Retreatment with interferon in chronic hepatitis C.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K Kurose.
Explore the source record for details and available documents.
Renal biopsy specimens from 42 children with IgA nephropathy and 23 with Henoch-Schönlein purpura nephritis (HSPN) were examined to investigate the relationship between intraglomerular and interstitial infiltrating macrophage populations and their clinicopathological findings. Macrophages were stained by monoclonal antibody (CD68) using the ABC method. Intraglomerular and interstitial macrophages were significantly increased in HSPN (2.48 +/- 2.71/glomerular cross-section: gcs, 11.54 +/- 11.67/mm2) compared with IgA nephropathy (1.36 +/- 1.09/gcs, 5.30 +/- 4.53/mm2). Infiltrating macrophages were significantly increased in both renal disease compared with minimal change nephrotic syndrome (0.29 +/- 0.12/gcs, 1.36 +/- 0.82/mm2). Infiltrating macrophages tended to decline with the lapse of time between the renal biopsy and the discovery of the renal disease, especially in HSPN. Increase in glomerular macrophages in HSPN was associated with the severity of their clinicopathological findings, but this was not the case in IgA nephropathy. Interstitial macrophages were increased in patients with severe clinicopathological findings in both disease. Patients having both proteinuria and hematuria showed many infiltrating macrophages compared to those with proteinuria or hematuria alone. These findings suggest that intraglomerular and interstitial infiltrating macrophages play important roles in the acute and early phase of IgA nephropathy and HSPN in children.
The intraglomerular and interstitial infiltrating macrophage population was studied in patients with IgA nephropathy (19 cases) and Henoch-Schönlein purpura nephritis (HSPN) (7 cases) who had undergone re-biopsy. Macrophages were stained by monoclonal antibody (CD68) using the ABC method. In HSPN, intraglomerular and interstitial infiltrating macrophages were significantly decreased in the second biopsy (0.57 +/- 0.56/gcs, 4.31 +/- 2.42/mm2) compared with the first (2.54 +/- 1.39/gcs, 18.37 +/- 11.96/mm2). In IgA nephropathy, fewer macrophages were noted at the second biopsy (0.78 +/- 0.44/gcs, 4.52 +/- 5.07/mm2) compared with the first (1.79 +/- 1.17/gcs, 5.98 +/- 4.88/mm2), and a statistical significance was found in intraglomerular macrophages, but not in the interstitium. Infiltrating macrophages were rapidly decreased in patients with improved clinicopathological findings at the second biopsy. Infiltrating macrophages tended to decline with the lapse of time from the discovery of the disease, without any relation to treatment.
The relationship between the intraglomerular infiltrating macrophage population and crescents was studied in IgA nephropathy (first biopsy: 468 glomeruli of 42 patients, re-biopsy: 183 glomeruli of 19 patients) and Henoch-Schönlein purpura nephritis (HSPN) (first biopsy: 275 glomeruli of 23 patients, re-biopsy: one glomeruli of 7 patients). Macrophages were stained by monoclonal antibody (CD68) using the ABC method. In the glomeruli with crescents and in patients having many crescents, many macrophages infiltrated in HSPN and at an early stage of IgA nephropathy, but not at the late stage of IgA nephropathy. Glomeruli with cellular crescents showed many macrophages compared with those with fibrocellular or fibrous crescents. In addition, 20.6% of intraglomerular macrophages were observed on the crescents. These findings suggest that macrophages play important roles in the early phase with cellular crescents in IgA nephropathy and HSPN.
A 14 years old boy experienced an anaphylactic reaction of dyspnea, vomiting, urticaria and hypotension after he ate sunflower seeds. Specific IgE-mediated hypersensitivity to sunflower seen extract was demonstrated by skin tests and radioallergosorbent test (RAST). By immunoblotting test analysis (SDS-PAGE, Western blotting method), the allergenic activity of sunflower seem were shown to be in the MW range of 13.5 Kd.
We report here a nine-year-old boy with oligomeganephronia. The patient had proteinuria and morphometric analysis of the renal biopsy specimen confirmed the diagnosis of oligomeganephronia. We employed a color image analyzer (OLYMPUS Corp.) to determine the glomerular surface area and the number of glomeruli per mm2 of the renal cortex of the patient. All the scanned glomeruli showed marked hypertrophy; the mean maximal surface area for the 5 glomeruli was 46 x 10(3) microns 2, which is approximately 4 times larger than that of normal children of the same age. The number of glomeruli per mm2 of the renal cortex of the patient had decreased to 1. 11 per mm2, which is approximately one fourth that of normal controls with IgA glomerulonephritis. The color image analyzer proved to be useful for the diagnosis of oligomeganephronia enabling the quantitative measurement of the glomerular surface area and the number of glomeruli per mm2 of the renal cortex.
We studied about the histological findings of the kidneys including of the infiltrated macrophages in one hour post-transplantation kidney biopsies (one hour biopsies) and re-biopsies on 11 patients. They were transplanted at 4-28 (ave. 15.1 +/- 3.8) years of age. The periods from transplantation to this study were 1.0-7.3 (ave. 3.3 +/- 1.9) years. 6 patients had acute rejections, and their renal function became normal after treatments. At this study, all grafts survived, and the patients had no abnormal findings except two (one had proteinuria, another had proteinuria and mild elevation of serum creatinine level). But histologically, five patients had chronic rejections among the 8 patients who had re-biopsies more than one year after transplantation. And we experienced 6 patients whose kidney had mesangial IgA deposits in one hour biopsies and 3 patients who had de novo type glomerulonephritis in re-biopsies (IgA neuropathy in 2 patients, membranous nephropathy in one). In one hour biopsies, the populations of macrophages in the interstitium were 4.18 +/- 2.84/mm2 in the patients who would have acute rejections (6 patients), 1.38 +/- 1.13/mm2 in the cases who would not have. It was suspected that the increase of the infiltrated macrophages in the interstitium in one hour biopsies could predict acute rejections. In re-biopsies, many macrophages infiltrated in the interstitium (8.34 +/- 4.86/mm2), particularly on patients who had chronic rejections.
We have encountered 2 cases of hemorrhagic vascular lesion in the external carotid artery system caused by facial injury. In case 1, treatment of epistaxis by nasal packing was unsuccessful. Good result was obtained by intravascular embolization in the internal maxillary artery using polyvinyl alcohol particles and gelatin sponge pieces. In case 2, massive subgaleal hemorrhage due to tearing of the middle meningeal artery caused by a skull base fracture appeared following surgery for open skull fracture. Hemostasis was performed successfully by intravascular embolization in the middle meningeal artery using microcoils and gelatin sponge pieces. In cases of facial injuries with hemorrhagic lesions in the external carotid artery system, hemostasis is generally difficult. Referring to these two cases, we think that the treatment of choice is angiography followed by intravascular embolization.
L1 (LINE-1) is a long interspersed repetitive sequence derived from a retrotransposon. Transfection studies using the CAT gene as a reporter demonstrated that the first 155bp in the human L1 sequence contains an element(s) responsible for the promoter activity in HeLa cells. The transcription was shown to initiate at the first nucleotide of the L1 sequence in the transgene. Three prominent nuclear protein binding sites were found in the 5' region of the L1 sequence by DNaseI footprint analysis. One of the binding sites, designated as site A located at +3 to +26, was shown to be essential for the L1 transcription because the mutation at the site A caused almost complete loss of the promoter activity. A sequence AAGATGGCC at +11 to +19 in the site A was defined as a target core element for the protein binding. The site A-binding protein (designated TFL1-A) was found in various types of cells including an embryonic teratocarcinoma cell line. These results indicate that an internal short element located at the very 5' terminal of L1 sequence and the nuclear factor binding to the element play a crucial role in the transcription of human L1.
We have previously found that neonatal administration of cytosine arabinoside (Ara-C) induces cerebellar malformation, including arrest of granule cell migration and destruction of glial palisade. In the present study, the expression of neural cell adhesion molecule (N-CAM) and its distribution were examined in the mouse malformed cerebellum induced by neonatal Ara-C administration. Western blot analysis demonstrated that, in the control group, the embryonic form of N-CAM (E-N-CAM) was expressed in the 7-day-old mouse (P7) cerebellum, but not in the P14 cerebellum which exhibited only the adult form of N-CAM (A-N-CAM). On the other hand, E-N-CAM was expressed in the Ara-C treated cerebellum not only at P7 but also at P14. Immunohistochemical studies revealed that E-N-CAM was observed in the area below the external granular layer (EGL) of the P7 cerebellum in both the control and Ara-C treated mice. In contrast, E-N-CAM immunoreactivity was found in the arrested EGL cells in the Ara-C treated cerebellum of P14 mice but not in the age-matched controls. Therefore, E-N-CAM was aberrantly expressed in the arrested EGL at P14. From the present and previous findings, it was speculated that the aberrant expression of E-N-CAM in the arrested EGL cells is attributed to abnormal cellular interactions, probably arrested EGL cell-to-Bergmann glia.
Recently, a new transthyretin (TTR) variant was described in the normal Portuguese and German populations. The same substitution was found associated with familial amyloidotic polyneuropathy (FAP) in an American family of Italian origin. Comparative isoelectric focusing studies showed a difference in the mobility pattern between the non-pathogenic and pathogenic variants. However, comparative DNA sequencing between them did not reveal any additional mutation. Comparative isoelectric focusing between the variants and TTR Asn 90 produced by recombinant techniques indicated that the non-pathogenic variant has the electrophoretic behaviour expected for the mutation. We suggest that an as yet unknown post-translational modification may have occurred in the FAP-associated Asn 90 variant, turning it into an amyloidogenic molecule.
Retinal projections in the house musk shrew (Suncus murinus) were determined by the anterograde transport of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP). Unilateral injection of WGA-HRP into the vitreous body resulted in the terminal labeling of the optic projections in the suprachiasmatic nucleus (SCH), the ventral (CGLv) and dorsal (CGLd) lateral geniculate nuclei, the intergeniculate leaflet (IGL), the pretectum, the superficial layers of the superior colliculus (CS), and the dorsal terminal nucleus (DTN) of the accessory optic system (AOS). Labeling of the SCH was bilateral, with ipsilateral predominance, and covered the whole dorsoventral extent of the nucleus. Immunohistochemical studies revealed that VIP-like immunoreactive neurons and fibers were present in almost all parts of the SCH. No hypothalamic regions other than the SCH received the optic fibers. The ipsilateral projections to the CGLv, CGLd, and IGL were sparse, and a considerable number of uncrossed retinal fibers were found in the pretectal olivary nucleus. No retinal projections to the lateral posterior thalamic nucleus (LP) were found. Ipsilateral optic fibers projected sparsely to the medial part of the CS. The AOS consisted of a small DTN with a very few crossed retinal projections but no lateral and medial terminal nuclei. In addition, the AOS had no inferior fascicle.
A monoclonal antibody (MAb-1E7), generated against bovine retinal homogenate, labeled the outer and inner segment layers of the vertebrate retina. Immuno-electron microscopic observation clearly demonstrated that antigen(s) bound by MAb-1E7 was localized in the cell membrane of the outer segment and the distal portion of the inner segment. Western blot analysis revealed that MAb-1E7 recognized 40 kD- and 27 kD-polypeptides. Mouse retina with hereditary photoreceptor degeneration (C3H/He and CBA strains) did not involve the MAb-1E7 immunoreactive structures. The present immunocytochemical observation demonstrated that MAb-1E7 was highly specific to the outer segment of the photoreceptor cells and, therefore, can be a useful marker for the cells.
The authors report a case of unilateral moyamoya disease which developed into moyamoya disease 3 years later. Unilateral moyamoya disease is generally defined as moyamoya disease, but the exact relationship is unknown. In this case, occlusive changes developed in the stenotic carotid fork, and in a similar portion contralaterally which was intact. Follow-up 4-vessel angiography is strongly recommended even for unilateral moyamoya disease.
A rare case of a type 2 proatlantal artery discovered following the rupture of a cerebral aneurysm in a 74-year-old female is reported. The aneurysm was clipped and the hematoma removed, but she died of severe vasospasm 9 days after surgery. The anomalous artery was thought to have been unrelated to rupture of the aneurysm.
Aequorin is a monomeric Ca2+-binding protein (Mr, 21,400) that emits light upon reacting with Ca2+. The protein has three Ca2+-binding sites, three cysteine residues, and a noncovalently bound chromophore that consists of coelenterazine and molecular oxygen. Light is emitted via an intramolecular reaction in which coelenterazine is oxidized by the bound oxygen. After light emission, aequorin may be regenerated by incubating the protein with coelenterazine, dissolved oxygen, EDTA, and 2-mercaptoethanol. To understand structure-function relationships in this protein, we used the technique of site-specific mutagenesis to replace the three cysteine residues with serine. Six of the seven modified aequorins had reduced luminescence activity, whereas the seventh with all three cysteines replaced by serine had luminescence activity equal to or greater than that of the wild-type aequorin. Further, the time required for the regeneration of the triply substituted aequorin was substantially increased compared to the time required for the regeneration of the wild-type aequorin. The results suggest that cysteine plays an important role in the regeneration of aequorin but not in its catalytic activity.
A 44-year-old female developed aphasia and visual disturbance of the left eye. Four-vessel angiography showed occlusion of the extra- and intracranial portions of the right internal carotid artery, severe stenosis of the left internal carotid fork, bilateral moyamoya vessels, and a persistent primitive hypoglossal artery on the left side. Measurement of cerebral blood flow by 133xe inhalation revealed decreased flow and no response to acetazolamide loading in the left cerebral hemisphere. The patient underwent superficial temporal artery-middle cerebral artery anastomosis, first on the left and then on the right side. There have been no other reported cases of moyamoya disease associated with a persistent primitive hypoglossal artery. Although the cause of moyamoya disease remains to be established, it is generally believed that stenotic changes of the carotid fork cause the development of moyamoya vessels as collateral pathways. According to this theory, there is no significant etiological relationship between moyamoya disease and persistent primitive hypoglossal artery. However, persistent primitive hypoglossal artery is compatible with moyamoya disease in terms of providing a collateral pathway via the vertebrobasilar system.
Spinal epidural cavernous hemangiomas are very rare; only 18 cases have been reported in the literature. The authors describe the case of a 38-year-old male whose first symptom was numbness of the foot, which, after 2 years, spread to the abdomen. On admission, he had no weakness but exhibited hyper-reflex of the lower limbs and hypalgesia below the 7th thoracic dermatome. Magnetic resonance imaging (MRI) revealed an extradural tumor at the level of the 7th thoracic vertebra, with erosion of the 7th vertebral body. T1-weighted images were obtained by inversion recovery with a repetition time (TR) of 2100 msec, an inversion time of 600 msec, and an echo time (TE) of 40 msec. T2-weighted images were obtained by a spin echo pulse sequence with a TR of 2000 msec and a TE of 120 msec. Compared with the spinal cord, the tumor showed low intensity on T1-weighted images and high intensity on T2-weighted images. The tumor was removed through a laminectomy. The histological diagnosis was cavernous hemangioma. After surgery, the patient's symptoms and signs improved. This is the first report of a spinal epidural cavernous hemangioma that includes MRI findings. It appears difficult to differentiate cavernous angiomas from neurinomas by MRI.