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S Nishiguchi

Publications and source records attributed to S Nishiguchi.

At least 163 records · Page 9Linked to original sources
PubMed1989

Liver-specific and high-level expression of human serum amyloid P component gene in transgenic mice.

To analyze the regulation of human serum amyloid P component (SAP) gene expression, we have produced seven transgenic mice. The 3.3 kb human SAP genes containing about 0.8 kb of 5' and 1.5 kb of 3' flanking region were injected into fertilized eggs of C57BL/6 mice. In five of the seven transgenic mice, human SAP was detected in the sera and serum concentrations were higher than that of human serum in three lines. The human SAP gene was expressed only in the liver. Amounts of human mRNA in the liver and serum concentrations of human SAP were roughly proportional to the copy number of the integrated gene. Human SAP production lowered the serum levels of mouse endogenous SAP. With the intraperitoneal administration of lipopolysaccharide, the mRNA levels in the liver and serum levels of mouse SAP increased several-fold in both the control and transgenic mice. On the other hand, neither the mRNA nor the serum levels of human SAP increased significantly.

Animals↗
PubMed1989

Relationship of the effects of interferon on chronic hepatitis B and the induction of 2',5'-oligoadenylate synthetase.

Two years or more after 35 patients (29 men and six women) with chronic hepatitis B were treated by interferon, we studied relationships of age, ALT activity, activity of serum DNA polymerase associated with the hepatitis B virus, serum levels of hepatitis B e antigen and activity of 2',5'-oligoadenylate synthetase in peripheral blood mononuclear cells when treatment started in comparison with treatment results. Seventeen patients were given human lymphoblastoid interferon-alpha; the other 18 patients were given interferon-beta. We measured the activity of 2',5'-oligoadenylate synthetase in these mononuclear cells and found the rate of increase in vivo and in vitro; the correlation between the two was r = 0.68. This enzyme activity in the patients who became negative for DNA polymerase after interferon treatment increased more both in vivo and in vitro than in patients who did not became negative. Also, both the in vivo and in vitro activity increased more in patients who became negative for the e antigen after interferon therapy than in those who remained positive. In the first group, interferon was considered to be effective; in the second, ineffective. Of the patients who became negative, some developed e antibodies and some did not; the increase in this enzyme activity in the two groups was not significantly different. The increase in the activity of 2',5'-oligoadenylate synthetase activity could be used to predict the results of interferon treatment and is an index that can be used before treatment to predict the response.

2',5'-Oligoadenylate Synthetase↗
PubMed1989

A female case of type VIII glycogenosis who developed cirrhosis of the liver and hepatocellular tumor.

The case of a 17-year-old female with a rare form of type VIII glycogenosis who developed cirrhosis of the liver and hepatocellular tumor is reported. Laparoscopy showed a tumor 50 mm in diameter in the lower portion of the right lobe of the liver. The tumor was biopsied under ultrasonic guidance, and tentatively diagnosed as adenomatous hyperplasia. The patient was also diagnosed as having type VIII glycogenosis (phosphorylase kinase deficiency).

Adolescent↗
PubMed1989

[Effects of interferon on the cell cycle of human hepatoma HLF cells analyzed by flow cytometry].

Growth inhibition by interferon (IFN) was investigated in human hepatoma HLF cells by use of flow cytometry to study the cell cycle. INF-alpha or -beta inhibited growth more than IFN-gamma. Use of either IFN-alpha or -beta and IFN-gamma at the same time inhibited growth more than with any one kind of IFN, but use of IFN-alpha and -beta together did not cause much inhibition. IFN inhibited growth by causing cells to accumulate in the S phase instead of moving on to the G2 phase. Accumulation in the S phase was less with IFN-gamma than with -alpha or -beta. It increased with the combination of IFN-alpha or -beta with IFN-gamma, but not with the combination of IFN-alpha and -beta.

Carcinoma, Hepatocellular↗
PubMed1989

[The clinical examination for posttransfusion hepatitis].

We studied viral hepatitis, type A, type B, type D and type non A non B. Type A hepatitis was diagnosed by the serological examination for IgM type anti-HA and total anti-HA. Several cases were negative for IgM type anti-HA within 2 weeks after the onset of type A hepatitis. Type B hepatitis was diagnosed by RIA for serum HBs antigen. Several cases of type B hepatitis were negative for serum HBs antigen but positive for IgM type anti-HBc, or hepatocytes were positive for HBs antigen. These cases had high titer of total anti-HBc. Type D hepatitis was diagnosed by RIA for anti-delta in serum and by PAP stain for delta antigen in hepatocytes. All cases of type D hepatitis were positive for anti-delta in their serum and positive for delta antigen in their hepatocytes, they were positive for HBs antigen. Incidence of HDV infection was 0.7% in HBV carrier. The incidence of non A non B hepatitis was 27.6% in 105 recipients and the incidence of its progression to the chronicity was 20.0%.

Adult↗
PubMed1989

Transgenic mouse model of familial amyloidotic polyneuropathy.

Familial amyloidotic polyneuropathy (FAP) is a dominantly inherited disorder, characterized by the extracellular deposition of amyloid fibrils composed of variant transthyretin (TTR), and by prominent peripheral nerve involvement. We demonstrate that the main cause of this disease is the presence of a point mutation in the TTR gene. However, neither the time of onset nor the clinical course is predictable. To elucidate the molecular pathogenesis of this disease, we constructed transgenic mice carrying and expressing the human mutant TTR gene. In these mice, amyloid is deposited in the alimentary tract as early as age six months, and becomes more remarkable with aging. These transgenic mice should be useful in elucidating factors which modulate the time of onset and the clinical course of FAP, and in establishing therapy for this intractable disorder.

Amyloidosis↗
PubMed1988

Structure of the mouse C-reactive protein gene.

A genomic DNA clone corresponding to the mouse C-reactive protein (CRP) has been isolated and characterized. The mouse CRP gene is 1.9-kilobase pairs in length and contains a single intron of 213-base pairs which interrupts the codon for the 2nd amino acid residue of the mature CRP protein. We compared nucleotide sequences of the mouse and human CRP genes and discussed structures of possible regulatory sequences. With this characterization, the isolation and sequence analyses of a set of mouse and human pentraxin genes, i.e. CRP and serum amyloid P component genes is not complete.

Amino Acid Sequence↗
PubMed1988

Structure of the mouse serum amyloid P component gene.

A genomic DNA clone corresponding to the mouse serum amyloid P component (SAP) has been isolated and characterized for the first time. The numbers of exons, the relative sites of intron/exon junctions, and the size of the coding region for mature SAP protein are all in complete agreement with those of the human SAP gene. In the 5'-flanking region of the mouse SAP gene, there is a small DNA segment (43-base pairs) which is highly homologous with the corresponding region of the human SAP gene. However, most parts of the 5'-flanking regions are not conserved between the mouse and human SAP genes, and several phorbol ester-responsive element-like sequences are present only in the mouse SAP gene.

Amino Acid Sequence↗
PubMed1988

Acute-phase response of mRNAs for serum amyloid P component, C-reactive protein and prealbumin (transthyretin) in mouse liver.

Acute-phase response of mRNAs for serum amyloid P component (SAP), C-reactive protein (CRP) and prealbumin was examined in C57BL/6 mouse liver by hybridization to specific cDNA probes. Although the level of SAP mRNAs in the unstimulated mouse was about one-tenth of that of CRP mRNAs, it increased up to 60-fold during the first 20 hr, and returned gradually to the original level at 69 hr after the administration of Escherichia coli lipopolysaccharide. On the other hand, the level of CRP mRNA rapidly increased up to 6-fold during the first 4 hr, and reverted to the original level as early as at 20 hr. In contrast, the level of mRNA for prealbumin decreased to about 0.5-fold during the first 20 hr, recovered and increased up to 1.6-fold of the original level during 32 to 69 hr.

Animals↗
PubMed1988

Inhibition of ornithine decarboxylase induction of interferon (alpha + beta) and its reversal by dibutyryl adenosine 3',5'-monophosphate.

Interferon (alpha + beta) given to C3H/HeN mice intraperitoneally inhibited increases in the activities of adenylate cyclase and ornithine decarboxylase after partial hepatectomy. The inhibition of ornithine decarboxylase was prevented by administration of dibutyryl cAMP. Core (2'-5')oligo(adenylate), i.e. A2'p5'A2'p5'A or (A2'p)2A, as well as interferon inhibited the increases in these two enzymes caused by partial hepatectomy. The inhibition by (A2'p)2A of ornithine decarboxylase activity was reversed by dibutyryl cAMP. These results suggested that the activity of interferon was similar to that of (A2'p)2A and that the inhibition of ornithine decarboxylase induction caused by these agents resulted from the inhibition of adenylate cyclase activity.

Animals↗
PubMed1986

Inhibition by interferon (alpha + beta) of mouse liver regeneration and its reversal by putrescine.

Mouse interferon (alpha + beta) given to mice by intraperitoneal injection suppressed both the accumulation of putrescine and stimulation of DNA synthesis in liver caused by partial hepatectomy. The suppression of DNA synthesis was completely reversed by exogenous putrescine. The same results were obtained when core 2',5'-oligoadenylate instead of interferon was given to partially hepatectomized mice. These results suggest that interferon inhibits putrescine formation through elevating the 2',5'-oligoadenylate level and thus inhibits DNA synthesis in the regenerating liver.

Animals↗