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Biomedical subjects

H Kitaguchi

Publications and source records attributed to H Kitaguchi.

At least 19 recordsLinked to original sources
PubMed2005

A brainstem variant of reversible posterior leukoencephalopathy syndrome.

Reversible posterior leukoencephalopathy syndrome (RPLS) is caused by various heterogeneous factors, the commonest being hypertension, followed by nonhypertensive causes such as eclampsia, renal diseases and immunosuppressive therapy. Patients with RPLS exhibit bilateral white and gray matter abnormalities in the posterior aspects of the cerebral hemispheres. However, this syndrome may affect the brainstem predominantly, and these cases are designated as hypertensive brainstem encephalopathy. We present here two patients with reversible brainstem encephalopathy: one with hypertension and the other without hypertension. These patients presented with swelling and diffuse hyperintensities of the brainstem in fluid-attenuated inversion-recovery (FLAIR) and T2-weighted MRI, but with relatively mild clinical symptoms. They recovered without major neurological deficits, but had residual lacunar lesions in the pons. Reversible brainstem encephalopathy with characteristic MRI features was found in both hypertensive and nonhypertensive patients. These patients were diagnosed with a brainstem variant of RPLS, which is potentially fully reversible after an adequate treatment, and therefore should be carefully differentiated from other brainstem disease conditions.

Aged↗
PubMed2001

Syk expression in endothelial cells and their morphologic defects in embryonic Syk-deficient mice.

Mice deficient in the Syk tyrosine kinase showed severe petechiae in utero and died shortly after birth. The mechanism of this bleeding, however, remains unknown. Here it is shown that this bleeding is caused by morphologic defects of Syk-deficient endothelial cells during embryogenesis. Immunoblot and reverse transcriptase-polymerase chain reaction Northern blot analysis indicated that Syk is expressed in several endothelial cell lines. Immunocytochemical analysis also confirmed that Syk is expressed in the normal embryonic endothelial cells and is absent in Syk-deficient mice. Furthermore, electron microscopic analysis of Syk-deficient mice revealed an abnormal morphogenesis and a decreased number of endothelial cells. The results indicate a critical role for Syk in endothelial cell function and in maintaining vascular integrity in vivo.

Animals↗
PubMed1997

Possible evidence of endothelial cell activation and disturbance in thalassemia: an in vitro study.

Activation of vascular endothelium is considered as an important facet of inflammation, thrombosis, and vasculitis. Activated endothelial cells express a number of immunologically relevant surface markers which are not detected in dormant condition. These surface markers on endothelial cell may involve in adhesion reaction and migration of blood cell components. We demonstrated increased level of the soluble adhesion molecules in circulating blood of both alpha- and beta-thalassemic patients. These adhesion molecules are theoretically known to be released from endothelial cells. The adhesion molecules included soluble Intercellular Adhesion Molecule-1 (sICAM-1), soluble E-Selectin (ELAM-1), soluble Vascular Cell Adhesion Molecule-1 (sVCAM-1), and von Willebrand Factor (vWF). The levels of these adhesion molecules were measured in serum from 32 thalassemic patients and 10 control healthy subjects. As compared to normal, increased sICAM-1 was found in beta-thal/HbE patients with non-splenectomy; BE-NS (p = 0.002), increased ELAM-1 in beta-thal/HbE patients with splenectomy; BE-S (p = 0.01) and HbH with Hb Constant Spring; HbH/CS (p = 0.001), and increased sVCAM-1 in BE-NS; (p = < 0.0001) and BE-S (p = 0.002). Significant increase in von Willebrand Factor (vWF), a marker for endothelial cell, was shown in BE-S (p = 0.04) as compared to normal. Adhesion molecules were also markedly demonstrated in the supernatant of in vitro culture of human vascular endothelial cell in the presence of 30% thalassemic serum, and these adhesion molecules were also detected on the surface of the cells by using the technic of laser scanning confocal microscope and direct immunofluorescence.

Adult↗
PubMed1997

Thalassemic serum inhibits endothelial cell mitosis in vitro.

Human umbilical vein endothelial cells were cultured in vitro using Iscove's Modified Dulbecco's Medium (IMDM) supplemented with either pooled normal human serum, or pooled thalassemic serum, or autologous umbilical cord serum, or fetal bovine serum. The mitotic activity was determined under the inverted phase contrast microscope and the number of mitotic cells was counted. Our results showed that the mitotic cells decreased in endothelial cell culture with thalassemic serum as compared with normal human serum, autologous umbilical cord serum or fetal bovine serum. The percentage of mitotic cells decreased on day 3 in the presence of beta-thalassemia/HbE serum from both splenectomized and non-splenectomized patients as compared with normal or autologous umbilical cord serum. In the presence of alpha-thalassemic serum, a similar outcome was also observed. From this study we can conclude that the thalassemic sera might contain factors which affect the endothelial cell growth and proliferation by inhibiting mitosis in vitro.

Cells, Cultured↗
PubMed1997

Surface and total tissue factor activity of endothelial cells.

With a technic that was developed by us, we found that normal human umbilical vein endothelial cells (HUVEC) in culture characteristically had very little tissue factor (TF) activity either on the surface or in the cells which had been disrupted. In the presence of endotoxin (E. coli O26:B6), a trigger for thrombosis in septicemic patients, we could not detect an increased TF activity of HUVEC on its surface. However, an increase in TF (total TF) was detected after disruption of the cells. The increase in total TF was dose-dependent. Endotoxin at the concentration of 10 micrograms/ml caused around 5 fold increase in total TF activity compared to that of HUVEC in the absence of endotoxin.

Cells, Cultured↗
PubMed1995

Alterations in vascular endothelial cell-related plasma proteins in thalassaemic patients and their correlation with clinical symptoms.

An increased level of plasma thrombomodulin (TM) in alpha- and beta-thalassaemia was demonstrated using an enzyme-linked immunosorbent assay (ELISA). Nonsplenectomized patients with beta-thalassaemia/haemoglobin E (BE) had higher levels of TM than splenectomized cases (BE-S). Patients with leg ulcers (BE-LU) were found to have the highest increase in TM level. Appearance of larger platelets in all types of thalassaemic blood was observed indicating an increase in the number of younger platelets. These data indicate that injury of vascular endothelial cells is present in thalassaemic patients.

Adolescent↗
PubMed1993

Synthetic Arg-Gly-Asp-Ser analogues of the cell recognition site of fibronectin that retain antimetastatic and anti-cell adhesive properties.

Synthetic peptide analogues of the Arg-Gly-Asp-Ser (RGDS) sequence of fibronectin in which the amino acid of Gly was substituted with another one, named X, i.e. Arg-X-Asp-Ser (R-X-DS), and N-terminal modified R-X-DS have been synthesized to examine their antimetastatic effects in murine lung or liver metastasis models, as well as the inhibitory effect on tumor cell invasion, migration and adhesion in vitro. R-X-DS [X = Leu (L) or D-Leu (1)], as well as RGDS at a high dose of 3000 micrograms, significantly reduced the number of lung tumor colonies when they were co-injected with B16-BL6 melanoma. At a dose of 1000 micrograms/mouse, N-terminal modified R-X-DS, i.e. acetyl-D-R-X-DS [AcDR-X-DS: X = G, L or I], showed a more potent inhibitory effect on the lung or liver metastasis of B16-BL6 melanoma or L5178Y-ML25 lymphoma cells, respectively, as compared with RGDS or R-X-DS. AcDRLDS and AcDRIDS prevented the invasion of B16-BL6 cells into Matrigel/fibronectin- and Matrigel/laminin- coated filters, haptotactic migration, and the adhesion of the cells to both fibronectin- and laminin-coated substrates, whereas AcDRGDS inhibited only fibronectin-mediated cell functions. The intermittent i.v. administration of a water soluble vinylpolymer [poly(carboxyethylmethacrylamide), poly(CEMA)] containing R-X-DS (X = L or 1) or RGDS, following the subcutaneous inoculation of B16-BL6 cells, significantly inhibited spontaneous Jung metastasis as compared with multiple administrations of RGDS, R-X-DS or the untreated control.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1992

Red blood cell and platelet induced differentiation of endothelial cells into capillary-like structure.

We cultivated endothelial cells of human umbilical vein origin in the presence of red blood cells and platelet-rich plasma, and observed the phenomena which occurred in the petri dish under phase contrast microscopy. Many small particles were observed after an overnight incubation. We washed the dish two times, then added thrombin to the dish. The network of thread-like strands appeared within 10 to 20 minutes of the addition, and at the same time the small particles adhered on the surface of the strands, swelled and fused gradually to cover the surface of the strands completely. Within 30 to 60 minutes the network of the strands changed into a capillary-like structure. These phenomena were not observed if we omitted red blood cells or platelet-rich plasma. Studies by transmission electron microscopy revealed that the inner surface of the lumen of the structure was covered with cells. The cells isolated from the lumen by trypsin grew to confluence in the conventional culture medium, and showed vWF antigen on their surface. These observations indicated that the method described is useful for in vitro study of angiogenesis.

Blood Platelets↗
PubMed1992

Interaction between endothelial cells and thalassemic red cells in vitro.

Erythrocytes from 45 patients with thalassemia and/or hemoglobinopathies were studied for their cytoadherence property to the vascular endothelial cells in vitro. In plasma free medium, erythrocytes from patients with beta-thal/Hb E both splenectomized and nonsplenectomized, HbH diseases (alpha-thal 1/alpha-thal 2 and alpha-thal 1/Hb Constant Spring genotypes) and homozygous Hb E subjects bind to endothelial cells at a greater number as compared to the binding cell number of normal erythrocytes (p-value < 0.05 in all types). Addition of autologous platelet-rich plasma or whole blood to the culture system causes further increase in the number of adhering beta-thalassemia red cells. Platelet-rich plasma had more enhancement effect than the whole blood. However, no such enhancement of both platelet-rich plasma and whole blood was demonstrated in the culture of normal or alpha-thalassemia erythrocytes. Increased binding between red cells and endothelial cells may contribute to the greater risk of vascular occlusion in thalassemic patients.

Blood Platelets↗
PubMed1992

Thalassemic serum impairs endothelial cell growth in vitro.

Endothelial cells cultured for 3 days in the presence of hemoglobin H pooled sera had significantly decreased cell proliferation compared to those in normal serum. Inhibition was demonstrated at a concentration of 20% pooled serum in the cultured medium. Further decrease was shown in the presence of 30% pooled hemoglobin H sera. Sera from two genotypes of Hb H disease (alpha-thal 1/alpha-thal 2 and alpha-thal 1/Hb Constant Spring) had the same degree of inhibitory effect. Pooled sera from beta-thal/Hb E patients (both splenectomized or nonsplenectomized cases) had no such inhibitory effect. However, at day 4 and 5, the growth pattern relatively declined. Bilirubin at a concentration greater than 4.0 mg% in the medium 199 also caused significant decrease in cell proliferation. Since the diluted Hb H serum had bilirubin less than 4.0 mg%, the inhibitory effect of the pooled HbH serum is thus not due to effect of bilirubin. The difference between HbH and beta-thal/HbE sera in terms of inhibition of endothelial cell proliferation is the new finding that needs further investigation to explain vascularization and hemostasis in the patients of these two genotypes.

Bilirubin↗
PubMed1991

Regioselective modification of Lysine's amino groups by proteases.

The regioselectivity of six serine proteases for the amino groups of lysine was investigated. alpha-Chymotrypsin showed a preference for the alpha-amino group, although the selectivity can be varied 10-fold depending on the reaction medium. Subtilisin Carlsberg and other bacterial proteases were highly specific for the epsilon-amino group, regardless of the reaction medium: they were used as catalysts for the preparative synthesis of isopeptides in anhydrous tert-amyl alcohol.

Amino Acid Sequence↗
PubMed1986

Increase in factor VIII clotting activity in the perfusate of isolated dog hind leg and heart by components of kallikrein-kinin system.

Transient increase in Factor VIII clotting (F.VIIIc) activity was observed by infusion of kallikrein or bradykinin (BK) to the isolated dog leg or heart preparation which was perfused with physiological solution, but the increase in Factor IX activity was not observed, suggesting that the increase in F.VIIIc activity was not due to contaminated plasma components of the perfusate. The increase coincided with the increase in prostacyclin (PGI2) which was determined by immunoassay of 6-keto-PGF1 alpha and by platelet aggregation inhibiting activity. Although increase in PGI2 by BK was inhibited by the pretreatment of the preparations with indomethacin or tranylcypromine, the increase in F.VIIIc activity was not inhibited, suggesting that the increase in F.VIIIc activity was not mediated by PGI2.

Animals↗
PubMed1985

Plasminogen activator activity of cultured endothelial cells derived from canine coronary vessel and human umbilical artery and vein.

The present study was undertaken to determine which cells participate in plasminogen activator (PA) release from the vascular wall. Canine coronary vessel was confirmed to release PA when various agents were administered in perfusion experiments. Endothelial cells from the coronary vessel were then isolated and cultured for 2 days. PA activity was observed in lysates of the cultured cells, and the medium used for the cultivation was found to contain little PA activity. This suggests that the endothelial cells participate in PA release from the vascular wall. In addition, the PA synthesis was also studied in cultured endothelial cells from human umbilical artery and vein. Both contained little PA activity, indicating that vascular endothelial cells may vary in PA synthesis and release according to the vessel.

Animals↗
PubMed1984

Prostacyclin release from the coronary vascular wall by vasoactive substances.

Which vasoactive substances that are synthesized in vivo could induce the release of a sufficient amount of prostacyclin (PGI2) to inhibit platelet aggregation from the vascular wall was investigated in the isolated dog heart perfused by a modified method of Langendorff. Infusion of 5 microM bradykinin or 25 u/ml crude thrombin into the heart for 30 sec resulted in the transient appearance of inhibitory activity of platelet aggregation. The inhibitory activity was stable at alkaline pH but unstable at acidic pH and thermolabile. The appearance of the inhibitory activity was prevented by treatment of the coronary vessel with 30 microM indomethacin or 1 mM tranylcypromine. These results indicated that the inhibitory activity was caused by PGI2. When 25 microM acetylcholine, 25 microM noradrenaline, 25 microM isoproterenol, 10 microM adenosine triphosphate (ATP), 5 microM adenosine, 1 microM angiotensin II, 25 microM histamine or 1 microM serotonin was infused for 30 sec, no inhibitory activity of platelet aggregation was observed. Bradykinin (5 X 10(-9) approximately 5 X 10(-6) M) and purified thrombin (1 X 10(-9) approximately 1 X 10(-7) M) induced a dose-dependent release of PGI2 which was assayed using a radioimmunoassay for 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha).

Adenosine↗