Mechanism of intermolecular dephasings on time-resolved anti-Stokes Raman scattering from a molecular ensemble.
Explore the source record for details and available documents.
Journal Article↗
Biomedical subjects
Y Fujimura
Publications and source records attributed to Y Fujimura.
Aggravation of subclinical diabetes insipidus during pregnancy.
BACKGROUND: Transient polyuria and polydipsia during pregnancy are rare, and their cause is not entirely clear. Possible explanations include the exacerbation of preexisting abnormalities in the secretion or action of vasopressin and abnormally large increases in plasma vasopressinase activity. METHODS: We studied two women in whom overt polyuria and polydipsia developed during the third trimester of pregnancy and disappeared after delivery. The secretion and action of vasopressin were studied both when the women had polyuria and polydipsia and later, when their water intake and urine volume were normal. RESULTS: One patient had partial nephrogenic diabetes insipidus. She had little increase in urine osmolality in response to water deprivation, hypertonic-saline infusion, and vasopressin injection and no response to desmopressin acetate (1-deamino-8-D-arginine vasopressin) during the immediate postpartum period. Her basal and stimulated plasma vasopressin concentrations were high (16.5 to 203.4 pmol per liter) before and during hypertonic-saline infusion 30 months post partum. The other patient had partial neurogenic diabetes insipidus. She had subnormal basal plasma vasopressin concentrations, a subnormal increase in the plasma vasopressin level and a subnormal decrease in urine flow in response to the administration of vasopressin, and a normal response to desmopressin. After pregnancy, when her urine volume was normal, she had no increase in plasma vasopressin in response to hypertonic-saline infusion, but she had a normal rise in the plasma vasopressin level and a normal renal response to vasopressin administration. CONCLUSIONS: Pregnancy may unmask subclinical forms of both nephrogenic and neurogenic diabetes insipidus. This exacerbation may result from both increased vasopressinase activity and diminished renal responsiveness to vasopressin.
Adult↗
Isolation and chemical characterization of two structurally and functionally distinct forms of botrocetin, the platelet coagglutinin isolated from the venom of Bothrops jararaca.
Two distinct forms of botrocetin, the von Willebrand factor (vWF)-dependent platelet coagglutinin isolated from the venom of the snake Bothrops jararaca, were purified and characterized structurally and functionally. The apparent molecular mass of the one-chain botrocetin was 28 kDa before and 32 kDa after reduction of disulfide bonds, while that of the two-chain botrocetin was 27 kDa before and 15/14.5 kDa after reduction. Amino acid composition of the two species revealed a similar high content of potentially acidic residues (greater than 60 Asx and Glx residues/molecule) but significant differences in the content of Cys and Phe residues. The NH2-terminal sequence of the one-chain botrocetin was Ile-Ile/Val-Ser-Pro-Pro-Val-Cys-Gly-Asn-Glu-. Two constituent polypeptides of the two-chain botrocetin showed similar but different NH2-terminal sequences, distinct from that of the one-chain species: (alpha) Asp-Cys-Pro-Ser-Gly-Trp-Ser-Ser-Tyr-Glu- and (beta) Asp-Cys-Pro-Pro-Asp-Trp-Ser-Ser-Tyr-Glu-. The carbohydrate content of both species was less than 2% of the total mass, and the pI was 4.0-4.1 for the one-chain species, and 4.6, 5.3-5.4, and 7.7-7.8 for the two-chain species. No free sulfhydryl group was detected in each species. Both types of botrocetin were resistant to proteolysis at neutral pH. Incubation of 125I-labeled one-chain botrocetin with the crude venom solution resulted in no detectable structural change. On a weight basis, the two-chain botrocetin was 34 times more active than the one-chain form in promoting vWF binding to platelets.(ABSTRACT TRUNCATED AT 250 WORDS)
Amino Acid Sequence↗
Studies on anti-von Willebrand factor (vWF) monoclonal antibody NMC-4, which inhibits both ristocetin- and botrocetin-induced vWF binding to platelet glycoprotein Ib.
Anti-von Willebrand factor (vWF) monoclonal antibody NMC-4 completely inhibited vWF binding to platelet glycoprotein (GP) lb induced by either ristocetin or botrocetin at an IgG concentration of approximately 10 micrograms/mL, and also blocked binding of asialo-vWF to GP lb. NMC-4 coupled beads isolated a 97-Kd fragment (Fr) from a whole tryptic digest of vWF. The N-terminal sequencing of the nonreduced 97-Kd Fr, in combination with amino acid analysis, showed it to be a homodimer of residues 449 through 728 of the constituent subunit. Present data, together with the results obtained from previous studies, confirm the existence of one or three possible inter-subunit disulfide bonds between cysteine residues 459, 462, and 464. NMC-4 bound to reduced vWF Fr(s) more weakly than to nonreduced Fr(s), but it did not react with Fr III-T2 of vWF, a disulfide-linked twin heterodimer of residues 273 through 511 and 674 through 728 (Marti et al, Biochemistry 26:8099, 1987). Fr III-T2 completely inhibited ristocetin-induced vWF binding at a concentration of 100 mumol/L but had no effect on botrocetin-induced binding. In addition, both the N- and C-terminal polypeptides, residues 449 through 549 and 674 through 728, generated by subdigestion of the 52/48-Kd Fr (Fujimura et al, J Biol Chem 261:381, 1986), inhibited preferentially ristocetin-induced vWF binding without affecting to botrocetin-induced vWF binding. These findings suggest that amino acid residues 512 through 673 of the vWF subunit are involved in botrocetin-induced vWF binding.
Antibodies, Monoclonal↗
Flow cytometric analysis of anti-platelet antibodies in patients with chronic idiopathic thrombocytopenic purpura (ITP) using acid-treated, formalin-fixed platelets.
Acid treatment of normal washed platelets prepared by albumin density gradient centrifugation followed by formalin fixation effectively eliminates HLA class I antigens from the platelet surface, without altering the immunoreactivity of platelet membrane glycoproteins Ib and IIb/IIIa complex. Using these platelets, flow cytometric analysis was performed on a total of 20 sera from different patients with chronic ITP, and revealed an inverse linear correlation between the platelet count and the mean fluorescence intensity which represents a relative amount of platelet-bound IgG. These results suggest that acid-treated, formalin-fixed platelets can be used as specimens to detect anti-platelet antibodies to differentiate from those to HLA-class I antigens.
Acids↗
Antiplatelet glycoprotein Ib monoclonal antibody (OP-F1) totally abolishes ristocetin-induced von Willebrand factor binding, but has minimal effect on the botrocetin-induced binding.
We describe here a new antiplatelet glycoprotein (GP) Ib monoclonal antibody (MoAb) designated OP-F1 (IgG1 kappa). Both OP-F1 and a well-characterized anti-GPIb MoAb, AP-1, totally abolished ristocetin-induced von Willebrand factor (vWF) binding to platelets and desialylated vWF binding to platelets at an IgG concentration of 2-8 micrograms/ml. AP-1 also blocked snake venom botrocetin-induced vWF binding at a similar IgG concentration, whereas OP-F1 had a minimal effect on botrocetin-induced binding. At a higher IgG concentration (150 micrograms/ml), OP-F1 inhibited botrocetin-induced binding by 50%. AP-1 (IgG) did not interfere with binding of [125I]OP-F1 (IgG) to platelets. Thus, the epitope involved in the binding of OP-F1 or AP-1 appears to be quite different. These results suggest that the vWF binding site(s) on the GPIb molecule generated by these inducers is in close proximity but not completely identical.
Antibodies, Monoclonal↗
[Domain structure of human von Willebrand factor, and its modulators involved in the platelet adhesion process in vitro].
von Willebrand factor (vWF), a macromolecular glycoprotein synthesized in endothelial cells and megakaryocytes circulates in blood as heterogenous multimers and plays a critical role in the formation of platelet plugs. vWF is composed of an identical subunit with a molecular weight (MW) of 270 kDa, which is held together by disulfide bonds. Functional domains of vWF for factor VIII, heparin, platelet glycoprotein (GP) Ib, collagen, and GP IIb/IIIa locate in this order from the N-to C-terminus of subunit. The GP Ib binding domain is cryptic in normal circulation and only becomes expressed when vWF is associated with the subendothelial matrix or with fibrin. In vitro, an antibiotic ristocetin or the snake venom botrocetin isolated from Bothrops jararaca mimics the active component of subendothelial matrix and causes the binding of vWF to GP Ib. To elucidate the mechanism of in vitro process of vWF-GPIb binding, we describe here the isolation and characterization of two distinct forms of botrocetin. Since ristocetin is a heavily glycosylated proteoid, it is hard to characterize the structure on the basis of amino acid analysis. The apparent MW of the one-chain botrocetin was 28 kDa before and 32 kDa after reduction of disulfide bonds, while that of the two-chain botrocetin was 27 kDa before and 15/14.5 kDa after reduction. Amino acid composition of the two species revealed a similar high content of potentially acidic residues (greater that 60 Asx and Glx residues/molecules) but significant differences in the content of Cys and Phe residues. The N-terminal sequence of the one-chain was Ile-Ile/Val-Ser-Pro-Pro-Val-Cys-Gly-Asn-Glu-.(ABSTRACT TRUNCATED AT 250 WORDS)
Amino Acid Sequence↗
Growth and cell viability of aortic versus pulmonic homografts in the systemic circulation.
Growth characteristics and cell viability of aortic and pulmonic valve homografts in the systemic circulation were compared in a growing sheep model. Seven aortic and seven pulmonic cryopreserved homografts were implanted in the descending aortae of recipient female lambs. Of seven sheep per group, three were killed at 8 months, three at 12 months, and one at 15 months. Tissue cultures were obtained on homograft valve and root wall specimens. Male donor cells were identified by chromosome analysis. Preimplant to explant changes in pulmonic homograft external diameters at the valve annulus and sinotubular junction increased significantly more than in aortic roots. The postoperative dimensions of the distal anastomotic diameter and length of the graft increased significantly more in pulmonic than in aortic roots by time of explant. Leaflet calcification and valvular stenosis did not develop in either pulmonic or aortic homografts over the period of observation. Calcification in the root wall was significantly less in pulmonic than aortic homografts. Growth on tissue culture was obtained from over 70% of homograft specimens. Viable donor cells were demonstrated in none and 43% of aortic and pulmonic leaflets, respectively, and 71% and 57% of aortic and pulmonary arterial homograft walls, respectively. In conclusion, both aortic and pulmonic homograft valves provide freedom from calcification and stenosis in this model. Continuing expansion of pulmonic root diameters under systemic pressure might lead to late aneurysm formation. Although host cell repopulation of grafts may be advantageous, the presence of viable donor cells in leaflet tissue does not seem necessary to prevent calcific degeneration.
Animals↗
Morphology and histology of the latissimus dorsi muscle.
Explore the source record for details and available documents.
Back↗
Enhanced botrocetin-induced type IIB von Willebrand factor binding to platelet glycoprotein Ib initiates hyperagglutination of normal platelets.
Botrocetin, a protein isolated from the venom of the snake Bothrops jararaca, induces platelet aggregation/agglutination by von Willebrand factor (vWF) binding to the membrane glycoprotein (GP) Ib, an action resembling that of ristocetin. However, some differences in the interaction between vWF and platelet GPIb induced by these two substances have been reported. We have recently shown that the GPIb binding domain on the vWF molecule, in both instances, resides in the tryptic 52/48 kDa fragment extending from amino acid residue 449 to 728 of the constituent subunit. In the present report, we demonstrate that botrocetin does not induce agglutination of formalin-fixed platelets from a patient with Bernard-Soulier syndrome congenitally lacking GPIb and GPIX as well as GPV, a finding similar to that shown with ristocetin. A monoclonal antibody against GPIb (AP-1) inhibits either ristocetin- or botrocetin-dependent vWF binding to formalin-fixed platelets from normal individuals. Therefore, botrocetin-induced vWF binding to formalin-fixed platelets may reflect the interaction between vWF and platelet GPIb. To strengthen this concept, we have now found that heightened botrocetin-induced type IIB vWF binding to platelet GPIb causes hyperagglutination of normal platelets.
Antibodies, Monoclonal↗
Measurement of microvilli of microfold cells (M-cells) and absorptive cells in follicle-associated epithelium of mouse Peyer's patches.
Explore the source record for details and available documents.
Animals↗
Distribution of microfold cells (M cells) in human follicle-associated epithelium.
Explore the source record for details and available documents.
Adolescent↗
Use of the argon beam electrocoagulator for performing pulmonary wedge resections.
The argon beam electrocoagulator (ABC) is a new form of electrocautery that is thought to be more effective than standard electrocautery. It has been used primarily in procedures associated with major blood loss such as liver transplantation and laparotomy for trauma. It has not been used in thoracic operations. We evaluated the safety and efficacy of the argon beam electrocoagulator for performing pulmonary wedge resections in an animal model by comparing it with standard electrocautery and suture closure. Variables used to compare the three methods of resection included perioperative blood loss, duration of chest tube air leak, and depth of necrosis and severity of inflammatory reaction in the lung at ten days and 3 weeks after resection. The argon beam electrocoagulator was as effective as standard electrocautery and suture closure in controlling air leaks, and caused less acute tissue injury than standard electrocautery. The argon beam electrocoagulator provides a safe and effective method for performing small pulmonary wedge resections, and should be evaluated in the clinical setting for this purpose.
Animals↗
Enhanced ristocetin-induced von Willebrand factor binding to platelet glycoprotein Ib in patients with steroid-responsive nephrotic syndrome.
To elucidate the mechanism of enhanced ristocetin-induced platelet aggregation (RIPA) in steroid-responsive nephrotic syndrome (SRNS), plasma levels of von Willebrand factor antigen (vWF:Ag) and ristocetin cofactor (RCof) were examined in 6 patients and the amount of ristocetin-induced vWF binding to platelets was determined. At the initial or relapse stage, the plasma vWF:Ag level was 415 +/- 137% and the RCof level was 364 +/- 117%. The ratio of RCof/vWF:Ag was 0.90 +/- 0.15 and no abnormalities of vWF:Ag multimers were observed, indicating that neither functional nor structural abnormalities were present in patient's plasma. The amount of ristocetin-induced normal vWF binding to nephrotic washed platelets, when ristocetin was used at concentrations of 0.5, 0.75, and 1.0 mg/ml, was 152-163% above the binding to normal platelets. In addition, nephrotic washed platelets resuspended in either normal or nephrotic plasma aggregated at a low concentration of ristocetin (0.75 mg/ml) which did not induce aggregation of normal platelets. In accordance with these observations, the decrease of Alcian blue 8GX binding to platelets, reflecting diminished surface negative charge, was also observed. These results appear to indicate that the plasma vWF level and the altered surface-negative charge in platelets both contribute to heightened vWF binding to GPIb, thus lowering the ristocetin concentration required for RIPA in SRNS.
Adolescent↗
[Left ventricular aneurysmectomy after myocardial infarction--comparative study between true aneurysms and functional aneurysms].
Postinfarction left ventricular aneurysms are pathophysiologically divided into true, functional and false aneurysm. On 14 patients treated by aneurysmectomy, we studied the difference of pre- and post-operative cardiac function between true aneurysms (9 patients) and functional aneurysms (5 patients). The aneurysm area, which is expressed as the end-diastolic perimeter (akinetic or dyskinetic area/left ventricular silhouette), was 51.6 +/- 7.7% in the true aneurysms versus 35.7 +/- 6.0% in the functional aneurysms. Preoperatively, patients with a true aneurysm had a more severe clinical status than those with a functional aneurysm (Six of nine patients with a true aneurysm were in New York Heart Association functional class III or IV). Postoperatively, all patients except one with a true aneurysm and one with a functional aneurysm improved in clinical status. Nonaneurysmal EF, that is the function of the nonaneurysmal left ventricle, has a significant correlation to postoperative LVEF (r = 0.57, p less than 0.05). Nonaneurysmal EF was 54 +/- 4% in the true aneurysm group versus 51 +/- 16% in the functional aneurysm group. LVEF improved significantly (p less than 0.05) from 31 +/- 11% preoperatively to 55 +/- 10% postoperatively in the group of true aneurysm, but did not improved significantly from 43 +/- 12% to 50 +/- 9% in the functional aneurysm group. The postoperative akinetic area was 8.1 +/- 9.1% in the true aneurysm group versus 17.8 +/- 11.5% in the functional group. We conclude that larger and more adequate resection of aneurysms improves the cardiac function in the true aneurysm group more than in the functional aneurysm group.
Adult↗
[A surgical case of Hodgkin's lymphoma originated from thymus].
We experienced a surgical case of large Hodgkin's lymphoma of the thymus. An 18 year-old male who had been complaining of a persistent cough was admitted to our hospital. Chest X-ray film showed an anterosuperior mediastinal tumor. But there was no superficial lymphadenopathy and hepatosplenomegaly. He received a surgical extirpation of the tumor approached by median sternotomy. The tumor expanded to the whole antero superior mediastinal region, which was 18.5 X 15 X 5.5 cm in size, surrounding the trachea and main branch of aortic arch and veins. The tumor directly invaded the bilateral pleura and left innominate vein, so these regions were resected with the tumor. The left innominate vein was reconstructed with a PTFE graft. The pathological diagnosis was Hodgkin's lymphoma nodular sclerosis type by LSG classification. A post operative course was uneventful.
Adolescent↗
[Significance of measuring Cu, Zn-superoxide dismutase (SOD) levels in open heart surgery].
Cu, Zn-SOD levels, free hemoglobin (Hb) and CPK-MB were measured in 18 patients undergoing open heart surgery. In order to evaluate the serum level of Cu, Zn-SOD, the ratio of Cu, Zn-SOD/free Hb was used to eliminate an influx of Cu, Zn-SOD released from erythrocytes during cardiopulmonary bypass. The value of Cu, Zn-SOD/free Hb was decreased significantly 30 minutes after aortic declamping and the minimal value was indicated 1 hour after the termination of cardiopulmonary bypass compared with the preoperative status. We thought that the decrease was due to the consumption of SOD competing against free radical generation. The correlation between the minimal value of Cu, Zn-SOD/free Hb and the ischemic time was apparent but the correlation between the minimal value of Cu, Zn-SOD/free Hb and the value of peak CPK-MB was not determined. It was suggested that the serum free radicals were not only derived from the heart but also from the lung or other parts of the body during open heart surgery.
Adult↗
Spontaneous platelet aggregation in type IIB Tampa von Willebrand disease is inhibited by the 52/48-kDa fragment of normal von Willebrand factor, which contains the GPIb binding domain.
The association of Type IIB von Willebrand disease (vWD) with chronic persistent thrombocytopenia and spontaneous platelet aggregation has recently been recognized. It has been shown that IIB von Willebrand factor (vWF) can initiate platelet aggregation by binding to the platelet glycoprotein (GP) lb receptor and inducing exposure of the GpIIb/IIIa fibrinogen receptor. In this study we demonstrate the increased binding of Type IIB Tampa vWF with normal platelets when compared with nonthrombocytopenic Type IIB vWF. Studies further demonstrate that spontaneous platelet aggregation initiated by IIB Tampa vWF can be blocked by a 52/48-kDa fragment of normal vWF, which contains the binding domain.
Binding Sites↗