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In writing this report, two objects were kept in mind, (1) to explain, if possible, the origin of the chromite deposits found in Sweetgrass and Stillwater Counties, and (2) to bring up to date all information on these deposits which had thus far been available. The work done consisted of study of the rocks and ores of the area under the microscope, both as thin sections and as polished sections, practically all of which was done at the Montana State School of Mines, during the school year of 1928 - 1929. The rock specimens and much information as to their locations and probable compositions were obtained from Mr. P. F. Minister, of the East Butte Copper Company. United States Geological Survey Bulletin 725-A, Deposits of Chromite in California, Oregon, Washington, and Montana, and the unpublished report on the Chromite deposits of the Boulder River, prepared by Prof. C. H. Clapp of the University of Montana, were frequently referred to and considerable material was drawn from them. The map of the Boulder River area is from Clapp's report.

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Recent demands for petroleum to carry on the war effort have resulted in widespread prospecting in the northern Great Plains. Nearly all oil wells now drilled are of a depth to penetrate the marine Jurassic formations. It is known that these strata differ in thickness from place to place, but information of distribution, thickness, and lithology has not yet been compiled.

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Pennsylvanian strata in Wyoming and adjacent areas have been the subject of much work and discussion. Most of the work has been due to the economic importance of the system as an oil producer in this region. Oil production from strata of Pennsylvanian age is rather recent history; and therefore, much of the available information is local­ized and incomplete.

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The accelerated post-war demand for petroleum products with resultant high prices and dwindling reserves has spurred producers to an extensive search for new fields and for ad­ditional production in known fields. Exploration and discov­ery is dependent on the collection and correlation of vast amounts of data both in the field and that found in liter­ature.

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In the past few years intensive studies have been going on concerning Cambrian formations as a locale for orebodies. Many of the dolomites and limestones of southwestern Montana are susceptible to replacement by mineralizing solutions, especially when overlain by a rather impervious layer of shale, as is the Pilgrim limestone of Upper Cambrian time.

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Oil and gas have been found in the Triassic strata of Wyoming. Although the Triassic has not as yet proven to be a large producing horizon it is very probable that ad­ditional oil will be found in Triassic strata in the future, and it is one of the goals at which oil well drillers aim their tools.

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OBJECTIVE: Mitogen-activated protein kinases (MAPKs), including JNK, p38, and ERK1/2, noticeably influence ischemia/reperfusion injury (IRI). The complement inhibitor dextran sulfate (DXS) associates with damaged endothelium denudated of its heparan sulfate proteoglycan (HSPG) layer. Other glycosaminoglycan analogs are known to influence MAPK signaling. Hypothetically therefore, targeted intravascular cytoprotection by DXS may function in part through influencing MAPK activation to reduce IRI-induced damage of the vasculature. METHODS: IRI of the infrarenal aorta of male Wistar rats was induced by 90 minutes clamping followed by 120 minutes reperfusion. DXS (5 mg/mL) or physiologic saline (NaCl controls) was infused locally into the ischemic aortic segment immediately prior to reperfusion. Ninety minutes ischemia-only and heparinase infusion (maximal damage) experiments, as well as native rat aorta, served as controls. Aortas were excised following termination of the experiments for further analysis. RESULTS: DXS significantly inhibited IRI-induced JNK and ERK1/2 activation (P = .043; P =.005) without influencing the p38 pathway (P =.110). Reduced aortic injury, with significant inhibition of apoptosis (P = .032 for DXS vs NaCl), correlated with decreased nuclear factor kappaB translocation within the aortic wall. DXS treatment clearly reduced C1q, C4b/c, C3b/c, and C9 complement deposition, whilst preserving endothelial cell integrity and reducing reperfusion-induced HSPG shedding. Protection was associated with binding of fluorescein labeled DXS to ischemically damaged tissue. CONCLUSIONS: Local application of DXS into ischemic vasculature immediately prior to reperfusion reduces complement deposition and preserves endothelial integrity, partially through modulating activation of MAPKs and may offer a new approach to tackle IRI in vascular surgical procedures. CLINICAL RELEVANCE: The purpose of the present study was to determine the role of dextran sulfate (DXS), a glycosaminoglycan analog and complement inhibitor, in modulating intracellular MAPK signaling pathways, reducing complement activation and ultimately attenuating ischemia/reperfusion injury (IRI) in a rat aortic-clamping model, in part a surrogate model to study the microvasculature. The study shows a role for DXS in ameliorating endothelial injury by reducing IRI-mediated damage and intravascular, local inflammation in the affected aortic segment. DXS may be envisaged as an endothelial protectant in vascular injury, such as occurs during vascular surgical procedures.

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