male scid beige mice  (Charles River Laboratories)

Journal: Translational Oncology

Article Title: A RIPK2 activity signature in prostate cancer: Modulation by RIPK2 inhibition and clinical association

doi: 10.1016/j.tranon.2026.102819

Figure Lengend Snippet: Ponatinib progressively suppresses the RIPK2 activity signature in vivo. (A) Schematic of the in vivo experimental design. Male immunodeficient SCID/Beige mice bearing ∼200 mm 3 subcutaneous (s.c.) 22Rv1 xenograft tumors were treated daily with ponatinib (Pon, 6 mg/kg) or vehicle (Veh) control by oral gavage for 3 or 7 days. Created with BioRender.com. (B) Tumor weights of 22Rv1 xenografts harvested after 3 or 7 days of treatment (n = 3 mice per group). (C) Immunoblot images (left) and corresponding densitometric quantification (right) of the indicated proteins in xenograft tumor lysates (n = 3). (D) Grouped dot plot showing log 2 -transformed fold changes (Log 2 FC) of the indicated RIPK2 signature genes in xenograft tumors relative to vehicle controls (n = 3). (E) Swarm plot of RIPK2 qPCR signature scores in xenografts (n = 3). Solid lines represent the mean signature scores. Nominal P-values were calculated using an unpaired two-tailed Student’s t-test. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; ns, not significant.

Article Snippet: A total of 100 μL of the cell suspension was injected subcutaneously into one flank of 6-week-old male SCID/Beige mice (n = 12; Charles River, #CRL:250; CB17.Cg-Prkdc scid Lyst bg-J /Crl).

Techniques: Activity Assay, In Vivo, Control, Western Blot, Transformation Assay, Two Tailed Test

Journal:

Article Title:

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Figure Lengend Snippet: SCID mice were infected intravenously with 1.0×10 6 CFU per animal of either Mabs ATCC 19977 WT, the dosRS KO mutant or the dosRS complemented mutant. AMK and AZI treatment of each group of mice began 28 d after infection, upon establishment of chronic infection. As of d 28, mice were treated daily (7 d/week) for 28 d with saline (gavage), AMK (150 mg/kg, subcutaneous injection) or AZI (200 mg/kg, gavage). Groups of mice were ethically euthanized on d 2, 28 and 56, and lungs and spleens were taken for bacterial enumeration (CFU). For each bacterial strain, the CFU results represent the average of 5 mice per time point, and bacterial loads are expressed as Log 10 CFU (± SEM). Asterisks denote statistically significant differences between antibiotic-treated WT and mutant- or complemented mutant-infected mice pursuant to the Student’s t -test (p* < 0.05; p** < 0.005).

Article Snippet: Fox Chase severe combined immunodeficiency (SCID) Beige mice were ordered from Charles River (North Wilmington, MA, USA).

Techniques: Infection, Mutagenesis, Saline, Injection

Journal:

Article Title:

doi:

Figure Lengend Snippet: ( A ) Exposure of OZ439 in Mabs ATCC 19977-infected SCID mice. In the acute model, mice received OZ439 orally (200 mg/kg) every other d for 14 d. In the chronic model, mice received OZ439 orally (50 mg/kg) every other d for 28 d. Shown are the averages (± SD) of lung and plasma concentrations 2 and 48 hs after the last dosing. Two mice were used per time point in the acute model. Four mice were used per time point in the chronic model. ( B ) Therapeutic efficacy testing in an acute SCID mouse model of MABSC infection. Mice (n=5 mice/group) were infected intratracheally with 1.0×10 6 CFUs of WT Mabs ATCC 19977. On d 12 post-infection, during the acute phase of infection, mice were treated daily (7 d/week) for 14 d, or every other day for OZ439, with vehicle used in the formulation of OZ439 (HPMC-SV), OZ439, AMK, AZI, IMI, CFZ, and the same four antibiotic treatments in combination with OZ439. See text for more details about the treatments. Bacterial loads were determined in the lungs, liver and spleen on d 2, 12 and 26. ( C ) Therapeutic efficacy testing in a chronic SCID mouse model of MABSC infection. Mice (five animals per group) were infected intravenously with 1.0×10 6 CFUs of WT Mabs ATCC 19977. On d 28 post-infection, upon establishment of chronic infection, mice were treated daily (7 d/week) for 28 d, or every other day for OZ439, with formulation vehicle, OZ439, AMK, AZI, IMI and CFZ, and the same four antibiotics in combination with OZ439. See text for more details about the treatments. Bacterial loads were determined in the lungs, liver, and spleen on d 2, 28 and 56. In ( B ) and ( C ), asterisks denote statistically significant differences between antibiotic-treated and antibiotic+OZ439-treated mice, or untreated and OZ439-treated mice pursuant to the Student’s t -test (*p < 0.05; **p < 0.005; ***p < 0.0005).

Article Snippet: Fox Chase severe combined immunodeficiency (SCID) Beige mice were ordered from Charles River (North Wilmington, MA, USA).

Techniques: Drug discovery, Infection, Clinical Proteomics, Formulation

Journal: bioRxiv

Article Title: Clinical-grade cryopreservation unlocks transplant-ready human pancreatic and stem cell–derived islets for diabetes therapy

doi: 10.64898/2026.04.25.720819

Figure Lengend Snippet: In all panels, native pancreatic islets (left) and SC-islets (right) are shown. ( A–D ) Human islet and SC-islet xenotransplantation in immunodeficient (SCID beige) mice: basal and intraperitoneal (IP) glucose-stimulated human serum insulin levels and corresponding stimulation indices. (n = 12–28 per group; paired Wilcoxon test). ( E-F ) Confocal images of explanted grafts stained for insulin (red), glucagon (green), and nuclei (DAPI, blue). Scale bars = 100 µm. ( G ) Reversal of hyperglycemia in chemically diabetic immunodeficient (NSG) mice transplanted with cryopreserved human islets (left) or SC-islets (right) stored for 1 day to 1 year. An intraperitoneal glucose tolerance test (IP-GTT) was performed on day 49, followed by nephrectomy of the graft-bearing kidney on day 50. Gray shading indicates the normoglycemic range. n = 5 for islet transplant and n = 4 for SC-islet grafts. Data are shown as box-and-whisker plots or mean ± SD. Abbreviations: DAPI, 4′,6-diamidino-2-phenylindole; NSG, NOD scid gamma; SC, stem cell; VR, vitrified and rewarmed.

Article Snippet: Male 8- to 10-week-old SCID Beige mice (Charles River Laboratories), weighing 19–24 g, were used as recipients for fresh and VR human islet and SC-islet grafts.

Techniques: Staining, Whisker Assay

Journal: Molecular cancer therapeutics

Article Title: NAPRT expression and epigenetic regulation in pediatric rhabdomyosarcoma as a potential biomarker for NAMPT inhibition

doi: 10.1158/1535-7163.MCT-25-0619

Figure Lengend Snippet: A-F. Tumor growth curves ( A-C ) and Kaplan-Meier plots ( D-F ) of Fox Chase SCID mice bearing RH30 (NAPRT+) ( A, D ), RH41 (NAPRT-) ( B, E ), RH41 NAPRT+ ( C, F ) following treatment with 30% cyclodextrin vehicle, 25 mg/kg OT82, and 25 mg/kg OT-82 in combination with 25 mg/kg NA. G-H. Total NAD + levels in tumors harvested from RH41 (NAPRT-) ( G ) and RH41 NAPRT+ ( H ) models treated with 1 cycle of 30% cyclodextrin vehicle, 25 mg/kg OT-82, and 25 mg/kg NAMPTi in combination with 25 mg/kg NA. I-J. Total NAD + levels in contralateral normal gastrocnemius muscle harvested from RH41 (NAPRT-) ( I ) and RH41 NAPRT+ ( J ) treated with 1 cycle of 30% cyclodextrin vehicle, 25 mg/kg OT-82, and 25 mg/kg NAMPTi in combination with 25 mg/kg NA. For G-J, each treatment cohort included 3 biological replicates, with 2 technical replicates per biological replicate. K. NAPRT expression by western blot in NAPRT-expressing PDX model (SJRHB13758). L. Cell viability in SJRHB13758 treated with increasing concentrations of OT-82 with and without 10 μM NA. M. NAPRT expression by western blot in PDX model, SJRHB010463_X16, confirming NAPRT-deficiency. N. Representative NAPRT IHC (left) and hematoxylin and eosin (H&E; right) images of SJRHB010463_X16, a NAPRT-deficient PDX model. O-Q. Tumor growth curves ( O ), Kaplan-Meier plots ( P ), and body weight plots ( Q ) of 6–8-week-old female Athymic Nude-Foxn1nu mice bearing RMS PDX SJRHB010463_X16. For A-F, each treatment group had 5 biological replicates (control N=5; OT82 N=5; OT82+NA N=5). For O-Q, each group had 6–9 biological replicates (control N=6; OT82 N=8; OT82+NA N=9). The data is plotted as mean with error bars indicating SEM. *p<0.05; **p<0.01; ***p<0.001; ****p<0.0001; n.s., not significant.

Article Snippet: Four- to six-week-old female Fox Chase SCID Beige mice (CB17.B6-Prkdc scid Lyst bg/Cr) from Charles River Laboratories (n = 3–5 mice per treatment group) were used for cell line xenograft experiments.

Techniques: Expressing, Western Blot, Control