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Biomedical subjects

Y Kondo

Publications and source records attributed to Y Kondo.

At least 883 records · Page 49Linked to original sources

A histopathologic study of early hepatocellular carcinoma.

In a series of 94 autopsy cases of hepatocellular carcinoma (HCC), 8 cases of minute HCC (less than 3.5 cm in diameter) were included. These cases had some additional nodular foci that revealed a possible histogenesis of HCC. The lesion was first noted as a group of basophilic liver cell cords in a limited area of a hyperplastic nodule. The cords showed acinar formation, bile congestion, and increase of stromal fibers with disappearance of sinusoids. When certain numbers of lobules were occupied by the basophilic liver cells, a dysplastic nodule was produced wherein the portal triads tended to disappear. Despite marked necrotic tendency, the liver cells proliferated actively and replaced the adjacent cirrhotic lobules. The process might be induced and enhanced by repeated episodes of necrosis and regeneration occurring in cirrhotic livers. Some minute HCC nodules had common features with those seen in the dysplastic nodule. Histologic findings of minute HCC nodules were also described and discussed in terms of their growth pattern.

Adult↗

Cytologic and ultrastructural studies of a rare breast carcinoma with osteoclast-like giant cells.

An unusual case of breast carcinoma with osteoclast-like giant cells (OGCs) was reported, for which the diagnosis was made by aspiration biopsy. The OGCs appeared to derive from large mononuclear cells, probably via their cellular fusion. The mononuclear cells had abundant lysosome-like granules, endoplasmic reticulum, and mitochondria. They were thought to be histiocytic cells, though active phagocytosis could not be demonstrated. Histologically, the tumor showed a pattern of well differentiated ductal adenocarcinoma, of which the stroma was crowded with histiocytic cells, OGCs, and lymphocytes. Marked hemorrhage and fibrosis were also seen. The tumor cells tended to be distorted and greatly diminished in accord with the accumulation of OGCs.

Biopsy, Needle↗

Existence of noradrenalin cells and serotonin cells in the pituitary gland of Rana catesbeiana.

The localization of catecholamine-synthesizing enzymes [tyrosine hydroxylase (TH), dopamine-beta-hydroxylase (DBH), and phenylethanolamine-N-methyltransferase (PNMT)], of serotonin (5-HT), and adrenocorticotropin (ACTH) in the pituitary of bullfrog (Rana catesbeiana), rat, hamster, and dog was examined by the immunofluorescence method. Many TH- and DBH-positive but PNMT-negative noradrenalin cells and 5-HT-positive serotonin cells were first observed in the pars distalis of the frog pituitary together with small numbers of ACTH-positive cells, in marked contrast to our previous findings that TH-positive but DBH-negative dopamine cells are rare in the anterior lobe of rat and dog pituitary. The entire population of cells of the pars intermedia showed a weak ACTH-like immunoreaction. Although most of these cells were TH- or 5-HT-negative, TH-positive but DBH-negative dopaminergic varicose fibers surrounded these cells. Among cells of the pars intermedia of the frog, 5-HT-positive cells with processes were also scattered. In the neural lobe, TH- and 5-HT-immunoreactive fibers were rarely seen.

Adrenocorticotropic Hormone↗

Intestinal metaplasia of the regenerative epithelia in 549 gastric ulcers.

Histopathologic changes in the regenerative epithelia of 549 foci of gastric ulcer were studied. About 70 per cent of the regenerative epithelia revealed intestinal metaplasia of the so-called complete or incomplete type. Parietal cells and chief cells were occasionally observed in the regenerative epithelia of ulcers located in fundic gland areas or at fundopyloric gland borders. It is possible that the regenerative epithelium frequently reverts to intestinal epithelium during the regenerative process, later redifferentiating into normal gastric mucosa or remaining as intestinal metaplasia and that, thus, only a few foci of intestinal metaplasia are precancerous lesions.

Cicatrix↗

Intracytoplasmic inclusions in the atrophic muscle fibers in Werdnig-Hoffmann disease.

In the biopsied muscle from a male infant having clinical and pathological characteristics of Werdnig-Hoffmann disease, unusual intracytoplasmic inclusions measuring from 1.5-7 micron in dimension were observed in approximately 3% of the atrophic fibers. Although the ultrastructural characteristics of the inclusion were almost identical to that of "cytoplasmic body" seen in various neuromuscular disorders, which showed somewhat different histochemical reactions. This unusual structure was assumed to have originated from degenerated myofibrils and possibly from mitochondria, while the significance of the body formation still remains to be solved.

Humans↗

Stimulation of tubulin-dependent ATPase activity in microtubule proteins from porcine brain by taxol.

Taxol, an antimitotic agent that induces microtubule assembly, stimulated tubulin-dependent Mg2+-ATPase activity of microtubule-associated proteins (MAPs). A concentration-dependent increase in the rate of ATP hydrolysis was observed. Taxol acted through its binding to the tubulin molecule on MAP ATPase, and maximal stimulation, which was found at approximately equal concentrations of taxol and tubulin, reached about 140% of the original level in the absence of taxol. Taxol enhanced ATP hydrolysis by a mixture of MAPs and tubulin, and this continued at a steady linear rate even when the polymerization had approached a plateau. In the presence of taxol, a large portion of ATPase activity and protein was recovered in the pellet after centrifugation at 70,000 g for 60 min at 25 degrees C. Both colchicine and podophyllotoxin inhibited taxol-stimulated ATPase activity via the same mechanism by which they inhibited taxol-induced microtubule polymerization. The stimulation by taxol was not found in the presence of Ca2+ alone but required Mg2+. We conclude that tubulin effectively stimulates Mg2+-ATPase activity of MAPs under conditions that induce tubulin polymerization.

Adenosine Triphosphatases↗

Biosynthesis of the common precursor to vasopressin and neurophysin in vitro in transplantable human oat cell carcinoma of the lung with ectopic vasopressin production.

Transplantable human oat cell carcinoma cells of the lung with ectopic vasopressin production were incubated with labeled amino acids and immunoreactive neurophysins in cell extracts were analyzed by isoelectric focusing. When the cells were incubated with L-(35S)-cysteine for 20 h, one major peak (isoelectric point; pI=5.3) and several minor peaks (pI=6.1, 5.7, 5.1, 4.9 and 4.7) of labeled proteins were observed. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the relative molecular mass (Mr) of the pI 5.7 protein was estimated to be 20,000 and that of the pI 6.1 species to be 19,000, while the remainder had a Mr of approximately 10,000. The result of the pulse-labeling experiment has clearly shown that the pI 5.7 and 6.1 proteins, which have affinity for concanavalin A, are biosynthetic precursors for the smaller form of neurophysin with a pI 5.3. When subjected to limited proteolysis with trypsin, the pI 5.7 protein generated a Mr 10,000 protein and a smaller peptide. The Mr 10,000 protein thus produced was identified as neurophysin on the basis of its pH-dependent affinity for vasopressin and the migration pattern on isoelectric focusing. The smaller peptide coeluted with synthetic arginine vasopressin and bound to neurophysin suggesting that it possesses a cysteine-tyrosyl sequence at its N-terminus. Similarly, the pI 6.1 protein liberated neurophysin and vasopressin-like peptide after incubation with trypsin. These results suggests that the glycosylated protein with a pI of 5.7 and a Mr of 20,000 is the common precursor to vasopressin and neurophysin in human oat cell carcinoma of the lung with ectopic vasopressin production. The pI 6.1 protein may be an intermediate in the conversion of the precursor to vasopressin and neurophysin.

Carcinoma, Small Cell↗

Polymorphism in Pg-1 (urinary pepsinogen-1) locus in the rat and its linkage analysis.

Cramer (1981) reported that Pg-1 (urinary pepsinogen) in the rat was loosely linked with albinism in the linkage group I. We performed a three point test on the loci of pg-1, c, and Hbb. We could reconfirm that pg-1 was autosomal trait with two co-dominant alleles of pg-1a and pg-1b. But in progeny of ((WF X IS) X WF) backcross, pg-1 was linked to neither c nor Hbb, while a close linkage between c and Hbb was detected. Also pg-1 was not linked to Mup-1 (LG II), a (LG IV), Es-3 (LG V), and h (LG VI). pg-1 will be one of the most valuable genetic markers of the rats, since pg-1 was highly polymorphic among inbred strains of rats, and not linked to LG I, II, IV, V, and VI.

Animals↗

Discovery, isolation and structure of novel cephamycins of Streptomyces chartreusis.

By the use of HPLC technique after treatment with beta-lactamases, two novel cephamycins, SF-1623 and SF-1623B, were discovered and isolated from the fermentation broth of Streptomyces chartreusis SF-1623. The structures of SF-1623 and SF-1623B were determined to contain 3-sulfothiomethyl and 3-hydroxymethyl groups respectively, by chemical and enzymatic transformation reactions. Studies on the fermentation condition and process for the large scale preparation of antibiotic SF-1623 are also described.

Bacteria↗

[60-CO organic complexes formed in the seawater by the addition of amino acids and their pretreatment for chemical analysis].

By sodium nickel ferrocyanide coprecipitation, 60Co and 137Cs are simultaneously collected by nearly 99% recoveries from the unaged seawater. But this coprecipitation is not effective for the recovery of the 60Co complexed with organic ligands which would exist in natural seawater. In order to obtain the effective recoveries for these complexed 60Co, various pretreatments were investigated by using model samples containing the 60Co aged with several amino acids. In the acidification of these samples by nitric acid as 1 pretreatment, a large portion of these complexed 60Co was dissociated, especially by heating samples at 90-95 degrees C. The recoveries of 60Co were ranging from 90 to 97%. On the other hand, the usage of potassium peroxodisulfate (4.0 x 10(-4)-2.0 x 10(-2) M) as another pretreatment method elevated the recoveries of these complexed 60Co by more than 99% by heating samples above 90 degrees C. These 2 pretreatment methods were also effective for recoveries of 137Cs ion.

Amino Acids↗

Association of hypercalcemia with tumors producing colony-stimulating factor(s).

Two human malignant tumors, which we previously reported to produce colony-stimulating factors (CSFs), were found to be accompanied by remarkable hypercalcemia. A patient with a CSF-producing lower jaw cancer (squamous cell carcinoma) developed a marked granulocytosis (150,000/microliters) and hypercalcemia (more than 215 mg/dl). The tumor was successfully transplanted into nude mice, which developed marked granulocytosis (300,000/microliters) and hypercalcemia (20 mg/dl). White blood cell and serum calcium concentrations of these mice decreased promptly to normal levels when the tumor was excised. Treatment with prednisolone (1.5 mg/kg) or indomethacin (5 mg/kg) had no effect on the serum calcium level of these mice. Parathyroid hormone or prostaglandin E was not increased in the serum of the mice or in the tumor tissue. However, the mice bearing the tumor excreted extremely large amounts of calcium in their urine, and their bony tissues contained less calcium and phosphorus than controls. Moreover, histology of bony tissues of these nude mice clearly demonstrated the decrease in trabecular tissues and cortical thickness as well as remarkable activation of osteoclasts. Another patient with a CSF-producing bronchogenic squamous cell carcinoma showed mild granulocytosis and hypercalcemia. The biopsied tumor tissue was transplanted into nude mice, which developed marked granulocytosis (300,000/microliters) and also severe hypercalcemia (18 mg/dl). These results suggest the presence of a new syndrome of granulocytosis and hypercalcemia associated with CSF-producing tumors. The causal mechanism of the hypercalcemia was shown to be some humoral factor which activates osteoclasts other than parathyroid hormone. Neither prostaglandins nor osteoclast-activating factor seemed to be the cause of the hypercalcemia.

Adult↗