Acta Medica Okayama 51巻 6号

High-resolution magnetic resonance venography (HR-MRV) of intracranial subependymal veins using a two-dimensional Fourier-transform time-of-flight technique was performed on normal volunteers and clinical cases of cerebral disease. For the pulse sequence, fast-field-echo sequence was used with the following parameters: TR/TE/ flip angle = 34ms/12ms/50deg., 256 x 256 matrix, 1 mm effective slice thickness, 150mm field of view, and one signal acquisition. Sequential vertical coronal sections were taken against the skull base. The anterior septal vein, the medial atrial vein, the anterior caudate vein and thalamostriate vein were detected in all subjects. In all clinical cases, HR-MRV was equal in diagnostic capability to conventional cerebral angiography.

Twelve cases of leptospirosis followed by the Infectious Diseases Clinic of the Cukurova University Medical School, Adana, Turkey, between January 1994 and November 1995 are reported. Included are their clinical manifestation, laboratory findings and serotype. Nine men and three women with an average age of 40.4 years were studied. Symptoms, clinical manifestations, laboratory findings and treatment of the disease are evaluated. All of the patients had fever and chills and the following symptoms: nausea and vomiting (91.6%), lower back pain and myalgia (58.3%), headache (50%), epistaxis (16.6%) and confusion (25%). The predominant clinical findings were jaundice (91.6%), hepatomegaly (41.6%), dyspnea (25%), conjunctival suffusion (33%), and nuchal rigidity (33%). Diagnosis was based on dark-field examination of the blood, cerebrospinal fluid and urine specimens. Also, microscopic agglutination tests (MAT) were carried out for serodiagnosis. MAT showed L. inter-rogans serovar icterohaemorrhagiae in 11 cases and L. interrogans serovar grippomosocova in one case. There was cross reaction with L. biflexa patoc in all cases. Agglutinations were tested in the same specimens twice and confirmed in the Microbiology Laboratory of the Etlik Veterinary Research Institute in Ankara. All cases were treated with penicillin and doxycycline. In the end; 83.3% of the patients were cured and 16.6% died due to hepatorenal failure.

Sections of the visual cortex of newborn (1-4 weeks after birth) and adult cats were stained with cationic iron colloid, aldehyde fuchsin or lectins (lectin Vicia villosa, soybean and Wisteria floribunda agglutinins). Many neurons in the adult cat visual cortex contained perineuronal sulfated proteoglycans detectable with cationic iron colloid and aldehyde fuchsin, or cell surface glycoproteins reactive to lectins. Double staining indicated that some of the lectin-labeled neurons were not stained with cationic iron colloid, and also that some of the cationic iron colloid-stained neurons were not labeled with lectins. The perineuronal sulfated proteoglycans and cell surface glycoproteins developed 3 weeks after birth. In the newborn cats 1-2 weeks after birth, no neurons were reactive to cationic iron colloid, aldehyde fuchsin or lectins. In the newborn cats 34 weeks after birth, it was clearly observed that the cytoplasm of the glial cells closely associated with the neurons containing the perineuronal sulfated proteoglycans showed an intense reaction to cationic iron colloid and aldehyde fuchsin, and that the Golgi complexes of the neurons with cell surface glycoproteins were intensely labeled with lectins. These findings suggest that the perineuronal sulfated proteoglycans are derived from the associated glial cells, and that the cell surface glycoproteins are produced by the associated nerve cells.

Characteristics of human hepatoma cell lines with the wild-type p53 were compared with those of human hepatoma cell lines with the mutant-type p53. The p21 protein located downstream of p53 was expressed in cell lines with the wild-type p53 but was not expressed in cell lines with the mutant-type p53. As to other tumor suppressor genes such as p16 and p27, there was no difference in their expression between both types of cell lines. In addition, no marked difference was observed in the activities of CDK2 and CDK4 between cell lines with the wild-type and the mutant-type p53. Phosphorylated Rb protein was detected in all cell lines except the HLE line, indicating that this cell line may have a deletion of and/or a mutation of the Rb gene. These results indicate that abnormalities of tumor suppressor genes other than p53, p16, p27, and Rb may be involved in hepatocarcinogenesis. The population doubling time of the wild-type p53 cells was significantly longer than that of the mutant p53 cells. Neither type of cell line showed a specific chromosome distribution which would indicate karyotype instability. The cell lines expressing the wild-type p53 produced tumors at lower frequency than those with the mutant p53 gene. Although there was no significant difference in effects of TGF-β1, EGF, cholera toxin, and db-cAMP on cell growth between the two types of cells, all three cell lines with the wild-type p53 were resistant to cytotoxicity of TNF-α, while two of the three with the mutant p53 were very sensitive to its cytotoxic effects.

This study was designed to investigate the induction of apoptosis during the reperfusion phase following warm liver ischemia in vivo. We evaluated apoptotic bodies (ABs) in sections stained with hematoxylin and eosin (H. E.) and positive hepatocytes in sections stained by the in situ nick end labeling method (TUNEL method) during the reperfusion phase up to 48 h after a 70% liver ischemia for 30 or 60min in duration (30 or 60 min group). The peak number of ABs in H. E.-stained sections was observed at 1 to 3 h in the 30 min group and 3 to 6 h in the 60 min group. The number of ABs gradually fell as the length of the perfusion period increased, and few ABs were observed at 24 and 48 h after reperfusion. A peak number of TUNEL-positive hepatocytes was recognized at 3 h after reperfusion in both groups, after which the numbers decreased gradually. DNA extracted from both groups was electrophoresed on a 1.5% agarose gel. In both groups, a ladder-like pattern over smear pattern was recognized at 3 h after reperfusion. These results show that hepatocyte apoptosis was induced during the early phase of reperfusion after rat liver ischemia morphologically and biochemically, which suggests that hepatocyte apoptosis may be associated with ischemia and reperfusion injury.

To clarify the nature of nitrogen metabolism between branched chain amino acid (BCAA) and glutamine (GIn) in liver failure, we measured arterial plasma concentrations of GIn and ¹⁵N uptake to amino-N and amide-N of GIn in normal and D-galactosamine-induced fulminant hepatic failure (FHF) rats after ¹⁵N-leucine (Leu) injection. Fifteen, 30 and 60 min after Leu injection, the arterial plasma concentrations of GIn were significantly higher in FHF rats than in controls. The concentrations of amino-¹⁵N GIn were also significantly higher in FHF rats than in controls at 5, 15, 30 and 60 min after injection. The concentrations of amide-¹⁵N GIn did not significantly differ between FHF and controls at 5, 15 and 30 min. However, at 60 min, the concentration was significantly higher in the FHF rats. The higher uptake of ¹⁵N to amino-N of GIn in FHF rats suggests the presence of an enhanced ability to synthesize GIn from Leu in FHF rats. The higher uptake of ¹⁵N to amide-N of GIn in FHF rats at 60 min after injection suggests that excessive administration of BCAA to patients with severely impaired urea-cycle capacity suffering with hepatic failure may lead to greater levels of hyperammonemia.

Two rare cases of carpal tunnel syndrome caused by calcification in the carpal tunnel are reported. One case involved a tumorous calcification consisting of basic calcium phosphate, and the other involved a diffuse calcification consisting of a mixture of calcium pyrophosphate dihydrate and basic calcium phosphate. These cases suggest that the shape of carpal tunnel calcifications is influenced by the nature of calcifying substance itself, i.e., whether it is heterogenous or homogenous.

Lumbar X-ray findings and clinical manifestations were investigated in 10 patients who underwent posterior fusion with or without Harrington instrumentation for idiopathic scoliosis between 1965 and 1975. The subjects were 4 men and 6 women, who ranged from 10 to 17 years of age at the time of surgery (mean, 12 years and 9 months). The postoperative follow-up period ranged from 20 to 30 years (mean, 24 years and 7 months). All patients were followed-up at our institution. Three patients received posterior fusion without instrumentation, and Harrington instrumentation was used in 7 from 1967 onwards. The distal end of the fusion was L2 in 4, L3 in 4, and L4 in 2 patients. Pain, evaluated by Moskowitz's criteria, was stage 1 in 5 and stage II in 5 patients (none of them had stage III or IV). In X-ray evaluation, graded according to Lawrence's classification, grade III changes were noted in 2 patients; one with thoracolumbar fusion with Harrington instrumentation to the L4 vertebra and the other patient was assessed at 30 years post-surgery. According to White-Panjabi's criteria, instability was noted in 1 patient with Harrington fixation including the L4 vertebra. Clinical manifestations and X-ray abnormalities were less severe than anticipated at 20 years plus post-surgery, although a tendency for deterioration was observed in patients with fusion including the L4 or patients followed up for more than 30 years post-surgery.