[Study of apoplexy by home visits of the patients and their families].
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Biomedical subjects
Publications and source records attributed to Y Taguchi.
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Percutaneous transhepatic biliary drainage (PTBD) guided by color Doppler echography was performed on nine patients. By color Doppler echography, the segmental and subsegmental branches of both the portal vein and the hepatic artery could be identified and discriminated from the bile ducts because of their color flow mapping. We could select the safe pathway of needle advance, which did not injure the vessels. Thus, complication of bleeding did not occur in any of the patients. Color Doppler echography seems a very useful and safe method for the guidance of PTBD.
A 4-month-old male infant had a fatal infantile mitochondrial disease associated with cardiomyopathy. He had elevated lactate concentrations in blood and cerebrospinal fluid and an increased lactate/pyruvate ratio. Histochemical analysis of muscle biopsy revealed several ragged-red fibers on modified Gomori trichrome stain and mildly decreased cytochrome c oxidase (complex IV) activity. Complex I and IV activities of the respiratory chain in muscle were decreased to about 35% of normal values biochemically; subunits of the two complexes were decreased nonselectively on immunoblotting. Mitochondrial DNA analysis failed to detect any mutation. Complex I and IV deficiencies should be considered as one of the causes of fatal infantile mitochondrial disease.
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In order to investigate the pathogenic role of bone resorption by osteoclasts in altered bone metabolism in non-insulin-dependent diabetes mellitus (NIDDM), the circulating levels of tartrate resistant acid phosphatase (TRACP) were simultaneously determined with osteocalcin, in rat models of NIDDM, i.e., genetic Wistar fatty rats and neonatally streptozotocin-induced diabetic rats (NSZ rats). In Wistar fatty rats exhibiting hyperglycemia and hyperinsulinemia, plasma TRACP was 40.0+/-0.4 U/l (mean+/-SE), significantly higher than that of 32.8+/-1.3 U/l in their lean littermates (p < 0.01). Bone length, bone strength, and weight of powdered bone in Wistar fatty rats were significantly decreased compared to control rats (p < 0.02-0.001). On the other hand, plasma TRACP in NSZ rats was 13.6+/-1.0 U/l, significantly lower than that of 31.4+/-1.2 U/l in their controls (p < 0.01). In addition, there were positive correlations between circulating TRACP and insulin levels in both NIDDM rat models (p < 0.05-0.01). Furthermore, plasma osteocalcin levels in these NIDDM models were significantly decreased than those of their corresponding controls (p < 0.001). Consequently, in Wistar fatty rats with hyperinsulinemia, it is suggested that the bone formation by osteoblasts was decreased, while the bone resorption by osteoclasts was increased. In contrast, in NSZ rats with hypoinsulinemia, both of bone formation and resorption were speculated to be decreased, indicating the decreased bone turnover. These results suggest that, although the deterioration in the osteoblastic function can be commonly observed in NIDDM animal models, the osteoclastic function is heterogeneous under NIDDM conditions.
1 The present study attempted to pharmacologically characterize the subtypes of alpha-adrenoceptors mediating the vasoconstriction in the isolated and perfused canine vesical artery. 2 Noradrenaline (NA) and phenylephrine (PE, an alpha1-adrenoceptor agonist) induced a dose-dependent vasoconstriction, whereas xylazine (an alpha2-agonist) did not induce any clear vascular constrictor response. 3 Prazosin at 0.01 microM and rauwolscine at 0.1 microM failed to affect the NA-induced vasoconstriction. Prazosin at 0.1 microM antagonized the vasoconstrictor responses to NA, with pKB value of 7.8. 4 WB 4101 at 0.01-0.1 microM dose-dependently inhibited the responses to NA, with a pKB value of 8.9. The vasoconstrictor responses to NA were not significantly affected by chloroethylclonidine (10-30 microM) or BMY 7378 (0.1 microM). 5 The present results indicate that the canine vesical arteries dominantly contain alpha1-adrenoceptors but have no alpha2-adrenoceptors, and the functional subtype of alpha1-adrenoceptor is characterized as an alpha1A-adrenoceptor subtype.
We report a case of metastatic pulmonary calcification that showed hyperintense signal on T1-weighted MRI. This uncommon MR appearance of calcification is similar to the MR characteristics of calcification in the brain due to abnormal calcium metabolism.
A 49-year-old man was admitted with the chief complaints of muscle weakness and gait disturbance. His neurological examination was compatible with peripheral neuropathy, and laboratory tests revealed IgA monoclonal gammopathy, increased protein content in the cerebrospinal fluid (CSF) without pleocytosis, and slow motor and sensory nerve conduction velocity. He was diagnosed as having chronic inflammatory demyelinating polyneuropathy with IgA monoclonal gammopathy of undetermined significance. The patient was treated with steroid, and plasmapheresis. He became so restless that antidepressant and haloperidol were administered. Then, he became unresponsive, and developed high fever, sweating, tachycardia, and tremor. Examination of CSF showed increased 3-methoxy-4-hydroxy-phenylglycol and decreased homovanillic acid. He was diagnosed as having neuroleptic malignant syndrome (NMS). However, his muscle tonus was still flaccid in his lower extremities that had been suffered from chronic polyneuropathy. Interestingly, his serum creatine kinase (CK) content was only slightly elevated. We suppose that the pathophysiological location of NMS might be primarily central, and that muscle rigidity and elevation of serum CK might not occur, if the peripheral nerves were completely impaired.
A total of 781 non-polypoid colorectal neoplasias harvested at 4 main Hospitals in Tokyo, Japan (n = 420) and at 4 different time-intervals at the Karolinska Hospital, Stockholm, Sweden (n = 361) were reviewed. By applying strict histologic definitions, the lesions were classified into adenomas with low grade dysplasia (LGD), with high grade dysplasia (HGD), intramucosal carcinomas (IMC) or submucosal carcinomas (SMC). Of the non-polypoid neoplastic lesions reviewed in Sweden, 82.8% (n = 299) had LGD. In Japanese patients only 42.6% (n = 179) had LGD (p < or = 0.001). On the other hand, as many as 42.4% (n = 178) of the non-polypoid lesions in Japanese patients had HGD, but only 14.1% (n = 51) of those in Swedish patients (p < or = 0.001). Whereas 15.0% (n = 63) of the non-polypoid neoplasias seen in Japan were IMC or SMC, only 3.0% (n = 11) of those seen in Sweden were IMC or SMC (p < or = 0.001). The cause(s) for these differences remains unclear. In Japan, however, a marked increased incidence of colonic cancer has been recorded in later years. Whether the "catching up phenomenon" by the Japanese with western colonic cancer incidence includes increased histologic aggressiveness of non-polypoid neoplastic polyps--as found in this survey--remains to be elucidated.
OBJECTIVE: To review the CT findings of BALTOMA, a low-grade malignant lymphoma originating from bronchus-associated lymphoid tissue (BALT). METHODS: The CT findings, symptoms, and clinical courses of BALTOMA in five patients were reviewed. The specimens obtained at operation were investigated, and the pathological findings were compared with the CT findings. RESULTS: There were no symptoms in four patients and normal laboratory data in all patients. One patient who complained of general malaise underwent surgery under suspicion of lung carcinoma. Four patients were observed from 4 months to 7 years and 1 month under the diagnosis of organizing pneumonia or chronic inflammatory processes. On CT images a localized lesion was seen in four cases, while multiple lesions were seen in one case. Attenuation of the lesions was between 39.15 and 60 HU on nonenhanced CT. Lesions were homogeneously enhanced by contrast material. The margins of the lesion were clearly demarcated by interlobular septa in one portion and were unclear in the other portion in all cases. Air bronchograms were seen in four cases. CT angiogram signs were seen in three of four cases in which contrast study was performed. There was no lymphadenopathy, pleural changes, or invasion to other organs. The pathological investigation revealed small lymphocytes that showed monoclonality in all cases. CONCLUSIONS: Awareness of the CT findings of BALTOMA can help to avoid misinterpreting BALTOMA as chronic inflammation and/or lung carcinoma. When a slowly progressive chronic pneumonia is being followed up, transbronchial lung biopsy and immunoglobulin staining of lymphocytes should be recommended for the correct diagnosis.
Histologic sections of endoscopically flat colorectal polyps removed in Tokyo and Stockholm were reviewed. A total of 178 flat colorectal neoplasias (88 from the Tokyo Medical College Hospital, Tokyo and 90 from the Karolinska Hospital, Stockholm) were classified following strict histologic criteria by two different pathologists (one Swedish and the other Japanese). The number of polyps with high grade dysplasia, with intramucosal carcinoma and with invasive carcinoma were significantly higher (p < 0.001) in Tokyo (61.4% or 54/88) than in Stockholm (15.0% or 14/90). The present results suggest that flat colorectal neoplasic polyps may be histologically more "severe" and more "aggressive" in Japanese than in Swedish patients. The possibility that more "advanced" lesions had been inadvertently removed in Tokyo was discounted as Japanese endoscopists were also instrumental in excising many of the flat colorectal polyps in Stockholm. Ethnic and/or environmental differences seem to play a crucial role in the evolution of flat colorectal neoplasic polyps from LGD and HGD, to intramucosal and to invasive carcinoma.
Cytokines that transduce their signals either through glycoprotein 130 (gp130) homodimers or gp 130/leukemia inhibitory factor (LIF) receptor beta heterodimers are potent inducers of osteoclast development in vitro as well as in vivo; and interleukin (IL)-6 has been recognized as an important pathogenic factor in diseases characterized by increased bone remodeling, such as the osteoporosis of sex steroid deficiency. Based on evidence that the same cytokines can also promote committed osteoblast differentiation and stimulate bone formation in vitro and in vivo and that mesenchymal cell differentiation toward the osteoblast lineage may be a prerequisite for osteoclastogenesis, we have investigated whether gp130 activation can affect the differentiation of uncommitted mesenchymal progenitors. Using as our model murine embryonic fibroblasts (EF), we found that IL-6 or IL-11 in combination with their soluble receptors (sIL-6R or sIL-11R) increased dose-dependently the number of alkaline phosphatase (AP)-positive cells in 3-6-day-long cultures. Moreover, EF cells maintained with IL-6/sIL-6R in the presence of ascorbic acid and beta-glycerophosphate expressed osteocalcin messenger RNA (mRNA) by 2 weeks and formed a matrix containing mineralized collagen fibers by 3 weeks. This prodifferentiation effect was specific for the osteoblastic lineage, as we found no evidence for increased differentiation of chondrocytes, adipocytes, or muscle cells. Unlike IL-6/sIL-6R, LIF, oncostatin M (OSM), and ciliary neurotrophic factor (CNTF) did not promote osteoblastic differentiation of EF cells. This pattern of specificity was accounted for by the finding that EF cells express gp130, but not the ligand-binding subunit of the IL-6 receptor (gp80) nor the LIF receptor beta. These observations add credence to the contention that increased production of gp130-utilizing cytokines and their receptors in pathological conditions like sex steroid deficiency is indeed responsible for not only the increased osteoclastogenesis, but also the increased osteoblastogenesis, and thereby for the increased rate of bone remodeling.