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Hitachi Ltd dox fluorescence
Selection and identification of DNA aptamers specific to ESCC. (A) Flow cytometry assays of the binding of the selected libraries to KYSE30 and Het-1A cells. (B) Flow cytometry assays of the binding of Z1-6 aptamer candidates to KYSE30 and Het-1A cells. (C) The binding signal-to-background ratio (SBR) calculation in B. <t>Fluorescence</t> intensity of random ssDNA was used as the background signal. (D) Confocal imaging of KYSE30 cells incubated with FAM-labeled Z1, Z2, and Z4 aptamers. The scale bar is 50 μm. (E) Determination of dissociation constant (K d ) of Z1, Z2, and Z4 aptamers for KYSE30 cells by flow cytometry. FAM-labeled random ssDNA was used as the negative control.
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Selection and identification of DNA aptamers specific to ESCC. (A) Flow cytometry assays of the binding of the selected libraries to KYSE30 and Het-1A cells. (B) Flow cytometry assays of the binding of Z1-6 aptamer candidates to KYSE30 and Het-1A cells. (C) The binding signal-to-background ratio (SBR) calculation in B. <t>Fluorescence</t> intensity of random ssDNA was used as the background signal. (D) Confocal imaging of KYSE30 cells incubated with FAM-labeled Z1, Z2, and Z4 aptamers. The scale bar is 50 μm. (E) Determination of dissociation constant (K d ) of Z1, Z2, and Z4 aptamers for KYSE30 cells by flow cytometry. FAM-labeled random ssDNA was used as the negative control.
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Selection and identification of DNA aptamers specific to ESCC. (A) Flow cytometry assays of the binding of the selected libraries to KYSE30 and Het-1A cells. (B) Flow cytometry assays of the binding of Z1-6 aptamer candidates to KYSE30 and Het-1A cells. (C) The binding signal-to-background ratio (SBR) calculation in B. <t>Fluorescence</t> intensity of random ssDNA was used as the background signal. (D) Confocal imaging of KYSE30 cells incubated with FAM-labeled Z1, Z2, and Z4 aptamers. The scale bar is 50 μm. (E) Determination of dissociation constant (K d ) of Z1, Z2, and Z4 aptamers for KYSE30 cells by flow cytometry. FAM-labeled random ssDNA was used as the negative control.
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Selection and identification of DNA aptamers specific to ESCC. (A) Flow cytometry assays of the binding of the selected libraries to KYSE30 and Het-1A cells. (B) Flow cytometry assays of the binding of Z1-6 aptamer candidates to KYSE30 and Het-1A cells. (C) The binding signal-to-background ratio (SBR) calculation in B. <t>Fluorescence</t> intensity of random ssDNA was used as the background signal. (D) Confocal imaging of KYSE30 cells incubated with FAM-labeled Z1, Z2, and Z4 aptamers. The scale bar is 50 μm. (E) Determination of dissociation constant (K d ) of Z1, Z2, and Z4 aptamers for KYSE30 cells by flow cytometry. FAM-labeled random ssDNA was used as the negative control.
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Brain homing ability, sequential targeting capability, and cytotoxicity assessment. (a) Illustration of Ang-Lip@BAY/GW1929 sequentially transported across the BBB, followed by targeting microglia. (b) Schematic of the BBB transwell model. (c) In vitro uptake by BV-2 cells of RhB-labeled Lip@BAY/GW1929 and Ang-Lip@BAY/GW1929 by fluorescent imaging (scale bar = 50 μm). (d, e f, and g) Fluorescent staining of (CD86 (d) and CD206 (f)), and quantification analysis ((e) and (g)) of the different conditions-treated BV-2 cells in an BBB model in vitro . (h) In vivo imaging of Cy5.5-labeled Ang-Lip@BAY/GW1929 in normoxia mice and CIH-induced mice. (i) Quantitative assessment of in vivo <t>fluorescence</t> intensity of brain at different time intervals under the Cy5.5 channel (n = 3). (j, k) In vitro cytotoxicity assay of Lip (j) and Ang-Lip@BAY/GW1929 (k) at different concentrations against BV-2 cells for 24 h. (l) Cytotoxicity of BV-2 cells treated with various samples. (m) CLSM images of BV-2 cells stained with calcein-AM (green, viable) and PI (red, dead) treated with Lip (G1), Lip@BAY (G2), Lip@GW1929 (G3), Lip@BAY/GW1929 (G4), and Ang-Lip@BAY/GW1929 (G5). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
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Hitachi Ltd f 7000 fluorescence spectrometer
Brain homing ability, sequential targeting capability, and cytotoxicity assessment. (a) Illustration of Ang-Lip@BAY/GW1929 sequentially transported across the BBB, followed by targeting microglia. (b) Schematic of the BBB transwell model. (c) In vitro uptake by BV-2 cells of RhB-labeled Lip@BAY/GW1929 and Ang-Lip@BAY/GW1929 by fluorescent imaging (scale bar = 50 μm). (d, e f, and g) Fluorescent staining of (CD86 (d) and CD206 (f)), and quantification analysis ((e) and (g)) of the different conditions-treated BV-2 cells in an BBB model in vitro . (h) In vivo imaging of Cy5.5-labeled Ang-Lip@BAY/GW1929 in normoxia mice and CIH-induced mice. (i) Quantitative assessment of in vivo <t>fluorescence</t> intensity of brain at different time intervals under the Cy5.5 channel (n = 3). (j, k) In vitro cytotoxicity assay of Lip (j) and Ang-Lip@BAY/GW1929 (k) at different concentrations against BV-2 cells for 24 h. (l) Cytotoxicity of BV-2 cells treated with various samples. (m) CLSM images of BV-2 cells stained with calcein-AM (green, viable) and PI (red, dead) treated with Lip (G1), Lip@BAY (G2), Lip@GW1929 (G3), Lip@BAY/GW1929 (G4), and Ang-Lip@BAY/GW1929 (G5). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
F 7000 Fluorescence Spectrometer, supplied by Hitachi Ltd, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Selection and identification of DNA aptamers specific to ESCC. (A) Flow cytometry assays of the binding of the selected libraries to KYSE30 and Het-1A cells. (B) Flow cytometry assays of the binding of Z1-6 aptamer candidates to KYSE30 and Het-1A cells. (C) The binding signal-to-background ratio (SBR) calculation in B. Fluorescence intensity of random ssDNA was used as the background signal. (D) Confocal imaging of KYSE30 cells incubated with FAM-labeled Z1, Z2, and Z4 aptamers. The scale bar is 50 μm. (E) Determination of dissociation constant (K d ) of Z1, Z2, and Z4 aptamers for KYSE30 cells by flow cytometry. FAM-labeled random ssDNA was used as the negative control.

Journal: Materials Today Bio

Article Title: Identification of a myosin 1B-binding aptamer for fluorescence imaging and targeted therapy of esophageal squamous cell carcinoma

doi: 10.1016/j.mtbio.2026.102867

Figure Lengend Snippet: Selection and identification of DNA aptamers specific to ESCC. (A) Flow cytometry assays of the binding of the selected libraries to KYSE30 and Het-1A cells. (B) Flow cytometry assays of the binding of Z1-6 aptamer candidates to KYSE30 and Het-1A cells. (C) The binding signal-to-background ratio (SBR) calculation in B. Fluorescence intensity of random ssDNA was used as the background signal. (D) Confocal imaging of KYSE30 cells incubated with FAM-labeled Z1, Z2, and Z4 aptamers. The scale bar is 50 μm. (E) Determination of dissociation constant (K d ) of Z1, Z2, and Z4 aptamers for KYSE30 cells by flow cytometry. FAM-labeled random ssDNA was used as the negative control.

Article Snippet: To investigate the Dox loading capacity, Dox was fixed at 2 μM, and various aptamer-to-Dox ratios (0, 1:20, 1:15, 1:10, 1:7.5, 1:5, 1:3, and 1:2) were prepared as above mentioned, and Dox fluorescence was examined by F-7000 fluorescence spectrometer (Hitachi, Japan).

Techniques: Selection, Flow Cytometry, Binding Assay, Fluorescence, Imaging, Incubation, Labeling, Negative Control

Flow cytometry assays of the binding of Z1 (blue), Z2 (orange), and Z4 (green) aptamers to different cell lines. Random ssDNA (red) was used as the control probe. Aptamers and random ssDNA were labeled with FAM group for collecting fluorescence signals.

Journal: Materials Today Bio

Article Title: Identification of a myosin 1B-binding aptamer for fluorescence imaging and targeted therapy of esophageal squamous cell carcinoma

doi: 10.1016/j.mtbio.2026.102867

Figure Lengend Snippet: Flow cytometry assays of the binding of Z1 (blue), Z2 (orange), and Z4 (green) aptamers to different cell lines. Random ssDNA (red) was used as the control probe. Aptamers and random ssDNA were labeled with FAM group for collecting fluorescence signals.

Article Snippet: To investigate the Dox loading capacity, Dox was fixed at 2 μM, and various aptamer-to-Dox ratios (0, 1:20, 1:15, 1:10, 1:7.5, 1:5, 1:3, and 1:2) were prepared as above mentioned, and Dox fluorescence was examined by F-7000 fluorescence spectrometer (Hitachi, Japan).

Techniques: Flow Cytometry, Binding Assay, Control, Labeling, Fluorescence

Fluorescence imaging of ESCC tissues with Cy5-labeled aptamer probes. (A) Representative images of ESCC and adjacent tissues stained with Cy5-labeled Z2 and Z4-6 aptamer probes. Cy5-labeled random ssDNA was used as the control probe. Scale bar is 50 μm. (B) Quantitative fluorescence intensity of ESCC and adjacent tissues stained with Cy5-labeled Z2 probes. (C) Quantitative fluorescence intensity of ESCC and adjacent tissues stained with Cy5-labeled Z4-6 probes. The asterisks indicate significance, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Journal: Materials Today Bio

Article Title: Identification of a myosin 1B-binding aptamer for fluorescence imaging and targeted therapy of esophageal squamous cell carcinoma

doi: 10.1016/j.mtbio.2026.102867

Figure Lengend Snippet: Fluorescence imaging of ESCC tissues with Cy5-labeled aptamer probes. (A) Representative images of ESCC and adjacent tissues stained with Cy5-labeled Z2 and Z4-6 aptamer probes. Cy5-labeled random ssDNA was used as the control probe. Scale bar is 50 μm. (B) Quantitative fluorescence intensity of ESCC and adjacent tissues stained with Cy5-labeled Z2 probes. (C) Quantitative fluorescence intensity of ESCC and adjacent tissues stained with Cy5-labeled Z4-6 probes. The asterisks indicate significance, ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Article Snippet: To investigate the Dox loading capacity, Dox was fixed at 2 μM, and various aptamer-to-Dox ratios (0, 1:20, 1:15, 1:10, 1:7.5, 1:5, 1:3, and 1:2) were prepared as above mentioned, and Dox fluorescence was examined by F-7000 fluorescence spectrometer (Hitachi, Japan).

Techniques: Fluorescence, Imaging, Labeling, Staining, Control

Selective cytotoxicity of Z4-6-Dox. (A) Schematic illustration of construction of Z4-6-Dox. (B) Fluorescence spectrum of Dox incubated with various concentration of Z4-6. Dox was fixed at 2 μM. (C) Flow cytometry assays of binding of Cy5-labeled Z4-6 and Z4-6-Dox to KYSE30 cells. Confocal imaging of KYSE30 (D) and Het-1A (E) cells treated with 4 μM Dox and 0.8 μM Z4-6-Dox. Cell nuclei were stained with Hoechst33342. CCK-8 assays of KYSE30 (F) and Het-1A (G) cells treated with 0.8 μM Z4-6 and Z4-6-Dox, and 4 μM Dox. The asterisks indicate significance, ∗∗∗ P < 0.001, ns indicates no significance. (H) Calcein-AM/PI imaging of KYSE30 and Het-1A cells treated with 0.8 μM Z4-6 and Z4-6-Dox, and 4 μM Dox. The green indicates Calcein-AM-stained live cells, and the red indicates PI-stained dead cells. (I) The percentage of dead cells was calculated. Untreated cells are the controls. The asterisks indicate significance, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Journal: Materials Today Bio

Article Title: Identification of a myosin 1B-binding aptamer for fluorescence imaging and targeted therapy of esophageal squamous cell carcinoma

doi: 10.1016/j.mtbio.2026.102867

Figure Lengend Snippet: Selective cytotoxicity of Z4-6-Dox. (A) Schematic illustration of construction of Z4-6-Dox. (B) Fluorescence spectrum of Dox incubated with various concentration of Z4-6. Dox was fixed at 2 μM. (C) Flow cytometry assays of binding of Cy5-labeled Z4-6 and Z4-6-Dox to KYSE30 cells. Confocal imaging of KYSE30 (D) and Het-1A (E) cells treated with 4 μM Dox and 0.8 μM Z4-6-Dox. Cell nuclei were stained with Hoechst33342. CCK-8 assays of KYSE30 (F) and Het-1A (G) cells treated with 0.8 μM Z4-6 and Z4-6-Dox, and 4 μM Dox. The asterisks indicate significance, ∗∗∗ P < 0.001, ns indicates no significance. (H) Calcein-AM/PI imaging of KYSE30 and Het-1A cells treated with 0.8 μM Z4-6 and Z4-6-Dox, and 4 μM Dox. The green indicates Calcein-AM-stained live cells, and the red indicates PI-stained dead cells. (I) The percentage of dead cells was calculated. Untreated cells are the controls. The asterisks indicate significance, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Article Snippet: To investigate the Dox loading capacity, Dox was fixed at 2 μM, and various aptamer-to-Dox ratios (0, 1:20, 1:15, 1:10, 1:7.5, 1:5, 1:3, and 1:2) were prepared as above mentioned, and Dox fluorescence was examined by F-7000 fluorescence spectrometer (Hitachi, Japan).

Techniques: Fluorescence, Incubation, Concentration Assay, Flow Cytometry, Binding Assay, Labeling, Imaging, Staining, CCK-8 Assay

In vivo fluorescence imaging with the Z4-6-Cy5 probe. Time-lapse fluorescence imaging of mice bearing KYSE30 tumors after injected with the Z4-6-Cy5 (A) and Random-Cy5 (C) probes. Fluorescence images of excised heart (1), liver (2), spleen (3), lung (4), kidney (5), tumor (6) tissues from mouse model injected with the Z4-6-Cy5 (B) and Random-Cy5 (D) probes. (E) The quantitative analysis of fluorescence intensity at tumor sites in mice treated with the Z4-6-Cy5 and Random-Cy5 probes. (F) The quantitative analysis of fluorescence intensity in excised tumors and major organs.

Journal: Materials Today Bio

Article Title: Identification of a myosin 1B-binding aptamer for fluorescence imaging and targeted therapy of esophageal squamous cell carcinoma

doi: 10.1016/j.mtbio.2026.102867

Figure Lengend Snippet: In vivo fluorescence imaging with the Z4-6-Cy5 probe. Time-lapse fluorescence imaging of mice bearing KYSE30 tumors after injected with the Z4-6-Cy5 (A) and Random-Cy5 (C) probes. Fluorescence images of excised heart (1), liver (2), spleen (3), lung (4), kidney (5), tumor (6) tissues from mouse model injected with the Z4-6-Cy5 (B) and Random-Cy5 (D) probes. (E) The quantitative analysis of fluorescence intensity at tumor sites in mice treated with the Z4-6-Cy5 and Random-Cy5 probes. (F) The quantitative analysis of fluorescence intensity in excised tumors and major organs.

Article Snippet: To investigate the Dox loading capacity, Dox was fixed at 2 μM, and various aptamer-to-Dox ratios (0, 1:20, 1:15, 1:10, 1:7.5, 1:5, 1:3, and 1:2) were prepared as above mentioned, and Dox fluorescence was examined by F-7000 fluorescence spectrometer (Hitachi, Japan).

Techniques: In Vivo, Fluorescence, Imaging, Injection

Brain homing ability, sequential targeting capability, and cytotoxicity assessment. (a) Illustration of Ang-Lip@BAY/GW1929 sequentially transported across the BBB, followed by targeting microglia. (b) Schematic of the BBB transwell model. (c) In vitro uptake by BV-2 cells of RhB-labeled Lip@BAY/GW1929 and Ang-Lip@BAY/GW1929 by fluorescent imaging (scale bar = 50 μm). (d, e f, and g) Fluorescent staining of (CD86 (d) and CD206 (f)), and quantification analysis ((e) and (g)) of the different conditions-treated BV-2 cells in an BBB model in vitro . (h) In vivo imaging of Cy5.5-labeled Ang-Lip@BAY/GW1929 in normoxia mice and CIH-induced mice. (i) Quantitative assessment of in vivo fluorescence intensity of brain at different time intervals under the Cy5.5 channel (n = 3). (j, k) In vitro cytotoxicity assay of Lip (j) and Ang-Lip@BAY/GW1929 (k) at different concentrations against BV-2 cells for 24 h. (l) Cytotoxicity of BV-2 cells treated with various samples. (m) CLSM images of BV-2 cells stained with calcein-AM (green, viable) and PI (red, dead) treated with Lip (G1), Lip@BAY (G2), Lip@GW1929 (G3), Lip@BAY/GW1929 (G4), and Ang-Lip@BAY/GW1929 (G5). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Journal: Materials Today Bio

Article Title: Intelligent nanoliposome ameliorate chronic intermittent hypoxia-mediated neuronal injury via a dual regulation microglial inflammation strategy

doi: 10.1016/j.mtbio.2026.102865

Figure Lengend Snippet: Brain homing ability, sequential targeting capability, and cytotoxicity assessment. (a) Illustration of Ang-Lip@BAY/GW1929 sequentially transported across the BBB, followed by targeting microglia. (b) Schematic of the BBB transwell model. (c) In vitro uptake by BV-2 cells of RhB-labeled Lip@BAY/GW1929 and Ang-Lip@BAY/GW1929 by fluorescent imaging (scale bar = 50 μm). (d, e f, and g) Fluorescent staining of (CD86 (d) and CD206 (f)), and quantification analysis ((e) and (g)) of the different conditions-treated BV-2 cells in an BBB model in vitro . (h) In vivo imaging of Cy5.5-labeled Ang-Lip@BAY/GW1929 in normoxia mice and CIH-induced mice. (i) Quantitative assessment of in vivo fluorescence intensity of brain at different time intervals under the Cy5.5 channel (n = 3). (j, k) In vitro cytotoxicity assay of Lip (j) and Ang-Lip@BAY/GW1929 (k) at different concentrations against BV-2 cells for 24 h. (l) Cytotoxicity of BV-2 cells treated with various samples. (m) CLSM images of BV-2 cells stained with calcein-AM (green, viable) and PI (red, dead) treated with Lip (G1), Lip@BAY (G2), Lip@GW1929 (G3), Lip@BAY/GW1929 (G4), and Ang-Lip@BAY/GW1929 (G5). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: The CIH-bearing mice and normoxia-treated mice (n = 3) were respectively fixed in the mouse tail vein injection holder and injected intravenously with Cy5.5-marked Ang-Lip@BAY/GW1929 (100 μg/mL, 100 μL) using a 1 mL syringe, and then monitored the fluorescence changes in the mouse brain during the specified time period (0.5, 2, 4, and 8 h) using in vivo fluorescence imaging (PerkinElmer IVIS Spectrum in vivo imaging system) after intraperitoneal anesthesia and quantified assessment.

Techniques: In Vitro, Labeling, Imaging, Staining, In Vivo Imaging, In Vivo, Fluorescence, Cytotoxicity Assay