Zeitschriftenaufsätze

Mollusks exhibit an unusually high diversity of genes encodingvoltage-gated proton channel homologs. In addition to the conventionalproton channels Hv1, Hv2, and Hv4, a structurally and functionally atypicalproton channel was previously identified in Aplysia californica (AcHv3,subsequently renamed AcHv3.1). [...]

Solar-induced chlorophyll fluorescence (SIF) is a rich source of information for understanding plant photosynthetic processes, carbon assimilation, functional status, and early stress symptoms of plants. As plants assimilate sunlight, they do so across the spectral range of photosynthetically active radiation. [...]

Ciltacabtagene autoleucel (cilta-cel), a B-cell maturation antigen (BCMA)–directed chimeric antigen receptor T-cell (CAR-T) therapy, has demonstrated deep and durable responses in patients with relapsed or refractory multiple myeloma and is rapidly moving into routine clinical practice worldwide.1, 2 While cytokine release syndrome (CRS) and immune-effector cell-associated neurotoxicity syndrome (ICANS) are well described, increasing attention is directed toward rarer but potentially severe neurotoxicity outside the ICANS spectrum.3, 4 Non-ICANS immune-effector cell-associated (IEC) toxicities reported after BCMA-directed CAR-T therapies include movement/neurocognitive treatment-emergent events with Parkinsonism-like features (IEC-PKS), cranial nerve palsies (IEC-NP), Guillain–Barré-syndrome-like presentations (IEC-GBS), and myelopathy.5 Phenotypes can overlap and evolve over weeks, complicating recognition and therapeutic decision-making.The biological basis of delayed non-ICANS neurotoxicity after BCMA-directed CAR-T therapy is an active area of investigation. Early reports have detected CAR-T in the cerebrospinal fluid (CSF) during neurotoxicity and, in individual cases, have described neuropathologic evidence of lymphocytic infiltration in affected brain regions, findings compatible with central nervous system (CNS) trafficking and the persistence of CAR-T, together with local inflammatory tissue injury.4 These observations have raised the possibility of an on-target/off-tumor mechanism in susceptible neural tissues, although causality has not been established.4, 6 At the cohort level, delayed non-ICANS neurotoxicity has been linked to pronounced CAR-T expansion and persistence and to heightened immune activation, often in patients with clinically relevant CRS and/or ICANS, suggesting that both cellular kinetics and inflammatory activation may contribute.3, 5-8 Despite these signals in clinical trials and real-world settings, non-ICANS neurotoxicity remains insufficiently characterized, and data from large in-label cohorts are limited. [...]

Background Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a well-established treatment for Parkinson’s disease (PD). Beyond basic omnidirectional, monopolar stimulation, advanced stimulation settings (AS), such as directional or vertical current steering, variation of pulse width and frequency, bipolar and interleaving stimulation are increasingly available. [...]