A Performance Comparison of Different YOLOv7 Networks for High-Accuracy Cell Classification in Bronchoalveolar Lavage Fluid Utilising the Adam Optimiser and Label Smoothing.

Accurate classification of cells in bronchoalveolar lavage (BAL) fluid is essential for the assessment of lung disease in pneumology and critical care medicine. However, the effectiveness of BAL fluid analysis is highly dependent on individual expertise. Our research is focused on improving the accuracy and efficiency of BAL cell classification using the "You Only Look Once" (YOLO) algorithm to reduce variability and increase the accuracy of cell detection in BALF analysis.

The Potential of Using Generative AI/NLP to Identify and Analyse Critical Incidents in a Critical Incident Reporting System (CIRS): A Feasibility Case-Control Study.

Background: To enhance patient safety in healthcare, it is crucial to address the underreporting of issues in Critical Incident Reporting Systems (CIRSs). This study aims to evaluate the effectiveness of generative Artificial Intelligence and Natural Language Processing (AI/NLP) in reviewing CIRS cases by comparing its performance with human reviewers and categorising these cases into relevant topics.

Methods: A case-control feasibility study was conducted using CIRS cases from the German CIRS-Anaesthesiology subsystem.

Energy metabolic pathways in neuronal development and function.

Neuronal development and function are known to be among the most energy-demanding functions of the body. Constant energetic support is therefore crucial at all stages of a neuron's life. The two main adenosine triphosphate (ATP)-producing pathways in cells are glycolysis and oxidative phosphorylation.

TORC1 regulation of dendrite regrowth after pruning is linked to actin and exocytosis.

Neurite pruning and regrowth are important mechanisms to adapt neural circuits to distinct developmental stages. Neurite regrowth after pruning often depends on differential regulation of growth signaling pathways, but their precise mechanisms of action during regrowth are unclear. Here, we show that the PI3K/TORC1 pathway is required for dendrite regrowth after pruning in Drosophila peripheral neurons during metamorphosis.

Developmental pruning of sensory neurites by mechanical tearing in Drosophila.

Mechanical forces actively shape cells during development, but little is known about their roles during neuronal morphogenesis. Developmental neurite pruning, a critical circuit specification mechanism, often involves neurite abscission at predetermined sites by unknown mechanisms. Pruning of Drosophila sensory neuron dendrites during metamorphosis is triggered by the hormone ecdysone, which induces local disassembly of the dendritic cytoskeleton.

AMPK adapts metabolism to developmental energy requirement during dendrite pruning in Drosophila.

To reshape neuronal connectivity in adult stages, Drosophila sensory neurons prune their dendrites during metamorphosis using a genetic degeneration program that is induced by the steroid hormone ecdysone. Metamorphosis is a nonfeeding stage that imposes metabolic constraints on development. We find that AMP-activated protein kinase (AMPK), a regulator of energy homeostasis, is cell-autonomously required for dendrite pruning.

PP2A phosphatase is required for dendrite pruning via actin regulation in Drosophila.

Large-scale pruning, the developmentally regulated degeneration of axons or dendrites, is an important specificity mechanism during neuronal circuit formation. The peripheral sensory class IV dendritic arborization (c4da) neurons of Drosophila larvae specifically prune their dendrites at the onset of metamorphosis in an ecdysone-dependent manner. Dendrite pruning requires local cytoskeleton remodeling, and the actin-severing enzyme Mical is an important ecdysone target.

Changes in neurovascular coupling during cycling exercise measured by multi-distance fNIRS: a comparison between endurance athletes and physically active controls.

It is well known that endurance exercise modulates the cardiovascular, pulmonary, and musculoskeletal system. However, knowledge about its effects on brain function and structure is rather sparse. Hence, the present study aimed to investigate exercise-dependent adaptations in neurovascular coupling to different intensity levels in motor-related brain regions.

Rab11 is required for neurite pruning and developmental membrane protein degradation in Drosophila sensory neurons.

Neurons, with their distinct neurites, require elaborate membrane trafficking pathways and regulation to uphold neurite identity and to be able to respond to neuronal or developmental stimuli. In a survey of trafficking regulators required for developmental dendrite pruning in Drosophila sensory neurons, we identified the small GTPase Rab11, a regulator of recycling endosomes. Dendrite pruning requires the developmentally regulated degradation of the cell adhesion molecule Neuroglian, and loss of Rab11 causes defects in the developmental degradation of Neuroglian and another target, the ion channel Ppk26.

Functions of Microtubule Disassembly during Neurite Pruning.

Large-scale neurite pruning, the developmentally regulated degeneration of axons or dendrites, is an important specificity mechanism during neuronal circuit formation. Pruning is usually restricted to single neurite branches and can occur by local degeneration or retraction. How this spatial regulation is achieved, and what triggers degeneration locally, are still poorly understood.

Differential Requirement for Translation Initiation Factor Pathways during Ecdysone-Dependent Neuronal Remodeling in Drosophila.

Dendrite pruning of Drosophila sensory neurons during metamorphosis is induced by the steroid hormone ecdysone through a transcriptional program. In addition, ecdysone activates the eukaryotic initiation factor 4E-binding protein (4E-BP) to inhibit cap-dependent translation initiation. To uncover how efficient translation of ecdysone targets is achieved under these conditions, we assessed the requirements for translation initiation factors during dendrite pruning.

Differential expression of Öbek controls ploidy in the blood-brain barrier.

During development, tissue growth is mediated by either cell proliferation or cell growth, coupled with polyploidy. Both strategies are employed by the cell types that make up the blood-brain barrier. During larval growth, the perineurial glia proliferate, whereas the subperineurial glia expand enormously and become polyploid.

Spatial regulation of microtubule disruption during dendrite pruning in .

Large-scale neurite pruning is an important specificity mechanism during neuronal morphogenesis. sensory neurons prune their larval dendrites during metamorphosis. Pruning dendrites are severed in their proximal regions, but how this spatial information is encoded is not clear.

The spliceosome-associated protein Mfap1 binds to VCP in Drosophila.

Posttranscriptional regulation of gene expression contributes to many developmental transitions. Previously, we found that the AAA chaperone Valosin-Containing Protein (VCP) regulates ecdysone-dependent dendrite pruning of Drosophila class IV dendritic arborization (c4da) neurons via an effect on RNA metabolism. In a search for RNA binding proteins associated with VCP, we identified the spliceosome-associated protein Mfap1, a component of the tri-snRNP complex.

PAR-1 promotes microtubule breakdown during dendrite pruning in .

Pruning of unspecific neurites is an important mechanism during neuronal morphogenesis. sensory neurons prune their dendrites during metamorphosis. Pruning dendrites are severed in their proximal regions.

Drosophila Valosin-Containing Protein is required for dendrite pruning through a regulatory role in mRNA metabolism.

The dendritic arbors of the larval Drosophila peripheral class IV dendritic arborization neurons degenerate during metamorphosis in an ecdysone-dependent manner. This process-also known as dendrite pruning-depends on the ubiquitin-proteasome system (UPS), but the specific processes regulated by the UPS during pruning have been largely elusive. Here, we show that mutation or inhibition of Valosin-Containing Protein (VCP), a ubiquitin-dependent ATPase whose human homolog is linked to neurodegenerative disease, leads to specific defects in mRNA metabolism and that this role of VCP is linked to dendrite pruning.

Neuronal remodeling and apoptosis require VCP-dependent degradation of the apoptosis inhibitor DIAP1.

The regulated degeneration of axons or dendrites (pruning) and neuronal apoptosis are widely used during development to determine the specificity of neuronal connections. Pruning and apoptosis often share similar mechanisms; for example, developmental dendrite pruning of Drosophila class IV dendritic arborization (da) neurons is induced by local caspase activation triggered by ubiquitin-mediated degradation of the caspase inhibitor DIAP1. Here, we examined the function of Valosin-containing protein (VCP), a ubiquitin-selective AAA chaperone involved in endoplasmic reticulum-associated degradation, autophagy and neurodegenerative disease, in Drosophila da neurons.

Control of the postmating behavioral switch in Drosophila females by internal sensory neurons.

Mating induces changes in the receptivity and egg-laying behavior in Drosophila females, primarily due to a peptide pheromone called sex peptide which is transferred with the sperm into the female reproductive tract during copulation. Whereas sex peptide is generally believed to modulate fruitless-GAL4-expressing neurons in the central nervous system to produce behavioral changes, we found that six to eight sensory neurons on the reproductive tract labeled by both ppk-GAL4 and fruitless-GAL4 can sense sex peptide to control the induction of postmating behaviors. In these sensory neurons, sex peptide appears to act through Pertussis toxin-sensitive G proteins and suppression of protein kinase A activity to reduce synaptic output.

Cdc48 (p97): a "molecular gearbox" in the ubiquitin pathway?

Cdc48 (p97), a conserved chaperone-like ATPase of eukaryotic cells, has attracted attention recently because of its wide range of cellular functions. Cdc48 is intimately linked to the ubiquitin pathway because its primary action is to segregate ubiquitinated substrates from unmodified partners. This 'segregase' activity is crucial for certain proteasomal degradation pathways and for some nonproteolytic functions of ubiquitin.

Functional division of substrate processing cofactors of the ubiquitin-selective Cdc48 chaperone.

Ubiquitin-dependent protein degradation usually involves escort factors that target ubiquitylated substrates to the proteasome. A central element in a major escort pathway is Cdc48, a chaperone-like AAA ATPase that collects ubiquitylated substrates via alternative substrate-recruiting cofactors. Cdc48 also associates with Ufd2, an E4 multiubiquitylation enzyme that adds further ubiquitin moieties to preformed ubiquitin conjugates to promote degradation.

A series of ubiquitin binding factors connects CDC48/p97 to substrate multiubiquitylation and proteasomal targeting.

Protein degradation in eukaryotes usually requires multiubiquitylation and subsequent delivery of the tagged substrates to the proteasome. Recent studies suggest the involvement of the AAA ATPase CDC48, its cofactors, and other ubiquitin binding factors in protein degradation, but how these proteins work together is unclear. Here we show that these factors cooperate sequentially through protein-protein interactions and thereby escort ubiquitin-protein conjugates to the proteasome.

Shp1 and Ubx2 are adaptors of Cdc48 involved in ubiquitin-dependent protein degradation.

Known activities of the ubiquitin-selective AAA ATPase Cdc48 (p97) require one of the mutually exclusive cofactors Ufd1/Npl4 and Shp1 (p47). Whereas Ufd1/Npl4 recruits Cdc48 to ubiquitylated proteins destined for degradation by the 26S proteasome, the UBX domain protein p47 has so far been linked exclusively to nondegradative Cdc48 functions in membrane fusion processes. Here, we show that all seven UBX domain proteins of Saccharomyces cerevisiae bind to Cdc48, thus constituting an entire new family of Cdc48 cofactors.