bluuebunny/crossref_metadata_2025 huggingface dataset:
Supplementary Figure S7 from Detecting Small Cell Transformation in Patients with Advanced EGFR Mutant Lung Adenocarcinoma through Epigenomic cfDNA Profiling
Authors: El Zarif Talal , Meador Catherine B. , Qiu Xintao , Seo Ji-Heui , Davidsohn Matthew P. , Savignano Hunter , Lakshminarayanan Gitanjali , McClure Heather M. , Canniff John , Fortunato Brad , Li Rong , Banwait Mandeep K. , Semaan Karl , Eid Marc , Long Henry , Hung Yin P. , Mahadevan Navin R. , Barbie David A. , Oser Matthew G. , Piotrowska Zofia , Choueiri Toni K. , Baca Sylvan C. , Hata Aaron N. , Freedman Matthew L. , Berchuck Jacob E.
Published: September 2024

Epigenomic datasets generated from cfDNA plasma samples from patients with metastatic lung cancer.
Supplementary Figure S5 from Detecting Small Cell Transformation in Patients with Advanced EGFR Mutant Lung Adenocarcinoma through Epigenomic cfDNA Profiling
Authors: El Zarif Talal , Meador Catherine B. , Qiu Xintao , Seo Ji-Heui , Davidsohn Matthew P. , Savignano Hunter , Lakshminarayanan Gitanjali , McClure Heather M. , Canniff John , Fortunato Brad , Li Rong , Banwait Mandeep K. , Semaan Karl , Eid Marc , Long Henry , Hung Yin P. , Mahadevan Navin R. , Barbie David A. , Oser Matthew G. , Piotrowska Zofia , Choueiri Toni K. , Baca Sylvan C. , Hata Aaron N. , Freedman Matthew L. , Berchuck Jacob E.
Published: September 2024

Number of differential H3K27ac, H3K4me3, DNA methylation, and open chromatin sites enriched in LUAD or SCLC PDXs before and after removal of peaks also present in WBCs.
Table 1 from Safety, Efficacy, and Biological Data of T-Cell–Enabling Oncolytic Adenovirus TILT-123 in Advanced Solid Cancers from the TUNIMO Monotherapy Phase I Trial
Authors: Pakola Santeri A. , Peltola Katriina J. , Clubb James H.A. , Jirovec Elise , Haybout Lyna , Kudling Tatiana V. , Alanko Tuomo , Korpisaari Riitta , Juteau Susanna , Jaakkola Marjut , Sormunen Jorma , Kemppainen Jukka , Hemmes Annabrita , Pellinen Teijo , van der Heijden Mirte , Quixabeira Dafne C.A. , Kistler Claudia , Sorsa Suvi , Havunen Riikka , Santos Joao M. , Cervera-Carrascon Victor , Hemminki Akseli
Published: September 2024

Patient demographics.
Figure 4 from Safety, Efficacy, and Biological Data of T-Cell–Enabling Oncolytic Adenovirus TILT-123 in Advanced Solid Cancers from the TUNIMO Monotherapy Phase I Trial
Authors: Pakola Santeri A. , Peltola Katriina J. , Clubb James H.A. , Jirovec Elise , Haybout Lyna , Kudling Tatiana V. , Alanko Tuomo , Korpisaari Riitta , Juteau Susanna , Jaakkola Marjut , Sormunen Jorma , Kemppainen Jukka , Hemmes Annabrita , Pellinen Teijo , van der Heijden Mirte , Quixabeira Dafne C.A. , Kistler Claudia , Sorsa Suvi , Havunen Riikka , Santos Joao M. , Cervera-Carrascon Victor , Hemminki Akseli
Published: September 2024

A, Virus staining (violet) in tumor biopsies from patient 20202 at different time points across the trial, showing productive virus replication in injected and noninjected lesions; scale bar, 50 mm. B, Tumor IHC from patient 20202 staining for DAPI, CD8, and CD56 showing increased numbers of effector lymphocytes in injected and non-injected lesions post-treatment; scale bar, 100 μm. C, Neutralizing antibodies (NAbs) against TILT-123 at baseline in all patients. D, Neutralizing antibody presence compared with disease control at day 78. Disease control defined as SMD or better at day 78. No disease control defined as PMD or NA at day 78. Groups compared with the Fisher’s exact test. E, Baseline neutralizing antibody presence compared with overall survival across trial. Groups compared with the MaxCombo log-rank test. F, Neutralizing antibody titer across trial in all dose cohorts. Baseline defined as day 1 pre-treatment value, for days 1 to 64 the highest titer shown for each day (pre-or post-treatment). G, Serum proteomic changes 16 hours after intravenous dosing of TILT-123, pooled patients from cohorts 1 to 5 (n = 15). H, Serum proteomic changes 16 hours after first dose of intratumoral dosing of TILT-123, pooled patients from cohorts 1 to 5 (n = 15). I, Serum proteomic changes 16 hours after second dose of intratumoral dosing of TILT-123, pooled patients from cohorts 1 to 5 (n = 15). For G–I, difference between pre‐and post-treatment protein calculated with the Mann–Whitney U test; ns, non-significant (P > 0.05).
Supplementary Table S9 from Multiplexed Spatial Profiling of Hodgkin Reed–Sternberg Cell Neighborhoods in Classic Hodgkin Lymphoma
Authors: Pourmaleki Maryam , Jones Caitlin J. , Mellinghoff Sabrina D. , Greenstein Brian D. , Kumar Priyadarshini , Foronda Miguel , Navarrete Daniel A. , Campos Carl , Roshal Mikhail , Schultz Nikolaus , Shah Sohrab P. , Schietinger Andrea , Socci Nicholas D. , Hollmann Travis J. , Dogan Ahmet , Mellinghoff Ingo K.
Published: September 2024

Supplementary Table S9. Comparison of EBV-positive NS and EBV-positive MC cHL.
Supplementary Table S4 from Multiplexed Spatial Profiling of Hodgkin Reed–Sternberg Cell Neighborhoods in Classic Hodgkin Lymphoma
Authors: Pourmaleki Maryam , Jones Caitlin J. , Mellinghoff Sabrina D. , Greenstein Brian D. , Kumar Priyadarshini , Foronda Miguel , Navarrete Daniel A. , Campos Carl , Roshal Mikhail , Schultz Nikolaus , Shah Sohrab P. , Schietinger Andrea , Socci Nicholas D. , Hollmann Travis J. , Dogan Ahmet , Mellinghoff Ingo K.
Published: September 2024

Supplementary Table S4. List of cell states.
Supplementary Table S2 from Multiplexed Spatial Profiling of Hodgkin Reed–Sternberg Cell Neighborhoods in Classic Hodgkin Lymphoma
Authors: Pourmaleki Maryam , Jones Caitlin J. , Mellinghoff Sabrina D. , Greenstein Brian D. , Kumar Priyadarshini , Foronda Miguel , Navarrete Daniel A. , Campos Carl , Roshal Mikhail , Schultz Nikolaus , Shah Sohrab P. , Schietinger Andrea , Socci Nicholas D. , Hollmann Travis J. , Dogan Ahmet , Mellinghoff Ingo K.
Published: September 2024

Supplementary Table S2. mpIF panel and antibody information.
Supplementary Data 2 from Identification of Therapy-Induced Clonal Evolution and Resistance Pathways in Minimal Residual Clones in Multiple Myeloma through Single-Cell Sequencing
Authors: Cui Jian , Li Xiaoyun , Deng Shuhui , Du Chenxing , Fan Huishou , Yan Wenqiang , Xu Jingyu , Li Xiaoqing , Yu Tengteng , Zhang Shuaishuai , Lv Rui , Sui Weiwei , Hao Mu , Du Xin , Xu Yan , Yi Shuhua , Zou Dehui , Cheng Tao , Qiu Lugui , Gao Xin , An Gang
Published: September 2024

Supplemental table 1-15.
Supplementary File S1 from Targeting AKR1B10 by Drug Repurposing with Epalrestat Overcomes Chemoresistance in Non–Small Cell Lung Cancer Patient-Derived Tumor Organoids
Authors: Suvilesh Kanve N. , Manjunath Yariswamy , Nussbaum Yulia I. , Gadelkarim Mohamed , Raju Murugesan , Srivastava Akhil , Li Guangfu , Warren Wesley C. , Shyu Chi-Ren , Gao Feng , Ciorba Matthew A. , Mitchem Jonathan B. , Rachagani Satyanarayana , Kaifi Jussuf T.
Published: September 2024

Supplementary File S1. Somatic single nucleotide polymorphic (SNP) mutations identified in PDTOs and matched patient tumors.
Supplementary Figure S10 from Targeting AKR1B10 by Drug Repurposing with Epalrestat Overcomes Chemoresistance in Non–Small Cell Lung Cancer Patient-Derived Tumor Organoids
Authors: Suvilesh Kanve N. , Manjunath Yariswamy , Nussbaum Yulia I. , Gadelkarim Mohamed , Raju Murugesan , Srivastava Akhil , Li Guangfu , Warren Wesley C. , Shyu Chi-Ren , Gao Feng , Ciorba Matthew A. , Mitchem Jonathan B. , Rachagani Satyanarayana , Kaifi Jussuf T.
Published: September 2024

Supplementary Figure S10. Dose titration of carboplatin and paclitaxel against resistant and sensitive PDTOs to determine Effective concentration (EC50).
Supplementary Figure S1 from Targeting AKR1B10 by Drug Repurposing with Epalrestat Overcomes Chemoresistance in Non–Small Cell Lung Cancer Patient-Derived Tumor Organoids
Authors: Suvilesh Kanve N. , Manjunath Yariswamy , Nussbaum Yulia I. , Gadelkarim Mohamed , Raju Murugesan , Srivastava Akhil , Li Guangfu , Warren Wesley C. , Shyu Chi-Ren , Gao Feng , Ciorba Matthew A. , Mitchem Jonathan B. , Rachagani Satyanarayana , Kaifi Jussuf T.
Published: September 2024

Supplementary Figure S1. Development and histomorphological characterization of patient-derived tumor organoid (PDTO) models.
Data from A Phase II Study of Potentiation of Pembrolizumab with Binimetinib and Bevacizumab in Refractory Microsatellite-Stable Colorectal Cancer
Authors: Lentz Robert W. , Friedrich Tyler J. , Blatchford Patrick J. , Jordan Kimberly R. , Pitts Todd M. , Robinson Hannah R. , Davis S. Lindsey , Kim Sunnie S. , Leal Alexis D. , Lee Mathew R. , Waring Meredith R.N. , Martin Anne C. , Dominguez Adrian T.A. , Bagby Stacey M. , Hartman Sarah J. , Eckhardt S. Gail , Messersmith Wells A. , Lieu Christopher H.
Published: September 2024

AbstractPurpose:
In this single-institution phase II investigator-initiated study, we assessed the ability of MAPK and VEGF pathway blockade to overcome resistance to immunotherapy in microsatellite-stable metastatic colorectal cancer (MSS mCRC).
Patients and Methods:
Patients with MSS, BRAF wild-type mCRC who progressed on ≥2 prior lines of therapy received pembrolizumab, binimetinib, and bevacizumab until disease progression or unacceptable toxicity. After a safety run-in, patients were randomized to a 7-day run-in of binimetinib or simultaneous initiation of all study drugs, to explore whether MEK inhibition may increase tumor immunogenicity. The primary endpoint was objective response rate (ORR) in all patients combined (by Response Evaluation Criteria in Solid Tumors v1.1).
Results:
Fifty patients received study drug treatment; 54% were male with a median age of 55 years (range, 31–79). The primary endpoint, ORR, was 12.0% [95% confidence interval (CI) 4.5%–24.3%], which was not statistically different than the historical control data of 5% (P = 0.038, exceeding prespecified threshold of 0.025). The disease control rate was 70.0% (95% CI, 55.4%–82.1%), the median progression-free survival 5.9 months (95% CI, 4.2–8.7 months), and the median overall survival 9.3 months (95% CI, 6.7–12.2 months). No difference in efficacy was observed between the randomized cohorts. Grade 3 and 4 adverse events were observed in 56% and 8% of patients, respectively; the most common were rash (12%) and increased aspartate aminotransferase (12%).
Conclusions:
Pembrolizumab, binimetinib, and bevacizumab failed to meet its primary endpoint of higher ORR compared with historical control data, demonstrated a high disease control rate, and demonstrated acceptable tolerability in refractory MSS mCRC.
Data from A Phase I/II Study of Valemetostat (DS-3201b), an EZH1/2 Inhibitor, in Combination with Irinotecan in Patients with Recurrent Small-Cell Lung Cancer
Authors: Choudhury Noura J. , Lai W. Victoria , Makhnin Alex , Heller Glenn , Eng Juliana , Li Bob , Preeshagul Isabel , Santini Fernando C. , Offin Michael , Ng Kenneth , Paik Paul , Larsen Christina , Ginsberg Michelle S. , Lau Yvonne , Zhang Xinyuan , Baine Marina K. , Rekhtman Natasha , Rudin Charles M.
Published: September 2024

AbstractPurpose:
Recurrent small-cell lung cancer (SCLC) has few effective treatments. The EZH2-SLFN11 pathway is a driver of acquired chemoresistance that may be targeted.
Patients and Methods:
This phase I/II trial investigated valemetostat, an EZH1/2 inhibitor, with fixed-dose irinotecan in patients with recurrent SCLC. Phase I primary objectives were to assess safety, tolerability, and a recommended phase II dose (RP2D). The phase II primary objective was overall response rate (ORR), with secondary objectives of determining duration of response (DoR), progression-free survival (PFS), and overall survival (OS). Correlative analyses included immunohistochemistry of pretreatment and on-treatment tumor biopsies and pharmacokinetics analysis.
Results:
Twenty-two patients were enrolled (phase I, n = 12; phase II, n = 10); one withdrew consent prior to treatment. Three dose-limiting toxicities (DLT) in dose-escalation resulted in valemetostat 100 mg orally daily selected as RP2D. Among 21 evaluable patients, the most frequent (≥20%) treatment-related adverse events were diarrhea, fatigue, nausea, and rash; three patients discontinued treatment for toxicity. Three of the first 10 patients in phase II experienced DLTs triggering a stopping rule. The ORR was 4/19 or 21% [95% confidence interval (CI), 6%–46%]. The median DoR, PFS, and OS were 4.6 months, 2.2 months (95% CI, 1.3–7.6 months), and 6.6 months (95% CI, 4.3 to not reached), respectively. SLFN11/EZH2 expression and SCLC subtyping markers did not correlate with response, but MHC-I expression did increase with treatment. Two responders demonstrated subtype switching on treatment.
Conclusions:
Combination valemetostat and irinotecan was not tolerated but demonstrated efficacy in recurrent SCLC. Valemetostat, combined with agents without overlapping toxicity, warrants further investigation in SCLC.
Data from Increased PVR Expression on Bone Marrow Macrophages May Promote Resistance to TIGIT Blockade in Multiple Myeloma
Authors: Lozano Ester , Mena Mari-Pau , Garrabou Glòria , Cardús Oriol , Díaz Tania , Moreno David F. , Mañé-Pujol Joan , Oliver-Caldés Aina , Battram Anthony , Tovar Natalia , Cibeira María-Teresa , Rodríguez-Lobato Luis-Gerardo , Bladé Joan , Fernández de Larrea Carlos , Rosiñol Laura
Published: September 2024

AbstractPurpose:
TIGIT blockade in our ex vivo model of bone marrow (BM) reduced the number of malignant plasma cells (PC) in only half of patients with multiple myeloma. Here, we wanted to investigate whether increased expression of TIGIT ligands may inhibit T-cell immune response promoting resistance to TIGIT blockade.
Experimental Design:
We first characterized the number and phenotype of BM macrophages in different stages of the disease by multiparameter flow cytometry. We assessed the effect of TIGIT ligands on PC survival by performing experiments in the ex vivo BM model and analyzed changes in gene expression by using NanoString technology and real-time PCR.
Results:
The frequency of BM macrophages was significantly decreased in multiple myeloma, which was accompanied by changes in their immunophenotype. Moreover, we found a higher number of malignant PC in ex vivo BM cells cultured onto the poliovirus receptor (PVR) and nectin-2 compared with control, suggesting that both ligands may support PC survival. In addition, the presence of PVR, but not nectin-2, overcame the therapeutic effect of TIGIT blockade or exogenous IL2. Furthermore, exogenous IL2 increased TIGIT expression on both CD4+ and CD8+ T cells and, indirectly, PVR on BM macrophages. Consistently, PVR reduced the number of cytotoxic T cells and promoted a gene signature with reduced effector molecules.
Conclusions:
IL2 induced TIGIT on T cells in the BM, in which increased PVR expression resulted in cytotoxic T-cell inhibition, promoting PC survival and resistance to TIGIT blockade.
Understanding and Overcoming Resistance to Selective FGFR Inhibitors across FGFR2-Driven Malignancies
Authors: Facchinetti Francesco , Loriot Yohann , Brayé Floriane , Vasseur Damien , Bahleda Rastislav , Bigot Ludovic , Barbé Rémy , Nobre Catline , Combarel David , Michiels Stefan , Italiano Antoine , Smolenschi Cristina , Tselikas Lambros , Scoazec Jean-Yves , Ponce-Aix Santiago , Besse Benjamin , André Fabrice , Olaussen Ken A. , Hollebecque Antoine , Friboulet Luc
Published: September 2024

Purpose:

Understanding resistance to selective FGFR inhibitors is crucial to improve the clinical outcomes of patients with FGFR2-driven malignancies.

Experimental Design:

We analyzed sequential ctDNA, ± whole-exome sequencing, or targeted next-generation sequencing on tissue biopsies from patients with tumors harboring activating FGFR2 alterations progressing on pan-FGFR–selective inhibitors, collected in the prospective UNLOCK program. FGFR2::BICC1 Ba/F3 and patient-derived xenograft models were used for functional studies.

Results:

Thirty-six patients were included. In cholangiocarcinoma, at resistance to both reversible inhibitors (e.g., pemigatinib and erdafitinib) and the irreversible inhibitor futibatinib, polyclonal FGFR2 kinase domain mutations were frequent (14/27 patients). Tumors other than cholangiocarcinoma shared the same mutated FGFR2 residues, but polyclonality was rare (1/9 patients). At resistance to reversible inhibitors, 14 residues in the FGFR2 kinase domain were mutated—after futibatinib, only the molecular brake N550 and the gatekeeper V565. Off-target alterations in PI3K/mTOR and MAPK pathways were found in 11 patients, often together with on-target mutations. At progression to a first FGFR inhibitor, 12 patients received futibatinib or lirafugratinib (irreversible inhibitors), with variable clinical outcomes depending on previous resistance mechanisms. Two patients with TSC1 or PIK3CA mutations benefited from everolimus. In cell viability assays on Ba/F3 and in pharmacologic studies on patient-derived xenografts, irreversible inhibitors retained better activity against FGFR2 kinase domain mutations, with lirafugratinib active against the recalcitrant V565L/F/Y.

Conclusions:

At progression to FGFR inhibitors, FGFR2-driven malignancies are characterized by high intra- and interpatient molecular heterogeneity, particularly in cholangiocarcinoma. Resistance to FGFR inhibitors can be overcome by sequential, molecularly oriented treatment strategies across FGFR2-driven tumors.
Supplementary Table S5 from Endoplasmic Reticulum Stress Potentiates the Immunosuppressive Microenvironment in Hepatocellular Carcinoma by Promoting the Release of SNHG6-Enriched Small Extracellular Vesicles
Authors: Liu Chengdong , Zhou Xiaohan , Zeng Hanyi , Yu Jiaping , Li Wenwen , Zhang Wanli , Liao Yanxia , Wang Haijian , Liu Li
Published: September 2024

Supplementary Table S5
Figure S7 from Nivolumab Reaches Brain Lesions in Patients with Recurrent Glioblastoma and Induces T-cell Activity and Upregulation of Checkpoint Pathways
Authors: Skadborg Signe K. , Maarup Simone , Draghi Arianna , Borch Annie , Hendriksen Sille , Mundt Filip , Pedersen Vilde , Mann Matthias , Christensen Ib J. , Skjøth-Ramussen Jane , Yde Christina W. , Kristensen Bjarne W. , Poulsen Hans S. , Hasselbalch Benedikte , Svane Inge M. , Lassen Ulrik , Hadrup Sine R.
Published: September 2024

Progression free survival and overall survival related to frequency of CD8+ T-cells expressing CD28.
Figure S10 from Nivolumab Reaches Brain Lesions in Patients with Recurrent Glioblastoma and Induces T-cell Activity and Upregulation of Checkpoint Pathways
Authors: Skadborg Signe K. , Maarup Simone , Draghi Arianna , Borch Annie , Hendriksen Sille , Mundt Filip , Pedersen Vilde , Mann Matthias , Christensen Ib J. , Skjøth-Ramussen Jane , Yde Christina W. , Kristensen Bjarne W. , Poulsen Hans S. , Hasselbalch Benedikte , Svane Inge M. , Lassen Ulrik , Hadrup Sine R.
Published: September 2024

Supplementary Figure 10 T cell analyses without tumor samples with IDH mutation.
Supplementary Figure S8 from PlexinB1 Inactivation Reprograms Immune Cells in the Tumor Microenvironment, Inhibiting Breast Cancer Growth and Metastatic Dissemination
Authors: Franzolin Giulia , Brundu Serena , Cojocaru Carina F. , Curatolo Aurora , Ponzo Matteo , Mastrantonio Roberta , Mihara Emiko , Kumanogoh Atsushi , Suga Hiroaki , Takagi Junichi , Tamagnone Luca , Giraudo Enrico
Published: September 2024

PLXNB1 inhibition did not directly affect tumor cells both in vitro and in vivo in EMT6 TNBC mouse model
Supplementary Table 4 from Intracellular Osteopontin Promotes the Release of TNFα by Mast Cells to Restrain Neuroendocrine Prostate Cancer
Authors: Sulsenti Roberta , Scialpi Giuseppina B. , Frossi Barbara , Botti Laura , Ferri Renata , Tripodi Irene , Piva Annamaria , Sangaletti Sabina , Pernici Davide , Cancila Valeria , Romeo Francesco , Chiodoni Claudia , Lecis Daniele , Bianchi Francesca , Fischetti Irene , Enriquez Claudia , Crivelli Filippo , Bregni Marco , Renne Giuseppe , Pece Salvatore , Tripodo Claudio , Pucillo Carlo E. , Colombo Mario P. , Jachetti Elena
Published: September 2024

Supplementary table 4 - transcript levels of the 29 TLR ligands measured by high throughput customized Taqman assay
Supplementary Figure S7 from Intracellular Osteopontin Promotes the Release of TNFα by Mast Cells to Restrain Neuroendocrine Prostate Cancer
Authors: Sulsenti Roberta , Scialpi Giuseppina B. , Frossi Barbara , Botti Laura , Ferri Renata , Tripodi Irene , Piva Annamaria , Sangaletti Sabina , Pernici Davide , Cancila Valeria , Romeo Francesco , Chiodoni Claudia , Lecis Daniele , Bianchi Francesca , Fischetti Irene , Enriquez Claudia , Crivelli Filippo , Bregni Marco , Renne Giuseppe , Pece Salvatore , Tripodo Claudio , Pucillo Carlo E. , Colombo Mario P. , Jachetti Elena
Published: September 2024

Supplementary Figure S7. Flow cytometry characterization of TNFa receptors and TNFa production. A. List of cytokines and chemokines tested through a multiplex immunoassay (Procarta-plex by Thermofisher) in the supernatants of ST4787 or T23 cells cultured either alone or in the presence of WT, OPN-/-, or MyD88-/- MCs. B.-C. Flow cytometry evaluation of TNFRs (CD120a and CD120b) on adenocarcinoma (T23 murine, 22Rv1 human) and NEPC (TC566 and TC411K murine, and LASCPC-01 human) cells. D. Gating strategy applied for intracellular detection of TNFa in MCs (CD49f-CD45+) by flow cytometry, in the co-cultures between MCs and tumor cells.
Supplementary Figure S3 from Intracellular Osteopontin Promotes the Release of TNFα by Mast Cells to Restrain Neuroendocrine Prostate Cancer
Authors: Sulsenti Roberta , Scialpi Giuseppina B. , Frossi Barbara , Botti Laura , Ferri Renata , Tripodi Irene , Piva Annamaria , Sangaletti Sabina , Pernici Davide , Cancila Valeria , Romeo Francesco , Chiodoni Claudia , Lecis Daniele , Bianchi Francesca , Fischetti Irene , Enriquez Claudia , Crivelli Filippo , Bregni Marco , Renne Giuseppe , Pece Salvatore , Tripodo Claudio , Pucillo Carlo E. , Colombo Mario P. , Jachetti Elena
Published: September 2024

Supplementary Figure S3. Toluidine blue for detection of MCs in mice. A. MC count reported as number of MCs/tumor area (cm2) in tumor samples from TRAMP mice with prostate intraepithelial neoplasia or adenocarcinoma (PIN/ADENO, n= 12), or TRAMP mice with NEPC (n= 3), as well as in prostatectomies from untreated patients with Gleason Score 7 (n= 10), Gleason Score 8 (n=10), or showing evidence of NEPC (n= 4). The histogram depict mean ± SD of biological replicates (represented by dots). B. Upper panels: representative images of toluidine blue staining in TRAMP, KitWsh-TRAMP, and OPN-/-TRAMP mice, or in KitWsh-TRAMP mice reconstituted with WT, OPN-/- or TNFa-/- MCs. Lower panels: representative images of toluidine blue staining in a prostate of a patient with adenocarcinoma. Scale bars indicate magnifications.
Figure S7 from Blockade of IL1β and PD1 with Combination Chemotherapy Reduces Systemic Myeloid Suppression in Metastatic Pancreatic Cancer with Heterogeneous Effects in the Tumor
Authors: Oberstein Paul E. , Dias Costa Andressa , Kawaler Emily A. , Cardot-Ruffino Victoire , Rahma Osama E. , Beri Nina , Singh Harshabad , Abrams Thomas A. , Biller Leah H. , Cleary James M. , Enzinger Peter , Huffman Brandon M. , McCleary Nadine J. , Perez Kimberly J. , Rubinson Douglas A. , Schlechter Benjamin L. , Surana Rishi , Yurgelun Matthew B. , Wang S. Jennifer , Remland Joshua , Brais Lauren K. , Bollenrucher Naima , Chang Eugena , Ali Lestat R. , Lenehan Patrick J. , Dolgalev Igor , Werba Gregor , Lima Cibelle , Keheler C. Elizabeth , Sullivan Keri M. , Dougan Michael , Hajdu Cristina , Dajee Maya , Pelletier Marc R. , Nazeer Saloney , Squires Matthew , Bar-Sagi Dafna , Wolpin Brian M. , Nowak Jonathan A. , Simeone Diane M. , Dougan Stephanie K.
Published: September 2024

Supplemental Figure 7: Macrophage subtypes are unaffected by treatment in patients in SR-1. (A) Baseline and on-treatment biopsies from patients (n = 6 paired samples) in the SR-1 trial were analyzed by multiplex immunofluorescence using the indicated antibodies. Representative image of the macrophage panel is shown. (B) Densities of total macrophages (CD68+ or CD163+ cells). (C) Densities of M1 polarized macrophages (CD86+IRF5+). (D) Densities of M2 polarized macrophages (CD206+CD163+).
Figure S3 from Blockade of IL1β and PD1 with Combination Chemotherapy Reduces Systemic Myeloid Suppression in Metastatic Pancreatic Cancer with Heterogeneous Effects in the Tumor
Authors: Oberstein Paul E. , Dias Costa Andressa , Kawaler Emily A. , Cardot-Ruffino Victoire , Rahma Osama E. , Beri Nina , Singh Harshabad , Abrams Thomas A. , Biller Leah H. , Cleary James M. , Enzinger Peter , Huffman Brandon M. , McCleary Nadine J. , Perez Kimberly J. , Rubinson Douglas A. , Schlechter Benjamin L. , Surana Rishi , Yurgelun Matthew B. , Wang S. Jennifer , Remland Joshua , Brais Lauren K. , Bollenrucher Naima , Chang Eugena , Ali Lestat R. , Lenehan Patrick J. , Dolgalev Igor , Werba Gregor , Lima Cibelle , Keheler C. Elizabeth , Sullivan Keri M. , Dougan Michael , Hajdu Cristina , Dajee Maya , Pelletier Marc R. , Nazeer Saloney , Squires Matthew , Bar-Sagi Dafna , Wolpin Brian M. , Nowak Jonathan A. , Simeone Diane M. , Dougan Stephanie K.
Published: September 2024

Supplemental Figure 3: Presence of canakinumab does not interfere with the ability to detect IL-1b in patient serum. Baseline serum from three randomly selected patients with pancreatic ductal adenocarcinoma was evaluated by cytokine bead array for IL-1b. For each patient sample, canakinumab was spiked in at the indicated concentrations. Note that measured IL-1b values were consistent across all samples from the same patient, regardless of the presence of canakinumab.
Figure S9 from MerTK Induces Dysfunctional Dendritic Cells by Metabolic Reprogramming
Authors: Zewdie Eden Y. , Edwards George M. , Hunter Debra M. , Earp Henry Shelton , Holtzhausen Alisha
Published: September 2024

Supplemental Figure 9
Figure S3 from MerTK Induces Dysfunctional Dendritic Cells by Metabolic Reprogramming
Authors: Zewdie Eden Y. , Edwards George M. , Hunter Debra M. , Earp Henry Shelton , Holtzhausen Alisha
Published: September 2024

Supplemental Figure 3
Supplementary Figure 10 from Iron Boosts Antitumor Type 1 T-cell Responses and Anti-PD1 Immunotherapy
Authors: Porte Sarah , Audemard-Verger Alexandra , Wu Christian , Durand Aurélie , Level Théo , Giraud Léa , Lombès Amélie , Germain Mathieu , Pierre Rémi , Saintpierre Benjamin , Lambert Mireille , Auffray Cédric , Peyssonnaux Carole , Goldwasser François , Vaulont Sophie , Alves-Guerra Marie-Clotilde , Dentin Renaud , Lucas Bruno , Martin Bruno
Published: September 2024

Body ferritin level does not modulate plasma concentrations of IL-6, IL-9, IL-10, IL-17A, IL-33 or TNFα following anti-PD1 immunotherapy in cancer patients.
Table S6 from Knocking Out CD70 Rescues CD70-Specific NanoCAR T Cells from Antigen-Induced Exhaustion
Authors: De Munter Stijn , Buhl Juliane L. , De Cock Laurenz , Van Parys Alexander , Daneels Willem , Pascal Eva , Deseins Lucas , Ingels Joline , Goetgeluk Glenn , Jansen Hanne , Billiet Lore , Pille Melissa , Van Duyse Julie , Bonte Sarah , Vandamme Niels , Van Dorpe Jo , Offner Fritz , Leclercq Georges , Taghon Tom , Depla Erik , Tavernier Jan , Kerre Tessa , Drost Jarno , Vandekerckhove Bart
Published: September 2024

Differentially expressed genes in bulk RNAseq data from CD70-4_1BB:ζ KO vs CD70-4_1BB:ζ WT
Supplemental Figure S3 from Knocking Out CD70 Rescues CD70-Specific NanoCAR T Cells from Antigen-Induced Exhaustion
Authors: De Munter Stijn , Buhl Juliane L. , De Cock Laurenz , Van Parys Alexander , Daneels Willem , Pascal Eva , Deseins Lucas , Ingels Joline , Goetgeluk Glenn , Jansen Hanne , Billiet Lore , Pille Melissa , Van Duyse Julie , Bonte Sarah , Vandamme Niels , Van Dorpe Jo , Offner Fritz , Leclercq Georges , Taghon Tom , Depla Erik , Tavernier Jan , Kerre Tessa , Drost Jarno , Vandekerckhove Bart
Published: September 2024

CD70 expression on nanoCAR T-cells.
Movie 2 from Knocking Out CD70 Rescues CD70-Specific NanoCAR T Cells from Antigen-Induced Exhaustion
Authors: De Munter Stijn , Buhl Juliane L. , De Cock Laurenz , Van Parys Alexander , Daneels Willem , Pascal Eva , Deseins Lucas , Ingels Joline , Goetgeluk Glenn , Jansen Hanne , Billiet Lore , Pille Melissa , Van Duyse Julie , Bonte Sarah , Vandamme Niels , Van Dorpe Jo , Offner Fritz , Leclercq Georges , Taghon Tom , Depla Erik , Tavernier Jan , Kerre Tessa , Drost Jarno , Vandekerckhove Bart
Published: September 2024

CD20-specific nanoCAR T-cells incubated with CD70+ JD033T organoid line
Data from Identification of Core Techniques That Enhance Genome Editing of Human T Cells Expressing Synthetic Antigen Receptors
Authors: Chang Ju-Fang , Wellhausen Nils , Engel Nils W. , Landmann Jack H. , Hopkins Caitlin R. , Salas-McKee January , Bear Adham S. , Selli Mehmet E. , Agarwal Sangya , Jadlowsky Julie K. , Linette Gerald P. , Gill Saar , June Carl H. , Fraietta Joseph A. , Singh Nathan
Published: September 2024

Abstract
Genome editing technologies have seen remarkable progress in recent years, enabling precise regulation of exogenous and endogenous genes. These advances have been extensively applied to the engineering of human T lymphocytes, leading to the development of practice changing therapies for patients with cancer and the promise of synthetic immune cell therapies for a variety of nonmalignant diseases. Many distinct conceptual and technical approaches have been used to edit T-cell genomes, however targeted assessments of which techniques are most effective for manufacturing, gene editing, and transgene expression are rarely reported. Through extensive comparative evaluation, we identified methods that most effectively enhance engineering of research-scale and preclinical T-cell products at critical stages of manufacturing.
Supplementary Table 5 from A Multicenter Real-life Prospective Study of Axicabtagene Ciloleucel versus Tisagenlecleucel Toxicity and Outcomes in Large B-cell Lymphomas
Authors: Stella Federico , Chiappella Annalisa , Casadei Beatrice , Bramanti Stefania , Ljevar Silva , Chiusolo Patrizia , Di Rocco Alice , Tisi Maria C. , Carrabba Matteo G. , Cutini Ilaria , Martino Massimo , Dodero Anna , Bonifazi Francesca , Santoro Armando , Sorà Federica , Botto Barbara , Barbui Anna M. , Russo Domenico , Musso Maurizio , Grillo Giovanni , Krampera Mauro , Olivieri Jacopo , Ladetto Marco , Cavallo Federica , Massaia Massimo , Arcaini Luca , Pennisi Martina , Zinzani Pier L. , Miceli Rosalba , Corradini Paolo
Published: September 2024

Supplementary Table 5 – List of centers and patients enrolled
Supplementary Table 1 from A Multicenter Real-life Prospective Study of Axicabtagene Ciloleucel versus Tisagenlecleucel Toxicity and Outcomes in Large B-cell Lymphomas
Authors: Stella Federico , Chiappella Annalisa , Casadei Beatrice , Bramanti Stefania , Ljevar Silva , Chiusolo Patrizia , Di Rocco Alice , Tisi Maria C. , Carrabba Matteo G. , Cutini Ilaria , Martino Massimo , Dodero Anna , Bonifazi Francesca , Santoro Armando , Sorà Federica , Botto Barbara , Barbui Anna M. , Russo Domenico , Musso Maurizio , Grillo Giovanni , Krampera Mauro , Olivieri Jacopo , Ladetto Marco , Cavallo Federica , Massaia Massimo , Arcaini Luca , Pennisi Martina , Zinzani Pier L. , Miceli Rosalba , Corradini Paolo
Published: September 2024

Supplementary Table 1 – Baseline variables associated with ORR at day 90, CRR at day 90, PFS, and OS
Supplemental Table 2 from Mis-splicing of Mitotic Regulators Sensitizes SF3B1-Mutated Human HSCs to CHK1 Inhibition
Authors: Sarchi Martina , Clough Courtnee A. , Crosse Edie I. , Kim Jason , Baquero Galvis Laura D. , Aydinyan Nelli , Wellington Rachel , Yang Feini , Gallì Anna , Creamer J. Philip , Stewart Sintra , Bradley Robert K. , Malcovati Luca , Doulatov Sergei
Published: September 2024

Supplemental Table 2. Splicing analysis of WT and SF3B1 K700E mutant K562 cells.
Supplemental Table 1 from Mis-splicing of Mitotic Regulators Sensitizes SF3B1-Mutated Human HSCs to CHK1 Inhibition
Authors: Sarchi Martina , Clough Courtnee A. , Crosse Edie I. , Kim Jason , Baquero Galvis Laura D. , Aydinyan Nelli , Wellington Rachel , Yang Feini , Gallì Anna , Creamer J. Philip , Stewart Sintra , Bradley Robert K. , Malcovati Luca , Doulatov Sergei
Published: September 2024

Supplemental Table 1. Splicing analysis of control and SF3B1 K700E edited cord blood (CB) and peripheral blood (PB) CD34+ cells.
Figure 3 from Disruption of KLHL6 Fuels Oncogenic Antigen Receptor Signaling in B-Cell Lymphoma
Authors: Meriranta Leo , Sorri Selma , Huse Kanutte , Liu Xiaonan , Spasevska Ivana , Zafar Sadia , Chowdhury Iftekhar , Dufva Olli , Sahlberg Eerika , Tandarić Luka , Karjalainen-Lindsberg Marja-Liisa , Hyytiäinen Marko , Varjosalo Markku , Myklebust June H. , Leppä Sirpa
Published: September 2024

KLHL6 interacts with BCR and forms homodimers and heterodimers that are differentially impacted by recurrent mutations. A, High-throughput proteomic approach to determine KLHL6 protein interactions and impact of recurrent mutations in DLBCL context. C-terminally tagged KLHL6 constructs encoding WT protein and different mutants or EmGFP (tagged and nontagged) controls were used in 4–8 biological replicate purifications in two batches of mass spectrometry. B, Volcano plot of DESeq2 model between WT KLHL6 and EmGFP pull-downs showing only the KLHL6 interacting proteins (positive fold-change). Labeled gene names of proteins denote high-confidence interactors detected by SAINT analysis. Plots on the right highlight interacting protein components of the Cop9-signalosome, immune proteasome, and BCR signaling. C, Representative IF microscopy images showing colocalization between endogenous KLHL6 and C-terminally V5-tagged KLHL7 and KLHL26 constructs. Scale bar, 10 µm. D and E, Volcano plots of differentially interacting proteins between WT KLHL6 (eight replicates) and (D) KLHL6L65P (four replicates) and (E) KLHL6L90F (eight replicates). Proteins with positive fold-change (log2) interact more strongly with the WT bait. F, Box plots of spectral counts of peptides from selected prey proteins in the pull-downs according to different baits. Dots represent biological replicates. Mann–Whitney U test for comparisons, P values shown. G and H, Bar and dot plots of spectral counts for specific peptides in BTB mutant KLHL6 pull-downs encoding either mutated or WT amino acids from (G) KLHL6L65P and (H) KLHL6L90F peptides. Dots represent individual replicates, and bars represent their means. All analyzed pull-downs contained mutant (bait) and WT (prey) peptides. I, Western blot analysis of SuDHL4 cells transduced with Strep-tagged WT and mutant KLHL6 constructs or EmGFP control. In the eluate, purified for Strep-tag, one protein (bait) is detected with HA-antibody, whereas two proteins (bait and prey) are detected with KLHL6 antibody confirming homodimerization. J, Balloon plot showing the interactors of WT and mutant KLHL6 baits according to SAINT analysis. K, Balloon plot of WT KLHL6 interactors compared with EmGFP control purifications identified with AP-MS across multiple lymphoma cell lines from different molecular backgrounds. Validated key interactors identified from SuDHL5 are shown.
Data from A Multicenter Real-life Prospective Study of Axicabtagene Ciloleucel versus Tisagenlecleucel Toxicity and Outcomes in Large B-cell Lymphomas
Authors: Stella Federico , Chiappella Annalisa , Casadei Beatrice , Bramanti Stefania , Ljevar Silva , Chiusolo Patrizia , Di Rocco Alice , Tisi Maria C. , Carrabba Matteo G. , Cutini Ilaria , Martino Massimo , Dodero Anna , Bonifazi Francesca , Santoro Armando , Sorà Federica , Botto Barbara , Barbui Anna M. , Russo Domenico , Musso Maurizio , Grillo Giovanni , Krampera Mauro , Olivieri Jacopo , Ladetto Marco , Cavallo Federica , Massaia Massimo , Arcaini Luca , Pennisi Martina , Zinzani Pier L. , Miceli Rosalba , Corradini Paolo
Published: September 2024

Abstract
This real-world prospective observational study across 21 Italian centers (CART-SIE) compares axicabtagene ciloleucel (axi-cel) and tisagenlecleucel (tisa-cel) outcomes in 485 patients with relapsed/refractory large B-cell lymphoma with baseline characteristics matched by stabilized inverse propensity score weighting. Axi-cel versus tisa-cel had higher all-grade cytokine release syndrome (78.6% vs. 89.3%, P = 0.0017) and neurotoxicity (9.9% vs. 32.2%, P < 0.0001) but also superior progression-free survival (PFS) at 1 year (46.5% vs. 34.1%, P = 0.0009). Even among patients who failed bridging therapy, axi-cel PFS was superior to tisa-cel (37.5% vs. 22.7%, P = 0.0059). Differences in overall survival and high-grade immune toxicities were not significant. The CAR-HEMATOTOX score not only predicted hematologic toxicity but also 1-year survival outcomes (51.5% in CAR-HEMATOTOX high vs. 77.2% in CAR-HEMATOTOX low, P < 0.0001). Twenty patients developed second primary malignancies, including two cases of T-cell neoplasms. These findings enable more informed selection of anti-CD19 CAR T-cell therapy, balancing bridging, safety, and efficacy considerations for individual patients.

Significance: The findings of this study on 485 patients with relapsed/refractory large B-cell lymphoma treated with commercial axi-cel and tisa-cel indicate axi-cel’s superior PFS after propensity score weighting. The predictive utility of CAR-HEMATOTOX in assessing not only toxicity but also outcomes across both CAR T-cell products may guide future risk-stratified management strategies.
Figure 4 from Anti-HDGF Antibody Targets EGFR Tyrosine Kinase Inhibitor–Tolerant Cells in NSCLC Patient-Derived Xenografts
Authors: Zhou Cindy Q. , Li Ariel , Ri Kaoru , Sultan Ahmed S. , Ren Hening
Published: September 2024

Effect of anti-HDGF antibody on EGFR signaling in osimertinib-treated TM00219 PDX tumor. Mice with established TM00219 PDX tumors were randomized into two arms (n = 6 each) to receive osimertinib or osimertinib plus anti-HDGF antibody H3. After 10 days of treatment, tumors were collected from euthanized animals and split for formalin-fixing and paraffin-embedding and Western blot analysis. A–D, IHC staining of tumor formalin-fixed, paraffin-embedded sections using (A) P-Erk1/2 (T202/Y204), (B) P-Akt1 (S473), (C) P-PRAS40 (T246), and (D) P-4EBP1 (T37/46). Representative fields of stained tumor at 4× view on OlyVIA (P-ERK and P-PRAS40) or 8× view on ImageScope (P-Akt and P-4EBP1) were shown. Tumors staining intensities in the two treatment arms were scored and plotted as the Cleveland dot graph. Naïve tumor staining is also shown for comparison. E, Western blots of protein extracts (10 μg/lane) from a matching set of tumors probed with indicated antibodies. The Western blot images were scanned and quantified using ImageJ. Mean density for each treatment group was plotted as a bar graph ± SD, with Y-axis showing image density relative to the naïve group. N, naive; O, osimertinib; OH, osimertinib plus anti-HDGF antibody H3. Asterisks mark the datasets in which there is a significant difference between the treatment arms.
Delineating the Clinical and Immunologic Characteristics: A Comparative Study of Inborn Errors of Immunity in Adult versus Pediatric Diagnosed
Authors: Karabiber Esra , Baris Safa
Published: September 2024

Introduction: Inborn errors of immunity (IEIs) are rare genetic disorders primarily identified in children due to their significant effects on immune system functionality. However, an increasing number of IEI cases are being diagnosed in adults, attributed to delayed presentation or advancements in diagnostic capabilities. This study explores the clinical and immunologic distinctions between IEIs diagnosed in adulthood versus childhood, shedding light on their differential presentations, the impact of diagnostic delays, and treatment outcomes. Methods: This study focused on 122 adult patients with IEI above 17 years old, diagnosed in adulthood or childhood. We collected comprehensive data on demographics, clinical presentations, genetic mutations, and therapeutic interventions. Results: The study revealed that 72.9% of participants were diagnosed in adulthood, facing a median diagnostic delay of 96 months. Diagnostic delays were longer in adults (132 months vs. 24 months) than in children. The most common clinical manifestations at onset were recurrent infections (46.7%) and autoimmunity (18%). Predominantly antibody deficiency was the most frequently diagnosed immunodeficiency (54.9%), followed by immunodysregulation at a rate of 26.2%. A higher incidence of immune thrombocytopenia or other complications, such as hepatomegaly and enteropathy, was observed in adult-diagnosed patients with IEI. Malignancies were more prevalent in patients with adult-onset IEI compared to those with childhood-onset (18.1% vs. 5.2%). Overall, 15 different malignancies were recorded in 13 patients (10.6%), including lymphomas and cancers of the stomach, thymus, skin, breast, and colon. Conclusions: The findings highlight a considerable diagnostic delay in recognizing IEI, especially in adults, and illustrate distinct differences in disease manifestation and progression between adult-onset and delayed-diagnosis groups.
СТАТЕВІ ОСОБЛИВОСТІ РОЗВИТКУ ОКСИДАТИВНОГО СТРЕСУ В ПЕЧІНЦІ ПІД ВПЛИВОМ КРАНІОСКЕЛЕТНОЇ ТРАВМИ ТА ЙОГО КОРЕКЦІЯ
Authors: ГУК Р. А. , ГУДИМА А. А.
Published: September 2024

Мета роботи: зʼясувати вплив експериментальної краніоскелетної травми на розвиток оксидативного стресу в печінці у щурів різної статі та оцінити ефективність 2-етил-6-метил-3-гідроксипіридину сукцинату в корекції виявлених порушень.
Матеріали і методи. В експериментах використано 78 білих щурів-самиць та 78 білих щурів-самців лінії Вістар масою 200–220 г. В умовах тіопенталонатрієвого наркозу в дослідній групі 1 моделювали краніоскелетну травму, у дослідній групі 2 щурам з краніоскелетною травмою проводили корекцію розчином 2-етил-6-метил-3-гідроксипіридину сукцинату. Контрольних щурів різної статі тільки вводили в наркоз. Щурів дослідної групи 1 виводили з експерименту через 1, 3, 7, 14 та 28 діб після моделювання травми. Щурів дослідної групи 2 виводили з експерименту через 7, 14 та 28 діб посттравматичного періоду. Для дослідження брали печінку, в гомогенаті якої визначали каталазну активність та вміст реагентів до тіобарбітурової кислоти. За їх співвідношенням розраховували антиоксидантно-прооксидантний індекс, величина якого свідчить про розвиток оксидативного стресу в печінці.
Результати. Під впливом модельованої травми у щурів-самців максимальне зниження величини антиоксидантно-прооксидантного індексу в печінці відмічали через 3 доби експерименту, у щурів-самиць – через 7 діб, з наступним підвищенням, яке у щурів обох статей до 28 доби не досягало рівня контролю. У всі терміни посттравматичного періоду величина показника була статистично вірогідно більшою у щурів-самиць, порівняно зі щурами-самцями. Під впливом 2-етил-6-метил-3-гідроксипіридину сукцинату, порівняно зі щурами без корекції, порушення величини антиоксидантно-прооксидантного індексу печінки виявилися меншими, що у щурів-самиць було статистично вірогідним через 7 діб експерименту, у щурів-самців – через 7, 14 та 28 діб експерименту. Отже, інтенсивність прооксидантних механізмів у відповідь на травму в печінці у щурів-самців є більшою, ніж у щурів-самок, проте ефективність 2-етил-6-метил-3-гідроксипіридину сукцинату у щурів-самців є вищою.
СТАТЕВІ ОСОБЛИВОСТІ РОЗВИТКУ ОКСИДАТИВНОГО СТРЕСУ В СЕРЦІ ЩУРІВ ІЗ МЕТАБОЛІЧНО АСОЦІЙОВАНОЮ СТЕАТОТИЧНОЮ ХВОРОБОЮ ПЕЧІНКИ І КОРЕКЦІЄЮ ЇЇ ПРЕПАРАТАМИ ІНОЗИТОЛУ
Authors: ЛЕВЧУК О. О. , ДЕНЕФІЛЬ О. В.
Published: September 2024

Мета роботи: вивчити особливості змін продуктів пероксидного окиснення ліпідів і антиоксидантної системи та прослідкувати морфологічні зміни у серці щурів різної статі із метаболічно асоційованою стеатотичною хворобою печінки (МАСХП) та при корекції патологічного процесу інозитолом.
Матеріали і методи. Досліди виконано на 96 щурах різної статі. Тварин поділено на 4 групи – контроль, МАСХП 4 місяці, МАСХП 4 місяці + міо-інозитол, МАСХП 4 місяці + D-chiro-інозито. У групі МАСХП 4 (2 група) тварини споживали замість води 20 % розчин фруктози протягом 4 місяців. Через 2 місяці від початку експерименту протягом 2 місяців їм інтрагастрально вводили міо-інозитол (400 мг/кг) або D-chiro-інозитол (30 мг/кг), відповідно 3 і 4 групи. Проводили забір серця для морфологічного і біохімічного досліджень; у гомогенаті серця визначали вміст дієнових і трієнових кон’югатів, основ Шиффа, ТБК-активних продуктів, супероксиддисмутазну і каталазну активність.
Результати. У серцях контрольної групи щурів-самців відмічено більшу активність процесів пероксидного окиснення ліпідів, порівняно з самицями. Метаболічно асоційована стеатотична хвороба печінки викликає активацію процесів пероксидного окиснення ліпідів, причому в самців зростають у більшій мірі первинні продукти пероксидного окиснення ліпідів та антиоксидантна активність, а в самиць – вторинні та кінцеві продукти пероксидного окиснення ліпідів. Інозитоли спричиняють зменшення оксидативного стресу в тварин обох статей. Морфологічна картина препаратів серця підтвердила виявлені біохімічні зміни.
Discovery of the male of Augochloropsis (Glyptochlora) Moure (Hymenoptera, Apidae, Halictinae), with a revised diagnosis for the subgenus
Authors: Celis Cindy Julieth , Raemakers Ivo , Melo Gabriel A. R.
Published: September 2024

Augochloropsis (Glyptochlora) Moure is a morphologically homogeneous and rare subgenus of Augochlorini, endemic to the Amazon Basin. So far, the subgenus was known only from females. Herein, we identified and studied the male of Augochloropsis (Glyptochlora) peruviana Celis & Melo. This specimen represents the first opportunity to document the male morphology of Augochloropsis (Glyptochlora). In addition to the description of the male, including genital capsule and metasomal sterna, we provide an updated diagnosis for A. (Glyptochlora).
Movimiento libertario y profetas del mercado en el Chile actual: las ideas de Axel Kaiser.
Authors: Morales Martín Juan Jesús
Published: September 2024

Axel Kaiser tornou-se nos últimos anos um dos mais proeminentes representantes do movimento libertário no Chile. Alguns de seus libros se tornaram verdadeiros best-sellers, como La fatal ignorancia. La anorexia cultural de la derecha frente al avance ideológico progresista (2014), La tiranía de la igualdad. Por qué el proyecto de la izquierda destruye nuestras libertades y arruina nuestro progreso (2015), La neoinquisición. Persecución, censura y decadencia cultural en el siglo XXI (2020), o El economista callejero. 15 lecciones de economía política para sobrevivir a políticos y demagogos (2021). Precisamente, o objetivo deste artigo é analisar as ideias mais representativas que esse intelectual público tem despejado em seus livros. Para tanto, o artigo fundamenta-se teoricamente na sociologia dos intelectuais e na sociologia das intervenções públicas. Além disso, é utilizado um modelo de análise de conteúdo aplicado nos livros de Axel Kaiser. O artigo discute e conclui como o movimento libertário no Chile está se tornando uma alternativa ideológica ao marxismo cultural; ele está construindo um novo senso comum baseado no liberalismo econômico e Axel Kaiser se destaca como um profeta intelectual do mercado que apela às emoções e à educação econômica.