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Biomedical subjects

H Arai

Publications and source records attributed to H Arai.

At least 217 records · Page 12Linked to original sources
PubMed1999

Oxidative modification of apolipoprotein E in human very-low-density lipoprotein and its inhibition by glycosaminoglycans.

The mechanism of metal ion-catalyzed oxidative modification of apolipoprotein E (apoE) in human very-low-density lipoprotein (VLDL) and its inhibition by glycosaminoglycan (GAG) was investigated in vitro. The VLDL oxidation catalyzed by Cu2+ led to the lipid peroxidation, the formation of aggregates, and covalent modification of apoE. The modified apoE lost heparin-binding activity. These results suggest that the lipid peroxidation of VLDL and modification of apoE cause impairment of lipid uptake by cells and deposit the oxidized lipids in the tissues. The lipid peroxidation and oxidative modification of apoE in VLDL mediated by Cu2+ and an aqueous radical generator were suppressed by GAG, heparan sulfate, heparin, and chondroitin sulfate A, even though GAGs demonstrated no ability to scavenge alpha,alpha-diphenyl-beta-picrylhydrazyl radical. There were no relationships between inhibitory activity of GAGs in the VLDL oxidation and their number of sulfate groups which possess chelating activity of metal ion. Therefore, it can be considered that the inhibition of VLDL oxidation by GAGs is possibly due to the interaction between GAG and VLDL which bring about the steric hindrance, interference with the reaction between VLDL particle and the reactive oxygen species. These studies suggest that GAGs preserve the biological functions of apoE from oxidative stress.

Adult↗
PubMed1999

Association of plasma levels of activated protein C with recanalization of the infarct-related coronary artery after thrombolytic therapy in acute myocardial infarction.

Protein C is one of the most important antithrombotic components. After activation by the thrombin-thrombomodulin complex on endothelial cells, activated protein C (APC) inactivates factors Va and VIIIa, which leads to the inhibition of thrombin formation. We examined the association of plasma levels of APC with the responsiveness to coronary thrombolytic therapy of the infarct-related coronary artery in patients with acute myocardial infarction (AMI). Plasma levels of APC, thrombin-antithrombin III complex (TAT), and plasminogen activator inhibitor (PAI) activity were measured in 32 consecutive AMI patients who underwent coronary angiography followed by thrombolytic therapy, and compared to the measurements in 23 control subjects. On admission, APC levels (ng/mL) were significantly elevated in patients with AMI, as compared with controls (2.5+/-0.4 vs. 1.2+/-0.2, 1.3+/-0.2, respectively, p<0.01). At discharge, plasma levels in AMI patients decline to values not significantly different from those in controls. (1.2+/-0.2, 1.3+/-0.2, respectively). TAT levels (ng/mL) were different among the groups in a fashion similar to that of APC (14.1+/-3.1 on admission vs. 3.3+/-0.4 at discharge, 1.8+/-0.1 in the control subjects, respectively, p<0.01). PAI activity levels (IU/mL) were higher on admission than at discharge and higher than the control subjects (19.7+/-1.8 vs. 10.5+/-1.0, 5.4 +/- 0.7, respectively, p<0.01). Thirty-two patients with AMI were classified into two groups according to the results of thrombolysis: the success group (24 patients) and the failure group (eight patients). APC levels were higher in the failure group than in the success group (5.1+/-0.7 vs. 1.6+/-0.2, p<0.01). TAT levels were also higher in the failure group than in the success group (30.8+/-9.6 vs. 8.6+/-1.7, p<0.01). PAI activity levels (IU/mL) were lower in the failure group than in the success group (13.5+/-3.1 vs. 21.7+/-2.1, p<0.05). There were correlations between APC and TAT levels both on admission (r=0.75, p<0.0001) and at discharge (r=0.71, p<0.0001). Elevated APC was thought to correlate with increased thrombin generation in patients with AMI. This study demonstrated that there was a significant relation between plasma APC level and the responsiveness to thrombolytic therapy of the infarct artery. This study may also indicate that increased thrombin generation is a cause of the resistance to thrombolytic therapy.

Acute Disease↗
PubMed1999

cDNA cloning and expression of human lactosylceramide synthase.

Lactosylceramide synthase is an enzyme that catalyzes the transfer of galactose from UDP-Gal to glucosylceramide, and thus participates in the biosynthesis of most glycolipids in mammals. We have isolated and sequenced the cDNA clone encoding human lactosylceramide synthase. The deduced amino acid sequence of the human lactosylceramide synthase showed 94.2% identity with rat lactosylceramide synthase. Northern blotting analysis revealed that lactosylceramide synthase mRNA was expressed in various tissues, with the highest level in brain and adrenal gland.

Amino Acid Sequence↗
PubMed1999

An alternative splicing form of phosphatidylserine-specific phospholipase A1 that exhibits lysophosphatidylserine-specific lysophospholipase activity in humans.

Phosphatidylserine-specific phospholipase A1 (PS-PLA1), which acts specifically on phosphatidylserine (PS) and 1-acyl-2-lysophosphatidylserine (lyso-PS) to hydrolyze fatty acids at the sn-1 position of these phospholipids, was first identified in rat platelets (Sato, T., Aoki, J., Nagai, Y., Dohmae, N., Takio, K., Doi, T., Arai, H., and Inoue, K. (1997) J. Biol. Chem. 272, 2192-2198). In this study we isolated and sequenced cDNA clones encoding human PS-PLA1, which showed 80% homology with rat PS-PLA1 at the amino acid level. In addition to an mRNA encoding a 456-amino acid product (PS-PLA1), an mRNA with four extra bases inserted at the boundary of the exon-intron junction was detected in human tissues and various human cell lines. This mRNA is most probably produced via an alternative use of the 5'-splicing site (two consensus sequences for RNA splicing occur at the boundary of the exon-intron junction) and encodes a 376-amino acid product (PS-PLA1DeltaC) that lacks two-thirds of the C-terminal domain of PS-PLA1. Unlike PS-PLA1, PS-PLA1DeltaC hydrolyzed exclusively lyso-PS but not PS appreciably. Any other phospholipids such as phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidic acid (PA), and their lyso derivatives were not hydrolyzed at all. These data demonstrated that PS-PLA1DeltaC exhibits lyso-PS-specific lysophospholipase activity and that the C-terminal domain of PS-PLA1 is responsible for recognizing diacylphospholipids. In addition, human PS-PLA1 gene was mapped to chromosome 3q13.13-13.2 and was unexpectedly identical to the nmd gene, which is highly expressed in nonmetastatic melanoma cell lines but poorly expressed in metastatic cell lines (van Groningen, J. J., Bloemers, H. P., and Swart, G. W. (1995) Cancer Res. 55, 6237-6243).

Alternative Splicing↗
PubMed1999

Role of class B scavenger receptor type I in phagocytosis of apoptotic rat spermatogenic cells by Sertoli cells.

Rat Sertoli cells phagocytose apoptotic spermatogenic cells, which consist mostly of spermatocytes, in primary culture by recognizing phosphatidylserine (PS) exposed on the surface of degenerating spermatogenic cells. We compared the mode of phagocytosis using spermatogenic cells at different stages of spermatogenesis. Spermatogenic cells were separated into several groups based on their ploidy, with purities of 60-90%. When the fractionated spermatogenic cell populations were subjected to a phagocytosis assay, cells with ploidies of 1n, 2n, and 4n were almost equally phagocytosed by Sertoli cells. All the cell populations exposed PS on the cell surface, and phagocytosis of all cell populations was similarly inhibited by the addition of PS-containing liposomes. Class B scavenger receptor type I (SR-BI), a candidate for the PS receptor, was detected in Sertoli cells. Overexpression of the rat SR-BI cDNA increased the PS-mediated phagocytic activity of Sertoli cell-derived cell lines. Moreover, phagocytosis of spermatogenic cells by Sertoli cells was inhibited in the presence of an anti-SR-BI antibody. Finally, the addition of high density lipoprotein, a ligand specific for SR-BI, decreased both phagocytosis of spermatogenic cells and incorporation of PS-containing liposomes by Sertoli cells. In conclusion, SR-BI functions at least partly as a PS receptor, enabling Sertoli cells to recognize and phagocytose apoptotic spermatogenic cells at all stages of differentiation.

Animals↗
PubMed1999

A comparison of tau protein in cerebrospinal fluid between corticobasal degeneration and progressive supranuclear palsy.

Many clinical and pathological discussions have been focused on the difficulty of differential diagnosis between corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP) in recent years. This study was conducted to evaluate the usefulness of tau proteins in cerebrospinal fluid (CSF) for the differentiation of these two diseases. Subjects consisted of 10 patients with CBD (four males and six females with a mean age of 67.9+/-5.8 years), 12 patients with PSP (eight males and four females with a mean age of 62.6+/-5.8 years) and 36 control subjects (CTL) (16 males and 20 females with a mean age of 65.8+/-9.9 years). The CBD group included patients with probable CBD, while all the patients in the PSP group satisfied the diagnostic criteria developed by the National Institute of Neurological Disorders and Stroke and Society for PSP (NINDS-SPSP). CSF tau proteins were measured with the sandwich ELISA method (Innogenetics, Belgium). The CSF tau protein level was 320.1+/-86.5 pg/ml in the CBD group, 151.5+/-52.7 pg/ml in the PSP group and 128.7+/-91.7 pg/ml in the CTL group. Significant differences were noted in tau protein levels between the CBD group and both the PSP group (P<0.001) and the CTL group (P<0.005). We suggested that the measurement of CSF tau proteins may be useful for the differentiation between CBD and PSP.

Aged↗
PubMed1999

Effect of nitrogen oxides on expression of the nir and nor genes for denitrification in Pseudomonas aeruginosa.

The activity of the promoters involved in transcription of the genes (nirS, nirQ and norC) required for anaerobic reduction of nitrite and nitric oxide was investigated in NIR- and NOR-deficient mutants of Pseudomonas aeruginosa. The transcriptional activity of these three promoters was induced by nitrite in a wild-type strain and the activity was low in an nirS mutant. In norCBD and nirQOP mutants, which were expected to accumulate nitric oxide because of a lack of nitric oxide reductase activity, the norC and nirQ promoters showed significantly enhanced activity in promoting transcription relative to the parental strain, even at low nitrite concentrations. These results suggest that the nirQ and norC promoters are regulated by the concentration of endogenous nitric oxide rather than that of nitrite.

Gene Expression Regulation, Bacterial↗
PubMed1999

Electrophoretic analysis of oxidative modification of apolipoprotein E in very low density lipoprotein from fresh human plasma.

Ferrous ion-induced oxidative modification of apoE in lipid peroxidation of human very low density lipoprotein (VLDL) and the role of the cysteinyl group, present in apoE3 but absent in apoE4, were examined. Fresh human VLDL was obtained from healthy volunteers with different apoE phenotypes as determined by isoelectric focusing (IEF). The VLDL was oxidized by incubating with FeSO4. The time course of the lipid peroxidation was determined by thiobarbituric acid (TBA) assay. The sequential oxidative modification of the apoE was demonstrated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting with an anti-apoE antibody. To modify the cysteinyl group of apoE3, the VLDL from the apoE3/3 subject was pretreated with cysteamine before the TBA assay and electrophoresis. The ferrous ion-induced peroxidation of the VLDL was pH-dependent, with increased reactivity at acidic pH ranges. In the initial stage of the lipid peroxidation of the VLDL, aggregates were formed involving apoE dimers and apoB via disulfide bonds, followed by the intra- and intermolecular cross-linkings of apoE monomers. The VLDL with apoE3/4 showed a shorter lag time than the VLDL with apoE3/3 in the TBA assay, suggesting a lower antioxidative effect with apoE3/4. The apoE3/3 pretreated with cysteamine showed the patterns of apoE3/4 in IEF and SDS-PAGE with immunoblotting, but it did not show the shortened lag time in the TBA assay. This suggests that factors other than cysteinyl groups contribute to the reduced antioxidative activity of apoE4.

Apolipoproteins B↗
PubMed1999

The cbbQ genes, located downstream of the form I and form II RubisCO genes, affect the activity of both RubisCOs.

Hydrogenovibrio marinus strain MH-110, an obligately lithoautotrophic hydrogen-oxidizing bacterium, possesses three sets of the genes for ribulose 1,5-bisphosphate carboxylase/oxygenase (RubisCO): namely, two form I type (cbbLS-1 and cbbLS-2) and one form II type (cbbM) enzymes. The cbbQ-m gene was located downstream of cbbM, and showed high similarity to other cbbQ genes and nirQ/norQ genes in denitrifying bacteria. Phylogenetic analysis of CbbQ and NirQ/NorQ indicated that CbbQ-m from Hv. marinus closely resembled CbbQ from Thiobacillus intermedius and Thiobacillus neapolitannus and less closely resembled NirQ and NorQ. The cbbQ-m gene has been shown to activate the form II RubisCO in E. coli cells, and the cbbQ-t from Hydrogenophilus thermoluteolus could also activate the form II RubisCO. Both cbbQ genes have also been shown to activate the form I RubisCO from Hp. thermoluteolus in E. coli cells. However, the activation levels of two form I RubisCOs from Hv. marinus were smaller than that of form I RubisCOs from Hp. thermoluteolus. Form II RubisCO activated by CbbQ-m (QM) was purified from E. coli cells. The result of the 8-anilino-1-naphthalenesulfonate binding assay and the circular dichroism spectra indicated that QM was conformationally different from Form II RubisCO that was not activated by CbbQ.

Amino Acid Sequence↗
PubMed1999

Induction of a critical elevation of povidone-iodine absorption in the treatment of a burn patient: report of a case.

A critical elevation of povidone-iodine absorption which occurred in a burn patient who was topically treated with 10% povidone-iodine (PI) gel is herein reported. A 65-year-old man was admitted to our hospital for deep second- and third-degree burns covering 26% of his total body surface area. The intravenous administration with lactated Ringer's solution and topical treatment with silver sulfadiazine were applied in addition to such treatments as debridement and skin grafting. However, wound infection occurred due to Pseudomonas aeruginosa. Topical treatment with PI gel was effective for this condition. Persistent nodal bradycardia with hypotension, metabolic acidosis, and renal failure occurred 16 days after the start of PI gel treatment. Iodine toxicosis caused by PI gel was suspected with a serum iodine level of 20600 microg/dl (normal range 2-9 microg/dl). The PI gel treatment was therefore discontinued immediately, and hemodialysis was scheduled. However, the patient's family refused hemodialysis and he died 44 days after admission. To our knowledge, only eight patients with iodine toxicosis have been reported in burn patients treated with PI gel.

Absorption↗
PubMed1999

Splenic artery aneurysm associated with systemic lupus erythematosus: report of a case.

We herein report on a 64-year-old Japanese female patient who presented with a splenic artery aneurysm (SAA) associated with systemic lupus erythematosus (SLE). The saccular aneurysm, which measured 3 cm in diameter, was located in the proximal third of the splenic artery from the pancreas with a portosystemic shunt. A double ligation of the splenic artery (the distal and proximal sides of the aneurysm) was performed without a splenectomy. The postoperative course showed acute pancreatitis without either splenic infarction or portal thrombus. To our knowledge, the closed association of SLE with an aneurysmal dilatation of the splenic artery has not been previously reported. Both the pathogenesis and the management of SAA associated with SLE are discussed following the presentation of this case. This is the first reported case of SAA associated with SLE.

Aneurysm↗
PubMed1999

Successful surgical treatment of a dural arteriovenous fistula at the craniocervical junction with reference to pre- and postoperative MRI.

We report a 62-year-old woman who presented with a myelopathy at the lower thoracic level. Left vertebral angiography revealed a dural arteriovenous fistula (DAVF) at the craniocervical junction, draining into an anterior spinal vein. Below the T7 level, the spinal cord gave high signal on T2-weighted images and enhanced with Gd-DTPA. The patient was successfully treated by simple clipping of vein draining the DAVF. The abnormal signal intensity and contrast enhancement rapidly regressed, except in the conus medullaris. Regression of the parenchymal abnormality on serial MRI following treatment corresponded closely with postoperative improvement of neurological function.

Arteriovenous Fistula↗
PubMed1999

A patient who survived total colonic type ulcerative colitis complicated by toxic megacolon, disseminated intravascular coagulation, methicillin-resistant Staphylococcus aureus infection and bilateral femoral phlebothrombosis.

We report a patient who survived total colonic type ulcerative colitis (UC) complicated by toxic megacolon (TM), disseminated intravascular coagulation (DIC), methicillin-resistant Staphylococcus aureus infection, and phlebothrombosis. A 69-year-old man was treated for about 4 months under the diagnosis of ischemic colitis at another hospital, and was transferred to our hospital. Based on endoscopic and pathological findings, we strongly suspected UC, and administered salazosulfapyridine and methylprednisolone, but TM and DIC developed, necessitating urgent subtotal colectomy. Despite his elderly age and the severe complications, he recovered and was discharged from our hospital about 4 months after admission. The mortality rate of UC complicated by TM and DIC in elderly patients is high, necessitating rapid initiation of high-dose steroid administration or surgical treatment.

Aged↗
PubMed1999

Hypertension as a paraneoplastic syndrome in hepatocellular carcinoma.

We report a 66-year-old man with hepatocellular carcinoma who was positive for hepatitis B surface antigen, and was hospitalized because of hypoglycemia and hypertension. His plasma renin activity was normal (2.3 ng/ml per h), but concentrations of angiotensin I (>2500 pg/ml) and II (86 pg/ml) were high. Increased angiotensin I level at sites proximal and distal from the confluence of the hepatic vein and the inferior vena cava indicated that the hypertension was provoked by overproduction of angiotensin I from the hepatocellular carcinoma. Previous reports of patients with hepatocellular carcinoma with hypertension due to abnormality of renin-angiotensin system are reviewed.

Aged↗
PubMed1999

Complications associated with transvenous embolisation of cavernous dural arteriovenous fistula.

Results are presented of transvenous embolisation, via either the inferior petrosal sinus (IPS) or the superior ophthalmic vein (SOV), for 19 patients with cavernous dural arteriovenous fistula with special emphasis on complications. In 17 patients (89%) there was complete angiographic elimination of the shunts and resolution of the symptoms. The remaining two patients also improved clinically, regardless of the minimal residual shunts. Complications included forehead dysaesthesia in one patient, blepharoptosis in two, and transient abducens nerve palsy in three. Injury of the supra-orbital nerve and levator muscle occurred in association with the exposure of the SOV in the patient with dysaesthesia of the forehead and in those with blepharoptosis, respectively. In two patients, abducens nerve palsy resulted from coil over-packing in the cavernous sinus and from dissection of the clival dura during guidewire penetration of the thrombosed IPS in one patient. We found that the complication rate decreased with time, because we became better with this procedure. We believe that transvenous embolisation is the best available treatment modality if one pays careful attention to avoid complications related to the procedure.

Aged↗