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Biomedical subjects

K Dohi

Publications and source records attributed to K Dohi.

At least 361 records · Page 20Linked to original sources
PubMed1994

Inhibitory effects of ginseng on proliferation of cultured mouse mesangial cells.

To evaluate the pharmacological action of ginseng, its effects on the proliferative activity of mesangial cells, which are thought to play an important role in the regulation of renal function, were determined in terms of [3H]thymidine uptake. When the extract was added to the medium of mesangial cell cultures, it suppressed the proliferation of mesangial cells, and similar proliferation-inhibitory activity was found in the total saponin and ginsenoside-Rd fractions, consistent with the renal effects observed in our previous in vivo studies. The inhibition of mesangial cell proliferation by the extract can thus be explained by the action of ginsenoside-Rd.

Animals↗
PubMed1994

Rapid measurement of urinary IL-6 by ELISA: urinary IL-6 as a marker of mesangial proliferation.

To determine whether the urinary level of interleukin 6 (IL-6) measured by enzyme-linked immunosorbent assay (ELISA) can be used as a marker of mesangial proliferation, we studied urinary levels of IL-6 in 124 patients with primary and secondary glomerulonephritis, using ELISA. Although urinary levels of IL-6 were correlated with the degree of mesangial proliferation, there was no correlation between urinary levels of IL-6 and urinary protein excretion or renal function. Urinary levels of low-molecular-weight proteins, which are parameters of tubular dysfunction, were not correlated with the urinary excretion of IL-6. These results suggest that the urinary level of IL-6 may be a useful marker for mesangial proliferation.

Adolescent↗
PubMed1994

[Unique association of p53 mutations with undifferentiated carcinoma of the thyroid].

In thyroid there is a wide variety of tumors varying from slowly growing differentiated adenocarcinomas to rapidly proliferating undifferentiated carcinomas. There has been some histopathological evidence that the undifferentiated thyroid carcinomas are derived from differentiated carcinomas. Moreover, it is suspected that some genetic events might be associated with such changes. To identify these genetic events that must be involved in thyroid tumor progression, we initially investigated p53 gene alterations in 10 papillary adenocarcinomas, 4 follicular adenocarcinomas, and 8 undifferentiated carcinomas. Base substitutional mutations in exons 5 to 8 and loss of heterozygosity (LOH) of the p53 gene were not detected in papillary or follicular adenocarcinomas. However, 7 of 8 undifferentiated carcinomasa were carrying base substitutional mutations, and LOH was detected in 3 of 5 informative cases. These results strongly suggest that the mutated p53 gene plays a crucial role in de-differentiation during the progression of thyroid tumors.

Adenocarcinoma↗
PubMed1993

The assessment of proliferating cell nuclear antigen immunohistochemical staining in small hepatocellular carcinoma and its relationship to histologic characteristics and prognosis.

BACKGROUND: A precise prognostic factor for small hepatocellular carcinoma (HCC), the diagnosis of which recently has increased in incidence because of the development of diagnostic imaging techniques, is desirable. It has been reported that proliferating cell nuclear antigen (PCNA) would be related to proliferating cells, and thus the PCNA labeling index may provide useful information about the biologic behavior of small HCC. METHODS: An assessment was made of proliferative activity by immunohistochemical staining using a monoclonal antibody against PCNA in 46 nodules of HCC less than 3 cm in diameter resected from 44 patients. A correlation between PCNA labeling index and clinicopathologic findings or prognosis was sought. RESULTS: The mean labeling index was 18.7% in HCC and 1.9% in nontumor liver tissue. The labeling index corresponded to the degree of histologic differentiation, and the labeling index of well differentiated HCC was significantly lower (P < 0.05) than that of moderately or poorly differentiated HCC. The incidence of capsule formation in the high labeling index group (labeling index > or = 20%) was significantly higher (P < 0.05) than that in the low labeling index group (labeling index < 20%). A high incidence of capsular and vascular invasion was found in the high labeling index group. The survival rate after resection was significantly higher (P < 0.05) and the recurrence rate significantly lower (P < 0.05) in the low labeling index group than in the high labeling index group. CONCLUSIONS: The PCNA labeling index was shown to be closely related to histologic characteristics, and proved to be a useful indicator of recurrence and survival in small HCC.

Adult↗
PubMed1993

In vitro irradiation is able to cause RET oncogene rearrangement.

Elevated risk of thyroid cancers among the atomic bomb survivors as compared to the nonexposed population suggests that some genetic events related to thyroid cancer must be caused by ionizing radiation. Accordingly, inducibility of RET oncogene rearrangements, i.e., the generation of the RET-PTC oncogene, specific for thyroid cancer, was investigated among human undifferentiated thyroid carcinoma cells (8505C), which do not have RET oncogene rearrangement, after 0, 10, 50, and 100 Gy of in vitro X-irradiation by means of reverse transcription polymerase chain reaction. After testing 10(8) cells at each dose point, 3 independent samples obtained with 50 Gy of X-irradiation and 6 independent samples obtained with 100 Gy of X-irradiation showed a rearranged RET oncogene amplified band. No rearranged transcripts were obtained from cells irradiated with 0 or 10 Gy. All of the transcripts were sequenced and found to contain the D10S170 and RET sequence. Interestingly, two types of rearrangements were included in these transcripts: one is specific for thyroid cancer and the other, which contains a 150-base pair insert, is atypical, not usually seen in vivo. This insert was found to be the exon of D10S170. Furthermore, in fibrosarcoma cells (HT1080), X-irradiation also induced RET oncogene rearrangements, which included the same two types of rearrangements observed in the X-irradiated thyroid cells (8505C). These results are in favor of the hypothesis that some radiation-induced thyroid cancers, including those among atomic bomb survivors, might have developed when a growth advantage was obtained through a specific form of RET oncogene rearrangement induced by radiation exposure.

Aged↗
PubMed1993

HLA antigens in anti-Ro(SS-A)-positive patients with recurrent annular erythema.

BACKGROUND: Recurrent annular erythema associated with the anti-Ro(SS-A) antibody response has recently been reported in Orientals. The association is assumed to represent a distinct clinical entity. OBJECTIVE: Our purpose was to extend knowledge on the immunogenetic spectrum of the disease. METHODS: Sixteen anti-Ro(SS-A)-positive Japanese patients with recurrent annular erythema and Sjögren's syndrome were studied. The standard complement-dependent microcytotoxicity assay was used to type the HLA-A, -B, -C, -DR, and -DQ, as well as the HLA-DRw52 and -DRw53 antigens. RESULTS: All 16 patients were positive for HLA-DRw52 antigens as compared with 52% of control subjects (p < 0.01 relative risk 14.8). No significant deviations were noted in the phenotype frequencies for HLA-A, -B, -C, and -DQ antigens. CONCLUSION: HLA-DRw52 is closely related to annular erythema in anti-Ro(SS-A)-positive Japanese patients with Sjögren's syndrome.

Adolescent↗
PubMed1993

Induction of natural suppressor-like cells from human adult peripheral blood lymphocytes by a K562-derived factor.

K562-AC1, a subclone of the human myeloid leukemia cell line K562, secreted an inhibitor of PHA-stimulated human T cell growth into the culture supernatant (K562sup). Kinetics and absorption assays in vitro revealed that the factor acts on PBMC during the very early growth phase. PBMC gained potent suppressor activity against autologous T cell growth after preculture with K562sup for 3 days in a dose-related manner. HLA class II negative and nylon wool-nonadherent subsets possessed higher suppressor potential than unfractionated PBMC. Treatment of K562sup-precultured PBMC with mAb followed by complement-lysing showed that the responsible suppressors belong to null cells expressing CD3-, CD4-, CD19-, CD14-, CD11b-, but partially CD2+. Exogenous IL-2 exhibited a synergistic effect on the activity of the suppressors committed by K562sup. However, K562sup inhibited IL-2-activated lymphocytes from generating anti-K562 cytolytic activity. Macrophages inhibited the induction of the suppressors, which was restored by adding indomethacin and/or IL-2. In conclusion, K562sup has the ability to induce efficient suppressor cells from human adult PBL, which belong to null cells without NK/lymphocyte-activated killer activity and are similar to natural suppressor cells.

Humans↗
PubMed1993

Genetic alterations in thyroid tumor progression: association with p53 gene mutations.

To identify the genetic events that must be involved in thyroid tumor progression, we initially investigated p53 gene alterations in 10 papillary adenocarcinomas, 4 follicular adenocarcinomas, and 8 undifferentiated carcinomas. Base substitutional mutations in exons 5 to 8 and loss of heterozygosity (LOH) of the p53 gene were not detected in papillary or follicular adenocarcinomas. However, 7 of 8 undifferentiated carcinomas were carrying base substitutional mutations, and LOH was detected in 3 of 5 informative cases. Furthermore, to verify that the p53 gene alterations are truly involved in tumor progression, DNA from individual foci of the four undifferentiated carcinomas coexisting with a differentiated focus and from one follicular adenocarcinoma with an undifferentiated focus was analyzed by direct sequencing and polymerase-chain-reaction-restriction-fragment-length polymorphism (PCR-RFLP). Base substitutional mutations in the p53 gene from exons 5 to 8 were identified exclusively in the undifferentiated foci, but not in the differentiated foci. LOH was observed in 3 of 4 informative undifferentiated foci. In one of these positive cases, LOH was observed in both papillary adenocarcinoma and undifferentiated carcinoma. However, a p53 gene mutation at codon 248 was detected in the undifferentiated carcinoma but not in the papillary adenocarcinoma. The results imply that LOH occurs first in papillary adenocarcinoma followed by a p53 mutation during the transition from papillary adenocarcinoma to undifferentiated carcinoma. Maintenance of LOH during tumor progression excludes the possibility that these different histological foci are derived from different origins and represents molecular evidence that undifferentiated carcinoma is very likely derived from preexisting papillary adenocarcinoma. Furthermore, these results strongly suggest that the mutated p53 gene plays a crucial role in de-differentiation during the progression of thyroid tumors.

Adenocarcinoma↗
PubMed1993

Induction of BCR-ABL fusion genes by in vitro X-irradiation.

The Philadelphia chromosome consists of a reciprocal translocation between the ABL oncogene at chromosome 9q34 and the BCR gene at chromosome 22q11, resulting in the expression of chimeric BCR-ABL mRNAs specific to chronic myelogenous leukemia (CML). Presence of the fusion gene can be detected with high specificity and sensitivity by means of reverse transcription and polymerase chain reaction. Using this assay, it was possible to detect BCR-ABL fusion genes induced among HL60 cells after 100 Gy of X-irradiation in vitro. In total, five fusion gene transcripts were obtained among 10(8) cells examined. These fusion genes contained not only CML-specific BCR-ABL rearrangements, but also other forms of BCR-ABL fusions. These latter genes had junctions of BCR exon 4/ABL exon 2 intervened by a segment of DNA of unknown origin, BCR exon 5/ABL exon 2, and BCR exon 4/ABL exon 2. The results appear to be direct evidence for the induction of the BCR-ABL fusion gene by X-irradiation. In terms of leukemogenesis, it appears that only those cells bearing certain CML-related BCR-ABL fusion genes are positively selected by virtue of a growth advantage in vivo.

Base Sequence↗
PubMed1993

Doppler echocardiographic assessment of left ventricular diastolic function in patients with progressive systemic sclerosis.

To investigate the diastolic function of the left ventricle in patients with progressive systemic sclerosis (PSS), 13 patients with PSS (3 males and 10 females; group PSS) were examined by Doppler echocardiography. As a control 8 age-matched healthy volunteers (3 males and 5 females; group H) were also examined. Pulse-wave transmitral Doppler flow velocity curves were digitized and curves of the first derivatives were obtained. In group PSS, total left ventricular wall thickness and left atrial dimension were increased, the ratio between the left ventricular end-diastolic dimension and the left ventricular wall thickness was decreased, late peak diastolic filling was increased, isovolumic relaxation time was prolonged, compared with group H. The patients with left ventricular wall thickening out of proportion to left ventricular end-diastolic dimension had decreased early peak diastolic filling. We conclude that patients with PSS have deterioration of left ventricular diastolic function, and the diastolic function is severely disturbed in patients with left ventricular wall thickening out of proportion to left ventricular end-diastolic dimensions.

Diastole↗