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4,004 results for “In vivo”
Data from: All-trans retinoic acid disrupts development in ex vivo cultured fetal rat testes. II: modulation of mono-(2-ethylhexyl) phthalate toxicity
Humans are universally exposed to low levels of phthalate esters (phthalates), which are used to plasticize polyvinyl chloride. Phthalates exert adverse effects on the development of seminiferous cords in the fetal testis through unknown toxicity pathways. To investigate the hypothesis that phthalates alter seminiferous cord development by disrupting retinoic acid signaling in the fetal testis, gestational day 15 fetal rat testes were exposed for 1-3 days to 10-6 M all-trans retinoic acid (ATRA) alone or in combination with 10-6 to 10-4 M mono-(2-ethylhexyl) phthalate (MEHP) in ex vivo culture. As previously reported, exogenous ATRA reduced seminiferous cord number. This effect was attenuated in a concentration-dependent fashion by MEHP co-exposure. ATRA and MEHP-exposed testes were depleted of DDX4-positive germ cells but not Sertoli cells. MEHP alone enhanced the expression of the retinoic acid receptor target Rbp1 and the ovary development-associated genes Wnt4 and Nr0b1, and suppressed expression of the Leydig cell marker, Star, and the germ cell markers, Ddx4 and Pou5f1. In co-exposures, MEHP predominantly enhanced the gene expression effects of ATRA, but the Wnt4 and Nr0b1 concentration-responses were non-linear. Similarly, ATRA increased the number of cells expressing the granulosa cell marker FOXL2 in testis cultures, but this induction was attenuated by addition of MEHP. These results indicate that MEHP can both enhance and inhibit actions of ATRA during fetal testis development and provide evidence that retinoic acid signaling is a target for phthalate toxicity in the fetal testis.
Data from: Polycaprolactone nanofibers loaded with 20(S)-Protopanaxadiol for in vitro and vivo antitumor activity study
In this work, 20(S)-Protopanaxadiol (PPD) loaded polycaprolactone (PCL) nanofibers were successfully fabricated by electrospinning technique using tween-80 as a solubilizer. Firstly, smooth and continuous nanofibers were collected by using suitable solvent and appropriate spinning conditions. Secondly, nanofiber mats were characterized by scanning electron microscope (SEM), thermogravimetric (TG) analysis, Fourier transform infrared spectroscopy (FTIR) and mechanical test. Finally, nanofibrous membranes were evaluated using water contact angle, in vitro drug release, biodegradation test, in vitro and vivo antitumor activity and cell apoptosis assay. As a result, scanning electron microscopy observations indicated that diameter of the drug-loaded nanofibers increased with drug concentration increasing. Thermogravimetric (TG) analysis and mechanical test showed nanofibers equipped with great thermal and mechanical properties. Biodegradation test exhibited that the structure of fabricated nanofibers had a certain degree of change after 15 days. In vitro release study showed that PPD from drug-loaded nanofibers could be released in a sustained and prolonged mode. The cytotoxic effect of drug-loaded nanofiber mats examined on the human laryngeal carcinoma cells (Hep-2 cells) demonstrated that the prepared nanofibers had a remarkable antitumor effect. Meanwhile, the drug-loaded fiber mats showed a super antitumor effect in vivo antitumor study. All in all, PCL nanofibers could be a potential carrier of PPD for cancer treatment.
Data from: Efficient and accurate extraction of in vivo calcium signals from microendoscopic video data
In vivo calcium imaging through microendoscopic lenses enables imaging of previously inaccessible neuronal populations deep within the brains of freely moving animals. However, it is computationally challenging to extract single-neuronal activity from microendoscopic data, because of the very large background fluctuations and high spatial overlaps intrinsic to this recording modality. Here, we describe a new constrained matrix factorization approach to accurately separate the background and then demix and denoise the neuronal signals of interest. We compared the proposed method against previous independent components analysis and constrained nonnegative matrix factorization approaches. On both simulated and experimental data recorded from mice, our method substantially improved the quality of extracted cellular signals and detected more well-isolated neural signals, especially in noisy data regimes. These advances can in turn significantly enhance the statistical power of downstream analyses, and ultimately improve scientific conclusions derived from microendoscopic data.
Data from: Lineage tracing of human B cells reveals the in vivo landscape of human antibody class switching
Antibody class switching is a feature of the adaptive immune system which enables diversification of the effector properties of antibodies. Even though class switching is essential for mounting a protective response to pathogens, the in vivo patterns and lineage characteristics of antibody class switching have remained uncharacterized in living humans. Here we comprehensively measured the landscape of antibody class switching in human adult twins using antibody repertoire sequencing. The map identifies how antibodies of every class are created and delineates a two-tiered hierarchy of class switch pathways. Using somatic hypermutations as a molecular clock, we discovered that closely related B cells often switch to the same class, but lose coherence as somatic mutations accumulate. Such correlations between closely related cells exist when purified B cells class switch in vitro, suggesting that class switch recombination is directed toward specific isotypes by a cell-autonomous imprinted state.
Data from: Human retinal pigment epithelium: in vivo cell morphometry, multispectral autofluorescence, and relationship to cone mosaic
Purpose: To characterize in vivo morphometry and multispectral autofluorescence of the retinal pigment epithelial (RPE) cell mosaic and its relationship to cone cell topography across the macula. Methods: RPE cell morphometrics were computed in regularly spaced regions of interest (ROIs) from contiguous short-wavelength autofluorescence (SWAF) and photoreceptor reflectance images collected across the macula in one eye of 10 normal participants (23–65 years) by using adaptive optics scanning light ophthalmoscopy (AOSLO). Infrared autofluorescence (IRAF) images of the RPE were collected with AOSLO in seven normal participants (22–65 years), with participant overlap, and compared to SWAF quantitatively and qualitatively. Results: RPE cell statistics could be analyzed in 84% of SWAF ROIs. RPE cell density consistently decreased with eccentricity from the fovea (participant mean ± SD: 6026 ± 1590 cells/mm2 at fovea; 4552 ± 1370 cells/mm2 and 3757 ± 1290 cells/mm2 at 3.5 mm temporally and nasally, respectively). Mean cone-to-RPE cell ratio decreased rapidly from 16.6 at the foveal center to <5 by 1 mm. IRAF revealed cells in six of seven participants, in agreement with SWAF RPE cell size and location. Differences in cell fluorescent structure, contrast, and visibility beneath vasculature were observed between modalities. Conclusions: Improvements in AOSLO autofluorescence imaging permit efficient visualization of RPE cells with safe light exposures, allowing individual characterization of RPE cell morphometry that is variable between participants. The normative dataset and analysis of RPE cell IRAF and SWAF herein are essential for understanding microscopic characteristics of cell fluorescence and may assist in interpreting disease progression in RPE cells.
Data from: Evidence for amino acid snorkeling from a high-resolution, in vivo analysis of Fis1 tail anchor insertion at the mitochondrial outer membrane
Proteins localized to mitochondria by a carboxyl-terminal tail anchor (TA) play roles in apoptosis, mitochondrial dynamics, and mitochondrial protein import. To reveal characteristics of TAs that may be important for mitochondrial targeting, we focused our attention upon the TA of the Saccharomyces cerevisiae Fis1 protein. Specifically, we generated a library of Fis1p TA variants fused to the Gal4 transcription factor, then, using next-generation sequencing, revealed which Fis1p TA mutations inhibited membrane insertion and allowed Gal4p activity in the nucleus. Prompted by our global analysis, we subsequently analyzed the ability of individual Fis1p TA mutants to localize to mitochondria. Our findings suggest that the membrane-associated domain of the Fis1p TA may be bipartite in nature, and we encountered evidence that the positively charged patch at the carboxyl-terminus of Fis1p is required for both membrane insertion and organelle specificity. Furthermore, lengthening or shortening of the Fis1p TA by up to three amino acids did not inhibit mitochondrial targeting, arguing against a model in which TA length directs insertion of TAs to distinct organelles. Most importantly, positively charged residues were more acceptable at several positions within the membrane-associated domain of the Fis1p TA than negatively charged residues. These findings, emerging from the first high-resolution analysis of an organelle targeting sequence by deep mutational scanning, provide strong, in vivo evidence that lysine and arginine can "snorkel," or become stably incorporated within a lipid bilayer by placing terminal charges of their side chains at the membrane interface.
Data from: Setup in a clinical workflow and impact on radiotherapy routine of an in vivo dosimetry procedure with an electronic portal imaging device
High conformal techniques such as intensity-modulated radiation therapy and volumetric-modulated arc therapy are widely used in overloaded radiotherapy departments. In vivo dosimetric screening is essential in this environment to avoid important dosimetric errors. This work examines the feasibility of introducing in vivo dosimetry (IVD) checks in a radiotherapy routine. The causes of dosimetric disagreements between delivered and planned treatments were identified and corrected during the course of treatment. The efficiency of the corrections performed and the added workload needed for the entire procedure were evaluated. The IVD procedure was based on an electronic portal imaging device. A total of 3682 IVD tests were performed for 147 patients who underwent head and neck, abdomen, pelvis, breast, and thorax radiotherapy treatments. Two types of indices were evaluated and used to determine if the IVD tests were within tolerance levels: the ratio R between the reconstructed and planned isocentre doses and a transit dosimetry based on the γ-analysis of the electronic portal images. The causes of test outside tolerance level was investigated and corrected and IVD test was repeated during subsequent fraction. The time needed for each step of the IVD procedure was registered. Pelvis, abdomen, and head and neck treatments had 10% of tests out of tolerance whereas breast and thorax treatments accounted for up to 25%. The patient setup was the main cause of 90% of the IVD tests out of tolerance and the remaining 10% was due to patient morphological changes. An average time of 42 min per day was sufficient to monitor a daily workload of 60 patients in treatment. This work shows that IVD performed with an electronic portal imaging device is feasible in an overloaded department and enables the timely realignment of the treatment quality indices in order to achieve a patient's final treatment compliant with the one prescribed.
Data from: In vivo dynamics of skeletal muscle Dystrophin in zebrafish embryos revealed by improved FRAP analysis
Dystrophin forms an essential link between sarcolemma and cytoskeleton, perturbation of which causes muscular dystrophy. We analysed Dystrophin binding dynamics in vivo for the first time. Within maturing fibres of host zebrafish embryos, our analysis reveals a pool of diffusible Dystrophin and complexes bound at the fibre membrane. Combining modelling, an improved FRAP methodology and direct semi-quantitative analysis of bleaching suggests the existence of two membrane-bound Dystrophin populations with widely differing bound lifetimes: a stable, tightly bound pool, and a dynamic bound pool with high turnover rate that exchanges with the cytoplasmic pool. The three populations were found consistently in human and zebrafish Dystrophins overexpressed in wild-type or dmdta222a/ta222a zebrafish embryos, which lack Dystrophin, and in Gt(dmd-Citrine)ct90a that express endogenously-driven tagged zebrafish Dystrophin. These results lead to a new model for Dystrophin membrane association in developing muscle, and highlight our methodology as a valuable strategy for in vivo analysis of complex protein dynamics.
Data from: Characterization of leukemia-inducing genes using a proto-oncogene/homeobox gene retroviral human cDNA library in a mouse in vivo model
The purpose of this research is to develop a method to screen a large number of potential driver mutations of acute myeloid leukemia (AML) using a retroviral cDNA library and murine bone marrow transduction-transplantation system. As a proof-of-concept, murine bone marrow (BM) cells were transduced with a retroviral cDNA library encoding well-characterized oncogenes and homeobox genes, and the virus-transduced cells were transplanted into lethally irradiated mice. The proto-oncogenes responsible for leukemia initiation were identified by PCR amplification of cDNA inserts from genomic DNA isolated from leukemic cells. In an initial screen of ten leukemic mice, the MYC proto-oncogene was detected in all the leukemic mice. Of ten leukemic mice, 3 (30%) had MYC as the only transgene, and seven mice (70%) had additional proto-oncogene inserts. We repeated the same experiment after removing MYC-related genes from the library to characterize additional leukemia-inducing gene combinations. Our second screen using the MYC-deleted proto-oncogene library confirmed MEIS1and the HOX family as cooperating oncogenes in leukemia pathogenesis. The model system we introduced in this study will be valuable in functionally screening novel combinations of genes for leukemogenic potential in vivo, and the system will help in the discovery of new targets for leukemia therapy.
Data from: The magnitude of ivacaftor effects on fluid secretion via R117H-CFTR channels: human in vivo measurements
We optically measured effects of orally available ivacaftor (Kalydeco®) on sweat rates of identified glands in 3 R117H subjects, each having a unique set of additional mutations, and compared them with 5 healthy control subjects tested contemporaneously. We injected β-adrenergic agonists intradermally to stimulate CFTR-dependent 'C-sweat' and methacholine to stimulate 'M-sweat', which persists in CF subjects. We focused on an R117H-7T/F508del subject who produced quantifiable C-sweat off ivacaftor and was available for 1 blinded, 3 off ivacaftor, and 3 on ivacaftor tests, allowing us to estimate in vivo fold-increase in sweat rates produced by ivacaftor's effect on the open probability (PO) of R117H-CFTR. Measured sweat rates must be corrected for sweat losses. With estimated sweat losses of 0.023 to 0.08 nl·gland-1·min-1, ivacaftor increased the average C-sweat rates 3-7 fold, and estimated function as % of WT were 4.1-12% off ivacaftor and 21.9-32% on ivacaftor (larger values reflect increased loss estimates). Based on single tests, an R117H-7T/ R117H-7T subject showed 6-9% WT function off ivacaftor and 28-43% on ivacaftor. Repeat testing of an R117H-5T/F508del subject detected only trace responding to ivacaftor. We conclude that in vivo, R117H PO is strongly increased by ivacaftor, but channel number, mainly determined by variable deletion of exon 10, has a marked influence on outcomes.
Data from: Understanding genetic variation in in vivo tolerance to artesunate: implications for treatment efficacy and resistance monitoring
Artemisinin-based drugs are the front-line weapon in the treatment of human malaria cases, but there is concern that recent reports of slow clearing infections may signal developing resistance to treatment. In the absence of molecular markers for resistance, current efforts to monitor drug efficacy are based on the rate at which parasites are cleared from infections. However, some knowledge of the standing variation in parasite susceptibility is needed to identify a meaningful increase in infection half-life. Here, we show that five previously unexposed genotypes of the rodent malaria parasite Plasmodium chabaudi differ substantially in their in vivo response to treatment. Slower clearance rates were not linked to parasite virulence or growth rate, going against the suggestion that drug treatment will drive the evolution of virulence in this system. The level of variation observed here in a relatively small number of genotypes suggests existing 'resistant' parasites could be present in the population and therefore, increased parasite clearance rates could represent selection on pre-existing variation rather than de novo resistance events. This has implications for resistance monitoring as susceptibility may depend on evolved traits unrelated to drug exposure.
Data from: Computer assisted detection of axonal bouton structural plasticity in in vivo time-lapse images
The ability to measure minute structural changes in neural circuits is essential for long-term in vivo imaging studies. Here, we propose a methodology for detection and measurement of structural changes in axonal boutons imaged with time-lapse two-photon laser scanning microscopy (2PLSM). Correlative 2PLSM and 3D electron microscopy (EM) analysis, performed in mouse barrel cortex, showed that the proposed method has low fractions of false positive/negative bouton detections (2/0 out of 18), and that 2PLSM-based bouton weights are correlated with their volumes measured in EM (r=0.93). Next, the method was applied to a set of axons imaged in quick succession to characterize measurement uncertainty. The results were used to construct a statistical model in which bouton addition, elimination, and size changes are described probabilistically, rather than being treated as deterministic events. Finally, we demonstrate that the model can be used to quantify significant structural changes in boutons in long-term imaging experiments.
Data from: An objective in vivo diagnostic method for inflammatory bowel disease
Inflammatory damage to the bowel, as occurs in inflammatory bowel disease (IBD), is debilitating to patients. In both patients and animal experimental models histological analysis of biopsies and endoscopic examinations are used to evaluate the disease state. However such measurements often have delays and are invasive, while endoscopy is not quantitatively objective. Therefore, a real-time quantitative method to assess compromised mucosal barrier function is advantageous. We investigated the correlation of in vivo changes in electrical transmural impedance with histological measures of inflammation. Four platinum (Pt) ball electrodes were placed in the lumen of the rat small intestine, with a return electrode under the skin. Electrodes placed within the non-inflamed intestine generated stable impedances during the 3 h testing period. Following intraluminal injection of 2,4,6-trinitrobenzene sulphonic acid (TNBS), an established animal model of IBD, impedances in the inflamed region significantly decreased relative to a region not exposed to TNBS (P < 0.05). Changes in intestinal transmural impedance were correlated (P < 0.05) with histologically assessed damage to the mucosa and increases in neutrophil, eosinophil and T-cell populations at 3 h compared with tissue from control regions. This quantitative, real-time assay may have application in the diagnosis and clinical management of IBD.
Data from: Impact of genetic reduction of NMNAT2 on chemotherapy-induced losses in cell viability in vitro and peripheral neuropathy in vivo
Nicotinamide mononucleotide adenylyl transferases (NMNATs) are essential neuronal maintenance factors postulated to preserve neuronal function and protect against axonal degeneration in various neurodegenerative disease states. We used in vitro and in vivo approaches to assess the impact of NMNAT2 reduction on cellular and physiological functions induced by treatment with a vinca alkaloid (vincristine) and a taxane-based (paclitaxel) chemotherapeutic agent. NMNAT2 null (NMNAT2-/-) mutant mice die at birth and cannot be used to probe functions of NMNAT2 in adult animals. Nonetheless, primary cortical cultures derived from NMNAT2-/- embryos showed reduced cell viability in response to either vincristine or paclitaxel treatment whereas those derived from NMNAT2 heterozygous (NMNAT2+/-) mice were preferentially sensitive to vincristine-induced degeneration. Adult NMNAT2+/- mice, which survive to adulthood, exhibited a 50% reduction of NMNAT2 protein levels in dorsal root ganglia relative to wildtype (WT) mice with no change in levels of other NMNAT isoforms (NMNAT1 or NMNAT3), NMNAT enzyme activity (i.e. NAD/NADH levels) or microtubule associated protein-2 (MAP2) or neurofilament protein levels. We therefore compared the impact of NMNAT2 knockdown on the development and maintenance of chemotherapy-induced peripheral neuropathy induced by vincristine and paclitaxel treatment using NMNAT2+/- and WT mice. NMNAT2+/- did not differ from WT mice in either the development or maintenance of either mechanical or cold allodynia induced by either vincristine or paclitaxel treatment. Intradermal injection of capsaicin, the pungent ingredient in hot chili peppers, produced equivalent hypersensitivity in NMNAT2+/- and WT mice receiving vehicle in lieu of paclitaxel. Capsaicin-evoked hypersensitivity was enhanced by prior paclitaxel treatment but did not differ in either NMNAT2+/- or WT mice. Thus, capsaicin failed to unmask differences in nociceptive behaviors in either paclitaxel-treated or paclitaxel-untreated NMNAT2+/- and WT mice. Moreover, no differences in motor behavior were detected between genotypes in the rotarod test. Our studies do not preclude the possibility that complete knockout of NMNAT2 in a conditional knockout animal could unmask a role for NMNAT2 in protection against detrimental effects of chemotherapeutic treatment.
Data from: Macrophage migration inhibitory factor is involved in ectopic endometrial tissue growth and peritoneal-endometrial tissue interaction in vivo: a plausible link to endometriosis development
Pelvic inflammation is a hallmark of endometriosis pathogenesis and a major cause of the disease's symptoms. Abnormal immune and inflammatory changes may not only contribute to endometriosis-major symptoms, but also contribute to ectopic endometrial tissue growth and endometriosis development. A major pro-inflammatory factors found elevated in peritoneal fluid of women with endometriosis and to be overexpressed in peritoneal fluid macrophages and active, highly vascularized and early stage endometriotic lesions, macrophage migration inhibitory factor (MIF) appeared to induce angiogenic and inflammatory and estrogen producing phenotypes in endometriotic cells in vitro and to be a possible therapeutic target in vivo. Using a mouse model where MIF-knock out (KO) mice received intra-peritoneal injection of endometrial tissue from MIF-KO or syngeneic wild type (WT) mice and vice versa, our current study revealed that MIF genetic depletion resulted in a marked reduction ectopic endometrial tissue growth, a disrupted tissue structure and a significant down regulation of the expression of major inflammatory (cyclooxygenease-2), cell adhesion (αv and β3 integrins), survival (B-cell lymphoma-2) and angiogenic (vascular endothelial cell growth) factorsrelevant to endometriosis pathogenesis, whereas MIF add-back to MIF-KO mice significantly restored endometriosis-like lesions number and size. Interestingly, cross-experiments revealed that MIF presence in both endometrial and peritoneal host tissues is required for ectopic endometrial tissue growth and pointed to its involvement in endometrial-peritoneal interactions. This study provides compelling evidence for the role of MIF in endometriosis development and its possible interest for a targeted treatment of endometriosis.
FIGURE 1 in Ex vivo three-dimensional reconstruction of Acutiramus: a giant pterygotid sea scorpion
FIGURE 1. The traditional reconstruction of Pterygotus from Clarke and Ruedemann (1912: pls. 67, 68): A. dorsal reconstruction; B. ventral reconstruction.
FIGURE 2 in Ex vivo three-dimensional reconstruction of Acutiramus: a giant pterygotid sea scorpion
FIGURE 2. Acutiramus and Erettopterus specimens showing the general morphology and arrangement of appendages and ventral structures. A, B. Acutiramus cummingsi from the Silurian (Pridoli), Bertie Group, Williamsville Formation, Bennett Quarry (= Buffalo Cement Company), Buffalo, NY (N 42.942, W 78.825). A. USNM PAL 60053 (Clarke and Ruedemann, 1912: pl. 72, fig. 1). B. NYSM 10193 (Clarke and Ruedemann, 1912: pl. 78, fig. 3). C. Acutiramus macrophthalmus (Hall, 1859) from the Silurian (Pridoli), Bertie Group, Fiddlers Green dolomite. No locality data. NYSM E3584. D. Erettopterus bilobus (Salter, 1856) from the Silurian (latest Llandovery and Wenlock) Patrick or Kip Burn formation, Scotland. NHMUK PI In 59342. A–C. Photographed under water. B, C. Photographs by Lisa Amati.
Figure 4 from: Obaid KA, Fawzi HA (2024) Evaluation of empagliflozin efficacy as a promising anti-aging treatment in mice: In-vivo study. Pharmacia 71: 1-9. https://doi.org/10.3897/pharmacia.71.e116184
Figure 4 Cross-sections of heart tissue of mice. A: In mice received normal saline only (G1); B: In mice received DGAL only (G2); C: In mice received DGAL and EMP 1 mg/kg after the end of induction (G4) (Olympus BX51microscpose and a software DP controller X40).
Figure 4 from: Mahmod AI, Oqal M, Khalid AM, Afifi FU, Talib WH (2024) Phytochemical analysis, antioxidant, and antitumor activity of Ligustrum ovalifolium leaves grown in Jordan: an in vitro and in vivo study. Pharmacia 71: 1-10. https://doi.org/10.3897/pharmacia.71.e111517
Figure 4 DPPH radical scavenging activity of L. ovalifolium extracts. Ascorbic acid is the positive control in this assay. Results are expressed as means of three independent experiments (bars) ± SEM (lines).
Figure 1 from: Mahmod AI, Oqal M, Khalid AM, Afifi FU, Talib WH (2024) Phytochemical analysis, antioxidant, and antitumor activity of Ligustrum ovalifolium leaves grown in Jordan: an in vitro and in vivo study. Pharmacia 71: 1-10. https://doi.org/10.3897/pharmacia.71.e111517
Figure 1 The antiproliferative activity of L. ovalifolium extracts against (A) T47D cell line (B) MDA-MB-231 cell line (C) HeLa cell line (D) Caco-2 cell line (E) PC3 cell line (F) EMT6/P cell line (G) Fibroblast cell line. Results are expressed as means of three independent experiments (bars) ± SEM (lines).
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.