A new material, an emulsion of poly(vinyl acetate) was experimentally developed and clinically used to overcome several disadvantages in currently used liquid embolisation materials. The emulsion microparticles, 0.3-0.7 microns in size, possessed cationic charge on the surface and hence aggregated immediately on contact with fluids containing anions. This inert polymer has the advantage that it does not induce a deleterious reaction in living tissue. Moreover, its medium is water and it is not adhesive, like the cyanoacrylates. Several concentrations of emulsion were injected into the renal arteries of dogs. For the investigation of tissue reactions and the possibility of recanalisation, the emulsion was injected into rats both subcutaneously and into the renal arteries. The renal artery injections in dogs showed adequate radiopacity and consistent complete occlusion. The lower the concentration of the emulsion, the smaller the arteries which could be occluded. Even at very low concentrations, however, venous occlusion did not occur. Histological study of the embolised rat kidney revealed no detectable damage in the vessel wall and no recanalisation for up to 6 months. The subcutaneously injected PVAc emulsion elicited mononuclear cell infiltration and gradual centripetal fibrosis, without any deleterious effect on the surrounding tissue. A cerebral arteriovenous malformation (AVM) was embolised using the material. Histology of the resected nidus showed findings similar to those in the animal experiments.

Resistance to freezing can be considered in connective tissue, blood vessels, and also epithelium and mature lymphocytes, but the tonsils are highly receptive to freezing, and thus during the 2 min two-cycle freezing the tonsils were able to be removed sufficiently. In addition, the edema in the peripheral tissue reached its peak in 12 to 24 hrs, and during this period it can be thought that dyspnoe could easily be induced. Histologically as well, necrosis was apparent after 12 hrs, with the peak coming during the first 3 days, and it was difficult to discern necrotic areas after 7 days. Revitalization of the epithelium, thrombosis, and fibrosis were also apparent as the 7th day. At the same time, dilated and regenerated capillary vellels were apparent. On the 14th day, collagen fibrosis of the deep layer tissue was found, and as of the 24-day collagen fibrosis up to the level of the epithelium was observed.

The diagnostic value of the nasal biopsy in the early diagnosis of Wegener's granulomatosis and its value in prognosis were examined in 11 patients with a clinicopathological diagnosis of the disease. The vascular lesions found included microabscess in the vascular walls in 82%, leukocytoclastic capillaritis in 73%, fibrinoid necrosis of blood vessels in 45%, leukocytoclastic endovasculitis in 27%, and palisading granuloma in vascular wall in 9% of cases. The extravascular lesions included palisading granuloma in all cases, microabscess in 91%, and diffuse granulomatous tissues in 82%. Palisading microgranuloma (82%) was more frequent than palisading macrogranuloma (45%). After therapy, complete remission occurred in 8 patients, but 3 patients died of sepsis, diffuse pulmonary haemorrhage, and cerebral haemorrhage. Comparison of the frequency of each finding in the nasal biopsy specimens between patients who achieved remission and those who died showed that leukocytoclastic vasculitis was found more commonly in fatal cases, and leukocytoclastic endovasculitis was observed only in fatal cases. Palisading granuloma as a vascular or extravascular lesion is the primary and most important finding in a histopathological diagnosis of Wegener's granulomatosis, microabscess in vascular walls is a secondary but the next most important finding, and leukocytoclastic vasculitis heralds dissemination of the disease and poor prognosis. It requires aggressive therapy.

Free amino acids in the tonsils of 20 individuals were measured column chromatographically. Those always found in readily detectable amounts included O-phosphoserine, taurine, O-phosphoethanolamine, aspartic acid, hydroxyproline, threonine, serine, glutamic acid, proline, glycine, alanine, α-amino-n-butyric acid, valine, cystine, methionine, isoleucine, leucine, tyrosine, phenylalanine, ornithine, γ-amino-butyric acid, lysine, histidine, and arginine. Results were compared for three clinical pathological groups and for four age groups. Some abnormal values may result from the pathological conditions.

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