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H Matsunami

Publications and source records attributed to H Matsunami.

At least 55 records · Page 3Linked to original sources
PubMed1995

Cadherin-11 expressed in association with mesenchymal morphogenesis in the head, somite, and limb bud of early mouse embryos.

Cadherin-11 (cad-11) is a novel member of the cadherin family of cell adhesion molecules, having recently been identified by means of the polymerase chain reaction. To study the function and expression of this molecule, we cloned mouse, cad-11 cDNA. Transfection of L cells with cDNA led them to acquire a typical cadherin-dependent cell-cell adhesiveness, and the L cells expressing cad-11 did not coaggregate with L cells expressing E-, P-, N-, or R-cadherin when they were mixed, indicating that this novel cadherin has a homophilic binding specificity, as found for other cadherins. To determine the developmental expression pattern of this molecule, we performed in situ hybridization analysis on early mouse embryos. Cad-11 first appeared in mesodermal layers only in the head and tail regions at the mid-to-late primitive streak stages. In the head, this appearance was followed by strong expression in mesenchymal tissues including branchial arches. In the trunk, the paraxial mesoderm initially did not express cad-11. However, as the somites formed, they expressed cad-11, and this expression was strictly correlated with their initial condensation and segregation from the presomitic mesoderm. The cad-11 expression in the somites was eventually restricted to sclerotome cells. As the limb buds developed, cad-11 appeared in the distal portion of the limb mesenchyme, and, at later stages, its expression was most evident at the peripheral mesenchyme. Cad-11 was thus expressed by restricted populations of mesenchymal cells in early embryos, although it was also expressed in parts of the neural tube, such as the optic vesicle and dorsal midline, and in part of the otic vesicle. As a step to investigate the role of cad-11 in mesenchymal cell adhesion, we dissociated the limb bud mesenchyme into single cells, pelleted them, and cultured them as aggregates. In these cultures, cad-11-positive cells clearly sorted out of the negative cell population, suggesting that cad-11 might be involved in selective association of mesenchymal cells. For comparison, we studied the expression of N-cadherin and found that the expressions of these two cadherins were differential, and complementary in some tissues. These results suggest that cad-11 is involved in specific associations of subsets of mesenchymal cells and also of some neural cells during early embryogenesis.

Amino Acid Sequence↗
PubMed1995

Fetal brain subdivisions defined by R- and E-cadherin expressions: evidence for the role of cadherin activity in region-specific, cell-cell adhesion.

We found that R-cadherin, a Ca2(+)-dependent cell--cell adhesion molecule, is expressed in restricted regions of the mouse fetal brain, as was found for E-cadherin previously. R-cadherin delineated a subset of alar domains within forebrain neuromeres and certain future nuclei, while E-cadherin was expressed in another distinctive pattern. When cells were collected from various local regions of the fetal brain, dissociated, and reaggregated under the conditions in which only cadherins are active for cell aggregation, R-cadherin-positive and -negative cells segregated from one another. Similar results were obtained for E-cadherin. Such segregation of cells was, however, suppressed when the cadherins were inactivated either by Ca2+ depletion or with blocking antibodies. These results suggest that cadherins confer region-specific adhesiveness on fetal brain cells and that this process may take part in brain segmentation.

Animals↗
PubMed1995

[Changes in coagulation parameters during the clinical courses of recipients of living-related partial liver transplantation].

We had rare opportunities to examine changes in fibrin degradation products (FDP)-D-dimer (DD), thrombin-antithrombin III complex (TAT), plasmin-alpha 2-plasmin inhibitor complex (PIC) and other coagulation parameters during the clinical courses of living-related partial liver transplantation (LRPLT). In seven out of eight recipients without severe rejection and/or disseminated intravascular coagulation (DIC), FDP-DD values reached their maximum at 5 to 10 days after transplantation, then gradually decreased. On the other hand, TAT values rose to the maximum at anhepatic or reperfusion phase of liver transplantation. These data represent hypercoagulation in consequence of tissue thromboplastin activation after extensive operation. Changes in PIC, tissue-type plasminogen activator, and plasminogen activator inhibitor-1 (PAI-1) in the clinical course of case 1 suggested that fibrinolysis was suppressed by relatively elevated level of PAI-1 around the operation, but thereafter was adversely accelerated by relatively lower levels of PAI-1. In comparison with patients with DIC, TAT was much higher but PIC was significantly lower in recipients of LRPLT. These findings indicated that marked hypercoagulation and mild to moderate hyperfibrinolysis occurred in recipients of LRPLT.

Antithrombin III↗
PubMed1995

Calculation of child and adult standard liver volume for liver transplantation.

Despite refinements in surgical techniques for liver transplantation, liver size disparity remains one of the most common problems in pediatric patients. Optimal liver graft size remains unknown and the volume of diseased liver in the recipient is not indicative of the volume (standard liver volume [LV]) optimal for the recipient's metabolic demands. To establish a formula for calculating the standard LV in the pediatric and adult populations for liver transplantation, whole LVs were measured using computed tomography (CT) in 96 patients (65 pediatric and 31 adolescent or adult subjects) with normal liver whose disease conditions did not seem to affect body weight (BW) or LV. In the 96 subjects, the ratio of estimated LV to BW decreased gradually as age increased until approximately 16 years, when it started to level off. On the other hand, there seemed to be a directly proportional relationship between the estimated LV in vivo and body surface area (BSA) (r = .981; r2 = .962; P < .0001) in the subjects as a whole, and the formula, LV (mL) = 706.2 x BSA (m2) + 2.4, was established from the measured data by simple regression analysis. Another predicting equation, LV (mL) = 2.223 x BW (kg)0.426 x body height (BH) (cm)0.682, was produced by multiple regression analysis (r2 = .969; P < .0001). Considering its simplicity of use, we adopted the first formula for predicting standard LV in an individual patient.

Adolescent↗
PubMed1995

[Studies on the blood coagulation factor XIII in patients with increased levels of FDP D-dimer].

Antigen levels of blood coagulation factor XIII (XIII) were determined in plasmas from patients with increased levels of fibrin degradation products-D-dimer (FDP-DD), including disseminated intravascular coagulation (DIC), by latex photometric immunoassay using polyclonal anti-XIII a subunit antibody-coated latex reagent. Since stable fibrin is directly degradated by plasmin and FDP-DD is produced, plasma FDP-DD levels correlate with plasmin-alpha 2-plasmin inhibitor complex levels, but not with thrombin-antithrombin III complex (TAT) or XIII levels. In order to clarify other causes of discordant relationships among the related three parameters, we studied the changes in plasma XIII, TAT and FDP-DD levels in fourteen DIC patients induced by various primary disorders. Only in two cases, XIII levels changed up and down irrelevant to the fluctuating levels of TAT and FDP-DD. In seven cases, plasma XIII levels remained low during the clinical courses, indicating possibilities that elevated condition of XIII consumption continued and/or production of XIII was low. On the other hand, in four patients, including two patients with nephrosis, XIII might be produced at higher rate than that of consumption. Same phenomenon was observed in one of eight recipients with living-related liver transplantation who showed remarkably increased levels of FDP-DD without DIC. In conclusion, plasma XIII level in patients with elevated FDP-DD may be influenced by the balance between consumption of XIII by unstable fibrin and/or surgical stress and the following tissue recovery etc. and production of XIII in liver, megakaryocytes and monocytes.

Disseminated Intravascular Coagulation↗
PubMed1994

Effect of platelet-activating factor on cold-preserved liver grafts.

Platelet-activating factor (PAF) may play an important role in graft injury in liver transplantation. Livers excised from male Wistar rats were preserved in University of Wisconsin solution for 6 h and then perfused with Krebs-Henseleit solution containing vehicle (bovine serum albumin) or PAF. Impairment of parenchymal cells was assessed by reference to tissue adenosine triphosphate levels, oxygen consumption and alanine aminotransferase activity in the effluent. The effect on non-parenchymal cells was evaluated by measurement of purine nucleoside phosphorylase and alanine aminotransferase levels in the effluent. Administration of as little as 1.0 ng kg-1 PAF caused a significant decrease in adenosine 5'-triphosphate concentration and oxygen consumption (P < 0.05), although non-parenchymal cell injury was not affected. PAF can therefore cause liver graft dysfunction with hepatocytes as the main target, even in the absence of microcirculatory disturbance secondary to interaction between blood cells and endothelial cells.

Adenosine↗
PubMed1994

Effect of granulocyte colony-stimulating factor on neutropenia in liver transplant recipients with hypersplenism.

The authors present details of their initial experience with use of recombinant human granulocyte colony-stimulating factor (rhG-CSF) for preventing neutropenia caused by hypersplenism, and, possibly, for reducing the risk of postoperative infections in pediatric liver transplant recipients. Seven patients with end-stage liver disease, three of whom had severe hypersplenism, underwent living related liver transplantation (LRLT). The rhG-CSF was administered to the latter three patients. Peripheral neutrophil counts decreased immediately after reperfusion (to 1500 +/- 300/microL) in the three patients, and returned to normal with use of rhG-CSF 3 to 10 days after transplantation. The dosage was adjusted to maintain peripheral leukocyte and granulocyte counts above 5,000/microL and 2,000/microL, respectively. This initial clinical trial showed that rhG-CSF administration restores the leukocyte counts of patients who have hypersplenism, without any significant adverse effects, and that rhG-CSF holds promise for reducing the risk of infections after liver transplantation.

Child↗
PubMed1994

[Changes in serum h-HGF levels after living-related liver transplantation].

It is well known that prognosis is very poor in patients with severe hepatic insufficiency such as congenital biliary atresia and fulminant hepatitis. The liver transplantation is only effective therapy for these patients and living-related liver transplantation is becoming popular in Japan. We observed the changes in serum human hepatocyte growth factor (h-HGF) levels of the recipients during the operation in 3 cases of congenital atresis and one of fulminant hepatitis. Serum h-HGF values in these patients reached the maximal levels (5-10-fold compared to the base line values) at the phase of portal or hepatic artery anastomosis during the operation. These observations suggest that the increase of h-HGF in the recipient is derived from the following three origins. (1) Wash outed h-HGF from the liver of the donor. (2) Induced h-HGF from other organs than the liver of the recipient. (3) The decreased catabolism of h-HGF in recipient due to total hepatectomy.

Adolescent↗