Quantum phase superoperator.
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Biomedical subjects
Publications and source records attributed to M Ban.
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A rare case of secondary syphilis showing mucous patches on the hard palate is reported. A 31-year-old male had two erosive patches which were slightly raised on his hard palate. A linear lesion was also present on the inside of his right alveolar process. Many red-brown macules on his abdomen and bilateral inguinal lymphadenopathy accompanied these symptoms. The serological tests for syphilis were positive: VDRL test 1:512, TPHA test 1:20,480, and IgM-FTA-ABS test 1:40. Immunohistochemical staining with rabbit monoclonal antibody to Treponema pallidum by the biotin-streptoavidin system detected treponemal organisms in the paraffin-embedded specimen from his mucous patch. A diagnosis of secondary syphilis was made, and he was given amoxicillin (AMPC) at 750 mg per day for 4 weeks. His eruptions, including the mucous patch, healed in a week.
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Complementary DNA encoding hen egg white lysozyme (HEWL) was subjected to site-directed mutagenesis to have the N-glycosylation signal sequence (Asn19-Tyr20-Thr21) by substituting Arg with Thr at position 21. The mutant lysozyme (R21T) was expressed in Saccharomyces cerevisiae carrying the yeast expression plasmid inserting the mutant HEWL cDNA. The mutant lysozyme was expressed in the glycosylated forms which are mainly a polymannosyl form with a small amount of oligomannosyl form. The polymannosyl lysozyme was susceptible to Endo H cleavage of the carbohydrate chain. The length of the polymannose chain was predicted to be approximately 340 residues/mol of lysozyme from carbohydrate analysis. According to the estimation with low-angle laser light scattering combined with HPLC, the average molecular weight of polymannosyl lysozyme was 75 kDa, which is consistent with the value obtained from the carbohydrate analysis. The size of polymannosyl lysozyme R21T is similar or somewhat larger than that of G49N reported previously. Thus, it was confirmed that the unusually large polymannose chain was attached to heterologous mutant lysozyme, regardless of the N-linked position, in yeast.
Male Swiss OF1 mice were injected subcutaneously with 20 mg/kg of cis-platinum (II) diamine dichloride (cis-platin). Examination of cryostat kidney sections stained for alkaline phosphatase (APP) revealed damage to about 10, 20, 40 and 50% of the proximal tubules after 7, 24, 48 and 72 h, respectively. Pretreatment with the glutathione synthesis inhibitor, buthionine sulfoximine (BSO), (i.p. 3 mmol/kg) potentiated the tubule damage of cis-platin. In contrast, pretreatment with organic anion transport inhibitor probenecid (i.p. 3 x 0.75 mmol/kg) reduced the number of damaged tubules by approximately 80% at 72 h after cis-platin injection. Pretreatment with the gamma-glutamyltranspeptidase (gamma-GT) inactivator acivicin (AT-125, 50 mg/kg p.o., plus 50 mg/kg i.p.) failed to prevent cis-platin induced renal toxicity. Pretreatment with the beta-lyase inactivator aminooxyacetic acid (AOAA, 2 x 100 mg/kg p.o.) and with the renal cysteine conjugate S-oxidase inhibitor methimazole (40 mg/kg i.p.) reduced the number of damaged tubules by approximately 40% and 75%, respectively in mice treated with cis-platin. The results suggest that the platinum-sulfhydryl group complexes formed are taken up by the kidney cells through an organic anion transport mechanism which is probenecid-sensitive. In the cells these complexes are stable for several hours, depending on the intracellular glutathione (GSH) level, and gradually undergo transformation to reactive metabolite(s) by renal intracellular beta-lyase and S-oxidase.
In chum salmon captured at the coastal sea and the natal river, the magnitudes of the olfactory nerve responses to the amino acids after perfusion of the olfactory epithelium with artificial pond water (APW) were similar to those after perfusion with artificial sea water (ASW), although the concentrations of Na+, Cl- and Ca2+ in ASW were 986, 430 and 27 times higher than those in APW, respectively. The findings suggest that the permeability of these ions across the apical membranes of olfactory cells do not essentially contribute to the transduction mechanism in the salmon.
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We developed a practically new central patient monitoring system for the operating room based on a system which had been developed in 1982. Since we introduced this system on May 19, 1992, we have utilized the system in more than 2,000 anesthesia cases. This system has been operating smoothly and accepted well by not only anesthesiologists but also surgeons and nurses. This system is easy to operate, and works automatically, contributing to the early detection of abnormalities in patient's condition. By introducing this system, the anesthesiologists have succeeded in controlling the patient during the operation more elaborately and effectively than before. Automated anesthesia recorder has reduced anesthesiologist's burden of the manual recording.
Recent advance in various diagnostic imagings has enabled the early diagnosis of pancreatic tumors. In pancreatic cancer, the tumor-demonstrability by US, CT, and MRI has reached 80% in the recent 6 years, which is superior to the rate in the past decade from 1978 and 1987. However, the prognosis of pancreatic cancer is still poor even if the cancer can be resected. To improve the outcome of surgical intervention, early detection of small cancers (< or = 2 cm in diameter) and appropriate intervention based on preoperative diagnosis of the tumor extension are proposed. The tumor detectability of small pancreatic cancer by US, CT, MRI was 67%, 25%, 20%, respectively, and thus US was the most valuable tool. In the prediction of tumor extension of serosal invasion (S factor), retroperitoneal invasion (Rp factor) and vessel invasion (PV factor), both US and CT were efficacious with an accuracy of more than 70%. In conclusion, recently-advanced imaging seems to be useful for detecting a small pancreatic cancer and evaluating the tumor extension, but it remains difficult to diagnose a carcinoma in situ; a truly early cancer.
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A 60-year-old woman with superficial spreading melanoma in situ, measuring 2.5 mm in diameter, was examined. She had noticed a very small pigmented lesion 1.2 mm in diameter on her left lower leg in April of 1989. By April of 1990, it had grown to 2.5 mm in diameter. Its edge was irregular, and its color was variegated black to brown. Skin surface markings had disappeared in the center portion. Histopathologically, the lesion was asymmetrical. Atypical large cells nested in the lower epidermis and were scattered singly in the mid and upper epidermis, as seen in Paget's disease. At the periphery of the lesion, single large tumor cells were scattered in the mid epidermis. The tumor cells reacted to monoclonal anti-melanoma antibody HMB-45.
Pregnant Sprague-Dawley rats were intraperitoneally injected with physiological saline solution (vehicle) or cadmium chloride (CdCl2) at 2.5 mg kg-1 body wt. on days 8, 10, 12 and 14 of gestation. Offspring were examined for renal alkaline phosphatase activity (ALP) on postnatal days (PND) 3 and 12, and for kidney metallothionein (MTh) and for liver, kidney and entire gastrointestinal tract 109Cd content at birth and on PND 3 and 12. No effects were observed on neonatal survival or on body, liver and kidney weights of pups up to PND 12. Newborns born and fed by mothers exposed to CdCl2 during pregnancy exhibited a significant decrease in ALP activity on PND 3. Conversely, no significant changes were observed in newborns lactated by surrogate non-treated mothers. Renal MTh increased with age but was not influenced by maternal treatment. Traces of 109Cd were present in the liver at birth (5-7 ng). Thereafter, 109Cd was mainly found in the gastrointestinal tract of newborns lactated by their biological mothers (610-690 ng on PND 12), with a marginal uptake in the liver (10-12 ng on PND 12). 109Cd was not detectable in the kidneys at any age (less than 4 ng). These results show that prenatal exposure to Cd cannot be the sole aetiological agent in the induction of the subtle and transitory changes in renal biochemistry observed in offspring born and fed by female rats intraperitoneally injected with 2.5 mg CdCl2 kg-1 body wt. on days 8, 10, 12 and 14 of gestation. The results also contradict the role of a direct effect on the kidney.
We report the case of a 49-year-old woman suffering from a malignant neoplasm of Langerhans cells (LC), documented by immunohistochemical and ultrastructural analysis, and review the literature to examine and characterize the clinical and laboratory features, therapy, and prognosis of malignant neoplasms of LC. Langerhans cell histiocytosis is now regarded as a disorder of immune regulation or an inflammatory process, rather than as a malignant neoplasm. Although LC share certain features in common with ordinary histiocytes or interdigitating dendritic cells, they also differ significantly from these cells in other respects. Therefore, we propose designating a malignant neoplasm of LC 'malignant Langerhans cell tumour' and that it should be considered as a separate entity from Langerhans cell histiocytosis or other malignant histiocytoses.
Male OF1 mice were injected subcutaneously with 80 mg/kg potassium dichromate (K2Cr2O7). Examination of cryostat kidney sections stained for alkaline phosphatase (APP) revealed damage to about 40-70% of the proximal tubules after 8 h. Pretreatment with the organic anionic transport inhibitor probenecid (i.p., 3 x 0.75 mmol/kg) reduced the number of damaged tubules by 60% in mice treated with potassium dichromate. Pretreatment with the gamma-glutamyltranspeptidase (gamma-GT) inactivator acivicin (AT-125, 50 mg/kg p.o., plus 50 mg/kg i.p.) failed to prevent chromate-induced renal toxicity. These results support the conclusion that a probenecid-sensitive transport process, but not a gamma-GT-catalyzed degradation, is involved in the mouse renal toxicity of potassium dichromate.
Male Sprague-Dawley rats were exposed to toluene diisocyanate (TDI) concentrations between 0.082 and 1.087 ppm for 4 h, and pulmonary lavage was carried out 24 h after initiation of the exposure. Cells recovered from the lavage effluents of TDI-exposed rat lungs were identified and counted, then pulmonary macrophages (PMs) resulting from cytocentrifuged preparations were examined for N-acetyl-beta-glucosaminidase (NAG) cytochemical staining. Exposure to TDI led to a parallel and concentration-dependent increase in the number of polymorphonuclear neutrophils (PMNs) and the proportion of PMs stained for NAG, suggesting that the same primary event initiates the two cell responses.