Single-cell sequencing unveils T-cell characteristic in acute myeloid leukemia.

Acute myeloid leukemia (AML) presents as a remarkably heterogeneous disease, and the intricate role of various T cell subtypes, including T helper (Th) cells and regulatory T (Treg) cells, in immune dysregulation and the promotion of leukemia cell proliferation and survival is not yet fully understood. In this study, we conducted a comparative analysis of transcriptome profiles in T cells derived from bone marrow samples of three leukemia patients, both before and after treatment, as well as from a relapse sample. This analysis was facilitated through the utilization of single-cell RNA sequencing. The T cell population was subcategorized into CD4 + T cells and CD8 + T cells. Intriguingly, the composition of CD8 + T cells exhibited a relatively stable pattern before and after treatment, while a substantial difference in composition was observed in CD4 + T cells, notably in Th17 and Treg cell populations. Pseudotime trajectory analysis of CD4 + T cell clusters provided further insights into the augmented transition between Th17-like and Treg cells in AML. This transition was characterized by changes in the expression of key genes, including STAT3, CCR6, IL23R, FOXP3, and CTLA4, along their developmental path. An increased cell-to-cell interaction between AML blast cells and all types of T cells appeared to contribute to the restoration of normal T cell proportions. Notably, the LGALS9-CD45 and LGALS9-CD44 pathways emerged as pivotal interactions between blast cells and Treg cells. Our findings unveil an imbalanced differentiation pattern in CD4 + T cells and elucidate the immunosuppressive profiles linked to leukemia cells, thereby enhancing our understanding of CD4 + T cell functionality in the context of AML.

Investigation of low-temperature partitioning with dispersive solid-phase extraction for quantification of pesticides in apples followed by electrospray-ionization mobility spectrometry: Comparison with conventional procedure.

Ion mobility spectrometry (IMS) has a promising application prospect in food surveillance. However, due to the complexity of food matrix and trace levels of pesticide residues, the effective and rapid detection of pesticides by IMS has been a challenge, especially when using electrospray ionization (ESI) as an ion source. In this study, low-temperature partitioning with dispersive solid-phase extraction (LTP-dSPE) was explored and compared with conventional procedures. Both methods were validated for the quantification of eight pesticides in apples, obtaining a limit of detection (LOD) of 0.02-0.12 mg/kg for LTP-dSPE and 0.02-0.09 mg/kg for conventional solid-phase extraction (SPE), lower than those usually stipulated by government legislation in food matrices. For LTP-dSPE, the matrx effect (ME) ranged from -16.3 to -68.6 %, lower than that for the SPE method, ranging from -70.0 to -92.9 %. The results showed satisfactory efficiency and precision, with recovery values ranging from 67.9 to 115.4 % for LTP-dSPE and from 62.0 to 114.8 % for conventional SPE, with relative standard deviations below 13.0 %. Notably, the proposed LTP-dSPE/ESI-IMS has been shown to be more cost-effective, easier to use, more environment-friendly, more accessible, and, most importantly, less matrix effect than the conventional method, thereby being suitably applicable to a wide range of food safety applications.

Regulation of the Notch signaling pathway by natural products for cancer therapy.

The Notch signaling pathway is an evolutionarily conserved pathway that modulates normal biological processes involved in cellular differentiation, apoptosis, and stem cell self-renewal in a context-dependent fashion. Attributed to its pleiotropic physiological roles, both overexpression and silencing of the pathway are associated with the emergence, progression, and poorer prognosis in various types of cancer. To decrease disease incidence and promote survival, targeting Notch may have chemopreventive and anti-cancer effects. Natural products with profound historical origins have distinguished themselves from other therapies due to their easy access, high biological compatibility, low toxicity, and reliable effects at specific physiological sites in vivo. This review describes the Notch signaling pathway, particularly its normal activation process, and some main illnesses related to Notch signaling pathway dysregulation. Emphasis is placed on the effects and mechanisms of natural products targeting the Notch signaling pathway in diverse cancer types, including curcumin, ellagic acid (EA), resveratrol, genistein, epigallocatechin-3-gallate (EGCG), quercetin, and xanthohumol and so on. Existing evidence indicates that natural products are feasible solution to fight against cancer by targeting Notch signaling, either alone or in combination with current therapeutic agents.

Ginger (Zingiber officinale Roscoe) preparations for prophylaxis of postoperative nausea and vomiting: A Bayesian network meta-analysis.

ETHNOPHARMACOLOGICAL RELEVANCE: Ginger has been proposed for prevention of postoperative nausea and vomiting (PONV), however it remains equivocal whether ginger can be an alternative option and which certain preparation is optimal for PONV prophylaxis. AIM OF THE STUDY: We conducted a network meta-analysis (NMA) to compare and rank relative efficacy for PONV control among all available ginger preparations collected in the databases. METHODS: Eligible records were identified by retrieving Medline (via Pubmed), Embase, Web of Science, CENTRAL, CNKI, WHO ICTRP and ClinicalTrials.gov for randomized controlled trials that investigated the efficacy of ginger therapies for the prophylaxis of PONV. A bayesian NMA within random-effects models was implemented. Certainty of evidence for estimates was investigated following GRADE framework. We prospectively registered the protocol (CRD 42021246073) in PROSPERO. RESULTS: Eighteen publications comprising 2199 participants with PONV were identified. Ginger oil (RR [95%CI], 0.39 [0.16, 0.96]) appeared to have the highest probability of being ranked best to decrease the incidence of postoperative vomiting (POV), with statistical significance compared with placebo, based on high to moderate confidence in estimates. With regard to reducing postoperative nausea (PON), statistically superiority was not observed in ginger regimens compared with placebo based on moderate to low certainty of evidence. Reduction in antemetic use and nausea intensity were noticed in ginger powder and oil. Ginger was significantly associated with better efficacy for Asian, older age, higher dosage, preoperative administration, hepatobiliary and gastrointestinal surgery. CONCLUSIONS: Ginger oil appeared to be superior to other ginger treatments for the prophylaxis of POV. With regard to reducing PON, ginger preparations indicated no obvious advantages.

Primary malignant melanoma of the cervix: A comprehensive analysis of case reports in the Chinese population.

PURPOSE: Malignant melanoma is a tumor generated from the basal melanocytes of human epidermis. Primary malignant melanoma of the cervix (PMMC) is derived from cervical melanocytes. It is an uncommon disease, mostly occurring in perimenopausal women. PMMC has a bad prognosis and lacks a defined protocol or treatment standards. The aim of this study was to analyze the impact of different surgical procedures and different adjuvant treatment modalities on their prognosis and to find risk factors for their prognosis by integrating published case report data based on the Chinese population. METHODS AND RESULTS: This study included 165 patients with PMMC in the Chinese population. We used the Kaplan-Meier method to build the survival curve, and the log-rank test to examine the variations among the subgroups. Prognostic factors were examined utilizing the Cox proportional hazards regression model. We found that patients who underwent radical hysterectomy-based surgery, those who underwent lymphadenectomy, and those who underwent other treatments in addition to surgery had significantly better survival rates. The overall analysis, showed that age, and FIGO Stage II, III, and IV, increased the risk of death. Moreover, radical hysterectomy (RH), total hysterectomy (TAH), lymphadenectomy, and adjuvant therapy were correlated with a decreased mortality risk. CONCLUSION: After summarizing the current data, we recommend radical hysterectomy, and lymphadenectomy treatment for patients with PMMC. For patients who had already undergone surgery, other treatment options had a positive effect on prognosis. For patients who had already undergone surgery, other treatment options had a positive effect on prognosis; therefore patient-specific treatment options need to be further discussed.

Recent advances in optical aptasensors for biomarkers in early diagnosis and prognosis monitoring of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) accounts for approximately 90% of all primary liver cancers and is one of the main malignant tumor types globally. It is essential to develop rapid, ultrasensitive, and accurate strategies for the diagnosis and surveillance of HCC. In recent years, aptasensors have attracted particular attention owing to their high sensitivity, excellent selectivity, and low production costs. Optical analysis, as a potential analytical tool, offers the advantages of a wide range of targets, rapid response, and simple instrumentation. In this review, recent progress in several types of optical aptasensors for biomarkers in early diagnosis and prognosis monitoring of HCC is summarized. Furthermore, we evaluate the strengths and limitations of these sensors and discuss the challenges and future perspectives for their use in HCC diagnosis and surveillance.

Association of urinary nickel levels with diabetes and fasting blood glucose levels: A nationwide Chinese population-based study.

Some epidemiological studies support a relationship between nickel exposure and diabetes in the general population. To address this, we tested the association of nickel exposure with diabetes in 10,890 adults aged ≥ 18 years old from the China National Human Biomonitoring study conducted in 2017-2018. Urinary nickel concentrations and fasting blood glucose (FBG) were measured, and lifestyle and demographic data were collected. Weighted logistic and linear regressions were used to estimate the associations of urinary nickel levels with diabetes prevalence and FBG. Restricted cubic splines (RCS) were used to test for the dose-response relationship. The odd ratio (95% confidence interval [CI]) of diabetes for the highest versus lowest quartiles of urinary nickel concentrations was 1.74 (1.28, 2.36) in the multivariate model (p trend =0.001). Each one-unit increase in log-transformed urinary nickel concentrations was associated with a 0.36 (0.17, 0.55) mmol/L elevation in FBG. The RCS curves showed a monotonically increasing dose-response relationship of urinary nickel with diabetes as well as FBG levels, and then tended to flatten after about 4.75 µg/L of nickel exposure. The nickel-diabetes association was stronger in individuals with lower than those with higher rice consumption (OR: 2.39 vs. 1.72). Our study supports a positive association between nickel exposure and diabetes prevalence in Chinese adults, especially in individuals with lower rice consumption. Further large-scale prospective studies are needed to validate our findings.

TP53 signal pathway confers potential therapy target in acute myeloid leukemia.

TP53 mutation is a frequent tumor suppressor mutation and a critical prognostic indicator across studies in many malignant tumors including hematologic malignancies. However, the role of TP53 and its correlative pathway in acute myeloid leukemia (AML) is enigmatic, which may provide possible emerging strategies with the potential to improve outcomes in AML. Accordingly, we focus not only on the TP53 mutation but also on the underlying mechanisms of the mutated TP53 signal pathway. While it is now generally accepted that TP53 mutations are widely associated with a dismal prognosis, resistance to chemotherapy, and high incidence of relapse and refractory AML. Hereby, the current therapeutics targeting TP53 mutant AML are summarized in this review. This will address emerging TP53-based therapeutic approaches, facilizing the TP53-targeted treatment options.

Integrative analysis indicates the prognostic value of circadian rhythm disruption in liver cancer: Potential for therapeutic targeting.

Circadian rhythms regulate various biological processes, such as cell division and metabolism. Circadian rhythm disruption (CRD) is often associated with malignant tumor progression and poor prognosis. However, the effect of CRD on liver cancer prognosis has not been systematically analyzed or fully elucidated. Here, we developed a method to quantify and assess intratumoral CRD in a single-cell transcriptomic analysis of liver cancer and systematically analyzed the role of CRD in tumor progression and prognosis. Furthermore, a LASSO-Cox regression model based on 14 CRD genes was used to predict overall patient survival across multiple datasets. We found that malignant cells with high CRD scores were enriched in specific metabolic pathways, such as fatty acid metabolism and the trichloroacetic acid cycle. Intercellular communication analysis suggested that CRD regulates chemokine-mediated interactions. With the bulk transcriptomic datasets, we determined that LiverCRD scores were significantly correlated with macrophage infiltration levels and could guide targeted immunotherapy and chemotherapy strategies. In addition, LiverCRD is also associated with the mutational landscape-for example, TP53 mutation frequency was higher in high-CRD samples. Finally, the 14-gene-based LASSO-Cox regression model could accurately predict overall patient survival across datasets. In conclusion, Our proposed analysis reflects the relationship between CRD and the immune environment in liver cancer, suggesting that CRD may serve as a potential prognostic indicator. Our results may help guide targeted anti-tumor strategies.

Ectopic viral integration Site-1 oncogene promotes NRAS pathway through epigenetic silencing of microRNA-124 in acute myeloid leukemia.

BACKGROUND: Acute myeloid leukemia (AML) is an aggressive hematological malignancy characterized by genetic mutations that promote proliferation of myeloid progenitors and prevent their differentiation. Over-expression of Ectopic Viral Integration site-1(EVI-1) is related to the poor prognosis in myeloid leukemia, but the underlying mechanism remains unclear. METHODS: Using qRT-PCR and western blotting, we quantified expressions of EVI-1, NRAS and ERK/p-ERK in leukemia cell lines and PBMCs. Using WTS-8 and cell cycle analysis, we further investigated whether downregulation of EVI-1 by siRNA can inhibit cell proliferation. Microscopic observation of peripheral blood cells from EVI-1 transgenic zebrafish and WT control were analyzed by Wright Giemsa staining. Using miR-seq, qPCR, dual-luciferase reporter and coimmunoprecipitation assays, we revealed the relationship between EVI-1, miR-124 and NRAS. RESULTS: EVI-1 was highly expressed in both primary AML and leukemia cell lines (THP-1 and K562). In a transgenic zebrafish model, EVI-1 mediated higher mortality and induced immature hematopoietic cells in the blood circulation, suggesting its oncogenic role. Furthermore, our results suggested that EVI-1 upregulated NRAS expression, thereby activating the RAS/ERK pathway through epigenetic silencing of a potent NRAS suppressor, miR-124. In this study, we found that EVI1 physically interacts with Dnmt3a to form a protein complex that targets and binds to regulatory elements of miR-124. CONCLUSIONS: Overall, the current findings demonstrate that EVI-1 overexpression converges on the regulation of miR-124 promoter methylation and activation of the RAS/ERK pathway in AML carcinogenesis, and suggest EVI-1 and/or miR-124 as therapeutic targets for this dismal disease.

Homoharringtonine Synergized with Gilteritinib Results in the Downregulation of Myeloid Cell Leukemia-1 by Upregulating UBE2L6 in FLT3-ITD-Mutant Acute Myeloid (Leukemia) Cell Lines.

FMS-like tyrosine kinase 3 (FLT3) mutant acute myeloid leukemia (AML) occurs in approximately 30% of all AML patients and still has a poor prognosis. This study is directed to investigate gilteritinib in combination with homoharringtonine (HHT) on FLT3-ITD-mutant AML cell lines. In our study, we found that cell proliferation was dramatically suppressed by the combination of gilteritinib and HHT. This combination therapy decreased the mitochondrial membrane potential, finally inducing apoptosis. We demonstrated that gilteritinib downregulated the expression of FLT3 and downstream signaling, further decreased the mRNA level of myeloid cell leukemia-1 (Mcl-1). HHT and combination therapy could upregulate UBE2L6, which induced the degradation of Mcl-1 via ubiquitin-proteasome system. Knockdown of UBE2L6 could protect Mcl-1 from deprivation through the ubiquitin-proteasome system. These findings may provide a novel theoretical basis for the treatment of AML patients with FLT3-ITD mutations.

Arsenic trioxide potentiates Gilteritinib-induced apoptosis in FLT3-ITD positive leukemic cells via IRE1a-JNK-mediated endoplasmic reticulum stress.

BACKGROUND: Acute myeloid leukemia (AML) patients with FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD) have a high relapse rate and poor prognosis. This study aims to explore the underlying mechanism of combining Gilteritinib with ATO at low concentration in the treatment of FLT3-ITD positive leukemias. METHODS: We used both in vitro and in vivo studies to investigate the effects of combination of Gilteritinib with ATO at low concentration on FLT3-ITD positive leukemias, together with the underlying molecular mechanisms of these processes. RESULTS: Combination of Gilteritinib with ATO showed synergistic effects on inhibiting proliferation, increasing apoptosis and attenuating invasive ability in FLT3-ITD-mutated cells and reducing tumor growth in nude mice. Results of western blot indicated that Gilteritinib increased a 160KD form of FLT3 protein on the surface of cell membrane. Detection of endoplasmic reticulum stress marker protein revealed that IRE1a and its downstream signal phosphorylated JNK were suppressed in Gilteritinib-treated FLT3-ITD positive cells. The downregulation of IRE1a induced by Gilteritinib was reversed with addition of ATO. Knockdown of IRE1a diminished the combinatorial effects of Gilteritinib plus ATO treatment and combination of tunicamycin (an endoplasmic reticulum pathway activator) with Gilteritinib achieved the similar effect as treatment with Gilteritinib plus ATO. CONCLUSIONS: Thus, ATO at low concentration potentiates Gilteritinib-induced apoptosis in FLT3-ITD positive leukemic cells via IRE1a-JNK signal pathway, targeting IRE1a to cooperate with Gilteritinib may serve as a new theoretical basis on FLT3-ITD mutant AML treatment.

Black liquor as biomass feedstock to prepare zero-valent iron embedded biochar with red mud for Cr(VI) removal: Mechanisms insights and engineering practicality.

Black liquor (BL) is an agro-industrial residue with high number of lignocellulosic components which could be recognized as a biomass feedstock. In this work, BL coupled with red mud (RM), were applied to prepare cost-effective zero-valent iron (ZVI) embedded in biochar. The oligomers in BL acted as reductants for RM to generate ZVI, while the organic components could be converted into biochar during pyrolysis. The RM/BL demonstrated excellent performance in the removal of Cr(VI) (349.5 mg/g), as the mechanisms were reduction and adsorption. The fixed-bed column study was conducted and 1.7 L simulated wastewater could be treated by 1.0 g RM/BL. After reaction, 95.5% ± 0.8% and 82.5%±3.2% Cr-loaded adsorbents could be recovered by an external magnet for batch and fixed-bed experiments, respectively. All these results shed light on valorizing these two widespread agro-industrial byproducts, and bridged the knowledge gap between magnetic bio-adsorbent preparation and its industrial practicality on wastewater purification.

One-step preparation of ZVI-sludge derived biochar without external source of iron and its application on persulfate activation.

Zero Valent Iron (ZVI) is an important and widely employed environmental remediation material in brownfield. However, the instability of fine size ZVI and the strong aggregation of nanoscale-ZVI limited its further application. To overcome these drawbacks, ZVI-Sludge Derived Biochar (SDBC) was prepared without external iron source through the one-step process of pyrolysis. The characterization results including SEM-EDX, XRD and XPS confirmed the successful loading of Fe0 on the surface of SDBC. The activation efficiency of persulfate (PS) in in-situ chemical oxidation system was studied. The environmental remediation properties of ZVI-SDBC/PS system were evaluated employing acid orange (AO7) and landfill leachate as target pollutants. ZVI-SDBC/PS system was highly efficient as that 99.0% of AO7 (0.06 mM) was removed by 0.925 mM of PS and 0.5 g L-1 of ZVI-SDBC. In addition, total organic carbon (TOC) and ammonia in leachate were removed by 62.8% and 99.8%, respectively. The removal efficiency of AO7 was nearly independent on initial pH as that 89.1% and 99.1% of AO7 were removed at pH of 9.08 and 2.13 respectively. Hydroxyl radicals dominated in the reaction under neutral and alkaline conditions with contribution rates of 71.9% and 86.1% respectively. Noticeably, not only free radicals but also non-radical species such as singlet oxygen contributed to the degradation, which favored the pH-independent performance. The reuse performance of ZVI-SDBC was higher than these of previously reported ZVI-based catalysts as that the first-order rate constant of AO7 removal decreased not much from 0.0718 to 0.0502 min-1 after the three-cycle reuse assays. In summary, ZVI-SDBC showed advantages such as the facile and chemical-saving preparation method, reliable disposal of municipal sewage sludge, remarkable efficiency and stability. These advantages proved ZVI-SDBC/PS system as an effective strategy of controlling waste by waste, and implicated its potential application in full-scale for environmental remediation in brownfield.

Modulation of FLT3 through decitabine-activated C/EBPa-PU.1 signal pathway in FLT3-ITD positive cells.

FMS-like tyrosine kinase 3 (FLT3)-mutant acute myeloid leukemia (AML) which occurs in approximately 30% of all AML patients still has a poor prognosis. This study aimed to examine the effect of decitabine (DAC) on FLT3-ITD positive AML. In our study, we found that expression of FLT3 and its downstream targets was decreased in FLT3-ITD mutant cell lines treated with DAC. DAC treatment could increase the percentage of apoptotic cells and CD11b positive cells tested by flow cytometry and upregulate the expression of cleaved caspase3, cleaved PARP, C/EBPa and PU.1 detected by western blot. To explore the effect of increased expression of PU.1 on FLT3 protein, we transiently transfected MOLM13 and MV4-11 cells with siRNA against PU.1 and a siRNA control. In both FLT3-ITD positive cells, the effect of DAC on downregulation of FLT3 was diminished in PU.1-konckdown MOLM13 and MV4-11 cells and there was a decrease of CD11b expression after PU.1 knockdown. Furthermore, the percentage of apoptotic cells was also decreased in PU.1-konckdown cells compared with siRNA control-expressing cells with the same dose of DAC. These findings indicated that DAC upregulated PU.1 to induce downregulation of FLT3 to trigger apoptosis. DAC was also found efficacious in mouse xenograft models of FLT3-ITD AML in our study. These findings may provide a novel theoretical basis for treatment of FLT3-ITD positive AML patients.

EVI-1 modulates arsenic trioxide induced apoptosis through JNK signalling pathway in leukemia cells.

High expression of the oncogene ecotropic viral integration site-1 (EVI-1) is an independent negative prognostic indicator of survival in leukemia patients. This study aimed to examine the effects of arsenic trioxide (ATO) on EVI-1 in acute myeloid leukemia (AML). Mononuclear cells were isolated from the bone marrow and peripheral blood of AML patients and healthy donors. EVI-1 expression in hematopoietic cells was evaluated by RT-qPCR and Western blot analysis. EVI-1 was highly expressed in both primary AML and leukemia cell lines (THP-1 and K562). ATO down-regulated EVI-1 mRNA in zebrafish in vivo as well as in primary leukemia cells and THP-1 and K562 cells in vitro. Additionally, ATO treatment induced apoptosis, down-regulated both EVI-1 mRNA and oncoprotein expression, increased the expression of pro-apoptosis proteins, and decreased the expression of anti-apoptotic proteins in leukemia cells in vitro. EVI-1 expression in leukemia cells (THP-1 and K562) transduced with EVI-1 siRNA was significantly reduced. Silencing EVI-1 had a significant effect on the activation of the JNK pathway and the induction of leukemia cell apoptosis. ATO may downregulate EVI-1 mRNA and oncoprotein levels and block the inhibitory effects of EVI-1 on the JNK pathway, which activates the JNK apoptotic pathway, thereby leading to the apoptosis of EVI-1 in AML patients.

Amentoflavone ameliorates cold stress-induced inflammation in lung by suppression of C3/BCR/NF-κB pathways.

BACKGROUND: Cold stress, which may lead to local and systemic injury, is reported to be related to the immune system, especially the complement system. At present, the lack of effective treatment is a critical issue. Amentoflavone (AF), which can inhibit cold stress-induced inflammation in lung by multiple mechanisms, is the main therapeutic ingredient in plants of the genus Selaginella. RESULTS: In the current study, we found that cold could induce lung inflammation related to the complement system and its downstream pathways. AF treatment significantly inhibited lung inflammation from cold exposure. We presented evidence that AF can bind to complement component 3 (C3) to regulate inflammation-related pathways involving Lck/Yes novel tyrosine kinase (Lyn), protein kinase B (Akt), nuclear factor-κB (NF-κB) and immune factors. Moreover, 30 mg/kg of AF caused significantly greater improvement than 15 mg/kg in reducing the level of C3 in lung tissue. CONCLUSIONS: AF can protect lung tissue from cold exposure. The protective effect may be achieved by inhibition of C3 and negative regulation of the B cell receptor (BCR)/NF-κB signaling pathways and high mobility group box 1 (HMGB1), which ultimately ameliorates the inflammatory response.

Upregulated microRNA-146a expression induced by granulocyte colony-stimulating factor enhanced low-dosage chemotherapy response in aged acute myeloid leukemia patients.

The selection of chemotherapy regimen for elderly patients with acute myeloid leukemia (AML) remains challenging. Here, we report that granulocyte colony-stimulating factor (G-CSF) upregulates the expression of microRNA (miR)-146a in a nuclear factor kappaB-dependent manner, leading to direct decreases in the expression of the target proteins CXCR4 and Smad4 in AML cells in vitro. The reduction in CXCR4 expression suppressed the migration abilities of leukemia cells. Downregulation of Smad4 promoted cell cycle entry in leukemia cells. Furthermore, an increase in apoptosis was observed when leukemia cells were treated sequentially with G-CSF and cytosine arabinoside in vitro. These findings suggest that G-CSF treatment may disrupt the protection of bone marrow niches from leukemia cells. In a review of data from 78 cases of primary AML, we found that a high miR-146a expression and/or upregulation of this miRNA during G-CSF priming chemotherapy was predictive of better clinical outcomes. Our findings suggest that miR-146a may be a novel biomarker for evaluating the clinical prognosis and treatment effects of a G-CSF priming protocol in elderly patients with AML.

Salicylate induces reactive oxygen species and reduces ultraviolet C susceptibility in Staphylococcus aureus.

This study demonstrates that growth of Staphylococcus aureus in the presence of salicylate reduces ultraviolet C (UVC)-induced cell death and increases the generation of reactive oxygen species (ROS). In addition, compounds that scavenge ROS (N-acetylcysteine, glutathione, catalase and superoxide dismutase) reverse the increased UVC survival induced by growth in the presence of salicylate, while ROS donors (tert-butylhydroperoxide, H2O2 and NaClO) enhance survival of salicylate challenged cultures. Collectively, these findings suggest that ROS production induced by growth in the presence of salicylate protects S. aureus from UVC-induced cell death.