Взрывоопасность угольной пыли и метана в горном деле

Данная статья посвящена проблеме предотвращения аварий на предприятиях горнодобывающей промышленности за счёт влияния. Рассматриваются причины повышения содержания газа в горных выработках. Дана сравнительная характеристика угольной пыли и метана по их опасности. Выявлено, что угольная пыль опаснее метана. Приведены меры по профилактике аварийности на горнодобывающих предприятиях. This article is devoted to the prevention of accidents in the mining industry at the expense of influence. It discusses reasons for the increase in gas content in mine workings. The author describes comparative characteristics of coal dust and methane at their danger. It is revealed that the coal dust is more dangerous than methane. The author gives measures for the prevention of accidents at mining enterprises

A Robust Solution Procedure for Hyperelastic Solids with Large Boundary Deformation

Compressible Mooney-Rivlin theory has been used to model hyperelastic solids, such as rubber and porous polymers, and more recently for the modeling of soft tissues for biomedical tissues, undergoing large elastic deformations. We propose a solution procedure for Lagrangian finite element discretization of a static nonlinear compressible Mooney-Rivlin hyperelastic solid. We consider the case in which the boundary condition is a large prescribed deformation, so that mesh tangling becomes an obstacle for straightforward algorithms. Our solution procedure involves a largely geometric procedure to untangle the mesh: solution of a sequence of linear systems to obtain initial guesses for interior nodal positions for which no element is inverted. After the mesh is untangled, we take Newton iterations to converge to a mechanical equilibrium. The Newton iterations are safeguarded by a line search similar to one used in optimization. Our computational results indicate that the algorithm is up to 70 times faster than a straightforward Newton continuation procedure and is also more robust (i.e., able to tolerate much larger deformations). For a few extremely large deformations, the deformed mesh could only be computed through the use of an expensive Newton continuation method while using a tight convergence tolerance and taking very small steps.Comment: Revision of earlier version of paper. Submitted for publication in Engineering with Computers on 9 September 2010. Accepted for publication on 20 May 2011. Published online 11 June 2011. The final publication is available at http://www.springerlink.co

Class I histone deacetylases 1, 2 and 3 are highly expressed in renal cell cancer

Background Enhanced activity of histone deacetylases (HDAC) is associated with more aggressive tumour behaviour and tumour progression in various solid tumours. The over-expression of these proteins and their known functions in malignant neoplasms has led to the development of HDAC inhibitors (HDI) as new anti-neoplastic drugs. However, little is known about HDAC expression in renal cell cancer. Methods We investigated the expression of HDAC 1, 2 and 3 in 106 renal cell carcinomas and corresponding normal renal tissue by immunohistochemistry on tissue micro arrays and correlated expression data with clinico-pathological parameters including patient survival. Results Almost 60% of renal cell carcinomas expressed the HDAC isoforms 1 and 2. In contrast, HDAC 3 was only detected in 13% of all renal tumours, with particular low expression rates in the clear cell subtype. HDAC 3 was significantly higher expressed in pT1/2 tumours in comparison to pT3/4 tumours. Expression of class I HDAC isoforms correlated with each other and with the proliferative activity of the tumours. We found no prognostic value of the expression of any of the HDAC isoforms in this tumour entity. Conclusion Class I HDAC isoforms 1 and 2 are highly expressed in renal cell cancer, while HDAC 3 shows low, histology dependent expression rates. These unexpected differences in the expression patterns suggests alternative regulatory mechanisms of class I HDACs in renal cell cancer and should be taken into account when trials with isoform selective HDI are being planned. Whether HDAC expression in renal cancers is predictive of responsiveness for HDI will have to be tested in further studies

Effect of Forest Site Preparation and Livestock Grazing on Stormflow and Water Quality in the South East

The commercial forestlands of East Texas and Louisiana are the most water-efficient producing areas of the two states. Current and projected water shortages for Texas makes this water-rich area extremely important to future growth and development of Texas. However, little is known about the influence of intensive forest practices or livestock grazing on water quality, yield or site productivity in Texas. This is the only instrumented watershed study in Texas or Louisiana that is currently evaluating the influence of livestock grazing on water and the second study evaluating the impact of intensive forest practices on water. This research is providing information that will enable forest managers, state and federal agencies to select livestock grazing and/or forest management practices that will maintain a productive forest environment and minimize off-site water quality impacts. It is imperative that if Texas in the next 30 years is: 1) to help meet the timber product demand that is projected to be placed on the Southeast, and 2) to meet the projected water shortages we need to understand the impact of intensive forest and livestock grazing practices on site productivity and water. This research is helping provide the basic information needed to manage Southeast forestlands for timber products, red meat and water. The southern states are currently producing half of the nation's wood supply with large demands to increase timber production expected in the next 20 years. The challenge facing forestry in the South is in developing technology and management to meet this increased demand and maintain an acceptable forest environment in the face of increased taxes, rising labor, equipment and energy costs. The intensive forest management practices of harvesting and site preparation have been identified as causing potential declines in site production and as sources of nonpoint pollution. The Clean Water Act (PL 92-500 and PL 95-217) requires identification and control of silvicultural activities and livestock grazing which contribute to nonpoint source pollution. Implementation of "best management practices", either voluntary or mandatory, are the suggested means for maintaining water quality and site productivity. Hydrologic impacts of livestock grazing result primarily from the interactions of climate, vegetation, soil, and intensity and duration of livestock use. Thus, grazing impacts will vary naturally from area to area due to the normal variability of these factors. Few studies have attempted to account for these natural variations. Documentation of the intensity and duration of livestock grazing has been poor or completely ignored in most studies. In East Texas, the impact of livestock grazing on water quality has had no research effort. Most research regarding the impact of grazing upon water quality has been conducted outside the Southern Region and, more importantly, outside of the Gulf Coastal Plains. Because geology, soils , topography, climate, etc. are different, extensions of that research to the East Texas and Louisiana areas may be misleading

Expression pattern of class I histone deacetylases in vulvar intraepithelial neoplasia and vulvar cancer: a tissue microarray study

BACKGROUND: Epigenetic regulation is an important mechanism leading to cancer initiation and promotion. Histone acetylation by histone deacetylases (HDACs) represents an important part of it. The development of HDAC inhibitors has identified the utility of HDACs as a therapeutic target. Little is known about the epigenetic regulation of vulvar intraepithelial neoplasia (VIN) and vulvar squamous cell cancer (VSCC). In this study, the expression of class I HDACs (HDAC 1, 2 and 3) was compared in a series of VIN and VSCC tissues. METHODS: A tissue micro array (TMA) with specimens from 106 patients with high-grade VIN and 59 patients with vulvar cancer was constructed. The expression of HDACs 1, 2 and 3 were analyzed with immunohistochemistry (IHC). The nuclear expression pattern was evaluated in terms of intensity and percentage of stained nuclei and was compared between vulvar preinvasive lesions and vulvar cancer. RESULTS: HDAC 2 expression was significantly higher in VIN than in VSCC (p < 0.001, Fisher's test). Also, 88.7% (n=94/106) of VIN samples and only 54.5% (n=31/57) of VSCC samples were scored at the maximum level. Conversely, HDAC 3 expression was significantly higher in VSCC (93%, 53/57) compared to VIN (73.6%, 78/106, p=0.003), whereas only a small difference in the expression of HDAC 1 was found between these two entities of vulvar neoplasia. CONCLUSIONS: These results suggest that epigenetic regulation plays a considerable role in the transformation of VIN to invasive vulvar neoplasia

Establishment of a patient-derived orthotopic osteosarcoma mouse model

Background: Osteosarcoma (OS) is the most common pediatric primary malignant bone tumor. As the prognosis for patients following standard treatment did not improve for almost three decades, functional preclinical models that closely reflect important clinical cancer characteristics are urgently needed to develop and evaluate new treatment strategies. The objective of this study was to establish an orthotopic xenotransplanted mouse model using patient-derived tumor tissue. Methods: Fresh tumor tissue from an adolescent female patient with osteosarcoma after relapse was surgically xenografted into the right tibia of 6 immunodeficient BALB/c Nu/Nu mice as well as cultured into medium. Tumor growth was serially assessed by palpation and with magnetic resonance imaging (MRI). In parallel, a primary cell line of the same tumor was established. Histology and high-resolution array-based comparative genomic hybridization (aCGH) were used to investigate both phenotypic and genotypic characteristics of different passages of human xenografts and the cell line compared to the tissue of origin. Results: A primary OS cell line and a primary patient-derived orthotopic xenotranplanted mouse model were established. MRI analyses and histopathology demonstrated an identical architecture in the primary tumor and in the xenografts. Array-CGH analyses of the cell line and all xenografts showed highly comparable patterns of genomic progression. So far, three further primary patient-derived orthotopic xenotranplanted mouse models could be established. Conclusion: We report the first orthotopic OS mouse model generated by transplantation of tumor fragments directly harvested from the patient. This model represents the morphologic and genomic identity of the primary tumor and provides a preclinical platform to evaluate new treatment strategies in OS

The FLASHForward Facility at DESY

The FLASHForward project at DESY is a pioneering plasma-wakefield acceleration experiment that aims to produce, in a few centimetres of ionised hydrogen, beams with energy of order GeV that are of quality sufficient to be used in a free-electron laser. The plasma wave will be driven by high-current density electron beams from the FLASH linear accelerator and will explore both external and internal witness-beam injection techniques. The plasma is created by ionising a gas in a gas cell with a multi-TW laser system, which can also be used to provide optical diagnostics of the plasma and electron beams due to the <30 fs synchronisation between the laser and the driving electron beam. The operation parameters of the experiment are discussed, as well as the scientific program.Comment: 19 pages, 9 figure

MEIS2 Is an Adrenergic Core Regulatory Transcription Factor Involved in Early Initiation of TH-MYCN-Driven Neuroblastoma Formation.

Roughly half of all high-risk neuroblastoma patients present with MYCN amplification. The molecular consequences of MYCN overexpression in this aggressive pediatric tumor have been studied for decades, but thus far, our understanding of the early initiating steps of MYCN-driven tumor formation is still enigmatic. We performed a detailed transcriptome landscaping during murine TH-MYCN-driven neuroblastoma tumor formation at different time points. The neuroblastoma dependency factor MEIS2, together with ASCL1, was identified as a candidate tumor-initiating factor and shown to be a novel core regulatory circuit member in adrenergic neuroblastomas. Of further interest, we found a KEOPS complex member (gm6890), implicated in homologous double-strand break repair and telomere maintenance, to be strongly upregulated during tumor formation, as well as the checkpoint adaptor Claspin (CLSPN) and three chromosome 17q loci CBX2, GJC1 and LIMD2. Finally, cross-species master regulator analysis identified FOXM1, together with additional hubs controlling transcriptome profiles of MYCN-driven neuroblastoma. In conclusion, time-resolved transcriptome analysis of early hyperplastic lesions and full-blown MYCN-driven neuroblastomas yielded novel components implicated in both tumor initiation and maintenance, providing putative novel drug targets for MYCN-driven neuroblastoma

Targeted ultra-deep sequencing reveals recurrent and mutually exclusive mutations of cancer genes in blastic plasmacytoid dendritic cell neoplasm

Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare haematopoietic malignancy characterized by dismal prognosis and overall poor therapeutic response. Since the biology of BPDCN is barely understood, our study aims to shed light on the genetic make-up of these highly malignant tumors. Using targeted high-coverage massive parallel sequencing, we investigated 50 common cancer genes in 33 BPDCN samples. We detected point mutations in NRAS (27.3% of cases), ATM (21.2%), MET, KRAS, IDH2, KIT (9.1% each), APC and RB1 (6.1% each), as well as in VHL, BRAF, MLH1, TP53 and RET (3% each). Moreover, NRAS, KRAS and ATM mutations were found to be mutually exclusive and we observed recurrent mutations in NRAS, IDH2, APC and ATM. CDKN2A deletions were detected in 27.3% of the cases followed by deletions of RB1 (9.1%), PTEN and TP53 (3% each). The mutual exclusive distribution of some mutations may point to different subgroups of BPDCN whose biological significance remains to be explored

HDAC1 Inactivation Induces Mitotic Defect and Caspase-Independent Autophagic Cell Death in Liver Cancer

Histone deacetylases (HDACs) are known to play a central role in the regulation of several cellular properties interlinked with the development and progression of cancer. Recently, HDAC1 has been reported to be overexpressed in hepatocellular carcinoma (HCC), but its biological roles in hepatocarcinogenesis remain to be elucidated. In this study, we demonstrated overexpression of HDAC1 in a subset of human HCCs and liver cancer cell lines. HDAC1 inactivation resulted in regression of tumor cell growth and activation of caspase-independent autophagic cell death, via LC3B-II activation pathway in Hep3B cells. In cell cycle regulation, HDAC1 inactivation selectively induced both p21WAF1/Cip1 and p27Kip1 expressions, and simultaneously suppressed the expression of cyclin D1 and CDK2. Consequently, HDAC1 inactivation led to the hypophosphorylation of pRb in G1/S transition, and thereby inactivated E2F/DP1 transcription activity. In addition, we demonstrated that HDAC1 suppresses p21WAF1/Cip1 transcriptional activity through Sp1-binding sites in the p21WAF1/Cip1 promoter. Furthermore, sustained suppression of HDAC1 attenuated in vitro colony formation and in vivo tumor growth in a mouse xenograft model. Taken together, we suggest the aberrant regulation of HDAC1 in HCC and its epigenetic regulation of gene transcription of autophagy and cell cycle components. Overexpression of HDAC1 may play a pivotal role through the systemic regulation of mitotic effectors in the development of HCC, providing a particularly relevant potential target in cancer therapy