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Biomedical subjects

H Mohri

Publications and source records attributed to H Mohri.

At least 127 records · Page 7Linked to original sources
PubMed1994

[Comparison of the late hemodynamics following corrective surgery of congenital heart diseases: ventricular septal defect, tetralogy of Fallot, Mustard operation and Fontan operation].

Late hemodynamics following corrective surgery for congenital heart diseases were evaluated in 65 patients. The patients were divided into 4 groups due to the operative procedures including closure of ventricular septal defect (VSD group = 15 patients), repair of tetralogy of Fallot (TOF group = 20), Mustard operation (Mustard group = 19) and Fontan operation (Fontan group = 11). The postoperative period was 3.8 +/- 3.8, 1.0 +/- 0.1, 5.7 +/- 4.3 and 3.2 +/- 4.9 years in VSD, TOF, Mustard and Fontan groups, respectively. Postoperative pulmonary to systemic arterial pressure ratio in VSD group significantly decreased to 0.38 +/- 0.13 from the preoperative value of 0.97 +/- 0.04. Pulmonary vascular resistance (Rp) in VSD group significantly decreased from 4.88 +/- 2.40 to 2.56 +/- 0.75 U.m2 and Rp in Fontan group significantly increased from 1.63 +/- 0.70 to 3.66 +/- 0.47 U.m2 postoperatively. Postoperative cardiac indices in VSD, TOF, Mustard and Fontan groups were 4.30 +/- 1.34, 4.28 +/- 0.72, 3.83 +/- 1.38 and 3.48 +/- 1.38 l/min/m2, respectively, without significant differences. Ejection fraction (EF) of the systemic ventricle (left ventricle) in VSD, TOF and Fontan groups were 0.66 +/- 0.06, 0.65 +/- 0.07 and 0.63 +/- 0.08, respectively. In Mustard group, EF of the systemic ventricle (right ventricle) was 0.56 +/- 0.12 and significantly less than left ventricular EF in the other 3 groups. The hemodynamic characteristics after these operative procedures should be considered for patient management.

Cardiac Surgical Procedures↗
PubMed1994

Experimental study of cerebral autoregulation during cardiopulmonary bypass with or without pulsatile perfusion.

Twenty-four adult mongrel dogs were divided into four equal groups according to the following method of cardiopulmonary bypass: normothermic continuous (so-called nonpulsatile) perfusion, normothermic pulsatile perfusion, hypothermic continuous perfusion, and hypothermic pulsatile perfusion. Cerebral blood flow was determined by measuring the volume of sagittal sinus venous blood outflow with a transit-time ultrasonic flowmeter. Cardiopulmonary bypass was initiated at a flow rate of 80 ml/kg per minute. Cerebral temperature was maintained at 37 degrees C in the normothermic groups and at 25 degrees C in the hypothermic groups. Arterial pH and carbon dioxide were maintained within the physiologic range by alpha-stat acid-base regulation. Mean cerebral perfusion pressure and blood flow were not affected during 90 minutes of the bypass. The respective values were 67.1 mm Hg and 37.1 ml/100 gm brain per minute with normothermic continuous perfusion, 72.8 mm Hg and 39.0 ml/100 gm per minute with nonpulsatile perfusion, 98.0 mm Hg and 23.0 ml/gm per minute with hypothermic continuous perfusion, and 86.8 mm Hg and 22.3 ml/100 gm per minute with hypothermic pulsatile perfusion. Pump flow rates were altered from 10 to 120 ml/kg per minute in a stepwise fashion to obtain graded changes of perfusion pressure. Cerebral blood flow, however, was not changed significantly by cerebral perfusion pressure so long as perfusion pressure was greater than 50 mm Hg. Conversely, cerebral blood flow changed proportionally with cerebral perfusion pressure at a pressure less than 50 mm Hg. The correlation between cerebral blood flow and perfusion pressure was described as two separate lines determined by linear regression. The slope of the regression line relating cerebral blood flow to perfusion pressure was 0.16 +/- 0.08 for a cerebral perfusion pressure above 50 mm Hg and 0.68 +/- 0.11 below 50 mm Hg in the normothermic continuous perfusion group; 0.14 +/- 0.09 and 0.32 +/- 0.09 with normothermic pulsatile perfusion; 0.10 +/- 0.04 and 0.62 +/- 0.18 with hypothermic continuous perfusion; 0.09 +/- 0.08 and 0.39 +/- 0.04 in the hypothermic pulsatile perfusion group. The slope above 50 mm Hg was significantly smaller and closer to zero in all groups than it was at a perfusion pressure below 50 mm Hg (p < 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

[The number and density of hypertensive vascular lesions of lung in advanced pulmonary hypertension--a computer 3-D morphometry in autopsy lung specimens of 5 patients with congenital cardiac anomaly].

To study how and to what degree the vascular bed of the lung is narrowed in patients with advanced pulmonary hypertension, the number and density of advanced pulmonary vascular lesions in lung tissue were determined by 3-dimensional morphometry. The material included 17 autopsy lung specimens taken from different lobes of 5 patients ranging from 2 to 17 years and dying of congenital cardiac anomalies. In each specimen, computer-aided 3-D reconstruction was performed from serial sections, and the number of grade 3 and 4 lesions was counted in the computer display, also with their densities calculated. The number and density of obstructive vascular lesions were found varying to an unexpected degree, with a marked difference among the individuals and among the site of the lung. The total number of plexiform lesion tends to be greater in the lower lobes. The degree of vascular bed narrowing, defined as the numerical ratio of the obstructed to the total of what we call "acinar arteries", was also various, suggesting that there can be patients who, having a bed not strongly narrowed, are operable even in the presence of plexiform lesion. On the other hand, the result of morphometry provided a basis on which the reliability of open lung biopsy is to be re-assessed: it disclosed the need of semi-serial sectioning of specimen in order not to be missed plexiform lesions particularly when their density in the lung is very low.

Adolescent↗
PubMed1994

[Autologous vs bovine pericardial valved patch for widening of the right ventricular outflow tract of tetralogy of Fallot].

Autologous or glutaraldehyde treated bovine pericardial valved patch was utilized for widening of the right ventricular outflow tract in 20 patients with tetralogy of Fallot (autologous pericardium group in 10 patients and bovine pericardium group in 10). Pericardial valve function of the both materials was evaluated by postoperative cardiac catheterization performed 1 year after the operation. There were no significant differences in pulmonary arterial and right ventricular pressures, and right ventricular ejection fraction and end-diastolic volume between the 2 groups. Pulmonary angiogram in the autologous pericardium group patients demonstrated the pulmonary regurgitation (PR) of grade 1 in 5 patients, grade 2 in 4 and grade 3 in 1. On the other hand, 1, 3 and 6 patients in the bovine pericardium group demonstrated no-PR, grade 1 PR and grade 2 PR, respectively. It was concluded that there were no significant differences between autologous and glutaraldehyde treated bovine pericardium as a material of valved patch for widening of the right ventricular outflow tract of tetralogy of Fallot.

Bioprosthesis↗
PubMed1993

Fibronectin inhibits platelet aggregation independently of RGD sequence.

Fibronectin binds to platelet membrane glycoprotein (GP) IIb-IIIa in Arg-Gly-Asp (RGD)-dependent and -independent manner. We have isolated and characterized the 29-kDa dispase fragment of fibronectin. Binding of 125I-fibronectin to thrombin-stimulated platelets was inhibited by the 29-kDa fragment and the GRGDSPA peptide with IC50 values of 1.5 +/- 0.4 and 8.1 +/- 0.9 microM, respectively. The NH2-terminal sequence of this fragment gave this result: Ala-Val-Thr-Thr-Ile-Pro-Ala-Pro-Thr-Asp. This established the position of this peptide within fibronectin as beginning with the residue tentatively designated 1597. Neither the RGDS sequence nor the RGD-independent binding domain of fibronectin (Bowditch, R. D., Halloran, C. E., Aota, S., Obara, M., Plow, E. F., Yamada, K. M., and Ginsberg, M. H. (1991) J. Biol. Chem. 266, 23323-23328) was contained in this fragment. The 29-kDa fragment inhibited ADP-induced aggregation of platelets and binding of fibrinogen to activated platelets. The fragment bound to immobilized GPIIb-IIIa. The 125I-labeled 29-kDa fragment directly bound to thrombin-stimulated platelets with 98,000 +/- 4,600 molecules/platelet (Kd = 4.6 +/- 0.5 x 10(-6) M). Direct binding was inhibited by the unlabeled 29-kDa fragment but was not blocked by either the GRGDSPA peptide or the monoclonal anti-GPIIb-IIIa antibody. These results indicate that the additional RGD-independent binding domain(s) to GPIIb-IIIa are present on fibronectin. This additional binding domain(s) on fibronectin may prevent thrombus formation by interfering with the interaction of fibrinogen with GPIIb-IIIa.

Adenosine Diphosphate↗
PubMed1993

Fibrinogen binds to heparin: the relationship of the binding of other adhesive proteins to heparin.

The binding of heparin to fibrinogen was characterized. We have used an assay employing heparin coupled to Sepharose CL-6B to show that 125I-fibrinogen binds to heparin in a time-dependent, divalent ion-independent, saturable, and reversible manner. A total of 1.75 mg of fibrinogen could bind to 1 ml of heparin-Sepharose CL-6B with a Kd of 4.03 x 10(-7) M. Binding was completely inhibited by other adhesive proteins including fibronectin, von Willebrand factor (vWF), and vitronectin with IC50s of 7.2-8.8 microM. The binding of 125I-fibrinogen to heparin-Sepharose CL-6B was blocked by a monoclonal antibody (52k-2) and a polyclonal antibody (FK-2). 52k-2 inhibits the binding of vWF, and FK-2 blocks the binding of fibronectin to heparin-Sepharose CL-6B. It is therefore likely that fibrinogen has a heparin-binding site(s) which may have some overlap with those of other adhesive proteins, although the physiological role of the fibrinogen heparin-binding domain is uncertain at present.

Antibodies, Monoclonal↗
PubMed1993

Effects of hybrid peptide analogs to receptor recognition domains on alpha- and gamma-chains of human fibrinogen on fibrinogen binding to platelets.

We synthesized a series of hybrid peptides that correspond to the gamma-chain dodecapeptide (400-411), variable numbers of glycine residues, and the RGDS peptide [Y-HHLGGAKQAGDV(G)nRGDS] to investigate the relationship of these receptor recognition domains of fibrinogen to platelet membrane glycoprotein IIb/IIIa. The tetrapeptide RGDS, the GRGDSPA peptide and the dodecapeptide inhibited binding of fibrinogen to GPIIb/IIIa by 50% (IC50) at concentrations of 17 +/- 1.6 microM, 15 +/- 2.1 microM, and 87 +/- 6.8 microM, respectively. The inhibitory effect of hybrid peptides increased as the number of glycine residues increased, plateauing with 9-11 glycine residues in hybrid peptide analogs, which had an IC50 of 0.68 +/- 0.14 microM. These hybrid peptides completely inhibited the binding of fibrinogen to activated platelets when used in sufficient concentrations. The peptide Y-HHLGGAKQAGDV(G)9RGDS blocked ADP-induced aggregation in citrated platelet-rich plasma with IC50 of 3.5 +/- 0.6 microM. When the peptide Y-HHLGGAKQAGDV(G)9RGDS was labeled with 125I to quantify its binding to platelets, maximal binding was observed within 30 min. The binding sites of the hybrid peptide were 43,600 molecules/platelet (Kd = 3.1 +/- 0.5 x 10(-7) M) to stimulated platelets and 12,500 molecules/platelet (Kd = 1.4 +/- 0.2 x 10(-7) M) to nonstimulated platelets. The hybrid peptides had the same binding affinity to platelets as fibrinogen and inhibited platelet function. Moreover, anti-GPIIb/IIIa antibody inhibited the binding of the labeled hybrid peptide to stimulated platelets. These results indicate that in the native fibrinogen molecule the presence of both RGD sequence or gamma-chain domain at optimal distances increased the binding affinity to GPIIb/IIIa.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1993

Quantitation of zidovudine-resistant human immunodeficiency virus type 1 in the blood of treated and untreated patients.

A nonselective ex vivo assay was used to directly detect and quantify zidovudine (AZT)-resistant human immunodeficiency virus type 1 (HIV-1) in the blood of treated and untreated patients. In contrast to previous reports, drug-resistant virus was detected in peripheral blood mononuclear cells of a few of the patients who had never received AZT. The AZT resistance of HIV-1 isolates from one untreated individual was confirmed by further susceptibility studies in vitro and by the finding of a characteristic mutation (Lys-->Arg at codon 70) in the reverse transcriptase. In patients who were clinically stable while on AZT, HIV-1 titers in plasma and mononuclear cells were generally low but resistant viruses already predominated. In those individuals who were deteriorating despite AZT administration, high levels of viremia were observed, and the resistance phenotype was nearly universal. These findings serve to emphasize the magnitude of the AZT-resistance problem in patients on drug treatment.

AIDS-Related Complex↗
PubMed1993

Triclonal gammopathy (IgA kappa, IgG kappa, and IgM kappa) in a patient with plasmacytoid lymphoma derived from a monoclonal origin.

We report the case of a 64-year-old woman with plasma cytoid lymphoma of the ileum and gastric wall. Serum protein electrophoresis and immunoelectrophoresis showed a triclonal IgG kappa, IgA kappa, and IgM kappa gammopathy. Biopsy of the tumor revealed three different cell types, which were stained with antibodies specific for IgG, IgA, and IgM. However, DNA analysis of immunoglobulin gene rearrangements using JH, C mu, and C kappa gene probes showed a monoclonal pattern. These results suggest that the three types of malignant cells producing different classes of immunoglobulins were derived from a single clone of B-cells that had undergone a "class switch".

Blotting, Southern↗
PubMed1993

Replacement of the transverse aortic arch for type A acute aortic dissection.

Surgical treatment of acute aortic dissection involving the segment of transverse aortic arch is difficult and often associated with a high mortality and morbidity. The high mortality and morbidity are primarily related to anatomic features and techniques of cerebral protection employed during the period of aortic branch occlusion needed for reconstruction. This study reports our experience of 20 consecutive cases of acute type A aortic dissection treated by repair or replacement of the transverse aortic arch during emergency operation. Ages of the patients ranged from 56 to 76 years. All patients were referred to us within 2 weeks of onset (mean time, 58 hours). Selective cerebral perfusion or deep hypothermia with complete circulatory arrest was employed during the period of aortic branch occlusion. Duration of cerebral perfusion, circulatory arrest, myocardial ischemia, and cardiopulmonary bypass averaged 106 minutes, 32 minutes, 127 minutes, and 248 minutes, respectively. There were three operative deaths. All three dissections were ruptured ones, and the patients died of hemorrhage, deep coma, or multiple organ failure. One patient died of infection 3 months after operation. The remaining patients are alive and well without any detectable neurological deficit 1 month to 4 years postoperatively. This experience emphasizes that repair or replacement of acute type A aortic dissection involving the aortic arch can be performed safely by adequate selection of patients, supportive measures, and operative methods.

Acute Disease↗
PubMed1993

Cardiac dilatation after cardiopulmonary bypass: ceramic plate technique for sternal splinting.

Intraoperative sternal closure after cardiopulmonary bypass in patients with cardiac dilatation and dysfunction may cause fatal deterioration of their hemodynamics. To avoid this complication, a ceramic plate made from methyl methacrylate was used for sternal splinting. This simple splint can avoid chest wall compression to the overdilated heart, maintaining stable hemodynamics after cardiopulmonary bypass without postoperative respiratory complications or mediastinal infection.

Bone Cements↗
PubMed1993

Protection of the brain during hypothermic perfusion.

The adequacy of the circuits for brain perfusion has been explored by hemodynamic assessment using the ability of the brain to autoregulate blood flow as an indicator, and by morphologic observation using carbon black or Evans blue infusion into the brain perfused antegradely or retrogradely. It is concluded that the safe pressure of cerebral perfusion needed to maintain cerebral integrity is between 40 and 50 mm Hg in both normothermic and hypothermic perfusions, a pressure that can be generated by nonpulsatile pump flows through the pump greater than 40 mL.kg-1 x min-1. Morphologic studies revealed development of focal infarctions in the brain and destruction of the blood-brain barrier by retrograde cerebral perfusion. The retrograde approach, therefore, is definitely inferior to the antegrade method. Antegrade perfusion for 90 minutes, however, produced minimal cerebral edema, suggesting the need for further improvement even in techniques of antegrade perfusion.

Animals↗
PubMed1993

Protection from postischemic spinal cord injury by perfusion cooling of the epidural space.

To avoid devastating spinal cord injury during aneurysm operations, we evaluated the protective effects of epidural space perfusion cooling during occlusion of the descending thoracic aorta in a canine model. Sixteen dogs were divided into three groups: group 1 (n = 5) underwent 60 minutes of aortic occlusion without epidural space perfusion cooling; group 2 (n = 6), 60 minutes of occlusion with perfusion cooling; and group 3 (n = 5), 120 minutes of occlusion with perfusion cooling. The development of motor disturbance and its severity were examined 7 days after the procedure. In group 1, 1 dog was normal and 4 dogs showed spastic paraplegia with rigidly extended hind limbs. In group 2, 5 dogs were normal and 1 dog was unable to walk although it could move both of its hind legs slightly. In group 3, all 5 dogs were normal. Groups 2 and 3 had a significantly better neurologic outcome than group 1. Histologic examination of the spinal cord in dogs with paraplegia revealed degeneration of gray matter with macrophage infiltration. Histologic examination of the spinal cord in dogs without neurologic deficit showed enlargement of the central canal, light edema, and a small number of dark neurons. We conclude that epidural space perfusion cooling is effective in reducing the incidence of spinal cord injury after temporary occlusion of the descending thoracic aorta.

Animals↗
PubMed1993

Localization of caldesmon and its dephosphorylation during cell division.

Mitosis-specific phosphorylation by cdc2 kinase causes nonmuscle caldesmon to dissociate from microfilaments during prometaphase. (Yamashiro, S., Y. Yamakita, R. Ishikawa, and F. Matsumura. 1990. Nature (Lond.). 344:675-678; Yamashiro, S., Y. Yamakita, H. Hosoya, and F. Matsumura. 1991. Nature (Lond.) 349:169-172). To explore the functions of caldesmon phosphorylation during cytokinesis, we have examined the relationship between the phosphorylation level, actin-binding, and in vivo localization of caldesmon in cultured cells after their release of metaphase arrest. Immunofluorescence studies have revealed that caldesmon is localized diffusely throughout cytoplasm in metaphase. During early stages of cytokinesis, caldesmon is still diffusely present and not concentrated in contractile rings, in contrast to the accumulation of actin in cleavage furrows during cytokinesis. In later stages of cytokinesis, most caldesmon is observed to be yet diffusely localized although some concentration of caldesmon is observed in cortexes as well as in cleavage furrows. When daughter cells begin to spread, caldesmon shows complete colocalization with F-actin-containing structures. These observations are consistent with changes in the levels of microfilament-associated caldesmon during synchronized cell division. Caldesmon is missing from microfilaments in prometaphase cells arrested by nocodazole treatment, as shown previously (Yamashiro, S., Y. Yamakita, R. Iskikawa, and F. Matsumura. 1990. Nature (Lond.). 344:675-678). The level of microfilament-associated caldesmon stays low (12% of that of interphase cells) when some cells start cytokinesis at 40 min after the release of metaphase arrest. When 60% of cells finish cytokinesis at 60 min, the level of microfilament-associated caldesmon is recovered to 50% of that of interphase cells. The level of microfilament-associated caldesmon is then gradually increased to 80% when cells show spreading at 120 min. Dephosphorylation appears to occur during cytokinesis. It starts when cells begin to show cytokinesis at 40 min and completes when most cells finish cytokinesis at 60 min. These results suggest that caldesmon is not associated with microfilaments of cleavage furrows at least in initial stages of cytokinesis and that dephosphorylation of caldesmon appears to couple with its reassociation with microfilaments. Because caldesmon is known to inhibit actomyosin ATPase and/or regulate actin assembly, its continued dissociation from microfilaments may be required for the assembly and/or activation of contractile rings.

Actin Cytoskeleton↗
PubMed1993

Biological cloning of functionally diverse quasispecies of HIV-1.

Twenty putative clones of HIV-1, derived by biological cloning from two different individuals, were characterized in vitro for functional activity and genotypic diversity. Many of the biological clones isolated by this method were genetically distinct, and could be further distinguished by differences in replication kinetics, host cell range, and/or cytopathicity. Our findings indicate that biological cloning by limiting dilution cultures is an effective method for isolating replication-competent, functionally diverse quasispecies of HIV-1.

Amino Acid Sequence↗
PubMed1993

Anti-fibrinogen antibody mediates fibrinogen binding to platelet membrane glycoprotein IIb-IIIa.

The binding of fibrinogen to platelets requires the agonist activation of platelet membrane glycoprotein IIb/IIIa. We have now found an anti-fibrinogen polyclonal antibody (YCU-R3) that increases the fibrinogen affinity of GPIIb/IIIa-binding function (activation) and subsequent platelet aggregation. The addition of intact IgG, F(ab)2 fragments or Fab fragments induced platelet aggregation. The antibody-mediated fibrinogen binding was specific and saturable. This binding was inhibited by native fibrinogen, the RGDS peptide, the peptide of the C-terminus gamma chain of fibrinogen (gamma 397-411), and the anti-GPIIb/IIIa monoclonal antibody (LJ-CP8). The antibody-dependent fibrinogen binding was similar to that induced by ADP. Moreover, after pretreatment with the anti-fibrinogen antibody and fibrinogen, formalin-fixed platelets bound to fibrinogen saturably. These results suggest that this anti-fibrinogen antibody may function as partial agonist.

Antibodies↗
PubMed1993

Increased viral burden and cytopathicity correlate temporally with CD4+ T-lymphocyte decline and clinical progression in human immunodeficiency virus type 1-infected individuals.

The rate of clinical progression is variable among individuals infected with human immunodeficiency virus type 1 (HIV-1). Changes in viral burden which correlate with disease status have been demonstrated in cross-sectional studies; however, a detailed longitudinal study of the temporal relationship between viral burden, CD4+ T-cell numbers, and clinical status throughout the course of infection has not been reported. Multiple longitudinal blood samples were obtained from four HIV-1-infected individuals with clinically divergent profiles. Levels of HIV-1 were measured in sequential samples of peripheral blood mononuclear cells, using both end-point dilution cultures and quantitative polymerase chain reaction methods. Serial HIV-1 isolates from each case were also evaluated to determine their biological properties in vitro. For the three patients with clinical progression, a dramatic increase in the level of HIV-1 was observed concurrent with or prior to a marked drop in CD4+ T lymphocytes. This increase in viral burden was temporally associated with the emergence of a more cytopathic viral phenotype. In contrast, consistently low levels of HIV-1 were observed in the one patient who was clinically and immunologically stable for more than a decade. Moreover, viral isolates from this patient were less cytopathic in vitro compared with HIV-1 isolates from those patients with disease progression. The temporal association between increased viral burden and CD4+ T-cell decline suggests a direct role for HIV-1 in the cytopathology of CD4+ T cells in vivo. Our results indicate that the pathogenic mechanisms responsible for CD4+ T-cell depletion may be related to both quantitative and qualitative changes in HIV-1.

Acquired Immunodeficiency Syndrome↗