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Lloyd, Albert L. "Germanic Evidence for a Neglected Indo-European Root." American Journal of Germanic Linguistics and Literatures 1, no. 1 (1989): 53–66. http://dx.doi.org/10.1017/s1470542700000064.
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ABSTRACTAn IE root *bhel(ə)- ‘strike, hit, hew, chop’, although not included in the standard IE etymological dictionaries, is shown to underly a number of etymologically obscure Germanic words, such as OHG bolz(o) ‘bolt’, Go. bliggwan ‘to beat’, OIcel. bella ‘to hit’, blak ‘slap, blow’, OHG blast ‘a throwing to the ground’, OHG bloh, bloc ‘block of wood’, and possibly OHG balko ‘beam’. Since related words can be found in Italic, Celtic, Baltic, and perhaps also Slavic and Greek, there would seem to be sufficient justification for the addition of this root to the inventory of recognized IE roots.
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Bartelt, Perry, Peter Bebi, Thomas Feistl, Othmar Buser, and Andrin Caviezel. "Dynamic magnification factors for tree blow-down by powder snow avalanche air blasts." Natural Hazards and Earth System Sciences 18, no. 3 (2018): 759–64. http://dx.doi.org/10.5194/nhess-18-759-2018.
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Abstract. We study how short duration powder avalanche blasts can break and overturn tall trees. Tree blow-down is often used to back-calculate avalanche pressure and therefore constrain avalanche flow velocity and motion. We find that tall trees are susceptible to avalanche air blasts because the duration of the air blast is near to the period of vibration of tall trees, both in bending and root-plate overturning. Dynamic magnification factors for bending and overturning failures should therefore be considered when back-calculating avalanche impact pressures.
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Aziz, Saeful, Qodri Hadi Putra, Aldo Brilianto, Ida Wayan Supriharta, and Rahmantha Purba Anggana. "IMPLEMENTASI METODE THROUGH SEAM BLAST DALAM MENDUKUNG OPERASIONAL PENAMBANGAN BATUBARA DI PIT C1 BLOK 8 BMO 2 PT BERAU COAL." Prosiding Temu Profesi Tahunan PERHAPI 1, no. 1 (2020): 337–48. http://dx.doi.org/10.36986/ptptp.v1i1.77.
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ABSTRAK Tujuan penelitian ini adalah untuk mengetahui: (1) kelayakan metode through seam blast untuk diimplementasikan pada area interburden dan batubara tipis dengan multi-seam. (2) Pengaruh terhadap peningkatan produktivitas, percepatan sekuen penambangan, kualitas batubara, dan konservasi batubara tipis. Dalam penelitian ini penulis bersama team yang yang dibentuk (terdiri dari pihak PT. Berau Coal site BMO 2, PT. Pamapersada Site BRCB, dan PT. DNX Site BMO 2) melakukan perencanaan menggunakan siklus plan, do, check, action (PDCA) terkait metode through seam blast dimana plan didukung dengan pendekatan konsep specipic, measurable, achievable, realistic dan timely (SMART). Pengumpulan data dilakukan dengan melakukan empat kali trial through seam blast. Hasil penelitian menunjukan bahwa : 1) Metode Through Seam Blast memungkinkan diimplementasikan di Pit C1 Blok 8 BMO 2 PT Berau Coal. (2) Terjadi peningkatan produktivitas alat gali muat sebesar 35 bcm/jam pada kelas PC-1200, mengurangi frekuensi blasting dari 2-3 kali menjadi 1 kali pada luasan area yang sama, adanya deviasi ash batubara tertambang (terhadap as batubara insitu) yang masih masuk dalam toleransi sebesar 2.75%, mine recovery tetap terjadi ≥98%. Kata kunci: through seam blast, produktivitas alat gali muat, frekuensi blasting, kualitas batubara, mine recovery ABSTRACT The purpose of this study is to determine: (1) the feasibility of the through seam blast method to be implemented in inter burden areas and thin coal with multi-seam. (2) Effects on increasing productivity, acceleration of mining sequences, coal quality, and conservation of thin coal. In this study the authors together with the team formed (consisting of PT. Berau Coal site BMO 2, PT. Pamapersada Site BRCB, and PT. DNX Site BMO 2) do the planning using the related cycle plan, do, check, action (PDCA) a through seam blast method where the plan is supported by a specific, measurable, achievable, realistic and timely (SMART) concept approach. Data collection was carried out by conducting four trial through seam blasts. The results showed that: 1) Through Seam Blast method is possible to be implemented in Pit C1 Block 8 BMO 2 PT Berau Coal. (2) An increase in the productivity of the loading and unloading tool by 35 bcm / hour in PC-1200 class, reducing the frequency of blasting from 2-3 times to 1 time in the same area, the deviation of mined coal ash (against the coal as in situ) still within tolerance of 2.75%, mine recovery still occurs ≥98%. Keywords: through seam blast, digger productivity, blasting frequency, coal quality, mine recovery
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Sazonov, S. I., N. S. Shubravyi, A. V. Knyshenko, M. D. Zhembus, A. V. Sukhomlin, and S. A. Kovalenko. "Forced blow-in of a blast furnace." Metallurgist 34, no. 12 (1990): 281. http://dx.doi.org/10.1007/bf00750118.
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Hayda, Roman, Robert M. Harris, and Cameron Dale Bass. "Blast Injury Research." Clinical Orthopaedics and Related Research 422 (May 2004): 97–108. http://dx.doi.org/10.1097/01.blo.0000128295.28666.ee.
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Langworthy, Michael J., John Sabra, and Mark Gould. "Terrorism and Blast Phenomena." Clinical Orthopaedics and Related Research 422 (May 2004): 82–87. http://dx.doi.org/10.1097/01.blo.0000128293.43913.ca.
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Di Stefano, Carla, Marco Tafani, Bruna Pucci, et al. "A Distinctive Pattern of Different Gene Expression in Chronic Myelogenous Leukemia Patients." Blood 112, no. 11 (2008): 4231. http://dx.doi.org/10.1182/blood.v112.11.4231.4231.
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Abstract Introduction: Molecular chaperones have many functions, such as protecting other proteins against aggregation, assisting in folding of nascent proteins/refolding of damaged proteins and targeting severely damaged proteins to degradation. As one of the molecular chaperones, Hsp90 functions to facilitate the folding of newly synthesized and denatured client proteins, including mutated p53, Bcr-Abl, p185ErbB2 and Raf-1. The Bcr-Abl fusion gene encodes for the p210Bcr-Abl tyrosine kinase (TK) implicated in the pathogenesis of chronic myelogenous leukemia (CML). Studies in cultured cells have identified many signal transduction pathways activated by Bcr-Abl, including activation of the Ras, MAPK, JNK/SAPK, phosphatidylinositol-3 kinase, nuclear factor-B and STAT pathways. Imatinib mesylate (imatinib IM) is a tyrosine kinase inhibitor that competitively inhibits ATP binding in the kinase domains of both the Bcr-Abl and c-Abl kinases. It has been suggested that resistance to imatinib stems from Bcr-Abl gene amplification, leading to overexpression of Bcr-Abl protein or point mutations in the Bcr-Abl gene However, several groups suggested that there might be other forms of Bcr-Abl-independent imatinib resistance Recently, it has been reported that changes in histone deacetylase (HDAC) expression in leukemic cells could be involved in mechanisms for abnormal cellular proliferation that operate through chromatin-independent pathways and thereby could lead to acquired drug resistance of the cells In the present study, we evaluated in primary leukemic blasts, obtained from chronic myelogenous leukemia patients at onset, patients in blast crisis and patients which were imatinib-resistant The espression the sirtuin members family and HSP70, HSP90 i-NOS and bcl-2 was evaluated by Nortern blot and Western blot analysis. Material and Methods: Primary leukaemia blasts We harvested primary blast rich mononuclear cells were obtained by gradient centrifugation on ficoll-hypaque of bone marrow and peripheral blood cells after obtaining appropriate informed consent. Northern blot Total RNAs from control or treated cells were isolated using Tri Reagent Aliquots of RNA were electrophoresed and blotted onto nylon membranes, that hybridized to 32P-labelled probe. Western Blot Cells were lysed and. then were centrifugated. Protein concentration was determined by the Bradford assay.. Equivalent amounts of protein loaded and electrophoresed and were transferred to nitrocellulose membranes, that were incubated with the different primary antibodies:, Result and Discussion:. In the present study, we evaluated a pattern of different gene expression by Northern Blot and Western Blot analysis in bone marrow and peripheral blood cells from 16 CML patients at onset, from 2 patients in blast crisis evolved under IM treatment, and 14 imatinib-resistant patients. Some RNAs were underexpressed in most or all samples tested and never overexpressed (eg SIRT2, SIRT3, SIRT4 and SIRT5), while others were overexpressed in the great majority of samples and rarely, if ever, underexpressed (eg SIRT1, SIRT7, HSP90, iNOS)Furthermore, we examined the level of heat-shock related proteins HSP90 and bcl-2 in 2 patients during treatment with IM. and one patient IM-resistant by western Blot analysis: HSP90 and BCl-2 increased one patient during treatment with IM, while both protein levels was very high in one one patient IM-resistant These results suggest that the difference of genes expression might contribute to patterns of clinical response.
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Rostovskii, A. V., A. E. Paren’kov, V. N. Loginov, G. G. Gavrilyuk, and M. A. Al’ter. "Optimum technologies for the blow-in of blast furnaces." Metallurgist 42, no. 6 (1998): 212–15. http://dx.doi.org/10.1007/bf02765996.
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Sinha, Pankhuri, Goutam Mukhopadhyay, and Sandip Bhattacharyya. "Investigation on Bulging of Blow Pipe in a Blast Furnace." Journal of Failure Analysis and Prevention 13, no. 3 (2013): 257–63. http://dx.doi.org/10.1007/s11668-013-9666-5.
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Shafat, Manar S., Matthew E. Fenech, Amina M. Abdul-Aziz, Jeremy Turner, Kristian M. Bowles, and Stuart A. Rushworth. "FABP4 Regulates Fatty Acid Transfer from Bone Marrow Adipocytes to Acute Myeloid Leukemia Blasts." Blood 126, no. 23 (2015): 3065. http://dx.doi.org/10.1182/blood.v126.23.3065.3065.
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Abstract Introduction The incidence of acute myeloid leukemia (AML) is strongly related to age with poor survival rates in the elderly population. AML blasts isolated from the bone marrow undergo spontaneous apoptosis in culture suggesting its microenvironment in the bone marrow (BM) contains cells and factors favorable to the progression of the disease. The BM microenvironment consists of many cell types not directly of the hematopoietic lineage, including bone marrow adipose tissue (MAT), which accounts for circa 50% of the BM volume in the axial skeleton of adults. We hypothesize that MAT may contribute to the cancerous hallmarks exhibited by the AML blasts in the bone marrow. Here we examine the relationship between cancer associated MAT and AML blast survival and proliferation. We describe how this association favors the survival of AML blasts by the transfer of free fatty acids (FFA) released from MAT to AML blasts via the chaperone protein fatty acid binding protein 4 (FABP4). We also show FABP4 to be a critical player in fatty acid transport and therefore the survival of AML blasts in the bone marrow. Methods To investigate the role of MAT in regulating AML survival we used primary AML blasts and marrow derived adipose tissue obtained from patient's bone marrow following an informed consent. MAT was co-cultured with primary AML blasts in vitro and the proliferation and survival of the blasts was determined by BrdU incorporation and Annexin V/PI staining respectively. Immunocytochemistry using lipid specific dye, CD34 antibody and nuclear staining was performed to determine lipid storage in primary AML blasts. Western blot analysis was used to determine the level of phosphorylated hormone sensitive lipase (HSL) and fatty acid binding protein 4 (FABP4) in adipocytes. ß oxidation in AML blasts was determined by transcript levels of CPT-1a and ACOX-1. FABP4 concentration was also assayed in MAT and MAT/AML co-cultures by ELISA. Adipocyte FABP4 was knocked down by shRNA and a small molecule inhibitor (BMS309403) was used for pharmacological inhibition. Results Results show that in vitro primary AML blasts demonstrate increased survival and proliferation when co-cultured on MAT. Immunocytochemistry using lipid specific dye on CD34+ primary AML blasts revealed presence of neutral lipids within the blasts, which following a 48 hour incubation in monoculture was significantly depleted. Primary AML blasts/MAT co-cultivation caused lipid accumulation in AML blasts and lipolysis of MAT indicated by increased levels of glycerol and FFA in the co-culture media compared to control. Immunoblotting of co-cultured MAT showed increased levels of lipolysis associated factors, phosphorylated HSL and perilipin with a decreased expression of FABP4 compared to MAT monocultures. An apparent increase in ß oxidation was also revealed in AML blasts indicated by the transcriptional activation of ß oxidation related genes. FABP4 MAT transcript levels were shown to increase significantly suggesting an increased production and subsequent trafficking of FABP4 from MAT. Pharmacological inhibition and shRNA mediated knock-down of FABP4 showed a significant decrease in survival and proliferation of AML blasts cultured with adipocytes. Finally investigations also revealed that AML blasts cultured with adipocytes had depleted lipid accumulation in response to FABP4 inhibition. Conclusion Here we report that lipid trafficking between MAT and AML supports survival and proliferation of the leukemic blasts in-vitro. We show that FABP4 is transcriptionally up-regulated in both AML and MAT which mediates the transport of FFA from adipocytes to the leukemic blast. Furthermore, the inhibition of FABP4 significantly reduces AML survival. Together, our data shows evidence for the relationship between MAT and AML blasts by fatty acid transfer identifying FA metabolism as a potential therapeutic target for this aggressive disease. Disclosures No relevant conflicts of interest to declare.
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van Luijn, Marvin M., Maaike E. Ressing, Emmanuel J. H. J. Wiertz, et al. "TAP- and Proteasome-Dependent Endogenous Antigen Loading of HLA Class II in Leukemic Blasts Introduces a Promising New Target for Generating Leukemia-Specific CD4+ T Cells." Blood 112, no. 11 (2008): 5443. http://dx.doi.org/10.1182/blood.v112.11.5443.5443.
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Abstract According to the classical HLA class II antigen presentation pathway, exogenous antigens are processed in the endosomal/lysosomal pathway and associate with HLA class II after exchange with the class II-associated invariant chain peptide (CLIP). For this reason, the relative amount of CLIP presented by HLA-DR (DR) molecules (CLIP/DR amount) can be considered as an indicator for HLA class II antigen loading. Previously, we showed that Invariant Chain (Ii) down-modulation in the Kasumi-1 and THP-1 AML cell lines led to marked declines in CLIP/DR amount [Van Luijn et al., Haematologica2008; 93(s1), Abstract 0029]. In addition, the total amount of cell surface-expressed DR was reduced on Kasumi-1 blasts, in line with the need of Ii for the transport of newly synthesized HLA class II molecules into the endosomal/lysosomal pathway. Surprisingly, in THP-1 blasts, Ii down-modulation hardly affected DR expression at the cell surface. In the present study, we further explored the Ii-independent pathway of HLA class II antigen presentation in leukemic blasts. Not only in the THP-1, but also in another AML cell line, the KG-1, Ii down-modulation had no effect on DR expression levels, as determined by flow cytometry. Since DR expression does require peptide binding, Ii-independency in these AML blasts may be achieved by endogenous antigen loading in the endoplasmic reticulum (ER). To test this hypothesis, supply of endogenously derived peptides into the ER was blocked by viral proteins interfering with the function of the transporter associated with antigen processing (TAP). As expected, TAP inhibition in KG-1 blasts by the viral UL49.5 protein (which changes the conformation of TAP and mediates its degradation) resulted in a strong down-regulation (7.7-fold) of HLA class I. Strikingly, TAP inhibition also induced a clear DR− KG-1 blast population (52.3% of total; MFI=1.4) next to the original DR+ KG-1 blast population (36.5% of total; MFI=288.9), demonstrating that DR expression is partly TAP-dependent in KG-1 blasts. Upon sorting of both populations, TAP−DR− blasts had a decreased expression of intracellular Ii as compared to TAP−DR+ blasts (3.9-fold) and wild type blasts (4.7-fold). Additionally, confocal microscopy revealed that in TAP−DR+ blasts, DR localised to the cell surface, indicating that Ii is able to rescue cell surface expression of DR. Indeed, Ii down-modulation in TAP−DR+ blasts caused a 2.3-fold decline in DR expression. The observed differences in TAP, Ii and DR expression between these KG-1 variants were confirmed by Western blot analysis. Furthermore, blocking of proteasome function by the specific inhibitors MG-132 and Bortezomib also caused a marked decrease of DR expression on KG-1 blasts (MFI declined from 289.2 to respectively 76.4 and 114.5). Accompanying reduction in HLA class I levels ascertained specific proteasome inhibition. This confirmed that at least part of the antigens presented by DR on KG-1 blasts was derived from endogenous sources. Similar results were obtained with THP-1 blasts, as both TAP and proteasome inhibition clearly affected DR expression. In line with our observations that in Kasumi-1 blasts, DR expression is Ii-dependent, addition of the TAP and proteasome inhibitors to Kasumi-1 blasts did not affect cell surface expression of DR. In conclusion, our data reveal an alternative Ii-independent, but TAP- and proteasome-dependent cross-presentation pathway in different AML cell lines, which involves HLA class II loading of endogenous antigens in the ER. Therefore, this alternative pathway may serve as a potent immunomodulatory target in leukemic blasts to activate CD4+ T cells specific for a broad range of leukemia-associated antigens.
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Yankovskii, A. S., M. F. Mar'yasov, A. V. Pol'shchikov, et al. "Blow-through of a blast furnace with the use of nitrogen." Metallurgist 32, no. 11 (1988): 347–48. http://dx.doi.org/10.1007/bf00749888.
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Schwerin, Susan C., Mitali Chatterjee, Elizabeth B. Hutchinson, et al. "Expression of GFAP and Tau Following Blast Exposure in the Cerebral Cortex of Ferrets." Journal of Neuropathology & Experimental Neurology 80, no. 2 (2021): 112–28. http://dx.doi.org/10.1093/jnen/nlaa157.
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Abstract Blast exposures are a hallmark of contemporary military conflicts. We need improved preclinical models of blast traumatic brain injury for translation of pharmaceutical and therapeutic protocols. Compared with rodents, the ferret brain is larger, has substantial sulci, gyri, a higher white to gray matter ratio, and the hippocampus in a ventral position; these attributes facilitate comparison with the human brain. In this study, ferrets received compressed air shock waves and subsequent evaluation of glia and forms of tau following survival of up to 12 weeks. Immunohistochemistry and Western blot demonstrated altered distributions of astrogliosis and tau expression after blast exposure. Many aspects of the astrogliosis corresponded to human pathology: increased subpial reactivity, gliosis at gray-white matter interfaces, and extensive outlining of blood vessels. MRI analysis showed numerous hypointensities occurring in the 12-week survival animals, appearing to correspond to luminal expansions of blood vessels. Changes in forms of tau, including phosphorylated tau, and the isoforms 3R and 4R were noted using immunohistochemistry and Western blot in specific regions of the cerebral cortex. Of particular interest were the 3R and 4R isoforms, which modified their ratio after blast. Our data strongly support the ferret as an animal model with highly translational features to study blast injury.
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Andreev, V. A., L. B. Unigovskii, V. N. Prokhorov, L. S. Tokarev, and A. V. Denisov. "Features of the blow-in and blow-out of a blast furnace during a class III overhaul." Metallurgist 32, no. 10 (1988): 321–23. http://dx.doi.org/10.1007/bf01160528.
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O'Nions, Jenny, and Martin J. Allday. "Proliferation and differentiation in isogenic populations of peripheral B cells activated by Epstein–Barr virus or T cell-derived mitogens." Journal of General Virology 85, no. 4 (2004): 881–95. http://dx.doi.org/10.1099/vir.0.19704-0.
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Human B cells isolated from peripheral blood were activated and induced to proliferate by either Epstein–Barr virus (EBV) or the T cell-derived mitogens CD40 ligand (CD40L) plus interleukin (IL)-4. Although both populations initially proliferated as B-blasts, significant differences were revealed over a longer period. EBV infection resulted in continuously proliferating lymphoblastoid cell lines (LCLs), whereas most of the CD40L/IL-4-stimulated B cells had a finite proliferative lifespan of 3–4 weeks. Cell cycle analysis, trypan blue staining and Western blot analysis for cleavage of poly(ADP-ribose) polymerase (PARP) all demonstrated that the decrease in proliferation in CD40L/IL-4-stimulated B cells is not due to cell death. Instead, these cells arrest, accumulate in G0/G1 and undergo alterations in cell surface marker expression, cellular morphology and immunoglobulin production, all consistent with plasmacytoid differentiation. In contrast, B cells infected with EBV continued to proliferate and retained a blast-like phenotype. Differences in both cytokine production and the expression of cell cycle regulators were identified between the two B-cell populations, which might contribute to the differentiation of the CD40L/IL-4-stimulated B cells and suggest potential mechanisms by which EBV may overcome this. The study has also identified a window of opportunity during which a comparison of isogenic populations of EBV- and mitogen-driven B blasts can be made.
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Kindler, Thomas, Frank Breitenbuecher, Andreas Marx, et al. "Efficacy and safety of imatinib in adult patients with c-kit–positive acute myeloid leukemia." Blood 103, no. 10 (2004): 3644–54. http://dx.doi.org/10.1182/blood-2003-06-2071.
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Abstract This phase 2 pilot study was conducted to determine the efficacy and safety of imatinib mesylate in patients with c-kit–positive acute myeloid leukemia (AML) refractory to or not eligible for chemotherapy. Twenty-one patients were enrolled and received imatinib 600 mg orally once daily. Five responses were seen primarily in patients, starting with relatively low blast counts in bone marrow (BM) and peripheral blood (PB): 2 patients who were considered refractory on chemotherapy on the basis of persistence of blasts in PB and BM met the criteria for complete hematologic remission, 1 patient had no evidence of leukemia, and 2 patients achieved a minor response. Treatment with imatinib demonstrated a good safety profile and was well tolerated. Western blot analysis and immunohistochemistry demonstrated c-Kit activation in primary AML cells. Further, imatinib treatment of primary AML cells inhibited c-Kit tyrosine-phosphorylation. Genomic DNA-sequencing of c-KIT showed no mutations in exons 2, 8, 10, 11, 12, and 17. Although some of the responses derived from relatively small reductions in leukemic blasts and may be attributable, in part, to prior chemotherapy, these cases suggest that imatinib has interesting clinical activity in a subset of patients with c-kit–positive AML. Further clinical trials are warranted to explore the clinical potential of imatinib in AML and to identify the underlying molecular mechanism.
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Rostovskii, A. V., A. E. Paren'kov, and P. I. Chernousov. "Refining theoretical combustion temperature during the blow-in of a blast furnace." Metallurgist 42, no. 12 (1998): 474–76. http://dx.doi.org/10.1007/bf02511767.
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Troeger, Anja, Ingo Schmitz, Ludmila Glouchkova, et al. "Upregulation of FLIPs upon CD40 Stimulation - A Novel Inhibititory Mechanism of CD95-Induced Apoptosis in Precursor B-ALL Blasts in Children." Blood 106, no. 11 (2005): 855. http://dx.doi.org/10.1182/blood.v106.11.855.855.
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Abstract The influence of the microenvironment on the activation status and behaviour of ALL blasts is critical for interactions with the immune system in vivo. The capacity of B cells to respond to CD40-ligand (CD40L) stimulation is critical for their sensitisation to immunological control mechanisms and susceptibility to apoptotic signals. Primary precursor B-ALL blasts (BCP-ALL; n=32) lack CD95-expression (mean±SE; 4.2±0.6% positive cells) and are resistant to apoptosis while significant up-regulation of CD95 is apparent upon CD40-stimulation in BCP-ALL blasts that reaches a plateau after 72 h. Yet, in spite of equivalent CD95-upregulation in ALL blasts (58.3±6.5%; n=17) and normal B cells (59.3±13.1%) specific apoptosis is markedly lower in ALL compared to mature B cells (19.1±3% vs 36.7±5.5%). Resistance to apoptosis in ALL blasts and its reversibility after cycloheximid treatment suggest that anti-apoptotic mechanisms prevent induction of cell death via CD95 ligation in CD40 activated blasts. In accordance, in CD40-activated ALL blasts caspase 8 and 3 activity is not enhanced upon CD95 ligation in contrast to an 1.8±0.3 and 1.7±0.3 fold increase in caspase activity in stimulated normal B cells (n=7), suggesting a block of the apoptotic cascade in BCP-ALLrelatively close to the receptor level. CD40L-activated ALL blasts and normal B cells were submitted to western blot analysis with respect to the molecules associated to the death-inducing signalling complex (DISC). FADD and the zymogen form of caspase-8 are constitutively expressed in both malignant and non malignant B cells with no modulation following CD40 ligation. In contrast, the anti-apoptotic short isoform of the c-FLICE inhibitory protein FLIPS is weakly expressed in naïve blasts and B cells, but strongly up-regulated upon 72h CD40-ligation in ALL with only barely detectable levels in CD40-activated normal B cells. We therefore propose, that prolonged induction of the FLIPS expression inhibits the onset of apoptosis despite high CD95 surface expression levels in BCP-ALL blasts. As an additional anti-apoptotic mechanism inhibiting the downstream effector caspases we demonstrated significant upregulation of the inhibitor of apoptosis protein (IAP) survivin in CD40-activated BCP-ALL (n=6) compared to the unstimulated control (632pg/ml±200pg/ml vs 180pg/ml±52pg/ml). Thus, we identified FLIPS as a CD40-regulated upstream anti-apoptotic element and concomitant downstream upregulation of survivin protein expression as critical mechanisms contributing to blast cell resistance to apoptosis.
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Gordin, Sergey, Ilya Zaychenko, Vera Sokolova, and Victoria Bazheryanu. "To calculate heat losses with flue gases of coal-fired boilers." E3S Web of Conferences 285 (2021): 07028. http://dx.doi.org/10.1051/e3sconf/202128507028.
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The article is devoted to solving the problem of increasing the efficiency of solid fuel boilers ’ blast control systems. Existing algorithms for calculating losses with outgoing gases, the value of which determines the efficiency of the boiler blow control system, have significant disadvantages due to either high complexity of calculations or insufficient accuracy of the Siegert formula. The authors of the article experimentally confirmed the limitations of practical application of the Siegert formula in the logic of solid fuel boiler blow control systems. To eliminate the identified shortcomings, a new formula for calculating losses with outgoing gases is proposed, which can be used in solid-fuel boiler blast control systems, which has a sufficiently high accuracy and, at the same time, low computational complexity.
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Lyalyuk, V. P. "Analysis of the blast furnace operations with a volume of 5000 m3 on tuyeres of different diameters from the positions of full mechanical energies of flows of combined blow and hearth gas." Ferrous Metallurgy. Bulletin of Scientific , Technical and Economic Information 76, no. 7 (2020): 691–99. http://dx.doi.org/10.32339/0135-5910-2020-7-691-699.
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In the commissioning period of the development of pulverized coal injection technology (PCI) on a blast furnace No. 9 with a volume of 5000 m3 of PJSC “ArcelorMittal Kryvyi Rih”, frequent cases of burnout of refrigerators of the cooling system of the shoulders and air tyueres appeared due to the highly developed peripheral gas flow. An attempt to limit the gas flow at the periphery by controlling the distribution of charge materials on the top produced a short-term result. Based on the prevailing ideas, that to reduce the intensity of the peripheral gas flow, it is necessary to increase the speed of the blast and, accordingly, the kinetic energy of the blast flow, flowing out of the air tuyeres of a blast furnace, it was decided to reduce their diameter. As a result of analysis of the operation of the specified blast furnace using the technology of PCI on tuyeres with a diameter of 150 and 140 mm, increased peripheral gas flow with a smaller diameter was established. Based on the results of the analysis, conclusions were made by many researchers and it was shown that with constant kinetic energy of the blast, flowing from the tuyeres of different diameters, the dimensions of the combustion zone are always larger before the tuyeres of a larger diameter. This is explained by the fact that the kinetic energy of the gas flow is only a part of their total mechanical energy. It was shown that to analyze the change in the size of the combustion zones and the depth of penetration of the hearth gas, it is necessary to use the full mechanical energy of the flows of the combined blast on the cut of the tuyere and hearth gas. It was established that the transition to PCI in a blast furnace instead of natural gas, it always causes an increase in the peripheral gas flow. The main reason for this phenomenon is associated with a decrease in the total mechanical energy of blast and hearth gas. It was recommended on a blast furnace with a volume of 5000 m3 with a hearth diameter of 14.7 m and the PCI technology to maintain the total mechanical energy of the blast flow at least 2100–2600 kJ/s, and the full mechanical energy of the hearth gas flow at least 5100–5300 kJ/s.
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Liu, Ying, Y. E. Liu, C. C. Tong, et al. "CD28 deficiency attenuates primary blast-induced renal injury in mice via the PI3K/Akt signalling pathway." BMJ Military Health 166, E (2019): e66-e69. http://dx.doi.org/10.1136/jramc-2019-001181.
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IntroductionPrimary blast affects the kidneys due to direct shock wave damage and the production of proinflammatory cytokines without effective treatment. CD28 has been reported to be involved in regulating T cell activation and secretion of inflammatory cytokines. The aim of this study was to investigate the influence of primary blast on the kidney and the effect of CD28 in mice.MethodsA mouse model of primary blast-induced kidney injury was established using a custom-made explosive device. The severity of kidney injury was investigated by H&E staining. ELISA was applied to study serum inflammation factors’ expression. Western blot assays were used to analyse the primary blast-induced inflammatory factors’ expression in the kidney. Immunofluorescence analysis was used to examine the PI3K/Akt signalling pathway.ResultsHistological examination demonstrated that compared with the primary blast group, CD28 deficiency caused a significant decrease in the severity of the primary blast-induced renal injury. Moreover, ELISA and western blotting revealed that CD28 deficiency significantly reduced the levels of interleukin (IL)-1β, IL-4 and IL-6, and increased the IL-10 level (p<0.05). Finally, immunofluorescence analysis indicated that PI3K/Akt expression also changed.ConclusionsCD28 deficiency had protective effects on primary blast-induced kidney injury via the PI3K/Akt signalling pathway. These findings improve the knowledge on primary blast injury and provide theoretical basis for primary blast injury treatment.
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Veszprémi, Anikó, Éva Katona, Csongor Kiss, et al. "Leukemic lymphoblasts, a novel expression site of coagulation factor XIII subunit A." Thrombosis and Haemostasis 96, no. 08 (2006): 176–82. http://dx.doi.org/10.1160/th06-05-0270.
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SummaryBlood coagulation factor XIII (FXIII) is a protransglutaminase circulating asa tetramer formed by two types of subunits (A2B2). The intracellular dimeric form of FXIII (A2) is present in platelets, megakaryocytes, monocytes and macrophages and has been detected in mono-and megakaryocytic leukemias. The aim of our study was to investigate FXIII-A expression in newly diagnosed B cell acute lymphoblastic leukemia (ALL) samples. We examined 47 de novo ALL cases of B cell origin by triple color labeling with flow cytometry. FXIII-A was detected by a FITC conjugated monoclonal antibody combined with CD34 and CD45 staining. In selected cases FXIII-A was investigated on slides prepared from blasts and visualized with a fluorescent microscope. In addition, blasts were studied by Western blot analysis and FXIII-A was measured by a highly sensitive ELISA method. By flow cytometry 19 samples of the 47 cases were found to be FXIII-A positive. Antigen concentration was 3.11± 1.19 fg/blast, while normal lymphoid precursors and mature lymphocytes from B-CLL did not contain FXIII-A. In the lysate of lymphoblasts that were positive by flow cytometry, a single band (82 kDa) corresponding to FXIII-A was detected on Western blots. Confocal laser scanning microscopic examination revealed the presence of FXIII-A in the cytoplasm of these lymphoblasts. This novel expression site of FXIII-A in leukemic lymphoblasts can be utilized as a diagnostic tool and may also gain functional significance in B-lineage ALL.
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Wang, Chunyu, Changjuan Shao, Li Zhang, et al. "Oxidative Stress Signaling in Blast TBI-Induced Tau Phosphorylation." Antioxidants 10, no. 6 (2021): 955. http://dx.doi.org/10.3390/antiox10060955.
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Traumatic brain injury caused by blast is associated with long-term neuropathological changes including tau phosphorylation and pathology. In this study, we aimed to determine changes in initial tau phosphorylation after exposure to a single mild blast and the potential contribution of oxidative stress response pathways. C57BL/6 mice were exposed to a single blast overpressure (BOP) generated by a compressed gas-driven shock tube that recapitulates battlefield-relevant open-field BOP, and cortical tissues were harvested at different time points up to 24 h after blast for Western blot analysis. We found that BOP caused elevated tau phosphorylation at Ser202/Thr205 detected by the AT8 antibody at 1 h post-blast followed by tau phosphorylation at additional sites (Ser262 and Ser396/Ser404 detected by PHF1 antibody) and conformational changes detected by Alz50 antibody. BOP also induced acute oxidative damage at 1 h post-blast and gradually declined overtime. Interestingly, Extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) were acutely activated in a similar temporal pattern as the rise and fall in oxidative stress after blast, with p38 showing a similar trend. However, glycogen synthase kinase-3 β (GSK3β) was inhibited at 1 h and remained inhibited for 24 h post blast. These results suggested that mitogen-activated protein kinases (MAPKs) but not GSK3β are likely involved in mediating the effects of oxidative stress on the initial increase of tau phosphorylation following a single mild blast.
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HATANO, Michiharu, Koichi KURITA, Hideyuki YAMAOKA, and Tsuyoshi YOKOI. "Computer Aided-analysis of Blow-in Operation by a Blast Furnace Dynamic Model." Transactions of the Iron and Steel Institute of Japan 25, no. 9 (1985): 933–40. http://dx.doi.org/10.2355/isijinternational1966.25.933.
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Birg, F., M. Courcoul, O. Rosnet, et al. "Expression of the FMS/KIT-like gene FLT3 in human acute leukemias of the myeloid and lymphoid lineages." Blood 80, no. 10 (1992): 2584–93. http://dx.doi.org/10.1182/blood.v80.10.2584.2584.
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Abstract FLT3, a receptor belonging to the FMS/KIT family and localized to 13q12, could play a role in the biology of early hematopoietic progenitor cells. Because FMS and KIT are expressed in both normal progenitors and myeloid leukemias, we looked for FLT3 expression in fresh human leukemic cells using Northern blot analysis. High levels of FLT3 expression were detected in 92% of the cases of acute myeloid leukemia (AML) tested, ranging from the M1 to the M5 stages of differentiation assessed in the French-American-British classification. Immature (MO) AML cells, biphenotypic leukemias, and AML with megakaryocytic differentiation (M7 subtype) also expressed the FLT3 transcript. FLT3 was also expressed at high levels in acute lymphoid leukemias of T and B origins. Finally, it was not expressed in chronic myeloid leukemias in chronic phase, whereas it was expressed in most blast crisis samples. This pattern of expression of FLT3 contrasts with the expression of FMS and KIT restricted to myeloid leukemias, and suggests that the FLT3 product could play a role in the expansion of the leukemic blasts of both the myeloid and lymphoid lineages.
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Birg, F., M. Courcoul, O. Rosnet, et al. "Expression of the FMS/KIT-like gene FLT3 in human acute leukemias of the myeloid and lymphoid lineages." Blood 80, no. 10 (1992): 2584–93. http://dx.doi.org/10.1182/blood.v80.10.2584.bloodjournal80102584.
Full textAbstract:
FLT3, a receptor belonging to the FMS/KIT family and localized to 13q12, could play a role in the biology of early hematopoietic progenitor cells. Because FMS and KIT are expressed in both normal progenitors and myeloid leukemias, we looked for FLT3 expression in fresh human leukemic cells using Northern blot analysis. High levels of FLT3 expression were detected in 92% of the cases of acute myeloid leukemia (AML) tested, ranging from the M1 to the M5 stages of differentiation assessed in the French-American-British classification. Immature (MO) AML cells, biphenotypic leukemias, and AML with megakaryocytic differentiation (M7 subtype) also expressed the FLT3 transcript. FLT3 was also expressed at high levels in acute lymphoid leukemias of T and B origins. Finally, it was not expressed in chronic myeloid leukemias in chronic phase, whereas it was expressed in most blast crisis samples. This pattern of expression of FLT3 contrasts with the expression of FMS and KIT restricted to myeloid leukemias, and suggests that the FLT3 product could play a role in the expansion of the leukemic blasts of both the myeloid and lymphoid lineages.
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Reeve, AE, CM Morris, and PH Fitzgerald. "Acquired homozygosity of the rearranged bcr allele during the acute leukemic phase of a patient with Ph-negative chronic myeloid leukemia." Blood 72, no. 1 (1988): 24–28. http://dx.doi.org/10.1182/blood.v72.1.24.24.
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Abstract A 45-year-old male patient with Ph-negative chronic myeloid leukemia (CML) had rearranged bcr-3′ and bcr-5#x2032; gene regions in Southern blot studies when leukemia was diagnosed. During development of terminal blast crisis, successive blood samples showed a progressive decrease in the amount of germline bcr DNA and its complete loss by full blast crisis. There were also increased amounts of rearranged bcr DNA consistent with acquired homozygosity. A similar result was obtained with an IgV lambda probe and indicated homozygosity of a significant part of chromosome 22. The bcr-abl gene complex behaves as a somatic dominant in CML, and we suggest that its acquired homozygosity is a mechanism of bcr-abl amplification similar to duplication of the Ph chromosome commonly found in the blast crisis of CML.
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Reeve, AE, CM Morris, and PH Fitzgerald. "Acquired homozygosity of the rearranged bcr allele during the acute leukemic phase of a patient with Ph-negative chronic myeloid leukemia." Blood 72, no. 1 (1988): 24–28. http://dx.doi.org/10.1182/blood.v72.1.24.bloodjournal72124.
Full textAbstract:
A 45-year-old male patient with Ph-negative chronic myeloid leukemia (CML) had rearranged bcr-3′ and bcr-5#x2032; gene regions in Southern blot studies when leukemia was diagnosed. During development of terminal blast crisis, successive blood samples showed a progressive decrease in the amount of germline bcr DNA and its complete loss by full blast crisis. There were also increased amounts of rearranged bcr DNA consistent with acquired homozygosity. A similar result was obtained with an IgV lambda probe and indicated homozygosity of a significant part of chromosome 22. The bcr-abl gene complex behaves as a somatic dominant in CML, and we suggest that its acquired homozygosity is a mechanism of bcr-abl amplification similar to duplication of the Ph chromosome commonly found in the blast crisis of CML.
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Langworthy, Michael J., Jeffrey M. Smith, and Mark Gould. "Treatment of the Mangled Lower Extremity after a Terrorist Blast Injury." Clinical Orthopaedics and Related Research 422 (May 2004): 88–96. http://dx.doi.org/10.1097/01.blo.0000129558.38803.c2.
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HATANO, Michiharu, Koichi KURITA, Hideyuki YAMAOKA, and Tsuyoshi YOKOI. "Computer Aided-analysis of Blow-out Operation of Blast Furnace by Mathematical Simulation Models." Transactions of the Iron and Steel Institute of Japan 25, no. 9 (1985): 941–48. http://dx.doi.org/10.2355/isijinternational1966.25.941.
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Chernov, N. N., V. E. Gritskov, V. G. Tret'yakov, and V. I. Timoshenko. "Features of the blow-in of a blast furnace after a class-I overhaul." Metallurgist 30, no. 9 (1986): 306–9. http://dx.doi.org/10.1007/bf00741793.
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Polyakov, N. S., V. N. Polyakov, S. T. Solodkov, and A. G. Bryukhov. "Use of schungite to blow in a blast furnace after a class II overhaul." Metallurgist 51, no. 3-4 (2007): 203–5. http://dx.doi.org/10.1007/s11015-007-0037-x.
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Folgiero, Valentina, Daniela Natale, Daria Pagliara та ін. "Indoleamine 2,3-Dioxygenase-1 (IDO1) Is Expressed by a Subset of Childhood Acute Myeloid Leukemias and Restrains IFN-γ Production by T Cells". Blood 120, № 21 (2012): 1430. http://dx.doi.org/10.1182/blood.v120.21.1430.1430.
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Abstract Abstract 1430 Background. Indoleamine 2,3-dioxygenase 1 (IDO1) degrades tryptophan (TRP) into kynurenine (KYN) and other immune suppressive molecules. The IDO1-driven production of KYN promotes the development, stabilization and activation of regulatory T cells (Treg), while suppressing effector T cells, all of which may contribute to immune system impairment in cancer-bearing individuals. It has been previously shown that IDO1 mRNA and protein are detectable in blast cells from 52% of adult patients with newly diagnosed acute myeloid leukemia (AML), in correlation with expanded Treg cells. Importantly, high copy numbers of IDO mRNA may be a negative independent predicting variable for overall and relapse-free survival in adult AML. Patients and methods. We investigated IDO1 expression and function in 21 children with acute leukemia [10 AML (median age 13 years, range 6–16), 9 B-cell precursor (BCP)-ALL, 1 infant acute leukemia with MLL rearrangement and 1 T-cell ALL] and in 1 patient with Ph+ chronic myeloid leukemia (CML). Amongst patients with AML, 3 children had secondary AML, 3 patients had core-binding factor (CBF)+ AML, 3 patients had FLT3-ITD+AML and 1 patient had AML with t(6;9). TRP and KYN levels were measured with reverse phase (RP)-HPLC. Results. Cells from either BCP-ALL or T-cell ALL expressed IDO1 neither constitutively nor after challenge with 100 ng/ml interferon (IFN)-γ, a prototypical inducer of IDO, whereas they up-regulated both phosphorylated STAT-3 and surface programmed death ligand 1 (PD-L1), an IFN-γ-inducible co-inhibitory receptor also implicated in tumor-induced immune evasion. By contrast, leukemia blast cells from 5 out of 10 AML and from Ph+ CML up-regulated IDO1 protein expression after in vitro challenge with IFN-γ (median 20-fold increase, range 11.9–120, compared with unstimulated AML cells). KYN levels significantly increased in supernatants of AML cells treated with IFN-γ for 72h (10.8 μM/L, range 8.15–20.5) compared with unstimulated cultures (1.4 μM/L, range 1.1–2.2), in parallel with TRP consumption (6.3 μM/L, range 3.0–14.1, after challenge with IFN-γ compared with 18.2 μM, range 13.7–20.9, in unstimulated cultures). The IFN-γ-induced increase of IDO expression was significantly inhibited by pre-treatment of leukemia cells with STAT3 inhibitors (median 1.95-fold compared with unstimulated AML cells, range 0.9–27.7), but not with STAT5 inhibitors. In line with these results, STAT3 inhibition prevented the IFN-γ-induced release of KYN in culture supernatants. Western blot runs of immuno-precipitated proteins with specific antibodies suggested a physical interaction between IDO and STAT3 in IFN-γ-challenged leukemia blasts, but not in unstimulated samples. In a mixed tumor cell lymphocyte culture (MTLC), AML blasts primed with IFN-γ significantly inhibited Th1 cytokine production by allogeneic CD8+ T cells, while enhancing IL-4 release by CD4+ T cells. These effects were potentiated by the supplementation of MTLCs with exogenous KYN. The intracellular levels of IL-17A were unaffected by the exposure of allogeneic T cells to AML blasts. The addition of D,L-1-methyl-tryptophan (1MT), an IDO inhibitor, to the co-cultures of T cells and AML blasts incompletely restored IFN-γ production by CD8+ T cells. By contrast, STAT3 inhibitors fully reverted the AML-induced skewing of IFN-γ/IL-4 secretion. Conclusions. Blast cells from a subset of childhood AML, but not those from BCP-ALL or T-cell ALL, express functional IDO1 and restrain IFN-γ secretion by CD8+ T cells, while enhancing IL-4 production by CD4+ T cells. From a therapeutic standpoint, STAT3 inhibitors may effectively interfere with IDO1 expression by AML cells, thus tipping the Th1/Th2 balance in favor of anti-leukemia immune responses. Disclosures: No relevant conflicts of interest to declare.
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Kurzrock, R., WS Kloetzer, M. Talpaz, et al. "Identification of molecular variants of p210bcr-abl in chronic myelogenous leukemia." Blood 70, no. 1 (1987): 233–36. http://dx.doi.org/10.1182/blood.v70.1.233.233.
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Abstract The aberrant abl protein product of a chronic myelogenous leukemia (CML) blast crisis cell line (K562) and of five Philadelphia chromosome- positive CML patients in blast crisis were analyzed by an immune complex kinase assay using two antipeptide sera generated against the hydrophilic domain of v-abl and a region within the third exon of the breakpoint cluster region (bcr) respectively. Both the anti-abl and anti-bcr sera detected a 210 kd band in extracts derived from K562 cells and from two CML patients with myeloid blast crisis. p210 was detected by the anti-abl but not the anti-bcr sera in three CML patients with myeloid (one patient) and lymphoid (two patients) blast crisis, indicating the absence of bcr exon 3 in this protein. Southern blot analysis on DNA derived from one of the patients in the latter group was consistent with the break on chromosome 22 occurring 5′ to bcr exon 3. Our observations demonstrate that the Philadelphia translocation results in the generation of a chimeric bcr-abl protein with at least two molecular variants, both of which are enzymatically active as protein kinases.
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Kurzrock, R., WS Kloetzer, M. Talpaz, et al. "Identification of molecular variants of p210bcr-abl in chronic myelogenous leukemia." Blood 70, no. 1 (1987): 233–36. http://dx.doi.org/10.1182/blood.v70.1.233.bloodjournal701233.
Full textAbstract:
The aberrant abl protein product of a chronic myelogenous leukemia (CML) blast crisis cell line (K562) and of five Philadelphia chromosome- positive CML patients in blast crisis were analyzed by an immune complex kinase assay using two antipeptide sera generated against the hydrophilic domain of v-abl and a region within the third exon of the breakpoint cluster region (bcr) respectively. Both the anti-abl and anti-bcr sera detected a 210 kd band in extracts derived from K562 cells and from two CML patients with myeloid blast crisis. p210 was detected by the anti-abl but not the anti-bcr sera in three CML patients with myeloid (one patient) and lymphoid (two patients) blast crisis, indicating the absence of bcr exon 3 in this protein. Southern blot analysis on DNA derived from one of the patients in the latter group was consistent with the break on chromosome 22 occurring 5′ to bcr exon 3. Our observations demonstrate that the Philadelphia translocation results in the generation of a chimeric bcr-abl protein with at least two molecular variants, both of which are enzymatically active as protein kinases.
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Filatov, S. V., A. I. Dagman, and V. N. Titov. "Energy efficient technology of hot metal smelting at PAO NLMK." Ferrous Metallurgy. Bulletin of Scientific , Technical and Economic Information 75, no. 1 (2019): 32–36. http://dx.doi.org/10.32339/0135-5910-2019-1-32-36.
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Decrease of energy expenditure for hot metal smelting is an actual task in blast furnace technology perfection. Under conditions of PAO NLMK regimes with maximum forcing of the BF process at the expense of pressure increase under furnace mouth and coke hot strength increase were chosen as one of priority ways to increase the BF operation energy efficiency. Data on blast furnaces productivity, specific coke rate, quantity of blow-in oxygen and fuel at different gas pressure levels under the furnace mouth quoted. A dependence between pulverized coal rate and total carbon consumption determined. It was shown, that application in PAO NLMK blast furnaces of coke having hot strength of 60–65% at maximum possible pressure under the furnace mouth and application of pulverized-coal fuel enabled in the period from 2012 through 2018 to decrease the coke rate by more than 100 kg. Also the total carbon consumption decreased by more than 30 kg per hot metal ton and to increase smelting products chemical composition stability.
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Berger, Gilead, Yehuda Finkelstein, and Moshe Harell. "Non-Explosive blast injury of the ear." Journal of Laryngology & Otology 108, no. 5 (1994): 395–98. http://dx.doi.org/10.1017/s002221510012688x.
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AbstractNon-explosive blast injury of the ear refers to the otological trauma caused by a blow to the ear that seals the external auditory meatus. It results in a sudden increase of air pressure within the ear canal that strikes the tympanic membrane. The present study portrays the various aspects of middle and inner ear damage in 91 patients resulting from an assault we entitled a ’non-explosive blast injury' to the ear. Sixty cases were caused by a slap or a fist, 13 patients suffered sport accidents, mostly in ball games, and 18 patients were injured during swimming and water sports activities. The common symptoms were hearing loss, earache, tinnitus, vertigo and otorrhoea. All 91 patients presented with acute perforations of their eardrums. The mean conductive hearing loss was 11.2 dB. A high tone sensorineural hearing loss was detected in only 20 per cent of the patients. A spontaneous closure of the perforation with a conservative management approach was observed in 94.8 per cent of the patientsHealing of the perforation was always associated with closure of the air-bone gap, while the results of the sensorineural hearing loss recovery were less favourable.
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Motomura, Sayuri, Toshiko Motoji, Minoko Takanashi, et al. "Inhibition of P-Glycoprotein and Recovery of Drug Sensitivity of Human Acute Leukemic Blast Cells by Multidrug Resistance Gene (mdr1) Antisense Oligonucleotides." Blood 91, no. 9 (1998): 3163–71. http://dx.doi.org/10.1182/blood.v91.9.3163.
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Abstract To overcome the problem of multidrug resistance, we investigated the effectiveness of phosphrothioate antisense oligonucleotides (MDR1-AS) in suppressing multidrug resistance gene (mdr1) expression in drug-resistant acute myelogenous leukemia (AML) blast cells and the K562 adriamycin-resistant cell line K562/ADM. The percentage of cells with the mdr1 gene product P-glycoprotein (P-gp) was decreased from 100% to 26% by 20 μmol/L MDR1-AS in the K562/ADM cells, and from 48.1% to 10.2% by 2.5 μmol/L MDR1-AS in the AML blast cells. Western blot analysis also showed a decrease in the amount of P-gp in the MDR1-AS–treated K562/ADM cells. This effect was specific to MDR1-AS, and not observed with sense or random control oligonucleotides. The expression of mdr1 mRNA in K562/ADM and AML blast cells treated with MDR1-AS was decreased compared with the random control. Intracellular rhodamine retention and [3H]daunorubicin also increased after antisense treatment. Chemosensitivity to daunorubicin increased in MDR1-AS–treated blast cells up to 5.9-fold in the K562/ADM cells and 3.0- to 6.4-fold in the AML blast cells. The expression of mdr1mRNA derived from colony cells decreased in the MDR1-AS–treated groups. No inhibitory effect of the oligonucleotides on normal bone marrow progenitors was observed. These findings suggest that MDR1-AS is useful to overcome multidrug resistance in the treatment of leukemia.
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Motomura, Sayuri, Toshiko Motoji, Minoko Takanashi, et al. "Inhibition of P-Glycoprotein and Recovery of Drug Sensitivity of Human Acute Leukemic Blast Cells by Multidrug Resistance Gene (mdr1) Antisense Oligonucleotides." Blood 91, no. 9 (1998): 3163–71. http://dx.doi.org/10.1182/blood.v91.9.3163.3163_3163_3171.
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To overcome the problem of multidrug resistance, we investigated the effectiveness of phosphrothioate antisense oligonucleotides (MDR1-AS) in suppressing multidrug resistance gene (mdr1) expression in drug-resistant acute myelogenous leukemia (AML) blast cells and the K562 adriamycin-resistant cell line K562/ADM. The percentage of cells with the mdr1 gene product P-glycoprotein (P-gp) was decreased from 100% to 26% by 20 μmol/L MDR1-AS in the K562/ADM cells, and from 48.1% to 10.2% by 2.5 μmol/L MDR1-AS in the AML blast cells. Western blot analysis also showed a decrease in the amount of P-gp in the MDR1-AS–treated K562/ADM cells. This effect was specific to MDR1-AS, and not observed with sense or random control oligonucleotides. The expression of mdr1 mRNA in K562/ADM and AML blast cells treated with MDR1-AS was decreased compared with the random control. Intracellular rhodamine retention and [3H]daunorubicin also increased after antisense treatment. Chemosensitivity to daunorubicin increased in MDR1-AS–treated blast cells up to 5.9-fold in the K562/ADM cells and 3.0- to 6.4-fold in the AML blast cells. The expression of mdr1mRNA derived from colony cells decreased in the MDR1-AS–treated groups. No inhibitory effect of the oligonucleotides on normal bone marrow progenitors was observed. These findings suggest that MDR1-AS is useful to overcome multidrug resistance in the treatment of leukemia.
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Hartman, Amy D., Annique Wilson-Weekes, Attaya Suvannasankha, et al. "In AML, Cbl Serves as Nexus for Signaling from Flt3, and Is Required for Coupling JNK1 in a Pathway of Survival and Proliferation Involving c-jun/AP-1." Blood 106, no. 11 (2005): 1203. http://dx.doi.org/10.1182/blood.v106.11.1203.1203.
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Abstract Here we demonstrate by immunoprecipitation and immunoblot, cbl is among the most heavily tyrosine phosphorylated adaptor proteins in primary AML blasts with Flt3 signaling, in the context of either mutation or overexpression/autocrine mechanisms. The human leukemic cell lines MV-4-11 and THP-1 model primary AML blasts in terms of Flt3 signaling by these respective criteria and demonstrate identical coupling between Flt3 and p85, the PI-3-kinase adaptor, by coimmunoprecipitation/blot experiments. Although cbl has no direct binding site on Flt3, it binds tightly to p85 SH2 by virtue of its tyrosine phosphorylation, also demonstrated by co-IP in cell lines and primary cells. Tyrosine phosphorylated cbl is a docking site for CrkII/L SH2’s and this provides a branch point for signals from Flt3 to PI-3-kinase or JNK, respectively, because CrkII(L) is known to bind JNK1 through SH3: polyproline interaction to serve as scaffolding; and interaction of JNK1 and CrkII/L was also observed by co-IP. In a survey of primary AML cases (n=33) there was a strict relationship between expression levels of (active) Flt3 and phospho-c-jun as readout for JNK activity level (p=0.001, r=0.54). To demonstrate the functional relevance of these interactions, siRNA knockdown of components was pursued in the cell lines and in primary AML blasts. JNK1 knockdown, and, to a much lesser degree, JNK2 knockdown, led to loss of phospho-c-jun expression in MV-4-11 and THP-1. Indeed, Flt3 signaling is required for JNK signaling because knockdown of Flt3 led to total loss of p-jun and c-jun expression in MV-4-11 and patient blast. By contrast, cbl knockdown led to selective loss of JNK signaling to p-jun without significantly affecting Flt3 or its downstream activating phosphorylation of AKT. Thus, despite binding by cbl to p85, cbl is not required for PI-3-kinase signaling because of redundancy supplied by the p85-Flt3 interaction. Further, by use of LY294002 to inhibit PI-3-kinase, PI-3-kinase is also not required for JNK signaling. However, selective inhibition of JNK signaling by the small molecule approach in these cell lines and in primary AML blasts leads to loss of proliferation, induction of apoptosis, and synergistic killing with daunorubicin. These observations form the platform for a phase I trial of JNK inhibition in refractory, multidrug-resistant, and Flt3-driven AML.
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Tsunoda, J., S. Okada, J. Suda, et al. "In vivo stem cell function of interleukin-3-induced blast cells." Blood 78, no. 2 (1991): 318–22. http://dx.doi.org/10.1182/blood.v78.2.318.318.
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Abstract The treatment of mice with high doses of 5-fluorouracil (5-FU) results in an enrichment of primitive hematopoietic progenitors. Using this procedure, we obtained a new class of murine hematopoietic colonies that had very high secondary plating efficiencies in vitro and could differentiate into not only myeloid cells but also into lymphoid lineage cells. The phenotypes of interleukin-3 (IL-3) induced blast colony cells were Thy-1-positive and lineage-marker-negative. We examined whether these blast colony cells contained primitive hematopoietic stem cells in vivo and could reconstitute hematopoietic tissues in lethally irradiated mice. Blast colony cells could generate macroscopic visible spleen colonies on days 8 and 12, and 5 x 10(3) blast cells were sufficient to protect them from lethally irradiation. It was shown that 6 or 8 weeks after transplantation of 5 x 10(3) blast cells, donor male cells were detected in the spleen and thymus of the female recipients but not in the bone marrow by Southern blot analysis using Y-encoded DNA probe. After 10 weeks, bone marrow cells were partially repopulated from donor cells. In a congenic mouse system, donor-derived cells (Ly5.2) were detected in the thymus and spleen 6 weeks after transplantation. Fluorescence-activated cell sorter analyses showed that B cells and macrophages developed from donor cells in the spleen. In the thymus, donor-derived cells were found in CD4, CD8 double-positive, single-positive, and double-negative populations. Reconstitution of bone marrow was delayed and myeloid and lymphoid cells were detected 10 weeks after transplantation. These results indicate that IL-3-induced blast cells contain the primitive hematopoietic stem cells capable of reconstituting hematopoietic organs in lethally irradiated mice.
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Tsunoda, J., S. Okada, J. Suda, et al. "In vivo stem cell function of interleukin-3-induced blast cells." Blood 78, no. 2 (1991): 318–22. http://dx.doi.org/10.1182/blood.v78.2.318.bloodjournal782318.
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The treatment of mice with high doses of 5-fluorouracil (5-FU) results in an enrichment of primitive hematopoietic progenitors. Using this procedure, we obtained a new class of murine hematopoietic colonies that had very high secondary plating efficiencies in vitro and could differentiate into not only myeloid cells but also into lymphoid lineage cells. The phenotypes of interleukin-3 (IL-3) induced blast colony cells were Thy-1-positive and lineage-marker-negative. We examined whether these blast colony cells contained primitive hematopoietic stem cells in vivo and could reconstitute hematopoietic tissues in lethally irradiated mice. Blast colony cells could generate macroscopic visible spleen colonies on days 8 and 12, and 5 x 10(3) blast cells were sufficient to protect them from lethally irradiation. It was shown that 6 or 8 weeks after transplantation of 5 x 10(3) blast cells, donor male cells were detected in the spleen and thymus of the female recipients but not in the bone marrow by Southern blot analysis using Y-encoded DNA probe. After 10 weeks, bone marrow cells were partially repopulated from donor cells. In a congenic mouse system, donor-derived cells (Ly5.2) were detected in the thymus and spleen 6 weeks after transplantation. Fluorescence-activated cell sorter analyses showed that B cells and macrophages developed from donor cells in the spleen. In the thymus, donor-derived cells were found in CD4, CD8 double-positive, single-positive, and double-negative populations. Reconstitution of bone marrow was delayed and myeloid and lymphoid cells were detected 10 weeks after transplantation. These results indicate that IL-3-induced blast cells contain the primitive hematopoietic stem cells capable of reconstituting hematopoietic organs in lethally irradiated mice.
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Qi, Min, and Yinong Yang. "Quantification of Magnaporthe grisea During Infection of Rice Plants Using Real-Time Polymerase Chain Reaction and Northern Blot/Phosphoimaging Analyses." Phytopathology® 92, no. 8 (2002): 870–76. http://dx.doi.org/10.1094/phyto.2002.92.8.870.
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Rice blast, caused by Magnaporthe grisea, is a serious fungal disease of rice worldwide. Currently, evaluation of the fungal pathogenicity and host resistance is mainly based on a disease rating or measurement of blast lesion number and size. However, these methods only provide visual estimation rather than accurate measurement of fungal growth in rice plants. In this study, DNA-based real-time polymerase chain reaction (PCR) and RNA-based northern blot/phosphoimaging analyses were evaluated to quantify M. grisea. Both methods were sensitive, specific, and reproducible and could accurately measure the relative growth and absolute biomass of M. grisea. The real-time PCR analysis showed that the growth of M. grisea in seedling leaves of susceptible cultivars (M201 and Wells) was ≈46 to 80 times higher than that of a resistant cultivar (Drew) at 4 and 6 days after inoculation. The data obtained from the real-time PCR assays also were consistent with that from northern blot/ phosphoimaging analysis. However, the real-time PCR approach was much faster and more convenient in most cases. Therefore, it is an excellent tool for in planta quantification of M. grisea and can be used for reliable assessment of fungal pathogenicity and host resistance
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Ciccone, E., O. Viale, C. Bottino, et al. "Antigen recognition by human T cell receptor gamma-positive lymphocytes. Specific lysis of allogeneic cells after activation in mixed lymphocyte culture." Journal of Experimental Medicine 167, no. 4 (1988): 1517–22. http://dx.doi.org/10.1084/jem.167.4.1517.
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These experiments were designed to define the ability of human TCR-gamma+ cells to recognize allogeneic cells. TCR-gamma+-enriched populations were obtained by treating peripheral blood E-rosetting cells with anti-CD4 and anti-CD8 mAbs. The resulting populations were CD2+4-8- expressed variable proportions of CD3+ cells (40-90%), and did not react with the WT31 mAb, which is specific for a framework determinant of the alpha/beta heterodimer that serves as receptor for antigen on most human T lymphocytes. After mixed lymphocyte culture with irradiated allogeneic cells for 7 d and 3 additional days in rIL-2 (100 U/ml), cells underwent proliferation in three of five individuals tested. In addition, MLC-derived cells lysed 51Cr-labeled PHA-induced blasts derived from the allogeneic cells used as stimulator, but not allogeneic unrelated or autologous blast cells. No cytotoxicity against autologous or allogeneic target cells could be induced by culturing CD3+4-8-WT31- lymphocytes in MLC with irradiated autologous cells. Surface iodination of allogeneic MLC-activated CD3+4-8-WT31- cells followed by lysis in 1% digitonin and immunoprecipitation with anti-CD3 mAb indicated that the CD3-associated molecules consisted of a major 45-kD band and a minor band of 43 kD. Northern blot analysis showed that mRNA for the gamma chain was expressed at high levels, whereas mRNAs for alpha and beta chains were missing. These data support the notion that TCR-gamma rather than TCR-alpha/beta is expressed in allospecific CD3-4-8-WT31- cell populations. Clones were further derived from MLC-stimulated CD3+4-8-WT31- populations. All the seven clones studied in detail maintained the surface phenotype as well as the cytolytic pattern of the original MLC populations, thus only specific allogeneic PHA-induced blasts were lysed. NK-sensitive as well as NK-resistant tumor targets were variably susceptible to lysis; therefore, specific cytolytic activity against allogeneic cells was not necessarily linked to the expression of MHC-nonrestricted cytotoxicity against tumor cells.
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Gorbatyuk, S. M., Yu S. Tarasov, I. A. Levitskii, A. G. Radyuk, and A. E. Titlyanov. "EFFECT OF A CERAMIC INSERT WITH SWIRLER ON GAS DYNAMICS AND HEAT EXCHANGE IN A BLAST FURNACE TUYERE." Izvestiya. Ferrous Metallurgy 62, no. 5 (2019): 337–44. http://dx.doi.org/10.17073/0368-0797-2019-5-337-344.
Full textAbstract:
The use of natural gas can reduce the amount of coke needed to produce cast iron. In a common tuyere natural gas is pressed against the surface of the air passage by a stream of hot blow and mixes poorly with it. It leads to incomplete burning of natural gas and its pyrolysis. One way to improve the mixing of natural gas and hot blow is to install the swirler in the air passage. In this case, however, intensification of natural gas burning inside the tuyere can lead to a burnout of the inner cylinder. In Ansys Fluent 18.2, using insulation insert with a swirler made in the form of a collar step at different places along the length of the insert, simulation of gas dynamics and its thermal state is carried out to solve the problem of mixing natural gas and hot blow in the air passage of tuyere. Simpler assumptions were adopted. Among which the simulation area included not only the fluid medium inside the air passage, but also the insulation insert, i.e. the associated problem of heat exchange was solved, and the processes of transfer of heat to water of the cooling system are taken into account in extended boundary conditions. The simplified calculation area scheme was created in the DesignModeler application, and the calculated grid was created in the AnsysMeshing application. The boundary conditions were set for blow (natural gas), as well as for the border of the insert with an air gap separating it from the internal cylinder and the fluid with the tuyere nose. Taking into account the symmetry of the computation region, the calculations were made for the half of tuyere. It has been found that mixing of natural gas and hot blow improves as the swirler moves along the length of the insert to the exit from the air passage. At the same time, in the swirler place the diameter of air passage is not less than downstream of the tuyere. The swirler`s shift toward the exit from air passage reduces the thermal load on the insert, thereby increasing its service life.
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Zhang, Shihong, Yi Wei, and Hongyu Pan. "Transgenic Rice Plants Expressing a Novel Antifreeze Glycopeptide Possess Resistance to Cold and Disease." Zeitschrift für Naturforschung C 62, no. 7-8 (2007): 583–91. http://dx.doi.org/10.1515/znc-2007-7-821.
Full textAbstract:
Freezing injury and disease are both restrictive factors in crop production. In order to improve the tolerance ability to these stresses, a better way is to carry out genetic engineering by transferring dualfunctional genes. A predicted rice antifreeze glycopeptide gene was purposefully selected from rice blast-induced cDNA library. Northern blot demonstrated that the gene is expressed not only in blast-infected rice leaves, but also in low temperature-treated rice. In addition, the expressed protein in Escherichia coli exhibits strong antifreeze activities. The gene was overexpressed in rice plants transformed via Agrobacterium tumefacient EHA105. Overall 112 T0 transformants were obtained in this research. Cold tolerance and disease resistance of T1 transformants were, respectively, investigated. The results showed that plants containing overexpressed transgene can withstand D1 ∞C for 24 h without severe chilling injury after thawed, and that disease symptoms of the parallel transformants are highly reduced in response to blast infection, when compared with controls. The relationship of the gene and several pathogenesis-related protein genes to be chosen was analyzed and discussed. All these results confirmed the dual role of the cloned gene, and implied that genetic engineering using this kind of gene is a promising method to reduce biotic and abiotic stresses
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Shcheglov, E. M., D. P. Kholodnyi, S. N. Grachev, et al. "Improving the Technology for the Blow-In of Blast Furnaces After Class-I and Class-II overhauls." Metallurgist 57, no. 11-12 (2014): 1082–87. http://dx.doi.org/10.1007/s11015-014-9849-7.
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Ferrari, S., MT Mariano, E. Tagliafico, et al. "Myeloperoxidase gene expression in blast cells with a lymphoid phenotype in cases of acute lymphoblastic leukemia." Blood 72, no. 3 (1988): 873–76. http://dx.doi.org/10.1182/blood.v72.3.873.873.
Full textAbstract:
Abstract By using a cDNA clone of the myeloperoxidase (MPO) gene, we have studied, by Northern blot analysis, the level of MPO mRNA in eight cases of acute lymphoblastic leukemia (ALL). The blast cell populations studied were characterized by morphologic, cytochemical, immunochemical, and molecular criteria. With all the methods used the populations were found to be highly homogeneous and showed a typical lymphoid phenotype. In particular, the Ig heavy-chain gene rearrangement was largely prevalent, and the germ line configuration was almost absent. However, in three of eight cases, high levels of MPO mRNA were detected. The remarkable homogeneity of the cell populations examined suggests that the MPO mRNA observed was present in cellular elements certainly identified as lymphoid. The absence of contamination by myeloid cells was confirmed by the results of Western blot analysis of the proteins of the cell population studied: no MPO protein was detectable. The levels of mRNA observed were high enough to be comparable to those observed in a promyelocytic cell population.
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Ferrari, S., MT Mariano, E. Tagliafico, et al. "Myeloperoxidase gene expression in blast cells with a lymphoid phenotype in cases of acute lymphoblastic leukemia." Blood 72, no. 3 (1988): 873–76. http://dx.doi.org/10.1182/blood.v72.3.873.bloodjournal723873.
Full textAbstract:
By using a cDNA clone of the myeloperoxidase (MPO) gene, we have studied, by Northern blot analysis, the level of MPO mRNA in eight cases of acute lymphoblastic leukemia (ALL). The blast cell populations studied were characterized by morphologic, cytochemical, immunochemical, and molecular criteria. With all the methods used the populations were found to be highly homogeneous and showed a typical lymphoid phenotype. In particular, the Ig heavy-chain gene rearrangement was largely prevalent, and the germ line configuration was almost absent. However, in three of eight cases, high levels of MPO mRNA were detected. The remarkable homogeneity of the cell populations examined suggests that the MPO mRNA observed was present in cellular elements certainly identified as lymphoid. The absence of contamination by myeloid cells was confirmed by the results of Western blot analysis of the proteins of the cell population studied: no MPO protein was detectable. The levels of mRNA observed were high enough to be comparable to those observed in a promyelocytic cell population.
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David, Sayd Farage, Felipe Farage David, and M. L. P. Machado. "Artificial Neural Network Model for Predict of Silicon Content in Hot Metal Blast Furnace." Materials Science Forum 869 (August 2016): 572–77. http://dx.doi.org/10.4028/www.scientific.net/msf.869.572.
Full textAbstract:
The growing focus on the efficiency of the reduction process in blast furnace generates an alteration in the way they operate. This modifies the conditions of transfer of silicon for the hot metal and can cause problems in the added value of your product. To evaluate the changes of the operational parameters of the reduction on the conditions of transfer of silicon process a mathematical model based on artificial neural networks has been implemented. Through this model it was possible to predict the silicon content to determine the influence of each operational parameter. Artificial neural networks were able to predict the silicon content through parameters of the reduction in blast furnace process, and this was verified by the precision of this model. The ANN showed that Theoretical flame temperature, Pressure blow and Coke rate have a positive influence on the silicon content in hot metal, and the Hot metal rate is inversely proportional to the silicon content of the hot metal.