The Journal of Pathology and Bacteriology

Our medical research library holds 6 studies published in The Journal of Pathology and Bacteriology (1947–1968). Each entry links to the study's record on PubMed and, where there is one, to the publisher's page and a free full text. 0 have an abstract, the authors' own summary as PubMed records it: open "Abstract" to read it. For 6 studies PubMed has no abstract for, we give the abstract printed in the article or, where there is none, a summary we wrote from it, each labeled as such.

About the journal

• Publisher: Oliver And Boyd
• Published: 1892–1968, England
• Language: English
• ISSN: 0368-3494 (print), 1555-2039 (electronic)
• Continued by: The Journal of Pathology
• Its record in the NLM Catalog

1960s

• The mechanism of formation of asbestos bodies. S.K. Botham, P.F. Holt. 1968;96(2):443-53. PubMed · Publisher

  Abstract

  Fibres of inhaled anthophyllite asbestos were found in the respiratory bronchioles of guinea-pigs 3 hr after the commencement of the inhalation period. After a further 3 hr, during which time the guinea-pigs inhaled no more asbestos dust, fibres were also found in the alveoli. The first pathological effect observed was haemorrhage from alveolar capillaries, which is followed by haemolysis of extravascular red cells and the formation of granules, which are iron-containing degradation products of haemoglobin (haemosiderin). These granules are found in macrophages together with a solubilised iron-containing product (? ferritin) diffusing throughout the cytoplasm. If the macrophage has also ingested asbestos fibres, the ferritin is then often adsorbed on to the asbestos. Almost invariably only one fibre becomes coated, this being usually the longest. Other fibres in the same macrophage remained uncoated for the duration of the experiment. The ferritin coating increases in thickness and, after about 4 wk, changes in the shape of the coating appeared. The cell meanwhile shrinks on to this structure, sometimes with rupture of the cell wall, and substances from the cytoplasm are adsorbed. The coating is first smooth, then corrugated and then it takes up a beaded form. After about 10 wk the structure becomes finely beaded and may begin to fragment.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

• A primary mesothelioma involving the rectovaginal septum and associated with beryllium. C. Gold. 1967;93(2):435-42. Case report PubMed · Publisher

  Abstract

  This paper describes an unusual case with serosal tumour deposits in the peritoneal cavity associated with a tumour, believed to be a mesothelioma, in the rectovaginal septum, and with a history of traumatic vaginal lesions repeatedly exposed by douching to hard water containing soluble beryllium compounds. Environmental contact with asbestos was a complicating factor. Analysis of the tumour tissue confirmed the presence of a significant amount of beryllium, which must be considered as a possible carcinogenic agent.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

• The mechanism of production of asbestos bodies from anthophyllite fibres. P.F. Holt, D.K. Young. 1967;93(2):696-9. PubMed · Publisher

  Abstract

  Histological studies of sections of guinea-pig lungs suggest that asbestos bodies are derived from the cytoplasm of macrophages that have attempted to ingest asbestos fibres. Proteins are probably adsorbed from the cytoplasm on to the asbestos and this leads to a shrinkage of the structure which produces corrugations or divides the structure into beads.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

• The early effects of chrysotile asbestos dust on the rat lung. P.F. Holt, J. Mills, D.K. Young. 1964;87:15-23. PubMed · Publisher

  Abstract

  Chrysotile dust of small particle size (<3 µm) rapidly produces fibrotic lesions in the lungs when inhaled by rats. It is suggested that asbestos is fibrogenic only when it can be ingested by phagocytes. The rapid fibrosis that can occur some years after asbestos has been inhaled by man may be due to the breakdown into large numbers of small fragments of fibres; these are then phagocytosed. Alternatively the small particles originally inhaled may act slowly and their effect may be enhanced by a superimposed infection.
  An apparatus that maintains an atmosphere containing small asbestos fibres at nearly constant concentration is described.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

• Histochemical demonstration of hyaluronic acid in pleural mesotheliomas. J.C. Wagner, D.E. Munday, J.S. Harington. 1962;84:73-8. PubMed · Publisher

  Abstract

  Diffuse pleural mesotheliomas secrete material that stains as an acid mucopolysaccharide and can be removed by prior digestion with either testicular or streptococcal hyaluronidase. Chemically, this material can be quantitatively precipitated by acetic acid, and its presence confirmed by prior treatment of pleural fluid with hyaluronidase. These methods have been used to differentiate between diffuse pleural mesothelioma and peripheral pulmonary adenocarcinoma, especially in asbestosis.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

1940s

• The effect of asbestos on tissue cultures; a comparative study with quartz and coal dust. T.H. Belt, I. Friedmann, E.J. King. 1947;59(1-2):159-64. PubMed · Publisher

  Abstract

  1. Phagocytosis, even of small particles of asbestos, took place slowly in tissue cultures and a considerable portion of the asbestos dust, approximately 50 per cent., remained untouched, though within range of phagocytes throughout the experiments. Compared with coal or quartz, asbestos was less readily phagocytosed, particle size being equal.
  2. Asbestos particles in small amount had little or no toxic effect on living cells in tissue cultures. The growth of fibroblasts was neither retarded nor accelerated and no necrosis of cells was observed as a result of contact with asbestos particles, while fatty change appeared to occur more slowly in asbestos phagocytes than in coal phagocytes.
  3. Asbestos particles underwent no visible change, and in particular no visible diminution in size, after having been ingested by phagocytes for as long as 5 weeks.
  4. The motility of wandering phagocytes was decreased after the ingestion of asbestos particles. This effect, not necessarily of a toxic character, may be deleterious in the case of cells within the lungs, since it tends to restrict the migration of cells and so favour the retention of particles within the lungs.
  5. Particles under 5 µm in length restricted cellular motility more than larger particles, for the reason that they were more readily phagocytosed. It would seem that wandering phagocytes are rarely able to ingest particles larger than 10 µm. Giant cells sometimes formed in tissue cultures, apparently by fusion of two or more ordinary phagocytes, and were then able to engulf larger particles or clusters of particles.
  6. There was no evidence of the formation of asbestos bodies in these experiments, nor have we noted the appearance of brown granular pigment like that seen in the lungs of experimental animals.

  PubMed has no abstract for this study. This is the authors' abstract, copied from the article.

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