[Morphological changes in rabbit pleura induced by Lactobacillus casei (LC9018)].
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Biomedical subjects
Publications and source records attributed to Y Fukuda.
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Flomoxef (FMOX, 6315-S) is a new antibiotic of oxacephem group with a broad antibacterial spectrum. Seven patients were treated by intravenous instillation of 1 g of FMOX twice daily. Seven-day treatment with FMOX was ineffective against chronic bronchitis caused by Escherichia coli in a patient who had received an operation for esophageal cancer 6 years previously. Seven-day treatment with FMOX was effective against acute pneumonia caused by Staphylococcus aureus in a patient with lung cancer. Nine-day treatment with FMOX was effective against pulmonary suppuration caused by Streptococcus pneumoniae in a patient with lung cancer. Six-day and 7-day treatment with FMOX were excellently or moderately effective against suspected obstructive pneumonia in 2 patients with lung cancer. Five-day and 6-day treatment with FMOX were ineffective against fever of unknown origins in 2 patients with lung cancer. Overall, FMOX was effective in 4 of the 7 patients evaluated.
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Danazol was given to 16 patients with endometriosis in daily doses of 200 to 400mg for 4 to 6 months, and the change in serum lipids and lipoproteins was analysed. Danazol decreased total cholesterol by an average of 22%, triglycerides by 56%, phospholipids by 29%, free fatty acids by 17% and lipid peroxides by 42%, among which reductions in total cholesterol (p less than 0.05) and lipid peroxides (p less than 0.01) were statistically significant when compared with the pretreatment levels. Levels of lipids in HDL and VLDL also fell: HDL-cholesterol by 43%, HDL-triglycerides by 68%, HDL-phospholipids by 40%, VLDL-cholesterol by 73%, VLDL-triglycerides by 71% and VLDL-phospholipids by 48%. The decrease in HDL-cholesterol (p less than 0.05), HDL-triglycerides (p less than 0.05) and HDL-phospholipids (p less than 0.001) was significant. Concurrently apolipoproteins and LCAT activity decreased: A-I by 28% (p less than 0.001), A-II by 7% (p less than 0.05) and LCAT by 35%. In contrast, LDL-cholesterol increased, though slightly. Therefore, the atherogenic index defined as the ratio of LDL-c/HDL-c rose as much as 98% of the initial value. These changes seem to have arisen from impairment in the VLDL-HDL cycle. The decrease in VLDL and increase in LDL indicated that VLDL was catabolised and converted to LDL at a normal rate while the formation of HDL was impaired probably due to the low activity of LCAT and low level of apo A-I and A-II.(ABSTRACT TRUNCATED AT 250 WORDS)
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For a study of the processes and mechanisms of pulmonary structural remodeling in fibrotic lungs and metaplastic squamous epithelial cells in fibrotic alveoli, immunohistochemical, ultrastructural, and light-microscopic morphometric observations were made of the lungs in acute and proliferative stages of diffuse alveolar damage (n = 40) obtained from biopsies and autopsies. Morphometry showed that intraalveolar fibrosis developed in the early proliferative stage and was more prominent than interstitial fibrosis. In the early proliferative stage, activated myofibroblasts migrated into intraalveolar spaces through gaps in the epithelial basement membrane. They then attached to the luminal side of epithelial basement membrane and produced intraalveolar fibrosis and coalescence of alveolar walls. This intraalveolar fibrosis was the essential factor in the remodeled lungs. Albumin, fibrinogen, immunoglobulins, and surfactant apoprotein were present throughout the hyaline membrane. Fibronectin was not found in hyaline membrane of the lesions in early acute stage but was demonstrated in later stages in outer layers of hyaline membranes and in the areas of intraalveolar fibrosis. Fibronectin may be responsible for the migration and proliferation of myofibroblasts in intraalveolar spaces. Metaplastic single-layered and stratified squamous epithelial cells were keratin-positive and surfactant apoprotein-negative. These metaplastic epithelial cells were frequently found in the alveoli with minimal Type II epithelial cell proliferation and in the grossly scarred alveoli.
Reduced glutathione (GSH, 10(-7)-10(-3) M) was found to exert a profound suppressive action on the Na+-independent and -dependent bindings of L-[3H]glutamic acid (Glu) in a temperature-independent manner. Similarly significant reduction of the bindings resulted from the addition of oxidized glutathione (GSSG). Scatchard analysis revealed that GSH as well as GSSG invariably decreased the affinity of the binding sites for [3H]Glu without significantly affecting the number of the binding sites. These results suggest that GSH (GSSG) may in part participate in the synaptic transmission at central Glu neurons through interaction with the receptors and/or the uptake sites for Glu.
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