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Biomedical subjects

H Ono

Publications and source records attributed to H Ono.

At least 235 records · Page 13Linked to original sources
PubMed1996

Expression of cell-cycle regulatory genes in HTLV-I infected T-cell lines: possible involvement of Tax1 in the altered expression of cyclin D2, p18Ink4 and p21Waf1/Cip1/Sdi1.

To understand how the growth of T-cells transformed by Human T-cell leukemia virus type I (HTLV-I) is deregulated, we analysed the expression of cell-cycle regulatory genes in HTLV-I infected and non-infected T-cell lines. We investigated the gene for 6 cyclins, 4 cyclin-dependent kinases, and 5 cyclin-dependent kinase inhibitors, and found the following: (1) HTLV-I infected T-cell lines preferentially expressed cyclin D2, whereas cyclin D3 was the major D-type cyclin in HTLV-I negative T-cell lines; (2) HTLV-I infected T-cell lines expressed strikingly low levels of p18Ink4 compared with those that were HTLV-I negative; (3) HTLV-I infected T-cell lines expressed high levels of p21Waf1/Cip1/Sdi1, whereas p21Waf1/Cip1/Sdi1 was undetectable in HTLV-I negative T-cell lines. These features were also found in T-cells immortalized by Tax1, which we established. Therefore, it is strongly suggested that Tax1 alters the expression of these cell-cycle regulatory genes.

Carrier Proteins↗
PubMed1996

Risk factors for lymph node metastasis from intramucosal gastric carcinoma.

BACKGROUND: Although regional lymph node metastasis from intramucosal early gastric carcinoma (EGC) is rare, it is very important to clarify the characteristics of patients having lymph nodal metastases in order to determine appropriate therapy. METHODS: The authors investigated 1196 patients with solitary intramucosal EGC who underwent resection at the National Cancer Center Hospital in Tokyo, with special reference to lymph node metastases. Eight clinicopathologic factors (age, sex, tumor: size, location, macroscopic type, histologic type, histologic ulceration of the tumor, and lymphatic vessel invasion) were investigated by univariate and multivariate analyses for their possible relationship to lymph node metastasis. RESULTS: Lymph node metastases were found in 43 patients (3.5%). Univariate analysis revealed that younger age (< 57 years), macroscopic depressed type, larger tumor size (> or= 30 mm), undifferentiated histologic type, histologic ulceration of the carcinoma, and lymphatic vessel invasion had a significant association with regional lymph node metastasis. Multivariate analysis revealed that lymphatic vessel invasion, histologic ulceration of the tumor, and larger size (> or = 30 mm) were independent risk factors for regional lymph node metastasis. The incidence of lymph node metastasis from intramucosal EGC negative for these 3 risk factors was only 0.36% (1 in 277 patients). CONCLUSIONS: Lymphadenectomy is unnecessary for patients with small intramucosal EGC with neither histologic ulceration of the tumor nor lymphatic vessel invasion because the incidence of regional lymph node metastasis is extremely low in those patients. The therapeutic options for such patients would be local resection or endoscopic resection.

Age Factors↗
PubMed1996

Effect of (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide on spinal motor systems in anesthetized intact and spinalized rats.

In the present study, we examined the effect of the 5-HT1A receptor agonist (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide (8-OH-DPAT), on the mono- and polysynaptic reflexes in intact and spinalized rats. 8-OH-DPAT (10 micrograms/kg i.v.) significantly potentiated the amplitude of the monosynaptic reflex in intact rats. In contrast, 8-OH-DPAT (30 and 100 micrograms/kg i.v.) produced a significant dose-related inhibition of the amplitude of the monosynaptic reflex in spinalized rats. These results suggest that 8-OH-DPAT predominantly excites spinal motor systems at the supraspinal site, and inhibits such systems at a spinal cord site.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

Free and island flap transfer for soft tissue defects in the hand and forearm.

Two hundred twenty patients with soft tissue defects in the hand and forearm were treated with 226 free and island flap transfers. Reconstructed sites involved the thumb in 74 cases, the fingers in 117, the hand in 30, and the forearm in 5. Seventy-nine patients received 82 free flaps, and 141 patients received 144 island flaps. Fifty-six finger reconstruction cases and 73 of 74 thumb reconstruction cases had sensory flap transfers. In the free flap transfer group, 77 flaps survived (93.9%), and 5 failed. In the island flap transfer group, 140 flaps survived (97.2%), and 4 failed. Of the five-failures in the free flap transfers, four were dorsalis pedis flaps, two of which were on patients with an arteriovenous fistula. Of the four failures in the island flap transfers, two were posterior interosseous flaps and two were digital island flaps. All four were reverse-flow island flaps.

Adolescent↗
PubMed1996

Internal stenting of the hepaticojejunostomy and pancreaticojejunostomy in patients undergoing pancreatoduodenectomy to promote earlier discharge from hospital.

Internal stenting of the hepaticojejunostomy and pancreaticojejunostomy was performed in 11 consecutive patients undergoing pancreatoduodenectomy between July 1992, and July 1994, to promote earlier discharge from hospital. Although minor leakage of the pancreaticojejunostomy occurred in 4 patients, this resolved within a short period and all 11 patients were able to be discharged by the 29th postoperative day in good health and without any intubation. Follow-up abdominal X-ray and computed tomography (CT) scans proved that all 22 of the stenting tubes had spontaneously fallen out by the 176th postoperative day. No complication related to the stenting tubes occurred in any of our patients.

Adult↗
PubMed1996

A point mutation in exon 7 of the C1-inhibitor gene causing type I hereditary angioedema.

The polymerase chain reaction and nucleotide sequence analysis have been used to characterize a point mutation in the seventh exon of one allele of the C1-inhibitor gene in a family with type I hereditary angioedema. A single base change (C-->T) at nucleotide 1482 in C1-inhibitor converted the codon for Gln-339 to a premature translation termination codon, TAG. Family studies suggest that this mutation is responsible for type I hereditary angioedema in a studied pedigree.

Amino Acid Sequence↗
PubMed1996

Learning to look with one eye: the use of head turn by normals and strabismics.

When asked to look through a tube, young children (normal, strabismic, monocularly enucleated) place it between the eyes, while older children turn the head or shut one eye. We videotaped 174 children (normals and strabismics, 2-17 yr of age) and 16 normal adults to find out when and why head turn occurs. In learning to look with one eye, children progressed through a sequence of four responses, categorized by age or amount of head turn. Binocular children use head turn apparently to avoid diplopia, then, most learn to shut one eye. Adults, forced to use the "non-preferred" eye, revert to turning the head.

Adolescent↗
PubMed1996

Midcarpal instability: is capitolunate instability pattern a clinical condition?

Five cases are presented with clinical findings of capito-lunate instability pattern of the wrist. All painful areas and tender points were dorsal, but variable in location and intensity. All plain radiographs and fluoroscopic instability series were normal. None of the cases had an explanation for the dorsal wrist pain other than a positive dorsal capitate-displacement test. Four out of five cases were treated in a cast for 4 weeks and two had subsequent splint immobilization. Although at short-term follow-up two of these five patients became pain-free, none was completely pain-free at long-term follow-up. Three patients treated with a cast had long-term follow-up. Only one could perform his original work. These findings support a clinical condition of midcarpal instability producing dorsal wrist pain reproduced with a simple stress test. Conservative, non-operative treatment will not usually produce long-term pain relief.

Adult↗
PubMed1996

Carbon dioxide induced panic attack in panic disorder in Japan.

1. The authors investigated the psychological and biochemical factors associated with challenge by 5% CO2-95% O2 inhalation for 20 min. While fifteen healthy people were used as control, thirteen cases who were diagnosed by DSM-III-R as suffering from panic disorder were used as subjects. CO2 inhalation induced panic in 38% of the panic disorder patients, but did not cause panic in any of the control cases (0%). 2. Acute panic inventory (API), heart rate and breathing rate of the panic group increased significantly after CO2 inhalation compared with the values in the control and non-panic groups. 3. Heart rates and systolic blood pressure were significantly higher those in the panic disorder and non-panic groups than in the control group prior to CO2 inhalation. The cortisol values in the panic and non-panic groups also were significantly higher than those in the control group before and after CO2 inhalation. 4. These results suggest elevated activity of the sympathetic nervous system during panic. The significantly higher heart rate, systolic blood pressure and cortisol values of the panic disorder subjects relative to the control before CO2 inhalation may have been due to circumstantial factors. The present findings of convincing evidence for behavioral, physiological, and biochemical hypersensitivity to CO2 in patients with panic disorders are consistent with a model of interoceptive conditioning in these patients.

Acute Disease↗
PubMed1996

Bicompartmentalization of the radiocarpal joint.

Seven wrists are presented with a septum connecting the lunotriquetral interosseous ligament and triangular fibrocartilage, resulting in bicompartmentalization of the radiocarpal joint. In all of the 7 wrists, having no history of trauma, the septums were suspected to be of congenital origin. The histopathology of the septum in 1 cadaver wrist showed a fibrocartilaginous structure. Two types of radiocarpal joint bicompartmentalization were identified by arthrography. Type 1 (2 wrists) had a septum with normal (intact) lunotriquetral interosseous ligament, and type 2 (5 wrists) had a septum with a communicating defect of the lunotriquetral interosseous ligament. The septum is most likely a congenital malformation caused by a disturbance of the vacuolization of the mesenchymal mass between the forearm and carpus.

Adult↗
PubMed1996

A case of bone marrow recurrence from gastric carcinoma after a nine-year disease-free interval.

We present a case of very late and unusual recurrence of gastric cancer. Nine years following total gastrectomy for gastric carcinoma, a 57-year-old man presented with disseminated intravascular coagulation associated with bone marrow recurrence. The primary tumor was a signet ring cell carcinoma invading the subserosal layer with lymph node metastasis. The patient was treated with sequential administration of methotrexate and 5-fluorouracil and went into remission. After treatment, he survived 10 months. Autopsy revealed diffuse bone marrow infiltration and distant lymph node metastasis with signet ring carcinoma cells.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1996

Hydrochlorothiazide exacerbates nitric oxide-blockade nephrosclerosis with glomerular hypertension in spontaneously hypertensive rats.

OBJECTIVE: To determine whether a diuretic can also reverse the clinical, systemic, renal and glomerular haemodynamic and pathological changes caused by nephrosclerosis. METHODS: Three groups of 20-week-old spontaneously hypertensive rats (SHR) were investigated: control male SHR; a similar group, administered 50 mg/l NG-nitro-L-arginine methyl ester (L-NAME) for 3 weeks; and SHR treated similarly with L-NAME but also with 80 mg/kg per day hydrochlorothiazide (HCTZ) by gavage for 3 weeks. RESULTS: The mean arterial pressure, cardiac output, effective renal plasma flow and glomerular filtration rate decreased as urinary volume increased in the SHR treated with HCTZ and L-NAME. A micropuncture study demonstrated increased glomerular capillary pressure (PG, 56 +/- 1 versus 68 +/- 3 mmHg) associated with increased efferent (2.1 +/- 0.2 versus 2.9 +/- 0.3 u) but no change in afferent arteriolar resistances compared with the SHR group treated with L-NAME only. In addition, HCTZ administration increased the juxtamedullary glomerular injury score (47 +/- 13 versus 114 +/- 29) associated with elevated urinary protein excretion (35 +/- 1 versus 53 +/- 13 mg/100 g body weight per 24 h) The afferent arteriolar injury score was not changed. The PG elevation was related not only to severe glomerulosclerosis but also to increased fibronectin and alpha-smooth muscle actin deposition. CONCLUSION: HCTZ administration exacerbated the changes in renal and micropuncture dynamics, proteinuria and histopathological nephrosclerosis produced by L-NAME in SHR.

Animals↗
PubMed1996

Hereditary angioedema caused by a point mutation of exon 7 in the C1 inhibitor gene.

Hereditary angioedema (HAE) is a genetic disease which may be detected serologically. We present a patient with HAE, in whom we examined the gene defect using the polymerase chain reaction. The patient presented with recurrent episodes of abdominal pain, or non-itchy swellings of the hands, feet, and penis. The serum levels of C1 inhibitor (C1-INH) and C4 were below normal. We determined that a single base change (C-->T) at nucleotide 1482 in the seventh exon was present in the C1-INH gene. This mutation converted the codon for the Gln-339 to a premature translation termination codon TAG. A point mutation in the C1-INH gene can cause type I HAE.

Adult↗
PubMed1996

Cysteine protease of Porphyromonas gingivalis 381 enhances binding of fimbriae to cultured human fibroblasts and matrix proteins.

It has been shown that Porphyromonas gingivalis 381, a suspected periodontopathogen, possesses fimbriae on its cell surface. The organism is also known to produce proteases which can degrade the host cell surface matrix proteins. In this study, we investigated the effect of protease on the binding of the purified P. gingivalis fimbriae to cultured fibroblasts or matrix proteins. A protease that can hydrolyze benzoyl-L-arginine p-nitroanilide was obtained from P. gingivalis 381 cells by sonication in phosphate-buffered 0.2% Triton X-100 and was purified by column chromatography. The molecular size of the protease was estimated to be 55 kDa by gel filtration or 47 kDa by sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis. The enzyme activity was markedly inhibited by sulfhydryl reagents, antipain, and leupeptin. The protease degraded various host proteins, including collagen and fibronectin, and cleaved the COOH terminus of the arginine residue in peptides such as benzoyl-L-arginine p-nitroanilide. However, P. gingivalis fimbriae were not degraded by protease activity. The enzyme activity was enhanced in the presence of reducing agents or CaCl2. When cultured fibroblasts were partially treated with the protease, the binding of the purified P. gingivalis fimbriae to the fibroblast monolayer was increased significantly. However, this enhancing effect was suppressed upon the addition of antipain and leupeptin. Similarly, binding of the fimbriae to the collagen or fibronectin immobilized on the microtiter wells was also enhanced. Addition of these host matrix proteins efficiently inhibited the binding of fimbriae to the fibroblast monolayer. The binding assay of fimbriae using dipeptidyl ligand affinity column chromatography demonstrated a clear interaction between fimbriae and the arginine residue. Taken together, these results indicate that the P. gingivalis protease at least partially degrades the host matrix proteins, which, in turn, may lead to an increased exposure of the cryptic ligands that can result in enhanced fimbria-mediated binding of this organism to periodontal tissues.

Amino Acid Sequence↗
PubMed1996

Successful erythropoietin treatment for severe anemia in nephrotic syndrome without renal dysfunction.

A 62-year-old woman presented with nephrotic syndrome and severe anemia although the renal function was not impaired. Renal biopsy revealed the histology of membranoproliferative glomerulonephritis, and the proteinuria was resistant to steroid therapy. Iron deficiency, bleeding and other causes of anemia were ruled out, however, her serum erythropoietin level was inappropriately low. The anemia was rapidly corrected by administration of recombinant human erythropoietin. It is suggested that inappropriately low erythropoietin level, in part at least, accounts for the anemia in nephrotic syndrome. It is proposed that erythropoietin therapy should be taken into consideration for severe anemia in nephrotic syndrome even when the renal function is not impaired.

Anemia↗
PubMed1996

ACE inhibition prevents and reverses L-NAME-exacerbated nephrosclerosis in spontaneously hypertensive rats.

Chronic nitric oxide inhibition exacerbates hypertension and nephrosclerosis in spontaneously hypertensive rats (SHRs). In this study, we determined whether angiotensin-converting enzyme (ACE) inhibition could prevent or reverse the systemic, renal, and glomerular hemodynamic alterations and the pathological changes of nephrosclerosis. Four groups of 20-week-old SHRs were studied: group 1, untreated controls; group 2, treated with N omega-nitro-L-arginine methyl ester (L-NAME, 50 mg/L for 3 weeks); group 3, L-NAME cotreated with quinapril (3 mg.kg-1.d-1 for 3 weeks); and group 4, L-NAME for 3 weeks followed by quinapril for 3 weeks (same doses). The results of this study demonstrated that both cotreatment (group 3) and posttreatment (group 4) with quinapril reduced mean arterial pressure (186 +/- 9 and 192 +/- 9 mm Hg, respectively, compared with group 2 SHRs, 221 +/- 5 mm Hg) and total peripheral resistance index associated with significant reductions in afferent and efferent arteriolar resistances; nephrosclerosis pathological scores; and urinary protein excretion (all at least P < .01). ACE inhibition also significantly increased stroke index, single-nephron glomerular filtration rate, and ultrafiltration coefficient compared with the L-NAME SHRs. Most notable were the findings that cotreatment with quinapril completely prevented the renal glomerular hemodynamic alterations with reduced glomerular capillary hydrostatic pressure and efferent arteriolar resistance compared with both the untreated and the L-NAME-treated SHRs (all at least P < .01). Posttreatment with quinapril also reversed the glomerular injury (subcapsular, -83%; juxtamedullary, -56%) and arteriolar (-87%) injury scores obtained from renal biopsy specimens (P < .005 and P < .0001, respectively). These changes were associated with decreased periarteriolar fibronectin and increased afferent arteriolar alpha-smooth muscle actin deposition (immunohistochemistry). These data, therefore, demonstrate that ACE inhibition not only prevents but also reverses L-NAME-exacerbated severe nephrosclerosis in SHRs, as indicated by improved systemic, renal, and glomerular hemodynamic changes, proteinuria, and histological alterations.

Analysis of Variance↗
PubMed1996

Receptor-mediated intrarenal angiotensin II augmentation in angiotensin II-infused rats.

Chronic low-dose angiotensin II (Ang II) infusion for 13 days mimics two-kidney, one clip Goldblatt hypertension and increase intrarenal Ang II levels. We performed studies to determine the time course for the enhancement of intrarenal Ang II levels and whether the increased intrarenal Ang II is a tissue-specific event and requires a receptor-mediated step. Male Sprague-Dawley rats were uninephrectomized, and either vehicle or Ang II (40 ng/min) was infused via a subcutaneous osmotic minipump. Plasma and renal Ang II levels were measured 3, 7, 10, and 13 days after minipump implantation. Compared with controls (126 +/- 2 mm Hg), systolic pressure in Ang II-infused rats exhibited a detectable increase by day 6 (146 +/- 2 mm Hg) and continued to increase to 189 +/- 5 mm Hg by day 12. Plasma Ang II levels were elevated by day 3, whereas intrarenal Ang II levels were not significantly elevated until 10 days of Ang II infusion. Renal injury characterized by focal and segmental glomerulosclerosis was evident after 13 days of Ang II infusion. Losartan (30 mg/kg per day) prevented the development of hypertension in the Ang II-infused rats for the duration of the infusion period (125 +/- 1 mm Hg) and reduced the degree of glomerular injury. Plasma renin activity was suppressed in the Ang II-infused group but was elevated markedly in both losartan-treated groups. Plasma Ang II levels were elevated in the Ang II-infused rats and were even higher during losartan treatment. Intrarenal Ang II levels were enhanced significantly (354 +/- 60 versus 164 +/- 23 fmol/g) in the Ang II-infused rats. However, losartan treatment prevented the augmentation of intrarenal Ang II caused by Ang II infusion. Heart and adrenal Ang II levels were not significantly increased in the Ang II-infused rats but were significantly elevated during losartan treatment. These results suggest that the tissue-specific elevations of intrarenal Ang II levels caused by chronic Ang II infusion are mediated by angiotensin type 1 receptor activation, which leads to either receptor-mediated internalization of Ang II, enhancement of intrarenal Ang II formation, or both.

Angiotensin II↗