Role of next-nearest-neighbor hopping in the t-t'-J model.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Tohyama.
Explore the source record for details and available documents.
Many factors have been suggested as possible mechanisms for the development of peritumoural oedema in meningioma. Venous compression by the tumor is thought to be one factor, but reports presenting a direct relationship between venous compression and the formation of oedema are rare. We have recently observed 6 meningioma patients in whom venous stasis contributed to peritumoural oedema. The stasis was due to 1) compression of an adjacent cortical vein by the tumour with stasis at the site of compression and/or its distal portion, 2) compression of adjacent brain by the tumour with prolonged perfusion and delayed venous return (visualized as pial staining in the capillary and venous phases), and 3) presence of an early draining vein linked to a nearby cortical vein with stasis at its periphery. Venous compression and stasis seem to be related not only to the formation of peritumoral oedema but also to the occurrence of haemorrhagic infarction after the resection of meningiomas.
This report describes the clinico-pathological features of a group of 36 patients with malignant lymphoma of the central nervous system (CNS) who were treated at one institution between 1970 and 1993. All cases were B cell type lymphomas. The authors summarize the most salient findings with respect to clinical course, pathology, treatment and disease outcome, and emphasize the value of diagnostic and therapeutic modalities in the management of patients with primary CNS lymphoma.
When pregnant women were tested for antibody to human T-cell leukemia virus-I, some were found to be positive although they had been negative during the previous pregnancy. In these women, HTLV-I infection was found from pedigree studies to have been acquired from their mothers rather than from their husbands. Furthermore, some of them had apparently remained HTLV-I antibody-negative for long periods after infection. When the breast-fed children of these women, in whom HTLV-I was acquired from their mothers but who were in an HTLV-I antibody-negative state, were also examined for evidence of HTLV-I infection, none was found.
Nestin is the major intermediate filament protein of embryonic central nervous system (CNS) progenitor cells. To identify proteins involved in early stages of lineage commitment in the developing human CNS we generated monoclonal antibodies to a TrpE-rat nestin fusion protein. This resulted in a monoclonal antibody (designated NST11) that did not recognize authentic human nestin, but did recognize a novel neuron-specific human polypeptide expressed in a subset of embryonic and adult CNS neurons as well as in medulloblastomas. NST11 immunoreactivity was abundant in developing spinal cord motor neurons, but was extinguished in these neurons by 17 weeks gestation. NST11 also labeled Purkinje cells at 17 weeks gestation, but Purkinje cells continued to express the NST11 antigen throughout gestation as well as in the adult cerebellum, and NST11 immunoreactivity was more abundant in Purkinje cells than in any other human CNS neurons. No NST11 immunoreactivity was detected in cells of the adult human peripheral nervous system or in a variety of adult non-neural human tissues. Further, NST11 almost exclusively stained cerebellar medulloblastomas. In Western blots of immature and mature human cerebral and cerebellar extracts, NST11 did not bind human nestin, but did detect an immunoband with a molecular weight of 220 kd. A similar immunoband was detected in medulloblastoma-derived cell lines with a neuron-like phenotype. These findings suggest that the NST11 monoclonal antibody recognizes a novel protein expressed by a subpopulation of immature and mature human CNS neurons, medulloblastomas, and medulloblastoma-derived cell lines.
Compared to other advanced countries, the field of mental health in Japan is characterized by a large hospitalized to general population ratio and a long mean hospitalization period. This is in large part attributable to the lack of appropriate housing as well as occupational recreational centers after discharge. At the same time the education of psychiatric medical staff has focused on the hospital environment, with little attention devoted to training at centers of community mental health. This hospital-dominant approach has been difficult to shed, and has persisted since the WHO report of Dr. Clark in 1968. Paralleling the introduction of the certified doctor system, at the Japanese Society of Psychiatry and Neurology recently, the manner of postgraduate training for psychiatrists and attempts to reform it were debated. In the midst of this debate, a consensus has emerged that study of community mental health is one of the minimum requirements to become a full-fledged psychiatrist. However, no adequate community mental health training programs have been established at any institution. At Nara Medical University hospitals, considerable weight has been placed on community mental health training, with such a training program designed and put into practice. In the present report, this training program is introduced and interim results reported, and the problems associated with community mental health training are discussed.
We review here recent data that have brought into sharper focus a number of important biological properties of the neoplastic cells in childhood primitive neuroectodermal tumors (PNETs) of the central nervous system (CNS). Studies of this group of tumors, as exemplified by posterior fossa medulloblastomas (MBs), suggest that neoplastic cells in PNETs partially recapitulate stages in the maturation of normal human neuroblasts. These findings may contribute to the elucidation of the mechanisms involved in tumor initiation and progression because oncogenes and antioncogenes appear to exert their effects in a cell type-specific manner that also depends on the maturational state of a given cell. Currently, a large body of data suggests that populations of cells in PNETs (e.g., MBs) exhibit one or more molecular defects in the sequence of maturational events leading to the exit of stem cells or partially committed neuron-like precursors from the cell cycle, followed by their terminal differentiation into neurons. This, together with the orchestrated interactions of as yet unidentified oncogenes and antioncogenes in these PNET cells, may represent a cluster of molecular abnormalities that underly the emergence of the highly malignant phenotype that characterizes childhood PNETs.
Nestin is a recently described member of the intermediate filament (IF) protein family that is especially abundant in neuroepithelial stem cells of the rat. The studies described here examine this class VI IF protein in the normal human developing central nervous system (CNS), human brain tumor-derived cell lines, and tissue samples of human CNS tumors. Human nestin exhibited biochemical and immunochemical properties similar to those of rat nestin. Further, as in the rat, nestin was detected immunohistochemically in several different types of immature human CNS cells, i.e. germinal matrix cells, neuroepithelial cells lining the central canal, radial glia and vascular cells. Nestin appeared in these cells at the earliest gestational age (i.e., 6 weeks) examined here and then it declined in all but the vascular cells at later embryonic stages. Nestin also was detected by immunocytochemistry in 6 of 7 primitive neuroectodermal tumor cell lines and in both of 2 malignant glioma cell lines examined. In these cell lines, nestin co-localized incompletely with bundles of IFs containing other IF proteins (i.e., vimentin, glial filament, neurofilament). Nestin was ubiquitous in a wide variety of brain tumors, but was most prominent in gliomas. The transient expression of nestin in primitive neuroepithelial cells at early stages of human embryogenesis and its abundance in neuroepithelial tumors suggest a role for nestin IFs in cellular events that precede the exit of embryonic CNS stem cells from the cell cycle and the commitment of the progeny of these stem cells to a specific lineage. The subsequent induction of different members of the IF protein family in phenotypically distinct CNS cells (i.e. neurons, glia) and the elimination of nestin from almost all differentiated CNS cells, imply that different classes of IFs subserve functions that are closely linked to the maturational state, as well as the lineage, of CNS cells.
Insights into the programmatic induction of neuronal and glial genes during human embryogenesis have depended largely on extrapolations of data derived from experimental mammals. However, the assumptions upon which these extrapolations are based have not been rigorously tested. Indeed, practically no information is available even on the human counterparts of the relatively small subset of well-characterized, developmentally regulated neuron and glial specific genes of the mammalian CNS. Thus, the developmental programs upon which human neural embryogenesis are based remain largely undeciphered. We have addressed this problem in immunohistochemical studies conducted on 22 human fetal spinal cords with gestational ages (GAs) that ranged from 6 to 40 weeks by using monoclonal antibodies to several classes of neuron or glial specific polypeptides. These polypeptides included: representatives of four different types (Types I-IV) of intermediate filament proteins, i.e., vimentin filament protein (VFP), glial fibrillary acidic protein (GFAP), different phospho-isoforms of the high (NF-H), middle (NF-M), and low (NF-L) molecular weight (Mr) neurofilament (NF) subunits, both acidic and basic cytokeratin (CK) proteins; three different microtubule associated proteins (MAPs), i.e., MAP2, MAP5, and tau; two different synaptic or coated vesicle proteins, i.e., synaptophysin (SYP) and clathrin light chain B (LCb); an oligodendroglial specific protein, i.e., myelin basic protein (MBP); and a receptor for a CNS trophic factor, i.e., the nerve growth factor receptor (NGFR).(ABSTRACT TRUNCATED AT 400 WORDS)
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A case is reported in which a diffuse subarachnoid dissemination occurred after successful removal of a posterior fossa hemangioblastoma. The patient was a 51-year-old man who suffered from headache and gait disturbance, and who was admitted to our hospital on September 25, 1985. Neurological examination revealed trunkal ataxia and increased intracranial pressure. A CT scan with contrast media revealed a high-density lesion with surrounding low-density area in the posterior fossa. Right vertebral angiography demonstrated a round tumor stain behind the medulla oblongata, which was fed by the right posterior inferior cerebellar artery. The complete resection of the tumor was carried out. A biopsy specimen from the tumor showed a picture characteristic of hemangioblastoma. Fourteen months later the patient was readmitted due to the sudden onset of disturbance of consciousness. A CT scan revealed a large intracerebral hematoma in the right putaminal region. Right carotid angiography demonstrated two small tumor stains in the right temporal lobe. An emergency operation to extirpate the hematoma was performed. But the disturbance of consciousness did not improve, and the patient died. At necropsy a lot of small round tumors were recognized at the surface of the bilateral cerebral and cerebellar cortex. They were present in the subarachnoid space and partially invaded the cerebral and cerebellar parenchyma, extending through Virchow-Robin's space. There was no recurrence of the tumor at the site of the original operation. No doubt, a subarachnoid dissemination had occurred. However the histological findings of tumors were similar to the findings recorded in the first biopsy.
A case of systemic lupus erythematosus (SLE) with mononucleosis-like hepatic injury was described. An emergent cesarean section was performed in a 25 yr-old house wife at 34 weeks gestation, followed by administration of several antibiotics. After the surgery she complained of high fever, hepatomegaly and dull right hypochondralgia, and mild liver dysfunction was also found. The liver biopsy showed prominent mononuclear cell infiltration in the sinusoids with minimum hepatocellular necrosis and mild triaditis, resembling hepatic lesion in infectious mononucleosis (mononucleosis-like injury). There were no clinical and serological features suggestive of infectious mononucleosis. This hepatic lesion was thought to be a manifestation of allergic reaction to drugs to which the lymphocyte stimulation test was found to be positive. Immunological abnormalities inherent in SLE might be related to occurrence of such allergic drug reaction.
Explore the source record for details and available documents.
The ratio of portal venous to hepatic blood flow was measured in chronic liver diseases by radionuclide angiography with 99mTc-Sn colloid and its clinical value was discussed. The ratio was proportionally decreased to the progression of the diseases (normal 74.5 +/- 7.3%, chronic hepatitis 58.8 +/- 9.2%, compensated liver cirrhosis 29.3 +/- 19.3%). In alcoholic liver diseases, the standard deviation of the ratio was large as 52.7 +/- 23.7%, and the low ratio in the early period of the disease increased within one or two months as the disease recovered. In comparison with the histological findings of the liver, the ratio in the alcoholic liver diseases was well correlated with the severity of liver fibrosis and liver cell swelling. In conclusion, this noninvasive and simple method is valuable in diagnosing the chronic liver disease, especially alcoholic liver diseases, and also in estimating its clinical course.
Medulloblastoma is the most common primitive neuroectodermal tumor (PNET) with the potential to differentiate along glial or neuronal lines. Thirty cases of medulloblastoma were tested by the peroxidase-antiperoxidase (PAP) method with anti-GFAP serum (DAKO) and by the avidin-biotin peroxidase complex (ABC) method with 68kd subunit of anti-NF antibody. All the cases were classified into three subtypes based on these immunohistochemical findings and were analyzed in relation to clinico-pathological features. Fifteen of thirty medulloblastomas contained GFAP positive cells, seventeen showed cells reacting to NF. The reactions for both proteins were present in eight medulloblastomas (PNET-BD, bipotential differentiation). Seventeen medulloblastomas reacted to only one protein (PNET-MD, monopotential differentiation). No reaction for either was found in five cases (PNET-NOS, not otherwise specified). The two year survival rate was 12.5% for PNET-BD compared to 49.2% for PNET-MD and 53.3% for PNET-NOS. Nine variables, i.e. age, tumor stage, metastatic stage, operation, radiotherapy, chemotherapy, histology, GFAP and NF, were analyzed using Cox's proportional hazard model. This revealed that the significant factors were tumor stage (p = 0.0002), GFAP (p = 0.0008) and operation (p less than 0.05). In conclusion, GFAP is the most important histological factor for prognosis and medulloblastoma without glial differentiation has a much better prognosis than one with glial differentiation.
The first case of hepatic injury induced by Venoplant, extracts of Aesculus Hippocastanum, having antiinflammatory activities, was described. A 37 yr-old man was admitted for treatment of pathological fracture of the left brachial bone. He had been received 65 mg Venoplant at another hospital several hours before admission. 17 days later, a liver function test showed mild abnormality and 60 days after injection, he complained of pruritus and jaundice. Laboratory studies revealed moderate elevation of total bilirubin, ALP, gamma-GTP and mild eosinophilia. CT studies and ERC showed no signs of extrahepatic obstructive jaundice. The lymphocyte stimulation test was positive. The liver biopsy demonstrated marked cholestasis with zonal necrosis in the centrilobular areas but showed little or no changes in the portal tracts. These features are consistent with drug-induced hepatic injury.
The influence of moderate obesity on the liver was assessed in 4613 male company employees including 534 moderately obese subjects (30-50 percent overweight). Serum levels of transaminases and gammaglutamyl transferase activities were significantly higher in moderately obese male non-drinkers than in non-obese non-drinkers. Twenty-four percent of male non-drinkers with moderate obesity had abnormal levels of sGPT and 47 percent of moderately obese male non-drinkers had significant hepatic steatosis as assessed by computed tomography. Although most previous studies on this subject were concerned with morbid obesity accompanying only those of more than 50 percent overweight or those who required surgery, the results of this study clearly indicate that moderately obese subjects also have frequent liver dysfunction.