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Biomedical subjects

Y Fujimura

Publications and source records attributed to Y Fujimura.

At least 37 records · Page 2Linked to original sources
PubMed2001

Stress caused by minimally invasive cardiac surgery versus conventional cardiac surgery: incidence of systemic inflammatory response syndrome.

The present study was conducted to evaluate the degree of stress in patients induced by minimally invasive cardiac surgery (MICS) in comparison with that caused by conventional cardiac surgery. We did this by assessing the incidence of systemic inflammatory response syndrome (SIRS). A total of 48 adult patients who underwent surgery for single valve disease were included in this study, 27 of whom underwent conventional surgery and 21 MICS. We evaluated the stress inflicted on the patients in these two groups by analyzing the duration and degree of SIRS and the level of C-reactive protein (CRP). SIRS was assessed by measuring body temperature, heart rate, respiratory rate, and white blood cell counts. There were no significant differences in the operating times, perfusion times, or aorta clamp times between the two groups; and the mean volume of blood transfusion did not differ significantly either. There was no significant difference in the incidence of SIRS or the mean duration of SIRS between the two groups. The CRP levels did not differ significantly between the two groups. Thus although MICS is superior to conventional cardiac surgery in that only a small skin incision is required, the stress experienced by the patient may be the same as that experienced by the patient undergoing conventional cardiac surgery.

Aged↗
PubMed2001

A new marker for cup cells in the rabbit small intestine: expression of vimentin intermediate filament protein.

Cup cells in the intestinal lining in mammals are largely limited to the ileum, suggesting a specific but undetermined function. The investigation of these cells has been hindered by the lack of a suitable marker for immunohistochemistry. The small intestine of rabbits was examined for a potential molecular marker. Segments of New Zealand white rabbit small intestine, with and without Peyer's patches, were removed, rinsed, fixed with periodate-lysine-2% paraformaldehyde (PLP), and frozen for immunohistochemistry, or fixed in 2.5% glutaraldehyde solution for electron microscopy. The sections were stained with monoclonal antibodies (V9, 3B4) against vimentin, which is known to be absent in enterocytes other than antigen-sampling M cells, and observed by immunohistochemistry and immunoelectron microscopy. Epithelial expression of vimentin intermediate filament proteins was limited to a subpopulation of villus-associated cells and to cells over Peyer's patch domes. Immunoreactivity with vimentin antibodies was selectively found in cells with a cup-like indentation in the brush border in villous epithelium and in M cells in Peyer's patch follicle epithelium. Immunoelectron microscopy revealed that the labeled cells in villous epithelium had shorter microvilli than the adjacent absorptive cells, and small, sparse, mitochondria, which are ultrastructural characteristics of cup cells. Vimentin filaments were recognized in the area surrounding the nucleus and extending beneath the plasma membrane of cup cells. In rabbit small intestine, vimentin is useful for the detection of cup cells, as well as M cells, and may facilitate the investigation of these little understood cells.

Animals↗
PubMed2001

Inhibition of human platelet aggregation by L-amino acid oxidase purified from Naja naja kaouthia venom.

L-Amino acid oxidase (LAO) widely exists in snake venoms. Purification of LAO from the Naja naja kaouthia (monocellate cobra) venom has been reported (Tan and Swaminathan, 1992), but its structural characterization and physiological function remained to be determined. The function of snake venom LAOs in hemostasis, especially their effect on platelet aggregation, has been controversial. We determined the N-terminal amino acid sequence of the N. n. kaouthia LAO named K-LAO to be DDRRSPLEECFQQNDYEEFLEIAKNGLKKTxNPKHVXxV (38 residues). The protein data base search revealed that the enzyme had high similarities with other snake venom LAOs. Further, platelet aggregation studies revealed that K-LAO functionally did not induce platelet aggregation in a platelet-rich plasma system, but that it inhibited platelet aggregation induced by agonists such as ADP, collagen and ristocetin in a dose-dependent manner. K-LAO diminished platelet aggregation more intensely under low than high shear stress. This inhibitory activity of K-LAO on either ristocetin-induced or shear-induced platelet aggregation was quenched by addition of catalase. These results indicate that K-LAO functions as an inhibitor to platelet aggregation through the formation of hydrogen peroxide. The enzyme may contribute to the development of a severe hematological disorder due to cobra envenomation.

Adenosine Diphosphate↗
PubMed2001

A tea catechin suppresses the expression of the high-affinity IgE receptor Fc epsilon RI in human basophilic KU812 cells.

Human basophilic KU812 cells express the high-affinity IgE receptor Fc epsilon RI, which plays a central role in the IgE-mediated allergic response. The effect of several major tea catechins, (+)-catechin, (-)-epicatechin, (-)-epigallocatechin, (-)-epicatechin gallate, and (-)-epigallocatechin gallate (EGCg), on the cell surface expression of Fc epsilon RI in KU812 cells was studied. Flow cytometric analysis showed that only EGCg was able to decrease the cell surface expression of Fc epsilon RI after a 24 h treatment in a dose-dependent manner. Moreover, immunoblot analysis revealed that the total cellular expression of the Fc epsilon RI alpha chain decreased upon treatment with EGCg. Fc epsilon RI is a tetrameric structure comprising one alpha chain, one beta chain, and two gamma chains. The level of mRNA production of each subunit in KU812 cells was investigated. KU812 cells treated with EGCg expressed lower levels of Fc epsilon RI alpha and gamma mRNA than nontreated cells. These results suggest that EGCg has an ability to down-regulate Fc epsilon RI expression, and this suppressive effect may be due to the down-regulation of Fc epsilon RI alpha and gamma mRNA levels.

Basophils↗
PubMed2001

Plasma of patients with Upshaw-Schulman syndrome, a congenital deficiency of von Willebrand factor-cleaving protease activity, enhances the aggregation of normal platelets under high shear stress.

Upshaw-Schulman syndrome (USS) is an autosomal recessive disorder characterized by repeated episodes of chronic thrombocytopenia and microangiopathic haemolytic anaemia (MAHA) that responds dramatically to infusions of fresh frozen plasma (FFP). Recent studies have provided consistent evidence that USS is a congenital deficiency of plasma von Willebrand factor-cleaving protease (VWF-CPase) activity and, therefore, unusually large VWF multimers (UL-VWFMs) are present in the plasma. However, the molecular mechanism of the clinical symptoms of USS is not well understood. We studied the relationship between UL-VWFMs and thrombocytopenia in two USS patients by analysing platelet aggregation using a mixture of the patient's plasma and normal washed platelets under high shear stress. Our results clearly showed a remarkably enhanced high shear stress-induced platelet aggregation (H-SIPA) by the patient's plasma. At 24 h after FFP infusion (approximately equal to 10 ml/kg body weight), the enhanced H-SIPA became almost completely normalized but, 2 d later, it began to return to the preinfusion level. These results were in accordance with the change in VWFM patterns. The specific effects of enhanced H-SIPA on VWF, platelet glycoprotein Ib and endogenous ADP released from platelets upon stimulation were confirmed using reagents that specifically inhibit their respective functions. Our present results clearly indicate that thrombocytopenia in USS patients is caused by a combination of the presence of UL-VWFMs, platelets and high shear stress generated in the microcirculation.

ADAM Proteins↗
PubMed2001

Effect of fluvoxamine on the pharmacokinetics of mexiletine in healthy Japanese men.

BACKGROUND AND OBJECTIVES: Fluvoxamine, a selective serotonin reuptake inhibitor, is known to inhibit several hepatic cytochrome P450 (CYP) isozymes, in particular CYP1A2. Mexiletine is mainly catalyzed by CYP2D6 and partially catalyzed by CYP1A2. Our objective was to study the potential pharmacokinetic interaction between fluvoxamine and mexiletine. METHODS: A randomized crossover design with two phases was used. A 7-day washout period separated the two treatment conditions. In the one phase, 6 healthy Japanese men received an oral dose of 200 mg of mexiletine alone (study 1); in the other phase, the men received fluvoxamine (50 mg twice a day) for 7 days, and on the eighth day they received oral mexiletine (200 mg) and fluvoxamine concomitantly (study 2). The concentrations of mexiletine were measured with HPLC. RESULTS: The area under the concentration-time curve and serum peak concentration of mexiletine in study 2 were significantly increased compared with those in study 1 (10.4 +/- 4.85 versus 6.70 +/- 3.21 microg x h/mL, P =.006 and 0.623 +/- 0.133 versus 0.536 +/- 0.164 microg/mL, P =.008, respectively). CONCLUSION: The effect of fluvoxamine on the mexiletine disposition is comparatively large, and when mexiletine and fluvoxamine are coadministered careful monitoring of mexiletine is needed.

Administration, Oral↗
PubMed2001

Traumatic subluxation of the axis after hyperflexion injury of the cervical spine in children.

Six cases of children (four boys and two girls, mean age 11 years) who had traumatic subluxation of the axis (C2) were reviewed retrospectively. Initial radiographs demonstrated no detectable vertebral fracture in any of the children. However, a slight anterior subluxation of C2 was observed in three of the patients. Radiographs, taken at 1 month after injury in all but one patient, revealed a progression of the subluxation and a local kyphosis in all of the patients. Four of the children were treated conservatively with a cervical brace, and an improvement of both the kyphosis and the anterior slippage of C2 was obtained accompanied by an anteroposterior growth of the C3 vertebral body. The kyphosis of two of the patients became severe and, ultimately, these patients underwent fusion surgery. At the follow-up, none of the patients presented with any significant symptom. For the correct diagnosis of traumatic subluxation of C2, sequential radiographs to confirm the progression of subluxation and local kyphosis are mandatory. Conservative treatment rather than early surgical treatment may be chosen for this injury, because mild and moderate kyphosis can be corrected spontaneously by remodeling of the cervical spine.

Adolescent↗
PubMed2001

Surgical management of idiopathic spinal cord herniation: a review of nine cases treated by the enlargement of the dural defect.

OBJECT: Spinal cord herniation is a rare cause of progressive myelopathy and can be corrected surgically. In most previous reports, closure of the dural defect was the recommended procedure. The object of this paper is to describe a new procedure in which spinal cord constriction is released by enlarging the hiatus; additionally the postoperative results will be discussed. METHODS: In nine patients with spinal cord herniation, enlargement of the dural defect was performed. In eight patients, neurological deficits resolved immediately after surgery. In one patient with a severe preoperative neurological deficit whose spinal cord herniated massively, deterioration occurred postoperatively. To date, no recurrence of herniation has been observed. CONCLUSIONS: The goals of surgery are to reduce the herniation, return the spinal cord to the normal position, and prevent the recurrence of herniation. The use of sutures to close the dural defect has been the method of choice to date. The surgical space in front of the spinal cord, however, is insufficient to accommodate this procedure safely. Because symptoms are caused by the constriction of the spinal cord at the hiatus, surgical expansion of the hiatus allows the goals of surgery to be achieved. This procedure, which is technically easier and less invasive with regard to the vulnerable spinal cord than the closure of the dural defect, could be a viable alternative for the treatment of this rare disease.

Adult↗
PubMed2000

Platelet-derived microparticles in patients with arteriosclerosis obliterans: enhancement of high shear-induced microparticle generation by cytokines.

We evaluated the plasma concentrations of cytokines and platelet-derived microparticles in patients with arteriosclerosis obliterans and studied the effect of cytokines on platelet-derived microparticle generation under high shear stress. Interleukin-6 levels peaked at 48 hours after vascular surgery, while thrombopoietin started to increase at 24 to 48 hours postoperatively and peaked on the seventh day. Platelet activation markers were increased in the arteriosclerosis obliterans patients preoperatively. Levels of P-selectin and CD63 both increased further, peaking at 6 to 24 hours postoperatively. Platelet-derived microparticle levels were also increased preoperatively. At 6 hours postoperatively, the plasma level of platelet-derived microparticles was significantly increased. Plasma platelet-derived microparticle level was lower at 12 hours but only returned to the preoperative value at 7 days after grafting. There was a difference in the platelet-derived microparticle level at 7 days between patients with or without antiplatelet therapy (cilostazol). The effect of cytokines on platelet activation under high shear stress was also studied. Interleukin-6 and thrombopoietin enhanced both P-selectin expression and platelet-derived microparticle generation under high shear stress. These results suggest that platelet-derived microparticles are released by platelet activation after vascular grafting when certain cytokines increase under high shear stress and that antiplatelet therapy may reduce platelet-derived microparticle levels postoperatively.

Aged↗
PubMed2000

Increased signal intensity of the spinal cord on magnetic resonance images in cervical compressive myelopathy. Does it predict the outcome of conservative treatment?

STUDY DESIGN: Correlation between a lesion of the spinal cord that elicits increased signal intensity (ISI) on magnetic resonance images (MRIs) and the outcome of conservative treatment for cervical compressive myelopathy was retrospectively investigated. OBJECTIVE: To investigate whether ISI could predict the outcome of conservative treatment for cervical compressive myelopathy. SUMMARY OF BACKGROUND DATA: It is unknown whether ISI is related to the outcome of conservative treatment for cervical compressive myelopathy. METHODS: Fifty-two patients with mild cervical myelopathy underwent conservative treatment with a cervical brace. The compressive lesions were spondylosis in 29 patients, disc herniation in 12, and an ossification of the longitudinal ligament in 11. They also underwent MRI (1.5 T), and ISI was evaluated on T2-weighted sagittal and axial images. The ISI areas were classified as focal or multisegmental. Thirty-nine patients underwent follow-up MRI after a mean interval of 2 years, 4 months. The transverse area of the spinal cord was also measured on T2-weighted axial images. The outcome of conservative treatment was assessed using the Japanese Orthopedic Association Score (JOA score). Patients showing either an improvement in the JOA score or with a JOA score of 15 or more were considered to have a satisfactory outcome. RESULTS: The average JOA score was 14.0 +/- 1.4 (range, 10-16) before conservative treatment and 14.4 +/- 1.9 (range, 10-17) at follow-up. The average gain in the JOA score was 0.4 points +/- 1.9 (range, -5 to +6). The outcome was satisfactory in 36 patients (69%). An area of ISI was observed in 34 patients (65%) before treatment (24 focal and 10 multisegmental). A satisfactory outcome was obtained in 78% of the patients without ISI, in 63% of those with focal ISI, and in 70% of those with multisegmental ISI. No statistically significant difference was seen among these three groups in the percentages of patients with satisfactory outcome, JOA scores before and after treatment or transverse spinal cord area. Of the 39 patients who were re-examined by MRI, 28 showed an area of ISI. The ISI regressed in five patients (18%). Satisfactory outcome was obtained in all 5 patients with regression of ISI, in 16 (70%) of the 23 patients without regression of ISI, and in 10 (91%) of the 11 patients without ISI apparent on the the first images (difference, not significant). CONCLUSIONS: Increased signal intensity was not related to a poor outcome of conservative treatment or severity of myelopathy in the patients with mild cervical myelopathy.

Adult↗
PubMed2000

Snake venom proteases affecting hemostasis and thrombosis.

The structure and function of snake venom proteases are briefly reviewed by putting the focus on their effects on hemostasis and thrombosis and comparing with their mammalian counterparts. Up to date, more than 150 different proteases have been isolated and about one third of them structurally characterized. Those proteases are classified into serine proteases and metalloproteinases. A number of the serine proteases show fibrin(ogen)olytic (thrombin-like) activities, which are not susceptible to hirudin or heparin and perhaps to most endogenous serine protease inhibitors, and form abnormal fibrin clots. Some of them have kininogenase (kallikrein-like) activity releasing hypotensive bradykinin. A few venom serine proteases specifically activate coagulation factor V, protein C, plasminogen or platelets. The venom metalloproteinases, belonging to the metzincin family, generally show fibrin(ogen)olytic and extracellular matrix-degrading (hemorrhagic) activities. A few venom metalloproteinases show a unique substrate specificity toward coagulation factor X, platelet membrane receptors or von Willebrand factor. A number of the metalloproteinases have chimeric structures composed of several domains such as proteinase, disintegrin-like, Cys-rich and lectin-like domains. The disintegrin-like domain seems to facilitate the action of those metalloproteinases by interacting with platelet receptors. A more detailed analysis of snake venom proteases should find their usefulness for the medical and pharmacological applications in the field of thrombosis and hemostasis.

Amino Acid Sequence↗
PubMed2000

The high molecular mass, glycoprotein Ib-binding protein flavocetin-A induces only small platelet aggregates in vitro.

The direct effects of snake venom glycoprotein (GP) Ib-binding proteins on platelet receptors during the formation of platelet aggregates were determined by a particle counting method using light scattering. Flavocetin-A induces small platelet aggregates, but not medium or large ones. However, neither jararaca GPIb-BP nor tokaracetin induce platelet aggregation. The flavocetin-A dose-response curve for formation of small aggregates is bell-shaped, with maximal effect at 1 to 2 microg/mL. The formation of small aggregates was not observed when fixed human platelets were used. Jararaca GPIb-BP, the anti-GPIb monoclonal antibody GUR83-35, prostaglandin I2, and ethylene diamine-N,N-dimethylformamide all inhibited flavocetin-A-induced small aggregate formation, but acetylsalicylic acid did not. Furthermore, anti-GPIIb/IIIa monoclonal antibodies, Abciximab, and YM337 significantly but partially inhibited aggregate formation, but the anti-von Willebrand factor monoclonal antibody NMC-4 had no effect. The formation of small aggregates required extracellular calcium, but flavocetin-A did not elevate cytosolic calcium. These results suggest that flavocetin-A binds to intact platelets, initiating platelet responses and inducing platelet aggregate formation by cross-linking platelets. Consequently, flavocetin-A may be a useful tool to study the mechanism of GPIb-mediated platelet activation and the structure-function relationships of GPIb.

Animals↗
PubMed2000

Evidence of M cells as portals of entry for antigens in the nasopharyngeal lymphoid tissue of humans.

The nasopharyngeal tonsils (adenoids) are prominent components of human nasal-associated lymphoid tissues (NALT). However, the role of the nasopharyngeal tonsils in antigen uptake for initiation of the mucosal immune response is unknown. The aims of this study were to describe the ultrastructure and function of the M cells of the human nasopharyngeal tonsils and to clarify their capacity for antigen uptake. Tissues obtained from eight patients undergoing adenectomy were examined by light and electron microscopy. Lymphoepithelium covers the nasopharyngeal lymphoid tissue and consists of ciliary epithelium, non-ciliary epithelial cells, M cells, goblet cells, and many intraepithelial lymphoid cells. M cells have irregular and broad cytoplasm-containing microvilli on their surface and small vesicles in their cytoplasm. Many lymphoid cells were enfolded by M cells. The uptake of horseradish peroxidase (HRP) in the tissue in organ culture was studied using histochemical techniques. Excised adenoid tissue was incubated in RPMI 1640 culture media with HRP for 10, 30, and 60 min. HRP which had adhered to the surface was taken up in vesicles and then transported in vesicles and tubules by M cells. The M cells of nasopharyngeal lymphoid tissue were ultrastructurally and functionally similar to those in human Peyer's patches and colonic lymphoid follicles. These findings indicate that NALT bears similarities to the gut-associated lymphoid tissue, and its antigen uptake capacity may be important for initiation of immunity in the upper aerodigestive tract.

Adenoidectomy↗
PubMed2000

Activation of protein-tyrosine kinase pathways in human platelets stimulated with the A1 domain of von Willebrand factor.

The binding of multimeric von Willebrand Factor (vWF) to its specific receptor on platelets, glycoprotein (GP)Ib, is a critical event, allowing platelet activation and subsequent thrombus formation in the vessels. In this study, the effects of the monomeric A1 domain, which contains the GPIb-binding site of the vWF molecule, on platelet activation were examined. The binding of the A1 domain to GPIb resulted in Syk activation and association with Src, as is the case with intact vWF. However, the A1 domain, in contrast to vWF, did not induce platelet cytoskeletal association of tyrosine kinases, Src and Lyn. When platelet functional responses, such as aggregation and intracellular Ca2+ mobilization, were monitored, the A1 domain failed to induce the responses by itself and blocked the responses induced by the multimeric vWF molecule. These results suggested that the A1 domain triggers at least some of tyrosine kinase-related signals via GPIb and may be a partial agonist as well as a competitive antagonist for the vWF-GPIb interaction.

Blood Platelets↗