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M Tani

Publications and source records attributed to M Tani.

At least 181 records · Page 10Linked to original sources
PubMed1996

Protection of ischemic myocardium by inhibition of contracture in isolated rat heart.

Protection of the ischemic myocardium by pretreatment with a high dose of 2,3-butanedione monoxime (BDM) is attributed to the enhancement of glycolytic ATP production rather than to the inhibition of contracture during mild ischemia. Our objective was to investigate whether the inhibition of contracture would protect the arrested heart during prolonged ischemia. Isolated perfused rat hearts were subjected to 30 min of low-flow ischemia followed by reperfusion. Ischemic hearts were treated with BDM (5 mmol/l) after beating stopped. BDM ameliorated the increase in intraventricular pressure after ischemia without significant changes in ATP levels and with a decreased accumulation of lactate. BDM treatment accelerated the recovery of function and high-energy phosphates with reduced myocardial Ca2+ overload. The results of this study suggested that inhibition of contracture can protect the heart from ischemia-reperfusion injury.

Adenosine Triphosphate↗
PubMed1996

Effect of stepwise normalization of perfusate pH on post-ischemic functional recovery and Ca2+ overload in isolated rat hearts.

The purpose of this study was to examine whether initial acidic reperfusion after ischemia followed by stepwise normalization of perfusate pH could improve functional recovery and to assess whether this is associated with a reduction in Ca2+ overload. Isolated rat hearts were subjected to global ischemia for 25 min, followed by 30 min of reperfusion. In the control group (Group C), the perfusate pH was 7.4 throughout reperfusion. In the acidic groups, the perfusate pH was 6.8 for the first 5 min, 7.1 for the second 5 min, and 7.4 for the remainder of reperfusion. Acidic buffer was produced either by adding HCl (metabolic acidosis, Group MA) or by bubbling with gas containing 12 to 24% CO2 (respiratory acidosis, Group RA). The recovery of ventricular function, Ca2+ uptake, and energy metabolites were analyzed. Thirteen of the 15 hearts in Group C, 14 of the 15 in MA and 8 of the 15 in RA recovered regular cardiac rhythm at the end of reperfusion. In these hearts which exhibited normal rhythm, the percent recovery in developed pressure was higher (MA: 73 +/- 8, RA: 68 +/- 6, C: 51 +/- 5%, p < 0.05) and left ventricular end-diastolic pressure was lower (MA: 5.1 +/- 1.4, RA: 5.9 +/- 1.3, C: 14.2 +/- 2.7 mmHg, p < 0.05) in the acidic groups. The improved recovery was associated with a significant reduction in Ca2+ uptake which persisted with the restoration of normal pH. These results demonstrate that early acidic reperfusion enhances contractile recovery and diminishes Ca2+ overload. Moreover, these salutary effects are maintained after stepwise normalization of the perfusate pH to physiological values.

Animals↗
PubMed1996

[Clinical significance and mechanism of ST-segment changes during the post-exercise recovery period in male patients with coronary artery disease].

The treadmill exercise test (TET) is evaluated by exercise-induced ST-segment depression (delta ST). However, the depression sometimes only appears during the post-exercise period. Depression appearing only during the post-exercise period may be as useful as depression during exercise to predict coronary artery disease, but little is known about factors that may affect ST depression after exercise. The clinical significance and mechanism of post-exercise ST depression were investigated in patients with coronary artery disease. Target heart rate- or symptom-limited TET was performed in 531 male patients with definitive effort angina pectoris or myocardial infarction using the Bruce protocol. Patients were divided into four groups according to delta ST during exercise and 1-2 min after exercise; 1) no TET or post-exercise delta ST (Nn, n = 192), 2) only post-exercise delta ST (Np, n = 36), 3) only TET delta ST (Pn, n = 112), 4) both TET and post-exercise delta ST (Pp, n = 66). Patient profiles, parameters during TET, echocardiographic and coronary angiographic findings and outcome during the year after TET were compared between the Nn and Np or Pn and Pp groups. The percentage of patients treated with beta-blocker was higher in the Np than that in the Nn group (Nn: 45%, Np: 64%, p < 0.05) and systolic blood pressure declined at 1 min after exercise from peak exercise in the Nn, but not in the Np group (Nn: 175 --> 167 mmHg, p < 0.05; Np: 170 --> 170 mmHg, not significant). There was no difference in age, other parameters during TET, echocardiographic and coronary angiographic findings and outcome between the Nn and Np group. The incidence of right coronary artery stenosis and that of patients with multi-vessel disease were higher in the Pp than those in the Pn group (Pn: 41%, 58%, Pp: 65%, 73%, both p < 0.05). The occurrence of chest pain during exercise was higher in the Pp than the Pn group in spite of less delta ST at peak exercise. However, systolic blood pressure declined after exercise in the Pn group, but not in the Pp group (Pn: 164 --> 158 mmHg, p < 0.05; Pp: 166 --> 164 mmHg, not significant). These results confirmed that the clinical significance of post-exercise delta ST in patients without TET delta ST differs from that in patients with TET delta ST and suggests that post-exercise delta ST without delta ST during exercise may be associated with an abnormal response to imbalances in the cardiovascular sympathetic system in the post-exercise period rather than with myocardial ischemia.

Blood Pressure↗
PubMed1996

Effect of brief hypoxia on reperfusion arrhythmias and release of Ca2+ by rat heart homogenate blocked by ryanodine.

OBJECTIVES: We previously reported that a brief period of hypoxic perfusion (BHP) prior to ischemia in rat hearts improved functional recovery upon reperfusion with reduced Ca2+ overload. The present study was designed to determine whether the effect of BHP would be associated with a reduction in reperfusion arrhythmias and a preservation of function of the sarcoplasmic reticulum (SR). METHODS: Hearts were subjected to 40 min of global ischemia and 30 min of reperfusion after a 20 min period of oxygenated perfusion (oxygenated group: OG), or a 10 min period of oxygenation and 10 min of hypoxic perfusion (hypoxic group: HG). We evaluated the release of Ca2+ by SR blocked by ryanodine, the recovery of left ventricular function, and the reperfusion induced ventricular tachycardia/fibrillation (VT/VF). RESULTS: Functional recovery improved and the incidence and duration of reperfusion VT/VF were reduced in HG. In HG the uptake of Ca2+ in SR decreased during ischemia, but this decrease was less than that in OG. However, recovery of Ca2+ uptake after reperfusion did not differ between groups. The release of Ca2+ by SR blocked by ryanodine was inhibited in HG throughout the ischemia-reperfusion sequence. CONCLUSIONS: Observations suggest that the benefits of BHP on recovery of function and reperfusion arrhythmias were associated with a decrease in release of Ca2+ by SR blocked by ryanodine.

Animals↗
PubMed1996

Identification of human cytochrome P450 isoforms involved in the stereoselective metabolism of mianserin enantiomers.

To identify cytochrome P450 (CYP) isoform(s) involved in the major metabolic pathways of mianserin (MS) enantiomers in humans, we examined the metabolites formed from S-(+)- and R-(-)-MS using human liver microsomes and eight recombinant human CYP isoforms (i.e., CYP1A2, 2A6, 2B6, 2C9, 2C19, 2D6, 2E1 and 3A4). The mean V(max)/K(m) values of the 8-hydroxylation and N-oxidation were greater for S-(+)- than for R-(-)-MS, whereas that of the N-demethylation gave the opposite observation. When relationships were evaluated in microsomes from 10 human livers between the metabolism of substrates toward the respective CYP isoforms and stereoselective metabolism of MS at a low (5 microM) and at a high (200 microM) MS concentration, significant correlations existed in: 2-hydroxylation of desipramine vs. 8-hydroxylation of S-(+)-MS (r = 0.94, P < .01), O-deethylation of phenacetin vs. N-demethylation of S-(+)-MS (r = 0.85, P < .01) and R-(-)-MS (r = 0.69, P < .05) or N-oxidation of S-(+)-MS (r = 0.94, P < .01) at the low concentration; and 6 beta-hydroxylation of testosterone vs. three metabolic reactions of both MS enantiomers at the high concentration (r = 0.68-0.93, P < .05-.01). Quinidine inhibited the 8-hydroxylation of both enantiomers by < 40% of the respective control values. Furafylline and alpha-naphthoflavone showed a potent inhibitory effect on the N-demethylation and N-oxidation of S-(+)-MS (by up to < 50% of the respective control activities). In addition, troleandomycin inhibited the N-demethylation and N-oxidation of R-(-)-MS by < 50% of the respective control activities. Among the recombinant human CYP isoforms, CYP2D6, 2B6, 3A4 and 1A2 catalyzed the 8-hydroxylation, and CYP1A2 and 3A4 were involved exclusively in the N-oxidation, whereas CYP2B6, 2C19, 1A2, 3A4 and 2D6 showed a catalytic activity for the N-demethylation, for either or both of MS enantiomers. Taken together, the 8-hydroxylation for both MS enantiomers is mediated mainly via CYP2D6, whereas the N-demethylation for both the enantiomers and N-oxidation for S-(+)-MS are catalyzed mainly via CYP1A2. The two in vitro experiments suggested that CYP3A is involved to a certain extent in each of the stereoselective MS metabolic pathways.

Cytochrome P-450 Enzyme System↗
PubMed1996

In situ hybridization analysis of glial fibrillary acidic protein mRNA reveals evidence of biphasic astrocyte activation during acute experimental autoimmune encephalomyelitis.

Reactive astrogliosis is a prominent pathological feature of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis. It is characterized by hypertrophy of astrocytes with increased content of glial fibrillary acidic protein (GFAP.) Studies of reactive astrocytes in acute experimental autoimmune encephalomyelitis have been complicated by the observation that the diffuse increase in GFAP immunohistochemical staining at the onset of central nervous system inflammation does not parallel the gradual increase in GFAP content probably because tissue edema enhances GFAP immunostaining. To characterize changes in GFAP expression, we performed in situ hybridization at 3- to 7-day intervals during the course of acute murine experimental autoimmune encephalomyelitis. We found a biphasic course of GFAP expression: an early phase of astrocyte reaction surrounding perivascular inflammatory cuffs and submeningeal infiltrates at the onset of central nervous system inflammation and clinical disease and a later phase of increased GFAP mRNA expression in regions of demyelination during resolution of inflammation and clinical improvement. IP-10, a member of a family of proinflammatory chemoattractant cytokines called chemokines, was expressed by astrocytes in a similar distribution as those expressing increased GFAP mRNA in the early phase of inflammation but was no detected in astrocytes in the later phase of activation. These results indicate that location and function of reactive astrocytes may vary during the course of immune-mediated demyelination.

Acute Disease↗
PubMed1996

Primary carcinoma of the gallbladder: role of external beam radiation therapy in patients with locally advanced tumor.

BACKGROUND/AIM: Several reports have demonstrated that occasional long-term survival might be obtained with external beam radiation therapy in patients with gallbladder cancer. However, there are few reports which evaluate the local effect of irradiation. The aim of our study was to investigate the local effect of radiation therapy. and to evaluate its role for locally advanced gallbladder cancer. PATIENTS AND METHODS: Twenty-two patients with locally advanced gallbladder cancer were treated with high-dose external beam radiation therapy. Tumor resection was performed in 5 patients, palliative surgery in 5, and the remaining 12 patients were treated by radiation therapy alone. RESULTS: Overall survival was 36% at 1 year, 18% at 3 years and 14% at 5 years. All but 2 patients developed local recurrence and died of disease at 1 to 99 months after radiation therapy. Among 17 patients who had not undergone tumor resection, partial response was obtained in 4 patients and no response in 13. Survival times in patients who achieved partial response were 14, 26, 47 and 99 months, whereas those of no response were 1 to 12 months with a mean of 4.8 months. Survival between these 2 groups (partial vs. no response) showed significant difference (p = 0.0008, logrank test). CONCLUSION: It is concluded that high-dose external beam radiation therapy could improve survival in some patients with unresectable gallbladder cancer.

Adenocarcinoma↗
PubMed1995

Clinical significance of quantitative analysis of carcinoembryonic antigen assessed by flow cytometry in fresh human gastric cancer cells.

The expression of carcinoembryonic antigen(CEA) on tumor cells freshly excised from 51 patients with gastric cancer was studied using flow cytometry. The expression of CEA by flow cytometry was more quantitative than that by immunohistochemical staining. There was no relationship between the fluorescence intensity assessed by flow cytometry and serum CEA levels, except for patients with a high titer of serum CEA. The patients with high grade CEA expression on tumor cells by flow cytometry had poor prognoses, compared to patients with low CEA expression in undifferentiated gastric cancer. Thus, it is suggested that the quantitative CEA expression on tumor cells by flow cytometry could be a useful prognostic marker in postoperative gastric cancer patients.

Adenocarcinoma↗
PubMed1995

Generation of CD4+ cytotoxic T lymphocytes stimulated by immobilized anti-CD3 monoclonal antibody and interleukin-2 in cancer patients.

The proliferation of autologous tumor-reactive cytotoxic T lymphocytes (CTL), induced by autologous mixed lymphocyte tumor-cell culture, was remarkably enhanced by activation with immobilized anti-CD3 monoclonal antibody (MAb) and interleukin-2 (IL-2), as compared with IL-2 alone. The activated CTL exhibited high cytotoxicity against autologous tumor cells. Cytotoxicity against autologous tumor cells was inhibited by anti-HLA-DR MAb. In negative selection with immunomagnetic beads, cytotoxicity against autologous tumor cells was inhibited by the elimination of CD4+ cells. The major cell-surface antigens of the activated CTL were CD3+, CD4+, CD25+, CD45RO+ and CD45RA-, suggesting helper T cells, and the activated CTL produced IL-2. It is concluded that the CTL activated by immobilized anti-CD3 MAb and IL-2 were CD4 cells that had both killer and helper functions. Our findings indicate that adoptive immunotherapy using these activated CTL would be effective in cancer patients.

Antibodies, Monoclonal↗
PubMed1995

An adenoviral vector can transfer lacZ expression into Schwann cells in culture and in sciatic nerve.

Although a number of genetic defects in the P0, peripheral myelin protein-22, and connexin-32 genes recently were shown to cause the demyelinating forms of Charcot-Marie-Tooth disease, there is yet no effective treatment for these patients. Recent studies showed that replication defective adenoviral vectors can efficiently introduce genes into muscle, brain, lung, and other tissues, suggesting that this vector system may be useful for the treatment of a number of genetic diseases. In this work, we demonstrated that a replication deficient adenovirus expressing the Escherichia coli beta-galactosidase gene (AdCMVLacZ) can introduce genes into Schwann cells, in culture as well as in sciatic nerve. Schwann cells cultured at a multiplicity of infection of 250:1 did not demonstrate cytopathic effects. Following injection of AdCMVLacZ into sciatic nerve of rats, lacZ-expressing, myelinating Schwann cells could be detected for at least 45 days. These data suggest that in the future, these vectors may be useful both in perturbing Schwann cell gene expression and in designing therapies for the treatment of Charcot-Marie-Tooth disease.

Adenoviruses, Human↗
PubMed1995

Central nervous system chemokine mRNA accumulation follows initial leukocyte entry at the onset of acute murine experimental autoimmune encephalomyelitis.

Central nervous system (CNS) expression of two chemokine mRNAs, encoding monocyte chemoattractant protein-1 (MCP-1) and IFN-gamma-inducible protein (IP-10), was previously shown to be closely related to the onset of clinical signs of murine experimental autoimmune encephalomyelitis (EAE). Chemokine mRNAs accumulated in a striking, transient burst within astrocytes, near inflammatory leukocyte infiltrates. It remained unclear if chemokines functioned to initiate leukocyte entry into CNS tissues, or to amplify the intrathecal inflammatory reaction. To address this issue, we determined the expression of chemokine mRNAs at the earliest evidence of CNS immune-mediated inflammation. For these experiments, mice were sacrificed in pairs at varying times after immunization. Only one member of each pair was symptomatic for EAE at the time of sacrifice. Symptom presence correlated well with histological inflammation at the time of sacrifice. RNA was prepared from two CNS sites, brain and spinal cord, and expression of chemokine mRNAs was analyzed by a sensitive and quantitative reverse transcriptase/polymerase chain reaction dot-blot hybridization assay. CNS expressions of MCP-1 and IP-10 gene were correlated tightly with histological inflammation; indeed, chemokine expression was never detected in the absence of leukocyte infiltrates. In situ hybridizations showed that astrocytes expressed chemokine transcripts. These findings provide new information about mechanisms controlling chemokine mRNA expression during immune-mediated inflammation in EAE and are consistent with a role for chemokines as amplifiers of CNS inflammatory reactions.

Animals↗
PubMed1995

Left ventricular dimensions and autonomic balance during head-up tilt differ between patients with isoproterenol-dependent and isoproterenol-independent neurally mediated syncope.

OBJECTIVES: This study sought to elucidate differences in mechanisms of neurally mediated syncope between patients with syncope induced by head-up tilt alone and those requiring isoproterenol infusion to induce syncope during head-up tilt. BACKGROUND: Some patients with neurally mediated syncope require isoproterenol to induce syncope during head-up tilt (isoproterenol dependent), and others do not (isoproterenol independent). Differences in mechanisms between these two groups have not been well elucidated. METHODS: A 60 degrees head-up tilt test was performed in 13 patients with isoproterenol-independent syncope (Group I, mean [+/- SD] age 28 +/- 12 years), 14 patients with isoproterenol-dependent syncope (Group II, mean age 34 +/- 14 years) and 20 control subjects without syncope (Group III, mean age 32 +/- 12 years). Left ventricular size and contractility were determined by echocardiography, and sympathovagal balance was determined with power spectral analysis of heart rate variability using a maximal entropy method. RESULTS: Group I patients had smaller left ventricular dimensions than Group II and III during baseline tilt. During head-up tilt with isoproterenol infusion (0.01 to 0.04 microgram/kg body weight per min), left ventricular dimensions decreased to the same extent in Groups II and III, but fractional shortening was greater in Group II than in Group III at the end of the tilt. The ratio of low (0.05 to 0.15 Hz) to high frequency (0.15 to 1.0 Hz) component became greater in Group I than in Groups II and III during the last period of baseline tilt. However, the ratio was greater in Group II than in Group III during the last period of the tilt with isoproterenol. CONCLUSIONS: Patients with isoproterenol-independent syncope had an exaggerated decrease in left ventricular size and sympathetic predominance preceding syncope during head-up tilt. In contrast, in patients with isoproterenol-dependent syncope, similar changes in autonomic nervous balance were evident only during isoproterenol infusion in addition to head-up tilt.

Adolescent↗
PubMed1995

Extracellular antigens of Actinobacillus actinomycetemcomitans Y4 in severe alveolar bone loss patients studied by two-dimensional electrophoresis and western blots.

The human immune response to extracellular substances (ES) from Actinobacillus actinomycetemcomitans Y4 were analyzed. Twenty-nine periodontal patients with generalized severe alveolar bone loss and 13 healthy volunteers were examined for serum IgG antibody titers against ES. Among the patients, 17 had higher antibody titers than healthy individuals (high-titer patients) but the remainder (low-titer patients) did not. Two-dimensional electrophoresis (2DE) and Western blots demonstrated that two proteins (40 and 37 kDa) and three smeared substances reacted with IgGs from high-titer patients, but not with IgGs from healthy volunteers. The low-molecular-mass smear at the acid side reacted with over 90% of all patients. This smear reacted with anti-A. actinomycetemcomitans lipopolysaccharide (LPS) monoclonal antibody which recognized LPS from each A. actinomycetemcomitans serotype. The high molecular mass smear at the acid side might be serotype-specific O-antigens of LPS. Another high molecular mass smear which located from the alkaline to the neutral side reacted with anti-serotype-b-specific capsular polysaccharide monoclonal antibody. Moreover, the 40- and 37-kDa proteins reacted with this anti-capsular polysaccharide antibody. This results suggested that 40- and 37-kDa proteins which reacted with 100% or 88% of high-titer patients might be glycoproteins linked with capsular polysaccharide.

Actinobacillus Infections↗
PubMed1995

Identification of human CYP isoforms involved in the metabolism of propranolol enantiomers--N-desisopropylation is mediated mainly by CYP1A2.

1. Studies using human liver microsomes and six recombinant human CYP isoforms (i.e. CYP1A2, 2A6, 2B6, 2D6, 2E1 and 3A4) were performed to identify the cytochrome P450 (CYP) isoform(s) involved in the ring 4-hydroxylation and side-chain N-desisopropylation of propranolol enantiomers in humans. 2. alpha-Naphthoflavone and 7-ethoxyresorufin (selective inhibitors of CYP1A1/2) inhibited the N-desisopropylation of R- and S-propranolol by human liver microsomes by 20 and 40%, respectively, while quinidine (a selective inhibitor of CYP2D6) abolished the 4-hydroxylation of both propranolol enantiomers almost completely. In contrast, sulphaphenazole (CYP2C8/9 inhibitor), S-mephenytoin (CYP2C19 inhibitor), troleandomycin (CYP3A3/4 inhibitor) and diethyldithiocarbamate (CYP2E1 inhibitor) elicited only weak inhibitory effects on propranolol metabolism via the two measured metabolic pathways. 3. Significant (P < 0.01) correlations were observed between the microsomal N-desisopropylation of both propranolol enantiomers and that for the O-deethylation of phenacetin among the 11 different human liver microsome samples (r = 0.98 and 0.77 for R- and S-propranolol, respectively). A marginally significant (r = 0.60, P congruent to 0.05) correlation was also observed between N-desisopropylation of S-, but not of R-propranolol and the 4'-hydroxylation of S-mephenytoin. No significant correlations were observed between the N-desisopropylation of propranolol enantiomers and the 2-hydroxylation of desipramine, the hydroxylation of tolbutamide or the 6 beta-hydroxylation of testosterone. 4. Significant (P < 0.01) correlations were observed between the microsomal 4-hydroxylation of R- and S-propranolol and the 2-hydroxylation of desipramine (r = 0.85 and 0.98, respectively). A weak (r = 0.66), albeit significant (P < 0.05) correlation was observed between the 4-hydroxylation of R-, but not of S-propranolol and the hydroxylation of tolbutamide. No significant correlations were observed between the 4-hydroxylation of propranolol enantiomers and the oxidation of other substrates for CYP1A2, 2C19, and 3A3/4. 5. Recombinant human CYP1A2 and CYP2D6 exhibited comparable catalytic activity with respect to the N-desisopropylation of both propranolol enantiomers; only expressed CYP2D6 exhibited a marked catalytic activity with respect to the 4-hydroxylation of both propranolol enantiomers.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1995

The effects of selective serotonin reuptake inhibitors and their metabolites on S-mephenytoin 4'-hydroxylase activity in human liver microsomes.

The inhibitory effects of four selective serotonin reuptake inhibitors (SSRIs), fluoxetine, sertraline, paroxetine and citalopram, and three metabolites (norfluoxetine, demethylcitalopram and didemethylcitalopram), on S-mephenytoin 4'-hydroxylation activities in human liver microsomes were studied. The 4'-hydroxylation of S-mephenytoin, a representative substrate toward CYP2C19, was competitively inhibited by all the SSRIs and their metabolites studied. The mean Ki values of fluoxetine, norfluoxetine, sertraline, paroxetine, citalopram, demethylcitalopram and didemethylcitalopram were 5.2, 1.1, 2.0, 7.5, 87.3, 55.8 and 7.7 microM, respectively. The findings suggest that some SSRIs and their metabolites with a low Ki value (e.g., fluoxetine, norfluoxetine) may reduce the clearance of drugs metabolized by this isoform of P450, thereby resulting in a possible drug-drug interaction, when administered simultaneously. In addition, SSRIs and their metabolites examined herein may be substrates toward CYP2C19.

Aryl Hydrocarbon Hydroxylases↗
PubMed1995

Detection of antigenic proteins in Porphyromonas gingivalis using two-dimensional electrophoresis and western blots.

Using two-dimensional (2D) electrophoresis and western blot assay, we analyzed antigenic proteins in Porphyromonas gingivalis uniquely recognized by antibodies in sera of periodontitis subjects. Proteins in the total membrane fraction of P. gingivalis 381 were resolved into at least 70 protein spots by 2D electrophoresis. In the gel stained with silver, the substance around 47 kDa protein on the acidic side (at an isoelectric point of about 4.5) was stained as a smear. Antigenic substances were characterized using purified IgGs from sera of 16 adult periodontitis (AP), 19 rapidly progressive periodontitis (RPP) and 14 periodontally healthy volunteers. Western blots demonstrated that 75 kDa protein reacted with IgGs from 75% of AP patients (p < 0.001), the antigenic substance around acidic 47 kDa protein reacted with IgGs from 81.3% of AP (p < 0.01) and 68.4% of RPP patients (p < 0.01) and the acidic 47 kDa protein reacted with 87.5% of AP (p < 0.01) and 78.9% of RPP patients (p < 0.01). The reaction frequency was significantly different from that of the healthy volunteers. Also 51 kDa and 41 kDa proteins reacted with 47 and 43 of 49 IgG samples, respectively. The substance around acidic 47 kDa protein reacted with mouse antiserum to P. gingivalis-LPS. After treatment with pronase or heat, the antigenic reactions disappeared not only from the proteins, but also from the area around the acidic 47 kDa protein. When the fraction was digested with lipase, the antigenic reaction of the area decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Hypocholesterolemic effect of 5 beta-cholane-3 alpha,7 beta,24-triol-24- sulfate in hamsters.

We studied the effect of 5 beta-cholane-3 alpha,7 beta,24-triol-24-sulfate (UDC-O-sulfate) on ileal active transport of cholyltaurine, on hepatic cholesterol 7 alpha-hydroxylase activity, on serum and liver cholesterol levels, on intestinal absorption of cholesterol, and on bile salt composition of gallbladder bile in hamsters. Experiments using the everted gut sacs show that UDC-O-sulfate inhibits the ileal active transport of cholyltaurine. In experiments feeding the diets with either UDC-O-sulfate, cholesterol, or both to hamsters, the addition of UDC-O-sulfate to the cholesterol-enriched diet reduced the elevation of serum and liver cholesterol levels caused by cholesterol feeding. Supplementation with UDC-O-sulfate to the standard diet was likely to reduce serum and liver cholesterol levels. Cholesterol 7 alpha-hydroxylase activity was higher in the two UDC-O-sulfate supplemented groups than in the two corresponding groups, the standard diet group and the cholesterol enriched diet group, respectively. Addition of UDC-O-sulfate to the standard and cholesterol diets did not change intestinal absorption of cholesterol. The change of the bile salt composition in hamsters fed UDC-O-sulfate may also suggest that the bile alcohol sulfate inhibits the intestinal absorption of endogenous bile salts. Hence the hypocholesterolemic activity of dietary UDC-O-sulfate is thought to be the effect of the partial interruption of the enterohepatic circulation of endogenous bile salts.

Animals↗