A type of chick embryo cell that fails to support formation of infectious RSV.
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Alpharetrovirus↗
Biomedical subjects
T Hanafusa
Publications and source records attributed to T Hanafusa.
A cell-associated factor essential for formation of an infectious form of Rous sarcoma virus.
Formation of a specific type of infectious Rous sarcoma virus called RSV(0) has been found to occur only in a certain type of chick embryo cell in the absence of avian leukosis virus. Although these chick cells lack any complete form of avian leukovirus, they appear to carry a genetic factor essential for formation of infectious RSV(0). A factor-deficient cell can be converted to a producer of infectious RSV(0) by infection with Rous sarcoma virus or avian leukosis virus which has been grown in factor-containing cells. Evidence is presented to show that the factor determines both the antigenic and host range specificity of RSV(0).
Animals↗
Recovery of a new virus from apparently normal chick cells by infection with avian tumor viruses.
Cells derived from the majority of chick embryos, although free of presently known avian tumor virus particles, appear to contain genetic materials similar to those found in this virus group. After infection of these cells with avian leukosis or Rous sarcoma virus, the genetic factor was recovered by incorporation into mature infectious virus. The newly isolated virus (RAV-60) did not require the assistance of another virus for its replication. The virus had most of the attributes of an RNA-containing avian leukosis virus, and its outer structure resembled the Rous sarcoma virus known as RSV(0).
Alpharetrovirus↗
Further studies on RSV production form transformed cells.
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Animals↗
Interaction among avian tumor viruses giving enhanced infectivity.
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Animals↗
Determining factor in the capacity of Rous sarcoma virus to induce tumors in mammals.
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Animals↗
Acarbose improved severe postprandial hypotension in a patient with diabetes mellitus.
Postprandial hypotension (PPH) is defined as a decrease of systolic blood pressure by more than 20 mmHg after meals. Severe PPH is a troublesome diabetic complication, which has no established means of treatment. We encountered a patient who had diabetes mellitus complicated by severe PPH and attempted to treat this problem using several medications (octreotide, midodrine hydrochloride, and acarbose). A 58-year-old male with diabetic triopathy complained of orthostatic dizziness and vertigo after meals. The blood pressure was monitored for 24 h with an ambulatory blood pressure monitor, revealing that the systolic blood pressure decreased markedly after breakfast and dinner by 45 and 50 mmHg, respectively. PPH was not improved by a subcutaneous injection of octreotide. Administration of midodrine hydrochloride reduced the frequency of hypotensive episodes from twice to once daily, but the magnitude of the postprandial fall in blood pressure was still around 30 mmHg. After the patient started to receive acarbose therapy, the postprandial fall in blood pressure was diminished to 18 mmHg and his symptoms largely disappeared. For the treatment of PPH in diabetic patients, our experience suggests that it may be appropriate to try first on alpha-glucosidase inhibitor like acarbose.
Acarbose↗
High glucose and hyperosmolarity increase secretion of interleukin-1 beta in cultured human aortic endothelial cells.
Interleukin-1 (IL-1) is secreted by endothelial cells (ECs) and smooth-muscle cells (SMCs), which are two major component cells of vessels and detected in atherosclerotic lesions. To evaluate the effect of hyperglycemia on the secretion of IL-1 beta in endothelial cells in diabetic patients, we investigated the effects of high glucose and hyperosmolar conditions on the secretion of IL-1 beta from cultured human aortic endothelial cells (HAECs). HAECs were treated with high concentration of glucose or hyperosmolar condition for 3 days. IL-1 beta in the supernatant was measured by high sensitive enzyme-linked immunosorbent assay (ELISA). Under high concentration of glucose (16.6 mmol/L) and hyperosmolar condition (glucose 5.5 mmol/L + mannitol 11.1 mmol/L), the secretion of IL-1 beta was significantly increased (41.0 +/- 2.8 and 26.3 +/- 5.9% increase, respectively, compared with that of 5.5 mmol/L glucose). In conclusion, high glucose and hyperosmolar condition increase the secretion of IL-1 beta in HAECs. The results suggest that diabetic macroangiopathies might be accelerated partly through the increase of IL-1 beta secretion in HAECs.
Aorta↗
Lectin-induced expression of DR antigen on human cultured follicular thyroid cells.
HLA-DR antigens, the human equivalent of mouse I region-associated or Ia products, are polymorphic cell surface sialoglycoproteins involved in initiation of the immune response. Their expression is normally restricted to B lymphocytes, macrophages, dendritic and other antigen-presenting cells and vascular endothelium and possibly some cells of the mucosa lining body cavities. HLA-DR expression can be modified during cell differentiation; B lymphocytes become negative on maturing to plasma cells and human T lymphocytes acquire these antigens when activated in vitro or in vivo. We report here that human thyroid follicular cells which are normally negative for HLA-DR molecules, can be induced to express these antigens when cultured with phytohaemagglutinin (PHA), concanavalin A (Con A) or pokeweed mitogen (PWM). These lectins exert their action directly on the thyroid cells with no concomitant mitogenic effect.
Animals↗
Loss of heterozygosity and analysis of mutation of p53 in hepatocellular carcinoma.
Thirty-six hepatocellular carcinoma (HCC) tissues obtained from 34 patients were classified according to histological diagnosis into six well-differentiated HCC, 20 moderately differentiated HCC and 10 poorly differentiated HCC. High molecular weight DNA was prepared from each tumour and the corresponding non-tumour tissue. Loss of heterozygosity (LOH) on chromosomes 4q, 5q, 10q, 11p, 16q, 17p, mutation of the p53 gene and polymorphism of intron 25 of the retinoblastoma (RB) gene were simultaneously analysed. The patients were composed of three cases of small HCC (the diameter of which was < 3 cm) and 31 cases of advanced HCC. Twenty-nine of 34 (85.3%) patients analysed had been exposed to hepatitis B virus and/or hepatitis C virus. The frequencies of LOH on seven chromosomes were 57.9% in 17p13.3, 45.1% in 17p, 45.1% in 11p, 41.9% in 5q, 41.9% in 16q24, 29.0% in 4q, 25.8% in 10q in advanced HCC (four of well differentiated, 18 of moderately differentiated and nine of poorly differentiated carcinoma). In contrast, LOH was observed on 4q, 5q, 16q and 17p in 33% (1/3) of the small HCC (two of well differentiated and one of moderately differentiated carcinoma). The mutation of the p53 genes and polymorphism of the RB gene were present in 25.8% (8/31) and 12.9% (4/31) of the advanced tumours, respectively, but the mutation was not found in small HCC. LOH on every chromosome and the p53 mutation were observed more frequently in more advanced tumours, and the genetic changes accumulated with the increase of the histopathological grade.(ABSTRACT TRUNCATED AT 250 WORDS)
Blotting, Southern↗
Retroperitoneal cellular schwannoma: report of a case diagnosed by the presence of S-100 protein.
A case of cellular schwannoma originating from the retroperitoneum is reported. The histological features of the tumor resembled those of a smooth muscle tumor. However, the tumor cells were positive for S-100 protein, which is almost exclusively identified within nerve sheath tumor cells. This finding confirmed the diagnosis of cellular schwannoma. This type of tumor is generally considered to be benign but is sometimes mistaken for a malignant tumor. These findings indicate that it is important to prove whether or not S-100 protein is present in the cells of a tumor of unknown origin especially arising in the mediastinum or retroperitoneum.
Adult↗
Expression of the midkine gene in human hepatocellular carcinomas.
BACKGROUND/AIMS: Aberrant expression of Midkine (MK) has been found in various human carcinomas including hepatocellular carcinoma (HCC). The aim of study is to identify the incidence of MK expression in tumor and surrounding non-tumor tissues of the liver, and to find the correlation of MK expression with other tumor markers. METHODOLOGY: Liver tissues were obtained from 16 patients with HCC and 4 with metastatic liver cancer. Background diseases of the HCC patients include liver cirrhosis and chronic hepatitis of type B or C. RNA was prepared from both cancerous and surrounding non-cancerous tissues, and analyzed for the presence of MK mRNA by RT-PCR, PCR-Southern blot, and Northern blot analysis. RESULTS: MK expression was detected in 12 (75%) of 16 HCCs by PCR-Southern blot analysis, the most sensitive of the 3 methods. Three of 9 surrounding cirrhotic tissues were weakly positive for MK expression, and none of chronic hepatitis and 4 normal tissues were negative. No significant difference was found in clinical and pathological parameters between MK negative and positive cases. Among metastatic cancers, 1 of gastric origin was positive for MK expression, but 1 each of chorangiocellular, gall bladder, and gastrinoma origin was negative. CONCLUSIONS: These results suggest that MK is expressed in the majority of HCC tissues and rarely in surrounding tissues in chronic liver diseases.
Aged↗
Accelerated decline of blood glucose after intravenous glucose injection in a patient with Cowden disease having a heterozygous germline mutation of the PTEN/MMAC1 gene.
The PTEN/MMAC1, a putative tumor suppressor, has been demonstrated to dephosphorylate phosphatidylinositol 3, 4, 5-triphosphate, a key molecule involved in the insulin signaling pathway. The PTEN may act, therefore, as a negative regulator of insulin signaling. The patient with Cowden disease, having a heterozygous PTEN/MMAC1 gene mutation, a C to T substitution of a single base at codon 130, was suspected to have decreased amount of PTEN protein with phosphatase signature motif. We thought that the patient might be more sensitive to insulin than normal subjects. As expected, administration of a bolus of glucose resulted in a more rapid clearance of blood glucose than was observed in 5 control subjects, indicating the presence of insulin hypersensitivity in the patient. The euglycemic hyperinsulinemic clamp study provided additional evidence.
Adult↗
Promoter-independent loss of mRNA and protein of the Rb gene in a human hepatocellular carcinoma.
BACKGROUND: Inactivation of the retinoblastoma (Rb) gene is considered to play a fundamental role in the genesis and progression of several human cancers. In retinoblastoma, the inactivation of Rb promoter by mutations or hypermethylation has been reported. Although genetic changes of Rb gene have been described in hepatocellular carcinoma (HCC), an epigenetic change such as hypermethylation of the Rb promoter as reported in retinoblastoma has not been described. MATERIALS AND METHODS: We examined the hypermethylation in the promoter region of Rb gene by restriction fragment length polymorphism in 19 HCCs, as well as the expression of Rb mRNA and protein by RT-PCR and by immunoblotting, respectively. RESULTS: We found no evidence of hypermethylation in the promoter region of the Rb gene in all HCCs analyzed. However, the expression of Rb mRNA and protein was lost in one HCC, and no mutation was detected in the Rb promoter region of this patient. The inactivation of Rb promoter by hypermethylation or by inhibition of binding of transcription factors due to point mutations did not contribute to the loss of mRNA and protein in the patient. CONCLUSIONS: Hypermethylation in the Rb promoter region appeared to have little causal effect on HCC.
Aged↗
Reciprocal gene expression of rat fibroglycan and beta-actin during the course of regeneration after D-galactosamine liver injury.
BACKGROUND/AIMS: Fibroglycan (FG) is a major heparan sulfate proteoglycan (HSPG) in the rat liver that is mainly distributed on the surface of hepatocytes. HSPG may play some important roles in the regeneration of liver by interacting with various growth factors such as bFGF and HB-EGF. However, little is known about the function of FG. We reported that after injury caused by D-galactosamine, regeneration started on the following day and peaked on day 2. To clarify the function of FG in liver regeneration, we investigated the gene expression of FG during regeneration after D-galactosamine injury. MATERIALS AND METHODS: Rats were given D-galactosamine on day 0. Liver RNA was collected from day 0 to day 7. The gene expression of FG and beta-actin (as a representative cytoskeleton) was examined by Northern and/or Slot blotting. RESULTS: FG gene expression was markedly decreased on day 2, but totally recovered on day 3. In contrast, beta-actin gene expression was markedly increased on day 2 and returned to the normal level on day 3. Expression of the FG and beta-actin genes was reciprocal. CONCLUSION: FG expression is transiently suppressed when cytoskeleton gene expression is enhanced at the early phase of liver regeneration.
Actins↗
Point mutations in the S and pre-S2 genes observed in two hepatitis B virus carriers positive for antibody to hepatitis B surface antigen.
Two hepatitis B virus (HBV) carriers who had antibodies to HBV surface antigen (anti-HBs) were studied. Case 1 was a 47 year old woman positive for hepatitis B e antigen (HBeAg), and case 2 was a 61 year old man positive for antibody to HBeAg (anti-HBe) and DNA-polymerase (DNA-p). Neither case had received the HBV vaccine. The nucleotide sequences of the HBV-DNA extracted from the patients' sera were determined within the pre-S2 and S genes. Seven out of nine S gene clones from case 1 and six out of nine S gene clones from case 2 had an amino acid replacement from Thr or Ile to Ser at codon 126 in the alpha-determinant of the S gene. Amino acid substitution of codon 145 of the S gene previously reported was not observed. Although two previous reports on HBV escape mutant carriers with both anti-HBs and HBeAg described some deletions in the pre-S2 gene, our cases did not show these deletions. Our analysis indicated that carriers with the HBV escape mutant did not always have pre-S2 gene deletions. We found two HBV escape mutant carriers who had amino acid substitutions at codon 126 in the S gene due to point mutation without any deletions in the pre-S2 gene.
DNA, Viral↗