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K Matsui

Publications and source records attributed to K Matsui.

At least 235 records · Page 13Linked to original sources
PubMed1997

[A prospective study on the timing of discontinuation of aspirin before coronary artery bypass grafting].

The effects of the timing of discontinuation of aspirin before coronary artery bypass grafting (CABG) on postoperative blood loss and blood requirements were examined in 22 patients undergoing elective CABG, who were randomly assigned into two groups. In Group I (11 patients), aspirin was discontinued two days before the operation and in Group II (11 patients), aspirin was continued up to the operation. The other 40 patients, who did not take aspirin for at least seven days before the operation, served as a control Group. There were no differences in preoperative data including the platelet count and the hemoglobin concentration, nor in operative variables such as operation time, cardiopulmonary bypass duration and aortic crossclamp time among the groups. Although postoperative blood loss (six hours' loss; Group I 218 ml, Group II 183 ml and control Group 172 ml) and red blood cells transfusion requirements were not different among the groups, platelet concentrates transfusion was more frequently required in Group II (54.5%) as compared with control Group (7.5%) and Group I (9.1%). The difference between Group II and the control Group reached statistical significance (p < 0.01), but there was no significant difference between Group I and control Group. This fact suggests that preoperative two days' discontinuation of aspirin works as effectively as seven days' discontinuation.

Aged↗
PubMed1996

IFN-gamma-inducing factor up-regulates Fas ligand-mediated cytotoxic activity of murine natural killer cell clones.

NK cells, non-T non-B immune effector lymphocytes, are localized in many organs, including liver, as well as in the circulation. To investigate the regulatory mechanism of killing apparatus in hepatic NK cells, we established IL-2-dependent NK cell clones from liver lymphocytes of BALB/c nude mice. To generate the NK cell clones, we incubated liver lymphocytes with a high dose of IL-2 in the presence of irradiated Kupffer cells, as feeder cells and as the source of IL-12, originally identified as NK cell stimulatory factor. Unless liver lymphocytes were incubated with both IL-2 and Kupffer cells, no cell growth was observed. Hepatic NK cell clones were established from this cell line by limiting dilution. The surface phenotypes of cloned NK cells were IL-2R beta-chain+ CD16+ CD3- IgM-. The clones did not express NK2.1, which is expressed by a half of NK-enriched spleen cells of BALB/c mice. Although the cells contained dense granules reactive to mAb against perforin, they exerted no conventional cytolytic activity against YAC-1. They constitutively expressed Fas ligand (FasL) and specifically killed Fas-positive target cells by fragmenting DNA. This Fas-FasL-mediated killing activity was enhanced by IFN-gamma-inducing factor, a recently identified novel cytokine produced by activated Kupffer cells, but was not affected by other Kupffer cell-produced cytokines, such as IL-12, IL-1beta, and TNF-alpha. Taken together, these findings suggest that hepatic NK cells participate in the immune response as effector cells through the Fas-FasL system in collaboration with cytokines from Kupffer cells.

Animals↗
PubMed1996

Calystegine B4, a novel trehalase inhibitor from Scopolia japonica.

GLC-MS analysis has been developed for screening plants of the family Solanaceae for new calystegines. GLC-MS analyses of the extract of Scopolia japonica showed the presence of a new tetrahydroxy-nor-tropane alkaloid in addition to the known calystegines A3, A5, B1, B2, B3, and C1. We gave this new alkaloid the trivial name calystegine B4. The structure of calystegine B4 was determined as 1 alpha, 2 beta, 3 alpha, 4 alpha-tetrahydroxy-nor-tropane from a variety of NMR spectral data. Calystegines B1, B2, and C1 are potent competitive inhibitors with Ki values ranging from 10(-6) to 10(-7) M for almond beta-glucosidase, while calystegine B4 inhibited this enzyme in a competitive manner, with a Ki value of 7.3 microM. Calystegine B2 is also a potent inhibitor of green coffee bean alpha-galactosidase, whereas calystegine B4 exhibited no significant activity for this enzyme. Among rat intestinal glycosidases, only trehalase was potently inhibited by calystegine B4, with an IC50 value of 9.8 microM. Furthermore, calystegine B4 potently inhibited pig kidney trehalase in a competitive manner, with a Ki value of 1.2 microM, but it was almost inactive against yeast and fungal trehalases.

Alkaloids↗
PubMed1996

Bell pepper fruit fatty acid hydroperoxide lyase is a cytochrome P450 (CYP74B).

Fatty acid hydroperoxide lyases cleave a C-C bond adjacent to a hydroperoxide group in lipoxygenase derived lipid hydroperoxides to form short-chain aldehydes and oxo-acids. Previously, we showed that fatty acid hydroperoxide lyase from bell pepper fruits is a heme protein whose spectrophotometric properties greatly resemble a cytochrome P450. In order to ascertain the relationship of it to the P450 gene family, we have cloned cDNA encoding fatty acid hydroperoxide lyase from immature bell pepper fruits. The cDNA encodes 480 amino acids, and shares homology with P450s mostly at the C terminus. The heme binding cysteine is recognizable at position 441. The most closely related P450 is allene oxide synthase (CYP74A), with which it has 40% identity. It qualifies the lyase as a member of a new P450 subfamily, CYP74B. From this finding, the enzyme is thought to be a novel member of P450 specialized for the metabolism of lipid peroxides.

Aldehyde-Lyases↗
PubMed1996

Two subsites on the active center of pig kidney trehalase.

A kinetic analysis of the active site of pig kidney trehalase was made by examining two types of inhibitors that are monosaccharide analogs and cause a competitive inhibition of the trehalase. Trehalase hydrolyzes trehalose (alpha-D-glycopyranosyl alpha-D-glucopyranoside) to give an equimolar mixture of alpha-D-glucose and, by inversion of configuration, beta-D-glucose. 1,4-Dideoxyl-1,4-imino-D-arabinitol is considered to be a transition state (glucosyl cation) analog, while methyl beta-D-glucoside, 1,5-dideoxy-1,5-imino-D-glucitol (1-deoxynojirimycin), fagomine, and 1-epivalidamine are considered to be analogs of the beta-D-glucose that is derived by hydrolysis of trehalose. These glucosyl cation inhibitor and beta-D-glucose analog inhibitors competed with each other at the same site on the active center of pig kidney trehalase and were therefore put together in one group (group A). Methyl alpha-D-mannoside and 1-deoxymannojirimycin were also competitive inhibitors of trehalase and competed with each other for the same site. However, an inhibitor in group A did not compete with the methyl alpha-D-mannoside or 1,5-dideoxy-1,5-imino-D-mannitol (1-deoxymannojirimycin). Thus these latter two inhibitors were placed in group B. These results support the hypothesis that the active center of trehalase may comprise two subsites, one for catalysis and one for recognition, that act separately on each of the glucose of the trehalose. The catalysis site requires the correct D-glucose configuration at carbons 2, 3, 4, and 5 or a good superimposition onto the glucosyl cation intermediate. The C2 equatorial OH group of a glucopyranosyl residue appears to be important for binding at the catalytic site since 1-deoxynojirimycin is more tightly bound by two orders of magnitude over its 2-deoxy derivative, fagomine. The beta-D-glucose and glucosyl cation analogs best fit this site. The recognition site is compatible with D-glucose and its analogs bearing the alpha configuration at the anomeric position. alpha-D-Mannose analogs are much more tightly bound than the corresponding D-gluco compound at this site. The extremely high affinity (Ki = 0.52 nM) of validoxylamine A, a mimic of the substrate in the transition state, derives from the synergistic interactions of two cyclitol units with two subsites. The value obtained by multiplying the Ki (1.2 microM) for 1-epivalidamine times that for 1-deoxymannojirimycin (Ki = 0.39 mM) is very close to that for validoxylamine A. The results described here may be applicable to other trehalase molecules.

Animals↗
PubMed1996

Construction of a new system for separate expression of mutagenesis proteins: the abilities to promote UV mutagenesis and interchangeability of MucA', MucB, SamA' and SamB proteins in Salmonella typhimurium.

The two distinct mucAB and samAB operons originally isolated from the plasmids of Salmonella typhimurium encode proteins engaged in induced mutagenesis. They represent two extreme cases among the so far characterized members of the enterobacterial umuDC family in respect to both the strength and the specificity of their effect. It is suggested that the MucA and SamA proteins are post-translationally processed to MucA' and SamA', respectively, which lack the N-terminal 25 amino acids and are the active species in mutagenesis. For the purpose of characterizing the individual activities of these proteins, we developed a new system for their SOS-independent separate and controllable expression in enterobacteria. Besides the matured forms of MucA', SamA' as well as MucB and SamB proteins we also expressed hybrid HisTag-MucA' and HisTag-SamA' proteins in which a synthetic 24 amino acid HisTag region replaces the natural 25 amino acid N-terminal leader present in the MucA and SamA precursors. In this study, we analyzed the effect of the mutagenesis proteins on the UV mutability of S. typhimurium YG5144. None of the proteins, if expressed alone, promoted UV mutagenesis. Different combinations of the proteins promoted mutagenesis to different extents in the order MucA' + MucB > SamA' + SamB > or = HisTag-MucA' + MucB > or = SamA' + MucB > MucA' + SamB > HisTag-SamA' + SamB. The mutagenesis enhancing potential of the combinations with MucB protein decreased as the expression of the proteins increased while the mutagenesis enhancing potential of the combinations with SamB protein increased together with the increase in the expression. The artificially expressed MucA' + MucB proteins were as active as their MucAB counterparts expressed from the plasmid pKM101 in promoting UV mutagenesis, but they were remarkably more efficient than their pKM101-born counterparts in promoting spontaneous mutagenesis. We conclude that the MucA'B and SamA'B proteins are partly interchangeable and the functionality of the resulting A' + B complex is largely dependent on the appropriate B-protein.

Amino Acid Sequence↗
PubMed1996

Effect of intranasal administration of thyrotropin-releasing hormone on ataxic gait in staggerer mice.

The ataxia ameliorating effect of an intranasal administration of thyrotropin-releasing hormone (TRH) was examined using normal and ataxic staggerer mutant mice. In the normal mice, the blood TRH level reached the maximum level 5 min after administration and was gradually eliminated during the following 60 min. The antiataxic effects of TRH in the staggerer mice was examined using an open field method. At lower doses, the intranasal administration of TRH in the staggerer mice was examined using an open field method. At lower doses, the intranasal administration of TRH did not exert any evident effect. However, at 3 mg or 4 mg, the fall index (the ratio of the number of falls to the movement score) was significantly decreased for 20 min after the administration. These results show that an intranasal administration of TRH can ameliorate the ataxia in staggerer mice, and may be promising for clinical use in patients with spinocerebellar degeneration.

Animals↗
PubMed1996

Marked elevation of plasma carcinoembryonic antigen and stomach carcinoma.

BACKGROUND: This study was undertaken to clarify the relationship between marked elevation of plasma carcinoembryonic antigen (CEA) and signet ring cell carcinoma of the stomach. METHODS: To elucidate the contributing factor of extreme elevation of plasma CEA value, the histologic and biochemical records for 310 cases of stomach carcinoma, including 202 advanced and 108 early, collected between 1980 to 1994 from the San-in Rosai Hospital and Tottori University Hospital were studied. Immunohistochemical localization of CEA in the stomach was performed using a peroxidase antiperoxidase (PAP) staining technique. RESULTS: Among 310 cases of gastric carcinoma, 44 (14%) had abnormal plasma CEA values. The positivity rates of early and advanced gastric carcinoma were 3.7% (4/18) and 19% (40/202), respectively. Concerning advanced gastric carcinoma, 20 cases had more than 51 ng/mL, and 20 cases had between 5 ng/mL and 50 ng/mL. Four cases with plasma CEA values of more than 1,000 ng/mL had histological signet ring cell carcinoma (one case), and poorly differentiated adenocarcinoma with signet ring cell carcinoma (2 cases). Three cases of signet ring cell carcinoma or poorly differentiated adenocarcinoma of the stomach were massive local infiltration rather than hepatic metastasis. Among 40 cases with elevated plasma CEA, a multivariate regression analysis showed that only one variable (lymph node metastasis) was an independent factor (P < 0.05). Significantly higher rates of peritoneal metastasis (P < 0.0001) and lymph node metastasis (P < 0.05) were observed in patients with marked elevations of plasma CEA than in patients with moderate elevations of plasma CEA. No correlation was obtained between plasma CEA value and several biochemical tests. CONCLUSIONS: Marked elevation of plasma CEA may be found in the absence of liver metastasis from signet ring or poorly differentiated gastric carcinoma. Patients with marked elevations of CEA also had lymphatic and peritoneal dissemination.

Adenocarcinoma↗
PubMed1996

Regulation of T-cell death genes: selective inhibition of FasL- but not Fas-mediated function.

Activation-induced cell death (AICD) requires coexpression of Fas and FasL. Hybridoma T-cells express detectable FasL mRNA 3 to 5 hr after culture in anti-CD3-coated wells. High and steady expression of FasL mRNA was observed after 8-10 hr of activation. Expression of FasL cytotoxicity and AICD is consistent with the time-course of FasL mRNA induction. Fas-Ig was effective in inhibiting AICD when added no later than 5 hr after activation, but was ineffective when added after 8-10 hr of activation. These observations suggest that FasL gene activation is a critical step for AICD. By contrast, Fas was constitutively expressed and the time-course study did not support the idea that up-regulation of Fas is critical for AICD. The critical role of FasL gene activation for AICD was confirmed by studies using inhibitors of AICD. Dexamethasone (Dex) inhibited FasL induction and Fas up-regulation, but not basal Fas expression of hybridoma T-cells. All-trans retinoic acid (RA) inhibited FasL induction, but had little effect on Fas up-regulation. Both agents inhibited FasL cytotoxicity. The Fas-mediated death pathway distal to Fas/FasL interactions remained intact in the protected hybridoma T-cells. These results demonstrate that FasL gene activation, but not Fas up-regulation, is critical for AICD and that Dex and all-trans RA selectively inhibits FasL but not Fas function. The system may prove useful for the identification of critical factors regulating T-cell death genes. It may also serve as a useful system to study gene regulation in AICD-dependent phenomena.

Animals↗
PubMed1996

The characterization of tyrosine phosphorylation of 78 and 92 kDa proteins in rat basophilic RBL-2H3 cells.

Previously, we have demonstrated that tyrosine phosphorylation of 78 and 92 kDa proteins in rat basophilic leukemia cells (RBL-2H3) is involved in a signal transduction system for high-affinity IgE receptor (Fc epsilon RI)-mediated histamine secretion. However, it is not clarified whether the tyrosine phosphorylation of 78 and 92 kDa proteins in RBL-2H3 cells is regulated by activation of protein kinase C (PKC) or phosphatidylinositol 3-kinase (PI3-kinase). In this study, therefore, the effect of depletion of PKC in RBL-2H3 cells, or the influence of PKC, PI3-kinase and tyrosine kinase inhibitors on histamine release from RBL-2H3 cells was examined. The elimination of PKC in RBL-2H3 cells induced significant suppression of histamine release, although the tyrosine phosphorylation of 78 and 92 kDa proteins was not inhibited. The inhibition of histamine release was also observed by the treatment with a PKC inhibitor such as H-7, calphostin C, a PI3-kinase inhibitor such as wortmannin or a tyrosine kinase inhibitor such as ST638, genistein, hervimycin A, although the tyrosine phosphorylation of both proteins was inhibited by only ST638. These results suggest that the 78 kDa protein in RBL-2H3 cells is not identical to the protein-tyrosine kinase PTK72 and the tyrosine phosphorylation of 78 and 92 kDa proteins in RBL-2H3 cells occurs upstream of PKC and PI3-kinase activation or is regulated independently of the PKC- and PI3-kinase-dependent signaling pathway.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1996

Comorbidity as a correlate of length of stay for hospitalized patients with acute chest pain.

OBJECTIVE: To determine whether comorbid medical conditions as measured with the Charlson Comorbidity Index are independent correlates of length of stay after adjusting for other clinical and socioeconomic data. DESIGN: Prospective cohort study. SETTING: Urban teaching hospital. PATIENTS: All 1,261 patient aged 30 years or more who were admitted to this hospital after coming to the emergency department with acute chest pain between October 1990 and May 1992. MEASUREMENTS AND OUTCOMES: Clinical data including comorbid medical conditions used in the Charlson index were prospectively recorded by the evaluating physician at the time of admission or by a research nurse who was blinded to the subsequent events. History of myocardial infarction was excluded from the calculation of the Charlson index score. Charlson index scores were 0 to 1 for 921 patients (73%), 2 to 3 for 263 (21%), and greater than 3 for 77 (6%). Unadjusted means (+/- SD) lengths of stay in these groups were 4.4 +/- 5.2, 5.2 +/- 5.9, and 7.5 +/- 9.3 days, respectively. In multiple linear regression analysis, compared with Charlson index scores of 0 to 1, scores of 2 to 3 and greater than 3 were significant (p < .01) independent correlates of the log transformation of length of stay after adjusting for clinical data from the initial presentation and subsequent course (model R2 = .510). In an analysis restricted to the 795 patients without clinical complications, a Charlson index score greater than 3 was an independent correlate of length of stay compared with scores of 0 to 1 (p < .01). Individual comorbid conditions were not significant correlates of length of stay after controlling for Charlson index score. CONCLUSIONS: In this population of patients with acute chest pain, comorbidity as measured with the Charlson index was independently associated with length of stay after adjustment for other clinical data. After adjusting for the Charlson index, no separate comorbid condition was significantly correlated with length of stay. These findings suggest that the Charlson index can be used to adjust for comorbidities in analyses of length of stay for patients with this condition.

Acute Disease↗
PubMed1996

Purification of a product from Salmonella typhimurium with the ability to inhibit mitogen-induced proliferation of murine splenic T-lymphocytes.

We attempted to purify a substance that inhibits mitogen-induced proliferation of murine splenic T-lymphocytes from Salmonella typhimurium. The soluble fraction of a suspension of bacteria disrupted by sonication was chromatographed serially on Mono Q HR, Superdex 200 HR and HiLoad Superdex 75 p.g. columns. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis revealed that the purified active substance migrated as a single band corresponding to a molecular mass of 87 kDa. We designated the purified substance S. typhimurium-derived inhibitor of T-cell proliferation (STI), which, at 0.2 microgram/ml and above, inhibited proliferation and augmented CD25 expression of phytohemagglutinin-stimulated murine splenic lymphocytes. These findings suggested that the immunosuppression induced by Salmonella infection may be attributable to STI.

Animals↗
PubMed1996

Randomised trial for the prevention of delayed emesis in patients receiving high-dose cisplatin.

Despite recent advances in control of acute emesis following cisplatin-based chemotherapy regimens, delayed emesis remains a significant cause of treatment-related morbidity and factors associated with delayed emesis have not yet been evaluated. A prospective randomised trial was conducted to compare the efficacy and toxicity of granisetron, dexamethasone plus prochlorperazine with granisetron alone in controlling cisplatin-induced delayed emesis and to identify the important factors that influence its occurrence and severity. Seventy cisplatin-naive patients with inoperable solid tumors participated in the trial. Patients who received 80 mg m-2 or 100 mg m-2 of cisplatin were randomly assigned to receive either granisetron 40 micrograms kg-1 intravenously (i.v.) on day 1, dexamethasone 20 mg i.v. on days 2 and 3 and prochlorperazine 5 mg orally thrice daily on days 1-5 or granisetron 40 micrograms kg-1 i.v. on day 1 alone. There was no difference in their acute antiemetic efficacy. A combination regimen was more effective than granisetron alone in preventing delayed symptoms, with superior rates of complete plus major responses of 77% vs 51% (P = 0.0460). Treatment arm was the only determinant factor for the occurrence of delayed emesis (P = 0.0101).

5-Hydroxytryptophan↗
PubMed1996

Structural continuity of filtration slit (slit diaphragm) to plasma membrane of podocyte.

Murine monoclonal antibody 5-1-6 was reported to bind to the slit membrane and closely related structures in rat renal glomeruli; it induced heavy, reversible proteinuria and appeared to redistribute onto the plasma membrane of epithelial cells after binding at the original target sites. This phenomenon of antigenic movement has not been analyzed in detail to date. In addition to normal kidneys we also studied localization of the antigen recognized by monoclonal antibody 5-1-6 in protamine sulfate-perfused rat kidneys, in which slit diaphragms are known to be functionally modified. Isolated glomeruli as well as ultrathin kidney cryosections were labeled by the immunogold technique to clarify the relation between this antigen and the slit diaphragm. Sequential localization of injected monoclonal antibody was visualized using a post-embedding immunogold method in rats 2 hours to 12 days after injection of antibody. Ultrastructural immunogold labeling demonstrated that under normal conditions antigenic molecules were expressed mainly in the area beneath the slit diaphragms. Occasionally labeling was found at the base of the foot process, facing the glomerular basement membrane. After protamine sulfate treatment antigenic sites were dislocated due to the lifting and disruption of slit diaphragms, indicating that this antigen is associated with slit diaphragms. Injected antibody was localized at the filtration slits at 2 hours, and by 12 hours it had moved onto the apical plasma cell membrane of foot process. In addition, from 3 days onwards patch or cap-like formation on the plasma cell membrane of podocytes was seen. Possible shedding of antibody from podocyte cell surface membrane was occasionally encountered, but internalization of antibody was a minor event. Elution experiments in isolated glomeruli at day 3 indicated that antigen and antibody were both localized on the podocyte cell surface membrane, suggesting redistribution of immune complexes. In conclusion, filtration slits (slit diaphragms) and the apical membrane of foot process of podocytes demonstrate structural continuity, as revealed by the movement of the antigen recognized by monoclonal antibody 5-1-6 as antigen-antibody complexes.

Animals↗
PubMed1996

IL-4 and anti-CD40 protect against Fas-mediated B cell apoptosis and induce B cell growth and differentiation.

Most Th2 clones, when activated, produce IL-4 and express CD40 ligand (CD40L) on their cell surface. Therefore, they can induce growth and differentiation of B cells by cognate help. In contrast, activated Th1 clones, which produce IFN-gamma and express both CD40L and Fas ligand (FasL) on their cell surface, often induce B cell apoptotic cell death. To understand the mechanism by which Th2 cells can induce B cell growth and differentiation in the presence of FasL-positive cells, we stimulated B cells with IL-4, anti-IgM and/or anti-CD40 in the presence of anti-Fas. We report here that addition of anti-Fas strongly inhibited anti-CD40-induced B cell proliferation without affecting anti-IgM-induced B cell proliferation. Furthermore we showed that stimulation of B cells with anti-CD40 induced the expression of Fas molecules on the B cells (approximately 30%) and rendered them highly sensitive to anti-Fas-mediated apoptotic cell death. Indeed, over 23% of anti-CD40-stimulated B cells showed hypodiploid DNA after being incubated with anti-Fas, while h2 cells could dominate over FasL-positive Th1 cells by production of CD40L and IL-4, which in combination induce antibody production and inhibit the Th1 cell-mediated immune response.

Animals↗
PubMed1996

Evaluation of the genotoxicity of stevioside and steviol using six in vitro and one in vivo mutagenicity assays.

Stevioside, a constituent of Stevia rebaudiana, is commonly used as a non-caloric sugar substitute in Japan. The genetic toxicities of stevioside and its aglycone, steviol, were examined with seven mutagenicity tests using bacteria (reverse mutation assay, forward mutation assay, umu test and rec assay), cultured mammalian cells (chromosomal aberration test and gene mutation assay) and mice (micronucleus test). Stevioside was not mutagenic in any of the assays examined. The aglycone, steviol, however, produced dose-related positive responses in some mutagenicity tests, i.e. the forward mutation assay using Salmonella typhimurium TM677, the chromosomal aberration test using Chinese hamster lung fibroblast cell line (CHL) and the gene mutation assay using CHL. Metabolic activation systems containing 9000 g supernatant fraction (S9) of liver homogenates prepared from polychlorinated biphenyl or phenobarbital plus 5,6-benzoflavone-pretreated rats were required for mutagenesis and clastogenesis. Steviol was weakly positive in the umu test using S.typhimurium TA1535/pSK1002 either with or without the metabolic activation system. Steviol, even in the presence of the S9 activation system, was negative in other assays, i.e. the reverse mutation assays using S.typhimurium TA97, TA98, TA100, TA102, TA104, TA1535, TA1537 and Escherichia coli WP2 uvrA/pKM101 and the rec-assay using Bacillus subtilis. Steviol was negative in the mouse micronucleus test. The genotoxic risk of steviol to humans is discussed.

Animals↗
PubMed1996

Identification of nekoflavin as 7 alpha-hydroxyriboflavin.

Nekoflavin, which was found in cat's choroids [Matsui, K. (1965) J. Biochem. 57, 201-206], was identified as 7 alpha-hydroxyriboflavin by comparing the physicochemical properties of nekoflavin acetate with those of chemically synthesized 7 alpha-hydroxyriboflavin pentaacetate. 7 alpha-Hydroxyriboflavin was synthesized from 4-chloro-2-methylbenzonitrile through 7-cyano-7-demethylriboflavin and 7 alpha-aminoriboflavin, which are also new flavins.

Animals↗