[Electroencephalography in patients with myoclonus epilepsy (Lafora type) and their family members].
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Biomedical subjects
Publications and source records attributed to T Ota.
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An inhibition enzyme-linked immunosorbent assay (inhibition-ELISA) was developed for the quantitative determination of human IgG (Gm) allotypes using rabbit anti-Gm antisera, alkaline-phosphatase-conjugated goat anti-rabbit IgG and, as the calibrant, purified human myeloma proteins possessing the relevant Gm allotype. The assay is reproducible and can detect as little as 10 ng/ml of G1m(a), G2m(n) or G3m(st), and 100 ng/ml of G1m(f) or G3m(g). Using this assay, the "gene dosage effect" and "allelic balance" in healthy Japanese were studied.
To use Albunex as a blood-flow tracer, the stability and consistency of microspheres under mixing conditions must be known. This study examined the effects of mixing conditions and machine settings on the size and echogenicity of Albunex solutions in vitro. Acoustic power, log compression, time-gain compensation, and transducer frequency were varied as Albunex solutions were imaged after mixing with magnetic stirring and pressurized. Higher acoustic power and lower transducer frequency decreased mean pixel intensity of Albunex solution images over time. Intensity, size, and number of Albunex microspheres were not significantly different between stirring speeds. The echogenicity of the Albunex solutions decreased with pressurization, and the critical pressure necessary to reduce the intensity to half its initial value increased with the logarithm of concentration (r = 0.91; p < 0.001). The microsphere size decreased with pressurization and remained smaller after pressure release (3.66 +/- 2.13 versus 1.47 +/- 0.95 microns; p < 0.01). These data indicate that acoustic power and transducer frequency may affect the physical properties of Albunex microspheres, decreasing mean videointensity. Pressure sensitivity of Albunex caused the decrease of videointensity and microsphere size.
The etiology and early events in the progression of epithelial ovarian carcinomas are among the least understood of all major human malignancies. There are no adequate means for early detection of these neoplasms and, as a result, they are usually diagnosed in late stages. The purpose of this review is to point out some of the peculiar problems and limitations that have hampered progress in ovarian carcinogenesis research and to summarize new approaches and recent advances in our understanding of this process. The review first presents an overview of the properties of the ovarian surface epithelium (OSE) which is thought to be the source of epithelial ovarian carcinomas, followed by a discussion of recent research based on human OSE. This includes sections on methodology for the attainment and study of OSE, investigations of OSE from women with predisposing mutations, and attempts to convert normal OSE to malignancy. This overview is followed by a discussion of the contributions, potential, and limitations of animal models. The knowledge gained by these approaches will likely lead to improvements in our ability to prevent, diagnose, and treat ovarian cancer.
In Drosophila, vitellogenins (yolk protein precursors) are synthesized by the female fat body, secreted into the hemolymph and subsequently taken up by the developing oocytes. The male fat body, on the other hand, does not do this even when immature ovaries are transplanted into the body cavity and grow. Thus, the hemolymph vitellogenins serve as an easily detectable sexually dimorphic biochemical marker.--We have examined hemolymph vitellogenins by SDS polyacrylamide gel electrophoresis in flies carrying various sex-transformation mutants (dsx, tra, tra-2 and tra-2OTF) singly and in all possible combinations. Chromosomal females homozygous for tra or tra-2 have no detectable hemolymph vitellogenins, while those homozygous for tra-2OTF exhibit appreciable levels of these proteins. Flies homozygous for dsx, both X/X and X/Y, have hemolymph vitellogenins, although the amount is consistently smaller in the latter. Indeed, X/Y; dsx/dsx is the only genotype in which hemolymph vitellogenins are detected in the X/Y flies. A clear hierarchy of epistasis exists among these sex-transformation mutants when they are examined in various combinations: dsx greater than tra, tra-2 greater than tra-2OTF. Moreover, an interaction between tra-2OTF and tra was seen in these experiments: X/X; tra-2OTF/tra-2OTF flies show the presence of only a trace of hemolymph vitellogenins when they are made heterozygous for tra. These results, combined with observations on gonad morphology, are discussed with respect to the Baker and Ridge (1980) hypothesis of sex determination.
To clarify what constitutes the adequate management of uterine endometrial carcinoma in young women, we reviewed clinicopathologically 31 patients aged 40 years and younger between January 1991 and June 2004. As a primary treatment, 12 cases chose hormonal treatment with medroxyprogesterone acetate (MPA; 600 mg/day) due to no findings of myometrial invasion and diagnosis of a grade 1, well-differentiated adenocarcinoma. In remaining 19 cases, surgery was performed. All the 19 patients who received surgery as a primary treatment are alive, with no evidence of a recurrence of the disease. In the 12 patients who received hormonal treatment, 8 patients eventually received a hysterectomy because of recurrence or no response to MPA. Of these eight patients, myometrial invasion was recognized in three patients. One of the eight patients died of the metastasized disease to the liver and brain after hysterectomy. After hormonal treatment, 4 of the 12 patients were exempted from surgery and showed no evidence of recurrence. Two patients had viable children. Progesterone receptor was negative in one case that died. Careful consideration should be given to hormonal treatment with MPA for the conservative management of endometrial carcinoma in young women. Moreover, MPA is not always a consistent management for every patient.
BACKGROUND: Hepatic ischemia/reperfusion (I/R) injury is an important clinical problem and leads to the release of the proinflammatory cytokines, TNF-alpha and IL-1. These cytokines play important roles in the induction of polymorphonuclear neutrophil (PMN) activation and infiltration, and induce not only localized hepatic injury but also remote organ injury, especially pulmonary injury. Using a total hepatic ischemia model in rats, we tested our hypothesis that suppression of TNF-alpha and IL-1 by FR167653 ameliorates I/R injury in the liver and lung. METHODS: Male Wistar rats, weighing 240-280 g, were divided into 3 groups, an FR group, a control group and a sham group. In the FR group, FR167653 (1 mg/kg/h) was administered continuously to the animals for 30 min prior to the onset of ischemia and for 2 h after reperfusion. The control group received normal saline. A porto-systemic shunt was placed between the cecal branch of the portal vein and the jugular vein, and total hepatic ischemia was produced for 90 min. The sham group was treated with placement of the porto-systemic shunt only. The 1-week survival rate, liver enzyme activity, hepatic tissue blood flow (HTBF), cytokine mRNA expression, myeloperoxidase (MPO) activity and histological results were studied. RESULTS: The 1-week survival rate and HTBF were significantly higher in the FR group than in the control group. Serum AST, ALT, and LDH levels were significantly lower in the FR group at 30 min, 1 h and 3 h after reperfusion. MPO levels in liver and lung tissue were also significantly lower in the FR group. The expression of IL-1beta mRNA remarkably decreased up to 6 h after reperfusion in the FR group. CONCLUSIONS: We concluded that the inflammatory cytokines, IL-1beta, play important roles in hepatic I/R injury. FR167653 might ameliorate I/R injury and be useful in liver surgery with ischemia.
The histogenesis of 3 types of rat renal cell tumors (basophilic cell, clear cell, and oncocytic) was stereologically analyzed, with particular attention paid to transitions from normal tubules. Early nitrosamine-induced preneoplastic lesions, including dysplastic tubules (altered tubules), epithelial hyperplasias, and small adenomas, were reconstructed using serially sectioned specimens processed for carbonic anhydrase type II (CA) and periodic acid-Schiff (PAS) (CA-PAS) double staining to allow easier distinction of the nephron segments: Proximal tubules had a PAS-positive brush border and were weakly positive for CA in the cytoplasm; distal tubules were PAS negative and weakly positive for CA; collecting ducts were PAS negative and strongly positive for CA. Similarly, cytochrome c oxidase (CytOx) and CytOx-PAS double staining was also applied to confirm the character of oncocytic lesions. All basophilic lesions (7 of 7) showed transition to proximal tubules. Clear cell lesions positive for CA, on the other hand, showed transition to distal tubules in 4 of 9 (44.4%) lesions and to collecting ducts in 4 of 9 (44.4%) lesions, but in only 1 of 9 (11%) to a proximal tubule. All oncocytic lesions (16 of 16), characterized by positivity for both CA and CytOx, showed transition to collecting ducts. The results indicate that the origins of renal cell neoplasia are proximal tubules for the basophilic cell lesions, either proximal or distal tubules for their clear cell counterparts, and collecting ducts for oncocytic lesions.
The aim of this study was to propose and validate a new method of making fused images from CT and FDG PET images for the upper abdominal area with no body surface marker. PET and CT were carried out in patients with pancreatic cancer (N = 5) and mass-forming pancreatitis (N = 2). First, we determined the midsagittal plane from PET and CT data. From the difference in location of the midsagittal planes, rotations of Y (from back to front) and Z axes (from foot to head) and X translation (from right to left) were calculated. An upper pole of the kidney was determined from PET and CT data. It showed Y and Z translations. The images of the three-dimensional data sets were fused on a workstation. Reproducibility was assessed with randomly misaligned PET and CT data sets. Pancreatic cancer and its lymph node metastases were identified easily on fused images. In reproducibility assessment, the average error of rotation was 0.77 degree. The average errors of translation were 3.43, 4.70, and 9.23 mm on the X, Y, and Z axes, respectively. In conclusion, this PET/CT image registration technique is feasible and practical. It allows precise anatomical assessment of normal and abnormal FDG accumulation.
Intravasation is essential for hematogenous metastasis in cancer cells, but its cellular determinants have not been well elucidated because of a lack of suitable experimental cell systems. Int-3LL was originally developed by in vivo sequential selection for intravasation from Lewis lung carcinoma (3LL) cells. Here, we found that these variant cells showed a highly penetrating ability in vitro as well as an augmented intravasating potential in vivo. In three-dimensional collagen-gel, Int-3LL cells formed diffusive colonies with less plating efficiency than their parental cells. Despite these properties, Int-3LL cells showed an ability of invasive migration in vitro similar to parental cells. On the other hand, a reduced adhesiveness and less spreading on extracellular matrices were revealed in Int-3LL cells. Analyses using anti-integrin antibodies indicated that the dysadhesion phenotype in Int-3LL cells was associated with integrin beta 4 dysfunction, which is known to produce epithelial detachment. Also, the types and the levels of integrins were not indistinguishable between Int-3LL and parental 3LL cells. Thus, the impaired function of integrin beta 4-mediated adhesion is considered to be an important factor in intravasation during metastasis.
We report a 73-year-old woman with intravascular malignant lymphomatosis (IML) who showed generalized telangiectasia as well as various neurological symptoms. In July 1998, she developed fever, dizziness, and confusion followed by left hemiparesis, and was admitted to our hospital on August 11, 1998. Laboratory tests indicated a normochromic normocytic anemia, thrombocytopenia, elevated serum lactic dehydrogenase (LDH), C-reactive protein (CRP), and cerebrospinal fluid protein. Magnetic resonance imaging (MRI) of the brain revealed an infarct-like lesion in the left frontal lobe and multiple white matter lesions. After admission, her neurological status deteriorated and lapsed into coma and quadriplegia. At the end of September 1998, generalized telangiectasia appeared, and she was diagnosed as IML on skin biopsy. Although combination chemotherapy failed to improve her neurological symptoms, telangiectasia disappeared in a few days, and the infarct-like lesion on MRI decreased in size. Serum LDH, CRP, and thrombocyte counts were normalized. Autopsy findings revealed perivascular clustering of B cell type lymphoma cells in the left frontal lobe where abnormal signal intensity was found on MRI, as well as the spleen and the bone marrow. This case emphasizes the importance of early diagnosis and treatment in IML.