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Biomedical subjects

Y Yaginuma

Publications and source records attributed to Y Yaginuma.

At least 37 records · Page 2Linked to original sources
PubMed1996

The habit of sniffing in nasal diseases as a cause of secretory otitis media.

To clarify the role of habitual sniffing caused by nasal diseases in the pathogenesis of middle ear diseases, 112 pediatric patients with secretory otitis media (183 ears) were examined for associated nasal diseases and habitual sniffing. Middle ear pressure and nasopharyngeal pressure were simultaneously measured during forceful sniffing. Fifty-four percent of the patients with secretory otitis media had allergic rhinitis and/or chronic sinusitis. Sixty percent of the patients with nasal diseases habitually sniffed, whereas only 30.8% of those without nasal diseases had this habit. In the patients with the habit of sniffing, a higher negative pressure tended to be created in the nasopharynx on forceful sniffing than in the patients who did not sniff. Thirty-one of 112 patients (27.7%) were positive on the sniff test. Of these 31 patients, 20 were associated with the habit of sniffing, and in 14 of the 20 patients, nasal diseases were considered to be the primary cause of the habit of sniffing. That is, in 14 of the 112 patients (12.5%) with secretory otitis media, the patients with nasal diseases frequently sniffed and their middle ears were evacuated. This study suggests that in many patients, sniffing provoked by nasal diseases plays an important role in the pathogenesis of secretory otitis media through the creation of negative nasopharyngeal pressure. This mechanism is presumed to be present in approximately one-tenth of pediatric patients with secretory otitis media.

Adolescent↗
PubMed1995

Analysis of the p53 gene in human choriocarcinoma cell lines.

In the present study, we analysed human choriocarcinoma cell lines for abnormalities in the tumour-suppressor gene p53 by Southern blotting, Northern blotting, non-radioisotopic single-stranded conformational polymorphism (SSCP) and complementary DNA sequencing. In all cell lines (Bewo, GCH-1, GCH-2, SCH, JAR, JEG-3, NUC-1 and HCCM-5), no p53 gene abnormality was detected by using Southern blotting. p53 mRNA of the expected size was detected in all cell lines tested by Northern blotting. SSCP analysis revealed abnormalities of p53 cDNA in the SCH cell line. Sequencing analysis of the entire coding region of the p53 gene revealed that both alleles were expressed in the JEG-3 cell line, and one of the alleles contained a point mutation (G to T) in codon 167 (Gln to His). In the NUC-1 cell line both alleles were point mutated. One allele had a point mutation (A to T) that resulted in a codon 17 change (Glu to Asp), and another had a point mutation (A to T) that caused a codon 24 change (Lys to Asn). In the SCH cell line, AGG was inserted between codon 249 and 250; this insertion resulted in an abnormal structure of the p53 protein. In three out of eight human choriocarcinoma cell lines, a p53 gene abnormality was detected. Therefore our data demonstrate that p53 gene abnormalities are associated with choriocarcinoma cell lines.

Base Sequence↗
PubMed1995

Pregnancy, labor and delivery in a woman with a damaged spinal cord.

We report here a case involving the pregnancy, labor and delivery of a woman with a damaged spinal cord. In our case, even though the cord was damaged below the Th11, continuous epidural anesthesia was needed to prevent autonomic hyperreflexia. The patient's and infant's subsequent courses were normal.

Adult↗
PubMed1994

[Analysis of p53 gene in gynecologic tumors].

The inactivation of the tumor suppressor gene p53 has been demonstrated in a variety of human tumors. Herein, we performed a p53 gene analysis of human gynecologic tumor cell lines and tumor tissues. In the SK-OV-3 cell line, Southern analysis suggested the presence of sequence deletions/rearrangements in at least one allele of p53 gene. Transcripts were not detectable by either Northern or PCR analysis. Sequencing analysis of the entire coding region revealed mutations changing the p53 amino acid composition in all six endometrial carcinoma cell lines tested (Ishikawa, Hec1-A, Hec1-B, KLE, RL95-2, and AN-3), and four cell lines in ovarian carcinoma cell lines (Caov-3, -4, OVCAR-3, and Kuramochi). Of the seven cervical carcinoma cell lines, two (HT-3 and C-33A) contained p53 codon changes. We were unable to detect the human papilloma virus (HPV) in these two cell lines. By contrast, five HPV-positive cervical carcinoma cell lines (HeLa S-3, Caski, SiHa, C-41, and ME-180) contained wild-type p53 gene sequences. Examination of loss of heterozygosity (LOH) by PCR revealed that about 30% of the human ovarian carcinoma tissues has LOH at the locus of p53 gene. We suggest that, in the HPV-positive cervical tumors, p53 inactivation occurred via the known mechanism of viral E6/cellular p53 protein association, whereas in all other tumors (ovarian carcinoma, endometrial carcinoma, HPV-negative cervical carcinoma) p53 function was compromised by changes in the amino acid sequence.

Base Sequence↗
PubMed1994

Pathogenesis of attic retraction pocket and cholesteatoma as studied by computed tomography.

It is hypothesized that blockade of the tympanic isthmus causes isolation of the attic and the adjacent middle ear spaces and that subsequent building up of the negative pressure in these spaces results in retraction of the pars flaccida, leading to formation of attic retraction pockets and cholesteatomas. To examine this theory, computerized tomographic (CT) findings of these conditions were evaluated in a series of 53 ears with retractions of the pars flaccida (attic retractions of Tos type II or deeper), including both retraction pockets and cholesteatomas. In 26 of 28 ears with attic retraction pockets, at least a portion of attic was aerated, and in 22 of these 26 ears, the mastoid antrum was also aerated. In contrast, in the 25 cases with attic cholesteatomas, these numbers decreased to 10 and 5, respectively, and the lack of aeration of the attic was demonstrated in 15 of 25 (60%) of the cases. In three cases of cholesteatoma, follow-up CT revealed either growth of a cholesteatoma from a retraction pocket or development of a small cholesteatoma into a large one. In these ears it was seen that the well-pneumatized attic and mastoid antrum seen in the initial CT was depleted by the growth of cholesteatoma that took place over a period of 4 months to 2 years. These results, showing good patency of the aditus and a pneumatized antrum in early stages of most cases of retraction pockets and cholesteatomas, are not in agreement with the hypothesis that the blockade of the tympanic isthmus is responsible for the pathogenesis of retraction pockets and cholesteatomas originating in the pars flaccida.

Adolescent↗
PubMed1993

Expression of superoxide dismutase (SOD) in adenomyosis.

OBJECTIVE: To assess the expression of Cu,Zn-SOD and Mn-SOD in peritoneal fluid and ectopic endometrium from women with adenomyosis. STUDY DESIGN: The levels of Cu,Zn-SOD and Mn-SOD were measured in peritoneal fluid from infertile women who did not have endometriosis (n = 27), women with adenomyosis (n = 22), and women with endometriosis (n = 15). The expression of Cu,Zn-SOD and Mn-SOD messenger ribonucleic acids in ectopic endometrium was investigated by Northern blot analysis. Mn-SOD in ectopic endometrium was investigated by immunohistochemical staining. RESULTS: The levels of Cu,Zn-SOD and Mn-SOD were significantly higher in the peritoneal fluid from women with adenomyosis than in those with endometriosis or infertile women. Mn-SOD was highly expressed in ectopic endometrium, but Cu,Zn-SOD was not. Mn-SOD was detected in ectopic endometrium of women with adenomyosis. CONCLUSIONS: These data show that reactive oxygen produced in adenomyosis may induce Mn-SOD in ectopic endometrium, which results in the release of relatively large amounts of this protein into the peritoneal fluid. These results suggest that free radicals may play a role in the pathogenesis of adenomyosis, the same as they do in other inflammatory processes.

Ascitic Fluid↗
PubMed1993

Immunohistochemical analysis of ras oncogene product p21 in human endometrial carcinoma.

Monoclonal antibody rp-28 directed against the ras gene product p21 has been used to evaluate ras p21 expression in endometrial lesions. Endometrial cancer showed a variable reactivity according to histological type: in well differentiated adenocarcinoma 63% were positive (12/19); in moderately differentiated adenocarcinoma 53% were positive (8/15); in poorly differentiated adenocarcinoma 40% were positive (2/5). The staining intensity of ras p21 seemed to be stronger in the more differentiated types of endometrial carcinoma. In endometrial carcinoma with premenopausal women, 27% were positive (3/11), and with postmenopausal women 71% were positive (20/28). The difference between premenopausal and postmenopausal groups was statistically significant (Mantel-Haenszel procedure, M-H chi 2 = 6.765, P < 0.01). The results suggest the existence of different carcinogenetic mechanisms in these two groups of endometrial cancer.

Adenocarcinoma↗
PubMed1993

[International normalized ratio (INR) for optimal anticoagulant therapy].

Optimal therapeutic ranges for an oral anticoagulant therapy has been discussed for many years. Prothrombin time, prothrombin time ratios (PTR) and thrombotest have been employed so far, but, recently, International Normalized Ratio of prothrombin time (PT-INR or INR) has been introduced. We investigated paying special interest to INR, the effectiveness of oral anticoagulant therapy in 170 prosthetic valve patients and in 157 patients with various cardiovascular diseases who received warfarin at two different centers. The thrombotest, prothrombin time and INR were measured at follow-up visits every month. Regarding the 170 patients with prosthetic valves with a mean follow-up period of 2.44 years, 9 thromboembolisms (TE) were reported. The average TT and INR values in TE-free patients among 101 in whom coagulability could be measured, were 21.1% and 1.73 respectively. The average TT and INR values in 5 patients with TE were 26.4% and 1.53 respectively and this was significantly (p < 0.01) higher (smaller) than in TE-free patients. 157 patients (mean age 55 +/- 12 y.o.) with various cardiovascular diseases (Table 2) were followed up for a mean of 4.9 +/- 3.2 years. As is seen in figure 4, mean INR values in TE patients were 1.28, in patients with bleeding complications 4.1, and in event free patients 2.07 respectively. In conclusion, with INR greater than 2.75, no thromboembolic complication occurred, but several hemorrhagic complications occurred at INR greater than 3. Therefore INR therapeutic ranges between 2.0-3.0 are recommendable both for the prevention of TE and bleeding complications.

Administration, Oral↗
PubMed1992

Abnormal structure and expression of the p53 gene in human ovarian carcinoma cell lines.

In an effort to analyze molecular mechanisms of human ovarian carcinogenesis, we studied the structure and expression of the p53 gene in different cell lines established from human ovarian carcinomas. In all six lines (PA-1, Caov-3 and -4, OVCAR-3, SK-OV-3, and Kuramochi), p53 abnormalities were detected. In the SK-OV-3 cell line, Southern analysis suggested the presence of sequence deletions/rearrangements in at least one allele of the p53 gene, and transcripts were not detectable by either Northern or polymerase chain reaction analysis. Sequence analysis of the entire coding region of the p53 gene revealed point mutations resulting in codon changes of a highly conserved region of the protein in four cell lines, Caov-3 and -4, OVCAR-3, and Kuramochi. In the Caov-3 cell line, the point mutation resulted in chain termination at codon 136. Quantitation of p53 protein by immunoprecipitation analysis revealed a 6-fold higher than control cell level in PA-1. By contrast, p53 protein was not detectable in lines Caov-3 and SK-OV-3. We conclude that altered levels of p53 gene expression and/or mutant forms of the p53 gene product are associated with all human ovarian cancer cells tested.

Base Sequence↗
PubMed1992

ras oncogene product p21 expression and prognosis of human ovarian tumors.

Monoclonal antibody rp-28 directed against the ras gene product p21 has been studied to evaluate ras p21 expression in malignant and benign ovarian tissues. Some ovarian carcinomas of serous and mucinous cystadenocarcinomas, undifferentiated adenocarcinomas, and clear cell carcinomas demonstrated intense staining of ras p21. The frequency and intensity of ras p21 staining were observed to increase with the degree of malignancy. There was no significant difference in ras p21 expression between early and late stages in ovarian tumors arising from the coelomic epithelium. With respect to prognosis, no differences between the ras p21-positive and -negative cases in ovarian tumors arising from the coelomic epithelium were observed. It is, therefore, possible to say that ras p21 expression was not related to clinical staging and prognosis. Expression of ras p21 in malignant lesions was higher than that in benign lesions of the ovary, and the expression is associated with the degree of malignancy in some types of ovarian tumors. Overexpression of ras p21 was observed in epithelial tumors; however, increased expression was not observed in germ cell and sex-cord stromal tumors. This differential expression of ras p21 is due to the different histogenesis of ovarian tumors. This fact may reflect a different carcinogenic mechanism for different types of malignancy.

Adult↗
PubMed1991

Analysis of the p53 gene in human uterine carcinoma cell lines.

The inactivation of the tumor suppressor gene p53 has been demonstrated in a variety of human tumors. In this study, we present a p53 gene analysis of 13 uterine carcinoma cell lines. Sequencing analysis of the entire coding region revealed mutations changing the p53 amino acid composition in all six endometrial carcinoma cell lines tested (Ishikawa, Hecl-A, Hecl-B, KLE, RL95-2, and AN-3). Of the seven cervical carcinoma cell lines, two (HT-3 and C-33A) contained p53 codon changes as well. We were unable to detect human papillomavirus in these two cell lines. By contrast, five human papillomavirus-positive cervical carcinoma cell lines (HeLa S-3, Caski, SiHa, C-4I, and ME-180) contained wild-type p53 gene sequences. We suggest that, in the human papillomavirus-positive cervical tumors, p53 inactivation occurred via the known mechanism of viral E6/cellular p53 protein association, whereas in all other tumors p53 function was compromised by changes in the amino acid sequence.

Base Sequence↗