Evolution from an antecedent chronic myeloid malignancy does not impact survival outcomes in NPM1-mutated AML.

Nucleophosmin-1 (NPM1)-mutated AML is a molecularly defined subtype typically associated with favorable treatment response and prognosis; however, its prognostic significance in AML evolving from an antecedent chronic myeloid malignancy is unknown. This study's primary objective was to determine the impact of mutated NPM1 on the prognosis of AML evolving from an antecedent chronic myeloid malignancy. We conducted a retrospective chart review including patients with NPM1-mutated de novo and sAML. sAML was defined as those with a preceding chronic-phase myeloid malignancy before diagnosis of AML. Of 575 NPM1-mutated patients eligible for inclusion in our study, 51 (8.9%) patients were considered to have sAML. The median time from diagnosis of NPM1-mutated chronic myeloid malignancy to sAML evolution was 3.6 months (0.5-79.3 months). No significant differences in leukemia-free (2-year LKFS 52.0% vs. 51.2%, p = .9922) or overall survival (2-year OS 56.3% vs. 49.4%, p = .4246) were observed between patients with NPM1-mutated de novo versus sAML. Our study suggests that evolution from a preceding myeloid malignancy is not a significant predictor of poor prognosis in the setting of an NPM1 mutation. Our study demonstrated a short time to progression to sAML in most patients, which further supports the consideration of NPM1 as an AML-defining mutation.

Development of Myelodysplastic Syndrome in a Patient With Pernicious Anemia During the Course of Replacement Treatment.

Megaloblastic anemia (MBA) is a reversible metabolic disorder that responds well to vitamin B12 supplementation. It contrasts with myelodysplastic syndrome (MDS), an irreversible neoplastic condition characterized by hematopoietic stem cell abnormalities. To date, no association has been identified between these two distinct etiologies, and they are considered independent diseases. However, despite their distinct classifications, both conditions present macrocytic anemia, similar bone marrow findings, and sometimes have common chromosomal abnormalities, which can lead to occasional misdiagnoses. Herein, we present a patient initially diagnosed with pernicious anemia (PA) who showed improvement with replacement therapy but subsequently became resistant to treatment and eventually developed MDS. Quantitative assessment of Wilm's tumor-1 (WT1) mRNA has emerged as a valuable tool for gauging MDS disease status and distinguishing it from related disorders, such as aplastic anemia. In our investigation of 30 patients with MBA, we explored WT1 mRNA expression. We observed its presence in 10 patients with PA, which suggests a potential link between PA and hematopoietic tumors.

Phytochemical Targeting of Nerve Growth Factor by Thymoquinone and Cuscutin: A Molecular Dynamics Simulation Study.

Background Nerve growth factor (NGF) is a novel target of pain therapeutics for oral cancer, and it plays a main role in the nociception of chronic pain. Surgery, along with chemotherapy or radiotherapy, is the gold standard for treating patients, but the side effects are significant as well. Newer effective interventions with natural phytochemicals could improve patient compliance and enhance the quality of life among patients with oral cancer. A literature search revealed a positive correlation between NGF and oral cancer pain. Nigella sativa (N. sativa) and Cuscuta reflexa (C. reflexa) have proven anticancer effects, but their activity with NGF is unexplored. Aims and objectives We aimed to identify the potential phytochemicals in N. sativa and C. reflexa. We also checked the NGF-blocking activity of the phytochemicals. Molecular docking and molecular dynamic (MD) simulations evaluated the binding energy and stability between the NGF protein and selected phytochemical ligands. Materials and methods We obtained protein NGF structure from UniProt (ID: 4EDX, P01138, Beta-nerve growth factor), ligand (thymoquinone) structure using PubChem ID: 10281, and ligand (cuscutin) structure using PubChem ID: 66065. Maestro protein (Schrödinger Inc., Mannheim, Germany) was used for molecular docking. Desmond Simulation Package (Schrödinger Inc., Mannheim, Germany) was used to model MD for 100 nanoseconds (ns). We have assessed the interaction between the protein and ligands by root mean square deviation (RMSD) values.  Results The interaction of thymoquinone and cuscutin with NGF was assessed. While interacting with thymoquinone, there was mild fluctuation from 0.6 Å to 2.5 Å up to 80 ns and ended up at 4.8 Å up to 100 ns. While interacting with cuscutin, mild fluctuation was seen from 0.8 Å to 4.8 Å till 90 ns and ended at 6.4 Å up to 100 ns. We found a stable interaction between our drug combination and the NGF receptor. Conclusion We have identified a stable interaction between thymoquinone, cuscutin, and NGF by our MD simulations. Hence, it could be used as an NGF inhibitor for pain relief and to control tumor progression. Further in vitro and in vivo evaluations of this novel drug combination with phytochemicals will help us understand their biological activities and potential clinical applications in oral cancer therapeutics.

Deubiquitinases at the interplay between hematopoietic stem cell aging and myelodysplastic transformation.

Hematopoietic stem cells (HSC) maintain blood production throughout life. Nevertheless, HSC functionality deteriorates upon physiological aging leading to the increased prevalence of haematological diseases and hematopoietic malignancies in the elderly. Deubiquitinating enzymes (DUBs) by reverting protein ubiquitination ensure proper proteostasis, a key process in HSC maintenance and fitness.

Structure-Based Identification of Novel Histone Deacetylase 4 (HDAC4) Inhibitors.

Histone deacetylases (HDACs) are important cancer drug targets. Existing FDA-approved drugs target the catalytic pocket of HDACs, which is conserved across subfamilies (classes) of HDAC. However, engineering specificity is an important goal. Herein, we use molecular modeling approaches to identify and target potential novel pockets specific to Class IIA HDAC-HDAC4 at the interface between HDAC4 and the transcriptional corepressor component protein NCoR. These pockets were screened using an ensemble docking approach combined with consensus scoring to identify compounds with a different binding mechanism than the currently known HDAC modulators. Binding was compared in experimental assays between HDAC4 and HDAC3, which belong to a different family of HDACs. HDAC4 was significantly inhibited by compound 88402 but not HDAC3. Two other compounds (67436 and 134199) had IC50 values in the low micromolar range for both HDACs, which is comparable to the known inhibitor of HDAC4, SAHA (Vorinostat). However, both of these compounds were significantly weaker inhibitors of HDAC3 than SAHA and thus more selective, albeit to a limited extent. Five compounds exhibited activity on human breast carcinoma and/or urothelial carcinoma cell lines. The present result suggests potential mechanistic and chemical approaches for developing selective HDAC4 modulators.

Modeling of Parkinson's Disease Progression and Implications for Detection of Disease Modification in Treatment Trials.

Background: Objectively measuring Parkinson's disease (PD) signs and symptoms over time is critical for the successful development of treatments aimed at halting the disease progression of people with PD. Objective: To create a clinical trial simulation tool that characterizes the natural history of PD progression and enables a data-driven design of randomized controlled studies testing potential disease-modifying treatments (DMT) in early-stage PD. Methods: Data from the Parkinson's Progression Markers Initiative (PPMI) were analyzed with nonlinear mixed-effect modeling techniques to characterize the progression of MDS-UPDRS part I (non-motor aspects of experiences of daily living), part II (motor aspects of experiences of daily living), and part III (motor signs). A clinical trial simulation tool was built from these disease models and used to predict probability of success as a function of trial design. Results: MDS-UPDRS part III progresses approximately 3 times faster than MDS-UPDRS part II and I, with an increase of 3 versus 1 points/year. Higher amounts of symptomatic therapy is associated with slower progression of MDS-UPDRS part II and III. The modeling framework predicts that a DMT effect on MDS-UPDRS part III could precede effect on part II by approximately 2 to 3 years. Conclusions: Our clinical trial simulation tool predicted that in a two-year randomized controlled trial, MDS-UPDRS part III could be used to evaluate a potential novel DMT, while part II would require longer trials of a minimum duration of 3 to 5 years underscoring the need for innovative trial design approaches including novel patient-centric measures.

To develop effective medicines that can slow down or stop the progression of Parkinson's disease (PD), it is important to accurately understand how the disease worsens over time. We used data from an observational study, led by the Michael J. Fox Foundation, called the Parkinson's Progression Markers Initiative (PPMI) to understand the natural progression of  PD. We simulated clinical trials on a computer using different scales to measure the progression of PD. We specifically looked at a physician-reported measure MDS-UPDRS part III, and at a patient-reported measure MDS-UPDRS part II of how PD symptoms worsen over time. To measure the effect of a new medicine slowing down the progression of PD using patient-reported measure MDS-UPDRS part II, we estimate that we may need to conduct a clinical trial of at least 3 to 5 years. On the other hand, to measure an effect using physician-reported measure MDS-UPDRS part III, the duration of the trial could be shorter than 2 years. We were also able to show that worsening recorded by the physician-reported measure MDS-UPDRS part III could be predictive of a later worsening recorded by the patient-reported measure MDS-UPDRS part II. We concluded that MDS-UPDRS part III may be a good endpoint for a clinical trial of a reasonable duration and that MDS-UPDRS part II could be measured in longer studies, for example, open-label extensions.

Alkaloid extract of seed Citrullus colocynthis as novel green inhibitor for mild steel corrosion in one molar HCl acid solution: DFT and MC/MD approaches.

The study was designed to explore the corrosion prevention capabilities of Citrullus colocynthis seeds alkaloid-rich extract (CSEA) on MS in a 1 M HCl environment by use of electrochemical and theoretical methods. Notably, Electrochemical Impedance Spectroscopy (EIS) and potentiodynamic polarization were used to probe the impact of immersion time and temperature. Energy-dispersive X-ray spectroscopy (EDX) and spanning electron microscopy (SEM) were used to confirm the presence of a protective layer on the substrate surface. Density functional theory (DFT) method was used to optimize the investigated species by use of B3LYP/6-31 + G(d, p) level of theory. The global and local quantum chemical reactivity descriptors were calculated to explore the inhibition corrosion efficiency and to identify the most favorable sites for electrophilic and nucleophilic attacks. Monte Carlo (MC) and molecular dynamics simulation (MDS) methods were used to study the interactions between corrosion inhibitor and metal surface. Noteworthy, results showed that CSEA exhibited an impressive inhibition efficiency, which reached 94.3% with a concentration of 2 g/L at 298 K. Potentiodynamic polarization revealed that the extract acted as a mixed-type inhibitor. Nyquist graphs showed that charge-transfer resistance and dæouble-layer capacitance both rised with increasing CSEA concentration, suggesting better inhibition efficiency. Notably, the Langmuir adsorption isotherm is well-aligned with the adsorption of inhibitor compounds. Importantly, all aforementioned theoretical methods were in agreement with the experimental findings. The outcome of the present work supported using Citrullus colocynthis seeds alkaloid-rich extract as ecofriendly agents to prevent corrosion.

Age-associated myeloid malignancies - the role of STAT3 and STAT5 in myelodysplastic syndrome and acute myeloid leukemia.

In the last few decades, the increasing human life expectancy has led to the inflation of the elderly population and consequently the escalation of age-related disorders. Biological aging has been associated with the accumulation of somatic mutations in the Hematopoietic Stem Cell (HSC) compartment, providing a fitness advantage to the HSCs leading to clonal hematopoiesis, that includes non-malignant and malignant conditions (i.e. Clonal Hematopoiesis of Indeterminate Potential, Myelodysplastic Syndrome and Acute Myeloid Leukemia). The Janus Kinase-Signal Transducer and Activator of Transcription (JAK-STAT) pathway is a key player in both normal and malignant hematopoiesis. STATs, particularly STAT3 and STAT5, are greatly implicated in normal hematopoiesis, immunity, inflammation, leukemia, and aging. Here, the pleiotropic functions of JAK-STAT pathway in age-associated hematopoietic defects and of STAT3 and STAT5 in normal hematopoiesis, leukemia, and inflammaging are reviewed. Even though great progress has been made in deciphering the role of STATs, further research is required to provide a deeper understanding of the molecular mechanisms of leukemogenesis, as well as novel biomarkers and therapeutic targets for improved management of age-related disorders.

The different faces of GATA2 deficiency: implications for therapy and surveillance.

GATA2 deficiency is one of the most common genetic predispositions to pediatric myelodysplastic syndrome (MDS) in children and adolescents. The wide spectrum of disease comprises, among others, hematological, immunological and pulmonary manifestations, as well as occasionally distinct organ anomalies. Due to the elevated risk of progression, nearly all individuals with GATA2-related MDS eventually undergo a hematopoietic stem cell transplantation (HSCT) at some point in their lives. Nevertheless, the optimal timing, method, and even the indication for HSCT in certain cases are still matter of debate and warrant further research. In this article, we report five patients with different hematological and immunological manifestations of GATA2 deficiency ranging from immunodeficiency and refractory cytopenia of childhood without chromosomal aberrations to relapsed MDS-related acute myeloid leukemia. We discuss the adopted strategies, including intensity of surveillance, indication and timing of HSCT, based on morphological, clinical and molecular markers, as well as individual patient needs. We conclude that a better characterization of the natural disease course, a better understanding of the prognostic significance of somatic aberrations and a thorough evaluation of patients´ perspectives and preferences are required to achieve a personalized approach aimed at improving the care of these patients.

Chronic myelomonocytic leukemia with ring sideroblasts/SF3B1 mutation presents with low monocyte count and resembles myelodysplastic syndromes with-RS/SF3B1 mutation in terms of phenotype and prognosis.

Introduction: Chronic myelomonocytic leukemia (CMML) and myelodysplastic syndromes (MDS) with ring sideroblasts (RS) or SF3B1 mutation (MDS-RS/SF3B1) differ in many clinical features, but share others, such as anemia. RS and SF3B1 mutation can also be found in CMML. Methods: We compared CMML with and without RS/SF3B1 and MDS-RS/SF3B1 considering the criteria established by the 2022 World Health Organization classification. Results: A total of 815 patients were included (CMML, n=319, CMML-RS/SF3B1, n=172 and MDS-RS/SF3B1, n=324). The percentage of RS was ≥15% in almost all CMML-RS/SF3B1 patients (169, 98.3%) and most (125, 72.7%) showed peripheral blood monocyte counts between 0.5 and 0.9 x109/L and low risk prognostic categories. CMML-RS/SF3B1 differed significantly from classical CMML in the main clinical characteristics, whereas it resembled MDS-RS/SF3B1. At a molecular level, CMML and CMML-RS/SF3B1 had a significantly higher frequency of mutations in TET2 (mostly multi-hit) and ASXL1 (p=0.013) and CMML had a significantly lower frequency of DNMT3A and SF3B1 mutations compared to CMML/MDS-RS/SF3B1. Differences in the median overall survival among the three groups were statistically significant: 6.75 years (95% confidence interval [CI] 5.41-8.09) for CMML-RS/SF3B1 vs. 3.17 years (95% CI 2.56-3.79) for CMML vs. 16.47 years (NA) for MDS-RS/SF3B1, p<0.001. Regarding patients with CMML and MDS, both with SF3B1 mutation, survival did not significantly differ. CMML had a higher risk of transformation to acute myeloid leukemia (24% at 8 years, 95%CI 19%-30%). Discussion: CMML-RS/SF3B1 mutation resembles MDS-RS/SF3B1 in terms of phenotype and clearly differs from CMML. The presence of ≥15% RS and/or SF3B1 in CMML is associated with a low monocyte count. SF3B1 mutation clearly improves the prognosis of CMML.

Molecular Targeting of the Isocitrate Dehydrogenase Pathway and the Implications for Cancer Therapy.

The advent of comprehensive genomic profiling using next-generation sequencing (NGS) has unveiled an abundance of potentially actionable genetic aberrations that have shaped our understanding of the cancer biology landscape. Isocitrate dehydrogenase (IDH) is an enzyme present in the cytosol (IDH1) and mitochondria (IDH2 and IDH3). In the mitochondrion, it catalyzes the irreversible oxidative decarboxylation of isocitrate, yielding the production of α-ketoglutarate and nicotinamide adenine dinucleotide phosphate (NADPH) as well as carbon dioxide (CO2). In the cytosol, IDH catalyzes the decarboxylation of isocitrate to α-ketoglutarate as well as the reverse reductive carboxylation of α-ketoglutarate to isocitrate. These rate-limiting steps in the tricarboxylic acid cycle, as well as the cytoplasmic response to oxidative stress, play key roles in gene regulation, cell differentiation, and tissue homeostasis. Mutations in the genes encoding IDH1 and IDH2 and, less commonly, IDH3 have been found in a variety of cancers, most commonly glioma, acute myeloid leukemia (AML), chondrosarcoma, and intrahepatic cholangiocarcinoma. In this paper, we intend to elucidate the theorized pathophysiology behind IDH isomer mutation, its implication in cancer manifestation, and discuss some of the available clinical data regarding the use of novel IDH inhibitors and their role in therapy.

Differential effects of air pollution exposure on mental health: Historical redlining in New York State.

Growing evidence suggests that ambient air pollution has adverse effects on mental health, yet our understanding of its unequal impact remains limited, especially in areas with historical redlining practices. This study investigates whether the impact of daily fluctuations in ambient air pollutant levels on emergency room (ER) visits for mental disorders (MDs) varies across neighborhoods affected by redlining. Furthermore, we explored how demographic characteristics and ambient temperature may modify the effects of air pollution. To assess the disproportional short-term effects of PM2.5, NO2, and O3 on ER visits across redlining neighborhoods, we used a symmetric bidirectional case-crossover design with a conditional logistic regression model. We analyzed data from 2 million ER visits for MDs between 2005 and 2016 across 17 cities in New York State, where redlining policies were historically implemented. A stratified analysis was performed to examine potential effect modification by individuals' demographic characteristics (sex, age, and race/ethnicity) and ambient temperature. We found that both PM2.5 and NO2 were significantly associated with MD-related ER visits primarily in redlined neighborhoods. Per 10µgm-3 increase in daily PM2.5 and per 10 ppb increase in NO2 concentration were associated with 1.04 % (95 % Confidence Interval (CI): 0.57 %, 1.50 %) and 0.44 % (95 % CI: 0.21 %, 0.67 %) increase in MD-related ER visits in redlined neighborhoods, respectively. We also found significantly greater susceptibility among younger persons (below 18 years old) and adults aged 35-64 among residents in grade C or D, but not in A or B. Furthermore, we found that positive and statistically significant associations between increases in air pollutants (PM2.5 and NO2) and MD-related ER visits exist during medium temperatures (4.90 °C to 21.11 °C), but not in low or high temperature. Exposures to both PM2.5 and NO2 were significantly associated with MD-related ER visits, but these adverse effects were disproportionately pronounced in redlined neighborhoods.

Atypical chronic myeloid leukemia found in a patient with eosinophilia for six years: a case report.

BACKGROUND: Atypical chronic myeloid leukemia (aCML) is a highly aggressive type of blood cancer that falls under the category of myelodysplastic/myeloproliferative neoplasms (MDS/MPN). In the fifth edition of the WHO classification of tumors, this category has been renamed MDS/MPN with neutrophilia. Although eosinophilia is commonly observed in blood cancers, it is rarely seen in aCML. CASE PRESENTATION: This study presents a case of aCML that was diagnosed six years after the patient developed eosinophilia. The patient had undergone tests to rule out other primary and secondary diseases, but the eosinophilia remained unexplained. Treatment with corticosteroids and hydroxyurea had proven ineffective. Six years later, the patient experienced an increase in white blood cells, primarily neutrophils. After ruling out other possible diagnoses, a combination of morphologic and molecular genetic findings led to the diagnosis of aCML. The patient responded well to treatment with azacitidine. CONCLUSIONS: This study summarizes the current state of aCML diagnosis and management and discusses the possible connection between eosinophilia and aCML.

Predicting which subsets of patients with myelodysplastic neoplasms are more likely to progress to overt chronic myelomonocytic leukemia.

The boundary between myelodysplastic syndromes (MDS) and chronic myelomonocytic leukemia (CMML) has been revised in the latest World Health Organization classification of myeloid malignancies. These changes were motivated by the description of a subgroup of MDS patients identified as oligomonocytic chronic myelomonocytic leukemia (OM-CMML) at risk of evolving into overt CMML. Various studies will be reviewed describing the clinical and biological features of MDS patients evolving to CMML. The efforts to discover biomarkers enabling the identification of these patients at the time of MDS diagnosis will be discussed. Finally, the molecular landscape of these patients will be presented with a specific focus on the biallelic inactivation of TET2 in light of its functional impact on hematopoietic stem cells, granule-monocytic differentiation, and its tight interplay with inflammation.

Deciphering the pH-dependent oligomerization of aspartate semialdehyde dehydrogenase from Wolbachia endosymbiont of Brugia malayi: An in vitro and in silico approaches.

The enzyme aspartate semialdehyde dehydrogenase (ASDH) plays a pivotal role in the amino acid biosynthesis pathway, making it an attractive target for the development of new antimicrobial drugs due to its absence in humans. This study aims to investigate the presence of ASDH in the filarial parasite Wolbachia endosymbiont of Brugia malayi (WBm) using both in vitro and in silico approaches. The size exclusion chromatography (SEC) and Native-PAGE analysis demonstrate that WBm-ASDH undergoes pH-dependent oligomerization and dimerization. To gain a deeper understanding of this phenomenon, the modelled monomer and dimer structures were subjected to pH-dependent dynamics simulations in various conditions. The results reveal that residues Val240, Gln161, Thr159, Tyr160, and Trp316 form strong hydrogen bond contacts in the intersurface area to maintain the structure in the dimeric form. Furthermore, the binding of NADP+ induces conformational changes, leading to an open or closed conformation in the structure. Importantly, the binding of NADP+ does not disturb either the dimerization or oligomerization of the protein, a finding confirmed through both in vitro and in silico analysis. These findings shed light on the structural characteristics of WBm-ASDH and offer valuable insights for the development of new inhibitors specific to WBm, thereby contributing to the development of potential therapies for filarial parasitic infections.

Unraveling the corrosion inhibition behavior of prinivil drug on mild steel in 1M HCl corrosive solution: insights from density functional theory, molecular dynamics, and experimental approaches.

The deterioration of mild steel in an acidic environment poses a significant challenge in various industries. The emergence of effective corrosion inhibitors has drawn attention to studies aimed at reducing the harmful consequences of corrosion. In this study, the corrosion inhibition efficiency of Prinivil in a 1M HCl solution through various electrochemical and gravimetric techniques has been investigated for the first time. The results demonstrated that the inhibition efficiency of Prinivil expanded from 61.37% at 50 ppm to 97.35% at 500 ppm concentration at 298 K. With a regression coefficient (R 2) of 0.987, Kads value of 0.935 and Ea value of 43.024 kJ/mol at 500 ppm concentration of inhibitor, a strong affinity of Prinivil for adsorption onto the metal surface has been significantly found. Scanning electron microscopy (SEM) and contact angle measurement analyses further support the inhibitory behavior of Prinivil, demonstrating the production of a defensive layer on the surface of mild steel. Additionally, molecular dynamics (MD) and Monte Carlo simulations were employed to investigate the stability and interactions between Prinivil and the metallic surface (Fe (1 1 0)) at the atomic level. The computed results reveal strong adsorption of Prinivil upon the steel surface, confirming its viability as a corrosion inhibitor.

Updates in biology, classification, and management of acute myeloid leukemia with antecedent hematologic disorder and therapy related acute myeloid leukemia.

Acute myeloid leukemia with antecedent hematologic disorder (AHD-AML) and therapy related AML (t-AML) constitute a heterogenous disease with inferior outcomes. It is often characterized by high-risk cytogenetic and molecular alterations associated with AHD or prior cancer therapy. Historically, the standard of care treatment has been intensive induction with "7 + 3", with an improved overall response rate and survival with CPX-351. Results from large registry-based studies suggested that allogeneic hematopoietic stem cell transplant is preferable to consolidation chemotherapy alone for achieving long-term survival in patients with AHD-AML. Prevalence of high-risk genetic features and advanced age and comorbidities in patients make AHD-AML and t-AML clinically challenging subgroups to treat with intensive approaches. Recent reports on less intensive treatment options, particularly the hypomethylating agent-venetoclax combination, have shown encouraging response rates in these patients. However, emerging resistance mechanisms compromise duration of response and overall survival. Several novel agents targeting apoptotic machinery, signaling pathways, and immune checkpoints are under clinical investigation, with an aim to truly improve overall outcomes in this subgroup. We reviewed updates in biology, classification, and clinical data comparing safety and efficacy of intensive and less intensive treatment options, and summarized ongoing studies with promising novel therapies in AHD-AML and t-AML.

GATA2 deficiency syndrome: A compensatory mechanism gone awry?

In their paper, using zebrafish models, Gioacchino et al. have demonstrated the GATA2 haploinsufficiency, the genetic hallmark of GATA2 deficiency syndrome, promotes erythroid and myeloid cytopenia, and have discovered a self-regulatory mechanism to compensate GATA2 levels and protein function. Commentary on: Gioacchino et al. GATA2 heterozygosity causes an epigenetic feedback mechanism resulting in myeloid and erythroid dysplasia. Br J Haematol 2024 (Online ahead of print). doi: 10.1111/bjh.19585.

Evaluating the impact of soil erosion on soil quality in an agricultural land, northeastern China.

The impact of soil erosion on soil quality is still not systematically understood. The purpose of this study was thus to quantify the impact of soil erosion on soil quality and its change with slope morphology in an agricultural field, northeastern China based on radionuclide 137Cs, unmanned aerial vehicle derived high resolution digital elevation model, and soil sampling. 137Cs method yielded an average soil erosion rate of - 275 t km-2 yr-1 ranging from - 1870 to 1557 t km-2 yr-1. The soil quality index derived from total dataset (SQI_TDS) can be well explained by that derived from minimum data set (SQI_MDS) with a determination coefficient R2 of 0.874. SOM, sand, and cation exchange capacity in the MDS play more important roles than other soil indicators. Soil quality was significantly affected by soil erosion, with Adj. R2 of 0.29 and 0.33 for SQI_TDS and SQI_MDS, respectively. The spatial variations of soil erosion and soil quality were both affected by slope topography. Soil erosion must be controlled according to topographic and erosion characteristics in northeastern China.