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S Kitagawa

Publications and source records attributed to S Kitagawa.

At least 145 records · Page 8Linked to original sources
PubMed1995

Induction of monocyte chemoattractant protein-1 synthesis in human monocytes during transendothelial migration in vitro.

Monocyte chemoattractant protein-1 (MCP-1, or monocyte chemotactic and activating factor) plays important roles in the recruitment of monocytes and thus in the development of atherosclerosis. In this study, we determined whether MCP-1 synthesis was induced by the cellular interaction between monocytes and endothelial cells during the process of transendothelial migration. We found that when human peripheral blood monocytes (2.5 x 10(6) cells) and umbilical vein endothelial cells (HUVECs; 5.0 x 10(5) cells) were cocultured for 5 hours, 7.9 ng/mL MCP-1 was secreted into the medium, whereas when the two were cultured separately, MCP-1 levels were 1.0 and 0.9 ng/mL, respectively. Furthermore, the use of interleukin-1 beta (IL-1 beta)-pretreated HUVECs in cocultures induced twice the levels of MCP-1 as in unstimulated HUVEC culture. Conditioned medium had transendothelial chemotactic activity for monocytes, and this activity was completely abolished by addition of anti-MCP-1 antibody. Although MCP-1 mRNA levels were very low or undetectable in HUVECs or monocytes alone, message could be detected after 2 hours of coculture in total mRNA preparations from both monocytes and HUVECs. mRNA levels increased by 4 hours and had declined slightly by 24 hours. The rapid induction of message suggests that cell contact between monocytes and HUVECs induces the de novo synthesis of MCP-1 protein. Anti-interleukin (IL)-1 alpha/beta and anti-tumor necrosis factor-alpha antibodies, or anti-lymphocyte function-associated antigen-1 and very late antigen-4 antibodies, had little or no inhibitory effects on MCP-1 secretion by cocultures.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Adhesion Molecules↗
PubMed1995

Parvovirus infection and generalized edema in adults.

We describe the clinical and laboratory findings of 7 adult patients with serological evidence of recent human parvovirus B19 (HPV) infection who presented with generalized edema. Six of the 7 patients had household contact with children with erythema infectiosum and had flu-like symptoms before visiting hospital. The interval between the flu-like episode and the development of edema ranged from 4 to 13 days (mean 7.0). In all 7 patients, there was serological confirmation of recent HPV infection, and all showed the development of edema following HPV infection without urine abnormalities or anemia. Two patients presented hypocomplementemia, and two patients showed signs of congestive heart failure. HPV may be considered a causative agent of generalized edema not only in the fetus but also in adults and HPV infection should be included in the differential diagnosis of generalized edema formation.

Adult↗
PubMed1995

Severe hypercalcemia and polyuria in a near-drowning victim.

A 73-year-old man was admitted because of near-drowning in a hot springs bath. Transient severe hypercalcemia and polyuria were seen during the first hospital day. It seemed that the hypercalcemia was due to acute intoxication from calcium contained in the water of the spring absorbed mainly through the alveoli. To our knowledge, this is the first case of acute hypercalcemia complicating a near-drowning in a hot spring. Analysis of serum and urine electrolytes during the polyuric phase revealed saline diuresis, which was probably due to interference by the hypercalcemia of the reabsorption of sodium and free water.

Aged↗
PubMed1995

Decreased expression of protein phosphatase type 2A in HL-60 variant (HL-60RAr) cells resistant to induction of cell differentiation by all-trans retinoic acid.

To evaluate the molecular basis for susceptibility of the cell differentiation induced by all-trans retinoic acid (ATRA), we examined biochemical activities and expression of protein phosphatases type 1 (PP1) and type 2A (PP2A) from HL-60 cells that are susceptible to differentiation induced by ATRA and HL-60RAr cells, HL-60 variant cells that are resistant to such induction. One nM of calyculin-A (CAL-A) achieved the enhancement of granulocytic differentiation in ATRA-treated HL-60 (1 microM) cells. ATRA exerted no differential action in HL-60RAr cells, but when used in combination with CAL-A, the differential activity was partly resumed at functional and phenotypic levels without change in morphology. The phosphatase activity in the cytosol from HL-60RAr cells was 50% of that from parental HL-60 cells, but the enzyme activities in either membrane or nuclear fractions showed similar values. The decreased phosphatase activity in the cytosol of HL-60RAr cells was mainly due to the decreased expression of the PP2A catalytic subunit. This low level of PP2A protein was reflected at a relative deficiency in expression of the PP2A beta gene in HL-60RAr cells. The exposure to 1 microM ATRA resulted in downregulation of PP2A catalytic subunit protein in HL-60 cells, but ATRA did not affect PP2A expression in HL60RAr cells. Both cell lines expressed the proteins of each PP1 catalytic subunit isozyme (i.e., PP1 alpha, PP1 gamma, and PP1 delta) at comparable levels. ATRA treatment had no effect on the levels of PP1 isozymes. Our results show a correlation between the extent of PP2A expression and the response of HL-60 and HL-60RAr cells to the differentiative effects of ATRA.

Blotting, Northern↗
PubMed1995

[Prevalence of urinary incontinence among institutionalized persons aged 60 and over in Japan].

In order to estimate the prevalence of persons experiencing urinary incontinence among the institutionalized aged 60 and over in Japan, a questionnaire survey was conducted in 16 prefectures in February 1991. The questionnaires were distributed and collected by the nurses in hospitals and in other facilities. A total of 10,022 residents were asked to answer a questionnaire on their urinary incontinence condition and 9,798 responses were analysed. The main results were as follows; 1) The prevalence rate of urinary incontinence occurring almost daily in hospitalized persons aged 60 and over was 23.3% for men, 23.8% for women. 2) The prevalence rate of urinary incontinence occurring almost daily in institutionalized persons aged 60 and over in special nursing homes was 64.2% of the aged 60 and over for men, 67.9% for women. 3) The prevalence of urinary incontinence increased with age for both sexes especially in hospitalized persons. 4) The 95% confidence interval estimate for the number of the hospitalized over 60 years old suffering from almost daily urinary incontinent incidents was estimated to be from 31,000 to 113,000 in men and from 60,000 to 182,000 in women. 5) The 95% confidence interval estimate for the number of the institutionalized in special nursing home over 60 years old suffering from almost daily urinary incontinent incidents was estimated to be from 34,000 to 50,000 in men and from 97,000 to 119,000 in women. 6) The 95% confidence interval estimate for the number of the institutionalized over 60 years old suffering from almost daily urinary incontinent incidents was estimated to be from 318,800 to 570,600 in both sexes. 7) A random sampling survey is required to elucidate the actual state of prevalence in all generations. 8) Future research should emphasize the assessment of preventive and medical interventions, as incontinence is preventable and medical and surgical treatment options are available.

Age Factors↗
PubMed1995

Stimulation and priming of human neutrophils by IL-1 alpha and IL-1 beta: complete inhibition by IL-1 receptor antagonist and no interaction with other cytokines.

Together, interleukin-1 alpha (IL-1 alpha) and IL-1 beta primed human neutrophils for enhanced release of superoxide (O2-) stimulated by chemotactic peptide, chemokine, and plant lectin, and alone, each triggered O2- release in a dose-dependent manner. The maximal priming and triggering effect was obtained by high concentrations (50 to 500 ng/mL) of IL-1 alpha or IL-1 beta, though IL-1 beta was more effective than IL-1 alpha at suboptimal concentrations. Priming effect of IL-1 was very rapid and maximal within 10 minutes, whereas O2- release triggered by IL-1 was gradual and continued for 90 to 120 minutes. Combined stimulation of human neutrophils with IL-1 plus granulocyte colony-stimulating factor (G-CSF) or granulocyte-macrophage CSF (GM-CSF) resulted in additive priming effect, and combined stimulation of neutrophils with IL-1 plus G-CSF, GM-CSF, or tumor necrosis factor (TNF) resulted in additive triggering effect, even when the maximal concentration of each cytokine was used. These priming and triggering effects of IL-1 alpha and IL-1 beta on the respiratory burst in human neutrophils were completely inhibited by IL-1 receptor antagonist (IL-1ra). Furthermore, only the net effect of IL-1 was inhibited by IL-1ra, even when human neutrophil was stimulated with IL-1 plus other cytokines to release O2-. Present results indicate that IL-1 does stimulate the respiratory burst activity in human neutrophils via receptor-mediated mechanism and suggest that the post-IL-1-receptor signaling pathways linked to the activation system of the respiratory burst are independent from those utilized by other cytokines in human neutrophils.

Adult↗
PubMed1995

Effects of endogenous endothelial interleukin-8 on neutrophil migration across an endothelial monolayer.

OBJECTIVE: Recent studies suggest that interleukin-8 (IL-8) is involved in the neutrophil infiltration of subendothelial myocardial tissue in the ischaemia/reperfusion injury associated with acute myocardial infarction. The aim of this study was to investigate the effects of IL-8 on transendothelial neutrophil migration using an in vitro three dimensional double chamber migration assay system. METHODS: Human neutrophils were incubated with human endothelial cell monolayers for 1 h, and adherent and migrated neutrophils were then counted. Expression of IL-8 mRNA and secretion of its protein by endothelial cells were analysed respectively by northern blotting and ELISA. RESULTS: Recombinant human (rh) IL-8 (50 ng.ml-1) placed in the lower compartment significantly increased neutrophil adhesion 1.7-fold and transmigration 2.3-fold, compared with control conditions using medium alone in both compartments. In contrast, rh IL-8 (50 ng.ml-1) in the upper compartment significantly inhibited neutrophil adhesion and transmigration by 53% and 61% respectively compared with controls. Neutrophil adhesion and transmigration was dependent on the IL-8 concentration gradient between upper and lower compartments. Unstimulated endothelial cells showed no IL-8 expression, but endothelial cells pretreated with IL-1 beta (25 U.ml-1) markedly induced endogenous IL-8 mRNA and protein accumulation. When endothelial cells were cocultured with neutrophils, enhanced endogenous IL-8 production was observed. Pretreatment of endothelial cells with IL-1 beta for 4 and 24 h increased neutrophil transmigration 2.8-fold and 3.0-fold respectively, compared with unstimulated endothelial cells. The addition of anti-IL-8 monoclonal antibody (12.5 micrograms.ml-1) to the upper compartment with IL-1 beta-pretreated endothelial cells further enhanced transmigration from 2.8- to 3.3-fold and from 3.0- to 4.3-fold respectively. CONCLUSIONS: Endogenous endothelial IL-8, secreted from activated endothelial cells into the apical side of endothelial cell monolayers, has an inhibitory effect on transendothelial migration of neutrophils, suggesting that IL-8 may prevent excessive neutrophil infiltration of myocardial tissue from circulating blood in the reperfusion injury associated with acute myocardial infarction.

Blotting, Northern↗
PubMed1995

Peutz-Jeghers syndrome.

Peutz-Jeghers syndrome is inherited as an autosomal dominant trait with variable incomplete penetrance. Patients with Peutz-Jeghers syndrome characteristically have hamartomatous polyps throughout their entire gastrointestinal tract, particularly in the small bowel, and mucocutaneous hyperpigmentation involving the lips, oral cavity, and skin. Although the intestinal hamartomatous polyps have a lower incidence of malignant change in the gastrointestinal tract than do adenomatous polyps, recent information suggests that the overall neoplastic transformation from Peutz-Jeghers syndrome is not a rare event.

Adenomatous Polyps↗
PubMed1995

[A case of carcinoma of the pancreas head associated with celiac axis compression syndrome].

We report a 51-year-old woman with pancreas head cancer associated with celiac axis compression syndrome (CACS). Angiography demonstrated that the inferior pancreatico-duodenal artery and the posterior superior pancreaticoduodenal artery dilated significantly. The lateral view of aortography showed compression of the celiac axis. We performed pancreatoduodenectomy safely with cutting the median arcuate ligament. Postoperative course was uneventful. Postoperative angiography demonstrated improvement of the compression. In CACS, celiac axis is compressed by the median arcuate ligament (seichu kyujo jintai in Japanese), not by the medial arcuate ligament (naisoku kyujo jintai in Japanese).

Abdominal Pain↗
PubMed1994

Release of endogenous ATP from the caudal artery in rats with arteriosclerosis.

Noradrenaline significantly increased (by a prazosin-sensitive mechanism) the overflow of ATP and its metabolites from the caudal arteries of rats treated with excess vitamin D2 and a high-cholesterol diet (arteriosclerotic rats), although the amount of the overflow was smaller than that in the normal rats. The arteries from the arteriosclerotic rats showed a marked increase in the calcium content and there was a significant negative correlation between the noradrenaline-induced overflow of ATP and the arterial calcium content. These findings indicate that ATP release from arteriosclerotic rat caudal arteries mediated by alpha 1-adrenoceptors is impaired in proportion to the extent of arterial calcification.

Adenosine Diphosphate↗
PubMed1994

Involvement of adhesion molecules in human monocyte adhesion to and transmigration through endothelial cells in vitro.

Although the accumulation of monocyte-derived foam cells in the subendothelium is a key step in early atherogenesis, the mechanism responsible for monocyte adhesion to and subsequent transmigration through endothelial cells (ECs) has not been defined fully. We investigated the kinetics and the role played by adhesion molecules in the adhesion and transmigration of human monocytes using an in vitro three-dimensional model system comprising ECs cultured on collagen gels. Monocyte adhesion to untreated EC layers increased with time, reached a maximum after 3 h, and then declined. Monocyte transmigration through untreated EC layers also increased with time and reached a plateau after 3-4 h. Prestimulation of ECs with interleukin-1 beta (IL-1 beta; 25 U/ml) for 4 h enhanced monocyte adhesion (40.7 +/- 1.4%) and transmigration (37.9 +/- 1.6%) significantly compared with the value for untreated EC layers. In unstimulated EC layers, anti-leukocyte function-associated antigen-1 (LFA-1) plus anti-intercellular adhesion molecule-1 (ICAM-1) monoclonal antibodies (mAbs) inhibited monocyte adhesion and transmigration significantly by 19% and 20%, respectively, whereas anti-very late antigen-4 (VLA-4) plus anti-vascular cell adhesion molecule-1 (VCAM-1) mAbs did not. In IL-1 beta-stimulated EC layers, anti-LFA 1 plus anti-ICAM-1 mAbs inhibited the adhesion and transmigration by 32% and 30%, respectively and anti-VLA-4 plus anti-VCAM-1 mAbs did so by 18% and 27%, respectively. These results suggest that the monocyte-EC interaction in unstimulated ECs is mediated, in part, by the LFA-1-ICAM-1 pathway and in IL-1 beta-stimulated ECs, in part, by both LFA-1-ICAM-1 and VLA-4-VCAM-1 pathways.

Antibodies, Monoclonal↗
PubMed1994

NG-nitro-L-arginine-resistant endothelium-dependent relaxation induced by acetylcholine in the rabbit renal artery.

Studies were designed to determine the extent of the involvement of endothelium-derived relaxing factor(s) other than nitric oxide (NO) in vascular relaxation in response to acetylcholine (ACh) in the rabbit renal artery. ACh (10(-9)-10(-6) M) induced concentration-dependent relaxation of isolated endothelium-intact arterial rings preconstricted with noradrenaline. NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase, partly inhibited the ACh-induced endothelium-dependent relaxation, whereas it almost completely abolished the production of cyclic-3', 5'-guanosine monophosphate (cGMP) in these rings in response to ACh. Methylene blue, an inhibitor of guanylate cyclase, had an essentially similar effect to L-NAME on the relaxation. Indomethacin, an inhibitor of cyclooxygenase, had no effect. High concentrations of potassium chloride (to inhibit endothelium-dependent hyperpolarization), tetraethylammonium (TEA) or 4-aminopyridine (4-AP), a voltage-dependent or Ca(2+)-dependent K+ channel blocker, partly inhibited the relaxation while, in contrast, glibenclamide, an ATP-sensitive K+ channel blocker, had no effect. Ouabain, an inhibitor of Na+, K(+)-ATPase, also partly inhibited the ACh-induced relaxation, especially the higher concentration effect. Application of L-NAME together with ouabain, TEA, or a high concentration of potassium chloride completely abolished the relaxation. These results suggest that ACh-induced endothelium-dependent relaxation in the rabbit renal artery is mediated by NO, and by an other factor(s), which relaxes the vascular smooth muscle through opening K+ channels other than ATP-sensitive ones, and/or through the activation of a Na+, K(+)-pump.

Acetylcholine↗
PubMed1994

In vivo and in vitro analysis of skin penetration enhancement based on a two-layer diffusion model with polar and nonpolar routes in the stratum corneum.

In vitro and in vivo skin penetration of three drugs with different lipophilicities and the enhancing effects of 1-geranylazacycloheptan-2-one (GACH) were studied in rats. In vivo drug absorption profiles obtained by deconvolution of urinary excretion profiles were compared to the corresponding in vitro data obtained with a diffusion experiment. In vivo skin penetration of lipophilic butylparaben was considerably greater than that observed in vitro, while hydrophilic mannitol and acyclovir showed low penetration in both systems without GACH pretreatment. On the other hand, GACH enhanced mannitol and acyclovir penetration, especially in the in vivo system. Analysis of absorption profiles, using a two-layer skin model with polar and nonpolar routes in the stratum corneum, suggested that the diffusion length of a viable layer (viable epidermis and dermis) was shorter in vivo than in vitro and the effective area of the polar route in the stratum corneum was larger in vitro without GACH pretreatment. GACH increased the partitioning of acyclovir into the nonpolar route to the same extent in both systems. In addition, GACH increased the effective area of the polar route in vivo, probably because of enhanced water permeability; however, this effect was smaller in vitro since the stratum corneum was already hydrated even without GACH pretreatment.

Acyclovir↗
PubMed1994

Differences in endothelium-dependent relaxation in various arteries from Watanabe heritable hyperlipidaemic rabbits with increasing age.

1. Endothelium-dependent relaxation in response to acetylcholine (ACh) and the calcium ionophore A23187 was examined in aorta, coronary, basilar and renal arteries isolated from Watanabe heritable hyperlipidaemic (WHHL) rabbits of 2, 6 and 12 months of age, with normolipidaemic heterozygous WHHL rabbits as controls. 2. In the rings of WHHL rabbit aortae and coronary arteries preconstricted with vasoconstrictors, endothelium-dependent relaxation in response to ACh was attenuated with age compared to the heterozygous WHHL rabbits. A significant negative correlation was found between the total cholesterol content and the relaxation response to ACh in the aortae or coronary arteries from 6 and 12 month old WHHL rabbits. 3. In the rings of basilar arteries, endothelium-dependent relaxations to ACh were not modified with age. Similarly, in the rings of renal arteries, the relaxation response to ACh was not changed with age, but in the 6 and 12 month preparations, after the age of 6 months, a contraction following the relaxation appeared at higher concentrations of ACh (10(-7) to 10(-6) mol/L). The contraction was endothelium-dependent and inhibited by indomethacin. 4. A23187-induced endothelium-dependent relaxations were also markedly attenuated in the aorta and significantly in the coronary artery with age. 5. Endothelium-independent relaxation to sodium nitroprusside was not changed in all arteries from WHHL rabbits of different ages. 6. These findings indicate that in the aorta and coronary artery of the WHHL rabbit, the endothelium-dependent relaxation to ACh and A23187 becomes impaired with increasing age (i.e., with the progression of cholesterol deposition in the arterial wall) but is preserved in the basilar and renal artery.

Acetylcholine↗
PubMed1994

[Studies based on biophysical chemistry on the mechanisms of modification of platelet functions by membrane reactive compounds].

Physico-chemical properties of the blood platelets and their membrane were investigated by fluorescence analysis and electron spin resonance spectrometry. Fluorescence analysis using diphenylhexatriene and its ionic derivatives revealed that the inner membrane compartment of the platelets is more fluid than the outer layer of the plasma membrane. Further, the relationship between the increase in membrane fluidity by membrane reactive compounds such as alcohols and their inhibitory effects on platelet function was clarified. These compounds seem to inhibit platelet function due to stimulation of adenylate cyclase, which is mediated by perturbation of the central region of the membrane lipid bilayer. The effects of monovalent cations and anions on platelet function was also examined and their mechanisms were studied. It was indicated that monovalent cations such as alkali metal cations modify platelet aggregation by changing fibrinogen binding. On the other hand, monovalent anions modified platelet function by quite different mechanism. Furthermore, generation of hydroxyl radicals by platelets and its enhancement accompanied with the activation of platelets were revealed. It was inhibited by inhibitors of platelet activation such as forskolin and phenolic antioxidants.

Adenylyl Cyclases↗