infinity reagents  (Thermo Fisher)

Journal: bioRxiv

Article Title: Gene dosage imbalance disrupts systemic metabolism in the Dp16 Down syndrome mouse model

doi: 10.64898/2026.01.13.699318

Figure Lengend Snippet: A-B) Overnight fasting insulin, blood glucose, serum triglyceride, cholesterol, non-esterified free fatty acids (NEFA), and β-hydroxybutyrate (ketone) in male (A) and female (B) Dp16 and WT mice. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 15). C-F) Impaired glucose tolerance as determined by the glucose tolerance test (GTT) in male (C) and female (E) Dp16 mice compared to WT controls. Impaired insulin sensitivity as determined by the insulin tolerance test (ITT) in male (D) and female (F) Dp16 compared to WT controls. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 15). G-H) Impaired triglyceride clearance in response to lipid gavage as determined by the lipid tolerance test (LTT) in male (G) and female (H) Dp16 relative to WT controls. Sample size for male mice (WT = 10; Dp16 = 14) and female mice (WT = 15; Dp16 = 15). I-J) Pooled mouse sera from male (I) and female (J) Dp16 and WT mice were fractionated by fast protein liquid chromatography (FPLC), and the triglyceride and cholesterol content of each fraction was quantified. Fractions corresponding to very-low density lipoprotein (VLDL), low-density lipoprotein (LDL), intermediate-density lipoprotein (IDL), and high-density lipoprotein (HDL) are indicated. All data are presented as mean ± SEM. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. For all tolerance tests, data were analyzed by 2-way ANOVA with Sidek post hoc tests.

Article Snippet: Following tissue extraction, total cholesterol content was quantified using the Infinity Cholesterol Reagent kit (Thermo Fisher Scientific, Middletown, VA) according to the manufacturer’s instructions.

Techniques: Fast Protein Liquid Chromatography

Journal: bioRxiv

Article Title: Gene dosage imbalance disrupts systemic metabolism in the Dp16 Down syndrome mouse model

doi: 10.64898/2026.01.13.699318

Figure Lengend Snippet: Quantification of hepatic TAG and DAG (by TLC method), and cholesterol (by infinity assay kit) levels in chow-fed Dp16 male (A-C) and female mice (D-F) and their corresponding WT controls. Sample size: male WT = 10 and Dp16 = 30; female WT = 15 and Dp16 = 10.

Article Snippet: Following tissue extraction, total cholesterol content was quantified using the Infinity Cholesterol Reagent kit (Thermo Fisher Scientific, Middletown, VA) according to the manufacturer’s instructions.

Techniques:

Journal: bioRxiv

Article Title: Gene dosage imbalance disrupts systemic metabolism in the Dp16 Down syndrome mouse model

doi: 10.64898/2026.01.13.699318

Figure Lengend Snippet: A-B) Overnight fasting insulin, blood glucose, serum triglyceride, cholesterol, non-esterified free fatty acids (NEFA), and β-hydroxybutyrate (ketone) in male (A) and female (B) Dp16 and WT mice on HFD. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 14). C-F) Exacerbated glucose intolerance as determined by the glucose tolerance test (GTT) in male (C) and female (E) Dp16 compared to WT controls on HFD. Exacerbated insulin resistance as determined by the insulin tolerance test (ITT) in male (D) and female (F) Dp16 compared to WT controls. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 14). G-H) The rate of triglyceride clearance in response to lipid gavage as determined by the lipid tolerance test (LTT) in male (G) and female (H) Dp16 and WT mice. Sample size for male mice (WT = 15; Dp16 = 12) and female mice (WT = 14; Dp16 = 14). I-J) Pooled mouse sera from male (I) and female (J) Dp16 and WT mice were fractionated by fast protein liquid chromatography (FPLC), and the triglyceride and cholesterol content of each fraction was quantified. Fractions corresponding to very-low density lipoprotein (VLDL), low-density lipoprotein (LDL), intermediate-density lipoprotein (IDL), and high-density lipoprotein (HDL) are indicated. All data are presented as mean ± SEM. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001. For all tolerance tests, data were analyzed by 2-way ANOVA with Sidek post hoc tests.

Article Snippet: Following tissue extraction, total cholesterol content was quantified using the Infinity Cholesterol Reagent kit (Thermo Fisher Scientific, Middletown, VA) according to the manufacturer’s instructions.

Techniques: Fast Protein Liquid Chromatography

Journal: Nature Communications

Article Title: Non-remnant triglyceride-rich lipoproteins due to lipoprotein lipase deficiency increase atherosclerosis in mice

doi: 10.1038/s41467-025-68193-3

Figure Lengend Snippet: A Lpl flox/flox /beta actin Cre mice (6 weeks) were injected intraperitoneally with tamoxifen (of 40 mg/kg × 4 days). The mice were maintained on a chow diet and 4 weeks later received LDLR ASO. Two weeks later blood was obtained to assess lipoproteins and the mice were then switched to a WD. B Plasma triglyceride (TG. **** p < 0.0001) and total cholesterol (TC, * p = 0.0105) levels on chow; C Lipoproteins were isolated by ultracentrifugation. VLDL (d < 1.006 g/mL) TG (** p = 0.0012) and cholesterol (** p = 0.0021). D LDL (d 1.019–1.053 g/mL) TG (* p = 0.0359) and cholesterol ( p = 0.9949). E HDL (d 1.063–1.22 g/mL) cholesterol (** p = 0.0034). F Sera from 3–5 mice were pooled, 200 µL was analyzed by FPLC and TG and cholesterol measured. Measurements for plasma TG and TC were performed in 12 Lpl fl/fl / Ldlr ASO (red) and 9 i Lpl −/− / Ldlr ASO mice (blue). A subset of 8 and 7 samples were fractionated for measurements of TRL and LDL TG and cholesterol measurements, and 3 samples per group were additionally fractionated to assess HDL cholesterol. Data are presented as mean ± SEM. Statistical analysis was performed by unpaired Student’s test (two-tailed).

Article Snippet: Total cholesterol (TC) was measured using Infinity Total Cholesterol Reagent (#TR13521, Thermo Scientific, Waltham, MA).

Techniques: Injection, Clinical Proteomics, Isolation, Two Tailed Test

Journal: Nature Communications

Article Title: Non-remnant triglyceride-rich lipoproteins due to lipoprotein lipase deficiency increase atherosclerosis in mice

doi: 10.1038/s41467-025-68193-3

Figure Lengend Snippet: Lpl fl/fl and i Lpl −/− after 12 weeks of LDLR knockdown using PCSK9 AAV and WD feeding. A TG levels. B Total TC levels. C , D Distribution of TG and cholesterol levels in plasma fractionated by size-exclusion chromatography. E Plasma TGs distribution on ultracentrifuge-fractionated lipoproteins. F Plasma cholesterol distribution on ultracentrifuge-fractionated lipoproteins. n = 21 Lpl fl/fl / Ldlr KD mice (red) and Lpl −/− / Ldlr KD mice (blue). Data are presented as the mean ± SEM. * p < 0.01; ** p < 0.005, *** p < 0.001, **** p < 0.0001 vs. Lpl fl/fl mice by unpaired Student’s test (two-tailed).

Article Snippet: Total cholesterol (TC) was measured using Infinity Total Cholesterol Reagent (#TR13521, Thermo Scientific, Waltham, MA).

Techniques: Knockdown, Clinical Proteomics, Size-exclusion Chromatography, Two Tailed Test

Journal: Nature Communications

Article Title: Non-remnant triglyceride-rich lipoproteins due to lipoprotein lipase deficiency increase atherosclerosis in mice

doi: 10.1038/s41467-025-68193-3

Figure Lengend Snippet: Chylomicrons were isolated from the plasma of control, high-cholesterol diet fed (termed 2wk HCD), or alloxan-treated rabbits fed a high-cholesterol diet (termed Alloxan), as well as from high-cholesterol diet fed Lpl −/− /Ldlr kd mice. A Representative electron microscope images of chylomicrons obtained from control (first panel), high-fat diet-fed (second panel), alloxan-treated rabbits (third panel), and Lpl −/− /Ldlr kd mice (fourth panel). n = 3 per group. B Mouse aortic ECs were treated with control (black) or SR-BI ASO (red) for 48hs, deprived of serum overnight, then exposed to DiI-labeled rabbit chylomicrons for 30 min. Cells were then fixed and imaged using a Leica SP8 confocal microscope to detect intracellular chylomicrons. SR-BI depletion significantly reduced the uptake of chylomicrons obtained from control and high-cholesterol diet-fed rabbits (left and middle panels and graphs), but not of chylomicrons obtained from alloxan-treated diabetic rabbits (right panels and graph). C Treatment with 10 mg/ml heparin (blue, control shown in black) significantly reduced EC uptake of chylomicrons obtained from Alloxan-treated but not control rabbits. D Chylomicrons from Alloxan-treated rabbits (green) undergo significantly less transcytosis than those obtained from control rabbits (black), as monitored by TIRF microscopy. Data for B and C are presented as mean ± SD of 9–12 independent experiments performed with technical duplicates. **** p < 0.0001 as compared to control, by unpaired Student’s t test (two-tailed). Transcytosis event rates ( D ) were measured in two samples obtained in two separate experiments. The graph shows the mean ± SEM. **** p < 0.0001 as compared to control, by ordinary one-way ANOVA.

Article Snippet: Total cholesterol (TC) was measured using Infinity Total Cholesterol Reagent (#TR13521, Thermo Scientific, Waltham, MA).

Techniques: Isolation, Clinical Proteomics, Control, Microscopy, Labeling, Two Tailed Test