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81.
We describe a 54-year-old woman with primary pulmonary adenocarcinoma showing a characteristic papillary architecture and prominent cilia formation. Immunohistochemically, the tumor cells were positive for carcinoembryonic antigen (CEA), epithelial membrane antigen (EMA) and Leu Ml, and negative for lactoferrin and surfactant apoprotein. An ultrastructural study also indicated differentiation toward bronchial surface epithelial cells. To our knowledge, this type of neoplasm has not been reported as peripheral-type adenocarcinoma of the lung. Acta Pathol Jpn 42: 745–750, 1992.  相似文献   
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This study was undertaken to clarify the effect of enzymes induced by ethanol consumption on the pharmacokinetics of trichloroethylene (TRI, a highly metabolised substance) and 1,1,1-trichloroethane (1,1,1-TRI, a poorly metabolised substance). Rats maintained on a control liquid diet or a liquid diet containing ethanol (2 g/day/rat) for not less than three weeks were exposed to either TRI (50, 100, 500, and 1000 ppm) or 1,1,1-TRI (50, 100, and 500 ppm) by inhalation for six hours and the concentration of each compound in the blood and the urinary excretion of metabolites (trichloroethanol and trichloroacetic acid) were measured over several hours. Ethanol, which increased the in vitro metabolism of both compounds about fivefold, enhanced the in vivo metabolism of TRI only at high levels of exposure (marginally at 500 and considerably at 1000 ppm), whereas the metabolism of 1,1,1-TRI was enhanced at all concentrations tested. Moreover, there was a definite difference in the effect of induction of enzymes between the two solvents: the enhanced metabolism of TRI in vivo was shown by a decrease in the blood concentration of TRI as well as by an increase in the urinary excretion of its metabolites, whereas that of 1,1,1-TRI was shown by an increase in the urinary excretion of its metabolites alone. These results suggest that the induction of enzymes differentially affects the pharmacokinetics of TRI and 1,1,1-TRI in human occupational exposure: TRI metabolism may be increased only at concentrations much higher than the current occupational exposure limit (mostly 50 ppm), whereas 1,1,1-TRI metabolism may be increased at an exposure similar to occupational exposure.  相似文献   
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Background Evidence suggests that, as a group, patients with schizophrenia have intellectual deficits that may precede the manifestation of psychotic symptoms; however, how successfully intelligence tests are able to discriminate schizophrenia from other psychotic disorders has yet to be investigated in detail. Methods Using Wechsler Adult Intelligence Scale – Revised (WAIS‐R) data for 55 inpatients with schizophrenia and 28 inpatients with non‐schizophrenic psychotic disorders (NSPD) (schizophreniform disorder, brief psychotic disorder, delusional disorder, psychotic disorder due to a general medical condition, and psychotic disorders not otherwise specified), intelligence performance was compared between schizophrenia and NSPD and among different subtypes of schizophrenia. Results There were no significant differences in intelligence quotient (IQ), verbal IQ (VIQ) and performance IQ (PIQ) discrepancy, and subtest scores of WAIS‐R between the patients with schizophrenia and those with NSPD. These diagnostic groups were not discriminated well by any WAIS‐R variables. Schizophrenia patients with prominent negative symptoms, on the other hand, had a significantly larger IQ discrepancy (VIQ > PIQ) than those without prominent negative symptoms and NSPD patients. Intelligence performance in schizophrenia did not differ with respect to diagnostic subtypes and longitudinal courses. Conclusions The current study failed to show diagnostic usefulness of WAIS‐R in discriminating schizophrenia and other psychoses. A diagnosis of schizophrenia does not significantly impact intellectual deficits in psychotic disorders.  相似文献   
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1. This study was undertaken to evaluate the preventive effects of locally administered argatroban, a competitive inhibitor of thrombin-induced platelet activation, on restenosis after balloon angioplasty. 2. A hydrogel-coated balloon catheter was immersed three times in argatroban/saline solution (1 mg/mL) for 60 s, inflated to a pressure of 606 kPa and left in the rabbit common carotid artery for 1 min. The same procedure was performed, without drug, as a control. The pharmacokinetics of delivered argatroban in the arterial wall were assessed using [14C]-argatroban. Platelet deposition 2h after balloon injury was quantified by fluorescence studies using antiplatelet antibody. Vascular smooth muscle cell (VSMC) proliferation 3 days after balloon injury was assessed by immunohistochemical staining for proliferative cell nuclear antigen (PCNA). In a clinical study, we divided 50 elective patients into two groups: argatroban and control. 3. In the experimental study, the mean quantities of argatroban at 0, 2 and 6 h after deflation wer. 24.63, 0.49 and 0.11 nmol/g wet weight of artery, respectively. Argatroban was undetected 24 h after deflation. Two hours after deflation, argatroban-treated arteries showed less platelet adhesion than saline-treated controls. The mean number of PCNA-positive cells was 16.9 and 43.8% in the argatroban and control groups, respectively (P < 0.01). In the clinical study, the mean late gain loss was 8.2 and 27.3% in the argatroban and control groups, respectively (P < 0.05). The mean late restenosis rate was 11.1 and 41.4% in the argatroban and control groups, respectively (P<0.05). 4. These data suggest that blood coagulation plays a significant role in VSMC proliferation after balloon injury and that locally administered argatroban using hydrogel-coated balloon catheter may prevent post-percutaneous transluminal coronary angioplast. restenosis.  相似文献   
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Radiographic studies of three cases of hypoplasia of the humeral trochlea were done. Several other anomalies were also detected, including a hypoplastic capitellum in case 2, a hyperplastic radial head in cases 2 and 3, and bulging of the loose joint capsule in case 3. Operations in cases 1 and 3, disclosed that ganglions and fibrous septa compressed the ulnar nerve. The cause of ulnar nerve palsy in patients with hypoplasia of the humeral trochlea is thought to be associated with the high incidence of ganglions in hypoplastic elbow joints. The ganglion may play a role.  相似文献   
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