Archives of Internal Medicine

SMITH, FRED M.

doi: 10.1001/archinte.1927.00130090030002pmid: N/A

Abstract Experimental ligation of the coronary arteries1 and observations on man following the occlusion of these vessels2 have demonstrated that the heart is extremely sensitive to a reduction in its blood supply. It would seem that a knowledge of the factors concerned in the regulation of the coronary circulation is important for a better understanding of impaired cardiac function. It is possible that a further study of this subject may furnish an explanation for the cause of cardiac failure in certain instances which are at present obscure and may perhaps suggest a more satisfactory means of treatment. The present report is concerned with studies of certain features of the coronary circulation in which the author has been interested during the last three years. INFLUENCE OF THE VAGI AND SYMPATHETIC NERVES ON THE CORONARY ARTERIES The action of the vagi and sympathetic nerves on the coronary arteries has been more extensively investigated References 1. Miller and Mathews: Effect on the Heart of Experimental Obstruction of the Left Coronary Artery , Arch. Int. Med. 3:476 ( (June) ) 1909.Crossref 2. Smith, F. M.: The Ligation of Coronary Arteries with Electrocardiographic Study , Arch. Int. Med. 22:8 ( (July) ) 1918.Crossref 3. Herrick, J. B.: Clinical Features of Sudden Obstruction of the Coronary Arteries , J. A. M. A. 59:2015 ( (Dec. 7) ) 1912Crossref 4. Thrombosis of Coronary Arteries , Herrick J. A. M. A. 72:387 ( (Feb. 8) ) 1919.Crossref 5. Lagendorff: Zentralbl. f. Physiol. 21:551, 1907. 6. Cow: J. Physiol. 42: 125, 1911. 7. Eppinger and Hess: Ztschr. f. exper. Path. u. Therap. 5:622, 1909.Crossref 8. Barbour: J. Exper. Med. 15:404, 1912.Crossref 9. Park: J. Exper. Med. 17:532, 1912.Crossref 10. Ishihara: Fuknoka-Ilwadaigaku-Zasshi. 14:3, 1921. 11. Barbour (footnote 3, fourth reference). 12. Cow (footnote 3, second reference). 13. Krogh; J. Physiol. 53:399, 1919-1920 14. Krogh J. Physiol. 55:412, 1921 15. The Anatomy and Physiology of Capillaries , Yale University, New Haven, 1922. 16. Wiggers: Am. J. Physiol. 24:391, 1909. 17. Smith, Miller and Graber: J. Clin. Investigation 2:157, 1925.Crossref 18. Brodie and Cullis: J. Physiol. 43:313, 1911-1912. 19. Sassa: Arch. f. d. ges. Physiol. 198:543, 1923.Crossref 20. Drury and Sumbal: Heart . 10:267, 1924. 21. Atzler and Frank: Arch. f. d. ges. Physiol. 181:144, 1920.Crossref 22. Morowitz and Zahn: Zentralbl. f. Physiol. 26:465, 1912 23. Deutsches. Arch. f. klin. Med. 116:364, 1914. 24. Sassa (footnote 10). 25. Smith, Miller and Graber: Relative Importance of Systolic and Diastolic Blood Pressure in Maintaining Coronary Circulation , Arch. Int. Med. 38:109 ( (July) ) 1926.Crossref 26. Markwalder and Starling: J. Physiol. 47:275, 1913-1914. 27. Nakagawa: J. Physiol. 56:340, 1922. 28. Anrep: Physiol. Rev. 6:596, 1926. 29. Barbour and Prince: J. Exper. Med. 21:330, 1915.Crossref 30. Bond: J. Exper. Med. 12:575, 1910.Crossref 31. Schafer: Zentralbl. f. Physiol. 19:218, 1905-1906. 32. Wiggers (footnote 7). 33. Meyer: Arch. f. Anat. u. Physiol. 1912, p. 223. 34. Morowitz and Zahn (footnote 13). 35. Wiggers (footnote 7). 36. Markwalder and Starling (footnote 15, first reference). 37. Drury and Smith: Heart 11:71, 1924. 38. Sumbal: Heart 11:285, 1924. 39. Smith, Miller and Graber: Am. J. Physiol. 77:1, 1926 40. Hunt and DeM. Taveau: Brit. M. J. 2:1788, 1906.Crossref 41. Dale: J. Pharmacol. & Exper. Therap. 6:147, 1914. 42. Hunt: Am. J. Physiol. 45:197, 1918. 43. Hunt (footnote 22, third reference). 44. Nakagawa (footnote 15, second reference). 45. Herlitzka: Tigerstadt Physiologie des Kreislaufes , Berlin, 1921, vol. 1, p. 319. 46. Langendorff: Arch. f. d. ges. Physiol. 78:423, 1899. 47. Porter: Am. J. Physiol. 1:141, 1898. 48. De Barenne: Arch. f. d. ges. Physiol. 177:217, 1919. 49. Smith, Miller and Graber (footnote 14, second reference). 50. Miyaka, quoted by Anrep (footnote 15, third reference). 51. Anrep (footnote 15, third reference). 52. Hammouda and Kinosita, quoted by Anrep (footnote 15, third reference). 53. Smith, Miller and Graber: Unpublished work. 54. Hedbom: Skandin. Arch. f. Physiol. 9:1, 1899. 55. Loeb: Arch f. exper. Path. u. Pharmakol. 51:64, 1903-1904. 56. Heathcot: J. Pharmacol. & Exper. Therap. 16:327, 1920. 57. Sakai and Saneyoshi: Arch. f. exper. Path. u. Pharmakol. 78:331, 1914-1915. 58. Guggenheimer and Sassa: Klin. Wchnschr. 2:1451, 1923.Crossref

OKADA, SEIZABURO;SAKURAI, EIICHI;IBUKI, TSUKIO;KABESHIMA, HARUTOSHI

doi: 10.1001/archinte.1927.00130090041003pmid: N/A

Abstract The basal metabolism in vitamin B starvation has been much discussed by various workers in recent years. The earliest article now available to us is that of Caspari and Moszkowski.1 After practical experience during research in New Guinea, Moszkowski concluded that the so-called beriberi of man is a disease of metabolism essentially due to the ingestion of polished rice, a view which was contradicted by other workers. To verify this opinion, Moszkowski offered to make experiments on himself. He was kept under observation by Caspari and others. About a month after the beginning of the rice diet, clinical symptoms began to appear, which eventually became significant. The chief symptoms were: general wandering neuralgia, tenderness of the muscles and skin, especially of the calf muscles, Lasègue's symptom, paresthesia and numbness of the hands and feet, weakness and somnolence, a sense of restriction in the chest, lability of the pulse, edema of References 1. Caspari, W., and Moszkowski, M.: Weiteres zur Beriberi-Frage , Berl. klin. Wchnschr. 50:1515, 1913. 2. Ramoino, P.: Contributo allo studio delle alimentazioni incomplete. Pathologica 7:101, 1915. 3. Abderhalden, E., and Schmidt, L.: Weitere Beiträge zur Kenntnis von organischen Nahrungsstoffen mit spezifischer Wirkung; III. Mitteil. , Pflüger's Arch. f. d. ges. Physiol. 185:141, 1920.Crossref 4. Abderhalden, E.: IV. Mitteil. , Pflüger's Arch. f. d. ges. Physiol. 187: 80, 1921Crossref 5. V. Mitteil. , Abderhalden Pflüger's Arch. f. d. ges. Physiol. 188:60, 1921.Crossref 6. Abderhalden, E., and Wertheimer, E.: VII. Mitteil. , Pflüger's Arch. f. d. ges. Physiol. 191:258, 1921.Crossref 7. Abderhalden, E.: VIII. Mitteil. , Pflüger's Arch. f. d. ges. Physiol. 191: 278, 1921Crossref 8. IX. Mitteil. , Abderhalden Pflüger's Arch. f. d. ges. Physiol. 192:163, 1921.Crossref 9. Abderhalden, E., and Wertheimer, E.: X. Mitteil. , Pflüger's Arch. f. d. ges. Physiol. 192:174, 1921Crossref 10. XIII. Mitteil. , Abderhalden Pflüger's Arch. f. d. ges. Physiol. 194:647, 1922Crossref 11. XVII. Mitteil. , Abderhalden Pflüger's Arch. f. d. ges. Physiol. 195:460, 1922.Crossref 12. Hess, W. R.: Die Rolle der Vitamine im Zellmechanismus , Ztschr. f. phys. Chem. 117:284, 1921. 13. Hess, W. R., and Messerle, N.: Untersuchungen über die Gewebeatmung bei Avitaminose , Ztschr. f. phys. Chem. 119:176, 1922. 14. Anderson, R. J., and Kulp, W. L.: A Study of the Metabolism and Respiratory Exchange in Poultry During Vitamin Starvation and Polyneuritis , J. Biol. Chem. 52:69, 1922. 15. Kinoshita, R.: Ueber den Gaswechsel bei der Reiskrankheit des Geflügers , Tr. Japanese Path. Soc. 12:186, 1922. 16. Okada, S.; Sakurai, E.; Ibuki, T., and Kabeshima, H.: On the Basal Metabolism in Vitamin B Starvation and in Beriberi , Ikai Jiho no. (1479) (Nov. 4) 1922 17. Japan M. World. 3:102 ( (May 15) ) 1923. 18. Groebbels, F.: Studien über das Vitaminproblem: I. Mitteil., Untersuchungen über das Gasstoffwechsel avitaminotisch ernährter weisser Mäuse , Ztschr. f. phys. Chem. 122:104, 1922Crossref 19. Klin. Wchnschr. 1548, 1922 20. II. Mitteil., Untersuchungen über den Einfluss der Vitaminzufuhr und des Hungerns auf Gasstoffwechsel, Gewicht und Lebensdauer vitaminfrei ernährter weisser Mäuse , Ztschr. f. phys. Chem. 131:214, 1923Crossref 21. III. Mitteil., Weitere Untersuchungen über den Einfluss der Vitaminzufuhr auf Gaswechsel, Gewicht und Lebensdauer vitaminfrei ernährter weisser Mäuse , Ztschr. f. phys. Chem. 137:14, 1924.Crossref 22. Knipping and Kowitz: Untersuchungen über die Avitaminose beim Menschen , München. med. Wchnschr. 70:46 ( (Jan. 12) ) 1923. 23. Magne, H., and Simonnet, H.: Sur les variations du quotient respiratoire chez le pegeon carencé , Bull. Soc. de chem. biol. 4:419, 1922. 24. Bickel, A.: Das Wesen der Avitaminose. Nach experimenteller Untersuchungen über die Abmagerungsform dieser Krankheit , Biochem. Ztschr. 146: 493, 1924 25. Weitere Untersuchungen über den Stoffwechsel bei der Avitaminose , Bickel Biochem. Ztschr. 166:251, 1925. 26. Yanagi, K.: The Oxygen Consumption in Vitamin B. Starvation , Nippon Naika Gakukwai Zasshi 13:189, 1925 27. Nippon Seikagakukai Kaiho 1:50, 1926. 28. Goh, T.: Nippon Byori Gakukwai Kaishi , 15:469, 1926. 29. Odaira, T.: Nissin Igaku , 15:1659, 1926.

KESSEL, LEO;HYMAN, HAROLD THOMAS

doi: 10.1001/archinte.1927.00130090063004pmid: N/A

Abstract In a previous article1 on exophthalmic goiter and the involuntary nervous system, we have recorded our observations on fifty unselected patients studied for two years. The following excerpt taken from this article will explain the system we followed in making our observations. In January, 1921, we instituted a study of fifty unselected cases of fully developed exophthalmic goiter.2 No specific therapeutic measures were employed "in order to determine the natural history (spontaneous course) of the disease,"3 and to establish an "index for the evaluation of therapeutic procedures."4 From the group were excluded (a) patients who had thyroid enlargement without other manifestations of exophthalmic goiter,5 and (b) those who, with or without thyroid enlargement, presented sympathomimetic symptoms, without significant elevation of the basal metabolism (autonomic imbalance).6 In the group studied, we included (1) patients with a significant elevation of metabolism on repeated readings; (2) patients whose illness was sufficiently severe to References 1. Hyman, H. T., and Kessel, Leo.: A Study of Exophthalmic Goiter and the Involuntary Nervous System , Arch. Surg. 8:149 ( (Jan.) ) 1924.Crossref 2. Kessel, Leo; Hyman, H. T., and Lande, Herman: A Study of Fifty Consecutive Cases of Exophthalmic Goiter , Arch. Int. Med. 31:433 ( (March) ) 1923.Crossref 3. Lieb, C. C.; Kessel, Leo, and Hyman, H. T.: Am. J. M. Sc. 165:384 ( (March) ) 1923.Crossref 4. Kessel, Leo; Hyman, H. T., and Lieb, C. C.: Exophthalmic Goiter and Involuntary Nervous System; Clinical and Laboratory Study of Involuntary Nervous System , J.A.M.A. 79:1213 ( (Oct. 7) ) 1922.Crossref 5. Kessel, Leo and Hyman, H. T.: Am. J. M. Sc. 165:387 ( (March) ) 1923.Crossref 6. Kessel, Leo and Hyman, H. T.: Am. J. M. Sc. 165:513 ( (April) ) 1923.Crossref 7. "1. Almost without exception, no patient in this series received iodid during the first month of observation and rarely within the first six weeks, during which time the greatest improvements were noted. 2. The administration of the iodids was not accompanied by any marked alteration in the rate of improvement in our experience: when benefit accompanied the exhibition of the drug, it was unusual to observe any changes other than a continuation of the amelioration of symptoms noted in the preceding weeks." There was no other routine medication. No purposeful psychotherapy was employed, but the patients were shielded, as far as possible, from psychic trauma, and attempts were made to adjust their social and economic difficulties. 8. Plummer, H.: Tr. A. Am. Phys. 1916, p. 138. 9. Graham, Allen: Exophthalmic Goiter and Toxic Adenoma , J. A. M. A. 87:628, ( (Aug. 28) ) 1926.Crossref 10. The readings of the basal metabolic rate have been made on the Roth-Collins machine by Dr. Herman Lande and his assistant, Miss A. K. Steiner. 11. Since the writing of this article, we were fortunately able to secure another basal metabolic rate on this patient on Jan. 18, 1927, when, with adequate cooperation from the patient, her rate was recorded at plus 17 per cent. 12. Since the writing of this article, the patient has reported for observation, and her basal metabolic rate is plus 4 per cent in the fifty-ninth month. 13. The majority of these patients were delivered by Dr. C. F. Jellinghaus at the Lying-In Hospital in New York.

RAPHAEL, THEOPHILE;SEARLE, OLIVE M.;HORAN, TOM N.

doi: 10.1001/archinte.1927.00130090077005pmid: N/A

Abstract Recently added emphasis has been given to the importance of the constitutional factor in disease through the work of Draper,1 Kretschmer2 and others. The work of these men has been based largely on structural or morphologic observations. It was felt that an approach to this problem from the standpoint of the basic physiologic pattern, as suggested by Draper, might also prove of interest. With this in view, a study of the distribution of the blood grouping was made in a series of tuberculous subjects, blood type being generally regarded as an outstanding constitutional quality, and tuberculosis as representing a somatic disorder of traditionally important genotypic relationship. The only previous work appearing in the literature is that of Alexander,3 who studied fifty cases with apparently negative results. Obviously, however, such a series is too small to warrant a valid conclusion. The series utilized in this study was comprised of 400 cases, References 1. Draper, G.: Human Constitution , Philadelphia, W. B. Saunders Co., 1924. 2. Kretschmer, E.: Körperbau u. Charakter , Berlin, Springer, 1921. 3. Alexander, W.: An Inquiry Into the Distribution of the Blood Groups in Patients Suffering from "Malignant Disease," Brit. J. Exper. Path. 2:66 ( (April) ) 1921. 4. Ottenberg, R.: A Classification of Human Races Based on Geographic Distribution of the Blood Groups , J. A. M. A. 84:1393 ( (May 9) ) 1925.Crossref 5. Moss, W. L.: A Simplified Method for Determining the Isoagglutinin Group in the Selection of Donors for Blood Transfusion , J. A. M. A. 68:1905 ( (June 23) ) 1917.Crossref 6. Sanford, A. H.: Blood Transfusion: Indications for Its Use, Methods of Selecting Donors and a Brief Consideration of Technic , M. Clin. N. Amer. 3:801 ( (Nov.) ) 1919. 7. Culpepper, W. L., and Ableson, M.: Report on Five Thousand Bloods Typed Using Moss's Grouping , J. Lab. & Clin. Med. 6:276 ( (Feb.) ) 1921. 8. Pinner, Max (Detroit Municipal Sanatorium) Personal Communication. 9. Guthrie, C. G., and Huck, J. G.: On the Existence of More than Four Isoagglutinin Groups in Human Blood , Bull. Johns Hopkins Hosp. 34:37, 80, 128 ( (Feb.) , March, April) 1923.

WILLIUS, FREDERICK A.;KILLINS, WENDELL A.

doi: 10.1001/archinte.1927.00130090081006pmid: N/A

Abstract The increasing use of the electrocardiograph in the clinical study of heart disease has brought forth many valuable graphic signs in the identification and the corroboration of myocardial disease, and also important facts bearing on prognosis. From time to time various observers have called attention to the relationship of electrocardiograms of low voltage to disease of the myocardium (Carter,1 Pardee and Master,2 Lutembacher,3 White and Burwell,4 Clerc and Bascourret,5 Oppenheimer and Rothschild6). Low voltage electrocardiograms have been recorded in patients with pericardial effusions, returning to normal after paracentesis and subsequent improvement in the patient's condition. Oppenheimer and Mann7 also called attention to them in connection with extensive pericardial and pleuropericardial effusions. The occurrence of low voltage records in myxedema and cretinism has been described by Zondek8 and by Thacher and White.9 A recent report by Sprague and White10 was based on fifty-seven cases observed during eleven years at the Massachusetts References 1. Carter, E. P.: Further Observations on the Aberrant Electrocardiogram Associated with Sclerosis of the Atrioventricular Bundle Branches and Their Terminal Arborization , Arch. Int. Med. 22:331 ( (Sept.) ) 1918.Crossref 2. Pardee, H. E. B., and Master, A. M.: Electrocardiograms and Heart Muscle Disease , J. A. M. A. 80:98 ( (Jan. 13) ) 1923.Crossref 3. Lutembacher, R.: The Heart in Hypertension , Bull. méd. 31:616, 1922. 4. White, P. D., and Burwell, C. S.: The Clinical Significance of Changes in the Form of the Electrocardiogram , M. Clin. N. Amer. 4:1839, 1920-1921. 5. Clerc, A., and Bascourret, M.: Les anomalies des complexes ventriculaires electriques et leur importance pronostique dans le cours de l'insuffisance cardiaque , Rev. de med. 41:587, 1924. 6. Oppenheimer, B. S., and Rothschild, M. A.: The Value of the Electrocardiogram in the Diagnosis and Prognosis of Myocardial Disease , Tr. A. Am. Phys. 39:247, 1924. 7. Oppenheimer, B. S., and Mann, Hubert: An Electrocardiographic Sign in Pericardial Effusion , Proc. Soc. Exper. Biol. & Med. 20:431, 1923. 8. Zondek, Hermann: Das Myxodemherz , München. med. Wchnschr. 65: 1180, 1918. 9. Thacher, C., and White, P. D.: The Electrocardiogram in Myxedema , Am. J. M. Sc. 171:61, 1926. 10. Sprague, H. B., and White, P. D.: The Significance of Electrocardiograms of Low Voltage , J. Clin. Investigation 3:109, 1926.

FRIED, B. M.

doi: 10.1001/archinte.1927.00130090089007pmid: N/A

Abstract Primary carcinoma of the lungs has become a clinical and pathologic entity of importance only in the last two decades. The pathologist of the nineteenth century was apparently under the influence of Virchow's statement to the effect that those organs which are frequently the seat of a metastatic involvement by malignant tumors are only in rare instances the seat of a primary new growth. The lungs were usually quoted as an example. Since from the circulatory point of view these organs are the convergent point of the body, malignant cells which happened to invade the blood or lymph streams invariably reach the lungs, where they form secondary nodules or masses, the latter not infrequently overshadowing that of the primary growth. Moreover, the failure of the pathologist to demonstrate grossly a secondary involvement of the lung by tumor is at present not regarded as being conclusive proof of the actual absence References 1. Schmidt, M. B.: Verbreitungswege der Carcinoma , Jena, 1903. 2. Goldmann, E. E.: Studien zur Biologie der Bösartigen Neubildungen , Beitr. z. klin. Chir. 72:1, 1911. 3. Lubarsch, O.: Einiger zur Sterblichkeits-und Leichenöffungs-statistik , Med. klin. 10:299 ( (March 9) ) 1924. 4. Seyfarth: Lungenkarzinome in Leipzig , Deutsche med. Wchnschr. 50:1497 ( (Oct. 31) ) 1924.Crossref 5. Kikuth, W.: Ueber Lungencarzinome , Virchows Arch. f. path. Anat. 255: 107, 1925.Crossref 6. Breckwoldt, Richard: Zur Frage der Zunahme der Lungenkrebse , Ztschr. f. Krebsforsch. 23:122, 1926.Crossref 7. Fuchs: Beitr. z. Kenntnis des Primären Geschwülstbildungen in der Lunge, Inaug. Dissert., Munich, 1886. 8. Pässler, H.: Ueber das Primäre Carcinome der Lunge , Virchows Arch. f. path. Anat. 146:191, 1896.Crossref 9. Wells, G. H.: Relation of Clinical to Necropsy Diagnosis in Cancer and Value of Existing Cancer Statistics , J. A. M. A. 80:737 ( (March 17) ) 1923Crossref 10. Cancer Statistics as they Appear to Pathologist , Wells J. A. M. A. 192388:399 ( (Feb. 5) )Crossref 11. 476 (Feb. 12) 1927. 12. Hanf, Dora: Zur Frage der Zunahme der Lungenkrebse in den letzten Jahren , Virchows Arch. f. path. Anat. 264:366, 1927.Crossref 13. Staehelin, R.: Ueber die Zunahme des Primären Lungenkrebses , Klin. Wchnschr. 4:1853 ( (Sept. 24) ) 1925.Crossref 14. Renaut, A.: Einige Belege und Betrachtungen zur Verbreitung und Statistik der Krebses, etc. , Schweiz. med. Wchnschr. 56:106 ( (Feb. 6) ) 15. 132 (Feb. 13) 1926. 16. Carrière, quoted by Imbert: L'augmentation du frequence du cancer est-elle reelle ou apparent? Bull. de l'assoc. franc, pour l'étude du cancer 15:141 ( (April) ) 1926. 17. Ménétrier, M. P.: La frequence du cancer , Bull. Acad. de méd. 95:177 ( (Feb. 23) ) 1926. 18. Thomas, B. A.: The Influence of Urology on Longevity , J. A. M. A. 86:1957 ( (June 26) ) 1926.Crossref 19. Apert, E.: La mort recule , Rev. de deux mondes , 27:121 ( (May) ) 1925. 20. Grove, J. S., and Cramer, S. E.: Primary Carcinoma of the Lungs , Am. J. M. Sc. 151:250, 1926.Crossref 21. Camp, de la, O.: Zur Klinik der Primären Bronchial Karzinom , Med. Klin. 20:1270, 1924. 22. Rist, E.: La differentiation clinique de la tuberculose pulmonaire d'avec les autres affections de voie respiratoires , Rev. de la tuberc. 4:125, 1926. 23. Graham, E. A.: The Surgical Treatment of Pulmonary Suppuration in Children , J. A. M. A. 87:806 ( (Sept. 11) ) 1926.Crossref 24. Fried, B. M.: Primary Carcinoma of the Lungs , Arch. Int. Med. 35:1 ( (Jan.) ) 1925.Crossref 25. Letulle, M.: Le poumon , Paris, A. Maloine et Fils, éditeurs, 1924. 26. footnote 18. 27. Letulle and Jacquelin ( Les "embolies bronchiques" cancereuses , Presse méd. 32:825, 1924) 28. Lubarsch, O.: Geschwülste. Blutferänderungen bei Carcinom. Ergebn. d. Allg. Path. 2:566, 1895 29. Uber destruirendes Wachstum und Bösartigkeit der Geschwülste , Ztschr. f. Krebsforsch. 5:114, 1907.Crossref 30. Fried, B. M.: Primary Carcinoma of the Liver , Am. J. M. Sc. 168:24 ( (Aug.) ) 1924.Crossref 31. Kitain, H. L.: Zur Kenntnis der Häufigkeit und der Localization von Krebsmetastasen, etc. , Virchows Arch. f. path. Anat. 238:288, 1922.Crossref 32. Pentimalli, F.: Ueber Metastasenbildung beim Hünersarcom , Ztschr. f. Krebsforsch. 22:64, 1924. 33. Haaland, M.: Die Metastasenbildung bei transplantierten Sarkomen der Maus , Ztschr. f. Krebsforsch. 5:122, 1907.Crossref 34. Dosquet: Ueber die Metastasenbildung bei Primären Lungen und Bronch. Krebses , Virchows Arch. f. path. Anat. 234:481, 1921.Crossref 35. Footnote 1 (first reference). 36. Footnote 1 (second reference). 37. Stern, A.: Das Schicksal eingeschwemmter Geschwülstzellen in der Lunge , Virchows Arch. f. path. Anat. 241:219, 1923.Crossref 38. Burrows, M. T.: The Mechanism of Cancer Metastasis , Arch. Int. Med. 37:454 ( (April) ) 1926.Crossref 39. Ewing, J.: Neoplastic Diseases , ed. 2-d., 1922, p. 86. 40. Grant, F. C.: Concerning Intracranial Malignant Metastases , Ann. Surg. 84:635, 1926. 41. Fishberg, Maurice: Diagnosis of Pulmonary Neoplasm , Arch. Int. Med. 37:445 ( (June) ) 1926.Crossref

NUZUM, FRANKLIN R.

doi: 10.1001/archinte.1927.00130090113008pmid: N/A

Abstract This paper is concerned with the changes found in the kidneys of three groups of rabbits that had been fed high protein diets for periods as long as twenty-four months. Many of the animals developed an increased blood pressure and clinical evidence of kidney injury.1 This evidence consisted first of albumin and casts in the urine, later of an increase of the nonprotein nitrogen and urea nitrogen of the blood and finally of a decrease of carbon dioxide of the blood plasma. The routine procedure in experiments were as follows: Forty-eight carefully selected young rabbits were placed in individual metabolism cages. None of these animals had a spontaneous nephritis or a systolic blood pressure higher than 74 of mercury. The cages were kept out doors the year around. The blood pressures were obtained once each month by a method previously described.2 At monthly intervals also, twenty-four hour samples of the References 1. Nuzum, F. R.; Osborne, Margaret, and Sansum, W. D.: The Experimental Production of Hypertension , Arch. Int. Med. 35:492 ( (April) ) 1925.Crossref 2. Nuzum, F. R.; Seegal, Beatrice; Garland, Ruth, and Osborne, Margaret: Arteriosclerosis and Increased Blood Pressure, Experimental Production , Arch. Int. Med. 37:733 ( (June) ) 1926.Crossref 3. Folin, O. F., and Wu, H.: A System of Blood Analysis , J. Biol. Chem. 38:81, 1919. 4. Van Slyke, W. D., and Cullen, G. E.: The Bicarbonate Concentration of the Blood Plasma; Its Significance, and Its Determination as a Measure for Acidosis , J. Biol. Chem. 30:289, 1917. 5. Newburgh, L. H., and Clarkson, Sarah: Renal Injury Produced in Rabbits by Diets Containing Meat , Arch. Int. Med. 32:850 ( (Dec.) ) 1923.Crossref 6. Polvogt, L. M.; McCollum, E. V., and Simmonds, Nina: The Production of Kidney Lesions in Rats by Diets Defective Only in that They Contain Excessive Amounts of Protein , Bull. Johns Hopkins Hosp. 34:168, 1923. 7. Evans, N., and Risley, E. H.: High Protein Ration as a Cause of Nephritis , California & West. Med. 23:437, 1925. 8. Drummond, J. C.; Crowder, G. P., and Hill, E. L. G.: Nutrition on High Protein Dietaries , J. Physiol 56:413, 1922. 9. Anderson, Hilding: Experimental Renal Insufficiency , Arch. Int. Med. 37:313 ( (March) ) 1923. 10. Jackson, Henry, and Riggs, Margaret D.: The Effect of High Protein Diets on the Kidneys of Rats , J. Biol. Chem. 68:101, 1923. 11. Osborne, T. B.; Mendel, L. B.; Park, E. A., and Winternitz, M. C.: Physiological Effects of Diets Unusually Rich in Protein or Inorganic Salts , J. Biol. Chem. 71:317, 1927. 12. Fischer, M. H.: Edema and Nephritis , J. Indiana M. A. 18:247, 1925.

WILSON, J. D.;GOODPASTURE, E. W.

doi: 10.1001/archinte.1927.00130090126009pmid: N/A

Abstract Acute yellow atrophy of the liver is a relatively rare malady in its clinically recognizable form, and when it is of a sufficient degree of severity to exhibit its classic clinical picture, it is almost invariably fatal. There are reasons for believing, however, that this disease of obscure etiology may exist in forms which are not of such rarity or fatality as are usually ascribed to it. For many years pathologists have described cases in which the lesions of the liver indicated a healing or healed stage of acute yellow atrophy, pointing to the probability, if not proving to the satisfaction of all, that recovery from a severe attack of the disease may occur. In 1895, Marchand1 clearly recognized the hyperplastic, regenerative nature of large nodules of hepatic cells which are commonly found in such livers, and which in some instances seem sufficient to carry on the function of the References 1. Marchand, F.: Beitr. z. Path. Anat. u. z. allg. Pathol. 17:206, 1895. 2. McDonald, S., and Milne, L. S.: J. Path. & Bact. 13:161, 1909. 3. Mallory, F. B.: Bull. Johns Hopkins Hosp. 22:69, 1911. 4. Umber, F.: Klin. Wchnschr. 1922 , 1:1585, 1922. 5. Seyfarth, C.: Deutsche med. Wchnschr. 47:1222, 1921. 6. Umber, F.: Deutsche med. Wchnschr. 45:537, 1919. 7. Huber, O., and Kausch, W.: Berl. klin. Wchnschr. 57:81, 1920. 8. Brütt, H.: Mitt, a. d. Grenzgeb. d. Med. u. Chir. 36:29, 1923. 9. Strumpell, Deutsche med. Wchnschr. 47:1219, 1921. 10. Pratt, J. H., and Stengel, A.: Tr. A. Am. Phys. 41:100. 1926.

VAUGHAN, WARREN T.

doi: 10.1001/archinte.1927.00130090135010pmid: N/A

Abstract The wide prevalence of hay-fever alone would justify presentation of any new concept offering possibilities of increased therapeutic efficiency. Conservative statisticians estimate that fully 1 per cent of the population of the United States is afflicted with hay-fever.1 The malady is sufficiently incapacitating, but when it is considered that 65 per cent of all persons with hay-fever finally become asthmatic,1 the need for further developments in treatment becomes even more obvious. Interest in these sufferers is not alone humanitarian, for the economic loss to the victim is often great. Those who do not have hay-fever know well the debilitating effect of an ordinary acute coryza, and realize the struggle of those who must work at full efficiency while semiprostrated for weeks or months with an unrelenting rhinitis. Even the welcome asylum of the hay-fever resort, usually located in a heavily timbered area in which weeds were few, has in great References 1. Balyeat, R. M.: Hay-Fever and Asthma , Philadelphia, F. A. Davis Company, 1926, p. 12. 2. Vaughan, Victor C.: Epidemiology and Public Health , St. Louis, C. V. Mosby Company, 1:65, 1922. 3. Manwaring and Crowe: J. Immunol. 2:517, 1917. 4. Weil, Richard, quoted by Zinsser: Infection and Resistance , New York, The Macmillan Company, 1923, p. 437. 5. Arthus: Compt. rend. Soc. de biol. 48:817, 1903. 6. Coca: Tice's Practice of Medicine , Hagerstown, Md., W. F. Prior Company, Inc., 1:110, 1920. 7. Van Leeuwen, W.: Allergic Diseases , Philadelphia, J. B. Lippincott Company, 1925. 8. Kolmer: Infection, Immunity and Biologic Therapy , Philadelphia, W. B. Saunders Company, 1924, p. 598. 9. MacKenzie, G. M.: Desensitization of Hay-Fever Patients by Specific Local Applications , J. A. M. A. 68:787 ( (March 18) ) 1922. 10. Kern: Ann. Clin. Med. 5:371, 1926. 11. Bernton, Harry S.: South, M. J. 20:257 ( (April) ) 1927.Crossref 12. Auer: Proc. Soc. Exper. Biol. & Med. 17:93, 1919. 13. Vaughan, W. T.: South. M. J. 27:749, 1924 14. Virginia M. Monthly 51:472, 1924. 15. Peshkin, M. M., and Rost, W. L.: Incidence of Protein Sensitization in Normal Child , Am. J. Dis. Child. 23:51 ( (Jan.) ) 1922. 16. Rackemann: Am. J. M. Sc. 163:87, 1922. 17. Vaughan, W. T.: Specific Treatment of Hay-Fever During the Attack , J. A. M. A. 80:245 ( (Jan. 27) ) 1923. 18. Duke: Asthma, Hay Fever, Urticaria and Allied Manifestations of Allergy , St. Louis, C. V. Mosby Company, 1925. 19. Phillips: Relief of Hay-Fever by Intradermal Injections of Pollen Extract , J. A. M. A. 86:182 ( (Jan. 16) ) 1926.

doi: 10.1001/archinte.1927.00130090145011pmid: N/A

This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract In the article by Dr. Albert H. Rowe, entitled "House Dust in the Etiology of Bronchial Asthma and of Hay-Fever" (Arch. Int. Med.39:498 [April] 1927), an error occurred in the last paragraph on page 501: 5 per cent salt solution was used, instead of 0.5 per cent solution, as there stated.