Nis elements ar software program

Manufactured by Nikon

Sourced in Japan

NIS-Elements-AR is a software program designed for image acquisition, analysis, and processing in research and microscopy applications. The software provides a comprehensive platform for managing and manipulating digital images from various types of microscopes and imaging devices.

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Lab products found in correlation

Gaasp multi detector unit, by Nikon (1 mentions) Antibody against gapdh, by Santa Cruz Biotechnology (1 mentions) Phospho erk1 2, by Cell Signaling Technology (1 mentions) Ab2402, by Abcam (1 mentions) Ab79758, by Abcam (1 mentions) Oct compound, by Sakura Finetek (1 mentions) Fura 2 acetoxymethyl ester, by Thermo Fisher Scientific (1 mentions) Eclipse, by Nikon (1 mentions)

6 protocols using nis elements ar software program

Multiphoton Imaging of Isolectin-Stained Livers

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The livers were harvested and incubated overnight in staining solution [1 ml
of phosphate buffered saline (PBS) containing 20 µl of isolectin conjugated
with FITC]. The isolectin-stained livers were then observed using a
multiphoton excitation fluorescence microscope. The excitation laser was
tuned at 920 nm and routed through an A1plus ×40 and ×60 water immersion
objective lens (Nikon Corporation). The stained liver was observed using a
bandpass emission filter 525/20 nm (for FITC) and 629/ 53 nm (for QDs655).
In general, 212 × 212 µm or 322 × 322 µm areas were scanned, and 20- to
30-µm z-series were acquired using a 0.6-µm step. The fluorescent signals
were detected using a GaAsP multi detector unit (Nikon Corporation). The
acquired images were analyzed and reconstituted using the NIS-Elements AR
software program (Nikon Corporation).

Yamada S., Yukawa H., Kitamura K., Mizumaki T., Yoshizumi Y., Oohara T., Nanizawa E., Hirano F., Sato K., Sugawara-Narutaki A., Ishikawa T, & Baba Y. (2023). In Vivo Real-Time Quantum Dots Imaging to Track Transplanted Adipose Stem Cells in Different Inflammatory States of Acute Liver Failure Mice. Cell Transplantation, 32, 09636897231176442.

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Evaluating JNK and ERK1/2-c-Myc-CXCR4 Signaling

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For evaluation of JNK and ERK1/2-c-Myc-CXCR4 signaling, PC-3 cells were treated for 24 h with RPMI-1640 medium containing 0.1 % serum and VCaP cells were treated for 24 h with Dulbecco modified Eagle medium (DMEM) containing 0.5 % serum. Then, cells were treated with 10 μg/ml GLIPR1-ΔΤΜ for 1 h followed by the addition of 1nM docetaxel with or without 1μΜ SP600125 and lysates were collected 24 h later (VCaP cells) and 48 h later (PC-3 cells). Antibodies against GLIPR1-ΔΤΜ (Myc-tag), phospho-JNK, JNK, phospho-ERK1/2, ERK1/2, c-Myc, and CXCR4 were all purchased from Cell Signaling Technology (Danvers, MA), and antibody against GAPDH was purchased from Santa Cruz. When indicated, densitometric analysis was performed and quantification of integrated density was assessed using the NIS-Elements-AR software program (version 3.0; Nikon) followed by GAPDH normalization.

Karanika S., Karantanos T., Kurosaka S., Wang J., Hirayama T., Yang G., Park S., Golstov A.A., Tanimoto R., Li L, & Thompson T.C. (2015). GLIPR1-ΔTM synergizes with docetaxel in cell death and suppresses resistance to docetaxel in prostate cancer cells. Molecular Cancer, 14, 122.

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In vitro BNB Leukocyte Trafficking Assay

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Untreated AIDP patient leukocyte trafficking across the BNB in vitro was studied in real time using a flow-dependent leukocyte trafficking assay. Intravital microscopy is not currently possible in rodent peripheral nerves. A parallel plate flow chamber was attached to cytokine-treated confluent primary endoneurial endothelial cells cultured on rat-tail collagen-coated CellBIND^® petri dishes, coupled to time-lapse video microscopy as previously described [37 (link),7 (link),26 (link)]. Videos were cropped, magnified and analyzed to determine the route of leukocyte transmigration at the BNB using the NIS-Elements AR software program (Nikon).

Dong C., Palladino S.P., Helton E.S, & Ubogu E.E. (2016). The pathogenic relevance of αM-integrin in Guillain-Barré syndrome. Acta neuropathologica, 132(5), 739-752.

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Investigating Cell Cycle Regulation Pathways

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For WB analysis of the effects of CDC6si, ARsi, TOPBP1si, AZD7762 and combinations of them, cells were transfected with siRNA for 24 hours and then, treated with DMSO or AZD7762 for 24 hours. Afterward, cells were treated with a serum-free medium overnight and then with full serum for 4 hours (synchronization) before protein extract preparation. For WB analysis of ENZ and AZD7762 effects, cells were treated with DMSO or ENZ for 24 hours. DMSO or AZD7762 was then added for 24 hours. Synchronization was achieved as above. Antibodies against CDC6 (3387), ATR (2790), P-ATR Ser428 (2853), Chk1 (2360), P-Chk1Ser317 (12302), Cdc25C (4688), P-Cdc25C Ser216 (9528), ATM (2873), P-ATM Ser1981 (13050) were purchased from Cell Signaling Technology. Antibodies against P-CDC6 Ser54 (ab75809), P-Chk1ser296 (ab79758), and TopBp1 (ab2402) were purchased from Abcam. Antibodies against GAPDH (365062) and AR (816) were purchased from Santa Cruz Biotechnology. When indicated, densitometric analysis was performed and quantification of integrated density was assessed using the NIS-Elements-AR software program (version 3.0; Nikon) followed by GAPDH normalization.

Karanika S., Karantanos T., Li L., Wang J., Park S., Yang G., Zuo X., Song J.H., Maity S.N., Manyam G.C., Broom B., Aparicio A.M., Gallick G., Troncoso P., Corn P.G., Navone N., Zhang W., Li S, & Thompson. T.C. (2017). Targeting DNA damage response in prostate cancer through inhibition of androgen receptor/CDC6-ATR-Chk1 signaling: Combined AR/CDC6 and Chk1/2 inhibition for PCa. Cell reports, 18(8), 1970-1981.

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Immunofluorescence Analysis of Brain Samples

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Immunofluorescence studies were performed as previously described57 (link). Briefly, animals were deeply anesthetized and perfused with 4% paraformaldehyde (PFA) in phosphate buffered saline (PBS). The brain was removed and immersed in 4% PFA overnight. The fixed brains were cryo-protected with 20 and 30% sucrose-containing PBS at 4 °C for 24 hours each, and frozen in O.C.T. compound (Sakura Finetek, Tokyo). Fixed samples were serially cut at 40 μm of thickness. Sections were blocked with Block Ace (Morinaga, Japan) and incubated overnight at 4 °C with primary antibodies (See Supplementary Table S2 for the list of primary antibodies). Alexa-488 and 555 (Life Technologies, Carlsbad, CA) were used for the secondary antibodies. DAPI was used for nuclear staining. The signal intensity of an immuno-labeled protein in the region of interest (ROI) was measured for a quantitative analysis using the NIS-elements AR software program (Nikon Corporation, Tokyo, Japan) and the levels in the control and Pten-cKO mice were compared. Morphological analysis was performed as described in Supplementary Methods.

Matsushita Y., Sakai Y., Shimmura M., Shigeto H., Nishio M., Akamine S., Sanefuji M., Ishizaki Y., Torisu H., Nakabeppu Y., Suzuki A., Takada H, & Hara T. (2016). Hyperactive mTOR signals in the proopiomelanocortin-expressing hippocampal neurons cause age-dependent epilepsy and premature death in mice. Scientific Reports, 6, 22991.

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Calcium Imaging of DRG Neurons

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Dissociated DRG cells were loaded with the ratio metric Ca²⁺ indicator dye Fura-2-acetoxymethyl ester (2 μM; Molecular Probes) for at least 40 min at 37 °C in 10 mM HEPES (pH 7.4) containing 140 mM NaCl, 5 mM KCl, 2 mM CaCl₂, 2 mM MgCl₂, and 11 mM glucose (extracellular solution). The cells were then transferred to a recording chamber placed on a microscope (Nikon Eclipse) and continuously perfused with the oxygenated (95% O₂ and 5% CO₂) extracellular solution (2 ml/min) at ambient temperature. The intracellular calcium concentration was expressed as the 340/380 ratio. The signals were captured and analyzed using the NIS-Elements AR software program (Nikon). All chemicals were directly applied to the bath. The MBP_84-104 or SCR peptide (5 or 10 μg/ml, each) was administered to female and male DRG. Where indicated, capsaicin (500 nM) was co-administered. Calcium imaging (ratio of 340/380) was used to record the DRG responses to the MBP_84-104 or SCR peptide and capsaicin.

Hullugundi S.K., Dolkas J., Chernov A.V., Yaksh T.L., Eddinger K.A., Angert M., Catroli G.F., Strongin A.Y., Dougherty P.M., Li Y., Quehenberger O., Armando A, & Shubayev V.I. (2024). Cholesterol-dependent LXR transcription factor activity represses pronociceptive effects of estrogen in sensory neurons and pain induced by myelin basic protein fragments. Brain, Behavior, & Immunity - Health, 38, 100757.

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