Two-dimensional SU(N) gauge theory on the light cone.
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Journal Article↗
Biomedical subjects
T Sugihara
Publications and source records attributed to T Sugihara.
Deformation of swollen erythrocytes provides a model of sickling-induced leak pathways, including a novel bromide-sensitive component.
Deoxygenation-induced red blood cell (RBC) sickling probably activates multiple cation leak pathways. In an attempt to model this, we examined the net passive K efflux ("K leak") from normal and sickle RBCs undergoing elliptical deformation in hypotonic media (200 mOsmol/L). This hypotonic deformation activates two deformation-dependent K leak pathways that are not detectable during the balanced leak (Kefflux = Nainflux) resulting from deformation of RBCs in isotonic medium. These are (1) a calcium-dependent leak component and (2) a novel leak pathway that is inhibited by substitution of bromide (but not sulfamate) for chloride, which converts the unbalanced K leak (Kefflux > Nainflux) of hypotonic deformation to a residual balanced leak. This dramatic effect of hypotonic deformation is reversible, is detected in both normal and sickle RBCs, and is inhibited significantly by 4,4'-diisothiocyano-2,2'-stilbene disulfonate. Remarkably, bromide also inhibits by 55% the K leak resulting from authentic deoxygenation-induced RBC sickling and, thereby, blunts the imbalance of accompanying monovalent cation leaks. The unique effect of bromide is not readily explainable on the basis of known behaviors of known ion leak/transport pathways. The mechanical threshold for triggering K leak during hypotonic deformation is at applied shear stress of 164 dyne/cm2, a value similar to the abnormal susceptibility we previously found for oxygenated sickle RBCs during isotonic deformation. These data suggest that membrane stretch accompanying hypotonic deformation activates the same multiple leak pathways that contribute to net K leak during authentic RBC sickling, including a previously unknown bromide-sensitive leak.
Anemia, Sickle Cell↗
Massive Schwinger model with SU(2)f on the light cone.
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Journal Article↗
Intravenous extended infusion of recombinant human soluble thrombomodulin prevented tissue factor-induced disseminated intravascular coagulation in rats.
This study demonstrated that intravenous infusion of recombinant human soluble thrombomodulin (rhs-TM) could inhibit disseminated intravascular coagulation (DIC) caused by 4 hr infusion of tissue factor (TF) in rats. Extended infusion of TF reduced fibrinogen and platelet counts and elevated serum FDP level. Pretreatment and coinfusion of rhs-TM could block changes of these DIC-parameters without prolongation of APTT. Heparin, which is a potent anti-DIC drug, could also inhibit these changes with extra prolongation of APTT and PT. Thus, these results suggest thrombomodulin prevent DIC less bleeding tendency than heparin.
Animals↗
Antithrombotic effects of recombinant human soluble thrombomodulin (rhs-TM) on arteriovenous shunt thrombosis in rats.
We examined the antithrombotic effect of recombinant human soluble thrombomodulin (rhs-TM) using an arteriovenous shunt thrombosis model and its influence on hemostasis in rats. Intravenous administration of rhs-TM (0.5-4 mg/kg) significantly inhibited thrombus formation and prolonged ex vivo activated partial thromboplastin time (APTT) in a dose-dependent manner. Thrombus formation was inhibited to the same extent in animals treated with heparin (25-200 U/kg) and in those treated with rhs-TM (0.5-4 mg/kg), but heparin had a much stronger effect on prolonging APTT. In the hemorrhagic study using the rat template bleeding time method, rhs-TM exhibited the prolongation of the bleeding time only at the highest effective dose (rhs-TM; 4 mg/kg) of the thrombosis experiments. Thus, rhs-TM exhibits the inhibitory effect on thrombus formation with less APTT prolongation in comparison with heparin and without significant pertubation of hemostasis.
Animals↗
"Turbo charging" the vertical rectus abdominis myocutaneous (turbo-VRAM) flap for reconstruction of extensive chest wall defects.
We report our experience using "turbo charging" of the vertical rectus abdominis myocutaneous (turbo-VRAM) flap in 7 patients with extensive chest wall defects. The turbo-VRAM flap provides augmented blood supply with microvascular anastomosis between the inferior epigastric system and available vessels of the axillary, brachial or cervical vascular system. All patients in this study had uncomplicated recovery. In 3 patients, the skin paddle of the flap, which was designed as a fish shape, was effectively used to cover a wide defect. One patient required resection of some lower costal cartilages located near the superior epigastric vascular system in order to extend the rotation distance of the flap. These technical options have made the turbo-VRAM flap more versatile. The turbo-VRAM flap allows successful coverage of extensive chest wall defects, including defects of the axilla, upper arm, shoulder, or neck.
Adult↗
Cleft lip mongolian spot: mongolian spot associated with cleft lip.
BACKGROUND: Mongolian spots in the cleft area of cleft lip have been found in some Japanese children. OBJECTIVE: Our purpose was to study the frequency of cleft lip mongolian spot in children with cleft lip of various severity. METHODS: Sixty-six babies with unilateral cleft lip were divided into three groups: namely, those with microform cleft lip (10 subjects), incomplete cleft lip (30 subjects), and complete cleft lip (26 subjects). The incidence of cleft lip mongolian spot in the three groups was studied. RESULTS: Thirty-six babies (55%) had a cleft lip mongolian spot. The mongolian spot was observed in no patients with microform cleft lip, in 18 patients (60%) with incomplete cleft lip, and in 18 patients (69%) with complete cleft lip. CONCLUSION: Cleft lip mongolian spot appears in high incidence when the cleft goes beyond the vermilion border.
Cleft Lip↗
Experience with arteriovenous malformations treated with flap coverage.
Fourteen patients with arteriovenous malformations were treated with surgical resection followed by well-vascularized tissue transfer. Free-tissue transfers were used in 12 of the patients and axial local flaps in 2 patients to reconstruct the region with arteriovenous malformations. The feeding arteries of the arteriovenous malformations were used as recipient vessels in all cases of free-tissue transfers without any trouble in microvascular anastomosis. With an average follow-up of 3 years and 2 months, 12 patients showed no clinical recurrence (86 percent). Follow-up angiography in seven patients showed complete disappearance of malformations in two patients and residual malformations not enlarged in three patients. Two patients had residual malformations that were noted to be increasing in follow-up angiograms, and they also had clinical evidence of recurrence. In these patients an intramaxillary recurrence in one and intraorbital in the other appeared at about 1 and 3 years, respectively, after surgery. This therapeutic concept can be expected to provide great remission in the treatment of arteriovenous malformations.
Adult↗
Facial reconstruction with free-tissue transfer.
The article provides a retrospective review of 25 free-tissue transfers for facial reconstruction on 24 recipient sites in 21 patients. The recipient sites of the face were classified into frontal (4 patients), orbital (2 patients), nasal (2 patients), buccal (11 patients), and oral region (5 patients). The transferred flaps included 16 fasciocutaneous flaps (6 forearm flaps, 5 scapular flaps, 2 anteromedial thigh flaps, 1 lateral arm flap, 1 dorsalis pedis flap, and 1 deltopectoral flap) and 8 myocutaneous flaps (6 latissimus dorsi myocutaneous flaps, 1 serratus anterior myocutaneous flap, 1 rectus abdominis myocutaneous flap, and 1 prefabricated flap). Thinning modifications such as the expansion, reduction, or extension techniques were performed in the myocutaneous flap to avoid having a bulky flap. In our view, the flap from the trunk matches the facial skin color better than that from the extremity. Satisfactory results were attained in all cases in which a complete replacement of the facial aesthetic unit was performed.
Adolescent↗
A cadaver investigation of the blood supply of the galeal frontalis flap.
The vascular anatomy of the galeal frontalis flap was studied in 12 fresh cadavers by an intraarterial dye injection technique. Special attention was directed to the length limit of this flap. The general belief that the galeal frontalis flap has a robust vascularity by means of the supratrochlear and supraorbital arteries was not demonstrated in this study. In the medial half of the forehead, superficial branches of both arteries penetrated the frontalis muscle immediately above the supraorbital rim and ran superficially in the subcutaneous tissue. In the lateral half, some of the superficial branches of the supraorbital artery traveled with the frontalis muscle and anastomosed with the frontal branch of the superficial temporal artery. Deep branches of the supratrochlear and supraorbital arteries showed an axial distribution on the periosteum only for a short distance. One or two branches of the supraorbital artery were found to take a superficial course within the subgaleal layer, pierce the frontalis muscle, and anastomose with the superficial temporal artery. These findings suggest that the galeal frontalis flap should be elevated in the lateral forehead. The preservation of the periosteum with the flap is recommended in order to ensure the temporoparietal extension.
Blood Vessels↗
Prognostic evaluation of cutaneous malignant melanoma based on the pTNM classification.
The prognoses of 100 consecutive melanoma patients were analyzed on the basis of Breslow's thickness and Clark's levels as well as according to stage employing the 1987 UICC pTNM classification. Among patients with lesions < or = 1.50 mm thick, the 10-year survival rate was 100% for both pT1 (n = 13) and pT2 (n = 6) disease, 73.4% for pT3a disease (n = 26), 62.2% for pT3b disease (n = 15), 69.3% for pT3 (n = 41) disease, and 38.7% for pT4 disease (n = 38). Significant differences in survival were found between the pT4 group and the pT1/pT3a or pT3 groups. The 10-year survival rate was 100% for level II (n = 13) and level III (n = 13) disease, 58.3% for level IV (n = 46) disease, and 34.5% for level V (n = 26) disease. Significant differences were found between level V and other levels. The survival rate at 10 years was 100% for stage I (n = 18), 63.3% for stage II (n = 24), and 52.5% for stage III (n = 55). In stage IV (n = 3), there was only one patient who survived for 42 months. There were significant differences in survival among all stages except I and II. The 10-year survival rate in 3 subgroups of stage III was 58.9% for pT4pN0M0 patients (n = 14), 63.2% for pT,pN1M0 patients (n = 31), and 20% for pT,pN2M0 patients (n = 10). Significant differences were found between the pT,pN1M0 and pT,pN2M0 subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Uniquely higher incidence of isolated or combined deficiency of band 3 and/or band 4.2 as the pathogenesis of autosomal dominantly inherited hereditary spherocytosis in the Japanese population.
To clarify the pathogenesis of hereditary spherocytosis (HS), red cell membrane protein components were analyzed by sodium dodecylsulfate-polyacrylamide gel electrophoresis (SDS-PAGE) with a 3.5-17% exponential gradient according to the method of Fairbanks et al. and of Laemmli in 47 HS cases from 32 unrelated Japanese families. The relative contents of each membrane protein fraction, which was stained by Coomassie blue, were expressed as their ratios to those of total membrane proteins. The density of each band of red cell membrane proteins in 47 HS patients was compared to that in 10 normal controls or in 4 high-reticulocyte controls. Various isolated or combined deficiencies of membrane proteins in these HS patients were detected by identifying the amounts of membrane proteins, which were > 1 S.D. (91%) or 2 S.D. (53%) of the mean values of normal controls, and > 1 S.D. (100%) or 2 S.D. (98%) of those of high-reticulocyte controls. Contrary to the commonly held belief that most of the autosomal dominantly-inherited HS demonstrate isolated or combined deficiency of ankyrin (ANK) and/or spectrin (SP), a much lower incidence of isolated or combined deficiency of SP and/or ANK was observed in these Japanese HS patients; 19% (> 1 S.D.) or 12% (2 S.D.) compared to normal controls, or 2% (1 S.D.) or 4% (2 S.D.) compared to high-reticulocyte controls. Instead, the incidence of isolated or combined deficiency of band 3 (B3) and/or band 4.2 (B4.2) was markedly elevated in these Japanese HS patients; 50% (1 S.D.) or 39% (2 S.D.) compared to normal controls, or 78% (1 S.D.) or 88% (2 S.D.) compared to high-reticulocyte controls. Other combined deficiencies were also observed, but the incidence was much lower. Therefore, distinct characteristics, i.e., higher incidence of isolated or combined deficiency of B4.2 and/or B3 with much lower incidence of ANK and/or SP deficiency, were observed in Japanese HS patients.
Anion Exchange Protein 1, Erythrocyte↗
Red cell membrane disorders in the Japanese population: clinical, biochemical, electron microscopic, and genetic studies.
Based on studies on 610 cases of hereditary red cell membrane disorders, the characteristic features of the incidence of these disorders in the Japanese population are described. These patients were screened by a protocol on red cell morphology (scanning electron microscopy), on red cell membrane proteins (sodium dodecylsulfate polyacrylamide gel electrophoresis, and kinetics of membrane proteins), biophysical studies (ektacytometry, mechanical stability and fluorescence recovery after the photobleaching method), membrane transport (sodium influx and efflux, and anion transport), gene analysis (spectrins, band 4.2 and band 3), surface markers (blood type antigens and sialic acid content), and development and expression of membrane proteins (using a two-phase liquid culture system). Among the molecular abnormalities detected, alpha-spectrin mutation appeared rare (only one family with spectrin alpha I/74), as opposed to two beta-spectrin mutations in Japan out of seven worldwide cases. Two unrelated kindreds with a chromosomal abnormality; that is, del (8) (p11.2-p21.1), were found that involved the possible contribution of ankyrin to the pathogenesis of hereditary spherocytosis. Anomalies of a transmembrane domain of band 3 were detected in two independent kindreds with impaired anion transport. Among 16 HE patients, 13 cases were partially band 4.1 deficient. Complete band 4.2 deficiency of the Nippon type (GCT-->ACT at codon 142 in band 4.2 gene) was observed in 17 cases of 13 unrelated kindreds. Other forms of band 4.2 deficiency without the mutation were also detected in three kindreds. Band 7 deficiency was found in seven cases with hereditary stomatocytosis independent of the presence or absence of cation transport abnormalities. A relatively high incidence of hereditary high red cell membrane phosphatidylcholine hemolytic anemia was disclosed by the analysis of red cell membrane lipids.
Anemia, Hemolytic, Congenital↗
[Concordant improvement of progressive systemic sclerosis and chronic myelogenous leukemia with interferon-alpha treatment].
A 44-year-old woman with progressive systemic sclerosis (PSS) visited our clinic because of leukocytosis and thrombocytosis. She was diagnosed as having chronic myelogenous leukemia (CML) with PSS, and was treated with interferon-alpha 2b (IFN-alpha) after pretreatment of hydroxyurea as a cytoreduction. Complete hematological remission was obtained two months later, and four months later minimal cytogenetic response was achieved by IFN-alpha. Her PSS symptoms were also improved to some extent as judged by Rodnan's total skin score, maximal opening distance of oral cavity, and range of motion of wrists. Our results suggest that IFN-alpha is probably beneficial not only for CML itself but also for PSS, too.
Adult↗
Electron microscopic and physicobiochemical studies on disorganization of the cytoskeletal network and integral protein (band 3) in red cells of band 4.2 deficiency with a mutation (codon 142: GCT-->ACT).
The role of band 4.2 deficiency in the pathogenesis of red cell membrane dysfunctions was studied in seven unrelated patients with complete band 4.2 deficiency with a point mutation (142 GCT-->ACT; 142 Ala-->Thr) on the cDNA of the band 4.2 gene. Two major types of abnormalities were detected in these patients; (A) abnormalities of the cytoskeletal network in the horizontal dimension, and (B) abnormalities of band 3 in the vertical dimension. Electron microscopy by the surface replica method and the quick-freeze deep-etching method demonstrated the markedly impaired cytoskeletal network (a disorganized cobblestone pattern, uneven distribution of junctional units, and the appearance of bulky aggregates after heat treatment). Ektacytometry showed a markedly decreased red cell deformability especially at 48 degrees C, although the cytoskeletal proteins themselves were essentially normal with normal mechanical stability of the Triton-shells. Electron microscopy by the freeze fracture method revealed a decreased number and a random distribution of intramembrane particles (IMPs) with a shift of the IMPs to a larger size. Fluorescence recovery after photobleaching studies on band 3 indicated the marked increase of its mobile fraction. The extractability of band 3 by Triton X in vitro was markedly enhanced, although the physico-biochemical properties of band 3 itself (the cleavage pattern of band 3 fragments, and the binding properties of band 3 to band 4.2 or ankyrin) were basically normal. These findings demonstrate that band 4.2 plays a crucial role in the maintenance of the normal structure and functions of both the cytoskeletal and integral proteins (band 3).
Anion Exchange Protein 1, Erythrocyte↗
Effects of recombinant human soluble thrombomodulin (rhs-TM) on a rat model of disseminated intravascular coagulation with decreased levels of plasma antithrombin III.
We reported that recombinant human soluble thrombomodulin (rhs-TM) is effective for disseminated intravascular coagulation (DIC) in vivo, in mice and rats. In the present work, we investigated the effects of decreased plasma antithrombin III (ATIII) levels on anticoagulant effects of rhs-TM, as compared to findings with heparin, of which effect is lowered by the decreased plasma ATIII levels in patients with DIC. Rat plasma ATIII levels decreased when we mixed plasma with anti-rat ATIII antibody and the potential of heparin to prolong APTT or PT was markedly diminished. The potential of rhs-TM to prolong APTT and PT was not affected. In rats injected with anti-rat ATIII antibody, plasma ATIII levels decreased immediately. When the rats were infused with tissue factor (TF), DIC was induced. At doses of rhs-TM and heparin which were equally effective at inhibiting the decrease in platelet count and fibrinogen level in control rats treated with TF, only rhs-TM remained effective in preventing DIC in rats with reduced ATIII levels. Heparin was not effective when administered to these rats with reduced ATIII levels. Therefore, rhs-TM effectively inhibits coagulation independent of ATIII levels, in contrast to heparin, which depends on the ATIII level.
Animals↗
[Secondary leukemia after etoposide treatment involved MLL gene rearrangement].
The 11q23 chromosomal abnormality is frequently observed in infantile leukemia and secondary leukemia, and the translocation associated gene in infantile leukemia is called mixed-lineage leukemia (MLL) gene. A 50-year-old man was admitted because of left axillary lymphadenopathy and IBL like T cell lymphoma was diagnosed by lymph node biopsy. The patient responded to the LSG-9 protocol with complete remission. After 10 months he was readmitted because of fever and was diagnosed acute myeloblastic leukemia by bone marrow aspiration. Chromosome analysis revealed 11q23 abnormality, suggesting that the leukemia was induced by etoposide treatment. Southern blot analysis demonstrated DNA rearrangement in the MLL gene at 11q23. It was suggested that the breakpoint region of the MLL gene in secondary leukemia is the same as that of infantile leukemia.
Chromosomes, Human, Pair 11↗
[Allogeneic cryopreserved marrow transplantation in a patient with chronic myelogenous leukemia].
A 45-year-old male with chronic myelogenous leukemia received cryopreserved allogeneic bone marrow from his HLA-identical sister. Bone marrow was harvested and cryopreserved prior to chemoradiotherapy since the donor had neurotic tendencies. The preconditioning regimen consisted of standard dosage of busulfan plus cyclophosphamide and total lymphoid irradiation (5Gy). A total of 3.1 x 10(7)/kg marrow mononuclear cells, containing 4.7 x 10(5) CD34+ cells/kg, and 8.0 x 10(6)/kg buffy coat cells collected from the donor at day 0 was infused. Marrow engraftment occurred by day 38 although hematological recovery was delayed and subsequent administration of GM-CSF, methylprednisolone and donor buffy coat cells were required. Mononuclear cells obtained from the patient's blood at day 28 had an inhibitory effect on CFU-GM formation of the donor's bone marrow mononuclear cells. We considered that this case suffered from a transient myelosuppression due to residual host cells after bone marrow transplantation.
Bone Marrow↗