Anomalous origin of the calcarine artery.
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Carotid Artery, Internal↗
Biomedical subjects
S Waga
Publications and source records attributed to S Waga.
Production of monocyte chemoattractant protein-1 by bovine glomerular endothelial cells.
To explore the role of glomerular endothelial cells (GEN) in the pathogenesis of glomerulonephritis, the in vitro production of monocyte chemoattractant protein-1 (MCP-1) by bovine GEN was determined by chemotaxis assay, and Western blot analysis, and immunocytochemistry. Monocyte chemotactic activity of GEN-conditioned media was detectable by a chemotaxis assay using human peripheral blood monocytes. Exposure to human recombinant interleukin-1 beta (IL-1 beta) and phorbol myristate acetate (PMA) significantly increased the chemotactic activity of GEN-conditioned media. A checkerboard analysis showed that the response of monocytes to GEN-conditioned media was truly chemotactic. Immunoadsorption with a monoclonal antibody to human MCP-1 reduced the chemotactic activity of GEN-conditioned media by 85%. Northern blot analysis revealed that MCP-1 mRNA was constitutively expressed by GEN and that IL-1 beta and tumor necrosis factor-alpha (TNF-alpha) increased MCP-1 mRNA levels in a dose- and time-dependent manner. Furthermore, PMA induced an increase in MCP-1 mRNA levels, whereas dibutyryl cyclic AMP and forskolin had minimal effects. Inhibition study using protein kinase inhibitors revealed that MCP-1 mRNA expression induced by IL-1 beta and TNF-alpha was suppressed by the tyrosine kinase inhibitor genistein, not by the protein kinase C inhibitors staurosporine or H-7, or the protein kinase A inhibitor H-89, suggesting an important role of tyrosine kinase in the cytokine-induced MCP-1 gene expression. Dexamethasone had a small inhibitory effect on constitutive MCP-1 mRNA expression, but no effect on the induction by TNF-alpha. By immunoperoxidase staining and Western blot analysis using an anti-MCP-1 monoclonal antibody. MCP-1 protein was detected in untreated GEN and increased by exposure to TNF-alpha. These results demonstrate the cytokine-induced production of MCP-1 by GEN at gene and protein levels as well as bioactivity, and suggest that GEN may participate in the development of glomerulonephritis through the production of MCP-1.
Blotting, Northern↗
[Medulla oblongata compression by tortuous vertebral artery: case report].
We reported a case of a 58-year-old woman who suffered from progressive tetraparesis and sensory disturbance caused by compression of the medulla oblongata brought about by bilateral tortuous vertebral arteries. The neurological examination on admission revealed tetraparesis, sensory disturbance in all modalities below the level of C2, onion-skin pattern sensory disturbance of the face, and motor weakness of the sternocleidomastoid muscles. X-ray films of the cervical spine showed OPLL at the level of C2.3, but on MRI the dural theca was not seen to be compressed at that level. MRI and vertebral angiography demonstrated ventrolateral compression of the medulla oblongata by bilateral tortuous vertebral arteries. After suboccipital craniectomy and C1.4 laminectomy, decompression of the medulla oblongata was performed. Both vertebral arteries were compressing the medulla oblongata at the ventrolateral side. Transposition of the vertebral arteries seemed impossible due to perforating branches to the medulla. After section of the dentate ligaments at C1 level, the medulla oblongata was decompressed and moved backward. Some small pieces of Dacron were inserted between the arteries and the medulla, in order to decrease the pulsatile effect of the vertebral arteries. Postoperatively, the patient's tetraparesis and sensory disturbance gradually improved. There are 6 reported cases concerning compression of the medulla oblongata by the vertebral artery. As MRI becomes more frequently used in neurological situations, it is important to keep the presence of such an entity in mind.
Female↗
[A case of successful acute revascularization using a long vein graft].
We experienced a case of successful acute revascularization using a long vein graft. A 68-year-old man was admitted to our department due to transient ischemic attack of the left hemiparesis. CT scan showed no infarction, but PAO-SPECT revealed moderate hypoperfusion in the right ACA and MCA area. Cerebral angiography demonstrated right IC occlusion at its origin and moderate collateral circulation via leptomeningeal anastomosis from the PCA area, and via the external carotid system, especially directly from STA. But the STA was very narrow. Three days after admission, left hemiparesis appeared again and deteriorated severely. This time the hemiparesis persisted. Although MRI demonstrated little infarction in the right frontal lobe, we decided to carry out revascularization on the same day. Right saphenous vein was harvested for a graft because of the narrow STA. The facial artery and angular artery was selected as a donor and a recipient respectively, to avoid a clamp of the EC and a craniotomy of the STA running area. Finally we performed a facial artery-vein graft-angular artery (M4) bypass. The patient showed no complication and the left hemiparesis improved enough to allow the patient to walk by himself. Revascularization using vein graft is dangerous for acute ischemia due to the possibility of a complication such as brain edema and hemorrhagic infarction. The usual style of vein graft bypass is an EC-vein graft-M2 or M3 bypass. Using this style, high pressure inside the EC is carried intracranially.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Disease↗
[The current view of molecular biology of DNA tumor virus].
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Animals↗
[Eukaryotic DNA replication: analysis of reconstitution of SV40 DNA replication].
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DNA Replication↗
Differential effects by the p21 CDK inhibitor on PCNA-dependent DNA replication and repair.
In mammalian cells, DNA damage increases the levels of the nuclear tumour-suppressor p53, resulting in elevated synthesis of p21, an inhibitor of cyclin-dependent kinases (CDK). p21 may also directly block DNA replication by inhibiting the proliferating-cell nuclear antigen (PCNA), an essential DNA replication protein. However, PCNA is also required for nucleotide-excision repair of DNA, an intrinsic part of the cellular response to ultraviolet irradiation. Using an in vitro system, we now show that p21 does not block PCNA-dependent nucleotide-excision repair, in contrast to its inhibition of simian virus 40 DNA replication. Furthermore, the short gap-filling DNA synthesis by PCNA-dependent DNA polymerases delta and epsilon is less sensitive to inhibition by p21 than is long primer-extension synthesis. The ability of p21 to inhibit the role of PCNA in DNA replication but not in DNA repair rationalizes in vivo data showing that genetic damage leads to inactivation of chromosomal replication while allowing damage-responsive repair.
Cell Line↗
Neuroprotection by glial cells through adult T cell leukemia-derived factor/human thioredoxin (ADF/TRX).
Adult T cell leukemia-derived factor (ADF) is a human homologue of thioredoxin (TRX) with many biological functions and is induced by various stimuli and stress. In the central nervous system (CNS), expression of ADF/TRX occurs in glial cells during ischemia and reperfusion. We showed that ADF/TRX was actively released from U251 astrocytoma cells upon exposure to a low concentration of H2O2. The addition of conditioned medium from H2O2-stimulated U251 cells or recombinant ADF (rADF) to the culture medium promoted the survival of neurons from embryonic mouse cortex and striatum, but the addition of mutant ADF (mADF), which has no reducing activity, did not. In addition to rADF, incubation with two other thiol compounds, 2-mercaptoethanol (2-ME) and N-acetyl-L-cysteine (NAC), also increased the neuronal cell survival rate. In contrast, L-buthionine-(S,R)-sulfoximine (BSO), which inhibited the synthesis of glutathione (GSH), decreased the neuronal cell survival rate. Intracellular GSH was increased by incubation with rADF for 24 h, as it is with 2-ME and NAC. Redox active molecules such as thiol compounds may be survival factors for central neurons in vitro, and this capacity may be supplied by endogenous molecules, such as ADF/TRX and glutathione, under certain pathologic conditions in vivo.
Acetylcysteine↗
The p21 inhibitor of cyclin-dependent kinases controls DNA replication by interaction with PCNA.
The p53 tumour-suppressor protein controls the expression of a gene encoding the p21 cyclin-dependent protein kinase (CDK) regulator. Levels of p21 protein are increased in senescent cells and p21 overexpression blocks the growth of tumour cells. In normal human cells, but not in many tumour cells, p21 exists in a quaternary complex with a cyclin, a CDK, and the proliferating-cell nuclear antigen (PCNA). p21 controls CDK activity, thereby affecting cell-cycle control, whereas PCNA functions in both DNA replication and repair. Here we use simian virus 40 DNA replication in vitro to show than p21 directly inhibits PCNA-dependent DNA replication in the absence of a cyclin/CDK. Furthermore, p21 blocks the ability of PCNA to activate DNA polymerase delta, the principal replicative DNA polymerase. This regulation results from a direct interaction between p21 and PCNA. Thus, during p53-mediated suppression of cell proliferation, p21 and PCNA may be important for coordinating cell-cycle progression, DNA replication and repair of damaged DNA.
Cell Division↗
Anatomy of a DNA replication fork revealed by reconstitution of SV40 DNA replication in vitro.
Complete enzymatic replication of DNA from the simian virus 40 origin has been reconstituted with T antigen and highly purified cellular proteins. DNA polymerase-alpha/primase functions primarily to synthesize RNA-DNA primers for initiation of DNA replication at the origin and for priming each Okazaki fragment. A polymerase switching mechanism requiring replication factor C and the proliferating cell nuclear antigen allows two molecules of DNA polymerase-delta to replicate both strands of the double helix conjointly.
Animals↗
Reconstitution of complete SV40 DNA replication with purified replication factors.
The identification and purification of human cell proteins required for the production of form I DNA following DNA replication from the simian virus 40 (SV40) origin is described. Using these proteins, complete SV40 DNA replication was reconstituted with only purified DNA replication factors: SV40 large tumor antigen (TAg), replication protein A (RPA), DNA topoisomerases I and II, DNA polymerase alpha-primase, replication factor C (RFC), the proliferating cell nuclear antigen (PCNA), DNA polymerase delta, maturation factor 1 (MF1), and DNA ligase I. MF1, a 5' to 3' exonuclease and DNA ligase I were both identified as essential components for production of covalently closed circular relaxed (form I) DNA. MF1 is probably the same exonuclease previously shown by others to function during DNA synthesis on artificial DNA templates or in conjunction with DNA polymerase alpha from the SV40 origin. Combined with these previous studies, our results suggest that MF1 functions to remove an RNA primer attached to every Okazaki fragment during lagging strand DNA synthesis. Interestingly, whereas mammalian DNA ligase I functioned in the reconstituted replication system, mammalian DNA ligase III did not substitute and the phage T4 DNA ligase functioned inefficiently, suggesting that DNA ligase I has a specific role as a replicative DNA ligase in eukaryotic cells.
Animals↗
Surgical treatment of ossification of the posterior longitudinal ligament in the thoracic spine.
Thoracic ossification of the posterior longitudinal ligament (OPLL) is a rare entity causing thoracic myelopathy. Its surgical decompression is still challenging. Three patients admitted with progressive myelopathy due to thoracic OPLL are described. A transthoracic anterolateral approach was used in the first and second cases, in which OPLL was located at the T3-T4 and T5-T6 and at the T7-T8 levels, respectively. In the third case, a transsternal approach was adopted for OPLL at the T1-T2 level. The OPLL, including dural ossification, was removed by microsurgical techniques as extensively as possible. Myelopathy in all three cases became relieved or stable postoperatively. Operative procedures are described in detail. From the viewpoint of surgical anatomy, the selection of operative approach depends on the level of the OPLL. The authors emphasize that a transthoracic anterolateral approach is the treatment of choice for extensive anterior pathology such as OPLL involving more than two thoracic bodies below the T4. A transsternal approach can provide excellent access to a lesion at the upper three thoracic bodies.
Aged↗
Microsurgical anatomy of the lower cervical spine and cord.
The authors dissected the cervical spine and its surrounding structures from 40 adult cadavers under a surgical microscope. The anterior part of the spine and spinal cord was examined after vertebrectomy. The posterior longitudinal ligament (PLL) consists of two layers; the anterior one is termed the deep layer, and the posterior one is termed the superficial layer. These two layers adhered together loosely. In the lateral portion of the spinal canal, the superficial layer joined the periradicular sheath at the level of the intervertebral disc spaces and joined the dura mater at the level of the vertebral bodies. After the removal of the deep layer, the anterior internal vertebral venous plexus was seen on top of the lateral part of the superficial layer. The venous plexus was embedded between the double-layered PLLs, was not located in the epidural space, and was not seen in the medial part of the PLL. The PLL without venous channels on top of it was about 10 mm in width at the levels of the intervertebral disc and about 5 mm at the levels of the vertebral body. The anterior root exit zone (AREZ) was an elliptical shape; the transverse length of the AREZ was about 2 mm, and the longitudinal length was 10 to 15 mm. The average number of anterior rootlets on the AREZ was 17 to 25 and tended to decrease in the lower cervical spinal cord. The posterior structures were examined after en bloc laminectomy.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Effect of serum from patients with mesangial proliferative glomerulonephritis on cultured rat mesangial cells.
We studied the effect of serum from patients with renal diseases characterized by mesangial proliferation on the proliferation of rat mesangial cells (MC) in culture. Indirect immunofluorescence technique with human anti-proliferating cell nuclear antigen (PCNA) antibody was utilized to detect proliferating MC in S-phase on microscope slides. MC from serum-starved culture medium containing 0.5% fetal calf serum (FCS) showed 6 +/- 2% of PCNA-positive MC, whereas those from complete medium containing 20% FCS showed 45 +/- 7%. This was confirmed by flow cytometry for MC from both conditions, in which 10.9% and 55.2% of S-phase MC were detected, respectively. Serum from 17 patients with IgA nephropathy as a prototype of mesangial proliferative glomerulonephritis produced more PCNA-positive MC than serum from 18 healthy controls (mean +/- S.D. = 21.5 +/- 9.9% vs. 4.4 +/- 5.9%, p < 0.001). In IgA nephropathy, this effect correlated tentatively with active histologic lesion in the glomeruli, but not with severity of urinary abnormalities. Serum from membrano-proliferative glomerulonephritis (MPGN) also produced significant PCNA-positive MC (mean +/- S.D. = 15.6 +/- 9.3%), compared to controls (p < 0.01), independent of the severity of urinary abnormalities. These findings suggest that serum effect on the proliferation of cultured rat MC may reflect an active histologic lesion in the glomeruli, and that anti-PCNA antibody to detect proliferating MC is, if not quantitative, relevant methodology to enumerate proliferating MC in culture.
Adolescent↗
[Primary spinal intramedullary malignant lymphoma: case report].
We report a case of primary spinal intramedullary malignant lymphoma. A 48-year-old man suffered from numbness and weakness of the left leg for 8 months. He was admitted to the hospital with progressive paraplegia and sudden onset of urinary retention. MRI revealed a low intensity mass on T1-weighted image with diffuse enhancement by Gd-DTPA in the thoracic spinal cord. An intramedullary spinal cord tumor was suspected and an urgent laminectomy (C7-Th5) was performed for decompression and confirmation. In the operation, the spinal cord was seen to be diffusely swollen, but no apparent tumor was identified either in color or consistency, and only biopsy was performed. The pathological diagnosis was malignant lymphoma (diffuse medium size-cell type). Investigations excluded the presence of lymphoma in other sites in the central nervous system and in the extraneural organs. We diagnosed a primary spinal intramedullary malignant lymphoma. Postoperative irradiation and chemotherapy were performed. After the irradiation with 16Gy to the tumor and 30Gy to the whole spinal axis, the tumor disappeared on MRI. One month later MRI demonstrated two markedly enhanced lesions in the right frontal lobe white mantle and the corpus callosum. He died of progressive respiratory disturbance 15 months after the beginning of his illness. Primary involvement of the spinal cord in malignant lymphoma is rare. Only 12 cases have been reported. The number of cases of malignant lymphoma in the central nervous system has gradually increased and it must be taken into consideration when diagnosing spinal cord tumors. We are looking forward to developing curative means including chemotherapy and radiotherapy.
Combined Modality Therapy↗
[The current view of molecular biology of DNA tumor virus].
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Animals↗
Regulation of eosinophil migration by adult T cell leukemia-derived factor.
Adult T cell leukemia-derived factor (ADF), originally defined as an IL-2 receptor alpha-chain (IL-2R alpha)/p55 (Tac) inducer, is a human thioredoxin homologue and has many cytokine-like activities. In this study, we examined the regulatory effect of ADF on eosinophil migration using human eosinophils and an eosinophilic subline of HL-60 human promyelocytic leukemia cells, YY-1. rADF induced migration of eosinophils from patients with hypereosinophilia, although rADF exhibited little activity on eosinophils from healthy donors. When human eosinophils were incubated with rADF (0.1-10 micrograms/ml) at 37 degrees C for 24 h, both chemotactic and chemokinetic activity of the complement anaphylatoxin peptide C5a on eosinophil migration was markedly enhanced in a dose-dependent manner. Similarly, this enhancing effect of rADF was observed in the migration assay using YY-1 cells. In contrast, rADF showed no modulation of migratory behavior of human eosinophils and YY-1 cells by IL-3, IL-5, nor granulocyte-macrophage colony-stimulating factor. Scatchard analysis of C5a receptors on YY-1 cells using 125I-C5a showed that rADF modulated neither the density nor the affinity of the cell membrane significantly. Furthermore, mutant ADF (mADF), which had no reducing activity, had no enhancing effect on C5a-induced eosinophil migration. These results indicate a possible involvement of ADF in the recruitment of eosinophils through redox regulation by a dithiol reductase activity.
Adult↗
Different behavior of chromatin domains encompassing fibroin heavy-chain gene in active, temporarily inactive, and permanently inactive transcriptional states in silk gland nuclei.
Chromatin structures of an approximately 46-kilobase pair region encompassing fibroin heavy chain gene of the silkworm, Bombyx mori, were compared in active (in the posterior silk gland nuclei of the fifth instar larvae), temporarily inactive (in the posterior silk gland nuclei of the fourth molting stage larvae), and permanently inactive (in the middle silk gland nuclei of the fifth instar larvae) transcriptional states. Chromatin structure of the second exon, the major body of the protein-encoding region, was highly sensitive to both DNase I and methidiumpropyl EDTA-Fe(II) in the active state but highly resistant to those agents in both temporarily and permanently inactive states, except that the fibroin "amorphous" region-encoding subregions remained relatively sensitive to DNase I. Distributions of DNase I hypersensitive sites in the 5' upstream region were generally similar between active and temporarily inactive states, but those of the permanently inactive state were markedly different. In the promoter-enhancer region, phosphodiester bonds between nucleotide positions -41 and -42 and also -42 and -43 were remarkably hypersensitive to DNase I in the active chromatin, but the same positions in the other two states were not.
Animals↗