Biomedical subjects
Publications and source records attributed to M Aihara.
A case of spontaneous urinary peripelvic extravasation secondary to an obstructing squamous cell carcinoma of the ureter is presented. A review of the literature reveals that peripelvic extravasation caused by tumor obstruction of the ureter is rare and most of its underlying lesions are metastatic retroperitoneal adenopathy.
A role of factor XIII (FXIII) on the interaction of human platelets with collagen was investigated using either formaldehyde fixed-washed platelets (FWP) or nonfixed platelets. The adhesion of FWP to bovine type I collagen was measured by using either an aggregometer or a collagen immobilized glass beads column. The interaction of non-fixed human platelets with collagen was measured with in vitro bleeding time (Thrombostat-4,000), which was performed by passing citrated whole blood through the filter covered with rat type I collagen under the constant shear stress. FWP adhesion to the collagen immobilized column (1,300 micrograms collagen) was not changed by the addition of commercial FXIII preparation (Fibrogammin); the adhesion was 42.7% in the presence of 1% human serum albumin, 42-43% in the presence of 1-2 U/ml of FXIII. The addition of rabbit antibody to FXIII to normal FWP did not change the degree of adhesion; 42.3% (1:100 anti-FXIII) and 46.1% (normal rabbit serum). Furthermore, platelets from the patient with congenital FXIII deficiency normally aggregated by bovine collagen and the adhesion of the patient FWP to the collagen was similar to that of normal FWP. Prolongation of partial thromboplastin time and the changes of thromboelastograph of normal plasma were observed after mixing with the collagen, and factor VIII, FXIII and von Willebrand factor were adsorbed by the collagen. The amount of FXIII in normal human plasma bound to collagen was 17, 23 and 54% at the concentration of the collagen 250, 500 and 1,000 micrograms/ml, respectively. The binding of plasma ristocetin cofactor was not different between normal control and the patient with FXIII deficiency. These data suggest that FXIII is not involved in human platelet interaction with the type I collagen, while FXIII in normal human plasma binds to the collagen.
Imipenem/cilastatin sodium (IMP/CS) was administered to patients with severe infections complicated by hematological disorders and solid tumors to assess its efficacy and safety. Primary diseases in this series of 76 cases included 37 cases of hematological disorders (acute leukemia in 25 cases, malignant lymphoma in 7 cases, aplastic anemia in 3 cases and 2 other diseases) and 38 cases of solid tumors (lung cancer in 7 cases, gastric cancer in 11 cases, esophageal cancer in 6 cases, pancreatic cancer in 3 cases, bile duct cancer in 4 cases, hepatocellular cancer in 3 cases, and 4 other diseases). Following results were obtained. 1. Types of infection in hematological diseases were sepsis in 5 cases, suspected sepsis in 24 cases, pneumonia in 5 cases and 3 others. The efficacy rates were 100% in sepsis, 62.5% in suspected sepsis, 80% in pneumonia and 73% in all cases. 2. Types of infection in solid tumors were sepsis in 2 cases, suspected sepsis in 13 cases, pneumonia in 10 cases, cholecystitis in 2 cases, cholangitis in 5 cases, liver abscess in 2 cases, and 4 others. The efficacy rates were 50% in sepsis, 69.2% in suspected sepsis, 80% in pneumonia, and 71.1% in all cases. 3. IPM/CS was administered in single use in 66 cases and in combination with other antibiotics in 9 cases. The efficacy rate in the single use was 72.7% and that in the combination use was 66.7%. 4. The efficacy rate in 35 cases of first use was 71.4% and that in 40 cases of second use was 72.5%.(ABSTRACT TRUNCATED AT 250 WORDS)
A 21-year-old man was admitted to our hospital because of anorexia and general malaise in July, 1988. On admission, the white blood cell count of 18,600/microliters with 72% leukemic cells. The bone marrow aspirate showed 76.8% immature monocytes, 10% mature and immature eosinophils. Leukemic cells were 66.6% myeloperoxidase positive cells, and 20.6% naphthylbutyrate esterase positive cells. The lysozyme activity in urine was high. Cytogenetic analysis revealed the presence of 46 XY inv (16) (p13 q22). Under the diagnosis of acute myelomonocytic leukemia with eosinophilia (M4Eo) associated with inv (16) (p13 q22), one course of DCMP induction therapy was performed. After complete remission, the bone marrow aspirate showed disappearance of inv (16) (p13 q22), and associated with decreased residual leukemic cells.
Thirty six hemophiliacs with HIV infection were treated with high-dose glycyrrhizin, Stronger Neo-Minophagen C (SNMC). The dose was 100-200 ml of SNMC in eighteen patients and 400-800 ml in the other 18. The patients were divided into an asymptomatic carrier (AC) group and AIDS related complex (ARC)/AIDS group. SNMC was administered intravenously daily for the first 3 weeks, every second day for the following 8 weeks to 36 HIV positive hemophilia patients in accordance with the protocol proposed by the Japanese National Research Committee. The CD 4/CD 8 ratio and CD 4 positive lymphocyte counts did not change during the treatment period. However, significant improvement was noted in some cases. A slight increase in mitogenic responsiveness to phytohemagglutinin, Concanavalin A and pokeweed mitogen was noted in most patients of both groups, especially in the AC group administered over 400 ml of SNMC. Furthermore, complete improvement was noted in liver dysfunction, which has been thought to be a major problem in hemophiliacs treated with blood products. Thus prophylactic administration of high-dose SNMC to HIV positive hemophiliacs having impaired immunological ability and liver dysfunction was considered to be effective to prevent the development from AC/ARC to AIDS.
Serum cortisol, prolactin (PRL), TSH, GH, LH and FSH levels were measured before and immediately after daily ACTH-Z therapy (0.01 mg/kg/day, 1-2 weeks) for 5 patients with infantile spasms and one patient with myoclonus epilepsy. Total number of ACTH-Z therapy were 8 times, and all patients became seizure free after ACTH-Z therapy. In 6 occasions, TRH, LH-RH and insulin tolerance tests were performed before and after daily ACTH-Z therapy. Serum cortisol levels were significantly increased after daily ACTH-Z therapy but all other hormone levels were significantly decreased. In TRH and LH-RH tolerance tests, peak levels and increments of PRL, LH and FSH were significantly decreased after daily ACTH-Z therapy and those of TSH were mildly decreased. In one case insulin tolerance test revealed an adequate decrease of blood glucose before and after ACTH-Z therapy, and there was a poor GH response after ACTH-Z therapy. Daily ACTH-Z therapy was thought to suppress secretion of anterior pituitary hormones.
The adhesion of human fixed washed platelets (FWP) to collagen was decreased after treatment with Serratia marcescens protease (SP), which removed 95% of the glycocalicin from platelet membrane glycoprotein (GP) Ib. However, the diminished adhesion of SP treated FWP to collagen could still be increased in the presence of purified von Willebrand factor (vWF). This ability to vWF to increase FWP adhesion to collagen is defined as collagen cofactor (CCo). The adhesion of FWP to collagen was not affected by a monoclonal antibody (MAb) to GP IIb/IIIa (10E5), that inhibits ADP and collagen induced platelet aggregation. On the other hand, it was decreased by 50% by a MAb to GP Ib (6D1), that inhibits ristocetin induced platelet aggregation. Adhesion of FWP in buffer to collagen was completely inhibited by Ricinus communis agglutinin I or concanavalin A, while Lens culinalis agglutinin and wheat germ agglutinin showed 50% inhibition. The FWP adhesion to collagen in the presence of vWF (normal plasma) was unaffected by MAbs to GP IIb/IIIa (10E5, P2, HPL1) but was decreased to 32-38% by MAbs to GP Ib (6D1, AN51, HPL11). A MAb to vWF (CLB-RAg 35), that inhibits ristocetin induced binding of vWF to platelets, decreased the CCo of normal plasma by 70%. The MAb, CLB-RAg 201, that inhibits the binding of vWF to collagen, completely inhibited the CCo of normal plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
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Collagen cofactor (CCo), an activity of von Willebrand factor (vWF) which increases the rate of adhesion of human fixed washed platelets (FWP) to collagen, was measured in plasma from normal individuals and individuals with von Willebrand's disease (vWD). CCo in vWD plasma was compared to vWF antigen (vWF:Ag), ristocetin cofactor (RCo), factor VIII (VIII) coagulant activity (VIII:C) and the quantitative bleeding time. There was close correlation between CCo and VIII:C (r = 0.909), vWF:Ag (r = 0.975), and RCo (r = 0.936). However, there was no correlation between CCo and the quantitative bleeding time. Plasma CCo in type IIA vWD was markedly lower than vWF:Ag and the ratio of CCo/vWF:Ag was 0.08, which was less than a mean value of 0.92 in type I vWD. CCo activity in normal plasma was completely inhibited by monoclonal antibody CLB-RAg 201, an antibody that inhibits the binding of vWF to collagen, suggesting that the binding of vWF to collagen is required for the expression of CCo. Furthermore, the partial inhibition of CCo by monoclonal antibody CLB-RAg 35 that inhibits the binding of vWF to platelet in the presence of ristocetin, suggests that CCo is partly mediated through platelet membrane glycoprotein Ib. Large multimers of vWF:Ag in normal plasma were preferentially absorbed by collagen. These studies demonstrate that CCo is another functional activity of vWF and the measurement of CCo may be useful for the detection of new variant forms of vWD.
Mice carrying the H-2b haplotype (e.g., inbred strains C57BL/6 and C57BL/10) are low responders to sperm whale myoglobin when tested in the T cell proliferation assay. Their response is improved by the removal of the Ly-2+ cells from the lymph node population, but it still remains significantly lower than that of cells cells from high-responder strains (e.g., DBA/2, H-2d). To determine whether T cells from the low and high-responder mice recognize the same or different epitopes on the immunizing antigen, we obtained sets of T cell clones from both strains and tested them against peptides representing different regions of the myoglobin molecule, as well as against myoglobins from species other than the sperm whale. Four types of T cell clones were obtained from the DBA/2 mice: 3 types responded to the peptide 107-120 (9 clones altogether), and 1 type responded to the peptide 133-149 (4 clones altogether). The 3 types responding to the peptide 107-120 could be distinguished by their response to horse myoglobin or by the restriction of the response (Ad vs. Ed). Similarly, 5 types of T cell clones were obtained from the C57BL/6 mice: 2 types responded to the peptide 10-22 (1 type, but not the other, responded to horse myoglobin); 1 type responded to the peptide 133-149; and 2 types did not respond to any of the peptides used (1 type, but not the other, responded to dog myoglobin). All 5 types (13 clones altogether) were presumably Ab restricted. These results demonstrate the diversity of epitopes in single antigenic regions and show equivalent heterogeneity of T cell repertoires in high and low responder mice. Attempts to demonstrate specific T cell suppression in the low responder mice failed; only partial, nonspecific suppression was observed.
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Changes in uterine weight and the estrogen receptor concentrations were examined in persistent estrous (PE) and persistent diestrous (PD) rats at 80 days of age. To prepare PE rats, 100 micrograms estradiol benzoate (EB) was injected sc into 3-day-old females. PD rats were obtained by daily injections of 10 micrograms EB into females for 10 consecutive days from the day of birth. The uterine weight in PE rats at 80 days was comparable to that in metestrous controls. The uteri of PD rats were smaller than those in PE rats. The concentrations of estrogen receptor in nuclear fractions in PE and PD rats were much lower than those in proestrous controls. Receptor concentrations in cytosol fractions were significantly lower in PE and PD rats than in control diestrous, proestrous and estrous rats. The dissociation constants and sedimentation coefficients of estrogen receptors in PE and PD rats were found to be in the same range as those in control rats. Thus, the reduction in the activity of cytosol receptors in these rats is attributable to a quantitative change in the amount of estrogen receptor protein. To study the response of the uterus to estrogen, ovariectomized rats were injected daily with 10 micrograms estradiol for 7 consecutive days. The uterine growth of PE and PD rats after administration of estradiol was less marked than in controls, indicating a reduction of estrogen sensitivity of the uterus. Seven daily administrations of estradiol continued to increase the concentration of uterine cytosol estrogen receptor in controls. In contrast, in PE and PD rats, the receptor concentrations continued to increase during the first 3 days, and then remained constant. These data suggest that EB in neonatal treatment may directly affect the mechanism of receptor synthesis in uterine tissues. This effect may contribute to the reduction of the uterine response to estrogen.
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