Blood typing and transfusion therapy in a patient with A2 subtype acute myeloid leukemia M2: A case report.

BACKGROUND: Acute myeloid leukemia (AML) is one of the most common types of leukemia in adults. However, AML is relatively rare in the population overall, accounting for only about 1 percent of all cancers. Treatment for AML can be very effective for some patients, yet it leaves others with serious and even life-threatening side effects. Chemotherapy is still the primary treatment for most AML, but over time, leukemia cells become resistant to chemotherapy drugs. In addition, stem cell transplantation, targeted therapy, and immunotherapy are currently available. At the same time, with the progression of the disease, the patient may have corresponding complications, such as coagulation dysfunction, anemia, granulocytopenia, and repeated infection, so transfusion supportive therapy will be involved in the overall treatment regime. To date, few articles have reported on blood transfusion treatment options for patients with ABO subtypes AML-M2. Blood transfusion therapy is an important supportive treatment for AML-M2, and accurate determination of patients' blood type is one of the most important steps in the treatment process. In this study, we explored blood typing and supportive treatment strategies for a patient with A2 subtype AML-M2 to provide the basis for treatment for all patients. CASE SUMMARY: In order to determine the blood type of the patient, serological and molecular biological methods were used for reference tests, and the genetic background was studied to determine the patient's final blood type and select the appropriate blood products for infusion treatment. According to the results obtained by serological and molecular biological methods, the blood type of the patient was A2 subtype; the genotype was A02/001; the irregular antibody screening was negative, and anti-A1 was found in the plasma. According to the overall treatment plan, active anti-infection, elevated cells, component blood transfusion support, and other rescue and supportive treatments were given, and the patient successfully passed the stage of myelosuppression after chemotherapy. Re-examination of bone marrow smears showed that AL was in complete remission of bone marrow signs, and minimal residual leukemia lesions suggested no cells with obvious abnormal immunophenotype (residual leukemia cells < 10-4). CONCLUSION: The infusion of patients with A2 subtype AML-M2 with A irradiated platelets and O washing red blood cells can meet the needs of clinical treatment.

Gibberellic acid alleviates cadmium toxicity in rice by regulating NO accumulation and cell wall fixation capacity of cadmium.

Gibberellic acid (GA) has been implicated in the response of plants to cadmium (Cd) stress, but the underlying mechanism remains unclear. In the present study, our aim was to confirm the role of GA in regulating the accumulation of Cd in rice. We found that Cd stress elevated the endogenous GA level in the rice roots. Exogenous GA application not only decreased the fixation of Cd in the root cell wall through reducing the hemicelluloses content, but also decreased the expression of OsNRAMP5 (Natural Resistance-Associated Macrophage Protein 5) and OsCd1 (a major facilitator superfamily gene). Both OsNRAMP5 and OsCd1 are related to Cd absorption, therefore, less Cd was accumulated in the roots. Furthermore, GA increased the expression of OsHMA3 (Heavy Metal ATPase 3) and OsCAL1 (Cadmium accumulation in Leaf 1), which are responsible for sequestering the Cd to the vacuoles and effluxing the Cd outside the cell, respectively, as a result, less Cd was accumulated in the shoots. In contrast, more Cd was accumulated in GA deficient lines. Furthermore, GA decreased the endogenous NO levels and the activity of antioxidant enzymes, while application of a NO scavenger-cPTIO diminished the alleviatory role of GA. In summary, the GA accelerated cell wall Cd exclusion mechanism probably improved rice tolerance to Cd toxicity via regulating the accumulation of NO.

The NAC transcription factor ANAC017 regulates aluminum tolerance by regulating the cell wall-modifying genes.

Aluminum (Al) toxicity is one of the key factors limiting crop production in acid soils; however, little is known about its transcriptional regulation in plants. In this study, we characterized the role of a NAM, ATAF1/2, and cup-shaped cotyledon 2 (NAC) transcription factors (TFs), ANAC017, in the regulation of Al tolerance in Arabidopsis (Arabidopsis thaliana). ANAC017 was localized in the nucleus and exhibited constitutive expression in the root, stem, leaf, flower, and silique, although its expression and protein accumulation were repressed by Al stress. Loss of function of ANAC017 enhanced Al tolerance when compared with wild-type Col-0 and was accompanied by lower root and root cell wall Al content. Furthermore, both hemicellulose and xyloglucan content decreased in the anac017 mutants, indicating the possible interaction between ANAC017 and xyloglucan endotransglucosylase/hydrolase (XTH). Interestingly, the expression of XTH31, which is responsible for xyloglucan modification, was downregulated in the anac017 mutants regardless of Al supply, supporting the possible interaction between ANAC017 and XTH31. Yeast one-hybrid, dual-luciferase reporter assay, and chromatin immunoprecipitation-quantitative PCR analysis revealed that ANAC017 positively regulated the expression of XTH31 through directly binding to the XTH31 promoter region, and overexpression of XTH31 in the anac017 mutant background rescued its Al-tolerance phenotype. In conclusion, we identified that the tTF ANAC017 acts upstream of XTH31 to regulate Al tolerance in Arabidopsis.

The MYB transcription factor MYB103 acts upstream of TRICHOME BIREFRINGENCE-LIKE27 in regulating aluminum sensitivity by modulating the O-acetylation level of cell wall xyloglucan in Arabidopsis thaliana.

Modification of the O-acetylation level of xyloglucan (XyG) appears to affect aluminum (Al) sensitivity in Arabidopsis by modulating its binding capacity to Al. However, the transcriptional regulation of this process remains largely unknown. In our previous studies, we found that the expression of TRICHOME BIREFRINGENCE-LIKE27 (TBL27), which is responsible for the O-acetylation of XyG, was downregulated under Al stress. In the present study, we showed that the expression of an R2R3-type transcription factor-encoding gene, MYB103, was also inhibited by Al exposure and exhibited a co-expression pattern with TBL27 in roots and siliques, suggesting a potential link between MYB103 and TBL27. The loss of function of MYB103 resulted in increased Al sensitivity, as indicated by more inhibited root growth and elevated root Al content compared with the wild type. Moreover, we also detected increased Al accumulation in the root cell wall and the hemicellulose fraction, which was attributed to the changes in the O-acetylation level of XyG rather than the XyG content itself. In addition, further analysis revealed that MYB103 positively activated TBL27 expression by directly binding to the TBL27 promoter region, and TBL27 overexpression in the myb103 mutant rescued the Al-sensitive phenotype of the mutant to the wild-type level. Taken together, we conclude that MYB103 acts upstream of TBL27 to positively regulate Al resistance by modulating the O-acetylation of the cell wall XyG.

[Effects of chitosan oligosaccharide on alveolar bone resorption, Th17/Treg balance and OPG/RANKL/RANK pathway in periodontitis rats].

PURPOSE: To investigate the effect of chitosan oligosaccharide on alveolar bone resorption, Th17/Treg balance and OPG/RANKL/RANK pathway in rats with periodontitis. METHODS: Rat model of periodontitis was established, and the periodontitis rats were randomly divided into model group, low-dose chitosan oligosaccharide group, middle-dose chitosan oligosaccharide group, high-dose chitosan oligosaccharide group and metronidazole group, with 12 rats in each group, another 12 rats were set as control group. After treatment, gingival index and alveolar bone absorption were evaluated. H-E staining was used to observe the pathological changes of periodontal tissues. The ratio of Th17/Treg cells in peripheral blood was detected by flow cytometry, the levels of serum IL-17, TGF-ß, RANKL and OPG were detected by ELISA, and the expressions of OPG and RANKL mRNA in periodontal tissues of rats in each group were detected by real-time fluorescent quantitative PCR(qRT-PCR). SPSS 24.0 software package was used to analyze the data. RESULTS: Compared with the control group, the periodontal tissue of the model group showed periodontal membrane fiber bundle rupture, disordered arrangement, capillary expansion, proliferation, inflammatory cell infiltration and other pathological damage. Gingival index, alveolar bone resorption value, Th17/Treg ratio, serum RANKL and IL-17 levels, and periodontal RANKL mRNA level were significantly increased(P<0.05), while the levels of serum OPG, TGF-ß and OPG mRNA in periodontal tissues were significantly decreased (P<0.05). Compared with the model group, the pathological damage of periodontal tissue in the low-middle-and high-dose chitosan oligosaccharide groups and metronidazole group was reduced; gingival index, alveolar bone resorption value, Th17/Treg ratio, serum RANKL and IL-17 levels, and periodontal RANKL mRNA level were significantly decreased(P<0.05), while the levels of serum OPG, TGF-ß and OPG mRNA in periodontal tissues were significantly increased(P<0.05); there was a dose-dependent relationship between the chitosan oligosaccharide groups, and there was no significant difference between the high-dose chitosan oligosaccharide group and metronidazole group(P>0.05). CONCLUSIONS: Chitosan oligosaccharide can promote Th17/Treg balance to return to normal, up-regulate OPG expression, down-regulate RANKL expression, inhibit alveolar bone resorption in periodontitis rats and improve their clinical symptoms.

Mining TCGA database for prognostic genes in head and neck squamous cell carcinoma microenvironment.

BACKGROUND/PURPOSE: Head and neck squamous cell carcinoma (HNSCC) is one of the most common malignant tumors. The aim of this study was to elucidate the effect of tumor microenvironment-related genes on the prognosis of HNSCC and to obtain tumor microenvironment-related genes that can predict poor prognosis in HNSCC patients. MATERIALS AND METHODS: The ESTIMATE algorithm was applied to the HNSCC transcriptomic data downloaded from the TCGA (The cancer genome atlas), and then the samples were divided into two groups: high and low immune scoring groups, and high and low basal scoring groups to screen for differentially expressed genes (DEGs) associated with poor patient outcomes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was performed to explore the potential functions of DEGs, and then to explore the potential prognostic value of individual DEGs. The results of survival analysis between DEGs and overall survival (OS) to explore tumor microenvironment-related genes relevant to the prognosis of HNSCC patients. RESULTS: Fifty-nine tumor microenvironment-related genes were screened for association of OS with HNSCC (P < 0.05). The GO and KEGG enrichment analysis showed that the selected DEGs may mediate immune response, extracellular matrix, and immunoglobulin binding via neutrophil activation in HNSCC. Six of these DEGs, GIMAP6, SELL, TIFAB, KCNA3, P2RY8 and CCR4 were most significantly associated with OS (P < 0.001). CONCLUSION: We identified six tumor microenvironment-related genes that were significantly associated with poor prognosis in HNSCC. These genes may inspire researchers to discover new targets and approaches for HNSCC treatment.

Long non-coding RNA FOXD2-AS1 promotes cell proliferation, metastasis and EMT in glioma by sponging miR-506-5p.

Long non-coding RNA forkhead box D2 adjacent opposite strand RNA 1 (FOXD2-AS1) has emerged as a potential oncogene in several tumors. However, its biological function and potential regulatory mechanism in glioma have not been fully investigated to date. In the present study, RT-qPCR was conducted to detect the levels of FOXD2-AS1 and microRNA (miR)-506-5p, and western blot assays were performed to measure the expression of CDK2, cyclinE1, P21, matrix metalloproteinase (MMP)7, MMP9, N-cadherin, E-cadherin and vimentin in glioma cells. A luciferase reporter assay was performed to verify the direct targeting of miR-506-5p by FOXD2-AS1. Subsequently, cell viability was analyzed using the CCK-8 assay. Cell migration and invasion were analyzed using Transwell and wound healing assays, respectively. The results demonstrated that FOXD2-AS1 was significantly overexpressed in glioma cells, particularly in U251 cells. Knockdown of FOXD2-AS1 in glioma cells significantly inhibited cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) and regulated the expression of CDK2, cyclinE1, P21, MMP7 and MMP9. Next, a possible mechanism for these results was explored, and it was observed that FOXD2-AS1 binds to and negatively regulates miR-506-5p, which is known to be a tumor-suppressor gene in certain human cancer types. Furthermore, overexpression of miR-506-5p significantly inhibited cell proliferation, migration, invasion and EMT, and these effects could be reversed by transfecting FOXD2-AS1 into the cells. In conclusion, our data suggested that FOXD2-AS1 contributed to glioma proliferation, metastasis and EMT via competitively binding to miR-506-5p. FOXD2-AS1 may be a promising target for therapy in patients with glioma.

Emergency Biosafety Management Practice in Laboratory of Shelter Hospital.

At the end of 2019, the novel coronavirus infection outbroke in Wuhan, Hubei Province. On Feb. 2, 2020, Wuhan, as the worst-hit region, began to build "shelter hospital" rapidly to treat patients with mild illness. The shelter hospital has multiple functions such as emergency treatment, surgical treatment and clinical test, which can adapt to emergency medical rescue tasks. Based on the characteristics that shelter hospital only treats patients with mild illness, tests of shelter laboratory, including coronavirus nucleic acid detection, IgM/IgG antibody serology detection, monitoring and auxiliary diagnosis and/or a required blood routine, urine routine, C-reactive protein, calcitonin original, biochemical indicators (liver enzymes, myocardial enzymes, renal function, etc.) and blood coagulation function test etc, were used to provide important basis for the diagnosis and treatment of the disease. In order to ensure laboratory biosafety, it is necessary to first evaluate the harm level of various specimens. In the laboratory biosafety management, the harm level assessment of microorganisms is the core work of biosafety, which is of great significance to guarantee biosafety. As an emergency deployment affected by the environment, shelter laboratory must possess strong mobility. This paper will explore how to combine the biosafety model of traditional laboratory with the particularity of shelter laboratory to carry out effective work in response to the current epidemic.