Societies and Academies


    LONDON. Royal Society, February 3.—Sir Archibald Geikie, K.C.B., president, in the chair.—F. D. Thompson: The thyroid and parathyroid glands throughout vertebrates.—Prof. E. A. Minchin and J. D. Thomson: The trans mission of Trypanosoma lewisi by the rat-flea (Ceratophyllus fasciatus). The experiments that form the subject of this communication are concerned essentially with the method of transmission and with questions connected there with. Incidentally, the fact of transmission is confirmed. All experiments were arranged so as to eliminate the possibility of infection other than by fleas, and to separate “direct” from “cyclical” infection. When preliminary experiments showed that infection, not “direct,” had taken place, further experiments were arranged to determine if fleas once infective retain infection so as to be capable of infecting a series of healthy clean rats without themselves being again exposed to infection, and at the same time to determine by direct observation and within narrow limits (1) the length of the incubation period in the flea, and (2) the length of the multiplication period in the rat. In all the experiments tame rats and fleas bred in captivity were used. The general arrangements and a detailed account of each experiment are given, but cannot be summarised briefly. A few observations on fleas dissected are recorded, and reference is made to Nuttall's experiments and conclusions. The following conclusions are drawn from the results of the experiments:—(1) The rat-flea (Ceratophyllus fasciatus) transmits T. lewisi from infected to non-infected rats. (2) Transmission takes place by the “cyclical” method. (3) Transmission by the “direct” method did not take place. (4) The incubation period in the flea has a minimum length of about six days, but may be longer. (5) The length of the multiplication period in the rat is about twelve days. (6) In the developmental cycle the establishment of the trypanosome in the flea begins with multiplication of Crithidia-like forms in the rectum. No flagellates have been found by the authors in any fleas which had not fed on infected rats.—Dr. F. Medigreceanu (Bucharest): The relative sizes of the organs of rats and mice bearing malignant new growths. The effects have been determined for rats and mice of the growth of transplanted carcinomata and sarcomata upon the weights of the principal organs of the body. The weights of the different organs of normal animals bear a relatively constant ratio to the total weight of the body. Weighing experiments on 200 mice and rats bearing trans planted tumours, and on four mice with spontaneous tumours, have shown (1) no disturbance of the normal ratio for the alimentary canal; (2) hypertrophy of the liver in all cases, and up to a certain point proportional to the weight of tumour; (3) hypertrophy of the heart, also in proportion to size of tumour; (4) no disturbance of normal ratio for the kidneys except in the case of a spindle-celled sarcoma, which induced hypertrophy; (5) varying ratios for the lungs. The most important result has been the discovery of an enlargement of the liver in animals bearing carcinomata and sarcomata, whether transplanted or naturally arising.—Dr. E. F. Bashford and Dr. B. R. G. Russell: Further evidence on the homogeneity, of the resistance to the implantation of malignant new growths. The principal object of the paper is to adduce further evidence that the resistance which animals already bearing transplanted tumours may offer to a second transplantation is identical in nature with the resistance offered by animals without tumours, after immunisation with normal or tumour tissue of the same species. A study of the processes at the site of the second implantation shows that, concomitantly with the establishment of the tumour developing from the first inoculation, an active resistance may be induced by the absorption of tumour tissue. Then the cancer cells implanted at the second inoculation fail to elicit the supporting connective tissue and vascular scaffolding necessary to their development into a tumour, and the process of resistance is exactly analogous to that previously described, when tumour tissue is implanted into mice after a preliminary immunisation with tumour or normal tissue of the same species. The assumption of a distinct form of resistance, “atreptic immunity,” is thereby rendered superfluous when tumour-bearing animals are resistant to a second inoculation. Prevailing conceptions of what constitutes immunity to cancer sensu strictiori are simplified further by experiments demonstrating that the active immunity to cancer which follows in rats after a preliminary inoculation of mouse cancer is not an immunity against cancer, but against the protein of a foreign species. Therefore hypotheses of cancer immunity, based upon a study of the behaviour of tumours in strange species, have at most only an indirect bearing upon the immunity to cancer of the same species. By actual observation of the processes occurring in animals immunised against the inoculation of cancer of their own species, only one form of induced resistance has been demonstrated to exist, consisting, so far as elucidated, in an inhibition of the chemiotactic powers the cancer cells normally exercise upon the connective tissue and vascular scaffolding of the host. This single explanation harmonises all the observed facts and rids the experimental study of cancer both of confusing hypotheses and of errors.—Dr. M. Haaland: The contrast in the reactions to the implantation of cancer after the inoculation of living and mechanically disintegrated cells. Inoculation of living tumour of normal tissue of the same species has been shown to induce resistance to subsequent transplantation of cancer. The present paper records experiments in which cancerous or normal tissues, after mechanical disintegration at -180° or 0° C., have been inoculated into mice. The experiments show that a complete disintegration of the cells entirely robs them of their immunising properties against a subsequent transplantation of cancer. There is no difference between tumour cells and normal cells in this respect. The absence of immunising power does not seem to be a question of dose of introduced material, because relatively enormous doses of dead material do not induce any resistance. In the same way the pressfluid, obtained from tumours and normal tissues by Buchner's press, is devoid of immunising properties. The immunising property is not bound up with the protein of the cell, but depends on a different principle. Living cells are necessary to induce resistance to transplantation of cancer. It seems necessary that these cells must not only remain alive, but also even grow for a certain time; without the fulfilment of these conditions the reaction inducing active resistance is not set up. The same consequences follow autolysis, the action of heat, radium, &c., upon tumour tissue and normal tissue. The reaction which the introduction of disintegrated cells calls forth is not only quantitatively different from that induced by living tissues, but also qualitatively different. Far from inducing any increased resistance, inoculation of disintegrated cells only seems to manure the soil for a subsequent growth of tumours. The failure to elicit the reactions of immunity to the transplantation of cancer by devitalised tissues reveals an important difference from the immunity reactions obtained against bacteria and their products and foreign proteids in general, in which cases the immunising properties are independent of the vitality of the organisms or cells.

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    Societies and Academies . Nature 82, 447–450 (1910).

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