reversible assembly and enables smart and fatigue‐resistant optoelectronic applications.

Abstract Antibiotic resistance is a growing threat, underscoring the need to understand the underlying mechanisms. Aminoglycosides kill bacteria by disrupting translation fidelity, leading to the synthesis of aberrant proteins. Surprisingly, mutations in fusA, a gene encoding translation elongation factor G (EF-G), frequently confer resistance, even though EF-G neither participates in mRNA decoding nor blocks aminoglycoside binding. Here, we show that EF-G resistance variants selectively slow ribosome movement along mRNA when aminoglycosides are bound. This delay increases the chance that the drug dissociates before misreading occurs. Over several elongation cycles, this selective silencing of drug-bound ribosomes prevents error cluster formation, preserving proteome and membrane integrity. As a result, fusA mutations confer resistance early in treatment by preventing self-promoted aminoglycoside uptake. Translation on drug-free ribosomes remains sufficiently rapid to sustain near-normal bacterial growth. This previously unrecognized resistance mechanism— selective silencing of corrupted targets—reveals a novel antibiotic resistance strategy with potential therapeutic implications.

Abstract: Although psychological research in continental Europe increasingly focuses on diversity and migration, it rarely centers racism as a context for understanding lived experience. With racism and far-right politics on the rise, such work is imperative. In this conceptual paper, we advocate for greater research in three key areas to more meaningfully understand and resist systemic racism across the continent. First, we need more work centering racially minoritized individuals, exploring processes of identity formation in the context of racialized Othering. Second, we need greater research on anti-Blackness, which may function differently and have distinct consequences from xenophobia or other forms of discrimination. Third, a critical interrogation of whiteness is needed, examining how diverse individuals alternately reinforce or resist exclusionary norms across contexts. To guide authors interested in taking up such work, we offer reflections and recommendations on terminology, methodology, theory, and researcher reflexivity.

Abstract Amyloids, classically associated with neurodegenerative disease, also play important roles in infection and immunity. Phenol-soluble modulins (PSMs) from Staphylococcus aureus are amyloid-forming virulence peptides that contribute to cytotoxicity, immune modulation, and biofilm stability. PSMα3 forms cross-α amyloid fibrils and shares sequence and α-helical self-assembly features with LL-37, a human host-defence peptide that forms non-amyloid α-helical assemblies. Here, we identify RNA as a context-dependent regulator of their assembly pathways and biological activity. RNA consistently reduces LL-37 cytotoxicity toward human cells without compromising its antibacterial function, suggesting a host-protective effect. In contrast, RNA preserves PSMα3 cytotoxic and antimicrobial activity over time by reshaping its assembly landscape, promoting liquid–liquid phase separation at low concentrations and stabilizing dynamic α-helical intermediates. At higher RNA concentrations, both peptides transition into distinct aggregated states, amorphous for LL-37 and fibrillar for PSMα3, correlating with divergent functional outcomes. The amyloid inhibitor EGCG abolishes the bioactivity of both peptides by redirecting assembly into non-functional aggregates, highlighting that activity depends on supramolecular architecture and reversibility rather than aggregation per se. Together, these findings establish RNA as an environmental regulator of α-helical peptide assemblies and reveal phase transitions as tuneable determinants of peptide function, with implications for microbial virulence, innate immunity, and therapeutic intervention in infectious and protein-aggregation–associated diseases.

Abstract. Enhanced transverse relaxation near rotary resonance conditions is a well-documented effect for anisotropic solid samples undergoing magic-angle spinning (MAS). We report transverse signal decay associated with rotary resonance conditions for rotating liquids, a surprising observation, since first-order anisotropic interactions are averaged at a much faster timescale compared with the spinning frequency. We report measurements of 13C and 1H signal intensities under spin lock for spinning samples of polybutadiene rubber, polyethylene glycol solution, and 99.96 % D2O. A drastic reduction in spin-lock signal intensities is observed when the spin-lock frequency matches 1 or 2 times the MAS rate. In addition, oscillations of the signal are observed, consistent with a coherent origin of the effect, a pseudo rotary resonance relaxation dispersion (pseudo-RRD). Through simulations, we qualitatively describe the appearance of pseudo-RRD, which can be explained by time dependence caused by sample rotation and an inhomogeneous field, the origin of which is an instrumental imperfection. Consideration of this effect is important for MAS experiments based on rotary resonance conditions and motivates the design of new MAS coils with improved radio frequency (RF)-field homogeneity.