Blood examinations in pulmonary fibrosis of haematite iron ore miners

Tubercle ◽  
1937 ◽  
Vol 19 (1) ◽  
pp. 8-18 ◽  
Author(s):  
J. Craw
1877 ◽  
Vol 4 (9) ◽  
pp. 406-410 ◽  
Author(s):  
Macdakin

The Ironstone Beds of Oolitic age in Lincolnshire have, during the last four years, yielded not only large quantities of brown hæmatite iron-ore, but some very interesting sections and borings, comprising thirty-one of the latter between four and seven miles to the south of Lincoln, and several extensive openings showing that the beds are much richer at this distance from Lincoln, but that they become very siliceous and pass into a ferruginous sand above Normanton about eighteen miles to the south.


1979 ◽  
Vol 40 (2) ◽  
pp. 213-232 ◽  
Author(s):  
L. A. Bursill ◽  
R. L. Withers
Keyword(s):  
Iron Ore ◽  

1871 ◽  
Vol 8 (81) ◽  
pp. 121-122 ◽  
Author(s):  
S. G. Perceval

On the 30th July last year I observed that a deposit of Websterite, subsulphate of alumina, had been cut into, in excavating for the new system of drainage in the Montpelier Road opposite the south end of Vernon Terrace. It occurs at a depthof 16 feet from the surface of the road, beneath a ferruginous deposit of varying depth, which overlies the chalk on the summit of the hill, consisting of ochreous clay with occasional flint-breccia and masses of hæmatite iron ore in some instances mammillated and associated with crystals of selenite. The iron ore is occasionally friable and of a cindery appearance, containing in its cavities angular pieces of chalk and occasional groups of crystals of selenite. The deposit of Websterite is about three feet wide at its junction with the overlying ferruginous mass, narrowing as it descends, apparently occupying a fissure in the chalk, which has at some time been filled with clay, or has been formed by some decomposing action on the chalk, the chalk intruding occasionally into the vein of Websterite. The mineral varies much in colour and appearance, consisting in some places of a soft white powder, which, I am informed by Sir W. C. Trevelyan, hehas observed in specimens at Newhaven, and which he has ascertained by the microscope to consist entirely of minute transparent crystals, the nature of which he believes has not yet been investigated; sometimes in masses of various size presenting the appearance of meerschaum, compact and structureless, or somewhat botryoidal in form, occasionally presenting a concentric structure, and rarely and only in a certain portion of the deposit exhibiting spherical concretions with a radiating structure. Specimens of these various forms I have presented to the British Museum. A mass of yellow clay with imbeddedchalk flints divides the summit of the vein of Websterite, and near the clay the mineral assumes the character of allophane, having a yellow ivory-like appearance, towards the chalk forming the wall of the vein of Websterite. The wall of the vein is marked by a dark line caused by the association of a soft black substance, oxide of manganese, with the Websterite.


Author(s):  
C. G. Plopper ◽  
C. Helton ◽  
A. J. Weir ◽  
J. A. Whitsett ◽  
T. R. Korfhagen

A wide variety of growth factors are thought to be involved in the regulation of pre- and postnatal lung maturation, including factors which bind to the epidermal growth factor receptor. Marked pulmonary fibrosis and enlarged alveolar air spaces have been observed in lungs of transgenic mice expressing human TGF-α under control of the 3.7 KB human SP-C promoter. To test whether TGF-α alters lung morphogenesis and cellular differentiation, we examined morphometrically the lungs of adult (6-10 months) mice derived from line 28, which expresses the highest level of human TGF-α transcripts among transgenic lines. Total volume of lungs (LV) fixed by airway infusion at standard pressure was similar in transgenics and aged-matched non-transgenic mice (Fig. 1). Intrapulmonary bronchi and bronchioles made up a smaller percentage of LV in transgenics than in non-transgenics (Fig. 2). Pulmonary arteries and pulmonary veins were a smaller percentage of LV in transgenic mice than in non-transgenics (Fig. 3). Lung parenchyma (lung tissue free of large vessels and conducting airways) occupied a larger percentage of LV in transgenics than in non-transgenics (Fig. 4). The number of generations of branching in conducting airways was significantly reduced in transgenics as compared to non-transgenic mice. Alveolar air space size, as measured by mean linear intercept, was almost twice as large in transgenic mice as in non-transgenics, especially when different zones within the lung were compared (Fig. 5). Alveolar air space occupied a larger percentage of the lung parenchyma in transgenic mice than in non-transgenic mice (Fig. 6). Collagen abundance was estimated in histological sections as picro-Sirius red positive material by previously-published methods. In intrapulmonary conducting airways, collagen was 4.8% of the wall in transgenics and 4.5% of the wall in non-transgenic mice. Since airways represented a smaller percentage of the lung in transgenics, the volume of interstitial collagen associated with airway wall was significantly less. In intrapulmonary blood vessels, collagen was 8.9% of the wall in transgenics and 0.7% of the wall in non-transgenics. Since blood vessels were a smaller percentage of the lungs in transgenics, the volume of collagen associated with the walls of blood vessels was five times greater. In the lung parenchyma, collagen was 51.5% of the tissue volume in transgenics and 21.2% in non-transgenics. Since parenchyma was a larger percentage of lung volume in transgenics, but the parenchymal tissue was a smaller percent of the volume, the volume of collagen associated with parenchymal tissue was only slightly greater. We conclude that overexpression of TGF-α during lung maturation alters many aspects of lung development, including branching morphogenesis of the airways and vessels and alveolarization in the parenchyma. Further, the increases in visible collagen previously associated with pulmonary fibrosis due to the overexpression of TGF-α are a result of actual increases in amounts of collagen and in a redistribution of collagen within compartments which results from morphogenetic changes. These morphogenetic changes vary by lung compartment. Supported by HL20748, ES06700 and the Cystic Fibrosis Foundation.


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