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Biomedical subjects

H Matsui

Publications and source records attributed to H Matsui.

At least 55 records · Page 3Linked to original sources

Epidemiological investigation of a fatal case of cholera in Japan by phenotypic techniques and pulsed-field gel electrophoresis.

A fatal case of cholera caused by Vibrio cholerae 01 El Tor serotype Ogawa occurred in Aichi Prefecture, Japan in 1995. The patient was identified locally, but the route of the infection was unknown. The causative isolate and 38 other domestic and imported V. cholerae O1 isolates, obtained between 1984 and 1997, were analysed by prophage typing, antimicrobial susceptibility testing and pulsed-field gel electrophoresis (PFGE). This was done to determine whether the isolate from this case differed from others associated with either mild cholera infections or asymptomatic carriage, and to elucidate the route of infection. Cholera toxin (CT) from 37 toxigenic isolates was assayed semi-quantitatively. The 39 isolates were divided into 12 temporary types in accordance with the results of the three typing techniques. The isolate from the fatal infection and nine other isolates were classified as temporary type IV. No difference in CT production was found between the isolate from the fatal case and the other 36 toxigenic isolates. Taken together, it is unlikely that a V. cholerae 01 isolate of distinguishable type was responsible for the fatal illness. Temporary type IV isolates were frequently present in both domestic and imported cases from 1994 to 1997 in Aichi, but they did not emerge before 1993. These results suggest that a new clone was introduced after 1993 from overseas and then disseminated into Aichi, and this may have been an important step in triggering the fatal case of cholera.

Adult↗

Impact of maintenance chemotherapy on disease-free survival in patients with stage Ic and II epithelial ovarian cancer.

PURPOSE OF INVESTIGATION: To evaluate the impact on disease free survival (DFS) with maintenance chemotherapy following complete surgery and adjuvant chemotherapy in patients with stage Ic and II epithelial ovarian cancer by a retrospective study. METHODS: One hundred and forty patients with stage Ic and stage II epithelial ovarian cancer were classified into three groups according to the modality of maintenance chemotherapy (no therapy, oral or intravenous administration of anti-cancer drugs). DFS was compared among the three groups, and independent predictive factors for relapse were analyzed. RESULTS: There were no statistically significant differences in DFS among the three groups for either stage Ic or II cancers, stage Ic and stage II. Multivariate analysis revealed that independent predictive factors for relapse were stage II (p = 0.004) in all patients and less than three cycles of adjuvant chemotherapy in stage II patients (p = 0.015). CONCLUSION: Maintenance chemotherapy had no impact on DFS in patients with stage Ic or II epithelial ovarian cancer.

Adenocarcinoma, Clear Cell↗

LIGHT, a member of the TNF superfamily, induces morphological changes and delays proliferation in the human rhabdomyosarcoma cell line RD.

LIGHT is a member of the tumor necrosis factor (TNF) superfamily, which binds two known receptors, lymphotoxin-beta receptor (LTbetaR) and the herpesvirus entry mediator (HVEM)/TR2. We investigated the effects of LIGHT on the human rhabdmyosarcoma cell line RD. LIGHT delayed cell proliferation and induced morphological changes of the cells. These effects were not shown by other TNF family ligands such as TNFalpha and LTalpha, which induced the transcriptional activity of nuclear factor-kappaB (NF-kappaB) and NF-kappaB-responsible chemokine productions in the same manner as did LIGHT. LTalpha1beta2, another TNF family ligand for LTbetaR, was shown to have similar activities in RD cells as LIGHT. Both LIGHT and LTalpha1beta2 induced the expression of muscle-specific genes such as smooth muscle (SM) alpha-actin, while TNFalpha and LTalpha did not. These findings indicate that LIGHT may be a novel inducer of RD cell differentiation associated with SM alpha-actin expression through the LTbetaR.

Actins↗

Identification and characterization of the human serotonin-4 receptor gene promoter.

The human serotonin-4 (5-HT(4)) receptor gene expression is highly regulated in various tissues. We isolated the human 5-HT(4) receptor gene containing the 5'-flanking region and characterized its promoter. By 5'-RACE (5'-rapid amplification of the cDNA ends) and inverse PCR, multiple transcription initiation sites were identified. The most 5' one (assigned to +1) was 5135 bp upstream to the translation start site. The 500-bp 5'-flanking region contained potential binding sites for transcription factor Sp-1, AP-2, AP-4, and GATA. However, this region lacked TATA- and CAAT-boxes. Transient transfection analyses in human choriocarcinoma T3M-3 (5-HT(4) receptor-positive) and HepG2 (5-HT(4) receptor-negative) cells revealed that the region (-210 to -105) is necessary for the basic and cell-type specific 5-HT(4) receptor gene expression. In addition, untranslated exon 1 contained negative (+112 to +182) as well as positive (+1 to +111) modulators, indicating that exon 1 plays a regulatory role in the 5-HT(4) receptor gene expression.

Base Sequence↗

The fate of autogenous free-fat grafts after posterior lumbar surgery: part 1. A postoperative serial magnetic resonance imaging study.

STUDY DESIGN: Time-related changes in free-grafted fat were investigated by postoperative serial magnetic resonance imaging in 22 patients with degenerative spinal disease who underwent posterior lumbar decompressive surgery. OBJECTIVES: To analyze the size and quality of the grafted fat on magnetic resonance imaging after posterior lumbar surgery. SUMMARY OF BACKGROUND DATA: Epidural fat grafts have been used to prevent epidural and perineural fibroses. Evaluations of changes in grafted fat have been reported, as observed on computed tomography scans. However, there are no published reports of clinical serial magnetic resonance imaging observations of grafted fat after posterior lumbar surgery. METHODS: Axial T1- and T2-weighted magnetic resonance imaging was performed at 3, 7, 21, and 42 days as well as 1 year after surgery. The signal intensity of the fat was classified on the T1-weighted image as Grade 1 (almost equal to subcutaneous fat tissue), Grade 2 (low-signal intensity as compared with subcutaneous fat tissue), Grade 3 (speckled intensity), or Grade 4 (signal void, suggesting the change to scar tissue. The time-related, cross-sectional area of the subarachnoidal space was measured from the T2-weighted image. RESULTS: The size of the grafted fat was reduced to approximately 57% after 42 days, and to about 33% after more than 1 year, as compared with the condition 3 days after surgery. In time, the shape of the grafted fat was changed along the shape of the dura mater. During the early stage (within 6 weeks after surgery), the signal intensity of the grafted fat was lower than that of normal subcutaneous fat tissue (Grades 2-4: 40.9-59.1%). However, the intensity had recovered to normal status (Grade 1) by 1 year after surgery. CONCLUSIONS: The total amount of grafted fat used in posterior lumbar surgery is reduced. However, as observed on magnetic resonance imaging, it is alive and remodeled along the shape of the dura mater in relation to its shrinkage and reexpansion. This remodeling of the grafted fat is meaningful and effective in protecting the spinal nerve. This report clarifies the fate of the grafted fat from the findings of postoperative serial magnetic resonance imaging after lumbar decompressive surgery.

Adipose Tissue↗

The fate of autogenous free-fat grafts after posterior lumbar surgery: part 2. Magnetic resonance imaging and histologic studies in repeated surgery cases.

STUDY DESIGN: Histologic changes of free-grafted fat were investigated from surgical specimens taken at repeated lumbar surgery in 18 patients with degenerative spinal disease who previously had undergone posterior lumbar decompression and free fat graft. OBJECTIVE: To clarify the clinical usefulness of free-grafted fat by histologic analysis. SUMMARY OF BACKGROUND DATA: The clinical postoperative serial magnetic resonance imaging studies in Part 1 showed that the size of grafted fat was reduced, and that the shape changed along with the shape of the dura mater. The shape of the grafted fat was remodeled in relation to the postoperative transient shrinkage and reexpansion of the dura mater. METHODS: From repeated surgery cases, the status of the previously grafted fat tissue in the virgin operation was analyzed. Sections from the specimens resected surgically during repeated surgery were stained with hematoxylin and eosin or osmium. The size and quality of the grafted fat globules were analyzed by computer. RESULTS: In all cases, grafted fat tissue was identified as a survival. Hematoxylin and eosin staining showed increased collagen fiber and hyperplasia of blood vessels entering the fat tissue that survived. From osmium staining, the size of fat globules was reduced. The shape and quality of the fat globules were analyzed by original staging. They showed various sizes, polymorphism, and vacuolar degeneration. CONCLUSIONS: Finding showed that the grafted fat used in posterior lumbar surgery reduced the size and quality of the fat globules, as compared with normal fat tissue. However, the grafted fat tissues were confirmed to be alive over the long term. This study clarified the fate of the grafted fat as observed by magnetic resonance imaging and histology from repeated surgery cases.

Adipose Tissue↗

ERK and p38 MAPK, but not NF-kappaB, are critically involved in reactive oxygen species-mediated induction of IL-6 by angiotensin II in cardiac fibroblasts.

We recently reported that angiotensin II (Ang II) induced IL-6 mRNA expression in cardiac fibroblasts, which played an important role in Ang II-induced cardiac hypertrophy in paracrine fashion. The present study investigated the regulatory mechanism of Ang II-induced IL-6 gene expression, focusing especially on reactive oxygen species (ROS)-mediated signaling in cardiac fibroblasts. Ang II increased intracellular ROS in cardiac fibroblasts, and the increase was completely inhibited by the AT-1 blocker candesartan and the NADH/NADPH oxidase inhibitor diphenyleneiodonium (DPI). We first confirmed that antioxidant N-acetylcysteine, superoxide scavenger Tiron, and DPI suppressed Ang II-induced IL-6 expression. Because we observed that exogenous H(2)O(2) also increased IL-6 mRNA, the signaling pathways downstream of Ang II and exogenous H(2)O(2) were compared. Ang II, as well as exogenous H(2)O(2), activated ERK, p38 MAPK, and JNK, which were significantly inhibited by N-acetylcysteine and DPI. In contrast with exogenous H(2)O(2), however, Ang II did not influence phosphorylation and degradation of IkappaB-alpha/beta or nuclear translocation of p65, nor did it increase NF-kappaB promoter activity. PD98059 and SB203580 inhibited Ang II-induced IL-6 expression. Truncation and mutational analysis of the IL-6 gene promoter showed that CRE was an important cis-element in Ang II-induced IL-6 gene expression. NF-kappaB-binding site was important for the basal expression of IL-6, but was not activated by Ang II. Ang II phosphorylated CREB through the ERK and p38 MAPK pathway in a ROS-sensitive manner. Collectively, these data indicated that Ang II stimulated ROS production via the AT1 receptor and NADH/NADPH oxidase, and that these ROS mediated activation of MAPKs, which culminated in IL-6 gene expression through a CRE-dependent, but not NF-kappaB-dependent, pathway in cardiac fibroblasts.

Angiotensin II↗

Two starch-branching-enzyme isoforms occur in different fractions of developing seeds of kidney bean.

The nature and enzymic properties of starch-branching enzyme (SBE) are two of the dominant factors influencing the fine structure of starch. To understand the role of this enzyme's activity in the formation of starch in kidney bean (Phaseolus vulgaris L.), a study was undertaken to identify the major SBE sequences expressed during seed development and to characterize the enzymic properties of the coded recombinant enzymes. Two SBE cDNA species (designated pvsbe2 and pvsbe1) that displayed significant similarity (more than 70%) to other family A and B SBEs respectively were isolated. Northern blot analysis revealed that pvsbe1 and pvsbe2 were differentially expressed during seed development. pvsbe2 showed maximum steady-state transcript levels at the mid-stage of seed maturation, whereas pvsbe1 reached peak levels at a later stage. Western blot analysis with antisera raised against both recombinant proteins (rPvSBE1 and rPvSBE2) showed that these two SBEs were located in different amyloplast fractions of developing seeds of kidney bean. PvSBE2 was present in the soluble fraction, whereas PvSBE1 was associated with the starch granule fraction. The differences in location suggest that these two SBE isoenzymes have different roles in amylopectin synthesis in kidney bean seeds. rPvSBE1 and rPvSBE2 were purified from Escherichia coli and their kinetic properties were determined. The affinity of rPvSBE2 for amylose (K(m) 1.27 mg/ml) was lower than that of rPvSBE1 (0.46 mg/ml). The activity of rPvSBE2 was stimulated more than 3-fold in the presence of 0.3 M citrate, whereas rPvSBE1 activity was not affected. The implications of the enzymic properties and the distribution of SBEs and amylopectin structure are discussed.

1,4-alpha-Glucan Branching Enzyme↗

Adenosine deaminase activity of insect-derived growth factor is essential for its growth factor activity.

Insect-derived growth factor (IDGF) was originally isolated from conditioned medium of NIH-Sape-4 cells derived from flesh fly embryos. Here we demonstrated that IDGF has adenosine deaminase activity. The substrate specificity of IDGF was similar to that of the mammalian cytoplasmic adenosine deaminase. The adenosine deaminase activity of IDGF was shown to be indispensable for its growth factor activity toward NIH-Sape-4 cells. We found that there are specific binding sites for IDGF on the surface of NIH-Sape-4 cells and that it binds to these sites with a K(d) value of 2.4 x 10(-10) m. We propose that the cell surface binding sites for IDGF are specific receptors modified with an adenosine moiety. When IDGF binds to these receptors, it may deaminate the adenosine moiety, and this process may be prerequisite for the signal transduction via this receptor.

Adenosine Deaminase↗

A high-efficiency protein transduction system demonstrating the role of PKA in long-lasting long-term potentiation.

Proteins and peptides have been demonstrated to penetrate across the plasma membrane of eukaryotic cells by protein transduction domains. We show that protein transduction by 11 arginine (11R) is an efficient method of delivering proteins into the neurons of brain slices. Here, we demonstrate that PKA inhibitory peptide, fused with 11R and nuclear localization signal, delivers the peptide exclusively into the nuclear compartment of neurons in brain slices. This inhibitory peptide blocked both cAMP responsive element-binding protein phosphorylation and long-lasting long-term potentiation (LTP) induction, but not early LTP. These results highlight transduction of proteins and peptides into specific neuronal subcellular compartments in brain slices as a powerful tool for studying neuronal plasticity.

Active Transport, Cell Nucleus↗

Effects of triphenyltin on cytosolic Na(+) and Ca(2+) response to glucose and acetylcholine in pancreatic beta-cells from hamster.

Oral administration of triphenyltin chloride (TPT) (60 mg/kg body wt) inhibits insulin secretion by perturbing the cytoplasmic Ca(2+) concentration ([Ca(2+)]i) in pancreatic beta-cells of the hamster. To test the possibility that the abnormal levels of [Ca(2+)]i induced by TPT administration could be due to a defect in the cytoplasmic Na(+) concentration ([Na(+)]i) in the beta-cells, we investigated the effects of TPT administration on the changes of [Na(+)]i and [Ca(2+)]i induced by glucose or acetylcholine (ACh) and on the [Na(+)]i induced by ouabain, a potent inhibitor of Na(+),K(+)-ATPase. The changes of [Na(+)]i and [Ca(2+)]i were measured in islet cells loaded with sodium-binding benzofuran isophthalate and fura 2, respectively. TPT administration strongly reduced the rise in [Ca(2+)]i induced by 15 mM glucose with and without extracellular 135 mM Na(+). TPT administration also significantly reduced the rise of [Ca(2+)]i by 100 microM ACh in the presence of 5.5 or 15 mM glucose but not the amplitude of [Ca(2+)]i by 100 microM ACh in Na(+)-free medium. TPT administration attenuated the rise in [Na(+)]i induced by 100 microM ACh in the presence of either 3 or 5.5 mM glucose. However, TPT administration did not impair the [Na(+)]i in the presence of glucose (3, 5.5, and 15 mM) or of 100 microM ouabain with 3 mM glucose. TPT administration significantly suppressed the insulin secretion induced by 15 and 27.8 mM glucose or 100 microM ACh in the presence of 5.5 mM glucose. Our study suggests that triphenyltin has inhibitory effects on the cellular Ca(2+) response due to a reduction of [Ca(2+)]i after Na(+)-dependent and Na(+)-independent depolarization in islet cells of the hamster.

Acetylcholine↗

Phylogenetic analysis of archaeal 16S rRNA libraries from the rumen suggests the existence of a novel group of archaea not associated with known methanogens.

Molecular diversity of rumen archaea was analyzed by PCR amplification and sequencing of two 16S rRNA clone libraries prepared from the bovine rumen fluid using two different archaea-specific primer sets. The first library of 19 clones which was generated with primers D30 and D33, produced essentially two groups of sequences, one affiliated with Methanomicrobium mobile (21% of clones) and the other -- with the uncultured archaeal sequences from anaerobic digester, which are distantly associated with Thermoplasma (79% of clones). The second library of 25 clones, which was generated with primers 0025e Forward and 1492 Reverse, produced a higher degree of diversity: in addition to the previous two groups, with the M. mobile- (56%) and Thermoplasma-associated sequences (20%), four clones (16%) were identified as Methanobrevibacter spp. The remaining two sequences were associated with unidentified archaeal sequences from the rumen and swine waste. Phylogenetic placement of eight almost complete 16S rRNA sequences revealed the existence of a novel cluster of the rumen Euryarchaeota, which is not affiliated with the known methanogenic archaea.

Animals↗

A mechanistic study of proliferation induced by Angelica sinensis in a normal gastric epithelial cell line.

It has been reported that an extract from Angelica sinensis mainly consisting of polysaccharides (95%) prevented ethanol- or indomethacin-induced gastric mucosal damage (Cho CH et al. Planta Med 2000;66:348-51). However, it is not known whether Angelica sinensis has a direct stimulatory effect on the healing of gastric mucosal lesions. To study the hypothesis that Angelica sinensis has a direct mucosal healing effect in rats and in isolated gastric epithelial cells, we assessed the wound repair in both animals and normal cell culture (RGM-1), as well as [3H]thymidine incorporation, ornithine decarboxylase (ODC) activity, and ODC protein and c-Myc protein expression after different treatments in RGM-1 cells. We found that Angelica sinensis crude extract (ASCE) dose-dependently enhanced gastric ulcer healing in rats and promoted wound repair in RGM-1 cells. It also significantly stimulated [3H]thymidine incorporation and ODC activity in RGM-1 cells in a concentration-dependent manner. ODC and c-Myc protein expression was also increased as a result of this process. DL-alpha-difluoromethyl-ornithine repressed the [3H]thymidine incorporation and ODC activity induced by ASCE. Pretreatment with c-Myc antisense oligodeoxynucleotides blocked the stimulatory action of ASCE on [3H]thymidine incorporation and ODC protein expression. These data suggest that ASCE has a direct mucosal healing effect on gastric epithelial cells, while ODC and c-Myc are closely associated with this effect.

Angelica sinensis↗

Recombinant core protein fragment of phosphacan, a brain specific chondroitin sulfate proteoglycan, promote excitotoxic cell death of cultured rat hippocampal neurons.

We investigated the role of phosphacan, a chondroitin sulfate proteoglycan that is constitutively expressed in the adult hippocampus, and recombinant core proteins of phosphacan in excitotoxic cell death of primary cultured rat hippocampal neurons. Phosphacan had no significant effect on excitotoxic neuronal death. Surprisingly, one of three recombinant proteins corresponding to N-terminal portions of phosphacan core protein dramatically promoted excitotoxic neuronal death. Moreover, the recombinant protein induced cell death of rat hippocampal neurons, even when neurons were not exposed to glutamate. These results suggest that proteolytic degradation of phosphacan and resultant core protein fragments may contribute to neuronal degeneration of hippocampal neurons in various neuropathological conditions.

Animals↗

Significance of perivascular lymphocytic infiltrates in endometrial carcinoma.

BACKGROUND: The objective of this study was to clarify the significance of perivascular lymphocytic infiltrates (PLI) in endometrial carcinoma. METHODS: The pathologic records of 127 patients with endometrioid type adenocarcinoma confined to the uterus were reviewed retrospectively. The patients were divided into 4 groups based on the presence or absence of vascular invasion (VI) and PLI: VI-PLI- (n = 87), VI-PLI+ (n = 7), VI+PLI+ (n = 22), and VI+PLI- (n = 11). Pathologic features including tumor grade, myometrial invasion, cervical involvement, vascular invasion-associated changes (VIAC; VI and/or PLI), tumor size, ovarian metastasis, and pelvic lymph node metastasis were assessed statistically. RESULTS: Selective pelvic lymphadenectomy was performed in 108 patients, and metastasis was identified in 6 cases (5.6%). Lymph node metastasis was the only independent variable related to recurrence (Cox regression analysis, P = 0.0008). Perivascular lymphocytic infiltrates correlated closely with VI (Fisher exact test, P < 0.0001). Vascular invasion-associated changes was the best predictor of lymph node metastasis (logistic regression analysis, P = 0.039), but among the three categories of VIAC, only the VI+PLI- group was significantly associated with lymph node metastasis (P = 0.0045). The odds ratios of VI+PLI- and VI+PLI+ cases for lymph node metastasis were 64.54 and 3.24, respectively. CONCLUSIONS: Although VIAC is the best predictor of lymph node metastasis, the presence of PLI is associated with a lower risk of lymph node metastasis among VIAC groups.

Endometrial Neoplasms↗

Relation of a common methylenetetrahydrofolate reductase mutation and plasma homocysteine with intimal hyperplasia after coronary stenting.

BACKGROUND: Hyperhomocysteinemia has been identified as an independent risk factor for coronary artery disease. Recent studies have shown that a common mutation (nucleotide 677 C-->T) in the methylenetetrahydrofolate reductase (MTHFR) gene may contribute to mild hyperhomocysteinemia and, therefore, to the incidence of coronary artery disease. No information exists, however, regarding the association between the mutation of the MTHFR gene or plasma homocysteine levels and morphological analysis of coronary atherosclerosis using intravascular ultrasound. METHODS AND RESULTS: To examine the potential influence of MTHFR genotype and homocysteine on coronaryarteries morphologically, we screened 62 patients with 65 lesions that were treated with 93 Palmaz-Schatz stents. The plasma homocysteine levels in the patients with the TT genotype were not significantly higher than those in the patients with non-TT (CC+CT) genotypes (13.1 +/- 5.5 versus 11.5 +/- 3.1 mmol/L, P=0.16). Angiographic analysis showed that the percent diameter stenosis in the patients with the TT genotype was significantly greater than that in those with non-TT genotypes (43.7 +/- 17.8% versus 29.0 +/- 22.0%, P=0.015). Intravascular ultrasound analysis showed that the TT genotype was significantly associated with greater intimal hyperplasia area (5.70 +/- 1.94 versus 3.72 +/- 1.38 mm2, P=0.001). In multiple stepwise regression analysis, the number of the T alleles was the only independent predictor of intimal hyperplasia after intervention (r2=0.21, P=0.004). CONCLUSIONS: The homozygous mutant genotype of the MTHFR gene may increase the risk of in-stent restenosis more than does the normal homozygous or heterozygous genotype.

Alleles↗

Expression of brain specific chondroitin sulfate proteoglycans, neurocan and phosphacan, in the developing and adult hippocampus of Ihara's epileptic rats.

Ihara's epileptic rats (IER) is an animal model of temporal lobe epilepsy with mycrodysgenesis, that exhibit abnormal migration of hippocampal neurons and recurrent spontaneous seizures. As an attempt to elucidate the roles of extracellular matrix molecules in the epileptogenecity and mossy fiber sprouting, immunohistochemical localization of brain specific chondroitin sulfate proteoglycans (CSPGs), neurocan and phosphacan, was examined in the hippocampus of postnatal IER and Sprague-Dawley (SD) rats using monoclonal antibodies 1G2 against neurocan and 6B4 against phosphacan. There was no difference in the expression of these two CSPGs between IER and SD rats in the 1st postnatal week. However, the expression of neurocan was poor in the hippocampus of IER in the 2nd and 3rd weeks whereas intense labeling of neurocan was present throughout the hippocampus of SD rats. Labeling of neurocan was almost absent in the hippocampus, while phosphacan was diffusely expressed in the stratum oriens and radiatum of Ammon's horn, and in the hilus and inner one-third molecular layer of the dentate gyrus at the 2nd month after birth. There was no difference in the expression of neurocan and phosphacan between IER and SD rats at the 2nd month after birth. By contrast, phosphacan was reduced in the inner molecular layer of the dentate gyrus in 8-month-old IER, while neurocan was reexpressed in the outer molecular layer and hilus in 3- and 8-month-old IER. It was suggested that the insufficient expression of neurocan may affect the development of neuronal organization in the hippocampus, and that the remodeling of extracellular matrix in the dentate gyrus may contribute to the mossy fiber sprouting into the inner molecular layer.

Aging↗

Suppression of apoptosis in hepatocytes by fructose-modified dendrimers.

By immobilizing fructose-modified dendrimers on a polystyrene culture plate, the number of initially adhered hepatocytes on it was increased. Moreover, increasing the number of generations of fructose-modified dendrimer (fructose-dendrimer) increased the number. Urea synthesis per unit area also was increased, corresponding to the increase in the number of initially adhered hepatocytes. This result suggests that the fructose-dendrimers do not cause a decline in cell function. On the other hand, apoptosis of hepatocytes occurs during cultivation, and results in a decrease in the number of adhered cells and a decline in cell function. Fructose-dendrimers were found to suppress apoptosis of hepatocytes. This characteristic is considered to be responsible for the increase in the number of initially adhered hepatocytes without a decline in cell function. Fructose-dendrimers are shown to be very suitable scaffolds for use in a high-performance bioartificial liver support system.

Animals↗