Biomedical subjects

M Yamazaki

Publications and source records attributed to M Yamazaki.

At least 253 records · Page 14Linked to original sources

PubMed1998

Suppressive effect on Theiler's murine encephalomyelitis virus-induced demyelinating disease by the administration of anti-IL-12 antibody.

We examined the role of IL-12, a cytokine critical to the evolution of cellular responses, in the development of Theiler's murine encephalomyelitis virus-induced demyelinating disease (TMEV-IDD). Treatment with mAbs to IL-12, especially during the effector phase, resulted in significant suppression of the development of this disease both clinically and histologically. In mice treated with these mAbs, the production of inflammatory and Th1-derived cytokines such as TNF-alpha and IFN-gamma in the spleen cells was decreased, and that of Th2-derived cytokines such as IL-4 and IL-10 was increased. The delayed type hypersensitivity and T cell proliferative response specific for TMEV were decreased by this treatment. These data suggest that IL-12 is critically involved in the pathogenesis of TMEV-IDD and that Abs to IL-12 could be a novel therapeutic approach in the clinical treatment of demyelinating diseases such as human multiple sclerosis.

Animals↗

PubMed1998

Immunological studies on the settlement-inducing protein complex (SIPC) of the barnacle Balanus amphitrite and its possible involvement in larva-larva interactions.

Immunological investigation has revealed that a settlement-inducing protein complex (SIPC), which induces cypris settlement of the barnacle Balanus amphitrite, is synthesized during larval development and accumulates in the cypris larva. We previously purified the SIPC from adult B. amphitrite, which was active when bound to a substratum. The SIPC is a glycoprotein of high molecular mass, consisting of three major subunits of 76, 88 and 98 kDa with lentil lectin (LCA)-binding sugar chains. In the present study, we prepared antiserum against each LCA-binding subunit of SIPC, and performed immunoblot analyses. Immunoblotting of adult extracts showed that anti-76-kDa antibody reacted only with the 76-kDa protein, whereas anti-88-kDa and anti-98-kDa antibodies reacted with both the 88-kDa and the 98-kDa proteins. Immunoblotting of larval extracts indicated that reactivity of the 76-kDa protein to anti-76-kDa antiserum increased during larval development and cyprid extracts reacted strongly. Moreover, by using immunostaining we found that the SIPC was contained in 'footprints' of cyprids, which have been shown to act as a settlement-inducing pheromone, and is secreted onto the antennular attachment discs. The results suggest that the SIPC (or SIPC-like proteins) is involved in both adult-larva and larva-larva interactions during settlement of the barnacle B. amphitrite.

Animals↗

PubMed1998

Alliinase [S-alk(en)yl-L-cysteine sulfoxide lyase] from Allium tuberosum (Chinese chive)--purification, localization, cDNA cloning and heterologous functional expression.

Alliinase [S-alk(en)yl-L-cysteine sulfoxide lyase], a pyridoxal-phosphate-(Pxy-P)-dependent enzyme, is responsible for the degradative conversion of S-alk(en)yl-L-cysteine sulfoxide to volatile odorous sulfur-containing metabolites in Allium plants. We have purified alliinase from shoots of Allium tuberosum (Chinese chive) to apparent homogeneity by SDS/polyacrylamide gel electrophoresis. A cDNA clone encoding alliinase was isolated from a cDNA library constructed from whole plants of A. tuberosum by hybridization screening with a synthetic 50-residue oligonucleotide encoding a conserved region of the alliinases from onion and garlic. The isolated cDNA encoded a protein of 476 amino acid residues with a molecular mass of 54083 Da. The deduced amino acid sequence exhibited 66-69% identities with those of reported alliinases from onion, garlic and shallot. The partial amino acid sequence, which was determined for a V8 protease-digested peptide fragment of the purified alliinase, was perfectly matched with the sequence deduced from the cDNA. An expression vector of recombinant alliinase cDNA was constructed in yeast. The catalytically active protein was in the soluble fraction of transformed yeast. Site-directed mutagenesis experiments indicated that Lys280 was essential for the catalytic activity and, thus, a possible Pxy-P-binding residue. The mRNA expression of the alliinase gene comprising a multigene family in the shoots of green plants was twofold higher than that in the roots of green plants; however, the expression in the shoots of etiolated plants was only 13% that in green shoots, although the expression in the roots was not remarkably different between in green and etiolated plants. Immunohistochemical investigation indicated that the alliinase protein is predominantly accumulated in the bundle sheath cells of shoots of A. tuberosum.

Allium↗

PubMed1998

Intermembrane distance in multilamellar vesicles of phosphatidylcholine depends on the interaction free energy between solvents and the hydrophilic segments of the membrane surface.

To investigate the interaction of the surface of biomembranes with solvents systematically, we have studied the structure and phase behavior of multilamellar vesicles of dipalmitoylphosphatidylcholine (DPPC) and 1-palmitoyl-2-oleoyl-phosphatidylcholine (POPC) in dimethylformamide (DMF)-water mixture by X-ray diffraction and differential scanning calorimetry. The solubility of phosphorylcholine, which is the same molecular structure as the head-group of phosphatidylcholine (PC), decreased with an increase in DMF concentration. This result indicates that DMF is a poor solvent for the hydrophilic segments of the surface of the PC membrane, and interaction free energy of the hydrophilic segments of the membrane surface with solvents increases with an increase in DMF concentration. X-ray diffraction data indicated that DPPC-MLVs were in the bilayer gel phase from 0 to 80% (v/v) DMF, and that the spacing (lamellar repeat period) and intermembrane distance of DPPC-MLV decreased with an increase in DMF concentration. Main transition temperature and pre-transition temperature of DPPC-MLV increased with an increase in DMF concentration, and above 50% (v/v) DMF there was no pre-transition. In the interaction of POPC-MLV with DMF, X-ray diffraction data indicated that POPC-MLVs were in L(alpha) phase (liquid-crystalline phase) from 0 to 80% (v/v) DMF, and that the spacing and intermembrane distance of POPC-MLV decreased with an increase in DMF concentration. These results are discussed by the change of the interaction free energy between the hydrophilic segments of the membrane surface and solvents. As DMF concentration increases, this interaction free energy may increase, resulting in the decrease of the intermembrane distance of PC-MLVs.

Journal Article↗

PubMed1998

Mapping of a novel human carbonyl reductase, CBR3, and ribosomal pseudogenes to human chromosome 21q22.2.

To find the genes contributing to Down syndrome, we constructed a 4-Mb sequence-ready map spanning chromosome 21q22.2 with megabase-sized cosmid/P1-derived artificial chromosome (PAC) contigs. The restriction map with rare cutting enzymes, followed by sequencing from the clustering sites, has defined CpG islands and revealed the genes associated with CpG islands (Accession No. D85771). Of these, two human carbonyl reductases (CBR; EC1.1.1.184) were found in a PAC 25P16 clone. CBR catalyzes the reduction of a large number of biologically and pharmacologically active carbonyl compounds to their corresponding alcohols and has been mapped in 21q22.1. To confirm these results, we sequenced the PAC clone in shotgun strategies and identified a novel carbonyl reductase, designated CBR3, 62 kb downstream from the original CBR. In addition, three ribosomal pseudogenes, L23a, S9, and L3, and some cDNAs with ESTs were mapped in the sequence. In conclusion, the sequence analysis for CpG islands predicted from the megabase-sized contigs will reveal and identify the genes involved in Down syndrome.

Alcohol Oxidoreductases↗

PubMed1998

Prothrombin fragment 1 + 2 measures treatment effect in patients with antiphospholipid syndrome.

Antiphospholipid syndrome (APS) is characterized by recurrent thrombosis. The anticoagulant management of APS thrombosis remains controversial. Few reports on markers of in vivo activation of coagulation have been reported. To determine whether plasma levels of prothrombin fragment 1 + 2 (F1 +2) correlate with thrombotic risk and treatment effect in patients with APS, plasma F1 + 2 levels were followed in 57 patients with this syndrome for more than 2 years. Clinical findings were also observed in these patients. Plasma levels of F1 + 2 in patients with APS were significantly higher when compared with control subjects (p<.05). These results suggest patients with APS are in a hypercoagulable state. Plasma levels of F1 + 2 significantly decreased following treatment with either aspirin, or aspirin plus warfarin (p<.05 and p<.01, respectively). Recurrent thromboses or spontaneous abortions occurred in all eight patients whose plasma levels of F1 + 2 remained higher than 1 nmol/l after treatment with either aspirin alone or no anticoagulants. These patients were subsequently treated with warfarin as well as aspirin, and plasma levels of F1 + 2 decreased to less than 1 nmol/l, with no additional thrombotic events over the remainder of the 2-year follow-up. No fatal bleeding was observed in treated patients. Our results suggest plasma levels of F1 + 2 are useful indicators of successful treatment. It is also suggested that warfarin plus mini-dose aspirin therapy is effective for patients with APS to protect from recurrent thromboses without harmful side effects. Further, prospective cohort studies are needed to substantiate these associations.

Antiphospholipid Syndrome↗

PubMed1998

The effect of pentoxifylline (PTX) on Theiler's murine encephalomyelitis (TMEV)-induced demyelinating disease.

Pentoxifylline (PTX) has been recently shown to have a variety of immunomodulatory effects. PTX suppresses the production of tumor necrosis factor-alpha (TNF-alpha) and T helper type 1 (Th1) cytokine, interferon-gamma (IFN-gamma), whereas it increases the production of Th2 cytokines, such as interleukin-4 (IL-4) and IL-10. In the pathogenesis of Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease (TMEV-IDD), encephalitogenic Th1 cells may play a major role. We examined the effect of PTX treatment on TMEV-IDD. We treated SJL/J mice, inoculated TMEV intracerebrally, with either PTX or saline from days -2 to 12 and days 14 to 27 postintracerebral infection. In the group of mice treated with PTX from days -2 to 12, the onset of TMEV-IDD was suppressed. On the other hand, in the group of mice treated with PTX from days 14 to 27 or saline, the onset of TMEV-IDD was not inhibited. The results of enzyme-linked immunospot (ELISPOT) assay of spleen cells of mice showed that the production of TNF-alpha and IFN-gamma was significantly inhibited (TNF-alpha and IFN-gamma, p < 0.001) and IL-4 and IL-10 production was significantly increased (IL-4, P < 0.001; and IL-10, P < 0.05, respectively) in the group of mice treated with PTX from days -2 to 12. These findings suggest that PTX suppresses the onset of TMEV-IDD by suppressing the production of TNF-alpha and modulating Th1-dominant immune responses into Th2-dominant ones.

Animals↗

PubMed1998

Multidrug resistance protein. Identification of regions required for active transport of leukotriene C4.

Multidrug resistance protein (MRP) is a broad specificity, primary active transporter of organic anion conjugates that confers a multidrug resistance phenotype when transfected into drug-sensitive cells. The protein was the first example of a subgroup of the ATP-binding cassette superfamily whose members have three membrane-spanning domains (MSDs) and two nucleotide binding domains. The role(s) of the third MSD of MRP and its related transporters is not known. To begin to address this question, we examined the ability of various MRP fragments, expressed individually and in combination, to transport the MRP substrate, leukotriene C4 (LTC4). We found that elimination of the entire NH2-terminal MSD or just the first putative transmembrane helix, or substitution of the MSD with the comparable region of the functionally and structurally related transporter, the canalicular multispecific organic anion transporter (cMOAT/MRP2), had little effect on protein accumulation in the membrane. However, all three modifications decreased LTC4 transport activity by at least 90%. Transport activity could be reconstituted by co-expression of the NH2-terminal MSD with a fragment corresponding to the remainder of the MRP molecule, but this required both the region encoding the transmembrane helices of the NH2-terminal MSD and the cytoplasmic region linking it to the next MSD. In contrast, a major part of the cytoplasmic region linking the NH2-proximal nucleotide binding domain of the protein to the COOH-proximal MSD was not required for active transport of LTC4.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1998

Interleukin 7 transgenic mice develop chronic colitis with decreased interleukin 7 protein accumulation in the colonic mucosa.

We have demonstrated that intestinal epithelial cells produce interleukin 7 (IL-7), and IL-7 serves as a potent regulatory factor for proliferation of intestinal mucosal lymphocytes expressing functional IL-7 receptor. To clarify the mechanism by which locally produced IL-7 regulates the mucosal lymphocytes, we investigated IL-7 transgenic mice. Here we report that transgenic mice expressing murine IL-7 cDNA driver by the SRalpha promoter developed chronic colitis in concert with the expression of SRalpha/IL-7 transgene in the colonic mucosa. IL-7 transgenic but not littermate mice developed chronic colitis at 4-12 wk of age, with histopathological similarity to ulcerative colitis in humans. Southern blot hybridization and competitive PCR demonstrated that the expression of IL-7 messenger RNA was increased in the colonic mucosal lymphocytes but not in the colonic epithelial cells. IL-7 protein accumulation was decreased in the goblet cell-depleted colonic epithelium in the transgenic mice. Immunohistochemical and cytokine production analysis showed that lymphoid infiltrates in the lamina propria were dominated by T helper cell type 1 CD4+ T cells. Flow cytometric analysis demonstrated that CD4+ intraepithelial T cells were increased, but T cell receptor gamma/delta T cells and CD8alpha/alpha cells were not increased in the area of chronic inflammation. Increased IL-7 receptor expression in mucosal lymphocytes was demonstrated in the transgenic mice. These findings suggest that chronic inflammation in the colonic mucosa may be mediated by dysregulation of colonic epithelial cell-derived IL-7, and this murine model of chronic colitis may contribute to the understanding of the pathogenesis of human inflammatory bowel disease.

Animals↗

PubMed1998

Nucleotide sequencing analysis of the 146-kilobase segment around the IkBL and MICA genes at the centromeric end of the HLA class I region.

To elucidate the complete gene structure and to identify new genes involved in the development of HLA class I antigen-associated diseases in the class I region of the human major histocompatibility complex on chromosome 6, a YAC clone (745D12) covering the 146-kb segment around the IkBL and MICA loci was isolated from a YAC library constructed from the B-cell line, BOLETH. A physical map of this region was constructed by isolation of overlapping cosmid clones derived from 745D12. Of these, five contiguous cosmids were chosen for DNA sequencing by the shotgun strategy to give a single contig of 146,601 bp from 2.8 kb telomeric of the IkBL gene to exon 6 of MICA. This region was confirmed to contain five known genes, IkBL, BAT1, MICB, P5-1, and HLA-X (class I fragment), from centromere to telomere, and their exon-intron organizations were determined. The 3.8-1 homologue gene (3.8-1-hom) showing 99.7% identity with the 3.8-1 cDNA clone, which was originally isolated using the 3.8-kb EcoRI fragment between the HLA-54/H and the HLA-G genes, was detected between MICA and MICB and was suggested to represent the cognate 3.8-1 genomic sequence from which the cDNA clone was derived. No evidence for the presence of expressed new genes could be obtained in this region by homology and EST searches or coding and exon prediction analyses. One TA microsatellite repeat spanning 2545 bases with as many as 913 repetitions was found on the centromeric side of the MICA gene and was indicated to be a potential hot spot for genetic recombination. The two segments of approximately 35 kb upstream of the MICA and MICB genes showed high sequence homology (about 85%) to each other, suggesting that segmental genome duplication including the MICA and MICB genes must have occurred during the evolution of the human MHC.

Carrier Proteins↗

PubMed1998

Proliferating cell nuclear antigen in hypertrophied spinal ligaments. Immunohistochemical localization of proliferating cell nuclear antigen in hypertrophied posterior longitudinal ligament of the cervical spine.

STUDY DESIGN: An experimental immunohistochemical investigation using an antibody for proliferating cell nuclear antigen. Surgically-extirpated specimens of posterior longitudinal ligament tissues from patients with hypertrophy of the posterior longitudinal ligament and other disorders of the cervical spine were analyzed. OBJECTIVE: To analyze the developmental mechanism of hypertrophy of the posterior longitudinal ligament, the authors evaluated the growth activity of cells in the posterior longitudinal ligament tissues by examining the immunolocalization of the proliferating cell nuclear antigen. SUMMARY OF BACKGROUND DATA: Although a number of cases of hypertrophy of the posterior longitudinal ligament have been reported, the pathophysiology of ligament hypertrophy is still unclear. It is well established that the proliferating cell nuclear antigen is a cell proliferation marker, and immunohistochemical analysis using an anti-proliferating cell nuclear antigen antibody is of value in assessing the cell growth activity of several tissues. METHODS: During anterior decompression surgery in the cervical spine, the authors extirpated posterior longitudinal ligament tissues in one piece from patients with hypertrophy of the posterior longitudinal ligament, ossification of the posterior longitudinal ligament, cervical disc herniation, and cervical spondylotic myelopathy. Midsagittal sections of the specimens were stained with an antibody against the proliferating cell nuclear antigen. RESULTS: In cases of hypertrophy of the posterior longitudinal ligament, immunostaining with the proliferating cell nuclear antigen was detected in cells in the posterior longitudinal ligament, not only at the vertebral endplate level, but also at the midvertebral level. A similar distribution of proliferating cell nuclear antigen-positive cells was observed in cases of ossification of the posterior longitudinal ligament. In cases of cervical disc herniation, however, proliferating cell nuclear antigen-positive cells in posterior longitudinal ligament tissues were restricted to the vertebral endplate level. No immunostaining with the proliferating cell nuclear antigen was seen in posterior longitudinal ligament tissues in cases of cervical spondylotic myelopathy. CONCLUSIONS: Cell growth activity was accelerated in posterior longitudinal ligament tissues in cases of hypertrophy of the posterior longitudinal ligament; such an unusual phenotype of posterior longitudinal ligament cells was also expressed in cases of ossification of cervical disc herniation and cervical spondylotic myelopathy. Therefore, up-regulation of the growth of posterior longitudinal ligament cells may contribute to the development of hypertrophy of the posterior longitudinal ligament, and some common regulatory mechanism(s) on the proliferation of posterior longitudinal ligament cells seem to underlie the development of hypertrophy of the posterior longitudinal ligament and ossification of the posterior longitudinal ligament.

Adult↗

PubMed1998

Vascular endothelial growth factor tightly regulates in vivo development of murine hepatocellular carcinoma cells.

Angiogenesis is essential for the development of a solid tumor, including hepatocellular carcinoma (HCC). HCC is a well-known hypervascular tumor. Vascular endothelial growth factor (VEGF) is one of the most potent angiogenic factors. Its role has not been clarified in vivo in HCC development. We used a self-contained, tetracycline-regulated retroviral vector system to elucidate the effect of VEGF on murine HCC development in a xenograft experimental model. By delivering the VEGF gene within the retroviral vector and under the control of a tetracycline-regulated promoter, we were able to manipulate VEGF expression in vivo tumor by providing tetracycline in the drinking water. Overexpression of VEGF showed a marked increase in tumor development accompanied by augmentation of neovascularization. The degree of tumor enlargement corresponded to the level of VEGF gene expression. Suppression of VEGF led to a decrease in tumor growth at the established tumor size, whether relatively small or large. The level of VEGF expression did not alter the proliferation of HCC cells in vitro. In a double-chamber chemoinvasion assay, the in vitro invasion activity of VEGF-transduced cells was not changed. In the presence of endothelial cells (EC), however, VEGF-transduced cells showed a marked increase in their in vitro invasion activity. These results suggested that VEGF plays a critical role in the development of HCC in cooperation with EC

Animals↗

PubMed1998

CD45RChighCD4+ intestinal mucosal lymphocytes infiltrating in the inflamed colonic mucosa of a novel rat colitis model induced by TNB immunization.

To clarify the role of CD4(+) intestinal mucosal lymphocytes in chronic intestinal inflammation, we developed a new rat colitis model by immunization with 2,4,6-trinitrobenzenesulfonic acid (TNB) in an emulsion with an adjuvant followed by transrectal administration of a low dose of TNB. Moreover, we assessed the therapeutic effect of anti-CD4 monoclonal antibody (mAb) on this model. In concert with the development ofserum anti-TNB Abs, transmural and segmental colitis that mimics some characteristics of human Crohn's disease was induced in the immunized rats. Immunohistochemical analysis showed the increase of infiltrating lamina propria CD4(+) T cells. Flow-cytometric analysis of isolated cells from inflamed mucosa revealed that CD45RChighCD4(+) T cells were significantly increased. Interestingly, intraperitoneal administration of anti-CD4 mAbs could suppress severe inflammation in the model with decrease of anti-TNB Ab titer. After the treatment with anti-CD4 mAbs, CD45RChighCD4(+) T cells in the lamina propria and interferon-gamma mRNA expression in the colonic lamina propria CD4(+) T cells were decreased. These results indicated that Th1 CD4(+) intestinal mucosal T cells have a role in the progress of inflamed lesions in chronic enteritis. They implicate that a therapy targeting mucosal T cells expressing CD4 may be feasible in the treatment of human Crohn's disease.

Animals↗

PubMed1998

Successful surgical management of penetrating cardiac injury.

A 60-year-old Asian man who suffered penetrating thoracoabdominal injuries was admitted to our hospital in a state of shock. Because the results of a chest computed tomogram (CT) strongly suggested a left ventricular injury, an emergency thoracotomy was performed. A laceration of the left ventricle (3 cm) was sutured and was closed without cardiopulmonary bypass, and coexisting lacerations of the superior mesenteric artery (SMA) and small bowel were surgically repaired. During the procedure, cardiac arrest occurred, but the patient recovered without any apparent neurologic deficit. Postoperative examinations using echocardiogram, CT, and cardiac catheterization revealed a delayed rupture of the left ventricle. On the 28th day after surgery, he was transferred to another hospital for elective cardiac surgery. Primary management of penetrating cardiac injury is discussed in this report.

Abdominal Injuries↗

PubMed1998

Involvement of insulin-like growth factor I in development of ossification of the posterior longitudinal ligament of the spine.

In order to investigate the pathogenesis of ossification of the posterior longitudinal ligament (OPLL) of the spine, we examined the distribution of insulin-like growth factor I (IGF-I) in the posterior longitudinal ligaments of OPLL patients, and analyzed the effects of IGF-I on the cultured spinal ligament cells. For that purpose we established eight varieties of OPLL and non-OPLL cell lines obtained from spinal ligaments of corresponding patients, respectively. In contrast to non-OPLL cases, all the OPLL cases were histologically shown to contain round-shaped cartilage-like cells in the transitional region from preossifying to ossifying ligaments, and these cells were strongly stained with an antibody for IGF-I. In the vicinity of preossifying cartilaginous tissues, ligament cells also had a rod-like appearance and were positive for IGF-I immunohistochemically. The effects of IGF-I on cultured spinal ligament cells were assayed by alkaline phosphatase (AP) activity, DNA synthesis, and the amounts of collagen produced. The number of OPLL cell lines that increased AP activity, responding to IGF-I irrespective of 1,25(OH)2D3, was significantly larger than that of non-OPLL cell lines, although IGF-I stimulated DNA and procollagen type I carboxyl-terminal peptide synthesis in most of both OPLL and non-OPLL cell lines. These data demonstrate the dominant expression of IGF-I in the posterior longitudinal ligaments of OPLL patients, and suggest that IGF-I preferentially induces osteogenic differentiation in OPLL cells rather than in non-OPLL cells. IGF-I, therefore, may be involved in the local ossification process of spinal ligaments observed in OPLL patients.

Adult↗

PubMed1998

Regional variations in the progression of bone loss in two different mouse osteopenia models.

Differences in trabecular and cortical bone loss have been demonstrated clinically, but differences in bone loss at different skeletal sites remain unclear. We examined regional variations in bone loss histomorphometrically in two strains of mice in which osteopenia progresses spontaneously: tiptoe-walking Yoshimura (twy) mice (from 4 to 37 weeks of age) and senescent ICR mice (from 4 to 88 weeks of age). Morphometrical measurements were obtained to investigate the changes with age in trabecular bone area and anterior cortical bone width in the lumbar vertebral body, trabecular bone area in the tibia, bone area in the parietal bone, and the cortical index in the humerus. Results showed that, in twy mice, trabecular turnover was higher than in ICR mice, and bone loss progressed in the following order: tibial trabecular bone, lumbar trabecular bone, parietal bone, lumbar anterior cortical bone, and the humerus. In ICR mice, bone formation declined after 60 weeks. Bone loss progressed in tibial trabecular bone and the parietal bone at 60 weeks of age, followed by lumbar trabecular bone, lumbar anterior cortical bone, and the humerus at 88 weeks of age. Bone loss varied at each site and between the two mouse strains, with different bone turnover rates. The findings of the present study indicate that special attention should be paid to regional variations in the progression of bone loss associated with differences in pathologic features.

Aging↗

PubMed1998

Neuroleptic malignant syndrome during haloperidol treatment in a cancer patient. A case report.

A case of neuroleptic malignant syndrome (NMS) in a 64-year-old man with cancer of the soft palate is reported. During haloperidol treatment for delirium, the patient showed consciousness disturbance with extrapyramidal signs. With discontinuation of haloperidol and replacement by dantrolene and bromocriptine, the patient recovered completely. Although major tranquilizers are widely used in clinical oncology to manage symptoms, NMS has been rarely reported in cancer patients, presumably because of lack of awareness. Early recognition of NMS and prompt treatment may improve the potentially fatal outcome.

Antipsychotic Agents↗

PubMed1998

Metastatic malignant meningioma of the liver with hypoglycemia: report of a case.

We herein present the case of a 68-year-old male who suffered an episode of hypoglycemic shock 2 years after undergoing total removal of a bifrontal parasagittal malignant meningioma. Imaging studies revealed three giant hypervascular tumors with a cystic portion in the right lobe, but no confirmed preoperative diagnosis could be made. At laparotomy, liver tumors were found in the medial segment of the left lobe as well as in the right lobe, and thus an extended right lobectomy was performed. All the resected tumors were histologically diagnosed as metastatic malignant meningiomas of the liver. Despite subsequent transarterial chemoembolization for a recurrence in the residual liver, the patient died 11 months after surgery. To the best of our knowledge, only one other case of a hepatectomy for liver metastases from an intracranial malignant meningioma has been reported in the literature, but there has never been any report of surgical treatment for a metastatic meningeal tumor in the liver associated with hypoglycemia. Although our surgical treatment provided effective palliation, the prognostic significance of a surgical strategy for such patients has yet to be established.

Aged↗