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Mice exhibit compensatory decreasing of diastolic blood pressure and increasing tissue perfusion to counteract the hemoglobin deoxygenation effect of Au@PEG NPs. Changes in physiological parameters of mice at different time points after tail vein injection of Au@PEG NPs: (A) Body weight, (B) Pulse rate, (C) Diastolic pressure, (D) Systolic pressure, (E) Pulse pressure (Systolic pressure − Diastolic pressure) ( n = 9). (F) Hepatic blood flow perfusion of mice was monitored at different time points after tail vein injection of Au@PEG NPs using laser speckle contrast imaging <t>(LSCI).</t> (G) Schematic diagram of the bright-field scope of the sampling area using LSCI. (H) Changes in hepatic blood flow perfusion of mice at different time points after tail vein injection of Au@PEG NPs. Physiological parameters measured before tail vein injection of Au@PEG NPs were set as the baseline. Changes in blood routine parameters of mice at different time points after tail vein injection of Au@PEG NPs: (I) WBCs, (J)RBCs, (K) PLTs. Relative expression of oxygen-sensing genes, (L) HIF-1α, (M) EPO, in kidney detected by real-time quantitative PCR and the 2 −ΔΔCT method. (N) Plasma erythropoietin (EPO) concentrations at different time points after tail vein injection of Au@PEG NPs. Asterisks indicate significance (* p < 0.05).
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Mice exhibit compensatory decreasing of diastolic blood pressure and increasing tissue perfusion to counteract the hemoglobin deoxygenation effect of Au@PEG NPs. Changes in physiological parameters of mice at different time points after tail vein injection of Au@PEG NPs: (A) Body weight, (B) Pulse rate, (C) Diastolic pressure, (D) Systolic pressure, (E) Pulse pressure (Systolic pressure − Diastolic pressure) ( n = 9). (F) Hepatic blood flow perfusion of mice was monitored at different time points after tail vein injection of Au@PEG NPs using laser speckle contrast imaging <t>(LSCI).</t> (G) Schematic diagram of the bright-field scope of the sampling area using LSCI. (H) Changes in hepatic blood flow perfusion of mice at different time points after tail vein injection of Au@PEG NPs. Physiological parameters measured before tail vein injection of Au@PEG NPs were set as the baseline. Changes in blood routine parameters of mice at different time points after tail vein injection of Au@PEG NPs: (I) WBCs, (J)RBCs, (K) PLTs. Relative expression of oxygen-sensing genes, (L) HIF-1α, (M) EPO, in kidney detected by real-time quantitative PCR and the 2 −ΔΔCT method. (N) Plasma erythropoietin (EPO) concentrations at different time points after tail vein injection of Au@PEG NPs. Asterisks indicate significance (* p < 0.05).
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Mice exhibit compensatory decreasing of diastolic blood pressure and increasing tissue perfusion to counteract the hemoglobin deoxygenation effect of Au@PEG NPs. Changes in physiological parameters of mice at different time points after tail vein injection of Au@PEG NPs: (A) Body weight, (B) Pulse rate, (C) Diastolic pressure, (D) Systolic pressure, (E) Pulse pressure (Systolic pressure − Diastolic pressure) ( n = 9). (F) Hepatic blood flow perfusion of mice was monitored at different time points after tail vein injection of Au@PEG NPs using laser speckle contrast imaging <t>(LSCI).</t> (G) Schematic diagram of the bright-field scope of the sampling area using LSCI. (H) Changes in hepatic blood flow perfusion of mice at different time points after tail vein injection of Au@PEG NPs. Physiological parameters measured before tail vein injection of Au@PEG NPs were set as the baseline. Changes in blood routine parameters of mice at different time points after tail vein injection of Au@PEG NPs: (I) WBCs, (J)RBCs, (K) PLTs. Relative expression of oxygen-sensing genes, (L) HIF-1α, (M) EPO, in kidney detected by real-time quantitative PCR and the 2 −ΔΔCT method. (N) Plasma erythropoietin (EPO) concentrations at different time points after tail vein injection of Au@PEG NPs. Asterisks indicate significance (* p < 0.05).
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Mice exhibit compensatory decreasing of diastolic blood pressure and increasing tissue perfusion to counteract the hemoglobin deoxygenation effect of Au@PEG NPs. Changes in physiological parameters of mice at different time points after tail vein injection of Au@PEG NPs: (A) Body weight, (B) Pulse rate, (C) Diastolic pressure, (D) Systolic pressure, (E) Pulse pressure (Systolic pressure − Diastolic pressure) ( n = 9). (F) Hepatic blood flow perfusion of mice was monitored at different time points after tail vein injection of Au@PEG NPs using laser speckle contrast imaging <t>(LSCI).</t> (G) Schematic diagram of the bright-field scope of the sampling area using LSCI. (H) Changes in hepatic blood flow perfusion of mice at different time points after tail vein injection of Au@PEG NPs. Physiological parameters measured before tail vein injection of Au@PEG NPs were set as the baseline. Changes in blood routine parameters of mice at different time points after tail vein injection of Au@PEG NPs: (I) WBCs, (J)RBCs, (K) PLTs. Relative expression of oxygen-sensing genes, (L) HIF-1α, (M) EPO, in kidney detected by real-time quantitative PCR and the 2 −ΔΔCT method. (N) Plasma erythropoietin (EPO) concentrations at different time points after tail vein injection of Au@PEG NPs. Asterisks indicate significance (* p < 0.05).
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Relapse and toxicity outcomes after <t>CD19-CAR.</t> (A) Cumulative incidence of relapse in the iBM (n = 21; green), EMD (n = 36; red), and CNS (n = 251; blue) cohorts, calculated using the Kaplan-Meier method. (B) <t>Post-CAR</t> <t>T-cell</t> relapse phenotype was assessed by flow cytometry and was reported as either CD19 + , CD19 − , lineage switch, or unknown. Relapse occurred in 134 patients (EMD n = 7; CNS n = 21; iBM n = 106). There were no statistical differences in the phenotypes among the cohorts. (C) Incidence of CRS in the different patient cohorts. Each pie chart represents 1 of the 3 cohorts as indicated. Displayed are patients with no CRS (blue), grade 1 to 2 CRS (gold), and grade 3 to 5 CRS (beige). CRS was graded by the reporting institution and included 126 of 308 (40.9%) cases graded according to the Lee criteria, 156 of 308 (50.6%) cases graded according to the University of Pennsylvania criteria, and 26 of 308 (8.4%) cases graded according to the American Society for Transplantation and Cellular Therapy guidelines. (D) The percentage of patients who developed neurotoxicity, as diagnosed by reporting institution, in the cohorts is indicated on the x-axis. (E) Reported reason for post-CAR HSCT in each individual cohort. Other encompasses 4 patients in the BM alone cohort who proceeded to transplant because of next-generation sequencing positivity in the absence of flow-detectable disease (n = 2), persistent BM aplasia (n = 1), and relapse with unknown phenotype characterized by the development of a scalp chloroma by day 28 after infusion (n = 1).
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Mice exhibit compensatory decreasing of diastolic blood pressure and increasing tissue perfusion to counteract the hemoglobin deoxygenation effect of Au@PEG NPs. Changes in physiological parameters of mice at different time points after tail vein injection of Au@PEG NPs: (A) Body weight, (B) Pulse rate, (C) Diastolic pressure, (D) Systolic pressure, (E) Pulse pressure (Systolic pressure − Diastolic pressure) ( n = 9). (F) Hepatic blood flow perfusion of mice was monitored at different time points after tail vein injection of Au@PEG NPs using laser speckle contrast imaging (LSCI). (G) Schematic diagram of the bright-field scope of the sampling area using LSCI. (H) Changes in hepatic blood flow perfusion of mice at different time points after tail vein injection of Au@PEG NPs. Physiological parameters measured before tail vein injection of Au@PEG NPs were set as the baseline. Changes in blood routine parameters of mice at different time points after tail vein injection of Au@PEG NPs: (I) WBCs, (J)RBCs, (K) PLTs. Relative expression of oxygen-sensing genes, (L) HIF-1α, (M) EPO, in kidney detected by real-time quantitative PCR and the 2 −ΔΔCT method. (N) Plasma erythropoietin (EPO) concentrations at different time points after tail vein injection of Au@PEG NPs. Asterisks indicate significance (* p < 0.05).

Journal: International Journal of Pharmaceutics: X

Article Title: PEGylated gold nanoparticles regulate metabolic flux in erythrocytes by inducing hemoglobin deoxygenation

doi: 10.1016/j.ijpx.2026.100495

Figure Lengend Snippet: Mice exhibit compensatory decreasing of diastolic blood pressure and increasing tissue perfusion to counteract the hemoglobin deoxygenation effect of Au@PEG NPs. Changes in physiological parameters of mice at different time points after tail vein injection of Au@PEG NPs: (A) Body weight, (B) Pulse rate, (C) Diastolic pressure, (D) Systolic pressure, (E) Pulse pressure (Systolic pressure − Diastolic pressure) ( n = 9). (F) Hepatic blood flow perfusion of mice was monitored at different time points after tail vein injection of Au@PEG NPs using laser speckle contrast imaging (LSCI). (G) Schematic diagram of the bright-field scope of the sampling area using LSCI. (H) Changes in hepatic blood flow perfusion of mice at different time points after tail vein injection of Au@PEG NPs. Physiological parameters measured before tail vein injection of Au@PEG NPs were set as the baseline. Changes in blood routine parameters of mice at different time points after tail vein injection of Au@PEG NPs: (I) WBCs, (J)RBCs, (K) PLTs. Relative expression of oxygen-sensing genes, (L) HIF-1α, (M) EPO, in kidney detected by real-time quantitative PCR and the 2 −ΔΔCT method. (N) Plasma erythropoietin (EPO) concentrations at different time points after tail vein injection of Au@PEG NPs. Asterisks indicate significance (* p < 0.05).

Article Snippet: Real-time hepatic microcirculation was quantified using LSCI technology (PeriCam PSI, Perimed) following established protocols ( ; ).

Techniques: Injection, Imaging, Sampling, Expressing, Real-time Polymerase Chain Reaction, Clinical Proteomics

Relapse and toxicity outcomes after CD19-CAR. (A) Cumulative incidence of relapse in the iBM (n = 21; green), EMD (n = 36; red), and CNS (n = 251; blue) cohorts, calculated using the Kaplan-Meier method. (B) Post-CAR T-cell relapse phenotype was assessed by flow cytometry and was reported as either CD19 + , CD19 − , lineage switch, or unknown. Relapse occurred in 134 patients (EMD n = 7; CNS n = 21; iBM n = 106). There were no statistical differences in the phenotypes among the cohorts. (C) Incidence of CRS in the different patient cohorts. Each pie chart represents 1 of the 3 cohorts as indicated. Displayed are patients with no CRS (blue), grade 1 to 2 CRS (gold), and grade 3 to 5 CRS (beige). CRS was graded by the reporting institution and included 126 of 308 (40.9%) cases graded according to the Lee criteria, 156 of 308 (50.6%) cases graded according to the University of Pennsylvania criteria, and 26 of 308 (8.4%) cases graded according to the American Society for Transplantation and Cellular Therapy guidelines. (D) The percentage of patients who developed neurotoxicity, as diagnosed by reporting institution, in the cohorts is indicated on the x-axis. (E) Reported reason for post-CAR HSCT in each individual cohort. Other encompasses 4 patients in the BM alone cohort who proceeded to transplant because of next-generation sequencing positivity in the absence of flow-detectable disease (n = 2), persistent BM aplasia (n = 1), and relapse with unknown phenotype characterized by the development of a scalp chloroma by day 28 after infusion (n = 1).

Journal: Blood Advances

Article Title: CD19 CAR T-cell outcomes in relapsed/refractory extramedullary B-ALL: a multisite, retrospective cohort review

doi: 10.1182/bloodadvances.2025018604

Figure Lengend Snippet: Relapse and toxicity outcomes after CD19-CAR. (A) Cumulative incidence of relapse in the iBM (n = 21; green), EMD (n = 36; red), and CNS (n = 251; blue) cohorts, calculated using the Kaplan-Meier method. (B) Post-CAR T-cell relapse phenotype was assessed by flow cytometry and was reported as either CD19 + , CD19 − , lineage switch, or unknown. Relapse occurred in 134 patients (EMD n = 7; CNS n = 21; iBM n = 106). There were no statistical differences in the phenotypes among the cohorts. (C) Incidence of CRS in the different patient cohorts. Each pie chart represents 1 of the 3 cohorts as indicated. Displayed are patients with no CRS (blue), grade 1 to 2 CRS (gold), and grade 3 to 5 CRS (beige). CRS was graded by the reporting institution and included 126 of 308 (40.9%) cases graded according to the Lee criteria, 156 of 308 (50.6%) cases graded according to the University of Pennsylvania criteria, and 26 of 308 (8.4%) cases graded according to the American Society for Transplantation and Cellular Therapy guidelines. (D) The percentage of patients who developed neurotoxicity, as diagnosed by reporting institution, in the cohorts is indicated on the x-axis. (E) Reported reason for post-CAR HSCT in each individual cohort. Other encompasses 4 patients in the BM alone cohort who proceeded to transplant because of next-generation sequencing positivity in the absence of flow-detectable disease (n = 2), persistent BM aplasia (n = 1), and relapse with unknown phenotype characterized by the development of a scalp chloroma by day 28 after infusion (n = 1).

Article Snippet: R.A.G. reports a consulting relationship with Moonlight Bio; and royalties from Bristol Myers Squibb related to CAR T-cell technologies.

Techniques: Flow Cytometry, Transplantation Assay, Next-Generation Sequencing