Biomedical subjects

K Ozono

Publications and source records attributed to K Ozono.

78 records · Page 5Linked to original sources

PubMed1989

Reflex control of mesenteric vein diameter and pressure in situ in rabbits.

We have directly demonstrated that the mesenteric veins actively constrict and dilate in response to reflex stimuli in the in situ preparation. A segment of small intestine of 23 chloralose-anesthetized rabbits was exposed in a specially designed bath. Small vein diameter and intravenous pressure (575-1,375 microns and 6.2-11.4 mmHg at rest, respectively) of the mesentery were measured continuously at the same site with the use of videomicrometer and micropressure systems during celiac ganglion stimulation (CGS), bilateral carotid occlusion (BCO), and aortic nerve stimulation (ANS). Innervation to the mesenteric vein was evident by a frequency-dependent venoconstriction in response to CGS, which was completely abolished by local application of tetrodotoxin. Vein diameter and intravenous pressure changed from an average of 1,042 +/- 32 to 1,003 +/- 32 microns (-3.8 +/- 0.3%, P less than 0.01) and from 8.1 +/- 0.3 to 9.0 +/- 0.3 mmHg (10.6 +/- 0.8%, P less than 0.01), respectively, during BCO. During ANS, vein diameter increased from 990 +/- 32 to 1,012 +/- 31 microns (2.4 +/- 0.2%, P less than 0.01), and intravenous pressure decreased from 8.5 +/- 0.3 to 7.9 +/- 0.2 mmHg (-6.1 +/- 0.6%, P less than 0.01), respectively. Vein diameter changes of -3.8 and 2.4% corresponded to volume changes of -7.6 and 4.9%, respectively. During BCO, vein diameter decreased while intravenous pressure increased, whereas during ANS vein diameter increased while intravenous pressure decreased. These results indicate that the reflex change in vein diameter is due to an active response.

Animals↗

PubMedDate not supplied

Brain natriuretic peptide as a hormonal marker of ventricular diastolic dysfunction in children with Kawasaki disease.

Although an increased level of serum brain natriuretic peptide (BNP) has been reported in children in the acute phase of Kawasaki disease (KD), no precise relation was documented between the serum BNP level and left ventricular (LV) systolic function. We hypothesized that the increased BNP levels may be explained by diastolic abnormalities in those with KD. We prospectively studied 25 patients in the acute phase of KD. Patients with abnormal systolic function were excluded. Pediatric cardiologists making the assessment of LV diastolic function were blinded to the BNP levels. Doppler interrogation was applied to measure LV inflow velocities, which were transformed to z scores using control measurements obtained from 83 healthy subjects. In the patients, the BNP levels ranged from 2.0 to 450.0 pg/ml, with a mean of 54.0 +/- 102.8 pg/ml. Six patients with abnormal velocities (> 2 SD in z score) showed significantly higher levels of BNP (152 +/- 173 pg/ml) than those in the remaining patients (p < 0.01). The BNP levels correlated positively with diastolic atrial velocity in z score (r = 0.51, p < 0.05), and negatively with diastolic early velocity to atrial velocity ratio in z score (r = -0.75, p < 0.01). This study suggests that LV diastolic dysfunction may occur in some children in the acute phase of KD, causing an increased level of BNP.

Adolescent↗

PubMedDate not supplied

Differential activities of 1alpha,25-dihydroxy-16-ene-vitamin D(3) analogs and their 3-epimers on human promyelocytic leukemia (HL-60) cell differentiation and apoptosis.

To clarify physiological role of the carbon 3 (C-3) epimerization of 1alpha,25(OH)(2)D(3) and biologic significance of a 3-epi metabolite of 1alpha,25(OH)(2)D(3), we examined biologic activities of the 3-epimers of 1alpha,25(OH)(2)D(3) and 1alpha,25(OH)(2)-16-ene-D(3) analogs in terms of modulation of cell cycle phase distribution and cell-surface CD11b antigen expression of HL-60 cells, transactivation of vitamin D target genes in transfected cells, stimulation of VDR/RXRalpha heterodimer formation in a rabbit reticulocyte lysates transcription/translation system, stimulation of VDR/RXRalpha/VDRE complex formation, and induction of HL-60 cell apoptosis. The analogs tested here were 1) 1alpha,25(OH)(2)D(3), 2) 1alpha,25(OH)(2)-3-epi-D(3), 3) 1alpha,25(OH)(2)-16-ene-D(3), 4) 1alpha,25(OH)(2)-16-ene-3-epi-D(3), 5) 1alpha,25(OH)(2)-16-ene-23-yne-hexafluoro(F(6))-D(3), 6) 1alpha,25(OH)(2)-16-ene-23-yne-hexafluoro(F(6))-3-epi-D(3), 7) 1alpha,25-(OH)(2)-16-ene-20-epi-23-yne-D(3), and 8) 1alpha,25(OH)(2)-16-ene-20-epi-23-yne-3-epi-D(3). When compared to the 3-natural (beta) analogs, the 3-epi (alpha) analogs were biologically significantly less active. The findings support the hypothesis that the C-3 epimerization is an inactivation pathway of 1alpha,25(OH)(2)D(3) and its analogs in vitamin D target tissues. We also found that the 3-epi analogs, but not the 3-natural (beta) analogs, were the potent inducers of apoptosis of HL-60 cells. These results suggest that the analogs could be divided into two groups, in which the 3-epi analogs were the potent inducers of apoptosis of HL-60 cells, and the 3-natural analogs were the potent modulators of HL-60 cell growth and differentiation. This is the first report demonstrating that the 3-epimerization of the hydroxyl group at C-3 of the A-ring of 1alpha,25(OH)(2)D(3) plays an important role to modulate HL-60 cell differentiation and apoptosis.

Animals↗

PubMedDate not supplied

(23S)- and (23R)-25-dehydro-1alpha-hydroxyvitamin D(3)-26,23-lactone function as antagonists of vitamin D receptor-mediated genomic actions of 1alpha,25-dihydroxyvitamin D(3).

We synthesized various analogues of 1alpha,25-(OH)(2)D(3)-26,23-lactone and examined the effects of them on HL-60 cell differentiation using the evaluation system of the genomic action of 1alpha,25-(OH)(2)D(3). We found that (23S)- and (23R)-25-dehydro-1alpha-OH-D(3)-26,23-lactone (TEI-9647 and TEI-9648) strongly bound to the VDR, but did not induce HL-60 cell differentiation. Intriguingly, TEI-9647 and TEI-9648 did inhibit that induced by 1alpha,25-(OH)(2)D(3), whereas they did not suppress that caused by retinoic acid or TPA. On the contrary, the similar 25-dehydrated 24-dehydro analogues, TEI-D1807 and TEI-D1808, weakly but significantly induced HL-60 cell differentiation, never showing inhibitory effect on HL-60 cell differentiation induced by 1alpha,25-(OH)(2)D(3). In other experiments, TEI-9647 and TEI-9648 markedly suppressed 25-OH-D(3)-24-hydroxylase gene expression induced by 1alpha,25-(OH)(2)D(3) in HL-60 cells. TEI-9647 also inhibited the heterodimer formation between VDR and RXRalpha, and the VDR interaction with co-activator SRC-1 according to the results obtained from the mammalian two-hybrid system in Saos-2 cells. Taking all these results into consideration, we reached a manifest conclusion that TEI-9647 and TEI-9648 are the specific and first antagonists of 1alpha,25-(OH)(2)D(3) action, specifically VDR-VDRE mediated genomic action.

Calcitriol↗

PubMedDate not supplied

Alternative splicing of fibronectin transcripts in osteochondrogenic tumors.

BACKGROUND: Fibronectin (FN) acts in many fundamental biological processes including cell adhesion, migration, proliferation and apoptosis. Although FN shows an ubiquitous expression pattern, alternative mRNA splicing modulates tissue-specific molecular heterogeneity at three regions: extra domain-B, extra domain-A and variable region. MATERIALS AND METHODS: In the present study, we analyzed the FN mRNA splicing in osteochondrogenic tumors as well as in various normal tissues using the RT-PCR method. RESULTS: Normal cartilage almost exclusively contained short mRNA lacking alternative exons in all regions. However, 14 osteochondrogenic tumors including osteochondroma, enchondroma, chondroblastoma, chondrosarcoma and osteosarcoma uniformly contained long mRNA with various patterns of alternative exons in the three regions. CONCLUSION: These results indicated that the lack of regulation excluding the alternative exons may be associated with tumorigenesis in chondrocytes.

Alternative Splicing↗

PubMedDate not supplied

Diagnosis of congenital cytomegalovirus infection by examination of placenta: application of polymerase chain reaction and in situ hybridization.

We examined the placentas of 12 patients in whom congenital cytomegalovirus (CMV) infection was suspected from serological and/or pathological evaluation. Seven patients died (including four intrauterine deaths) and five survived. On histological examination, the characteristic inclusion bodies were detected in only three placentas, and villitis with plasma cell infiltration was seen in eight placentas. Immunohistochemistry using a specific antibody against CMV improved the sensitivity of CMV deletion (10 cases were positive). With the polymerase chain reaction (PCR) following the extraction of DNA from formaldehyde-fixed placenta samples, CMV DNA was detected in seven cases. All 12 subjects were diagnosed with CMV infection by additional Southern blot analysis after the PCR. CMV DNA was also detected by an in situ hybridization method in all cases. With current molecular biological techniques the placenta can be reliably used for the diagnosis of congenital CMV infection.

Cytomegalovirus↗