[Clinico-pathological study of 32 autopsy cases of atypical mycobacteriosis].
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Biomedical subjects
Publications and source records attributed to Y Tajima.
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It is essential to develop animal models for human diseases with disease onset mechanisms the same as those of humans to study the causes, and therapeutic and preventive methods for human disease, as well as to develop new drugs. In the past, many beneficial experiments were performed by selecting animals with symptoms similar to those of humans from nature or breeding colonies. Experimental systems using induced disease models have been developed and provided useful results. The current basis of biology has reached the molecular level, and various phenomena of life have come to be understood through clarification of the expression of genes (DNA). Human diseases are one of these life phenomena, and the study of the relation between life phenomena and genes (DNA) has already started in the field of genetics. The next step appears to be the manipulation of genes to produce animal models for various human diseases. Progress has already been made in genetic and cellular engineering and embryonic manipulation on the basis of their respective methodologies and principles. One of the topics for future studies will be the development of models for human diseases through the integrated application of these fields. It is clear from documents on medical history that experiments using animals have been performed from the earliest period of ancient medical research. Therefore, pioneers in each period continued such studies and by the time of Claude Bernard, animal experiments had become an essential part of medical research. He stated in 1865 in his "Introduction to the Study of Experimental Medicine" that "I not only conclude that experiments made on animals from the physiological, pathological and therapeutic points of view have results that are applicable to theoretic medicine, but I think that without such comparative study of animals, practical medicine can never acquire a scientific character." Following this, animal experiments were widely performed in all fields of medical research, but the animals used in such experiments were only improved to the level they have reached today through the modernization movement which started in Europe, the United States and Japan from the end of the 1940's through the beginning of the 1950's. From the 1960's, the term "biomedical research" came into use in the United States to describe experiments using animals in the fields of medical research.(ABSTRACT TRUNCATED AT 400 WORDS)
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A striking resistance to lethal damage from a single dose of 6-8 Gy of X rays has been found in mice which had received various pretreatments to induce metallothionein (MT) synthesis in the liver prior to irradiation. Mice were injected with manganese (10 mg Mn/kg) or cadmium (3 mg Cd/kg) salt subcutaneously, or a patch of dorsal skin (2 X 2 cm2) was excised 1 or 2 days prior to irradiation. The increased tolerance of these mice to radiation was established by a marked decrease of mortality rate, an increase of mean survival time, a reduction of weight loss, and a smaller decrease in the number of leukocytes as compared with the control group. The LD50/30 for control mice was 6.3 Gy, while the corresponding values for the groups pretreated with Mn, Cd, and skin excision were 7.5, 7.7, and 7.9 Gy, respectively. The normal level of MT in mouse liver was approximately 25 micrograms/g tissue. This level increased 2.5- to 3-fold 24 h after 6.3 Gy irradiation. The MT levels of mice pretreated with Cd, Mn, and skin excision were increased 8-, 5-, and 7-fold, respectively, prior to irradiation as compared with the preirradiation control. These results indicate that the induction of MT in mouse liver is a significant factor in the mechanism of protection against radiation.
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The binding of wheat germ agglutinin (WGA) to the extracellular matrix of rat tracheal cartilage was studied at both the light and electron microscopic levels. The detection of binding sites was accomplished by a postembedment method using the direct fluorescence technique for light microscopy and the avidin-biotin bridging system for electron microscopy. Distinct fluorescence was observed in the pericellular region of chondrocytes, and this fluorescence was completely removed after treatment with 4 M guanidine hydrochloride. By electron microscopy, the reaction products as found in the pericellular region were not observed in the interterritorial collagenous matrix, confirming a similar distribution as found by fluorescence microscopy. These results show that WGA-binding sites are present in pericellular matrical substances, which are known to be rich in proteoglycan and glycosaminoglycan complexes and which exhibit similar staining with antibodies to proteoglycans or with cationic dyes. As WGA binds to N-acetyl-glucosamine and N-acetyl-neuraminic acid residues, the pericellular matrix of rat tracheal cartilage appears to consist of proteoglycan having a high concentration of these saccharides.
A mucus-secreting presacral cyst was found in a 49-year-old woman who complained of dysuria. A routine rectal digital examination revealed a retrorectal mass. Diagnostic imaging demonstrated a large presacral cystic tumor. The cyst was removed through a transsacral approach. Histologically, the cyst membrane consisted of squamous and columnar mucus-secreting epithelium, and was diagnosed as a mucus-secreting presacral cyst.
Both the adenylate cyclase activity and the motility of human sperm were stimulated by bicarbonate with the same concentration dependency. The correlation between bicarbonate levels in semen and the motility of sperm from the patients with male infertility was investigated. Bicarbonate in semen was found to originate mainly from the seminal vesicles, and a significant positive correlation was observed between bicarbonate levels and volume of semen. The motility of infertile sperm was also found to correlate positively to the seminal levels of bicarbonate. These results suggest that the lowered levels of bicarbonate in semen are at least in part responsible for the poor sperm motility in infertile patients, as a result of the failure in the activation of sperm adenylate cyclase.
An unusual case and they of dentinogenic ghost cell tumor, a peculiar variant of calcifying odontogenic cyst, is reported. The tumor consisted predominantly of ghost cells with occasional areas of "dentinoid" in close proximity to masses of ghost cells. The presence of ameloblastoma-like nests of epithelium was characteristic of the present case and they were interpreted as a degenerative phenomenon exhibiting an inductive effect with formation of abundant ghost cells, occurring within a pre-existing ameloblastoma. The term of "dentinogenic ghost cell tumor" is employed for this unique lesion presented in this report. The literature describing the neoplastic potential of the calcifying odontogenic cyst is briefly reviewed.
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Recently, a low molecular weight factor, which specifically stimulates sperm adenylate cyclase, was found in porcine seminal plasma (Okamura, N., and Sugita, Y. (1983) J. Biol. Chem. 258, 13056-13062). The purified factor was analyzed by 1H NMR, 13C NMR, infrared spectroscopy, and elementary analysis and identified as sodium bicarbonate. The effects of sodium bicarbonate both on adenylate cyclase activity in porcine spermatozoa and on sperm motility have been studied. Sperm adenylate cyclase was found to be specifically activated by bicarbonate over the physiological concentration range. In contrast, the adenylate cyclase activity in other tissues was not affected. The same concentration range of bicarbonate which resulted in activation of adenylate cyclase also stimulated sperm motility. The motility and enzyme activity of spermatozoa in all species so far tested (human, bovine, rat, mouse, and dog) were found to be similarly sensitive to bicarbonate concentration. These results show that the bicarbonate-sensitive adenylate cyclase system regulates sperm motility and suggest that this system is common to all mammals.
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Plasma volume (PV) and extracellular fluid volume (ECF) were determined in 7 patients with essential hypertension (controls) and in 10 patients with primary aldosteronism, while on a high Na diet (342 mEq/day) and on a low Na diet (12 mEq/day). The volume studies were repeated in 6 of the primary aldosteronism patients during treatment with spironolactone for over 3 months. Plasma renin activity (PRA), plasma aldosterone concentration (PAC), cortisol concentration, and serum Na and K concentrations were measured in all patients while on a Na-restricted diet (85 mEq/day) as well as on high-Na and low-Na diets. There were no significant changes in arterial pressure during different Na diets in any groups of patients with essential hypertension, or primary aldosteronism with and without spironolactone therapy. Spironolactone treatment normalized the arterial pressure in patients with primary aldosteronism at all Na intakes. These patients had greater values for PV and ECF than did those with essential hypertension. Spironolactone treatment reduced PV during the low-Na diet, but did not alter it during the high-Na diet. Spironolactone did not produce significant changes in ECF during either the high-Na or low-Na diets. Although there were no changes in PV and ECF in patients with primary aldosteronism due to changes in Na intake, both PV and ECF were significantly less in these patients during spironolactone treatment and in patients with essential hypertension during low-Na intake than during high-Na intake. With primary aldosteronism, PRA was depressed and PAC was elevated when compared to essential hypertension, these were not altered by different Na diets in the patients with primary aldosteronism as they were in those with essential hypertension. During treatment with spironolactone the PRA was restored to normal and showed normal changes with variations in dietary Na, but PAC remained elevated during spironolactone. Plasma cortisol was the same among those with essential hypertension and patients with untreated and spironolactone-treated primary aldosteronism. Serum K was less in untreated primary aldosteronism during all Na diets than in essential hypertension, but during spironolactone it was restored to normal. These results suggest that in primary aldosteronism the reduction in arterial pressure by spironolactone treatment does not occur simply by reductions in body fluid volumes. The long-term treatment of patients with primary aldosteronism with spironolactone does not inhibit the production of aldosterone, possibly because of enhanced activity of the renin-angiotensin system and an increase in serum K.