Multifunctional CoFe2O4@MXene-AgNWs/Cellulose Nanofiber Composite Films with Asymmetric Layered Architecture for High-Efficiency Electromagnetic Interference Shielding and Remarkable Thermal Management Capability.

Developing high-efficiency electromagnetic interference (EMI) shielding composite films with outstanding flexibility and excellent thermal management capability is vital but challenging for modern integrated electronic devices. Herein, a facile two-step vacuum filtration method was used to fabricate ultrathin, flexible, and multifunctional cellulose nanofiber (CNF)-based composite films with an asymmetric layered architecture. The asymmetric layered structure is composed of a low-conductivity CoFe2O4@MXene/CNF layer and a highly conductive silver nanowires (AgNWs)/CNF layer. Benefiting from the rational placement of the impedance matching layer and shielding layer, as well as the synergistic effect of electric and magnetic losses, the resultant composite film exhibits an extremely high EMI shielding effectiveness (SE) of 73.3 dB and an average EMI SE of 70.9 dB with low reflected efficiency of 4.9 dB at only 0.1 mm thickness. Sufficiently reliable EMI SE (over 95% reservation) is attained even after suffering from continuous physical deformations and long-term chemical attacks. Moreover, the prepared films exhibit extraordinary flexibility, strong mechanical properties, and satisfactory thermal management capability. This work offers a viable strategy for exploiting high performance EMI shielding films with attractive thermal management capacity, and the resultant films present extensive application potential in aerospace, artificial intelligence, advanced electronics, stealth technology, and the national defense industry, even under harsh environments.

Facile construction of core-shell Carbon@CoNiO2 derived from yeast for broadband and high-efficiency microwave absorption.

Manufacturing dielectric/magnetic composites with hierarchical structure is regard as a promising strategy for the progress of high-performance microwave absorption (MA) materials. In this paper, the nano-grass structured CoNiO2 magnetic shell was uniformly anchored on the yeast-derived carbon microspheres by in-situ one-pot synthesis method. Profiting from the unique nano-grass and core-shell structure, capable dielectric/magnetic loss, along with improved impedance matching, the prepared absorber realizes desirable MA performance. The minimum reflection loss (RLmin) reaches up to -44.06 dB at 6.56 GHz. Moreover, the effective absorption bandwidth (EAB, reflection loss (RL) < -10 dB) accomplishes 7.04 GHz under a low filler loading of 20 wt%. This work endeavors a valuable insight for designing innovative core-shell structured materials with high-efficiency MA and broad bandwidth.

DNA methylation is a common molecular alteration in colorectal cancer cells and culture method has no influence on DNA methylation.

The present study aimed to explore whether culture method had an influence on DNA methylation in colorectal cancer (CRC). In the present study, CRC cells were cultured in two-dimensional (2D), three-dimensional (3D) and mouse orthotopic transplantation (Tis) cultures. Principal component analysis (PCA) was used for global visualization of the three samples. A Venn diagram was applied for intersection and union analysis for different comparisons. The methylation condition of 5'-C-phosphate-G-3' (CpG) location was determined using unsupervised clustering analysis. Scatter plots and histograms of the mean ß values between 3D vs. 2D, 3D vs. Tis and Tis vs. 2D were constructed. In order to explore the biological function of the genes, gene ontology and Kyoto Encyclopedia of Gene and Genomes (KEGG) pathway analyses were utilized. To explore the influence of culture condition on genes, quantitative methylation specific polymerase chain reaction (QMSP) was performed. The three samples connected with each other closely, as demonstrated by PCA. Venn diagram analysis indicated that some differential methylation positions were commonly shared in the three groups of samples and 16 CpG positions appeared hypermethylated in the three samples. The methylation patterns between the 3D and 2D cultures were more similar than those of 3D and Tis, and Tis and 2D. Results of gene ontology demonstrated that differentially expressed genes were involved in molecular function, cellular components and biological function. KEGG analysis indicated that genes were enriched in 13 pathways, of which four pathways were the most evident. These pathways were pathways in cancer, mitogen-activated protein kinase signaling, axon guidance and insulin signaling. Furthermore, QMSP demonstrated that methylation of mutL homolog, phosphatase and tensin homolog, runt-related transcription factor, Ras association family member, cadherin-1, O-6-methylguanine-DNA-methyltransferase and P16 genes had no obvious difference in 2D, 3D and Tis culture conditions. In conclusion, the culture method had no influence on DNA methylation in CRC cells.

DNA methylation is related to the occurrence of breast cancer and is not affected by culture conditions.

The present study aimed to explore the relationship between DNA methylation and breast cancer under different cell culture conditions. MCF­7 breast cancer cells were cultured in two­dimensional (2D), three­dimensional (3D) and orthotopic transplantation (Ti) adhesion substrates. Principal component analysis (PCA) was used for global visualization of these three samples. The methylation status of CpG sites was examined by unsupervised clustering analysis. Scatter plots and histograms were constructed from the mean ß­values from 3D vs. 2D, 3D vs. Ti and Ti vs. 2D analysis. In addition, analyses of Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were conducted to explore the putative biological functions in which mutL homolog (MLH), phosphatase and tensin homolog (PTEN), runt­related transcription factor (RUNX), Ras association domain family (RASSF), cadherin 1 (CDH1), O­6­methylguanine­DNA methyltransferase (MGMT) and P16 may serve a role. Quantitative methylation­specific polymerase chain reaction (QMSP) was performed to determine the influence of culturing conditions on important gene expression. Results from PCA analysis indicated that the three samples were closely connected with each other. Venn diagrams revealed that certain differential methylation positions were common among the three sample groups, and 116 CpG positions were identified that appeared to be hypermethylated. The methylation patterns were more similar between 3D vs. 2D cultures compared with those between 3D vs. Ti or between Ti vs. 2D. Results of GO term and KEGG pathway analyses indicated that genes were enriched in four pathways, including transporter activity and G­protein coupled receptor activity. In addition, QMSP analysis identified no notable differences in the methylation status of MLH, PTEN, RUNX, RASSF, CDH1, MGMT and P16 under 2D, 3D and Ti culture conditions. In conclusion, abnormal DNA methylation is related with breast cancer, and the methylation status did not change in breast cancer cells cultured in different conditions.

Acute arrest of hematopoiesis induced by infection with Staphylococcus epidermidis following total knee arthroplasty: A case report and literature review.

Infection is one of the most severe complications of total knee prosthesis implantation. The present study reported the case of a 74-year-old female that developed a Staphylococcus epidermidis infection following a cemented total knee arthroplasty. A routine blood test revealed neutropenia and anemia, while S. epidermidis was detected in the peripheral blood and bone marrow. In the present case, S. epidermidis infection led to acute arrest of hematopoiesis (AAH), also known as aplastic crisis, which is the temporary cessation of red cell production. The development of AAH secondary to S. epidermidis infection is rare and, to the best of our knowledge, this is the first case reported in the literature. The present study increased our knowledge of this rare disease and its characteristics, which will enable physicians to be aware of the development of AAH as a rare complication of S. epidermidis infection.

Male accessory breast cancer successfully treated with endocrine therapy: A case report.

Male accessory breast cancer is an extremely rare tumor. Several risk factors have been identified, including genetic and hormonal abnormalities. Accessory breast carcinoma usually occurs under the axilla or in the inguinal region. Clinical diagnosis is frequently delayed due to the general lack of awareness among physicians and patients. In the present study, the case of a 63-year-old male patient who was diagnosed with accessory breast cancer at a local advanced stage was reported. However, the patient was successfully treated with endocrine therapy.

Langerhans cell histiocytosis with multisystem involvement in an infant: A case report.

Langerhans cell histiocytosis (LCH) is a proliferative disease of histiocyte-like cells, with a wide range of clinical presentations that vary from a solitary lesion to more severe multifocal or disseminated lesions. The disease can affect any age group; however, the peak incidence rate is in infants aged between 1 and 3 years-old. Diagnosis of LCH should be based on the synthetical analysis of clinical presentations, in addition to features of imaging and histopathology. Although certain cases regress spontaneously, other patients require systemic chemotherapy together with the administration of steroids. The present study reports the case of an infant with LDH with multisystem involvement, including that of the bone, skin, orbit, spleen and lungs. The patient received chemotherapy and obtained rapid improvement in the involved systems. A total of 2.5 years after completion of the therapy, the patient still remains in follow-up and no evidence of active disease has been noted.

Pulmonary MALT lymphoma: A case report and review of the literature.

Mucosa-associated lymphoid tissue (MALT) lymphoma is an extranodal low-grade B-cell lymphoma. Pulmonary MALT lymphoma is considered to originate from bronchial MALT and is also referred to as bronchial-associated lymphoid tissue lymphoma. Pulmonary MALT lymphoma is a rare disease, but it is the most frequent subset of primary pulmonary lymphoma. The median age at diagnosis of pulmonary MALT lymphoma is 50-60 years, with only few patients aged <30 years. This is the case report of a 19-year-old patient with pulmonary MALT lymphoma presenting with a multiple pulmonary consolidation pattern on computed tomography scans, who underwent successful chemotherapeutic treatment with a chlorambucil-based regimen.

Clinicopathological significance and potential drug target of p15INK4B in multiple myeloma.

Multiple myeloma (MM) is a clonal malignancy characterized by the proliferation of malignant plasma cells in the bone marrow and the production of monoclonal immunoglobulin. In addition to genetic changes, gene hypermethylation is an alternative mechanism of tumor suppressor gene inactivation in MM. The cyclin-dependent kinase inhibitor 1 (CDKN2B or p15(INK4B) ) gene lies adjacent to the tumor suppressor gene, cyclin-dependent kinase inhibitor 2 (CDKN2A), and is frequently mutated and deleted in a wide variety of tumors, including MM. However, there is a lack of systematic analysis of p15 epigenetic modification such as methylation in MM from different studies that can provide more powerful estimation of an effect. In this study, we have systematically reviewed the studies of p15(INK4B) promoter methylation in MM and quantified the association between p15(INK4B) promoter methylation and MM using meta-analysis methods. We observed that the frequency of p15(INK4B) methylation is significantly higher in MM patients than in normal healthy controls. The pooled odds ratio (OR) from ten studies including 394 MM and 99 normal individuals is 0.08, while confidence interval (CI) is 0.03-0.21 (P<0.00001). This indicates that p15(INK4B) inactivation through methylation plays an important role in the pathogenesis of MM. In addition, the frequency of p15(INK4B) methylation was significantly higher in patients with MM than in those with asymptomatic monoclonal gammopathy of undetermined significance. The pooled OR from four studies is 0.40, 95% CI =0.21-0.78 (P=0.007). These results suggest that silencing of p15(INK4B) gene expression by epigenetic modification such as promoter hypermethylation plays a role not only in the initiation of MM but also in plasma cell malignant transformation, disease progression, and development.

Text mining and network analysis of molecular interaction in non-small cell lung cancer by using natural language processing.

Lung cancer including non-small cell lung cancer (NSCLC) and small cell lung cancer is one of the most aggressive tumors with high incidence and low survival rate. The typical NSCLC patients account for 80-85 % of the total lung cancer patients. To systemically explore the molecular mechanisms of NSCLC, we performed a molecular network analysis between human and mouse to identify key genes (pathways) involved in the occurrence of NSCLC. We automatically extracted the human-to-mouse orthologous interactions using the GeneWays system by natural language processing and further constructed molecular (gene and its products) networks by mapping the human-to-mouse interactions to NSCLC-related mammalian phenotypes, followed by module analysis using ClusterONE of Cytoscape and pathway enrichment analysis using the database for annotation, visualization and integrated discovery (DAVID) successively. A total of 70 genes were proven to be related to the mammalian phenotypes of NSCLC, and seven genes (ATAD5, BECN1, CDKN2A, FNTB, E2F1, KRAS and PTEN) were found to have a bearing on more than one mammalian phenotype (MP) each. Four network clusters centered by four genes thyroglobulin (TG), neurofibromatosis type-1 (NF1 ), neurofibromatosis type 2 (NF2 ) and E2F transcription factor 1 (E2F1) were generated. Genes in the four network modules were enriched in eight KEGG pathways (p value < 0.05), including pathways in cancer, small cell lung cancer, cell cycle and p53 signaling pathway. Genes p53 and E2F1 may play important roles in NSCLC occurrence, and thus can be considered as therapeutic targets for NSCLC.

Recurrence of histiocytic necrotizing lymphadenitis: A case report and literature review.

Histiocytic necrotizing lymphadenitis (HNL) is a unique form of self-limiting lymphadenitis with an unknown cause. The majority of cases resolve within several months and the disease has a low recurrence rate of 3-4%. In the present study, a prolonged recurrent case of HNL was reported. A 44-year-old female developed recurrent HNL with generalized lymphadenopathy 14 years after the original episode.

Restoration of INK4a/ARF gene inhibits cell growth and cooperates with imatinib mesylate in Philadelphia chromosome-positive leukemias.

VSV-G-pseudotyped lentiviral vectors expressing p16(INK4a) or p14(ARF) were used to infect at high-efficiency Philadelphia chromosome (Ph)-positive leukemia cell lines lacking endogenous transcripts. Restoration of p16(INK4a) accumulated cells in the G0/G1 phase of cell cycle and restoration of p14(ARF) induced their apoptosis, followed by significant growth inhibition. Transduction of primary blast cells from chronic myeloid leukemia in blast crisis (CML-BC) and Ph-positive acute lymphoblastic leukemia (ALL) with p16(INK4a) or p14(ARF) virus also resulted in cell growth inhibition and/or apoptosis with a patient-to-patient variation, whereas clonal growth and differentiation of cord blood progenitor cells were not affected by enforced expression of INK4a/ARF. Furthermore, upon viral transduction at low multiplicity of infection, INK4a/ARF potentiated the effect of imatinib mesylate on Ph-positive leukemia cell lines in an additive but not synergistic manner. These results suggest that INK4a/ARF protein-mimetic agents may be promising options for Ph-positive leukemias in combination with imatinib mesylate.

[Effect of up-regulated expression of tumor suppressor gene p14(ARF) on apoptosis of chronic myeloid leukemia cells].

OBJECTIVE: To investigate the effect of up-regulated expression of tumor suppressor gene p14(ARF) on apoptosis of chronic myeloid leukemia (CML) cells and its interaction with imatinib. METHODS: Tumor suppressor gene p14(ARF) was transduced into K562 (K562-p14(ARF)) and 4 blast crisis primary CML cells (CML-BC 1-4) using vesicular stomatitis virus glycoprotein (VSV-G) pseudotyped lentiviral vector with cells transduced by empty vector as control. Fluorescence microscopy and flow cytometry were applied to measure transduction efficiency, and Western blotting assay was used to detect p14(ARF) protein of K562 cells. WST-8 method was used to determine cell growth inhibition rate of K562 cells transduced by the target gene under different concentrations of imatinib (0, 0.015, 0.062, 0.125, 0.25, 0.5, 1.0, 2.0 µmol/L). Cell apoptosis and leukemic cellular colony-forming ability were detected by Annexin V-FITC/PI dyeing using flow cytometry (FCM) and semi-solid culture method respectively. RESULTS: Fluorescence microscopy and FCM showed that transduction efficiency (GFP positive cells) of K562-p14(ARF), K562-VSV and CML-BC1 cells were close to 100%, and CML-BC 2-4 cells were 80% to 90% on average. Results of Western blotting showed that the levels of ARF protein expression of K562 cells transduced by p14(ARF) were significantly higher than of untransduced cells; the apoptosis rate of K562-p14(ARF) was 20%; the mean apoptosis rate of 4 primary leukemic cells transduced by the p14(ARF) [(71.1±22.4)%] was significantly higher than of control group [(12.4±6.2)%] (P<0.05). Imatinib significantly inhibited the proliferation of K562-p14(ARF) cells in a dose-dependent manner. The mean leukemic cellular colony-forming unit of 4 primary leukemic cells transduced by the p14(ARF) (41.5±13.2) was significantly lower than of the control group (88.5±7.9) (P<0.05). CONCLUSION: Increased p14(ARF) gene expression could induce apoptosis of CML cells; Moreover, it could enhance inhibitory effect on cell proliferation when combined with imatinib.

Evaluation of clinical value of single nucleotide polymorphisms of dihydropyrimidine dehydrogenase gene to predict 5-fluorouracil toxicity in 60 colorectal cancer patients in China.

Dihydropyrimidine dehydrogenase (DPD) activity could be affected by single nucleotide polymorphisms (SNPs), resulting in either no effect, partial or complete loss of DPD activity. To evaluate if SNPs of DPD can be used to predict 5-FU toxicity, we evaluated five SNPs of DPD (14G1A, G1156T, G2194A, T85C and T464A) by TaqMan real time PCR in 60 colorectal cancer patients. Clinical data demonstrated that there was higher correlation between DPD activity and toxic effects of 5-FU (p<0.05). Six patients were positive for G2194A detection, which were all heterozygous. Two patients had lower DPD activities (< 3) with higher toxic effects (≥ stage III) while one patient was also positive for T85C detection. Ten patients were positive for T85C detection. Two patients were homozygous with lower DPD activities and higher toxic effects. Two patients were positive for the T464A detection, which were heterozygous with lower DPD activity and higher toxic effects and also positive for T85C detection. These data clearly indicated that the T464A and homozygous of the T85C are stronger biomarkers to predict the 5-FU toxicity. Our study significantly indicated that the detection for G2194A, T85C and T464A could predict ~13% of 5-FU severe toxic side effects.

[Influence of gene transduction mediated by lentivirus vector on gene expression of human CD34+ cord blood cells].

OBJECTIVE: To investigate the influence of gene transduction mediated by lentivirus vector on human CD34+ cord blood cell (CBCs) gene expression. METHODS: CD34+ cells were isolated and transduced with the third-generation self-inactivating ( SIN) lentiviral vector carrying green fluorescent protein (GFP). The total RNA from transduced cells was extracted and the differences of genotypes between the transduced and non-transduced CD34+ cells were determined with cDNA microarray analysis. RESULTS: In 23000 genes two were upregulated and six downregulated. These changes were not confirmed by semi-quantitative RT-PCR method. CONCLUSIONS: Lentiviral vector used in this study do not influence significantly on the gene expression of CD34+ CBCs, and the vector system may be a useful and safe one in clinical gene therapy.

[Reversal of mdrl gene-dependent multidrug resistance in multidrug resistance human leukemia cell line K562/ADM using short hairpin RNA expression vectors].

OBJECTIVE: To explore the role of reversal multidrug resistance (MDR) using short hairpin RNA (shRNA) expression vectors in multidrug resistance human leukemia cell line K562/ADM. METHODS: The oligonucleotides with 19-mer hairpin structure were synthesized. The shRNA expression vectors were constructed and introduced into K562/ADM cells. Expression of mdr1 mRNA was assessed by RT-PCR, and P-gp expression was determined by Western blot. The apoptosis and sensitivity of the K562/ADM cells to doxorubicin were quantified by flow cytometry and methyl thiazolyl tetrazolium (MTT) assays, respectively. Cellular daunorubicin accumulation was assayed by laser confocal scanning microscope (LCSM). RESULTS: In positive clones of K562/ADM cells stably transfected with pSilencer 3.1-HI neo mdr1-A and mdr1-B shRNA expression vectors, RT-PCR showed that mdr1 mRNA expression was significantly reduced to 35.9% (P < 0.05), 27.5% (P < 0.01), respectively. Western blot showed that P-gp expression was significantly and specifically inhibited. Resistance against doxorubicin was decreased from 79-fold to 38-fold (P < 0.05), 30-fold (P < 0.01) respectively. Furthermore, the fluorescence intensity of K562/ADM cells was increased significantly compared with the control. shRNA vectors significantly enhanced the cellular daunorubicin accumulation. The percent of the apoptosis cell was significantly enhanced to 18.1% (P < 0.05) , 54.4% (P < 0.01) respectively. CONCLUSIONS: shRNA expression vectors can effectively reverse MDR, and restore the sensitivity of drug-resistance K562/ADM cells to conventional chemotherapeutic agents.

[Study of apoptosis gene expression in U937 cells induced by adhesion culture with mesenchymal stem cell].

OBJECTIVE: To compare apoptosis gene expression profiling of U937 cells in suspension culture with that cultivated with mesenchymal stem cells (MSCs), and find out the relationship between drug resistance of leukemia cells and hemopoietic microenvironment. METHODS: U937 cells were cultivated in adhesion culture with MSCs and in suspension culture for 48 hours. Cell cycle was determined by flow cytometry and gene expression profiling by cDNA microarray. RESULTS: Compared with that in suspension, G(0)/G(1) fraction of U937 cells increased in adhesion culture (45.3 +/- 3.1)% vs (32.6 +/- 2.1)%, respectively (P < 0.05), whereas G(2)/M fraction and apoptosis rate were decreased. After 48 h twenty-eight differential expression genes were screened out in 487 apoptosis-related genes, among which 27 were up-regulated and were mainly apoptosis-suppressor genes, apoptosis-promoter genes, cell cycle positive control genes and cell cycle negative control genes. But Bcl-XL was up-regulated most obviously. The only one gene down-regulated was an apoptosis promoter gene. CONCLUSION: Adhesion culture with MSCs can lead to growth suppression and decrease natural apoptosis of U937 cells. The mechanism was multiple gene effects, but Bcl-XL may be of the most importance.

Study on the bone marrow mesenchymal stem cells induced drug resistance in the U937 cells and its mechanism.

BACKGROUND: The hematopoietic microenvironment (HM) plays a critical role in malignant cell growth, patient survival, and response to chemotherapy in hematologic malignancies. However, mechanisms associated with this environmental influence remain unclear. In this study, we investigated the role of bone marrow derived mesenchymal stem cells (MSCs) in U937 cell line, to find out the relations between leukemia drug resistance and the MSCs. METHODS: U937 cells were cultured in suspension or grew adherently with MSCs. The cell growth curve was drawn and the cell cycle was measured by flow cytometry. Apoptosis and sensitivity of U937 to daunoblastina (DNR) were quantified by DNA ladder detection and trypan blue exclusion assays, respectively. The gene expression profile chip technology was used to determine and analyze the changes in apoptosis-related gene expression after adherent culture and the expression of MDR1 mRNA was assessed by reverse transcriptional polymerase chain reaction (RT-PCR) at the same time. RESULTS: In the adherent culture, the proliferation of the U937 cells was inhibited, the G0/G1 phase cells increased (F = 64.9726, P < 0.0001), G2/M phase cells were decreased (F = 98.1361, P < 0.0001) and the natural apoptosis rate was decreased (F = 24.0866, P < 0.0001) compared with those in the suspended culture. U937 cell viability was enhanced and cell apoptosis was blocked during DNR treatment in adherent culture with MSCs. Thirty-nine differently expressed genes were screened from the 487 apoptosis related genes in the adherent culture U937 cells. Among the 37 upregulated genes, Bcl-XL was upregulated most significantly. Two genes were downregulated. Adherent culture did not induce MDR1 mRNA expression in U937 cells. CONCLUSIONS: MSCs play a role in modulating the proliferation of U937 cells and response of U937 cells to DNR, and Bcl-XL apoptosis-inhibiting gene may be most important in determining the sensitivity of leukemic cells to treatment, which is not related to MDR1.