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@article{faucris.267813294,
abstract = {A Summary: Creating 3D animations from microscopy data is computationally expensive and requires high-end hardware. We therefore developed 3Dscript.server, a 3D animation software that runs as a service on dedicated, shared workstations. Using 3Dscript as the underlying rendering engine, it offers unique features not found in existing software: rendering is performed completely server-side. The target animation is specified on the client without the rendering engine, eliminating any hardware requirements client-side. Still, defining an animation is intuitive due to 3Dscript's natural language-based animation description. We implemented a new OMERO web app to utilize 3Dscript.server directly from the OMERO web interface; a Fiji client to use 3Dscript.server from Fiji for integration into image processing pipelines; and batch scripts to run 3Dscript.server on compute clusters for large-scale visualization projects.},
author = {Schmid, Benjamin and Tripal, Philipp and Winter, Zoltan and Palmisano, Ralf},
doi = {10.1093/bioinformatics/btab462},
faupublication = {yes},
journal = {Bioinformatics},
note = {CRIS-Team WoS Importer:2022-01-07},
pages = {4901-4902},
peerreviewed = {Yes},
title = {{3Dscript}.server: true server-side {3D} animation of microscopy images using a natural language-based syntax},
volume = {37},
year = {2021}
}
@article{faucris.239306987,
abstract = {Loss-of-function mutations of NaV1.7 lead to congenital insensitivity to pain, a rare condition resulting in individuals who are otherwise normal except for the inability to sense pain, making pharmacological inhibition of NaV1.7 a promising therapeutic strategy for the treatment of pain. We characterized a novel mouse model of NaV1.7-mediated pain based on intraplantar injection of the scorpion toxin OD1, which is suitable for rapid in vivo profiling of NaV1.7 inhibitors. Intraplantar injection of OD1 caused spontaneous pain behaviors, which were reversed by co-injection with NaV1.7 inhibitors and significantly reduced in NaV1.7−/− mice. To validate the use of the model for profiling NaV1.7 inhibitors, we determined the NaV selectivity and tested the efficacy of the reported NaV1.7 inhibitors GpTx-1, PF-04856264 and CNV1014802 (raxatrigine). GpTx-1 selectively inhibited NaV1.7 and was effective when co-administered with OD1, but lacked efficacy when delivered systemically. PF-04856264 state-dependently and selectively inhibited NaV1.7 and significantly reduced OD1-induced spontaneous pain when delivered locally and systemically. CNV1014802 state-dependently, but non-selectively, inhibited NaV channels and was only effective in the OD1 model when delivered systemically. Our novel model of NaV1.7-mediated pain based on intraplantar injection of OD1 is thus suitable for the rapid in vivo characterization of the analgesic efficacy of NaV1.7 inhibitors.
2+ [half-maximal inhibitory concentration (IC50) = 13 μM] > Cd2+ (IC50 = 38 μM) > Ni2+ (IC50 = 62 μM) > Cu2+ (IC50 = 200 μM). Zn2+ proved to be a weak (IC50 = 27 μM) and only partial inhibitor of the channel function, whereas Mg2+, Mn2+ and La3+ did not exhibit any substantial effect. Co2+, the most potent channel blocker, was able not only to compete with Ca2+ but also to pass with it through the open channel of TRPV1. In response to heat activation or vanilloid treatment, Co2+ accumulation was verified in TRPV1-transfected cell lines and in the TRPV1+ dorsal root ganglion neurons. The inhibitory effect was also demonstrated in vivo. Co2+ applied together with vanilloid agonists attenuated the nocifensive eye wipe response in mice. Different rat TRPV1 pore point mutants (Y627W, N628W, D646N and E651W) were created that can validate the binding site of previously used channel blockers in agonist-evoked 45Ca2+ influx assays in cells expressing TRPV1. The IC50 of Co2+ on these point mutants were determined to be reasonably comparable to those on the wild type, which suggests that divalent cations passing through the TRPV1 channel use the same negatively charged amino acids as Ca2+.
in silico molecular modelling of the receptor by promoting easier establishment of boundary conditions. The better understanding of the structure-function relationship of TRPV1 may promote discovery of new, promising, more effective and safe drugs for treatment of neurogenic inflammation and pain-related diseases and may offer new opportunities for therapeutic interventions.
+ T cells. This goes along with a mildly decreased frequency of IL-10-expressing B cells. We did not observe consistent effects on the phenotype and function of innate immune cells, including cytokine production, costimulatory molecule expression, and phagocytic capacity. Hence, our study reveals that low VD intake promotes lupus pathology, likely via the deviation of adaptive immunity, and suggests that the correction of VD deficiency might not only exert beneficial functions by preventing osteoporosis but also serve as an important module in prophylaxis and as an add-on in the treatment of lupus and possibly other immune-mediated diseases. Further research is required to determine the most appropriate dosage, as too-high VD serum levels may also induce adverse effects, possibly also on lupus pathology.},
author = {Kraemer, Antoine N. and Schäfer, Anna Lena and Sprenger, Dalina T.L. and Sehnert, Bettina and Williams, Johanna P. and Luo, Aileen and Riechert, Laura and Al-Kayyal, Qusai and Dumortier, Hélène and Fauny, Jean Daniel and Winter, Zoltan and Heim, Kathrin and Hofmann, Maike and Herrmann, Martin and Heine, Guido and Voll, Reinhard E. and Chevalier, Nina},
doi = {10.3389/fimmu.2022.933191},
faupublication = {yes},
journal = {Frontiers in Immunology},
keywords = {autoimmune; autoimmunity; choleacliferol; diet; lupus; mice; SLE; vitamin D},
note = {CRIS-Team Scopus Importer:2022-12-16},
peerreviewed = {Yes},
title = {{Impact} of dietary vitamin {D} on immunoregulation and disease pathology in lupus-prone {NZB}/{W} {F1} mice},
volume = {13},
year = {2022}
}
@article{faucris.312691132,
abstract = {Purpose: To study the tissue architecture, isthmus (connection between two lobes) of the lacrimal gland using preclinical 7T MRI in combination with histology and electron microscopy. Methods: Ten lacrimal glands from Caucasian body donors (mean age 78.7 years) were studied using 7T-MRI (N = 5; scanned at 75-μm intervals), histology, and electron microscopy (N = 5) and 3D cinematic rendering (CR) techniques. Results: 3D CR images showed uniform-sized lobules (widest lobule diameter, 1.68 ± 0.19 mm in orbital lobe, 1.68 ± 0.17 mm in palpebral lobe) in both lobes, separated by septae (size, 0.29 ± 0.09 mm). The internal framework of the gland resembled a honeycoomb pattern. In CR and histology, the isthmus contained glandular acini, large blood vessels, nerves, and no more than two ducts having a tortuous course towards the conjunctival surface. On assigning a color display to the rendered lacrimal gland, all glands showed a blood vessel originating from the main lacrimal artery just 5 mm beyond the hilum and making it course to the palpebral lobe via isthmus. The distance between the conjunctiva and the central substance of the orbital and palpebral lobe was 9.4 ± 0.2 mm and 2.8 ± 0.7 mm, respectively. Electron microscopy of the palpebral lobe revealed compact subepithelial layer in the overlying conjunctiva, followed by loosely scattered collagen bundles that contained the gland lobules. Conclusion: 3D-CR can be used to study the lacrimal gland microstructure, help fabricate a 3D scaffold for lacrimal gland bioprinting, and serve as guide for transconjunctival lacrimal gland targeted therapies i.e., 2.9 & 9 mm long needle to reach the orbital and palpebral lobe center, respectively in normal-size glands.},
author = {Singh, Swati and Winter, Zoltan and Necker, Fabian and Bäuerle, Tobias and Scholz, Michael and Bräuer, Lars and Paulsen, Friedrich},
doi = {10.1016/j.jtos.2023.09.010},
faupublication = {yes},
journal = {Ocular Surface},
keywords = {3D printing; 7T MRI; Cinematic rendering; Dry eye disease; Lacrimal gland; Palpebral lobe},
note = {CRIS-Team Scopus Importer:2023-10-13},
pages = {204-212},
peerreviewed = {Yes},
title = {{New} insights into lacrimal gland anatomy using {7T} {MRI} and electron microscopy: {Relevance} for lacrimal gland targeted therapies and bioengineering},
volume = {30},
year = {2023}
}
@article{faucris.254751623,
abstract = {Teeth are composed of many tissues, covered by an inflexible and obdurate enamel. Unlike most other tissues, teeth become extremely cold sensitive when inflamed. The mechanisms of this cold sensation are not understood. Here, we clarify the molecular and cellular components of the dental cold sensing system and show that sensory transduction of cold stimuli in teeth requires odontoblasts. TRPC5 is a cold sensor in healthy teeth and, with TRPA1, is sufficient for cold sensing. The odontoblast appears as the direct site of TRPC5 cold transduction and provides a mechanism for prolonged cold sensing via TRPC5's relative sensitivity to intracellular calcium and lack of desensitization. Our data provide concrete functional evidence that equipping odontoblasts with the cold-sensor TRPC5 expands traditional odontoblast functions and renders it a previously unknown integral cellular component of the dental cold sensing system.},
author = {Bernal, Laura and Sotelo-Hitschfeld, Pamela and König, Christine and Sinica, Viktor and Wyatt, Amanda and Winter, Zoltan and Hein, Alexander and Touska, Filip and Reinhardt, Susanne and Tragl, Aaron and Kusuda, Ricardo and Wartenberg, Philipp and Sclaroff, Allen and Pfeifer, John D. and Ectors, Fabien and Dahl, Andreas and Freichel, Marc and Vlachova, Viktorie and Brauchi, Sebastian and Roza, Carolina and Boehm, Ulrich and Clapham, David E. and Lennerz, Jochen K. and Zimmermann, Katharina},
doi = {10.1126/sciadv.abf5567},
faupublication = {yes},
journal = {Science Advances},
note = {CRIS-Team WoS Importer:2021-04-09},
peerreviewed = {Yes},
title = {{Odontoblast} {TRPC5} channels signal cold pain in teeth},
volume = {7},
year = {2021}
}
@article{faucris.239305458,
abstract = {Transient Receptor Potential Vanilloid 1 (TRPV1) confers noxious heat and inflammatory pain signals in the peripheral nervous system. Clinical trial of resiniferatoxin from Euphorbia species is successfully aimed at TRPV1 in cancer pain management and heading toward new selective painkiller status that further validates this target for drug discovery efforts. Evodia species, used in traditional medicine for hundreds of years, are a recognised source of different TRPV1 agonists, but no antagonist has yet been reported.In a search for painkiller leads, we noted for the first time a TRPV1 antagonist activity in the fresh fruits of Tetradium daniellii (Benn.) T.G. Hartley (syn. Evodia hupehensis Dode).Through a combination of extraction and purification methods with functional TRPV1-specific Ca2+ uptake assays (bioactivity-guided fractionation/isolation/purification); we isolated a new painkiller candidate that is a distant structural homologue of capsiate exovanilloids and endovanilloids such as anandamide, but a putative competitive inhibitor of the TRPV1. Four additional inactive compounds (N-isobutyl-4,5-epoxy-2E-decadienamide, geranylpsoralen, 8-(7',8'-epoxygeranyloxy)psoralen, and xanthotoxol) were also co-purified with pellitorine. Their structures were established by extensive 1D- and 2D-NMR spectroscopic analysis.1H- and 13C NMR determination of the chemical structure revealed it to be pellitorine, (2E,4E)-N-(2-methylpropyl)deca-2,4-dienamide, which can compete structurally with algesics released in inflammation. In contrast to previous isolates from Evodia species, pellitorine blocked capsaicin-evoked Ca2+ uptake with an IC50 of 154 µg/ml (0.69 mM/l). N-Isobutyl-4,5-epoxy-2E-decadienamide and geranylpsoralen, 8-(7',8'-epoxygeranyloxy)psoralen, and xanthotoxol did not affect the TRPV1.This is the first evidence that pellitorine, an aliphatic alkylamide analogue of capsaicin, can serve as an antagonist of the TRPV1 and may inhibit exovanilloid-induced pain.
Objectives:
Resiniferatoxin, the most potent agonist of inflammatory pain/vanilloid receptor/cation channel (TRPV1) can be used for neuron subtype specific ablation of pain generating cells at the level of the peripheral nervous system by Ca2+-excytotoxicity. Molecular neurosurgery is an emerging technology either to alleviate severe pain in cancer or treat/prevent different local neuropathies. Our aim was determining sensory modalities that may be lost after resiniferatoxin treatment.
Newborn or adult mice were treated with resiniferatoxin, then changes in chemical and heat sensitivity were correlated with alterations of the cell composition of sensory ganglions.
Only mice treated at adult age became less sensitive to heat stimuli, while both treatment groups lost sensitivity to specific vanilloid agonists of TRPV1 and, interestingly, to allyl-isothiocyanate, a selective agonist of TRPA1. Our in vivo and post mortem analytical results confirmed that TRPV1 and TRPA1 function together and resiniferatoxin-mediated neurosurgery removes both sensor molecules
In adult mice resiniferatoxin causes: i) desensitization to heat and ii) sensitization to cold. Cold hyperalgesia, an imbalance in thermosensation, might be conferred by a prominent cold receptor that is expressed in surviving resiniferatoxin-resistant sensory neurons and compensates for pain signals lost with TRPA1 and TRPV1 double positive cells in the peripheral nervous system.