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Charles River Laboratories balb c mice
Balb C Mice, supplied by Charles River Laboratories, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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In Vivo:

Article Title: Linking tumor viability and immune infiltration with dual-nucleus MRI in preclinical models
Article Snippet: .. To assess the function of the mOatp1a1 reporter in vivo, bilateral orthotopic 4T1 mammary fat pad tumors were established in BALB/c mice (Charles River, Canada). ..

Injection:

Article Title: Oncostatin M cytokine promotes breast cancer progression by remodelling the extracellular matrix and activating integrin signalling in cancer cells
Article Snippet: Cells were injected into the fourth right mammary fat pad of anaesthetized (with 4% isoflurane) 6- to 8-week-old female mice purchased from Charles River. .. For the syngeneic 4T1 orthotopic tumour experiment, 5.000 viable murine parental 4T1 cells were injected into syngeneic BALB/C mice (Charles River) and therapeutic neutralization of OSM was performed with a murine OSM inhibitor (iOSM), consisting on an Fc-tagged soluble OSMR–gp130 fusion protein , . ..

Neutralization:

Article Title: Oncostatin M cytokine promotes breast cancer progression by remodelling the extracellular matrix and activating integrin signalling in cancer cells
Article Snippet: Cells were injected into the fourth right mammary fat pad of anaesthetized (with 4% isoflurane) 6- to 8-week-old female mice purchased from Charles River. .. For the syngeneic 4T1 orthotopic tumour experiment, 5.000 viable murine parental 4T1 cells were injected into syngeneic BALB/C mice (Charles River) and therapeutic neutralization of OSM was performed with a murine OSM inhibitor (iOSM), consisting on an Fc-tagged soluble OSMR–gp130 fusion protein , . ..

other:

Article Title: A fully human pan VL9 HLA-E TCRm antibody enables functional dissection of HLA-E biology and checkpoint signaling
Article Snippet: BALB/c mice were purchased from Charles River Laboratories.

Article Title: Carprofen and buprenorphine delivery using micropipette-guided drug administration (MDA) in mice.
Article Snippet: Male and female C57BL/6 N (N= 30 per sex) and BALB/c mice (N= 30 per sex) were sourced from Charles River Laboratories (Sulzfeld, Germany) at the age of 10 weeks.

Expressing:

Article Title: Monoclonal antibodies for intracellular delivery of payloads
Article Snippet: .. Antibody generation was achieved by immunization of Balb/c mice (Charles River Laboratories, Wilmington, MA) with a living murine mammary epithelial cell line expressing a cDNA encoding the human dystroglycan (DG) protein. ..



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Biocompatibility of hydrogels. (A-C) Hydrogels were incubated in the respective cell culture media for 72 h, and the obtained extracts were used to assess their effects on the metabolic activity of huMECs (A), vSMCs (B), and NHDFs (C) after 48 h of culture. (D, E) Hydrogel extracts were added to primary human monocytes obtained from five independent donors. The differentiation efficiency of these immune cells into M1 (D) or M2 (E) macrophages was analyzed by flow cytometry using specific markers. (F) Anti-factor Xa activity of HA c and sHA c was determined in comparison with Hep using a chromogenic assay. (A-F) One-way ANOVA: ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. (G) In-vivo assessment of GelMA and GelMA/sHA c hydrogels loaded with TIMP-3. Experimental overview: TIMP-3-loaded GelMA and GelMA/sHA c hydrogels were implanted subcutaneously <t>into</t> <t>BALB/c</t> mice for 14 days. (H) Representative histological images of explanted gels stained for MPO (neutrophils), CD68 (macrophages), CD31 (microvessels), and Sirius red (collagen deposition). The granulation tissue between the muscle tissue and the implant is highlighted by dotted yellow lines. (I-L) Quantification of MPO + and CD68 + cells, CD31 + events, and Sirius red intensity (three ROIs per sample). Statistical analysis was performed using an unpaired t -test with Welch's correction: ∗p < 0.05, ∗∗p < 0.01.
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IL-17A + γδT cells are increased and induce the inflammatory response in experimental BA. Experimental BA was induced in <t>neonatal</t> <t>Balb/c</t> mice through intraperitoneal injection of RRV; after RRV injection, (A) IL-17A levels in the liver homogenate supernatant of the murine BA model were dynamically measured through ELISA (n=5/group per time point), and (B) IL-17A + γδT cells were dynamically analyzed through flow cytometry on days 3, 7 and 14 (n=5/group per time point). (C) After knocking out <t>the</t> <t>Tcrδ</t> gene in Balb/c mice, the dynamic change in IL-17A content in the liver tissue of the Tcrδ −/− murine BA model was measured through ELISA (n=5/group per time point). (D) On day 7 of the Tcrδ −/− murine BA model, immunohistochemical staining with CK19 (upper panels, original magnification, ×100) was used to observe the morphology of intrahepatic bile ducts, and H&E staining (original magnification, ×100) was used to observe liver inflammation (middle panels) and extrahepatic bile duct morphology (lower panels) (n=5/group). (E) Incidence of BA and survival analysis in the Tcrδ −/− murine BA model (n=28 for Tcrδ −/− + RRV group, n=34 for WT + RRV group). (F-H) After adoptive transfusion of murine IL-17A + γδT cells into Tcrδ −/− mice, the aforementioned indicators were observed. (F) Dynamic changes in hepatic IL-17A levels were measured by ELISA (n=5/group per time point). (G) Liver inflammation, intrahepatic bile duct morphology and extrahepatic bile duct morphology were analyzed by immunohistochemical staining with CK19 (left panels, original magnification, ×100) and H&E staining (middle panels for liver inflammation and right panels for extrahepatic bile duct morphology, original magnification, ×100) (n=5/group). (H) Incidence of BA and survival analysis (n=32 for Tcrδ −/− + RRV + RPMI 1640 group, n=34 for Tcrδ −/− + RRV + IL-17A + γδT group). Data are presented as the mean ± standard deviation of at least three repeated experiments. *** P<0.001; ns, not significant. BA, biliary atresia; CK19, cytokeratin 19; H&E, hematoxylin and eosin; MEM, minimum essential medium; RRV, rhesus rotavirus; WT, wild-type.
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IL-17A + γδT cells are increased and induce the inflammatory response in experimental BA. Experimental BA was induced in <t>neonatal</t> <t>Balb/c</t> mice through intraperitoneal injection of RRV; after RRV injection, (A) IL-17A levels in the liver homogenate supernatant of the murine BA model were dynamically measured through ELISA (n=5/group per time point), and (B) IL-17A + γδT cells were dynamically analyzed through flow cytometry on days 3, 7 and 14 (n=5/group per time point). (C) After knocking out <t>the</t> <t>Tcrδ</t> gene in Balb/c mice, the dynamic change in IL-17A content in the liver tissue of the Tcrδ −/− murine BA model was measured through ELISA (n=5/group per time point). (D) On day 7 of the Tcrδ −/− murine BA model, immunohistochemical staining with CK19 (upper panels, original magnification, ×100) was used to observe the morphology of intrahepatic bile ducts, and H&E staining (original magnification, ×100) was used to observe liver inflammation (middle panels) and extrahepatic bile duct morphology (lower panels) (n=5/group). (E) Incidence of BA and survival analysis in the Tcrδ −/− murine BA model (n=28 for Tcrδ −/− + RRV group, n=34 for WT + RRV group). (F-H) After adoptive transfusion of murine IL-17A + γδT cells into Tcrδ −/− mice, the aforementioned indicators were observed. (F) Dynamic changes in hepatic IL-17A levels were measured by ELISA (n=5/group per time point). (G) Liver inflammation, intrahepatic bile duct morphology and extrahepatic bile duct morphology were analyzed by immunohistochemical staining with CK19 (left panels, original magnification, ×100) and H&E staining (middle panels for liver inflammation and right panels for extrahepatic bile duct morphology, original magnification, ×100) (n=5/group). (H) Incidence of BA and survival analysis (n=32 for Tcrδ −/− + RRV + RPMI 1640 group, n=34 for Tcrδ −/− + RRV + IL-17A + γδT group). Data are presented as the mean ± standard deviation of at least three repeated experiments. *** P<0.001; ns, not significant. BA, biliary atresia; CK19, cytokeratin 19; H&E, hematoxylin and eosin; MEM, minimum essential medium; RRV, rhesus rotavirus; WT, wild-type.
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IL-17A + γδT cells are increased and induce the inflammatory response in experimental BA. Experimental BA was induced in <t>neonatal</t> <t>Balb/c</t> mice through intraperitoneal injection of RRV; after RRV injection, (A) IL-17A levels in the liver homogenate supernatant of the murine BA model were dynamically measured through ELISA (n=5/group per time point), and (B) IL-17A + γδT cells were dynamically analyzed through flow cytometry on days 3, 7 and 14 (n=5/group per time point). (C) After knocking out <t>the</t> <t>Tcrδ</t> gene in Balb/c mice, the dynamic change in IL-17A content in the liver tissue of the Tcrδ −/− murine BA model was measured through ELISA (n=5/group per time point). (D) On day 7 of the Tcrδ −/− murine BA model, immunohistochemical staining with CK19 (upper panels, original magnification, ×100) was used to observe the morphology of intrahepatic bile ducts, and H&E staining (original magnification, ×100) was used to observe liver inflammation (middle panels) and extrahepatic bile duct morphology (lower panels) (n=5/group). (E) Incidence of BA and survival analysis in the Tcrδ −/− murine BA model (n=28 for Tcrδ −/− + RRV group, n=34 for WT + RRV group). (F-H) After adoptive transfusion of murine IL-17A + γδT cells into Tcrδ −/− mice, the aforementioned indicators were observed. (F) Dynamic changes in hepatic IL-17A levels were measured by ELISA (n=5/group per time point). (G) Liver inflammation, intrahepatic bile duct morphology and extrahepatic bile duct morphology were analyzed by immunohistochemical staining with CK19 (left panels, original magnification, ×100) and H&E staining (middle panels for liver inflammation and right panels for extrahepatic bile duct morphology, original magnification, ×100) (n=5/group). (H) Incidence of BA and survival analysis (n=32 for Tcrδ −/− + RRV + RPMI 1640 group, n=34 for Tcrδ −/− + RRV + IL-17A + γδT group). Data are presented as the mean ± standard deviation of at least three repeated experiments. *** P<0.001; ns, not significant. BA, biliary atresia; CK19, cytokeratin 19; H&E, hematoxylin and eosin; MEM, minimum essential medium; RRV, rhesus rotavirus; WT, wild-type.
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Biocompatibility of hydrogels. (A-C) Hydrogels were incubated in the respective cell culture media for 72 h, and the obtained extracts were used to assess their effects on the metabolic activity of huMECs (A), vSMCs (B), and NHDFs (C) after 48 h of culture. (D, E) Hydrogel extracts were added to primary human monocytes obtained from five independent donors. The differentiation efficiency of these immune cells into M1 (D) or M2 (E) macrophages was analyzed by flow cytometry using specific markers. (F) Anti-factor Xa activity of HA c and sHA c was determined in comparison with Hep using a chromogenic assay. (A-F) One-way ANOVA: ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. (G) In-vivo assessment of GelMA and GelMA/sHA c hydrogels loaded with TIMP-3. Experimental overview: TIMP-3-loaded GelMA and GelMA/sHA c hydrogels were implanted subcutaneously into BALB/c mice for 14 days. (H) Representative histological images of explanted gels stained for MPO (neutrophils), CD68 (macrophages), CD31 (microvessels), and Sirius red (collagen deposition). The granulation tissue between the muscle tissue and the implant is highlighted by dotted yellow lines. (I-L) Quantification of MPO + and CD68 + cells, CD31 + events, and Sirius red intensity (three ROIs per sample). Statistical analysis was performed using an unpaired t -test with Welch's correction: ∗p < 0.05, ∗∗p < 0.01.

Journal: Bioactive Materials

Article Title: Glycosaminoglycan-functionalized hydrogels for sustained delivery of tissue inhibitor of metalloproteinase-3 mediating matrix metalloprotease inhibition and extracellular matrix stabilization

doi: 10.1016/j.bioactmat.2026.02.010

Figure Lengend Snippet: Biocompatibility of hydrogels. (A-C) Hydrogels were incubated in the respective cell culture media for 72 h, and the obtained extracts were used to assess their effects on the metabolic activity of huMECs (A), vSMCs (B), and NHDFs (C) after 48 h of culture. (D, E) Hydrogel extracts were added to primary human monocytes obtained from five independent donors. The differentiation efficiency of these immune cells into M1 (D) or M2 (E) macrophages was analyzed by flow cytometry using specific markers. (F) Anti-factor Xa activity of HA c and sHA c was determined in comparison with Hep using a chromogenic assay. (A-F) One-way ANOVA: ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001. (G) In-vivo assessment of GelMA and GelMA/sHA c hydrogels loaded with TIMP-3. Experimental overview: TIMP-3-loaded GelMA and GelMA/sHA c hydrogels were implanted subcutaneously into BALB/c mice for 14 days. (H) Representative histological images of explanted gels stained for MPO (neutrophils), CD68 (macrophages), CD31 (microvessels), and Sirius red (collagen deposition). The granulation tissue between the muscle tissue and the implant is highlighted by dotted yellow lines. (I-L) Quantification of MPO + and CD68 + cells, CD31 + events, and Sirius red intensity (three ROIs per sample). Statistical analysis was performed using an unpaired t -test with Welch's correction: ∗p < 0.05, ∗∗p < 0.01.

Article Snippet: To investigate the in-vivo function of the gels, GelMA + TIMP-3 und GelMA/sHA c + TIMP3 gels were subcutaneously transplanted into the flanks of eight 14-week-old BALB/c mice (Janvier Labs, Le Genest-St-Isle, France).

Techniques: Incubation, Cell Culture, Activity Assay, Flow Cytometry, Comparison, Chromogenic Assay, In Vivo, Staining

IL-17A + γδT cells are increased and induce the inflammatory response in experimental BA. Experimental BA was induced in neonatal Balb/c mice through intraperitoneal injection of RRV; after RRV injection, (A) IL-17A levels in the liver homogenate supernatant of the murine BA model were dynamically measured through ELISA (n=5/group per time point), and (B) IL-17A + γδT cells were dynamically analyzed through flow cytometry on days 3, 7 and 14 (n=5/group per time point). (C) After knocking out the Tcrδ gene in Balb/c mice, the dynamic change in IL-17A content in the liver tissue of the Tcrδ −/− murine BA model was measured through ELISA (n=5/group per time point). (D) On day 7 of the Tcrδ −/− murine BA model, immunohistochemical staining with CK19 (upper panels, original magnification, ×100) was used to observe the morphology of intrahepatic bile ducts, and H&E staining (original magnification, ×100) was used to observe liver inflammation (middle panels) and extrahepatic bile duct morphology (lower panels) (n=5/group). (E) Incidence of BA and survival analysis in the Tcrδ −/− murine BA model (n=28 for Tcrδ −/− + RRV group, n=34 for WT + RRV group). (F-H) After adoptive transfusion of murine IL-17A + γδT cells into Tcrδ −/− mice, the aforementioned indicators were observed. (F) Dynamic changes in hepatic IL-17A levels were measured by ELISA (n=5/group per time point). (G) Liver inflammation, intrahepatic bile duct morphology and extrahepatic bile duct morphology were analyzed by immunohistochemical staining with CK19 (left panels, original magnification, ×100) and H&E staining (middle panels for liver inflammation and right panels for extrahepatic bile duct morphology, original magnification, ×100) (n=5/group). (H) Incidence of BA and survival analysis (n=32 for Tcrδ −/− + RRV + RPMI 1640 group, n=34 for Tcrδ −/− + RRV + IL-17A + γδT group). Data are presented as the mean ± standard deviation of at least three repeated experiments. *** P<0.001; ns, not significant. BA, biliary atresia; CK19, cytokeratin 19; H&E, hematoxylin and eosin; MEM, minimum essential medium; RRV, rhesus rotavirus; WT, wild-type.

Journal: International Journal of Molecular Medicine

Article Title: IL-17A + γδT cell activation via the HMGB1-TLR2/4-NF-κB signaling pathways in biliary atresia

doi: 10.3892/ijmm.2026.5852

Figure Lengend Snippet: IL-17A + γδT cells are increased and induce the inflammatory response in experimental BA. Experimental BA was induced in neonatal Balb/c mice through intraperitoneal injection of RRV; after RRV injection, (A) IL-17A levels in the liver homogenate supernatant of the murine BA model were dynamically measured through ELISA (n=5/group per time point), and (B) IL-17A + γδT cells were dynamically analyzed through flow cytometry on days 3, 7 and 14 (n=5/group per time point). (C) After knocking out the Tcrδ gene in Balb/c mice, the dynamic change in IL-17A content in the liver tissue of the Tcrδ −/− murine BA model was measured through ELISA (n=5/group per time point). (D) On day 7 of the Tcrδ −/− murine BA model, immunohistochemical staining with CK19 (upper panels, original magnification, ×100) was used to observe the morphology of intrahepatic bile ducts, and H&E staining (original magnification, ×100) was used to observe liver inflammation (middle panels) and extrahepatic bile duct morphology (lower panels) (n=5/group). (E) Incidence of BA and survival analysis in the Tcrδ −/− murine BA model (n=28 for Tcrδ −/− + RRV group, n=34 for WT + RRV group). (F-H) After adoptive transfusion of murine IL-17A + γδT cells into Tcrδ −/− mice, the aforementioned indicators were observed. (F) Dynamic changes in hepatic IL-17A levels were measured by ELISA (n=5/group per time point). (G) Liver inflammation, intrahepatic bile duct morphology and extrahepatic bile duct morphology were analyzed by immunohistochemical staining with CK19 (left panels, original magnification, ×100) and H&E staining (middle panels for liver inflammation and right panels for extrahepatic bile duct morphology, original magnification, ×100) (n=5/group). (H) Incidence of BA and survival analysis (n=32 for Tcrδ −/− + RRV + RPMI 1640 group, n=34 for Tcrδ −/− + RRV + IL-17A + γδT group). Data are presented as the mean ± standard deviation of at least three repeated experiments. *** P<0.001; ns, not significant. BA, biliary atresia; CK19, cytokeratin 19; H&E, hematoxylin and eosin; MEM, minimum essential medium; RRV, rhesus rotavirus; WT, wild-type.

Article Snippet: The Tcrδ −/− , Tlr2 −/− and Tlr4 −/− Balb/c mice (n=2 male mice and 4 female mice per genotype; age, 8-10 weeks; weight, 20-25 g) were produced by Shanghai Model Organisms Center, Inc., using a proprietary CRISPR-Cas9 gene targeting platform.

Techniques: Injection, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Immunohistochemical staining, Staining, Standard Deviation