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Opposing a great power is a means of asserting one's own power, and several countries aspire to be great powers regionally if not globally. One expression of power is the [...]

During the past decade, radiophosphorus has become a widely accepted agent for the treatment of primary polycythemia, and favorable experience with it has been reported by a number of investigators.1In the eight year period from Jan. 1, 1942 through Dec. 31, 1949, 199 patients who had primary polycythemia have been treated with radiophosphorus at the Mayo Clinic. This group included 78 women and 121 men varying in age from 25 to 73 years, with a mean age of 54 years. The case records of this entire series were of value in the analysis of most pretreatment features. In the consideration of posttreatment features, inadequacy of treatment, failure to return, and recentness of treatment have reduced this total group to 148 patients.In addition to the foregoing, we have considered a group of 32 patients with primary polycythemia who were treated with means other than radiophosphorus (phlebotomy, phenylhydrazine, and

By the term leukemoid reaction is meant a blood picture that closely resembles, or is indistinguishable from, that of the various types of leukemia. At necropsy, however, leukemic changes in the organs and tissues of the body are lacking. Reactions of the leukemoid type have been recognized for many years, and it is now known that they occur with a wide variety of pathologic conditions. Our experience leads us to believe that they are much more frequently encountered than was formerly thought. Since it is essential that these reactions be distinguished from the leukemias, it is important that practitioners in all branches of medicine have a general idea concerning those diseases with which leukemoid reactions may be encountered.In attempting to group these leukemoid reactions, we realize that some of them might well be placed under two headings. As time goes on, however, other groups of cases will undoubtedly be

The hemorrhagic phenomena, so often a complication of hepatic disease, has long presented a serious medical problem, particularly when the disease is severe and of long duration. The isolation of vitamin K and its application to control of the hemorrhagic tendency in hepatic disease created the impetus for study which has increased appreciation of the role of the liver in the synthesis of factors necessary for normal coagulation of blood. For many years thrombin has been known to play a definite part in coagulation of blood, and its precursor, prothrombin, has been shown to be a product of hepatic metabolism. It now is known that a normally functioning liver is one factor necessary for the maintenance of a normal level of prothrombin in the plasma.1Experimentally and clinically, it has been demonstrated that in certain diseases of the liver, a diminished level of prothrombin in the blood often is

Neutropenia can result from various causes, which include inhibition of granulopoiesis in the bone marrow, arrest of maturation and excessive destruction of neutrophils. It is also a common associated finding in other blood dyscrasias and in some infections and infectious diseases. Neutropenia that arises from depression of bone marrow often is associated with corresponding reduction of other elements formed in the marrow, for example, erythrocytes and platelets. This reduction occurs in the various types of aplastic anemia; in anemia secondary to roentgen and radium irradiation, to exposure to benzene and to the administration of various chemicals, such as derivatives of the benzene ring, arsphenamine, sulfonamide compounds and gold compounds, and in anemia in which the etiologic factor is unknown. The myelophthisic anemias that accompany myeloma, osteosclerosis, Hodgkin's disease, involvement of the marrow by metastatic carcinoma or tuberculosis, leukopenic forms of leukemia and Gaucher's disease often are associated with neutropenia.In

Pernicious anemia, first described by Combe1 in 1824, was not recognized as a clinical entity until Addison's reports2 appeared in 1849 and 1855. It invariably terminated fatally until the epochal discovery of Minot and Murphy3 in 1926 that the oral administration of liver was effective in controlling the anemia and certain other clinical manifestations of the disease. Neurologic manifestations, however, were not well controlled by oral therapy. Later, extracts of liver were introduced which could be administered parenterally. These yielded far better clinical and hemopoietic responses. Progression of neurologic manifestations was prevented, and in cases in which neurologic involvement was of recent onset improvement frequently occurred.Search for the active factor or factors in liver that possessed anti-pernicious-anemia properties resulted in the discoveries of folic acid in 1945 and of vitamin B12 in 1948. While folic acid elicited hemopoietic responses in patients with pernicious anemia in

About 30% of the patients with metastatic malignancy develop significant effusions in the pleural, peritoneal, or pericardial cavities.1 Rarely, the fluid has the characteristics of a transudate, as in some cases of mediastinal adenopathy, or a high content of fats, as in chylous effusions. More commonly, its physical properties resemble those of an exudate, with a specific gravity in the neighborhood of 1.016, a protein content higher than 3.5 Gm.%, and a high number of cells in the sediment. It was for the latter type of exudative effusions that the intracavitary administration of radioisotopes and alkylating agents was proposed; it was presumed that the effectiveness of this form of therapy was due to high local concentration of the cancerocidal agent coming into direct contact with the malignant tumor implants on the serosa surfaces.2In general, it is estimated that with either radioisotopes or chemotherapeutic agents it is possible