In a previous report the population dynamics of emigrafive macrophages in rats was described (1). The macrophages were obtained from foci of acute nonbacterial inflammation provoked on abraded skin surfaces or in subcutaneous tissues at varying intervals with respect to the time of a single injection of trifiated thymidine (TdR-H3). The results indicated that the macrophages which adhered to glass cover slips in contact with the sites of inflammation were the progeny of rapidly and continuously dividing precursors. Similar conclusions have been reached by others in a variety of experimental situations (2-5). It was also shown that the macrophages emigrating to cutaneous and subcutaneous loci of acute nonbacterial inflammation originated predominantly from bone marrow (6). The origin of peritoneal macrophages from donors' bone marrow has been demonstrated by Balner (7) and Goodman (8) in lethally irradiated mice. However, the traditional view, among whose proponents have been Cappell (9), and more recently Felix and Dalton (10), is that the majority of peritoneal mononuclear cells arise from local elements.The purpose of the present study has been to determine whether the macrophages of experimentally induced peritoneal exudates have isotopic labeling features which suggest their derivation from the same precursors as those macrophages previously characterized (1, 6). Evidence is presented which supports this idea. Lymphocytelike cells in the exudates were also shown to be members of a rapidly proliferating population with precursors in bone marrow. Materials and MethodsAnimals.--Randomly-bred Columbia-Sherman rats of both sexes weighing between 100 to 200 g were used in most of the experiments. Only highly inbred BN rats (Microbiological Associates Inc., Walkersville, Maryland.) were used as partners in parabiosis experiments and as donors and recipients of cell transfusions. All operative procedures were carried out with the rats under ether anesthesia.

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Rats infected intravenously with Salmonella enteritidis develop a chronic destructive polyarthritis. The joint lesions resemble those of human rheumatoid arthritis in distribution and pathology. On the basis of histological and microbiological studies, involvement does not appear to be the result of intra-articular sepsis. Instead, the data favor the view that transient infection incites an immunological response that localizes in the joint and becomes destructive.

In order to assess the diagnostic accuracy of survey radiography for canine congenital cardiac anomalies, thoracic radiographs of 57 dogs with congenital cardiac anomalies, 31 normal dogs and 27 dogs with acquired cardiac disease were mixed, and reviewed by two independent observers, who were blinded to any patient information. The congenital anomalies were aortic stenosis (n=25), pulmonic stenosis (n=10), patent ductus arteriosus (n=9), ventricular septal defect (n=8), tricuspid dysplasia (n=3) and mitral dysplasia (n=2). Both observers were moderately accurate at identifying dogs with cardiac disease. Their ability to distinguish dogs with congenital versus acquired cardiac disease was poorer and this assessment was probably influenced by the recognition of patients that were skeletally immature, which biased observers towards a diagnosis of congenital cardiac anomaly. The diagnosis rate for specific congenital anomalies was also poor (the differential list included a correct diagnosis in only 40 and 37 per cent of cases). Radiographic signs of specific cardiac chamber enlargement or pulmonary vascular abnormalities were recognised by both observers in only 20 per cent of instances in which they might be expected. They were, however, recognised more frequently in dogs with anomalies that imposed a volume load on the heart than in dogs with anomalies that induced a pressure load on the organ. It is concluded that survey radiography is an inaccurate method for diagnosis of canine congenital cardiac anomalies because of the difficulty of recognising radiographic signs, which are not present in many cases.

Acquired resistance in tuberculosis (1), brucellosis (2), listeriosis (3), and salmonellosis (4) is primarily cell mediated. The macrophages, which act as effectors of this type of antimicrobial immunity are derived mainly from circulating monocytes (5). The abundance of macrophages in tissue lesions may be due in part to the state of delayed-type hypersensitivity (DTH) 1 which develops during these infections (6). In this connection, there is evidence that a high proportion of the macrophages which accumulate within a DTH reaction site arise from the further differentiation or maturation of inonocytes that emigrate from the blood (7). The expression of peripheral delayed hypersensitivity is, in fact, dependent upon the presence of such macrophages in the test sites (8, 9). Monocytes in most mammalian species constitute only a small proportion of the circulating white blood cells. It follows that in systemic infections of this type the demand for macrophages within infective foci could deplete the blood of monocytes unless compensatory mechanisms were operative. Still, there is little information concerning the activity of such mechanisms within the monocyte system. The strongest evidence for an operative homeostasis is in fact the constancy of the blood monocyte count. Most evidence on this point is inferential and based on data derived from studies of nonspecific inflammation. Thus, virtually nothing is known concerning the capacity of the monocyte system to meet the demands imposed by infection or the means by which the delivery of monocytes can be increased in such circumstances.The present studies were therefore addressed to the problem of monocyte mobilization in response to Salmonella infection in the rat. This model was chosen on the basis of unpublished observations that the rapid development of immunity in rats infected with Salmonella enteritidis was associated with abundant granulomatous accumulations of macrophages in the liver and spleen, an absolute monocytosis in the blood, and the development of high levels of cutaneous DTH. The cytokinetic changes underlying the obvious and rapid mobilization of monocytes in these animals were *