same patient; or are they connected through a link which is still unknown to us, thereby forming one affection or disease? If these questions could be solved, there might be some hope of discovering some rational mode of treatment, so as to prevent albuminuria from setting in, in which case all is lost. In another chapter we find the calculation of the amount of urea excreted in several chronic diseases, such as obesity, syphilis and athrepsy. Here it is easy to make a mistake, and still more so to err in trying to interpret the results obtained, because here the nourishment taken by the patient plays an important part, which is easily overlooked, e. g., in fleshy persons. Azoturia may be produced either by excess of food, or by abstaining from farinaceous food. The only way of ascertaining if the combustive functions are really exaggerated in a patient would be to compare the amount of chlorates contained in the secretions with the weight of the patient. Since Brouardel published his paper, on what he termed the uropoietic functions of the liver, several experiments have been made to ascertain the amount of urea excreted in diseases of this organ. The results have been very contradictory, but it is certain that large quantities of urea have been found in the urine of patients whose liver was completely degenerated.—_London Medical Record._ EXPERIMENTS CONCERNING ERYSIPELAS. Observations “were undertaken” by H. Fillman, of Leipzig, “in order, if possible to obtain further and more accurate information upon some contested points regarding erysipelas.” The experimenter has addressed himself here, especially to the answering of the four following questions: I. Is it possible to convey erysipelas by inoculation from a diseased to a healthy individual? In other words, do those fluids obtained from the tissues of an erysipelatous part and employed for inoculation (_e. g._, lymph, blood, the contents of bullæ, pus, etc.,) exercise a specific, _i. e._, contagious action on healthy individuals when inoculated, or do they not? II. What is the action of carbolic acid upon those erysipelatous animal fluids which produced the same disease on being inoculated into healthy individuals, and therefore in all probability contained the erysipelas poison? III. In what way is it possible (apart from direct conveyance) to produce erysipelas in healthy animals by the application of different morbid matters? IV. What do we learn from the results of anatomical and experimental investigation regarding the presence and significance of bacteria? What relation have they to erysipelas?