Quantum decoherence and classical correlation in quantum mechanics.
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Biomedical subjects
Publications and source records attributed to M Morikawa.
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We investigated the effect of 2,3-dibenzylbutane-1,4-diol (DBB), a mammalian lignan, on superoxide production and [Ca2+]i mobilization in human neutrophils. DBB did not generate superoxide production by itself, but enhanced the FMLP or A23187-induced superoxide production in a dose dependent manner. DBB did not influence the OAG-induced superoxide production. The priming effect of DBB was inhibited by W-7 or trifluoroperazine, but not by H-7 or staurosporine. And the priming effect of DBB was observed in the presence or absence of extracellular Ca2+. DBB enhanced the low dose FMLP-induced [Ca2+]i mobilization. These results suggest that the priming effect of DBB in human neutrophils may be caused by the activation of the calcium-calmodulin pathway but not the protein kinase pathway.
The human leukemic cells HL-60, U937, KG-1 and THP-1 incubated with transforming growth factor-beta 1 (TGF-beta 1) were studied by examining cell surface antigens and macrophage-specific activities. The addition of 0.5 ng/ml (20 pM) of TGF-beta 1 with 1 alpha, 25-dihydroxyvitamin D3 [1 alpha, 25(OH)2D3] induced more Leu-M3 (CD14)-positive cells (approximately 80%) than 5 X 10(-8) M 1 alpha, 25(OH)2D3 alone did (30 to 50%), although original HL-60 cells did not express any Leu-M3 antigen at all. Tumor necrosis factor-alpha (TNF-alpha) with TGF-beta 1 and 1 alpha, 25(OH)2D3 was found to potentiate the expression of these surface antigens. Furthermore, the phagocytic activity was also induced strongly. The expression of CR3 (CD11b) antigen was also increased, and all Leu-M3-positive cells were found CR3-positive when HL-60, U937, and THP-1 cells were treated with these stimulants. In contrast, CR3 but not Leu-M3 was induced in KG-1 cells after the same treatment. This may indicate that the responsiveness of leukemic cells to TGF-beta 1 and 1 alpha, 25(OH)2D3 might vary depending on a differentiation stage of the target cells. Furthermore, K562 cells originated from a more undifferentiated precursor, were not able to respond to these two inducers. These results suggested that some of TGF-beta superfamily proteins might represent potent modulators in hematopoiesis, especially in the development of monocytes-macrophages or their precursors.
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1. In rabbit aorta, quinacrine, but not indomethacin nor nordihydroguaiaretic acid, inhibited contractile responses to norepinephrine and KCl. Amiloride and nifedipine did not affect the effect of quinacrine. 2. In Ca2(+)-free medium, quinacrine (3 x 10(-6)-10(-4) M) inhibited the norpinephrine response less than that to a subsequent addition of Ca2+. 3. M&B 22, 948, nitroglycerin and forskolin inhibited the Ca2+ response. The effect of quinacrine was inhibited by M&B 22,948, but not by forskolin and potentiated by nitroglycerin. 4. Quinacrine and M&B 22,948 potentiated the nitroglycerin-relaxation. The effect of quinacrine plus M&B 22,948 was not different from that of quinacrine. 5. These results indicate that the effect of quinacrine may be different from that of nifedipine but is related to cGMP.
A sixty-two-year-old man who underwent coronary angiography and received acute thrombolytic and anticoagulant therapy for acute myocardial infarction developed multisystemic injury, including renal insufficiency and cutaneous manifestations. Fundoscopic examination and skin biopsy specimen led to the diagnosis of multiple cholesterol embolization syndrome (MCES). Discontinuation of anticoagulants and administration of hemostatic (carbazochrome, tranexamic acid, reptilase, and vitamin K) and antihyperlipidemic (cholestyramine and probucol) drugs resulted in temporary improvement of cutaneous and renal disorders and extended survival for about one year. Besides severe aortic atherosclerosis, postmortem examination revealed numerous cholesterol emboli to multiple organs. MCES is a rare but serious complication of left heart catheterization and anticoagulant therapy, and the optimal treatment remains to be established. The authors suggest here that the above-mentioned therapy might be effective for management of MCES.
High-strength denture teeth (HS teeth) were developed in order to improve the hardness and wear resistance of conventional plastic denture teeth (PL teeth), while retaining their feature of easy occlusal adjustment. The objective of this study was to evaluate the abrasive wear resistance of HS teeth. We conducted wear tests and measured surface roughness using six types of anterior artificial teeth, i.e., three types of HS teeth and three types of PL teeth, the latter serving as the control. The results of the toothbrush abrasion test revealed that the HS teeth had about 5 times greater wear resistance than the PL teeth. It was also found that the type of artificial teeth and the number of abrasive wear-testing strokes had a significant (P less than 0.05) influence on the surface roughness of artificial teeth.
Subarachnoid phenol block was applied to four traumatic spinal cord injury patients who had been suffering from urinary incontinence caused by detrusor hyperreflexia. Two were females with complete thoracic cord injury, the others were males with incomplete cervical cord injury. In all patients, detrusor hyperreflexia and urinary incontinence disappeared after 0.3-0.6 ml injection of 10% phenol glycerin. Vesicoureteral reflux observed in three ureters of two patients disappeared or improved. Two obtained sufficient bladder capacity for urine storage, while the others who had been treated by continuous urine drainage for a long time prior to the block could not obtain sufficient bladder compliance. The cause seemed to be organization of the bladder wall.
2,3-Dibenzylbutane-1,4-diol (DBB) is a mammalian lignan derived from human urine. To investigate the pharmacological actions of mammalian lignans, the effects of DBB on high K(+)-induced contraction in rabbit femoral artery were studied. High K+ induced a transient contraction followed by sustained contraction, and both depended on extracellular Ca2+. DBB inhibited transient contraction as well as sustained contraction. Verapamil or nifedipine inhibited sustained contraction more effectively than transient contraction. DBB inhibited the transient contraction remaining in the verapamil- or the nifedipine-pretreated preparation in a concentration-dependent manner. Moreover, DBB inhibited sustained contraction elicited by Bay K 8644 (Ca2+ channel activator). These results indicate that DBB effects not only the sensitive Ca2+ channels but also the insensitive channels.
Long-term results of mitral valve replacement using glutaraldehyde-treated porcine bioprostheses were evaluated. The subjects were 77 patients with the Hancock valve (Hancock group) and 60 with the Liotta valve (Liotta group) who survived operation. The maximum follow-up was 14 years and 8 years, and the cumulative follow-up was 631 patient-year (p-y) and 301 p-y in the Hancock and Liotta groups. The actuarial survival rate at 8 years was 80.1 +/- 4.6% for the Hancock group and 88.1 +/- 4.2% for the Liotta group, and there was no significant difference in survival rate between the both groups. The actuarial survival rate at 14 years was 74.3 +/- 5.9% for the Hancock group. The valve-related complications in the Hancock and the Liotta groups were as follow; thromboembolism 1.9%/p-y vs 1.3%/p-y, bleeding 0 vs 0.7%/p-y, perivalvular leak 0.3% vs 0, infection 0.3%/p-y vs 0.7%/p-y, primary tissue failure (PTF) 3.3%/p-y and all valve-related complications 5.9%/p-y vs 6.0%/p-y. There was no significant difference in valve-related complications between the both groups. However, the actuarial event free rate of PTF was significantly lower in the Liotta group than the Hancock group between 4 and 7 years after operation (100% vs 88.8 +/- 4.3% in the 4th year p less than 0.01, 87.7 +/- 4.4% vs 73.5 +/- 8.0% in the 7th year, p less than 0.05). Although the both anti-thrombogenicity and anti-inflammation were acceptable in the porcine bioprostheses, this prosthesis is now used only in the selected patients because of the limited long term durability of this valve.
The clinical efficacy of norfloxacin (NFLX) was evaluated on 40 patients. They had subjective symptoms suggestive of prostate inflammations and more than five white blood cells (WBC)/hpf in their prostatic secretions (EPS) or VB3. Of these, gram negative rods were isolated from the EPS in 3 patients and gram positive cocci were obtained in 26 patients. The overall clinical efficacy was determined at the second week. The effectiveness rate of the subjective symptoms was 82.5%. The effectiveness rate of the WBC in the EPS was 47.4%. The effectiveness rate of the bacteria in the EPS was 64.3%. The overall clinical effectiveness rate was 77.8%. A subjective side effect was observed only in one patient who had skin eruption like urticaria. Mild liver dysfunction of blood chemistry analysis was shown only in two patients but they had had long standing chronic hepatitis. We conclude that NFLX is an effective drug for the patients with chronic prostatitis.
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Arginine 115 in the subsite F of human lysozyme (peptidoglycan N-acetylmuramoylhydrolase, EC 3.2.1.17) was replaced with lysine, histidine, glutamine or glutamine acid by site-directed mutagenesis. The conversions which conserve positive charge, Arg115 to Lys or His (at acidic pH), have little affected on either the kinetic parameters for Micrococcus lysodeikticus cells or the activity against glycol chitin, nor on the cleavage patterns of hexa(N-acetylglucosamine) [(GlcNAc)6] and penta(N-acetylglucosamine) [(GlcNAc)5]. On the other hand, the conversions which cause loss of the positive charge, Arg115 to His (neutral and alkaline pH), Gln or Glu, not only reduced the activity against glycol chitin but also changed the cleavage patterns for (GlcNAc)6 and (GlcNAc)5. These results suggest that Arg115 is structurally required not for the specific hydrogen bonding interaction with a sugar residue but for the positively charged character in the construction of subsite F in human lysozyme.
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From January 1978 through February 1989, 110 tricuspid annuloplasties (De Vega's procedure) were performed in association with mitral and combined mitral and aortic valve disease. Preoperatively, 106 (96%) of 110 patients were in New York Heart Association functional class III or IV. There were seven early deaths (6.3%), and 3 patients, 2 with mitral lesions and 1 with a combined lesion, died during a follow-up period of 3 to 52 months (mean follow-up, 22 months). Four patients (3.6%) required reoperation because of biological mitral valve failure at 5 to 8 years after tricuspid annuloplasty (mean period, 6.6 years). Twenty-three (62%) of 37 randomly selected patients evaluated by echocardiography and 14 (70%) of 20 patients evaluated by right ventriculography showed complete disappearance of tricuspid regurgitation after tricuspid annuloplasty in 1 to 18 months (mean period, 3.3 months). Seventy-seven (96%) of the survivors were in functional class I or II after tricuspid annuloplasty. The actuarial survival rate for the TAP series including early deaths was 85.8% +/- 7.4% at 10 years and the actuarial rate of freedom from reoperation on the tricuspid valve was 96.7% +/- 1.4%. Our surgical experience indicates that the De Vega's annuloplasty, as the method of first choice, is a simple, reliable procedure and resulted in improvement in 90% of patients with moderate to severe functional tricuspid regurgitation.