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Biomedical subjects

M Abe

Publications and source records attributed to M Abe.

At least 397 records · Page 22Linked to original sources
PubMed1998

Histiocytic sarcoma of the spleen associated with hypoalbuminemia, hypo gamma-globulinemia and thrombocytopenia as a possibly unique clinical entity--report of three cases.

We report three patients with histiocytic sarcoma of the spleen associated with severe hypoalbuminemia, hypo gamma-globulinemia and thrombocytopenia. After the clinical diagnosis of splenic tumor of unknown origin was made, all three patients underwent splenectomy. The histiocytic origin of the tumor was confirmed histopathologically and immunohistochemically using a panel of antibodies. In contrast to malignant histiocytosis (MH), which typically reveals severe generalized clinical manifestations and a rapidly fatal course caused by the disseminated proliferation of neoplastic histiocytes, these patients were asymptomatic or showed only mild clinical symptoms for a long period of time until the recurrence was detected by which time the tumor cells had already spread to other organs. All three cases were characteristically associated with hypoalbuminemia, hypo gamma-globulinemia and thrombocytopenia, which returned to normal after splenectomy. Splenic histiocytic sarcoma with the features described here may represent a unique clinical entity, distinct from MH.

Adult↗
PubMed1998

Blood blisterlike aneurysms of the internal carotid artery.

OBJECT: An aneurysm arising from the anterior wall of the internal carotid artery (ICA) is a poorly understood entity. A small hemispherical bulge from the anterior wall of the ICA, which is called a "blood blisterlike aneurysm" (BBA), may be confused with a tiny berry aneurysm although the clinical features are distinctly different. This paper summarizes the clinical course of patients with this lesion to clarify the nature of the BBA. METHODS: Six patients with BBAs who presented with subarachnoid hemorrhage (SAH) are described. In all patients, the initial angiogram obtained soon after SAH showed only a small bulge from the anterior wall of the ICA. In three of the six patients this bulge had progressed to a saccular appearance within a few weeks. The wall of the lesion was so thin and fragile that the aneurysm ruptured at the base during clipping or within a few hours after clipping in two patients. CONCLUSIONS: From the authors' experience, as well as a review of the literature, which includes an autopsy study of similar cases, it is inferred that these lesions are focal wall defects covered only with thin fibrous tissue and that they are therefore not true aneurysms. Direct clipping often causes laceration of the lesion, whereas complete wrapping or clipping after wrapping is effective, but may fail to prevent growth of the aneurysm. Endovascular occlusion of the cervical ICA with or without bypass surgery, which is less risky than direct surgery, is another option.

Adult↗
PubMed1998

[Relationship between aging and morphological bone changes of the condyle in temporomandibular disorders].

In order to clarify the clinical significance of morphological bone changes of the mandibular condyle in temporomandibular disorders, the relationship between radiographic bone changes and aging was clinically studied. The subjects of the study were 1,120 patients (812 females and 308 males). The average age was 33 years +/- 15 years (from 10 to 81 years of age). The 1,120 patients were divided into six age brackets (10 to 19 years, 20 to 29 years, 30 to 39 years, 40 to 49 years, 50 to 59 years, 60 to 81 years). According to radiograms taken by lateral oblique transcranial projection, orbitcondyle projection and orthopantomography, the morphological bone changes were classified into seven groups, erosion, osteophyte, eburnation, flattening, deformity, concavity and sclerosis. The results were as follows: 1. The incidence of the patients with radiographic bone changes of the mandibular condyle increased with aging and showed significantly different age distribution from that without bone changes (Mann-Whitney U test: p < 0.01). 2. The incidence of erosion did not increase with aging and showed significantly different age distribution from osteophyte or eburnation (Mann-Whitney U test: p < 0.01, 0.05). The incidence of flattening also did not increase with aging and showed significantly different age distribution from osteophyte, eburnation or deformity (Mann-Whitney U test: p < 0.01, 0.05, 0.05).

Adolescent↗
PubMed1998

[A study of clinical significance of leucocyte migration test in drug eruption].

In 202 patients suspected of drug eruption, the identification of the allergenic drugs were performed by leucocyte migration test (LMT). Leucocyte migration activating factor (LMAF) was detected in 94 cases (46.5%) and Leucocyte migration inhibitory factor (LMIF) in 93 cases (46.0%) for tests either without patients' serum or with patient's serum. Either LMAF or LMIF was detected in 158 cases (78.2%). LMAF was detected in 46 cases (22.8%) for tests only without patient's serum, and in 68 cases (33.7%) for tests only with patient's serum. Accordingly, LMAF was found significantly more frequently with patient's serum than without patient's serum (p < 0.01, chi 2-test). The drugs showing either LMAF-positive or LMIF-positive were detected in 193 of all 647 suspected drugs, in which 53 drugs (27.5%) were beta-lactam antibiotics and 36 (28.0%) were non-steroidal antiinflammatory drugs. LMAF was detected significantly higher than LMIF in beta-lactam antibiotics-induced eruptions (p < 0.01, chi 2-test), which LMIF was detected significantly higher than LMAF in non-steroidal antiinflammatory drugs-induced eruptions (p < 0.01, chi 2-test). Our finding indicate that both LMAF and LMIF may be involved in the pathogenesis of drug eruptions, that the detection of either LMAF or LMIF may be valuable to identify the allergenic drugs in drug eruption by means of LMT and that the production of LMAF may be enhanced in the presence of patients' sera. Furthermore, the pathogenic mechanism of beta-lactam antibiotics-induced eruption may be different from that of non-steroidal antiinflammatory drugs-induced eruption.

Adolescent↗
PubMed1998

[Hemorrhagic shock death caused by not so severe injury during the medication of anticoagulants].

A 73-year-old man receiving anticoagulants (warfarin potassium) orally with a history of prosthetic heart valve replacement was struck by a truck. When admitting to the hospital, he complained of lumbago with laboratory findings of anemia and prolongation of prothrombin times. Twenty-two hours after the accident, he died suddenly in the hospital and forensic autopsy was performed 9 hours after his death. Autopsy findings revealed marked subcutaneous and intramuscular hematoma in the lumbar and gluteal region and anemic change of viscera. Furthermore, 854 ng/ml of warfarin which was well accordance with the therapeutic levels was detected in the serum obtained from cadaver by using gas chromatography-mass spectrometry. Therefore, we concluded that the man had died of hemorrhagic shock caused by the force acting to the lumbar region accompanied by the influence of anticoagulant action of warfarin. To our knowledge, this is the first report to detect the warfarin from cadaver's serum. In dealing with the unnatural death of the patient receiving the anticoagulants, it is valuable to survey the medications and detect the presence of anticoagulants in cadaver.

Accidents, Traffic↗
PubMed1998

[A case of sellar T cell type malignant lymphoma].

A case of primary T cell type malignant lymphoma of the sellar region was reported. This 53-year-old male was admitted to our neurosurgical service because of slowly progressive occipitalgia and diplopia over the previous 5 months. On admission neurological examination revealed a slight limitation of the lateral movement of the left eye. Endocrinological examination showed no abnormalities. Despite a mild neurological deficit, a CT scan revealed an extensive bony destruction around the sellar region including the dorsum sellae, the bilateral petrous apices, and the upper two thirds of the clivus. Magnetic resonance imaging (MRI) disclosed that the tumor was slightly hypointense on T1-weighted image, isointense on T2-weighted image, and faintly and homogeneously enhanced after administration of Gd-DTPA. Since the tumor was enhanced faintly on MRI, it was diagnosed as an invasive pituitary adenoma, but it was thought that chordoma and germinoma should be considered. The patient underwent a transsphenoidal surgery. A firm, grayish and avascular tumor was partially removed. The histopathological examination using monoclonal surface marker of the specimen revealed the tumor was stained with UCHL-1 and CD3 antibodies directed against T cells, and diagnosed as T cell type malignant lymphoma of the sellar region (diffuse, large cell type; LSG). Postoperatively he received radiation therapy. His symptoms much improved and no regrowth of the residual tumor has been found in follow-up studies to the present. Primary malignant lymphomas very rarely occur in the skull base. As far as we are aware, this is the only second case of primary T-cell lymphoma in the sellar region reported so far in the medical literature. Although preoperative diagnosis is extremely difficult because of a paucity of data, malignant lymphomas should be kept in mind in the differential diagnosis of sellar tumors, especially if neuroimaging studies show an extensive bony destruction in the skull base.

Combined Modality Therapy↗
PubMed1997

Cancer cells isolated from malignant pleural and peritoneal effusions inhibit phospholipase A2 activity in human polymorphonuclear leukocytes.

We studied the influence of cancer cells on the LTB4 production by human polymorphonuclear leukocytes (PMN). The cancer cells were isolated from malignant pleural effusion specimens taken from two patients or from a peritoneal effusion specimen of one patient. While human PMN produced LTB4 following stimulation with A23187, the addition of cancer cells inhibited LTB4, 5-HETE and 12-HETE production by PMN in a cell number-dependent manner, while the cancer cell lines also showed a similar inhibition. The addition of lysate of the breast cancer cells also inhibited in a dose-dependent manner the production of LTB4 by PMN following stimulation with A23187. The addition of arachidonic acid completely reversed the inhibition of PMN-LTB4 production by the addition of the breast cancer cell lysates, thus suggesting inhibition at the phospholipase A2 level. The addition of this lysate to the partially purified human cytosolic PLA2 also inhibited the PLA2 activity. In contrast, the addition of lymphoma cells isolated from metastatic lymphnodes did not inhibit the LTB4 production from PMN. Since LTB4 is one of the important chemotactic factors for PMN and monocytes, these findings suggest that the inhibition of the PLA2 activity by the cancer cells thus results in a reduced production of LTB4 from PMN and contributes to a predisposition to develop severe infection in patients with advanced cancer.

Ascitic Fluid↗
PubMed1997

Both hypertrophic and dilated cardiomyopathies are caused by mutation of the same gene, delta-sarcoglycan, in hamster: an animal model of disrupted dystrophin-associated glycoprotein complex.

Cardiomyopathy (CM) is a primary degenerative disease of myocardium and is traditionally categorized into hypertrophic and dilated CMs (HCM and DCM) according to its gross appearance. Cardiomyopathic hamster (CM hamster), a representative model of human hereditary CM, has HCM and DCM inbred sublines, both of which descend from the same ancestor. Herein we show that both HCM and DCM hamsters share a common defect in a gene for delta-sarcoglycan (delta-SG), the functional role of which is yet to be characterized. A breakpoint causing genomic deletion was found to be located at 6.1 kb 5' upstream of the second exon of delta-SG gene, and its 5' upstream region of more than 27.4 kb, including the authentic first exon of delta-SG gene, was deleted. This deletion included the major transcription initiation site, resulting in a deficiency of delta-SG transcripts with the consequent loss of delta-SG protein in all the CM hamsters, despite the fact that the protein coding region of delta-SG starting from the second exon was conserved in all the CM hamsters. We elucidated the molecular interaction of dystrophin-associated glycoproteins including delta-SG, by using an in vitro pull-down study and ligand overlay assay, which indicates the functional role of delta-SG in stabilizing sarcolemma. The present study not only identifies CM hamster as a valuable animal model for studying the function of delta-SG in vivo but also provides a genetic target for diagnosis and treatment of human CM.

Amino Acid Sequence↗
PubMed1997

Isolation of human and fission yeast homologues of the budding yeast origin recognition complex subunit ORC5: human homologue (ORC5L) maps to 7q22.

Orc5p is a subunit of the origin recognition complex in the budding yeast Saccharomyces cerevisiae, which has been shown to play a critical role in both chromosomal DNA replication and transcriptional silencing. We have cloned cDNAs from both human and fission yeast Schizosaccharomyces pombe that encode proteins homologous to the budding yeast and Drosophila Orc5p. Human Orc5p showed 35.1, 22.3, and 19.4% identity to the Drosophila, S. pombe, and S. cerevisiae Orc5p, respectively. We have localized the human ORC5 gene (ORC5L) to chromosome 7 using Southern and PCR analysis of DNA isolated from a panel of human/rodent somatic cell hybrids and mapped the gene locus to 7q22 using fluorescence in situ hybridization. We have identified a YAC clone that contains human ORC5L and maps to chromosome band 7q22.1. We have identified the S. pombe ORC5 gene and located it in a cosmid mapped on chromosome II.

Amino Acid Sequence↗
PubMed1997

Possible role of P-450 metabolite of arachidonic acid in vasodilator mechanism of angiotensin II type 2 receptor in the isolated microperfused rabbit afferent arteriole.

Although angiotensin II type 2 (AT2) receptor has recently been cloned, its functional role is not well understood. We tested the hypothesis that selective activation of AT2 receptor causes vasodilation in the preglomerular afferent arteriole (Af-Art), a vascular segment that accounts for most of the preglomerular resistance. We microperfused rabbit Af-Arts at 60 mmHg in vitro, and examined the effect of angiotensin II (Ang II; 10(-11)-10(-8) M) on the luminal diameter in the presence or absence of the Ang II type 1 receptor antagonist CV11974 (CV; 10(-8) M). Ang II was added to both the bath and lumen of preconstricted Af-Arts. Ang II further constricted Af-Arts without CV (by 74+/-7% over the preconstricted level at 10(-8) M; P < 0.01, n = 7). In contrast, in the presence of CV, Ang II caused dose-dependent dilation; Ang II at 10(-8) M increased the diameter by 29+/-2% (n = 7, P < 0.01). This dilation was completely abolished by pretreatment with an AT2 receptor antagonist PD123319 (10(-7) M, n = 6), suggesting that activation of AT2 receptor causes vasodilation in Af-Arts. The dilation was unaffected by inhibiting either nitric oxide synthase (n = 7) or cyclooxygenase (n = 7), however, it was abolished by either disrupting the endothelium (n = 10) or inhibiting the cytochrome P-450 pathway, particularly the synthesis of epoxyeicosatrienoic acids (EETs, n = 7). These results suggest that in the Af-Art activation of the AT2 receptor may cause endothelium-dependent vasodilation via a cytochrome P-450 pathway, possibly by EETs.

8,11,14-Eicosatrienoic Acid↗
PubMed1997

Biphasic modulation in the trigeminal nociceptive neuronal responses by the intracerebroventricular prostaglandin E2 may be mediated through different EP receptors subtypes in rats.

To determine which prostaglandin E2 (PGE2) receptor subtypes are involved in the brain-derived PGE2-induced changes in nociception, we injected synthetic EP1, EP2 and EP3 receptor agonists (0.01 fmol to 10 nmol) into the lateral cerebroventricle (LCV) of urethane-anesthetized rats and observed the changes in the responses of the wide dynamic range (WDR) neurons in the trigeminal nucleus caudalis to noxious pinching of facial skin. The enhancement and suppression of the nociceptive responses of the WDR neurons were observed after the LCV injection of MB28767 (an EP3 receptor agonist) at a low dose range (1-100 fmol) and 17-phenyl-omega-trinor PGE2 (an EP1 receptor agonist) at high doses (1-10 nmol), respectively. Furthermore, the suppression of nociceptive neuronal responses after the LCV injection of PGE2 (1 nmol) was completely blocked by SC19220 (an EP1 receptor antagonist, 300 nmol). On the other hand, butaprost (an EP2 receptor agonist) at any doses tested (0.1 fmol to 1 nmol) had no effect on the nociceptive responses. The LCV injection of MB28767 (10 fmol) and 17-phenyl-omega-trinor PGE2 (1 nmol), which respectively enhanced and suppressed the nociceptive neuronal responses, did not affect the responses of the low threshold mechanoreceptive neurons to innocuous tactile stimuli. These results provide electrophysiological evidence that brain-derived PGE2 induces mechanical hyperalgesia and hypoalgesia through EP3 and EP1 receptors, respectively, in the rat.

Analgesics↗
PubMed1997

Immunotherapy of multiple myeloma with a monoclonal antibody directed against a plasma cell-specific antigen, HM1.24.

Multiple myeloma remains an incurable malignancy because of marked resistance of tumor cells to conventional chemotherapeutic agents. Alternative strategies are needed to solve these problems. To develop a new strategy, we have generated a monoclonal antibody (MoAb), which detects a human plasma cell-specific antigen, HM1.24. In this report, we evaluated the in vivo antitumor effect of unconjugated anti-HM1.24 MoAb on human myeloma xenografts implanted into severe combined immunodeficiency (SCID) mice. Two models of disseminated or localized tumors were established in SCID mice by either intravenous or subcutaneous injection of human myeloma cell lines, ARH-77 and RPMI 8226. When mice were treated with a single intraperitoneal injection of anti-HM1.24 MoAb 1 day after tumor inoculation, the development of disseminated myeloma was completely inhibited. In mice bearing advanced tumors, multiple injections of anti-HM1.24 MoAb reduced the tumor size and significantly prolonged survival, including tumor cure, in a dose-dependent manner. The proliferation of cultured human myeloma cells was inhibited in vitro by anti-HM1.24 IgG-mediated complement-dependent cytotoxicity, but not by the antibody alone. Moreover, spleen cells from SCID mice mediated antibody-dependent cell cytotoxicity against RPMI 8226 cells. These results indicate that anti-HM1.24 MoAb can be used for immunotherapy of multiple myeloma and related plasma cell dyscrasias.

Animals↗
PubMed1997

The murine DNA-PKcs gene consists of 86 exons dispersed in more than 250 kb.

The DNA-PKcs gene encodes the 465-kDa catalytic subunit of DNA-dependent protein kinase (DNA-PK), which associates with heterodimeric autoantigens Ku70 and Ku80 and exhibits protein kinase activity depending on DNA double-strand breaks. The gene is also responsible for the aberration in severe combined immune deficiency (SCID) mice, which exhibit a high sensitivity to ionizing radiation and abnormal DNA rearrangement of immunoglobulin and T cell receptor genes. There is further evidence that DNA-PKcs phosphorylates various proteins involved in DNA replication, transcription, repair, and recombination. Nevertheless the structure/function relationship in this huge molecule is virtually unknown. We determined the exons and introns of the murine DNA-PKcs gene by the long-distance polymerase chain reaction method. The murine DNA-PKcs gene consists of 86 exons distributed in a region of more than 250 kb. The average size of the exons is 140 bp. All the splicing sites conform to the GT/AG rule. The SCID mutation site (Tyr4046) has been identified in exon 85. The genomic structure of the DNA-PKcs gene provides clues for the study of various functional domains in this macromolecule.

Amino Acid Sequence↗
PubMed1997

Precursor B cells for autoantibody production in genomically Fas-intact autoimmune disease are not subject to Fas-mediated immune elimination.

The Fas/Fas ligand (FasL) system participates in regulation of the immune system through the apoptotic process. However, the extent to which abnormalities in this system are involved in the loss of self-tolerance and development of autoimmune disease not associated with Fas/FasL mutations remains unknown. The present study addresses this issue in Fas/FasL-intact, systemic lupus erythematosus (SLE)-prone (NZB x NZW) (NZB/W) F1 mice. While splenic B cells from 2-month-old mice before overt SLE expressed Fas poorly, in vitro stimulation with an agonistic anti-CD40 mAb up-regulated their Fas expression, thus revealing the existence of two populations: one was Fashigh and highly susceptible to anti-Fas mAb-induced apoptosis, and the other was Faslow and apoptosis-resistant. The Faslow cells were included in the CD5(+) B cell subpopulation and contained most of the cells that produced IgM anti-DNA antibodies. The isotype of anti-DNA antibodies switches from IgM to IgG in NZB/W F1 mice at ages beginning at about 6 months. These IgG anti-DNA antibodies were produced almost exclusively by a subpopulation of splenic B cells that spontaneously expressed low levels of Fas in vivo and were apoptosis-resistant. The findings indicate that precursor B cells for autoantibody production and presumably autoantibody-secreting cells in these mice are relatively resistant to Fas-mediated apoptosis, a finding supporting the concept that abnormalities of Fas-mediated apoptotic process are involved in the development of autoreactive B cells in Fas/FasL-intact autoimmune disease.

Animals↗
PubMed1997

External and intraoperative radiotherapy for resectable and unresectable pancreatic cancer: analysis of survival rates and complications.

PURPOSE: Clinical results of intraoperative radiotherapy (IORT) and/or external beam radiotherapy (EBRT) for both resectable and unresectable pancreatic cancer were analyzed. METHODS AND MATERIALS: Between 1980 and 1995, 332 patients with pancreatic cancer were treated with surgery and/or radiation therapy (RT). Of the 332 patients, 157 patients were treated with surgical resection of pancreatic tumor, and the remaining 175 patients had unresectable pancreatic tumors. Among the 157 patients with resected pancreatic cancer, 62 patients were not treated with RT, while 40 patients were treated with EBRT alone (mean RT dose; 46.3 Gy) and 55 patients with IORT (25.2 Gy) +/- EBRT (44.0 Gy). On the other hand, among the 175 patients with unresectable pancreatic cancer, 58 patients were not treated with RT, 46 patients were treated with EBRT alone (39.2 Gy), and the remaining 71 patients with IORT (29.3 Gy) +/- EBRT (41.2 Gy). RESULTS: For 87 patients with curative resection, the median survival times (MSTs) of the no-RT, the EBRT, and the IORT +/- EBRT groups were 10.4, 13.0, and 15.5 months, respectively, without significant difference. For 70 patients with noncurative resection, the MSTs of the no-RT, the EBRT, and the IORT +/- EBRT groups were 5.3, 8.7, and 6.5 months, respectively. When the EBRT and the IORT +/- EBRT groups were combined, the survival rate was significantly higher than that of the no RT group for noncuratively resected pancreatic cancers (log rank test; p = 0.028). The 2-year survival probability of the IORT +/- EBRT group (16%) was higher than that of the EBRT group (0%). For unresectable pancreatic cancer, the MSTs of 52 patients without distant metastases were 6.7 months for palliative surgery alone, 7.6 months for EBRT alone, and 8.2 months for IORT +/- EBRT. The survival curve of the IORT +/- EBRT group was significantly better than that of the no-RT group (p < 0.05), and the difference between the IORT +/- EBRT and the EBRT alone groups was marginally significant (p = 0.056). In addition, the 2-year survival probability for the IORT +/- EBRT group was 14%, while no 2-year survival was observed in the no RT or the EBRT groups. Multivariate analysis using the Cox proportional hazards model revealed that tumor size, stage (Stages 1, 2 vs. Stages 3, 4), and curability of resection were significant variables for resectable pancreatic cancer, while distant metastases and performance of IORT were significant variables for unresectable pancreatic cancer. The dose of EBRT was a marginally significant factor for both resectable and unresectable tumors (both p = 0.06). In terms of complications, ulcers of gastrointestinal tract were noted in 14% of the 126 patients treated with IORT. CONCLUSION: Although prolongation of the MST by IORT was not remarkable, long survivals (>2 years) were obtained by IORT +/- EBRT for noncuratively resected and unresectable pancreatic cancer. IORT combined with EBRT is indicated for noncurative resected or unresectable pancreatic cancer without distant metastases.

Adult↗
PubMed1997

Src tyrosine kinase mediates stimulation of Raf-1 and mitogen-activated protein kinase by the tumor promoter thapsigargin.

Thapsigargin is a non-phorbol ester-type tumor promoter that elevates the intracellular Ca2+ (Ca(i)2+) levels by blocking the microsomal Ca2+ ATPase. At present, the consequence of this Ca(i)2+ increase and the nature of the tumorigenicity of thapsigargin still remain to be elucidated. Previously, we demonstrated that thapsigargin activates the mitogen-activated protein (MAP) kinase via Ca(i)2+ but independently of protein kinase C or Ca2+ influx. Here, we show that thapsigargin also rapidly stimulates the Src tyrosine kinase. Transfection of a v-Src gene into a hippocampal cell line (H19-7) renders a constitutive activation of MAP kinase, whereas transfection of a kinase-deficient Src mutant blocks the activation by thapsigargin, suggesting that Src is required for the thapsigargin-induced MAP kinase activation. Cotransfection of a dominant-inhibitory Raf-1 and the v-Src genes into H19-7 cells results in an inhibition of the otherwise constitutively elevated MAP kinase activity, suggesting that Raf-1 is required for the Src-dependent activation of MAP kinase. Similarly, in the LA-90 cells, expression of a temperature-sensitive allele of v-Src constitutively activates Raf-1 and MAP kinase, whereas expression of a dominant-inhibitory Raf-1 mutant abolishes the MAP kinase activation induced by either v-Src or thapsigargin treatment. Together, these results suggest that thapsigargin stimulates MAP kinase signaling via Src and Raf-1. The activation of this Src-MAP kinase pathway suggests a biochemical mechanism for the tumorigenic nature of thapsigargin.

Animals↗