In order to investigate the mechanism of synthesis and secretion of lysozyme (LZ) by human mononuclear phagocytes, the ultrastructural localization of LZ was studied by a pre-embedding direct immunoperoxidase method. Blood monocytes showed a reaction product for LZ in cytoplasmic granules, whereas cultured monocytes showed the reaction product in phagosomes as well as granules at 5 h of culture and in numerous large granules at 3 days of culture. In Kupffer cells, LZ was present in cytoplasmic granules, vacuoles and phagosomes. Some Kupffer cells showed a positive reaction for LZ in the rough endoplasmic reticulum, perinuclear cisterna and Golgi apparatus. Macrophages in the lymph nodes contained LZ in cytoplasmic granules. Bone marrow macrophages contained numerous phagosomes with electron-dense degradation products of erythrocytes, but the reaction product for LZ could not be clearly identified. The present study demonstrated that LZ is present in the granules of human mononuclear phagocytes and released into phagosomes. An in-vitro culture study, furthermore, demonstrated that macrophages produce LZ-containing large granules distinct from those of monocytes. However, findings that indicate the synthesis and secretion of LZ by cultured monocytes, as suggested previously by other investigators, were not observed in this study.
The authors report an autopsied case of systemic lupus erythematosus (SLE) with pulmonary hypertension. The patient was a forty-five-year-old female who had been troubled by obstinate Raynaud's phenomenon for ten years before the definite diagnosis of pulmonary hypertension was made. Microscopic examination of the pulmonary vasculature yielded findings consistent with plexogenic pulmonary arteriopathy. However, the deposition of immune complexes in the pulmonary vascular endothelium was not detected by enzyme antibody study. This case suggests, therefore, that "pulmonary Raynaud's phenomenon" is a possible pathogenesis of pulmonary hypertension in patients with SLE.
Summary.-Oral administration of N -methyl -N'-nitro -N-nitrosoguanidine (MNNG) to hamsters at a concentration of 50-83 ,tg/ml in the drinking water resulted in a high incidence of tumours in the glandular stomach. Short-term administration of MNNG for 4-6 months resulted in more adenocarcinomata in the glandular stomach than long-term administration for 7-8 months. One case of metastasis of an adenocarcinoma of the glandular stomach to the liver and 2 cases of metastasis to the regional lymph nodes were found. Spindle cell sarcomata in the glandular stomach and adenocarcinomata in the duodenum were also often produced.Oral administration of MNNG at the very high concentration of 500-2000 vg/ml induced a hepatic cell carcinoma, intrahepatic bile duct carcinomata, bile duct cystadenomata and cystic dilatation, and a haemangioma in the liver but no tumour in the glandular stomach.Sequential morphological studies on the glandular stomach of hamsters receiving 50 ,ug/ml of MNNG in the drinking water showed 3 stages of change of the mucosa. The mucosa became atrophic and eroded in the first 16 weeks. Irregular atypical glands developed at the margins of erosions and proliferation of spindle cells in the submucosa were found after 18 weeks. Spindle cell sarcomata developed in animals after 20 weeks. Adenocarcinomata developed between 25 and 32 weeks.
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