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Biomedical subjects

K Takeuchi

Publications and source records attributed to K Takeuchi.

At least 181 records · Page 10Linked to original sources
PubMed2000

Increased plasma fibrinogen level and future risk of coronary artery disease after repair of abdominal aortic aneurysm.

BACKGROUND: Cardiovascular disease such as coronary artery disease is a major cause of late death after repair of abdominal aortic aneurysm (AAA). But risk factors are not well known. So, we investigated the incidence of cardiovascular events after surgery and examined the prognostic factors. STUDY DESIGN: We retrospectively reviewed 270 patients who underwent elective surgery for AAA from 1985 to 1995. Kaplan-Meier survival analysis was used to estimate survival rates and the probability of coronary, cerebrovascular, and cardiovascular events. The risk factors for each endpoint were investigated using multivariate analysis. RESULTS: The overall survival rate was 87.3% at 3 years, 76.4% at 5 years, and 52.3% at 10 years. Current cigarette use, renal insufficiency, advanced age (> or = 70 years old), and higher plasma fibrinogen level (> or = 300 mg/dL) were significant factors influencing survival. The probability of a coronary event was 4.9% at 3 years, 7.1% at 5 years, and 20.7% at 10 years. Plasma fibrinogen level and cerebrovascular disease were significant prognostic factors for coronary events. The probability of a cerebrovascular event was 5.3% at 3 years, 7.6% at 5 years, and 18.0% at 10 years. No significant prognostic factors for cerebrovascular events existed. The probability of a cardiovascular event was 10.3% at 3 years, 14.9% at 5 years, and 33.6% at 10 years. Plasma fibrinogen level was a significant risk factor for cardiovascular events. But the presence of coronary artery disease did not affect survival or the incidence of coronary, cerebrovascular, or cardiovascular events. CONCLUSIONS: Plasma fibrinogen level is an independent risk factor of future coronary events after surgery for AAA, and the increased risk of coronary artery events contributes to the impaired survival. Patients with higher plasma fibrinogen level need careful surveillance for cardiovascular disease after surgery.

Adult↗
PubMed2000

Acid secretory changes in streptozotocin-diabetic rats: different responses to various secretagogues.

We examined gastric acid secretion in response to various stimuli in streptozotocin (STZ) induced diabetic rats and characterized the alteration of acid secretory responses in diabetic conditions. Animals were injected STZ (70 mg/kg, intraperitoneally) and used after five weeks of diabetes with blood glucose >350 mg/dl. Under urethane anesthesia, the experiment was performed in a chambered stomach or a whole stomach preparation, and the acid secretion was measured at pH 7.0 using a pH-stat method and by adding 100 mM NaOH. The acid secretion was stimulated by intravenous infusion of either histamine (4 mg/kg/hr), pentagastrin (60 microg/kg/hr), or carbachol (20 microg/kg/hr) or by intraluminal application of peptone solution (4%), or vagal electrical stimulation (2 msec, 3 Hz, 0.5 mA). In normal rats, acid secretion was increased in response to either histamine, pentagastrin, carbachol, peptone, or electrical vagal stimulation. In STZ diabetic rats, however, changes in acid secretion varied depending on the stimuli; the acid response to histamine remained unchanged, but the responses to vagal electrical stimulation or pentagastrin and carbachol were significantly decreased or enhanced, respectively, as compared to normal rats. Likewise, the acid response to peptone was also markedly enhanced in STZ-diabetic rats, and this response was significantly blocked by atropine and YM022 (a CCKB/gastrin antagonist) as well as famotidine in both normal and diabetic rats. Both pentagastrin and carbachol increased the luminal release of histamine in normal rats, and these responses were significantly augmented in STZ-diabetic rats. The altered acid response and histamine release induced by pentagastrin in STZ diabetic rats were partially reversed by daily injection of insulin. These results suggest that STZ-diabetic rats showed different changes in gastric acid secretion in response to various stimuli. The increased acid secretory response may be associated with an enhanced release of mucosal histamine, while the decreased response may be due to vagal neuropathy.

Animals↗
PubMed2000

Polaprezinc exerts a salutary effect on impaired healing of acute gastric lesions in diabetic rats.

We examined the influence of diabetes mellitus (DM) on the healing of HCl-induced gastric lesions and the healing promoting effect of polaprezinc [N-(3-aminopropionyl)-L-histidinato zinc] on these lesions. Studies were performed on rats injected intraperitoneally with streptozotocin (STZ, 70 mg/kg) five weeks prior to experiments. Diabetic rats had blood glucose levels (BGLs) higher than 350 mg/100 ml. Randomly chosen animals were treated subcutaneously with insulin (4 IU/day/rat) starting 1 week after STZ. Animals were given 1 ml of 0.6 N HCl by oral gavage (per os) following 18 hr of fasting; they were fed normally from 1 hr later and killed at various time points after HCl administration. Polaprezinc (3-30 mg/kg) or its components ZnSO4/7H2O and L-carnosine were given orally, twice daily for four days following HCl treatment. Gastric lesions induced by HCl healed macroscopically to quiescence within 10 days. DM and insulin did not affect the development of HCl-invoked gastric lesions, but the healing of such lesions was markedly impaired in animals with DM. Daily administration of insulin returned high BGLs to significantly lower ranges (190-208 mg/100 ml) and markedly antagonized the healing impairment. Polaprezinc (>10 mg/kg) significantly reversed the delay observed in diabetic rats without any notable effects on BGLs or acid secretion. Similar trends were observed with ZnSO4/7H2O or a mixture of ZnSO4/7H2O and L-carnosine, but not by L-carnosine alone. The mucosal expression of insulin-like growth factor-1 (IGF-I) mRNA was significantly lower in diabetic rats, a dysregulation partially corrected by insulin and polaprezinc. In addition, the delayed healing in diabetic rats was also significantly promoted by the repeated subcutaneous administration of rhIGF-I (>10 microg/kg, twice daily) without any notable effect on BGLs or acid secretion. These results suggest that DM exerted a deleterious influence on the healing of acute gastric lesions in both insulin- and zinc-sensitive manner. The salutary effects of polaprezinc on the impaired healing of gastric lesion in STZ-diabetic animals may at least be partly explained by enhancement of mucosal IGF-I mRNA expression in the stomach.

Acute Disease↗
PubMed2000

Alterations of GTP-binding proteins (Gsalpha and Gq/11alpha) in gastric smooth muscle cells from streptozotocin-induced and WBN/Kob diabetic rats.

We investigated possible impairment of the signal transduction system in gastric myocytes of streptozotocin-induced diabetic (STZ) and spontaneous diabetic WBN/Kob (WBN/Kob) rats. Gastric motility 10 weeks after the onset of diabetes mellitus was significantly reduced in both diabetic rats compared with control, and the decreased motility was not recovered by the administration of insulin to maintain normal blood glucose levels. There was no significant difference between both types of diabetic rats and control rats in total number of [3H]quinuclidinyl benzilate ([3H]QNB) binding sites (Bmmax: 545-587 fmol/mg protein) on gastric smooth muscle cell membranes or in the affinity of [3H]QNB for the binding sites (Kd: 0.06-0.07 nM). Immunoblot analysis using polyclonal anti-G-protein antibodies indicated increased expression of Gsalpha in gastric smooth muscle cell membranes, but no significant change in Gialpha or Gq/11alpha expression in STZ rats, and decreased expression of Gq/11alpha with no significant change in Gsalpha and Gialpha in WBN/Kob rats. The cAMP production in gastric smooth muscle cell membranes was augmented in the absence and presence of 100 microM isoproterenol, and 100 microM forskolin in STZ rats, whereas no significant change of cAMP production was observed in WBN/Kob rats irrespective of the presence of the stimulants. These findings suggest that long-standing diabetes may induce alterations in signal transduction at downstream receptors in gastric myocytes, resulting in the impairment of gastric motility, although the mechanism of reduced contractile activity may differ between STZ and WBN/Kob rats.

Adenylyl Cyclases↗
PubMed2000

Comparative nucleotide sequence analyses of the entire genomes of B95a cell-isolated and vero cell-isolated measles viruses from the same patient.

Experimental infection of monkeys with the IC-B strain of measles virus (MV), which was isolated in marmoset B lymphoblastoid B95a cells from an acute measles patient, caused clinical signs typical for measles, while infection by the IC-V strain isolated in African green monkey kidney Vero cells from the same patient did not cause any clinical signs in infected monkeys. The IC-B strain replicated only in B95a cells, whereas the IC-V strain replicated in both B95a and Vero cells (3,6). To clarify which gene or mutation(s) was responsible for the difference in these phenotypes, the nucleotide sequences of the entire genomes of the IC-B and IC-V strains were determined. Comparative nucleotide sequence analyses revealed only two nucleotide differences, one in the P/V/C gene and the other in the M gene, predicting amino acid differences in the P, V and M proteins and a 19 amino acid deletion in the C protein of the IC-V strain. The truncation in the C protein was confirmed for the IC-V strain by immunoprecipitation using the C protein specific antiserum. No nucleotide difference was found in the envelope H gene. These results indicated that nucleotide difference(s) in the P/V/C or/and M gene, and not H gene, was responsible for the different cell tropism and pathogenicity of MV in this case.

Animals↗
PubMed2000

Histopathology of a human allografted kidney with clinically sufficient function.

To clarify the clinico-pathological significance of protocol biopsy and clinically silent rejection in the management of renal graft recipients, we selected a total of 139 (23%) from 604 biopsy specimens according to the following criteria: 1) less than 1.4 mg/dL of serum creatinine and 2) more than 1,500 mL/d of urine volume at time of biopsy. Clinical indications for the biopsy were classified into five categories: i) protocol biopsy (73 specimens), including 69 cases at discharge post-transplantation; ii) slight increase in serum creatinine (32); iii) proteinuria (20); iv) evaluation of pulse-therapy (13); and v) fever elevation (1). Except for the last category, the specimens were histopathologically diagnosed as being normal in 50 (68%), 6 (17%), 1 (5%), and 5 (38%) specimens, respectively. Even borderline changes, and mild acute rejection, as well as drug-induced nephropathy were included, implying the existence of clinically silent rejection or drug-induced nephropathy. Obvious diversity in the histopathological diagnosis was noted in category iii) showing proteinuria, which was mainly caused by chronic rejection, drug-induced nephropathy and glomerulonephritis. The graft survival rate was no different among the four categories, except for category v). These results indicate that biopsies obtained from functionally sufficient renal grafts could provide useful information in the management of the recipients. The clinical significance of protocol biopsy awaits further clarification by the analysis of a large number of cases.

Biopsy↗
PubMed2000

Prevention of autoimmune hearing loss in MRL/lpr mice by bone marrow transplantation.

We examined the effects of bone marrow transplantation (BMT) on immune-mediated inner ear diseases in MRL/Mp-lpr/lpr (MRL/lpr) mice, which manifest not only lupus nephritis but also sensorineural hearing loss (SNHL) at the age of 20 weeks. These mice were treated with cyclophosphamide (CY) and irradiation (5 Gy x 2), followed by the transplantation of bones plus bone marrow cells from allogeneic normal C57BL/6 mice at the age of 12 weeks. Hematolymphoid cells were reconstituted with donor-derived cells 3 months after BMT. Thus-treated MRL/lpr mice showed neither lupus nephritis nor SNHL even 24 weeks after BMT. No pathological findings were observed in either glomeruli or cochleae. These findings suggest that BMT can be used to prevent the development of autoimmune SNHL in MRL/lpr mice.

Animals↗
PubMed2000

The roles of nitric oxide and prostaglandins in alterations of ulcerogenic and healing responses in adjuvant-induced arthritic rat stomachs.

AIM: To examine alterations of gastric ulcerogenic and healing responses in adjuvant-induced arthritic rats. METHODS: Arthritis was induced in male Dark Agouti rats by injection of Freund's complete adjuvant into the right hind paw. RESULTS: The gastric ulcerogenic response to indomethacin was markedly increased in AA rats, depending on the degree of arthritic change. By contrast, HCl/ethanol-induced gastric lesions were significantly suppressed in arthritic rats when compared with normal rats. The increased ulcerogenic response to indomethacin was significantly prevented by L-NAME and antineutrophil serum but not by FR167653, while the reduced ulcerogenic response to HCl/ethanol was significantly prevented by L-NAME and partly by indomethacin or NS-398. On the other hand, the healing of chronic gastric ulcers induced by thermal cauterization was also significantly delayed in arthritic rats when compared with normal rats. This delayed healing of gastric ulcers was affected by neither L-NAME, indomethacin nor FR167653. The gastric mucosa of arthritic rats showed a significant increase in both inducible nitric oxide synthase (iNOS) activity and prostaglandin (PG) E2 contents. CONCLUSIONS: Gastric ulcerogenic and healing responses were altered in arthritic rats. The ulcerogenic response to indomethacin was increased while that to HCl/ethanol was decreased. These changes in ulcerogenic responses may both be accounted for by increased production of NO/iNOS, with the latter also being partially related to elevated production of PGs/COX-2. Moreover, the healing of gastric ulcers was also delayed in arthritic rats, but the mechanism was related to neither NO nor PGs.

Animals↗
PubMed2000

The roles of prostaglandin E receptor subtypes in the cytoprotective action of prostaglandin E2 in rat stomach.

AIM: To investigate the EP receptor subtype involved in the gastroprotective action of prostaglandin (PG) E2 using various EP receptor agonists in rats, and using knockout mice lacking EP1 or EP3 receptors. METHODS: Male SD rats and C57BL/6 mice were used after an 18-h fast. Gastric lesions were induced by oral administration of HCl/ethanol (150 mM HCl in 60% ethanol). Rats were given various EP agonists i.v. 10 min before HCl/ethanol: PGE2, sulprostone (EP1/EP3 agonist), butaprost (EP2 agonist), 17-phenyl-omega-trinorPGE2 (17-phenylPGE2: EP1 agonist), ONO-NT012 (EP3 agonist) and 11-deoxyPGE1 (EP3/EP4 agonist). In a separate study, the effect of PGE2 on HCl/ethanol lesions was examined in EP1- and EP3-receptor knockout mice. RESULTS: Gastric lesions induced by HCl/ethanol were dose dependently prevented by PGE2: this effect was mimicked by sulprostone and 17-phenylPGE2 and was significantly antagonized by ONO-AE-829, an EP1 antagonist. Neither butaprost, ONO-NT012 nor 11-deoxyPGE1 exhibited any protective activity against HCl/ethanol-induced gastric lesions. PGE2 caused an inhibition of gastric motility as well as an increase of mucosal blood flow and mucus secretion, the effects being mimicked by prostanoids activating EP1 receptors, EP2/EP3/EP4 receptors and EP4 receptors, respectively. On the other hand, although HCl/ethanol caused similar damage in both wild-type mice and knockout mice lacking EP1 or EP3 receptors, the cytoprotective action of PGE2 observed in wild-type and EP3-receptor knockout mice totally disappeared in mice lacking EP1 receptors. CONCLUSION: The gastric cytoprotective action of PGE2 is mediated by activation of EP1 receptors. This effect may be functionally associated with inhibition of gastric motility but not with increased mucosal blood flow or mucus secretion.

Animals↗
PubMed2000

Interactive roles of endogenous prostaglandin and nitric oxide in regulation of acid secretion by damaged rat stomachs.

BACKGROUND: The acid inhibitory mechanism in the damaged stomach is known to involve endogenous nitric oxide (NO) as well as prostaglandin (PG). AIM: To investigate the interaction between PG and NO in regulation of acid secretion in the stomach following damage. METHODS: Under urethane anaesthesia, a rat stomach was mounted in an ex vivo chamber and perfused with saline. Acid secretion, luminal PGE2, NO metabolites (NOx) and histamine output were measured before and after application of 20 mM taurocholate Na (TC) for 30 min, with or without pre-treatment with indomethacin and/or N(G)-nitro-L-arginine methyl ester (L-NAME). RESULTS: Exposure of the stomach to TC caused a decrease in acid secretion, with concomitant increase of both luminal NOx and PGE2. Either L-NAME or indomethacin reduced the decrease in acid secretion in response to TC, but only L-NAME allowed acid secretion to increase over basal values. L-NAME prevented the increase of luminal NOx after TC treatment, while indomethacin inhibited PGE2 release during and after exposure to TC. The increase in acid secretion in the presence of L-NAME was prevented when indomethacin was given concomitantly. TC treatment increased histamine output in the lumen, a process that was enhanced by L-NAME but reduced by indomethacin. CONCLUSIONS: Damage to the stomach increases both NO and PG in the lumen, and decreases acid secretion. Inhibiting NO production increases acid secretion in the damaged stomach, but only when PG biosynthesis is intact. It is assumed that endogenous PG has a dual role in the regulation of acid secretion in the damaged stomach: an inhibitory effect at the parietal cell and an excitatory effect probably through enhancing the release of mucosal histamine.

Animals↗
PubMed2000

The Vdelta1 T cell receptor repertoire in human nasal mucosa.

The gamma/delta T cells play important roles as the first line of defence in mucosal immunity. Vdelta1 bearing T cells comprise the major population of gamma/delta T cells in the human nasal mucosa. Recently, it was reported that certain receptors are predominant at given anatomical locations. The purpose of this study was to elucidate the gamma/delta T-cell receptor repertoire in human nasal mucosa. Nasal epithelia were scraped and peripheral blood were obtained from three healthy volunteers. We performed reverse-transcription polymerase chain reaction (RT-PCR) analysis and characterized the junctional sequences of Vdelta1 T-cell receptor (TCR) transcripts. Vgamma and Vdelta gene usage in intraepithelial lymphocytes (IELs) in right and left nasal mucosa were almost the same, but they were different from those in peripheral blood lymphocytes (PBLs). The VDJ sequence of nasal Vdelta1 T-cell receptor transcripts showed diversity and were different for each individual. Vdelta1 in the IELs were rearranged to Jdelta1 and Vdelta1 in the PBLs were rearranged not only to Jdelta1 but also to Jdelta3. Vdelta1 sequences in the IELs in the nasal mucosa showed no overlap with those in the PBLs. These results indicate that gamma/delta T cells in the nose are organ specific lymphocytes.

Adult↗
PubMed2000

Independent pathways leading to apoptotic cell death, oxidative burst and defense gene expression in response to elicitin in tobacco cell suspension culture.

We characterized pharmacologically the hypersensitive cell death of tobacco BY-2 cells that followed treatments with Escherichia coli preparations of INF1, the major secreted elicitin of the late blight pathogen Phytophthora infestans. INF1 elicitin treatments resulted in fragmentation and 180 bp laddering of tobacco DNA as early as 3 h post-treatment. INF1 elicitin also induced rapid accumulation of H2O2 typical of oxidative burst, and the expression of defense genes such as phenylalanine ammonia-lyase (PAL) gene at 1 h and 3 h after elicitin treatment, respectively. To investigate the involvement of the oxidative burst and/or the expression of defense genes in the signal transduction pathways leading to hypersensitive cell death, we analyzed the effect of several chemical inhibitors of signal transduction pathways on the various responses. The results indicated that (a) the cell death required serine proteases, Ca2+ and protein kinases, (b) the oxidative burst was involved in Ca2+ and protein kinase mediated pathways, but elicitin-induced AOS was neither necessary nor sufficient for cell death and PAL gene expression, and (c) the signaling pathway of PAL gene expression required protein kinases. These results suggest that the three signal transduction pathways leading to cell death, oxidative burst and expression of defense genes branch in the early stages that follow elicitin recognition by tobacco cells.

Algal Proteins↗
PubMed2000

Regulatory mechanism of acid secretion in the damaged stomach: role of endogenous nitric oxide.

The present article overviews the regulatory mechanism of acid secretion in the stomach after damage with taurocholate (TC), one of the bile acids. Mucosal exposure of a rat stomach to 20 mmol/L TC for 30 min caused a decrease of acid secretion with a concomitant increase in nitric oxide (NO) and prostaglandin (PG) E2 (PGE2) as well as Ca2+ in the luminal contents. Prior administration of N(G)-nitro-L-arginine methyl ester (L-NAME), as well as indomethacin, significantly attenuated the reduction of acid secretion by TC and acid secretion was even increased in the presence of L-NAME. The acid stimulatory effect of L-NAME in the damaged stomach was not mimicked by aminoguanidine and was antagonized by co-administration of L-arginine but not D-arginine. Increased NO release in the damaged stomach was suppressed by pretreatment with L-NAME or co-application of EGTA and the latter also inhibited the increase in luminal Ca2+. The enhanced acid secretory response in the presence of L-NAME was also inhibited by cimetidine, FPL-52694 (a mast cell stabilizer) or sensory deafferentation. Mucosal exposure to TC caused an increase in luminal histamine output, together with a decrease in the number of mucosal mast cells in the stomach. These changes were prevented by FPL-52694 and sensory deafferentation and were also partly suppressed by indomethacin. In addition, the acid stimulatory action of L-NAME in the damaged stomach was significantly mitigated when indomethacin was administered together with L-NAME. We conclude that: (i) damage in the stomach may activate acid a stimulatory pathway in addition to a PG-, NO- and Ca2+-dependent inhibitory mechanism, but the latter effect overcomes the former, resulting in a decrease in acid secretion; (ii) acid stimulation in the damaged stomach is mediated by histamine released from the mucosal mast cell, a process interacting with capsaicin-sensitive sensory nerves; (iii) the increase in luminal Ca2+ plays a role in increasing NO production and, hence, in regulating acid secretion; and (iv) PG may have a dual role in the regulation of acid secretion in the damaged stomach: an inhibitory effect at the parietal cell and an excitatory effect, probably through enhancing the release of mucosal histamine.

Animals↗
PubMed2000

Duodenal somatostatinoma: a case report and review of 31 cases with special reference to the relationship between tumor size and metastasis.

Somatostatinomas are rare functioning neoplasms usually arising in the pancreas and duodenum. We report a case of somatostatinoma in a 42-year-old male with neither neurofibromatosis nor somatostatinoma syndrome. A large tumor in the descending duodenum had given rise to multiple lymph node metastases. An additional 31 duodenal somatostatinoma cases were also reviewed. Most originated in the descending part of the duodenum, with the ampulla and peri-ampullary area as the most common sites (60%). Frequent manifestations were abdominal pain (25%), jaundice (25%), or cholelithiasis (19%), the latter two reflecting obstruction of the bile duct by tumors. Only two cases showed a possible somatostatinoma syndrome (6%). The tumors with metastases, lymph nodes (10) and liver (2), were significantly larger than average than those without (2.91 +/- 1.49 cm vs 1.36 +/- 0.71 cm, P < 0.05). With a cut-off point of 2.0 cm, diagnostic accuracy for metastasis was 77.78% with 87.50% specificity and 63.64% sensitivity. The smallest tumor with metastases was 0.8 cm and the largest without metastases was 3.0 cm. These results indicate that duodenal somatostatinomas are malignant by nature and the risk of metastasis significantly increases with tumors larger than 2.0 cm.

Adult↗
PubMed2000

Cardiac strangulation in a neonatal case: a rare complication of permanent epicardial pacemaker leads.

A newborn female underwent pacemaker implantation with epicardial pacing leads for the treatment of bradycardia caused by congenital atrioventricular block. At 10 months after pacemaker implantation, she was admitted with congestive heart failure. The epicardial leads were seen to encircle the heart, and myocardial ischemia was suggested. During cardiac catheterization she collapsed: emergency operation was performed, but she died on postoperative day 6.

Bradycardia↗