A Carbon Nanocomposite Material Used in the Physical Modelling of the Overburden Subsidence Process.

Carbon nanomaterial is widely used in structural health monitoring due to the advantage of sensitivity and good mechanical properties. This study presents a novel approach employing carbon nanocomposite materials (CNMs) to characterize deformation and damage evolution in physical modelling. As the primary measurement method, the CNM is used to investigate the deformation characteristics of a 200-400 m thick sandstone bed at a 1 km deep longwall mine. The sandstone unit is identified as an ultra-thick key stratum (UTKS), with its thicknesses varying across different mining panels of the UTKS. The results of CNM monitoring show that the UTKS remains stable even after a consecutive excavation of 900 m in width. This stability impedes the upward propagation of overlying strata failure, leading to minimal surface subsidence. The study demonstrates the huge potential of CNM in the mining area, which can be useful for investigating material damage in physical modelling studies. The findings suggest that the cumulative extraction width in individual mining areas of the mine should be controlled to avoid a sudden collapse of the UTKS, and that special attention should be paid to where the UTKS's thickness changes substantially. The substantial variation in UTKS thickness significantly impacts the pattern of overburden subsidence.

Influence of stress distribution in coal seams of non-uniform extremely thick key stratum and disaster-causing mechanisms.

This paper analyzes the influence of the overlying extremely thick primary key stratum on the strong mine pressure hazard at the large mining face in Gaojiapu coal mine. The analysis of the distribution characteristics of the primary key stratum in the Gaojiapu coal mine reveals the bow-shaped structural characteristics of the overlying thick primary key stratum. An elastodynamic model was developed using the variational method to calculate and analyze the influence of the movement of the primary key stratum on the stress and energy of the underlying weak rock. The results show that the arch structure of the overlying extremely thick primary key stratum can significantly affect the distribution pattern of stress and strain energy in the coal body, and the stress and strain energy in the coal body are transferred to the middle of the coal column, and the middle region of the coal column enters a high stress state. These results suggest that the change in thickness of the overlying primary key stratum at Gaojiapu in the coal column area is a major factor in the frequent occurrence of impact ground pressure events at the mine. This study explains the causes of frequent impact ground pressure in the lower coal rock mass of the extremely thick primary key stratum, and provides a reference for the prevention and control of impact hazards in the extremely thick primary key stratum.

The field monitoring experiment of the high-level key stratum movement in coal mining based on collaborative DOFS and MPBX.

The deformation and movement characteristics of high-level key stratums in overlying strata are important for estimating ground subsidence and understanding failure characteristics of ultrathick strata during mining. In this study, a distributed optical fiber sensor (DOFS) and multipoint borehole extensometers (MPBXs) were collaboratively employed to monitor the deformation of high-level key stratums in situ during the mining process at working face 130,604 of the Maiduoshan Coal Mine. DOFS monitoring results showed that the distance from advance influence of mining on the ground surface is 219.2 m. The deformation of the shallow stratums were greater and was affected earlier than that of the deep stratums. The deformation in the strata did not occur continuously and the boundary curve of the impact from advance mining was not a straight line with the advancement of the working face. By the MPBX technology, we measured the strata movement and obtained four-stage characteristics of high-level key stratum movement. The subsidence of the primary key stratum and the sub key stratum were monitored to reach 1389 and 1437 mm; their final relative displacement differed by 48 mm. No bed separation was observed in between the strata, and the key stratums tended to sink as a whole with the advancement of the working face. This research guides the analysis the movement of thick high-level key stratums.

Sequencing and characterization of mitochondrial genome of Idaea effusaria (Lepidoptera: Geometridae).

The Idaea effusaria belongs to Geometridae in Lepidoptera. The complete mitogenome of I. effusaria was described in this study, which is typically circular duplex molecules and 16,161 bp in length, containing the standard metazoan set of 13 protein-coding genes, 22 transfer RNA genes, 2 ribosomal RNA genes, and an A + T-rich region. The gene order is same with other lepidopterans. Except for cox1 started with CGA, all other PCGs started with the standard ATN codons. Most of the PCGs terminated with the stop codon TAA, whereas cox2 has the stop codon CAT. The phylogenetic tree showed that Larentiinae is close to Sterrhinae. The species of Ennominae form a monophyly.

14,15-Epoxyeicosatrienoic acid suppresses cigarette smoke condensate-induced inflammation in lung epithelial cells by inhibiting autophagy.

Epoxyeicosatrienoic acids (EETs) are metabolic products of free arachidonic acid, which are produced through cytochrome P-450 (CYP) epoxygenases. EETs have anti-inflammatory, antiapoptotic, and antioxidative activities. However, the effect of EETs on cigarette smoke-induced lung inflammation is not clear. Autophagy is believed to be involved in the pathogenesis of chronic obstructive pulmonary disease. In addition, nuclear erythroid-related factor 2 (Nrf2), a transcription factor that regulates many antioxidant genes, is thought to regulate antioxidant defenses in several lung diseases. In addition, interaction between EETs, autophagy, and Nrf2 has been reported. The aim of this study was to explore the effect of 14,15-EET on cigarette smoke condensate (CSC)-induced inflammation in a human bronchial epithelial cell line (Beas-2B), and to determine whether the underlying mechanisms involved in the regulation of Nrf2 through inhibition of autophagy. Autophagy and expression of autophagy signaling pathway proteins (LC3B, p62, PI3K, Akt, p-Akt, and p-mTOR) and anti-inflammatory proteins (Nrf2 and HO-1) were assessed via Western blot analysis. Autophagosomes and autolysosomes were detected by adenoviral mRFP-GFP-LC3 transfection. Inflammatory factors (IL-6, IL-8, and MCP-1) were detected by ELISA. Lentiviral vectors carrying p62 short hairpin RNA were used to interfere with p62 expression to evaluate the effect of p62 on Nrf2 expression. Nrf2 expression was determined through immunocytochemistry. 14,15-EET treatment resulted in a significant reduction in IL-6, IL-8, and MCP-1 secretion, and increased accumulation of Nrf2 and expression of HO-1. In addition, 14,15-EET inhibited CSC-induced autophagy in Beas-2B cells. The mechanism of the anti-inflammatory effect of 14,15-EET involved inhibition of autophagy and an increase in p62 levels, followed by translocation of Nrf2 into the nucleus, which then upregulated expression of the antioxidant enzyme HO-1. 14,15-EET protects against CSC-induced lung inflammation by promoting accumulation of Nrf2 via inhibition of autophagy.

The complete mitochondrial genome sequence of Hemibagrus nemurus (Siluriformes: Bagridae).

Hemibagrus nemurus (Valenciennes, 1840) is a kind of tropical freshwater catfish which is native to Asian waters. It is economically valued for its importance in fisheries and aquaculture. At present, there exist some confusion in species identification in Bagridae. In this paper, we sequenced and characterize the complete mitogenome of H. nemurus. The genome was 16,526 bp in length, and typically consists of 37 genes, including 13 protein-coding genes, 2 rRNAs, 22 tRNA, 1 origin of replication on the light-strand (OL) and a single large control region (CR). The gene organization is identical to that of a typical bony fish. The overall base composition was 31.5%, 26.6%, 26.7%, and 15.2% for A, T, C, and G, respectively, with a slight bias on AT content (58.1%). This result is expected to provide useful molecular data and contribute to further taxonomic and phylogenetic studies of Hemibagrus and Bagridae.

The complete mitochondrial genome of Carposina sasakii (Lepidoptera: Carposinidae).

The peach fruit moth, Carposina sasakii belongs to Carposinidae in Lepidoptera. In this paper, we described the complete mitogenome of C. sasakii. It is 15,611 bp in length, including 13 PCGs, 2 rRNAs, 22 tRNAs and a major noncoding A + T-rich region, which revealed the typical gene content found in other metazoan mitogenomes. The overall base composition is 42.0% A, 39.5% T, 7.75% G and 10.75% C. The A + T-rich region is located between rrnS and trnM. There is a motif ATAGA in downstream of rrnS followed by a 19 bp Poly-T stretch. The Poly-A is not found in upstream of trnM, and the position of Poly-A is replaced by a stem-loop structure. There are eight mononucleotide repeat sequences (Tn/An) with the length of 7 bp-19bp, three dinucleotide repeat sequences (TA)n/(AT)n, and a longer repeat sequence (AATATATA)5 in A + T-rich region. The mononucleotide repeat sequences occur repeatedly in A + T-rich reigion of C. sasakii, which is special in insects sequenced of Lepidoptera.

The complete mitochondrial genome sequence of Colossoma macropomum (Characiformes: Serrasalmidae).

Colossoma macropomum (Cuvier, 1816) is the largest characin of South America. This species and its congeners mainly feed on zooplankton, insects, snails and decaying plants. In this paper, we sequenced and annotated the complete mitogenome of C. macropomum. The total length is 16,703 bp, and it typically consist of 37 genes, including 13 protein-coding genes, two rRNAs, 22 tRNA, a light-strand replication origin (OL) and a large control region (D-loop). The overall base composition is 29.9%, 24.6%, 29.5% and 15.9% for A, T, C and G, respectively, with a slight bias on AT content (54.6%). All protein-coding genes share the start codon ATG, except for COI, which begins with GTG. Most of them have TAA or TAG as the stop codon, except COII, ND4 use AGA and COI, Cytb use an incomplete stop codon T. This information could provide useful molecular data and contribute to further phylogenetic studies of Characiformes and Serrasalmidae.

[Effect of WS070117M1 on chronic obstructive pulmonary disease in mice and the underling mechanisms of anti-inflammation].

The aim of this study is to investigate the anti-inflammatory effect of the adenosine derivative N6-(3-hydroxylaniline) adenosine (WS070117M1) on cigarette smoke plus LPS (lipopolysaccharide)-induced chronic obstructive pulmonary disease (COPD) in mice and its mechanism. COPD model was established by exposing male BALB/c mice to cigarette smoke and challenged with LPS inhalation. Supernatants of bronchoalveolar lavage fluid (BALF) were harvested and IL-1ß, IL-6, IL-8 and TGF-ß1 levels were measured by ELISA (enzyme-linked immunesorbent assay). The number of total white blood cells and neutrophils in bronchoalveolar lavage fluid was counted separately. Lung tissue was stained with Mayer 's hematoxylin and eosin for histopathologic examination. pAMPKa protein expression and distribution of lung tissue were analyzed by immunohistochemistry method. In vitro, levels of AMPKα phosphorylation in phorbol-12- myristate-13-acetate (PMA) differentiated THP-1 cells was detected by immunohistochemistry, IL-8 level in supernatants of cigarette smoke condensate stimulating PMA differentiated THP-1 cells was measured by ELISA. The results showed that WS070117M1 treatment significantly activated AMPKa in the lung tissue. It also resulted in down regulation of IL-1ß, IL-6, IL-8 and TGF-ß1 levels in bronchoalveolar lavage fluid and IL-8 level in cigarette smoke condensate stimulating PMA differentiated THP-1 cells. In addition, WS070117M1 could inhibit the recruitment of total white blood cells and neutrophils. These results suggest that WS070117M1 may alleviate the airway inflammation by activating AMPK in the lung tissue.

[Recent advances in the study of Nrf2 and inflammatory respiratory diseases].

Nuclear factor-erythroid 2 related factor 2 (Nrf2) is an ubiquitous and important transcription factor. It regulates antioxidant response elements (AREs)-mediated expression of antioxidant enzyme and cytoprotective proteins. A large body of research showed that Nrf2-Keap1 (Kelch-like ECH-associated protein 1, Keap 1)-ARE signaling pathway is involved in the endogenous antioxidant defense mechanisms. Nrf2 increases the expression of a number of cytoprotective genes, protects cells and tissues from the injury of a variety of toxicants and carcinogens. As a result, Nrf2 enhances the expression of glutathione and antioxidants such as superoxide dismutase and glutathione S-transferase, and subsequently scavenging free radicals. Air pollution especially from PM2.5 particles, is associated with an increasing morbidity of inflammatory pulmonary diseases and their deterioration. More and more studies demonstrated that Nrf2 was a novel signaling molecule in the modulation of inflammatory responses in these inflammatory respiratory diseases, such as asthma, acute lung injury (ALI) and COPD. Therefore, Nrf2 targeting might be a therapeutic target, which will provide clinical benefit by reducing both oxidative stress and inflammation in asthma, acute lung injury (ALI) and COPD. This review focused on the relationship between Nrf2 and inflammatory respiratory diseases and oxidative stress.

Novel nitric oxide-releasing derivatives of brusatol as anti-inflammatory agents: design, synthesis, biological evaluation, and nitric oxide release studies.

Brusatol, a biologically active natural product, was modified in four distinct positions through the covalent attachment of a furoxan moiety, which acts as a nitric oxide (NO) donor. Forty derivatives were synthesized and evaluated for their inhibitory effects on excess NO biosynthesis in activated macrophages. Among them, compound 75 demonstrated inhibition (IC50 = 0.067 µM) comparable to that of brusatol but were less cytotoxic. More importantly, even at very low doses (2 µmol/kg/day), compound 75 also showed substantial inhibitory efficacy against chronic obstructive pulmonary disease (COPD)-like inflammation in the mouse model induced by cigarette smoke (CS) and lipopolysaccharide (LPS). Particularly, this compound was over 100-fold less toxic (LD50 > 3852 µmol/kg) than brusatol and could be a promising lead for further studies. Notably, the improved properties of this derivative are associated with its NO-releasing capability.

Cancer in inflammatory bowel disease.

Patients with long-standing inflammatory bowel disease (IBD) have an increased risk of developing colorectal cancer (CRC). Many of the molecular alterations responsible for sporadic colorectal cancer, namely chromosomal instability, microsatellite instability, and hypermethylation, also play a role in colitis-associated colon carcinogenesis. Colon cancer risk in inflammatory bowel disease increases with longer duration of colitis, greater anatomic extent of colitis, the presence of primary sclerosing cholangitis, family history of CRC and degree of inflammation of the bowel. Chemoprevention includes aminosalicylates, ursodeoxycholic acid, and possibly folic acid and statins. To reduce CRC mortality in IBD, colonoscopic surveillance with random biopsies remains the major way to detect early mucosal dysplasia. When dysplasia is confirmed, proctocolectomy is considered for these patients. Patients with small intestinal Crohn's disease are at increased risk of small bowel adenocarcinoma. Ulcerative colitis patients with total proctocolectomy and ileal pouch anal-anastomosis have a rather low risk of dysplasia in the ileal pouch, but the anal transition zone should be monitored periodically. Other extra intestinal cancers, such as hepatobiliary and hematopoietic cancer, have shown variable incidence rates. New endoscopic and molecular screening approaches may further refine our current surveillance guidelines and our understanding of the natural history of dysplasia.

A critical role for the host mediator macrophage migration inhibitory factor in the pathogenesis of malarial anemia.

The pathogenesis of malarial anemia is multifactorial, and the mechanisms responsible for its high mortality are poorly understood. Studies indicate that host mediators produced during malaria infection may suppress erythroid progenitor development (Miller, K.L., J.C. Schooley, K.L. Smith, B. Kullgren, L.J. Mahlmann, and P.H. Silverman. 1989. Exp. Hematol. 17:379-385; Yap, G.S., and M.M. Stevenson. 1991. Ann. NY Acad. Sci. 628:279-281). We describe an intrinsic role for macrophage migration inhibitory factor (MIF) in the development of the anemic complications and bone marrow suppression that are associated with malaria infection. At concentrations found in the circulation of malaria-infected patients, MIF suppressed erythropoietin-dependent erythroid colony formation. MIF synergized with tumor necrosis factor and gamma interferon, which are known antagonists of hematopoiesis, even when these cytokines were present in subinhibitory concentrations. MIF inhibited erythroid differentiation and hemoglobin production, and it antagonized the pattern of mitogen-activated protein kinase phosphorylation that normally occurs during erythroid progenitor differentiation. Infection of MIF knockout mice with Plasmodium chabaudi resulted in less severe anemia, improved erythroid progenitor development, and increased survival compared with wild-type controls. We also found that human mononuclear cells carrying highly expressed MIF alleles produced more MIF when stimulated with the malarial product hemozoin compared with cells carrying low expression MIF alleles. These data suggest that polymorphisms at the MIF locus may influence the levels of MIF produced in the innate response to malaria infection and the likelihood of anemic complications.

The anemia of malaria infection: role of inflammatory cytokines.

Death from malaria occurs from the complications of the infection: cerebral manifestations leading to coma and a severe and refractory anemia leading to hypoxia and cardiac decompensation. Several mechanisms have been identified to play a role in the pathogenesis of malarial anemia, such as erythrocyte lysis and phagocytosis, and sequestration of parasitized red blood cells, but recent data indicate that these mechanisms (singly or in combination) do not adequately explain the severity of this anemia. By contrast, hematologic studies have shown that bone marrow suppression and ineffective erythropoiesis contribute importantly to the severe anemia of malaria infection. The host mechanisms responsible for suppression of erythropoiesis may involve an excessive or sustained innate immune response or a pathologic skewing of the T-cell differentiation response with the attendant production of certain proinflammatory cytokines. Experimental data also indicate that severe malarial anemia is associated with the immunologic expression of a circulating inhibitor of erythropoiesis that functionally antagonizes the action of erythropoietin. We review the clinical and experimental basis for these concepts and discuss ongoing experimental and genetic studies aimed at unraveling the molecular basis of this malaria-induced bone marrow suppression.