Uptake of Au(III) Ions by Aluminum Hydroxide and Their Spontaneous Reduction to Elemental Gold (Au(0)).

The behavior of AuCl(4)(-) ions during the formation of aluminum hydroxide at pH 6 was examined. With an increase in NaCl concentration, the content of gold taken up by aluminum hydroxide decreased, suggesting that chloro-hydroxy complexes of Au(III) ion were taken up due to the formation of Al-O-Au bonds. It was found unexpectedly that the Au(III) ions taken up were spontaneously reduced to elemental gold without addition of a specific reducing reagent and then colloidal gold particles were formed. The mechanisms for the uptake of Au(III) ions by aluminum hydroxide and for their spontaneous reduction are discussed. Copyright 2001 Academic Press.

[Evaluation of a respiratory care unit on a 45-bed hospital ward].

With a limited number of beds for patients undergoing medical and surgical treatment for respiratory diseases, we set aside 6 of 45 beds on one floor to be used as a respiratory care unit. During the past 5 years, 1820 patients (1225 medical and 595 surgical) were admitted to the respiratory care unit; they were treated for an average of 5.02 days. Of the patients being treated medically, 451 received mechanical ventilatory support. The majority of those patients had acute exacerbations of chronic respiratory failure due to emphysema or to sequelae of pulmonary tuberculosis. Acute respiratory distress associated with asthma or with pneumonia were also relatively common, as was the adult respiratory distress syndrome. A total of 119 patients on home oxygen therapy are being seen as out-patients, and the respiratory care unit was found to be quite useful whenever they needed intensive management. Only 148 (8.1%) of the patients admitted to the respiratory care unit died before discharge, and the ratio of cost to performance was good. The respiratory care unit was most effective in allowing for continuity of care from the onset of respiratory distress, and including exacerbations, surgical interventions, postoperative management, and out-patient care.

Accessory middle cerebral artery and duplication of middle cerebral artery--terminology, incidence, vascular etiology, and developmental significance.

A series of 455 bilateral carotid angiographies included 14 accessory middle cerebral arteries (Acc-MCAs) and seven duplication of middle cerebral arteries (Dup-MCAs). The branching patterns of Dup-MCA could be classified as "direct bifurcation" from the internal carotid artery, since most lacked the essential bifurcation or trifurcation at the distal end of the M1 portion. On the other hand, Acc-MCAs are probably residual congenital arteries. These anomalous MCAs were apparently associated with epilepsy. Five Acc-MCAs were associated with anterior communicating artery aneurysm at the origin. In addition, a rare case of Dup-MCA with arteriovenous malformation at its origin was found.

Monoclonal antibody against ependymoma-derived cell line.

Mouse myeloma cells were fused with spleen cells from mice that had been immunized with a human ependymoma derived cell line, KMS II. Hybridomas producing monoclonal antibodies (MAbs) were screened and cloned. Specificity of the antibody was determined by enzyme-linked immunosorbent assay (ELISA) and/or indirect immunofluorescence assay. One of the MAbs, designated Ep-C4 (subclass = IgG1), reacted with two cell lines derived from ependymoma but did not react with 17 cell lines derived from other types of brain tumor nor with 4 neuroblastoma cell lines or 19 cell lines derived from carcinoma, hematopoietic tumors and amnion. Indirect immunofluorescence and immuno-electron microscopy studies revealed that the antigen recognized by MAb Ep-C4 was located on cell surface membrane. The membrane antigen of KMS II cells, immunoprecipitated by MAb Ep-C4, was a protein of 81,000 dalton. The reactivity of MAb Ep-C4 was further examined using immunofluorescence and/or immunoperoxidase methods and frozen sections and short-term cultures of various types of brain tumors. No cross-reactivity with normal adult or fetal brain tissues was detected by absorption assay and immunoperoxidase staining. Our results suggest that the antigen defined by MAb Ep-C4 is specific for ependymoma cells, and different from the antigens of glioma cells or other neuroectodermal-derived cells previously described.

[Improvement of ischemic symptoms and cerebral blood flow after percutaneous transluminal angioplasty for renovascular hypertension. Report of a case with multiple cerebrovascular occlusive disease].

A 53-year-old male complained of frequent left motor-sensory transient ischemic attack for 4 months. On admission, he demonstrated mild right hemiparesis, dysarthria, and right hemisensory disturbance of all modalities. Cerebral angiography demonstrated complete occlusion of the left internal carotid artery just above the origin of the ophthalmic artery and a stenotic lesion at the horizontal segment of the right middle cerebral artery. Renal angiography showed severe stenosis of the right renal artery. Systolic blood pressure was over 200 mmHg and marked circadian variation of blood pressure was noted. Serum renin was 4.0 ng/ml/hr. Four months after superficial temporal artery-middle cerebral artery anastomosis, left carotid angiography showed good patency of the bypass and the ischemic symptoms completely disappeared. Single photon emission computed tomography (SPECT) showed increased cerebral blood flow (CBF), especially in the left hemisphere after surgery. Six months after the bypass surgery, he complained of mild right hemiparesis again. Shortly after percutaneous transluminal angioplasty (PTA) for renal arterial stenosis, his hemiparesis was improved and the systolic blood pressure stabilized to 150-170 mmHg. SPECT showed the CBF had also recovered in both hemispheres. The improvement in ischemic symptoms and increased CBF after PTA were probably related to stabilization of the systemic blood pressure or inhibition of serum renin-angiotensin.

Microvascular decompression for hemifacial spasm. Patterns of vascular compression in unsuccessfully operated patients.

To determine the causative factors of unsuccessful microvascular decompression for hemifacial spasm, the follow-up results in 53 patients were assessed retrospectively. The mean follow-up period was 36 months. There were 32 patients who had compression of the seventh cranial nerve ventrocaudally by an anterior inferior cerebellar artery (AICA) or a posterior inferior cerebellar artery. Of these 32 patients, 30 (94%) had excellent postoperative results. Of 14 patients with more severe compression by the vertebral artery, nine (64%) had excellent results, three (21%) had good results, and two (14%) had poor results; in this group, three patients with excellent results experienced transient spasm recurrence. There were seven patients in whom the meatal branch of the AICA coursed between the seventh and eighth cranial nerves and compressed the dorsal aspect of the seventh nerve; this was usually associated with another artery compressing the ventral aspect of the nerve ("sandwich-type" compression). Of these seven patients, five (71%) had poor results including operative failure in one and recurrence of spasm in four. The authors conclude that the clinical outcome was closely related to the patterns of vascular compression.

[Diagnostic value of short latency somatosensory evoked potentials for various intracranial lesions].

Diagnostic value of short latency somatosensory evoked potentials (SSEP) was studied in 124 patients with various intracranial lesions. Abnormal SSEPs were recorded in 58 of 124 patients (46.8%) and were classified into three types. Type I (6 cases) showed abnormality of late components with N18 being preserved. All patients with type I abnormality had cortical or subcortical lesions in the parietal lobe. Type II (20 cases) was characterized by abnormality of N18 and late components with N16 being preserved, and mainly seen in patients with a lesion involving thalamus and internal capsule. Type III (31 cases) showed abnormality of N16 and N18 which was elicited by unilateral stimulation (IIIa: 11 cases), or bilateral stimulation (IIIb: 21 cases), and this indicated brainstem impairment. The incidence of SSEP abnormality was as high as 93.1% in patients with sensory disturbance, and 23.1% in patients without such disturbance, and it was suggested that SSEP is useful to detect subclinical dysfunction in the somatosensory pathway. The SSEP grades defined by Anderson et al were found to be well correlated with the outcome of patients with severe head injury, and the SSEP was more reliable for predicting the outcome of patients than the auditory brainstem evoked responses. The SSEP grades were also fairly well correlated with the outcome of patients with cerebrovascular accidents, although the outcome was not consistent in patients with moderately abnormal SSEP.

Influence of vasopressin level on osmotic pressure and sodium concentration in plasma and cerebrospinal fluid in patients with intracranial lesions.

To study the influence of the vasopressin level on osmotic pressure and sodium concentration in plasma and cerebrospinal fluid (CSF), plasma and CSF were sampled simultaneously in 27 patients with central nervous system lesions. A significant elevation of arginine vasopressin (AVP) levels in plasma and CSF and a significant increase in the osmotic pressure gradients of plasma and CSF were observed in hyponatremic patients. The significant increases in the osmotic pressure gradients may be attributable to hemodilution and CSF concentration resulting from the elevated AVP level, because the sodium concentration gradients of plasma and CSF did not significantly increase. The elevated AVP levels in plasma and CSF and the increased osmotic pressure gradients of plasma and CSF normalized in parallel with improvement of consciousness. These findings suggest that the increased osmotic pressure gradients of plasma and CSF, derived from increased AVP secretion into blood and CSF, exacerbates brain edema induced by the primary lesion and may contribute to the clinical deterioration of some patients with intracranial lesions.

[Uptake and localization of neocarzinostatin in malignant glioma. Experimental study by immunofluorescent staining method].

The authors studied the localization of neocarzinostatin (NCS) in cultured cells and in tumor-bearing rats by means of immunofluorescent staining. Anti-NCS antibody was obtained through immunization of rabbits with NCS. Cellular uptake of NCS was dose-dependent (1.0 to 1000 micrograms/ml) in 9L rat gliosarcoma cells in monolayer. In monolayer cells of 9L, KMG-4 (derived from human glioblastoma), and KMS II (human ependymoma) treated with 1 mg/ml of NCS, drug uptake occurred within a few seconds. Accumulation was much higher in the cytoplasm than in the nucleus and, although nuclear uptake increased slightly over time, there appeared to be no increase in total cellular uptake. Mitotic cells, which were spherical in culture, showed greater intracellular accumulation than other cells. There was no significant difference in uptake among non-mitotic cells. Cells surviving 20 hours of treatment retained accumulation as high as that in killed cells. In KMG-4 monolayers, cytoplasmic and nuclear NCS distribution still differed, whereas 9L monolayers exhibited more even intracellular distribution. In 9L spheroid models treated with 1 mg/ml of NCS, the drug permeated almost all layers within 10 minutes, and at 120 minutes had heavily accumulated in the central necrotic areas. In rats with transplanted brain tumors, NCS selectively accumulated in neoplastic tissues following intra-arterial administration. However, NCS uptake by arterial endothelium was also seen, which suggests the potential for vascular toxicity. The therapeutic value of NCS is discussed in terms of its pharmacokinetic characteristics.

[Pharmacokinetics of neocarzinostatin in patients with malignant glioma. Quantitative analysis of tissue concentration].

Because of technical difficulties, the pharmacokinetics of neocarzinostatin (NCS) have not been thoroughly evaluated in patients with malignant glioma. The authors produced anti-NCS antibody by immunizing rabbits with NCS and established a means of quantifying tissue levels of NCS with enzyme-linked immunosorbent assay. In one patient given a bolus injection of 1 mg of NCS intra-arterially, the concentration of drug in neoplastic tissue at 25 minutes (0.1136 micrograms/g) was higher than that in blood at 20 minutes and was retained for a longer period. Rapid entry of NCS into the tumor cavity was observed at 5 minutes. In two postoperative cases, NCS applied topically to the tumor site (50 and 100 micrograms) was retained at high levels (0.2941 and 3.33 micrograms/ml) even after 48 hours, although no NCS was detected in blood after 60 minutes. NCS concentrations as low as 1 microgram/ml demonstrated cytocidal effects, and a delay in tumor growth was observed even at an NCS level of 0.1 microgram/ml, despite the fact that the half-life of NCS is extremely short (3 seconds in serum). Because its cytotoxic effect seems to be very rapid, it appears more important to obtain a high initial NCS concentration than to maintain a constant blood level.

[Immunological function in head-injured patients. Relationship with severity of injury and age].

The immunological function of 29 head-injured patients was investigated, with special reference to the relationships between changes in immunity and both severity of head injury and age. The patients were classified according to Glasgow Coma Scale scores (15, 9 to 14, and 3 to 8) and age (under 35, 35 to 65, and over 65 years). T cell subsets (OKT4 and OKT8) and Leu-11a cells were studied by flow cytometry with the use of monoclonal antibody. Lymphocyte stimulation indices were also evaluated. The percentage of OKT4 cells was significantly decreased in the young patients with severe head injury, whereas the percentage of OKT8 cells remained almost within the normal range. Thus, the ratio of OKT4 to OKT8 cells was decreased. The percentage of Leu-11a cells showed no correlation with severity of injury or age. Lymphocyte stimulation indices were reduced in cases of severe head injury. In this study, patients with severe head injury were immunosuppressed, particularly those under age 35.

Import and processing of precursor to mitochondrial aspartate aminotransferase. Structure-function relationships of the presequence.

The precursor protein of pig mitochondrial aspartate aminotransferase (pre-mAspAT) contains a 29-residue presequence (Joh, T., Nomiyama, H., Maeda, S., Shimada, K., and Morino, Y. (1985) Proc. Natl. Acad. Sci. U. S. A. 82, 1-5). Pre-mAspAT produced in an in vitro transcription and translation system was avidly imported into pig and rat liver mitochondria to be processed to the mature form of the enzyme. The pre-mAspAT was also processed to the mature form upon incubation with mitochondrial extracts. We synthesized precursor proteins with alterations within the presequence and compared quantitatively the effects of these mutations on the rates of both import and processing. Single and multiple substitutions of four basic residues with neutral amino acids at positions 5, 8, 18, and 28 showed that each residue contributes differentially to import and processing. Substitutions of His5 and Arg8 with glycines abolished the import activity but did not appreciably affect the rate of processing. Substitution of Arg28 with leucine at the position adjacent to the cleavage site seriously impaired the processing without appreciably affecting the rate of import. Analysis of deletions revealed that the amino-terminal region from position 2 to 8 was essential for both the import and processing. Thus the positive charges in the amino-terminal region are critical for import while the amino-terminal peptide segment and the cleavage site region appear to be requisite for recognition by a processing protease.

[Clinical significance of sialic acid in the CSF; in relation to the malignancy and leptomeningeal dissemination].

We examined the level of sialic acid in cerebrospinal fluid (CSF) in 20 patients with brain tumor, and 5 patients with non-neoplastic disease of central nervous system. CSF concentration of sialic acid in the patients with malignant and semi-malignant or benign brain tumor was 5.26 +/- 2.39 mg/dl, and 1.82 +/- 1.61 mg/dl, respectively. In patients with non-neoplastic disease, it was 1.64 +/- 1.53 mg/dl. The difference between groups was statistically significant (p less than 0.005). In two patients with malignant brain tumor, the level of sialic acid was decreased by radiation therapy or intrathecal chemotherapy. In conclusion, CSF concentration of sialic acid was significant of diagnosis of brain tumor character of malignancy, and effect of therapy for CSF dissemination.

[Lipid metabolism of the patients with subarachnoid hemorrhage due to ruptured intracranial aneurysm--with special reference to the occurrence of cerebral angiospasm].

Lipid metabolism, which can be an important factor for arteriosclerosis, was studied in the patients with subarachnoid hemorrhage due to ruptured intracranial aneurysm. Total cholesterol, LDL-cholesterol, HDL-cholesterol, triglyceride and Atherogenic Index were determined in 131 patients, who were admitted to our hospital since May, 1984 to March, 1986. Those results were analyzed in relation to the grading on admission, outcome and especially cerebral angiospasm. Serum levels of LDL-cholesterol and Atherogenic Index tended to correlate with the grading on admission. Total cholesterol, Atherogenic Index well correlated with the recovery of the patients and the activity of daily life. In this study, we especially examined the relationship with cerebral angiospasm. The results suggested that the role of cerebral arteriosclerosis caused by disturbance of lipid metabolism was rather negative to the development of cerebral angiospasm after subarachnoid hemorrhage.

[A case of cerebral gumma].

A case of cerebral gumma in the left trigonal region is reported. A 74-year-old man was admitted to our hospital on Apr. 23, 1985 with unsteady gait and memory disturbance. Neurological examination revealed slight disorientation, memory disturbance, right homonymous hemianopsia and right hemiparesis. Serological reaction for syphilis was strongly positive, and so was CSF. The CSF showed slight pleocytosis (8/3 lymphocytes) and increased protein content (130 mg/dl). DSA showed no hypervascularity nor tumor stain. Ga brain scan showed no abnormality. The CT scan revealed an irregular low density area near the left trigone with abnormal contrast enhancement. Because of the radiological findings a malignant lymphoma was diagnosed and biopsy was performed, however, histological investigation confirmed the diagnosis of cerebral gumma. The patient was treated with penicillin and reduction of the tumor size was observed on CT scan. Cerebral gumma has been reported only rarely during the last few decades, and there are only a few descriptions of the neuroradiological characteristics of this disease. An accurate diagnosis can be made only by taking into consideration the clinical findings and course, the serological results, and the effect of the antisyphilitic treatment. When dealing with CT imaging similar to an intracranial malignant lymphoma, syphilitic disease of the brain should be regarded as possibly being present.

Immunohistochemical localization of apolipoprotein E in human glial neoplasms.

Immunocytochemical analyses revealed the presence and distribution of apolipoprotein E (apo E) in normal human brain tissue as well as in 77 human intracranial neoplasms. In normal brain tissues, the perikarya of astrocytes exhibited a strong positive reaction, whereas the Bergmann glia were stained to a moderate degree. However, no immunoreactivity was observed with neurons, oligodendrocytes, ependymal cells, and choroidal epithelium. Among the intracranial neoplasms, oligodendroglioma, choroid plexus papilloma, hemangioblastoma, primary malignant lymphoma, neurinoma, meningioma, pituitary adenoma, and craniopharyngioma were all negative. Immunoreactivity in the peripheral neuroblastoma was nil. However, the perikarya of astrocytomas and glioblastomas showed a positive reaction. Analyses on the degree of anaplasia and the amount of apo-E as an intensity of immunostaining showed a negative correlation. The astrocytic elements were stained in mixed oligoastrocytomas and medulloblastomas with glial differentiation. A few cases of ependymomas showed weak perikaryal immunostaining. Western blot analyses with anti-apo E antibody of a freshly prepared surgical specimen with astrocytomas revealed a single band with a molecular weight of approximately 37,000. The well differentiated cultured human astrocytoma cells secreted apo E into the medium. These lines of evidence suggest that apo E may serve as a potential marker specific for astrocytomas and glioblastomas, as well as an indicator of astrocytic tumor cell differentiation. The apo E localization in human brain tumors could be clinically relevant and diagnostically useful.