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Journal articles on the topic 'Mine blast pathology'

Author: Grafiati

Published: 28 May 2022

Last updated: 31 July 2025

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1

Denisov, Alexey V., Vladimir V. Khominets, Stanislav M. Logatkin, Alexey V. Anisin, and Aleksandr P. Bozhchenko. "Development of mine-blast trauma severity score for lower extremities in men." Bulletin of the Russian Military Medical Academy 23, no. 3 (2021): 195–204. http://dx.doi.org/10.17816/brmma73198.

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This study presented the results of the analysis of existing approaches to the assessment of the severity of lower extremity injuries protected with explosion-proof shoes in case of mine-explosive ammunition explosion. An increasing number of mine explosives are used in modern local wars and armed conflicts. At present, more than 110 million mines are planted and activated. Every year, nearly 10 thousand individuals are killed by explosive demolitions, and more than 20 thousand civilians sustain injuries. The necessity to clear minefields and to destroy located ammunition increases the risks o

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2

Vorobiev, A. A., A. S. Mazunov, E. V. Venskel, et al. "Clinical observation of the effective use of the passive exoskeleton in complex habilitation and rehabilitation of a patient with post-traumatic brachioplexopathy due to mine-blast injury." Russian Journal of Operative Surgery and Clinical Anatomy 9, no. 2 (2025): 110. https://doi.org/10.17116/operhirurg20259022110.

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Background. The use of passive exoskeletons seems to be a promising method of comprehensive habilitation and rehabilitation for severe combat wounds of the brachial plexus, which leads to disability of a third of patients with this pathology. Objective. To demonstrate the possibilities of using the passive exoskeleton in the habilitation and rehabilitation of a patient with brachial plexopathy, complicating mine-explosive injury. Material and methods. Anamnesis collection, analysis of medical documentation, physical examination, and dynamic somatometry were carried out. Results. In a disabled

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3

Usenko, O. Y., A. V. Sydyuk, O. Y. Sydyuk, et al. "A clinical case of treatment for anaerobic infection in a patient with mine blast trauma in the intensive care unit." EMERGENCY MEDICINE 20, no. 5 (2024): 309–19. http://dx.doi.org/10.22141/2224-0586.20.5.2024.1729.

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Anaerobic infection is one of the severe wound infections caused by anaerobic microorganisms. According to statistical data, patients with complications of anaerobic infection have a high mortality rate, so early diagnosis and appropriate therapy are a key to the effective treatment of this pathology. To date, very few clinical cases with a combined effective treatment for anaerobic wound infection have been described. This article considers the step-by-step diagnosis and treatment for anaerobic infection in a serviceman who was injured as a result of military operations.

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4

Kozlova, Yu V., A. V. Kosharnij, M. A. Korzachenko, and I. V. Kytova. "Retrospective Analysis and Current State of Experimental Models of Blast-induced Trauma." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 5, no. 6 (2020): 66–71. http://dx.doi.org/10.26693/jmbs05.06.066.

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Combat pathology, particularly mine-blast injury is the main cause of military casualties. In our country, as a factor of destabilization, are widely used terrorist attacks using explosive devices of different capacities. Blast injury over 60% is cause of military casualties during armed conflicts. It is known that the condition for the formation of air-shock wave is creating waves of pressure, which is distributed at supersonic speed as possible with pulsed gas explosion and expansion of compression ambient air. The brain, chest, abdomen, and bladder are the most sensitive parts of the human

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5

Korshnyak, Volodymyr O., Julia V. Bovt, Oleksandr R. Pulyk, and Oleksandr M. Stoyanov. "MINE-BLAST TRAUMA AS A FACTOR IN THE EARLY DEVELOPMENT OF VASCULAR DISEASES OF THE BRAIN." Wiadomości Lekarskie 76, no. 6 (2023): 1485–90. http://dx.doi.org/10.36740/wlek202306123.

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The aim of this study is to investigate the state of bulbar conjunctival vessels, rheological properties of blood, catecholamines (adrenaline, norepinephrine), lipid metabolism, alkaline proteins of blood serum in patients with consequences of mild combat traumatic brain injury. Materials and methods: 76 individuals aged 28 to 41 years were examined. The duration of the injury lasted from 2 to 4 years. The control group consisted of 28 individuals aged 45 to 49 years with primary cerebral atherosclerosis and manifestations of cerebral circulation disorders. The state of the bulbar conjunctiva

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6

Wang, Chunyu, Changjuan Shao, Li Zhang, et al. "Oxidative Stress Signaling in Blast TBI-Induced Tau Phosphorylation." Antioxidants 10, no. 6 (2021): 955. http://dx.doi.org/10.3390/antiox10060955.

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Traumatic brain injury caused by blast is associated with long-term neuropathological changes including tau phosphorylation and pathology. In this study, we aimed to determine changes in initial tau phosphorylation after exposure to a single mild blast and the potential contribution of oxidative stress response pathways. C57BL/6 mice were exposed to a single blast overpressure (BOP) generated by a compressed gas-driven shock tube that recapitulates battlefield-relevant open-field BOP, and cortical tissues were harvested at different time points up to 24 h after blast for Western blot analysis.

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7

Wang, Hongxing, Yi Ping Zhang, Jun Cai, et al. "A Compact Blast-Induced Traumatic Brain Injury Model in Mice." Journal of Neuropathology & Experimental Neurology 75, no. 2 (2016): 183–96. http://dx.doi.org/10.1093/jnen/nlv019.

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8

Rajakumar, Sujeetha A., Eniko Papp, Kathy K. Lee, et al. "B cell acute lymphoblastic leukemia cells mediate RANK-RANKL–dependent bone destruction." Science Translational Medicine 12, no. 561 (2020): eaba5942. http://dx.doi.org/10.1126/scitranslmed.aba5942.

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Although most children survive B cell acute lymphoblastic leukemia (B-ALL), they frequently experience long-term, treatment-related health problems, including osteopenia and osteonecrosis. Because some children present with fractures at ALL diagnosis, we considered the possibility that leukemic B cells contribute directly to bone pathology. To identify potential mechanisms of B-ALL–driven bone destruction, we examined the p53−/−; Rag2−/−; Prkdcscid/scid triple mutant (TM) mice and p53−/−; Prkdcscid/scid double mutant (DM) mouse models of spontaneous B-ALL. In contrast to DM animals, leukemic T

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9

Wang, Xiaoli, Cing Siang Hu, Virginia Gillespie, Cecile Marie Krejsa, and Ronald Hoffman. "Navtemadlin (KRT-232), a Small Molecule MDM2 Inhibitor, Is More Effective Than Decitabine Against Myeloproliferative Neoplasm-Blast Phase in a Patient-Derived Xenograft Model." Blood 138, Supplement 1 (2021): 3591. http://dx.doi.org/10.1182/blood-2021-153071.

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Abstract Patients with myeloproliferative neoplasm-blast phase (MPN-BP) have a particularly dismal prognosis with a median survival of less than 6 months with currently available therapies (Mesa Blood 2015). Decitabine is the standard of care for MPN-BP. Recently, using xenotransplantation assays, we have shown that MPN-BP originates at the hematopoietic stem cell (SC) level (Wang Blood 2018) and that MPN-BP CD34 + cells contain higher levels of MDM2 protein compared with their normal counterparts (% of MDM2 + CD34 + cells: MPN-BP: 76.4±3.3; Normal: 17.5±6.4. P &lt;0.05). MDM2 negatively r

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10

Spohr, Corinna, Teresa Poggio, Geoffroy Andrieux, et al. "Gab2 deficiency prevents Flt3-ITD driven acute myeloid leukemia in vivo." Leukemia 36, no. 4 (2021): 970–82. http://dx.doi.org/10.1038/s41375-021-01490-0.

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AbstractInternal tandem duplications (ITD) of the FMS-like tyrosine kinase 3 (FLT3) predict poor prognosis in acute myeloid leukemia (AML) and often co-exist with inactivating DNMT3A mutations. In vitro studies implicated Grb2-associated binder 2 (GAB2) as FLT3-ITD effector. Utilizing a Flt3-ITD knock-in, Dnmt3a haploinsufficient mouse model, we demonstrate that Gab2 is essential for the development of Flt3-ITD driven AML in vivo, as Gab2 deficient mice displayed prolonged survival, presented with attenuated liver and spleen pathology and reduced blast counts. Furthermore, leukemic bone marrow

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11

Benito, Juliana M., Volgin Y. Andrei, Ye Chen, et al. "Leukemia Microenvironment and Pathologic Hypoxia: Sensitivity to Hypoxia-Activated Cytotoxin TH-302." Blood 120, no. 21 (2012): 1523. http://dx.doi.org/10.1182/blood.v120.21.1523.1523.

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Abstract Abstract 1523 We have recently demonstrated that the leukemic bone marrow (BM) niche is highly hypoxic and that hypoxia promotes resistance of leukemic cells to chemotherapy (Benito et al., PLoS One 2011, e23108). Our preliminary data indicate that AML cells surviving chemotherapy in the human xenograft mouse models of leukemia reside within hypoxic areas of BM microenvironment as documented by staining with the hypoxia marker CAIX. These findings support utility of hypoxia-activated pro-drugs with the goal to eliminate leukemic blasts and leukemic stem cells residing in hypoxic BM mi

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12

Satoh, Yasushi, Yoshiyuki Araki, Masashi Kashitani, et al. "Molecular Hydrogen Prevents Social Deficits and Depression-Like Behaviors Induced by Low-Intensity Blast in Mice." Journal of Neuropathology & Experimental Neurology 77, no. 9 (2018): 827–36. http://dx.doi.org/10.1093/jnen/nly060.

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13

Ramsey, Joanne Margaret, Glenda Joanne Dickson, Janetta Jacoba Bijl, et al. "Differential Gene and MicroRNA Expression In a HOXA9-MEIS1 Model of Leukemia." Blood 116, no. 21 (2010): 64. http://dx.doi.org/10.1182/blood.v116.21.64.64.

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Abstract Abstract 64 Altered expression of the HOX-MEIS axis is associated with leukemia, particularly AML, where it plays a role in increased proliferation and impaired differentiation. Particular focus has been placed on the role of HOX-MEIS in leukemia with MLL gene rearrangements and MLL-fusion induced models that represent this poor prognostic subgroup. However more recently, we and others have identified altered expression of HOX-MEIS in AML with normal karyotype (AML-NK) that accounts for the vast majority of patients with this disease. The prognostic outcome of this large subgroup of p

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14

Johnson, Radia, Eniko Papp, Ildiko Grandal, et al. "A Novel Mutational Mechanism Drives Over-Expression of Ligand-Independent FLT3 in a Murine Model of B-Precursor ALL." Blood 118, no. 21 (2011): 640. http://dx.doi.org/10.1182/blood.v118.21.640.640.

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Abstract Abstract 640 To identify dysregulated transcriptional and signaling networks that contribute to the development of acute lymphoblastic leukemia (ALL), our laboratory has generated and characterized p53−/−Prkdcscid/scid double mutant (DM) mice and Rag-2−/−p53−/−Prkdcscid/scid triple mutant (TM) mice. Both strains develop CD19+ B-precursor ALL by 8–16 weeks of age, but with distinct cytogenetic abnormalities and clinical sequelae. Interestingly, TM but not DM leukemic mice exhibited dissemination of leukemic blasts to the leptomeninges of the central nervous system (CNS), a characterist

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15

Spohr, Corinna, Teresa Poggio, Geoffroy Andrieux, et al. "Abstract 945: Gab2 deficiency protects against Flt3-ITD driven acute myeloid leukemia in vivo." Cancer Research 82, no. 12_Supplement (2022): 945. http://dx.doi.org/10.1158/1538-7445.am2022-945.

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Abstract Internal tandem duplications (ITD) of the FMS-like tyrosine kinase 3 (FLT3) frequently co-exist with inactivating DNMT3A mutations and predict poor prognosis in acute myeloid leukemia (AML). In vitro studies implicated the docking protein Grb2-associated binder 2 (GAB2) as FLT3-ITD effector. By utilizing a Flt3-ITD knock-in, Dnmt3a haploinsufficient mouse model, we demonstrate that Gab2 is essential for the development of Flt3-ITD driven AML in vivo, as Gab2 deficient mice survived significantly longer, had reduced blast counts and exhibited an attenuated spleen and liver pathology as

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16

USENKO, O. Y., O. Y. SYDYUK, V. V. ANTONENKO та ін. "CLINICAL CASE OF THE FIRST KIDNEY TRANSPLANTATION IN UKRAINE TO A SERVICEMAN OF THE ARMED FORCES OF UKRAINE WHO RECEIVEDWITH MINES BLAST TRAUMA(MВT) AS A RESULT OF THE ARMED AGGRESSION OF THE RUSSIAN FEDERATION AGAINST UKRAINE". PAIN, ANAESTHESIA & INTENSIVE CARE, № 2(107) (30 червня 2024): 64–68. http://dx.doi.org/10.25284/2519-2078.2(107).2024.308318.

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Kidney injury is one of the most common parenchymal organ injuries in military personnel because of military actions. This pathology requires a comprehensive approach to diagnosis (both instrumental and laboratory) and surgical and conservative treatment. One of the effective methods of surgical treatment is kidney transplantation. This surgical intervention is a method of renal replacement therapy in end-stage renal disease. The outcome is influenced by many factors: the age and weight of the donor and recipient, the presence of cardiovascular complications, and others. Patients are also asse

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Kato, Itaru, Akira Niwa, Megumu Saito та ін. "Establishment of a Novel CNS Infiltrated Xenograft Model through Engraftment of Patient-Derived Acute Lymphoblastic Leukemic Cells Into NOD/SCID/γc Null Mouse". Blood 116, № 21 (2010): 3248. http://dx.doi.org/10.1182/blood.v116.21.3248.3248.

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Abstract Abstract 3248 Background and Purpose: Acute lymphoblastic leukemia (ALL) is the most common type of childhood hematologic malignancy. Although improvements in treatment regimen have raised the 5-year survival rate as high as 80% for pediatric ALL patients, a minority of patients with various risk factors, including central nervous system (CNS) infiltration continue to have poor prognosis. Recently, bone marrow (BM) microenvironments which support leukemic stem cells have become noticed as an important element which can influence treatment response and relapse of the disease. Although

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18

Collins-Underwood, Racquel, Christopher B. Miller, James R. Downing, and Charles G. Mullighan. "Ikzf1 Haploinsufficiency Contributes to the Pathogenesis of BCR-ABL1 Positive Acute Lymphoblastic Leukemia." Blood 114, no. 22 (2009): 678. http://dx.doi.org/10.1182/blood.v114.22.678.678.

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Abstract Abstract 678 Expression of the constitutively active tyrosine kinase BCR-ABL1 is the hallmark of two diseases with distinct pathologic and clinical features: chronic myeloid leukemia (CML), an expansion of relatively mature granulocytes that typically responds well to kinase inhibition, and pre-B cell acute lymphoblastic leukemia (ALL), an aggressive malignancy of lymphoid progenitors that has a dismal prognosis. The basis for this dichotomy has been poorly understood. Recent studies profiling genome-wide DNA copy number alterations in CML and ALL have identified a near-obligate delet

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19

Resar, Linda, Francescopaolo Di Cello, Surajit Dhara, et al. "Inactivation of the INK4A/ARF (CDKN2) locus Cooperates with HMGA1 in T-Cell Leukemogenesis." Blood 114, no. 22 (2009): 3969. http://dx.doi.org/10.1182/blood.v114.22.3969.3969.

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Abstract Abstract 3969 Poster Board III-905 Because T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive lymphoid leukemia with a high rate of relapse in both children and adults, research is urgently needed to discover molecular pathways that could be targeted in therapy. Recent studies have identified NOTCH1 activating mutations, genomic classifiers, and other molecular pathways that are disrupted in T-ALL, although these findings have not yet translated into better therapy or improved long-term survival. Thus, we are investigating molecular pathways that play a causative role in T-A

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20

Zorko, Nicholas, Susan P. Whitman, Kelsie Bernot, et al. "The Mll PTD and Flt3 ITD Double Knock-In Mouse Develops Acute Leukemia and Recapitulates Phenotypic, Molecular and Epigenetic Characteristics of the Counterpart Human Acute Myeloid Leukemia." Blood 116, no. 21 (2010): 150. http://dx.doi.org/10.1182/blood.v116.21.150.150.

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Abstract Abstract 150 Background. The Mll PTD and Flt3 ITD are co-present in a subset of adult patients (pts) with cytogenetically normal (CN) acute myeloid leukemia (AML) and poor clinical outcomes. While the single mutant knock-in (KI) mice (Mll PTD or Flt3 ITD) exhibit enhanced myeloid progenitor self-renewal or reduced apoptosis, respectively, neither model develops acute leukemia. We hypothesized that with mutant expression driven via the endogenous promoters, the two mutations may cooperate in vivo to induce an acute leukemia that mimics the human counterpart. Methods. Single mutant hete

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Frisch, Benjamin J., John M. Ashton, Craig T. Jordan, and Laura M. Calvi. "Microenvironmental Changes In An In Vivo Model of Myeloid Leukemia Negatively Regulate Osteoblastic Cells." Blood 116, no. 21 (2010): 1219. http://dx.doi.org/10.1182/blood.v116.21.1219.1219.

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Abstract Abstract 1219 Patients with myelogenous leukemias can present with symptoms of bone pain and pathologic fractures, however little is known about the interactions between malignant cells and the bone marrow microenvironment. Additionally leukemia is known to severely interfere with normal hematopoiesis. To further characterize interactions between leukemic cells and the microenvironment, we used a model of blast crisis CML (bcCML) in which immature murine hematopoietic cells are engineered to express the BCR/ABL and Nup98/HoxA9 translocation products. Injection of these cells into naï

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Xu, Yaqun, Kathy Chan, Siu Ping Fok, Toni Ki Fong Man, Chi Kong Li, and Kam Tong Leung. "Histone Hypoacetylation-Driven CD9 Repression Arrests Differentiation and Evades Immunosurveillance in Pediatric Acute Myeloid Leukemia." Blood 138, Supplement 1 (2021): 3311. http://dx.doi.org/10.1182/blood-2021-152503.

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Abstract Acute myeloid leukemia (AML) is a genetically heterogeneous hematologic malignancy characterized by uncontrolled proliferation of myeloid progenitor cells accompanied by impaired terminal differentiation. Despite intensive treatment regimes, the clinical outcomes remain poor, underscoring the need to decipher the underlying pathology and implement therapeutic interventions. Emerging evidence suggest myeloblasts could evolve machineries to evade T cell patrol and hinder immunotherapies. Here, we present a new mechanism driving immune escape in the context of pediatric AML, based on our

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Rizo, Aleksandra, Sandra Olthof, OS van Ronald, et al. "The Polycomb Gene BMI1 Collaborates with BCR-ABL in Leukemic Transformation of Human Cord Blood CD34+ Cells." Blood 112, no. 11 (2008): 1350. http://dx.doi.org/10.1182/blood.v112.11.1350.1350.

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Abstract Previously, we demonstrated that BMI1 acts as a stem cell maintenance factor for human stem/progenitor cells. Here, we report that BMI1 collaborates with BCR-ABL in inducing leukemogenic transformation of human cord blood (CB) CD34+ cells. BMI1 and BCR-ABL were co-expressed into CB CD34+ cells (further referred as B/B cells) using a retroviral approach and cells were transplanted into NOD-SCID mice. In two out of five mice we observed leukemia within 4 months after transplantation. Chimerism levels reached 80–90% in the bone marrow and peripheral blood and morphological analysis revea

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Zhang, Xiuyan, Yu Wang, Lun Xiao, Haixia Zhou, Li Zhu, and Yun Zhao. "Zinc Finger Protein X-Linked Exhibits Pro-Leukemia Activity Via WNT3 in Chronic Myeloid Leukemia Stem/Progenitor Cells." Blood 132, Supplement 1 (2018): 4247. http://dx.doi.org/10.1182/blood-2018-99-114663.

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Abstract Zinc Finger protein, X-linked (ZFX) is a transcriptional regulator, which controls the self-renewal of both embryonic and hematopoietic stem cells and participates in pathogenesis of various cancers. Zfx deficiency impairs Notch intracellular domain (NotchIC) induced acute T-cell leukemia (T-ALL) or MLL-AF9 induced acute myeloid leukemia (AML) in mice models. However, the function of ZFX in chronic myeloid leukemia (CML) stem/progenitor cells has not been elucidated yet. In the present study, qRT-PCR analysis showed that ZFX expression was significantly higher in CD34+ cells from CML

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Collins-Underwood, J. Racquel, Nidal Boulos, Debbie Payne-Turner, Shann-Ching Chen, Richard Williams, and Charles Mullighan. "The Role of Dominant-Negative IKAROS Mutations In the Pathogenesis and Treatment Responsiveness of BCR-ABL1 positive Acute Lymphoblastic Leukemia." Blood 116, no. 21 (2010): 540. http://dx.doi.org/10.1182/blood.v116.21.540.540.

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Abstract Abstract 540 Expression of the constitutively active tyrosine kinase BCR-ABL1 is the hallmark of two diseases with distinct pathologic and clinical features: chronic myeloid leukemia (CML), an expansion of relatively mature granulocytes that typically responds well to kinase inhibition, and pre-B cell acute lymphoblastic leukemia (ALL), an aggressive malignancy of lymphoid progenitors that has a dismal prognosis. The basis for this dichotomy has been poorly understood. Recent studies profiling genome-wide DNA copy number alterations in CML and ALL have identified common deletions of I

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26

Forrester, A. Michael, Ellen R. Boyd, Clemens Grabher, et al. "NUP98-HOXA9 Reprograms Embryonic Hematopoiesis, Suppresses Cellular Apoptosis, and Causes Malignant Tissue Infiltrates in Transgenic Zebrafish." Blood 114, no. 22 (2009): 3961. http://dx.doi.org/10.1182/blood.v114.22.3961.3961.

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Abstract Abstract 3961 Poster Board III-897 The NUP98-HOXA9 fusion oncogene results from a t(7;11)(p15;p15) chromosomal translocation and is associated with inferior prognosis in de novo and treatment-related acute myeloid leukemia (AML), as well as blast crisis in chronic myeloid leukemia (CML). HOXA9 belongs to the highly-conserved HOX gene family of developmental transcription factors and is critical for vertebrate hematopoiesis. Upregulation of HOXA9 is a frequent phenomenon in human AML, implicating a central role in myeloid disease. Thus, elucidating the activity of oncogenic NUP98-HOXA9

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Lechman, Eric R., Karin G. Hermans, Stephanie M. Dobson, et al. "Modeling the Multi-Step Pathogenesis of Acute Myeloid Leukemia of Down Syndrome." Blood 124, no. 21 (2014): 3579. http://dx.doi.org/10.1182/blood.v124.21.3579.3579.

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Abstract The multistep pathogenesis of Down Syndrome (DS)-associated pre-leukemia and subsequent progression to acute leukemia is one of the better characterized of all human blood malignancies. Children with DS have a 150 fold increased risk of developing acute megakaryoblastic leukemia (AMKL) and greater than 30 fold increased risk of developing B cell acute lymphoblastic leukemia (B-ALL). DS-AMKL is often preceded in late fetal development or soon after birth by a pre-leukemic syndrome termed transient myeloproliferative disorder (TMD), which is characterized by high numbers of abnormal meg

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Sha, Xiaojin, Barbara Hoffman, and Dan Liebermann. "Loss of Stress Sensor GADD45a and GADD45b Accelerates BCR-ABL-Driven Leukemogenesis Via Distinct Signaling and Cellular Pathways." Blood 116, no. 21 (2010): 1217. http://dx.doi.org/10.1182/blood.v116.21.1217.1217.

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Abstract Abstract 1217 The bcr/abl oncogene causes chronic myelogenous leukemia (CML) in humans. BCR/ABL is known to localize to the cytoskeleton and to display a constitutively active tyrosine kinase activity that leads to the recruitment of downstream effectors of cell proliferation and survival. This is accomplished via several adapter proteins and signaling pathways, including Ras, PI3K-AKT, PkD2-NFkB and JAK-STAT5, all of which are believed to participate in the pathogenesis of CML. The complex nature of these signaling pathways and how they contribute to the initiation and progression of

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Fu, Yu-Hsuan, Lianjun Zhang, Ying-Chieh Chen, et al. "Single-Cell RNA-Seq Reveals Intermediate Cell States and Identifies Features Defining Cellular Heterogeneity in Inv(16) Acute Myeloid Leukemia (AML)." Blood 142, Supplement 1 (2023): 5683. http://dx.doi.org/10.1182/blood-2023-182484.

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AML is an aggressive hematological malignancy with heterogeneous genetic abnormalities. One recurrent chromosomal translocation common in AML is chromosome 16 inversion, inv(16)(p13.1q22), which results in the leukemogenic fusion gene CBFB- MYH11. Using a conditional Cbfb-MYH11 (CM) knock-in mouse model to mimic the somatic expression of the CM fusion gene, we demonstrated that CM expression leads to impaired hematopoietic differentiation as well as accumulation of phenotypic hematopoietic stem cells (HSC) and pre-megakaryocyte/erythrocyte (Pre-Meg/E) progenitors, which are predisposed to leuk

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30

Dang, Yujia, Xiao Huang, Yurong Qin, et al. "Abstract 7323: LBL-043, a novel LILRB4xCD3 T cell engager, for the treatment of relapsed/refractory multiple myeloma." Cancer Research 85, no. 8_Supplement_1 (2025): 7323. https://doi.org/10.1158/1538-7445.am2025-7323.

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Abstract Background: Multiple myeloma (MM) is a clonal plasma cell proliferative disorder characterized by abnormal increase of monoclonal immunoglobulins. Despite newly developed novel therapeutic agents have greatly improved the outcome of MM patients in the past decades, MM is still an incurable hematological malignancy. Several CD3 bispecific immunotherapies that harness T cells against MM are at various stages of preclinical and clinical development, but most of them are hampered by the refractory and resistant mechanisms. Leukocyte immunoglobulin-like receptor B4 (LILRB4) is an immune ch

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Hu, Chao, Xi Jiang, Bryan Ulrich, et al. "Mircrorna-550 Functions As a Critical Tumor Suppressor in Acute Myeloid Leukemia." Blood 126, no. 23 (2015): 1240. http://dx.doi.org/10.1182/blood.v126.23.1240.1240.

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Abstract Background: Acute Myeloid leukemia (AML) is one of the most common and fatal form of hematologic malignancies. Recurring chromosomal aberrations and gene mutations have been shown to contribute to AML pathogenesis and clinical outcomes. However, no effective therapy is available to selectively target the cytogenetic and molecular abnormalities, except for PML-RARA in acute promyelocytic leukemia (APL) which can be targeted by all-trans retinoic acid (ATRA) and arsenic trioxide (ATO). As a result, the majority of AML patients are suffering from unsatisfied treatment of standard chemoth

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Kerr, Nadine A., Rachele Sangaletti, Winston Walters, and Suhrud M. Rajguru. "Association of Blast‐induced Hearing Loss with Progression of Alzheimer’s Disease Pathology." Alzheimer's & Dementia 20, S1 (2024). https://doi.org/10.1002/alz.089629.

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AbstractBackgroundExposures to hazardous noise causes irreversible injury to the structures of the inner ear, leading to changes in hearing and balance function with strong links to age‐related cognitive impairment. While the role of noise‐induced hearing loss in long‐term health consequences, such as progression or development of Alzheimer’s Disease (AD) has been suggested, the underlying mechanisms and behavioral and cognitive outcomes or therapeutic solutions to mitigate these changes remain understudied. This study aimed to characterize the association between blast exposure, hearing loss,

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Kimura, Eiko, Kunio Mizutari, Takaomi Kurioka, et al. "Effect of shock wave power spectrum on the inner ear pathophysiology in blast-induced hearing loss." Scientific Reports 11, no. 1 (2021). http://dx.doi.org/10.1038/s41598-021-94080-0.

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AbstractBlast exposure can induce various types of hearing impairment, including permanent hearing loss, tinnitus, and hyperacusis. Herein, we conducted a detailed investigation of the cochlear pathophysiology in blast-induced hearing loss in mice using two blasts with different characteristics: a low-frequency dominant blast generated by a shock tube and a high-frequency dominant shock wave generated by laser irradiation (laser-induced shock wave). The pattern of sensorineural hearing loss (SNHL) was low-frequency- and high-frequency-dominant in response to the low- and high-frequency blasts,

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Thomas, Chloe N., Alexandra Bernardo-Colón, Ella Courtie, et al. "Effects of intravitreal injection of siRNA against caspase-2 on retinal and optic nerve degeneration in air blast induced ocular trauma." Scientific Reports 11, no. 1 (2021). http://dx.doi.org/10.1038/s41598-021-96107-y.

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AbstractOcular repeated air blast injuries occur from low overpressure blast wave exposure, which are often repeated and in quick succession. We have shown that caspase-2 caused the death of retinal ganglion cells (RGC) after blunt ocular trauma. Here, we investigated if caspase-2 also mediates RGC apoptosis in a mouse model of air blast induced indirect traumatic optic neuropathy (b-ITON). C57BL/6 mice were exposed to repeated blasts of overpressure air (3 × 2 × 15 psi) and intravitreal injections of siRNA against caspase-2 (siCASP2) or against a control enhanced green fluorescent protein (si

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Boehme, Nickolas A., Adam Hedberg-Buenz, Nicole Tatro, et al. "Axonopathy precedes cell death in ocular damage mediated by blast exposure." Scientific Reports 11, no. 1 (2021). http://dx.doi.org/10.1038/s41598-021-90412-2.

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AbstractTraumatic brain injuries (TBI) of varied types are common across all populations and can cause visual problems. For military personnel in combat settings, injuries from blast exposures (bTBI) are prevalent and arise from a myriad of different situations. To model these diverse conditions, we are one of several groups modeling bTBI using mice in varying ways. Here, we report a refined analysis of retinal ganglion cell (RGC) damage in male C57BL/6J mice exposed to a blast-wave in an enclosed chamber. Ganglion cell layer thickness, RGC density (BRN3A and RBPMS immunoreactivity), cellular

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Puangmalai, Nicha, Nemil Bhatt, Alice Bittar, Cynthia Jerez, Nikita Shchankin, and Rakez Kayed. "Traumatic brain injury derived pathological tau polymorphs induce the distinct propagation pattern and neuroinflammatory response." Alzheimer's & Dementia 20, S1 (2024). https://doi.org/10.1002/alz.089310.

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AbstractBackgroundThe misfolding and aggregation of the tau protein into neurofibrillary tangles constitute a central feature of tauopathies. Traumatic brain injury (TBI) has emerged as a potential risk factor, triggering the onset and progression of tauopathies. Our previous research revealed distinct polymorphisms in soluble tau oligomers originating from single versus repetitive mild TBIs. However, the mechanisms orchestrating the dissemination of TBI brain‐derived tau polymorphs (TBI‐BDTPs) remain elusive.MethodWe explored whether TBI‐BDTPs could initiate pathological tau formation, leadin

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Gibson‐Corley, Katherine N., Georgina Ofori‐Amanfo, Mariah R. Leidinger, and Allyn M. Lambertz. "How Different Are We? Performing Formalin Fixed Paraffin Embedded Tissue Immunohistochemistry Across Species." FASEB Journal 30, S1 (2016). http://dx.doi.org/10.1096/fasebj.30.1_supplement.51.6.

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The Comparative Pathology Laboratory (CPL) at the University of Iowa is affiliated with both a teaching hospital and a research university, which provides the opportunity to work with tissues from humans and a variety of research animals, including mice, rats, ferrets, rabbits, sheep and pigs. The CPL has developed procedures for immunohistochemical (IHC) antibodies on organisms for which the antibody has not previously been validated. In many instances, non‐standard research organisms are not referenced on antibody datasheets. Peer‐reviewed journal articles are referenced, but infrequently me

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Honig, Marcia G., Nobel A. Del Mar, Desmond L. Henderson, et al. "Raloxifene Modulates Microglia and Rescues Visual Deficits and Pathology After Impact Traumatic Brain Injury." Frontiers in Neuroscience 15 (October 29, 2021). http://dx.doi.org/10.3389/fnins.2021.701317.

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Mild traumatic brain injury (TBI) involves widespread axonal injury and activation of microglia, which initiates secondary processes that worsen the TBI outcome. The upregulation of cannabinoid type-2 receptors (CB2) when microglia become activated allows CB2-binding drugs to selectively target microglia. CB2 inverse agonists modulate activated microglia by shifting them away from the harmful pro-inflammatory M1 state toward the helpful reparative M2 state and thus can stem secondary injury cascades. We previously found that treatment with the CB2 inverse agonist SMM-189 after mild TBI in mice

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Li, Chao, Shanyan Chen, Heather R. Siedhoff, et al. "Low-intensity open-field blast exposure effects on neurovascular unit ultrastructure in mice." Acta Neuropathologica Communications 11, no. 1 (2023). http://dx.doi.org/10.1186/s40478-023-01636-4.

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AbstractMild traumatic brain injury (mTBI) induced by low-intensity blast (LIB) is a serious health problem affecting military service members and veterans. Our previous reports using a single open-field LIB mouse model showed the absence of gross microscopic damage or necrosis in the brain, while transmission electron microscopy (TEM) identified ultrastructural abnormalities of myelin sheaths, mitochondria, and synapses. The neurovascular unit (NVU), an anatomical and functional system with multiple components, is vital for the regulation of cerebral blood flow and cellular interactions. In t

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Badash, Ido, Patricia M. Quiñones, Kevin J. Oghalai, et al. "Endolymphatic Hydrops is a Marker of Synaptopathy Following Traumatic Noise Exposure." Frontiers in Cell and Developmental Biology 9 (November 5, 2021). http://dx.doi.org/10.3389/fcell.2021.747870.

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After acoustic trauma, there can be loss of synaptic connections between inner hair cells and auditory neurons in the cochlea, which may lead to hearing abnormalities including speech-in-noise difficulties, tinnitus, and hyperacusis. We have previously studied mice with blast-induced cochlear synaptopathy and found that they also developed a build-up of endolymph, termed endolymphatic hydrops. In this study, we used optical coherence tomography to measure endolymph volume in live CBA/CaJ mice exposed to various noise intensities. We quantified the number of synaptic ribbons and postsynaptic de

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Barker, Sarah, Edwin Vázquez‐Rosa, Salvatore Caradonna, et al. "Reducing tau acetylation rescues cognitive deficits in a mouse model of traumatic brain injury‐induced acceleration of Alzheimer’s disease." Alzheimer's & Dementia 20, S1 (2024). https://doi.org/10.1002/alz.091710.

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AbstractBackgroundTBI is the 3rd greatest risk factor for developing AD, behind genetics and aging. TBI is associated with a 3‐4 year earlier onset of cognitive impairment, and increased cortical thinning and amyloid plaques in people with AD. The underlying mechanisms of this relationship are not understood, and as a result there are no treatments that protect patients from accelerated AD after TBI. We reported that tau is pathologically acetylated after TBI. Acetylated tau is significantly more elevated in the brains of human AD subjects with a history of TBI, compared to AD alone and health

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Fonseca, Gabriela Rodrigues e., Ana Laura Grossi de Oliveira, Ramayana Morais de Medeiros Brito, et al. "Immunogenic mapping of potential epitopes from Tc-CTL-1 for the diagnosis of murine toxocariasis." Memórias do Instituto Oswaldo Cruz 120 (2025). https://doi.org/10.1590/0074-02760240111.

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BACKGROUND Toxocariasis is a neglected global zoonosis. The immunological diagnosis has setbacks that hinder further knowledge about its pathology, epidemiology, and public control measures, and lack of financial support and attention prevents innovative research. Although studies on synthetic peptides are common for several infectious pathologies, none evaluated chemically synthetic peptides for toxocariasis diagnosis. OBJECTIVE This study aimed to identify potential synthetic peptides from C-type lectin 1 (Tc-CTL-1) from Toxocara canis. METHODS In silico analyses were made by five B-cell pep

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Antypiuk, Ada, Steven Vance, Richa Sharma, et al. "Genetic iron overload aggravates and pharmacological iron restriction improves MDS pathophysiology in a preclinical study." Blood Journal, October 22, 2024. http://dx.doi.org/10.1182/blood.2024026135.

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Although iron overload is a common feature in myelodysplastic syndromes (MDS), it remains unclear how iron excess is detrimental for disease pathophysiology. Taking advantage of complementary approaches, we analyzed the impact of iron overload and restriction achieved through genetic activation (FPNC326S) and pharmacologic inhibition (vamifeport) of the iron exporter ferroportin in a MDS mouse model, respectively. While FPNC326S-induced iron overload did not significantly improve the late stages of erythroid maturation, vamifeport-mediated iron restriction ameliorated anemia and red blood cell

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