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Abstract Background Many polycyclic aromatic hydrocarbons (PAHs) can cause DNA adducts and initiate carcinogenesis. Mixed exposures to coal dust (CD) and PAHs are common in occupational settings. In the CD and PAH-exposed lung, CD increases apoptosis and causes alveolar type II (AT-II) cell hyperplasia but reduces CYP1A1 induction. Inflammation, but not apoptosis, appears etiologically associated with reduced CYP1A1 induction in this mixed exposure model. Many AT-II cells in the CD-exposed lungs have no detectable CYP1A1 induction after PAH exposure. Although AT-II cells are a small subfraction of lung cells, they are believed to be a potential progenitor cell for some lung cancers. Because CYP1A1 is induced via ligand-mediated nuclear translocation of the aryl hydrocarbon receptor (AhR), we investigated the effect of CD on PAH-induced nuclear translocation of AhR in AT-II cells isolated from in vivo-exposed rats. Rats received CD or vehicle (saline) by intratracheal (IT) instillation. Three days before sacrifice, half of the rats in each group started daily intraperitoneal injections of the PAH, β-naphthoflavone (BNF). Results Fourteen days after IT CD exposure and 1 day after the last intraperitoneal BNF injection, AhR immunofluorescence indicated that proportional AhR nuclear expression and the percentage of cells with nuclear AhR were significantly increased in rats receiving IT saline and BNF injections compared to vehicle controls. However, in CD-exposed rats, BNF did not significantly alter the nuclear localization or cytosolic expression of AhR compared to rats receiving CD and oil. Conclusion Our findings suggest that during particle and PAH mixed exposures, CD alters the BNF-induced nuclear translocation of AhR in AT-II cells. This provides an explanation for the modification of CYP1A1 induction in these cells. Thus, this study suggests that mechanisms for reduced PAH-induced CYP1A1 activity in the CD exposed lung include not only the effects of inflammation on the lung as a whole, but also reduced PAH-associated nuclear translocation of AhR in an expanded population of AT-II cells.

The objective of this work was to study the impact of deficiency of certain macro and microelements on clinical, hematobiochemical and electrocardiographic changes in sheep. The survey study was carried out on a total of 300 sheep, of which 250 suffered from mineral deficiency and 50 apparent healthy were used as control. Clinical investigations of diseased sheep revealed change wool color, easily detached wool, alopecia, pale mucous membrane, and diarrhea. Clinical examination showed significant elevation (p< 0.05) of respiratory rate and heart rate. Hematological examination revealed significant (P<0.05) decrease in Hb, RBCs, WBCs and HCT, with increase in MCV, MCH. Biochemically, there was a statistically significant (P<0.05) decline in Ca, Mg, P, Cu, Zn, Se, Fe, TP and albumin, whereas ALT, ALP, LDH, cTnI, and creatinine levels increased significantly (P<0.05). Electrocardiographic examination showed different changes, including abnormal T-waves (wide and enlarged), premature ventricular depolarization and cardiac arrhythmia. It was concluded that macro-micro element deficiency is associated with clinical, biochemical, hematological and ECG alterations. In addition, they have been related to dysfunctions of internal organs including liver, heart and kidney. Therefore, it is recommended to prescribe a proper feeding management program containing the necessary macro- and micro elements for sheep flocks and do not rely only on the grazing as a main source of feed to maintain the health and production of sheep. [ABSTRACT FROM AUTHOR]

In this work, the effects of rotational and traverse speeds on the 1.5 mm butt joint performance of friction stir welded 2024-T4 aluminum alloy sheets have been investigated. Five rotational speeds ranging from 560 to 1800 rpm and five traverse speeds ranging from 11 to 45 mm/min have been employed. The characterization of microstructure and the mechanical properties (tensile, microhardness, and bending) of the welded sheets have been studied. The results reveal that by varying the welding parameters, almost sound joints and high performance welded joints can be successfully produced at the rotational speeds of 900 rpm and 700 rpm and the traverse speed of 35 mm/min. The maximum welding performance of joints is found to be 86.3% with 900 rpm rotational speed and 35 mm/min traverse speed. The microhardness values along the cross-section of the joints show a dramatic drop in the stir zone where the lowest value reached is about 63% of the base metal due to the softening of the welded zone caused by the heat input during joining. [ABSTRACT FROM AUTHOR]

Background: Many polycyclic aromatic hydrocarbons (PAHs) can cause DNA adducts and initiate carcinogenesis. Mixed exposures to coal dust (CD) and PAHs are common in occupational settings. In the CD and PAH-exposed lung, CD increases apoptosis and causes alveolar type II (AT-II) cell hyperplasia but reduces CYP1A1 induction. Inflammation, but not apoptosis, appears etiologically associated with reduced CYP1A1 induction in this mixed exposure model. Many AT-II cells in the CD-exposed lungs have no detectable CYP1A1 induction after PAH exposure. Although AT-II cells are a small subfraction of lung cells, they are believed to be a potential progenitor cell for some lung cancers. Because CYP1A1 is induced via ligand-mediated nuclear translocation of the aryl hydrocarbon receptor (AhR), we investigated the effect of CD on PAH-induced nuclear translocation of AhR in AT-II cells isolated from in vivo-exposed rats. Rats received CD or vehicle (saline) by intratracheal (IT) instillation. Three days before sacrifice, half of the rats in each group started daily intraperitoneal injections of the PAH, beta-naphthoflavone (BNF)., Results: Fourteen days after IT CD exposure and 1 day after the last intraperitoneal BNF injection, AhR immunofluorescence indicated that proportional AhR nuclear expression and the percentage of cells with nuclear AhR were significantly increased in rats receiving IT saline and BNF injections compared to vehicle controls. However, in CD-exposed rats, BNF did not significantly alter the nuclear localization or cytosolic expression of AhR compared to rats receiving CD and oil., Conclusion: Our findings suggest that during particle and PAH mixed exposures, CD alters the BNF-induced nuclear translocation of AhR in AT-II cells. This provides an explanation for the modification of CYP1A1 induction in these cells. Thus, this study suggests that mechanisms for reduced PAH-induced CYP1A1 activity in the CD exposed lung include not only the effects of inflammation on the lung as a whole, but also reduced PAH-associated nuclear translocation of AhR in an expanded population of AT-II cells.