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Biomedical subjects

A Ito

Publications and source records attributed to A Ito.

At least 19 recordsLinked to original sources

Fretting corrosion resistance and fretting corrosion product cytocompatibility of ferritic stainless steel.

To avoid nickel ion release from SUS317L as an implant material, a new type of nickel, commercially free, of high purity, and high chromium ferritic stainless steel, was developed. The new stainless steel (FJ) was studied for aspects of fretting corrosion and cytocompatibility compared with SUS317L. A pin-on-plate fretting corrosion test in an artificial physiologic solution, and cell culture in media with the addition of the artificial physiologic solution used for fretting was conducted. Resistance to the fretting induced crevice corrosion of FJ was higher than that of SUS317L because of the favorable electrochemical stability of the FJ alloy. The amount of iron ion or colloidal fine particles released from FJ was about a quarter of that from SUS317L, although the weight loss of a pin of FJ was almost 5/3 that of SUS317L. The artificial physiologic solution used for SUS317L fretting was more harmful to the growth of L929 and MC3T3-E1 cells than that used for FJ fretting. FJ was therefore superior to SUS317L as a biomaterial, judging from the resistance to fretting-induced crevice corrosion, electrochemical stability, and the cytocompatibility of fretting corrosion products.

3T3 Cells

Bending strength of synthetic OH-carbonated hydroxyapatite single crystals.

Although hydroxyapatite (HAP) is applied to medical implants because of its biocompatibility, no data on mechanical strength of HAP single crystals were yet available, partly due to the difficulty in obtaining sufficiently large single crystals. In the present study the bending strength of OH-carbonated hydroxyapatite (CHAP) single crystals containing carbonate of 0.09 CO2 wt % prepared hydrothermally was determined in three-point bending tests. The three-point bending tests were performed using a modified ultra micro-hardness tester with a span of 380 micrograms and a bending direction of <210>. The CHAP single crystals were broken in air, water, and air after immersion in alpha minimum essential medium (alpha MEM) + 10% fetal bovine serum (FBS) for 3 weeks. The average bending strength of the CHAP single crystals was 468 +/- 205, 361 +/- 199 and 501 +/- 212 MPa in air, water, and air after immersion in alpha MEM + 10% FBS, respectively. In all cases the maximum strength at each crystal thickness value decreased in inverse proportion to the thickness.

Animals

Compartmental analysis of asialoglycoprotein receptor scintigraphy for quantitative measurement of liver function: a multicentre study.

A multicentre study on multicompartmental analysis of hepatic scintigraphy using technetium-99m labelled galactosyl serum albumin (GSA), which binds to the asialoglycoprotein receptor, was carried out at seven institutions in Japan. Seventy-four patients with liver disease received 3 mg (185 MBq) of 99mTc-GSA by intravenous injection. Sequential scanning was performed 30 min after injection to obtain anterior images of the heart and liver, followed by single-photon emission tomography (SPET). The indices included in this analysis were hepatic blood flow (Q) and maximal receptor binding rate (Rmax), which showed a good correlation with semiquantitative ratio indices for 99mTc-GSA, namely the retention rate in blood (HH15) and the hepatic uptake rate (LHL15). Q and Rmax also showed a significant correlation with other measures of hepatic function. When patients were grouped according to the severity of chronic liver damage (hepatocellular functional damage), Q was reduced in the moderate and severe groups, while Rmax was reduced in proportion to the functional stage. Both parameters showed no inter-institution difference using analysis of co-variance with the functional stage as a co-variant. With regard to the hepatic uptake rate, anterior planar images and SPET images gave similar results for Q and Rmax. Acquisition times of 15 or 30 min provided the same results. The multicompartmental model analysis permitted comparable results to be obtained at institutions using different gamma cameras, and is therefore considered a universally applicable method. These results indicate that Q and Rmax are useful general indices for evaluating the functional reserve capacity of the liver.

Asialoglycoprotein Receptor

Human Taenia eggs develop into cysticerci in scid mice.

The intermediate hosts for Taenia saginata and T. solium are cattle and pigs (and humans for the latter), respectively. In vitro-hatched (but not activated) oncospheres of both Asian Taenia (T. saginata asiatica, a new subspecies of T. saginata or T. asiatica, a new species) and T. solium injected subcutaneously into the backs of mice with severe combined immunodeficiency (scid) developed into fully matured cysticerci. Five-month-old metacestodes of Asian Taenia had no hooklets and were bigger in size than those previously reported and similar to those of T. saginata. Their morphology suggested that the cysticerci were more advanced than those in the intermediate host animals. It is suggested that scid mice are valuable experimental animal models for studying human taeniid cestode infections.

Animals

Endotoxin-induced upregulation of type I interleukin-1 receptor mRNA expression in hepatocytes of mice: role of cytokines.

Interleukin-1 (IL-1) signal is transduced through the type I IL-1 receptor (IL-1RI). Although regulation of IL-1R expression has been extensively studied in vitro, little is known about it in vivo. By using RT-PCR analysis, we investigated the regulation of the IL-1RI mRNA expression level in various organs of mice at 2, 6, and 24 h following lipopolysaccharide (LPS) administration. IL-1RI mRNA expression in response to LPS appeared to be different in various organs. As a marked and sustained increase of IL-1RI mRNA expression in the liver was observed, we investigated the mechanism of the upregulation. IL-1, IL-6, and tumor necrosis factor (TNF) all increased the mRNA expression in the liver when administrated in vivo. In situ hybridization revealed that upregulation of IL-1R mRNA was observed in parenchymal liver cells (hepatocytes) in response to LPS administration. When primary cultured hepatocytes were treated in vitro, IL-1, IL-6, conditioned medium from LPS-treated mouse macrophages, and serum from LPS-treated mouse upregulated IL-1RI mRNA expression, but LPS, TNF, and prostaglandin E2 failed to do so. Therefore, these results suggest that the upregulation of IL-1RI mRNA in the hepatocytes by LPS administration is mediated by cytokines, especially by IL-1 and IL-6. The results also indicate that the regulation is different in different organs, and microenvironmental factors may be important.

Animals

Hormonal regulation of matrix metalloproteinase 9/gelatinase B gene expression in rabbit uterine cervical fibroblasts.

Since the degradation of uterine cervical extracellular matrix is an essential process in cervical ripening and dilatation at term, we examined the effect of pregnancy on the level of pro-matrix metalloproteinase 9 (proMMP-9)/progelatinase B in the rabbit uterine cervix and its regulation in uterine cervical fibroblasts. Uterine cervices shortly before term parturition contained high levels of proMMP-9 compared with those of nonpregnant rabbits. Uterine cervical fibroblasts prepared from rabbits at 23 days of gestation did not produce proMMP-9; in contrast, interleukin (IL)-1 alpha, IL-1 beta, or phorbol 12-myristate 13-acetate (PMA) induced proMMP-9 production along with an increase of proMMP-9 mRNA, and the IL-1-mediated induction of proMMP-9 was synergistically enhanced by PMA. On the other hand, physiological concentrations of progesterone suppressed IL-1-and/or PMA-mediated production of proMMP-9 in a dose-dependent manner. This suppressive effect of progesterone on proMMP-9 production was accompanied by a decrease in matrix metalloproteinase 9 (MMP-9) mRNA, indicating that progesterone down-regulates the production of proMMP-9 at the transcriptional level. These results indicate that in the rabbit uterine cervix, IL-1 alpha and IL-1 beta are effective inducers of the proMMP-9 production, and progesterone is a physiological suppressor. Thus, MMP-9 and progesterone are very likely to play essential roles in cervical ripening and dilatation in the rabbit, and the production of MMP-9 in the cervix is finely regulated during pregnancy.

Animals

Inflammatory cytokines cause coronary arteriosclerosis-like changes and alterations in the smooth-muscle phenotypes in pigs.

We recently developed a porcine model in which chronic, local treatment with interleukin-1 beta (IL-1 beta) causes coronary arteriosclerosis-like changes and hyperconstrictive responses. This study was designed to examine whether or not other major inflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha) might also cause similar coronary responses and whether those responses are associated with alterations in the smooth-muscle phenotypes. A segment of the porcine coronary artery was aseptically wrapped with cotton mesh, absorbing IL-1 beta, TNF-alpha, and IL-1 alpha. Two weeks after the operation, coronary arteriography showed the development of mild stenotic lesions at the cytokine-treated sites, where hyperconstrictive responses were repeatedly induced by intracoronary serotonin or histamine. Histologically mild intimal thickening was noted at those cytokine-treated sites. Immunostaining and immunoblotting demonstrated that all three myosin heavy chain isoforms, SM1, SM2 (smooth-muscle type), and SMemb (nonmuscle type), were noted in the normal coronary segments, whereas in the segments treated with inflammatory cytokines, SM1 and SM2 were markedly reduced, and only SMemb was noted. These results indicate that inflammatory cytokines all have a similar ability to induce coronary arteriosclerosis-like changes and hyperconstrictive responses, which are associated with alterations in smooth-muscle phenotypes toward dedifferentiation.

Animals

Immunodiagnosis of alveolar echinococcosis by enzyme-linked immunosorbent assay using a partially purified Em18/16 enriched fraction.

An improved enzyme-linked immunosorbent assay (ELISA) system using partially purified Eml8/16 enriched fraction (PP-Em18/16) prepared by isoelectric focusing was evaluated for serodiagnosis of alveolar echinococcosis (AE). The PP-Em18/16-ELISA was compared with Em2plus-ELISA by using sera from AE and cystic echinococcosis (CE) patients in China, where both AE and CE are endemic; sera from CE patients in Australia, where only CE exists; and sera from patients with cysticercosis, paragonimiasis, or sparganosis in Korea, where no indigenous AE or CE exists. We used Em2plus-ELISA as a standard ELISA and found 24.6% (17 of 69 specimens) cross-reactivity with sera from CE. Furthermore, some of the sera from paragonimiasis, sparganosis, and cysticercosis patients were also cross-reactive in the Em2plus-ELISA. When we tested for similar cross-reactivity in the same sera from CE patients by PP-Em18/16-ELISA (23.2%, 16 of 69), it became evident that the specificity of the PP-Em18/16-ELISA was better than that of the Em2plus-ELISA, since no sera from patients with the examined parasitic diseases except CE showed cross-reactivity. Some CE patients from China showed exceptionally high levels of antibody in comparison with those of CE patients from Australia, where no AE occurs. It is speculated that these patients with strongly positive cases of CE from China may have been exposed to both species of Echinococcus.

Animals

[Morphological characterization and classification of air cells in temporal bone by digital processing of CT images].

We determined the extent of pneumatization in the temporal bone and reconstructed three-dimensional structures of air cells by computer-assisted digital processing of high resolution CT images of the bone. We attempted morphological classification of temporal bone air cells by characterization of the three-dimensional structures obtained. A total of 52 ears in 33 normal subjects (18 males and 15 females; mean age 51 years) was examined. The volume of pneumatization in the temporal bone, as measured by CT, ranged from 2.08 to 20.05 ml (mean 6.40 +/- 4.09). The morphological characteristics of air cells in the three-dimensional images were examined with reference to the volume of air cells and the direct on of their growth. The three-dimensional structures were observed from four directions (lateral, supralateral, anterolateral and supramedial). Large air cells existed plentifully in all directions. Anteriorly, air cells were growing in two directions; laterally and toward the petrous apex. The growth in the latter direction was especially marked, and this contributed to the growth in the medial direction. Air cells that grew anteriorly had two directions of growth (lateral and toward the petrous apex). The directional difference in growth varied with the ear. On examining the suprainferior growth, air cells that grew large in the anterior direction were found to grow large in the suprainferior direction and those that did not grow large in the anterior direction were found contrarily to grow poorly in the suprainferior direction. With the above morphological characteristics taken into consideration, morphological classification of air cells into five types was attempted by the volume of air cells and the direction of their growth.

Adolescent

[Tuberculosis in the crew of a submarine].

We report the apparent spread of mycobacterial tuberculosis among a submarine crew from a crew member with a low grade of infectivity. The air-conditioning system of submarines requires completely closed recirculation of ambient air. If a person with pulmonary tuberculosis were in a submarine, one would expect to find a high incidence of tuberculosis among others on the ship. The index patient was a 35-year-old member of a submarine crew. An abnormal shadow was found on a chest roentgenogram during an annual medical checkup, and he was hospitalized for examination. Acid-fast bacilli were found in his gastric secretions, but he did not complain of coughing and no tuberculosis bacilli were found in his sputum. All members of the submarine crew were examined, and some who were on board with the index patient reacted strongly. Because those who were also suspected to be infected were usually not close to the index patient's living quarters and had little contact with the patient in the submarine, we strongly suspect that the closed ventilation system contributed to the spread of the infection. Control of tuberculosis in a sealed environment requires detailed investigation of the environment and completion of chemoprophylaxis. Adequate ventilation and ultraviolet radiation are more effective than decontamination with disinfectants for the control of infectious droplet nuclei. Ships should be equipped with those systems.

Adult

Tumor necrosis factor alpha (TNFalpha) induces pro-matrix metalloproteinase 9 production in human uterine cervical fibroblasts but interleukin 1alpha antagonizes the inductive effect of TNFalpha.

We have examined the regulation of precursor of matrix metalloproteinase 9 (proMMP-9)/progelatinase B production by tumor necrosis factor alpha (TNFalpha) and interleukin 1alpha (IL-1alpha) using human uterine cervical fibroblasts. TNFalpha, but not IL-1alpha, induces the production of proMMP-9 in the cervical cells. IL-alpha, however, suppresses the TNFalpha-induced proMMP-9 production. 12-0-tetradecanoylphorbol 13-acetate (TPA) also stimulates the cervical cells to produce proMMP-9, and IL-1alpha synergistically enhances its production. TNFalpha-induced proMMP-9 production is not mediated by protein kinase C (PKC), whereas the effect of IL-1alpha is through PKC. By contrast, proMMP-3/prostromelysin 1 is up-regulated by TNFalpha or TPA in the presence of IL-1alpha, whose modulation is PKC-dependent. The suppressive effect of IL-1alpha on the TNFalpha-induced proMMP-9 production is a new biological effect of IL-1 on MMP production.

Alkaloids

Conformational change in DNA induced by cationic bilayer membranes.

The effect of synthetic cationic lipids on the structure of DNA was studied. The fluorescence enhancement of ethidium bromide on intercalation into DNA was suppressed by the addition of bilayer-forming lipids, but not by micellar ones. Results on the fluorescence depolarization index suggest that ethidium bromide is not released from DNA by lipids intercalated into DNA. CD spectra of the DNA-lipid complexes revealed that the structure of DNA was changed only by bilayer-forming lipids at temperatures lower than their Tc values. Thus, the conformation of DNA is forced to change by cationic lipids forming the rigid bilayer membrane so that ethidium bromide fluorescence might be reduced, and the conformation can be controlled by selection of the appropriate lipid and temperature.

Cations

Coronary artery spasm does not depend on the intracellular calcium store but is substantially mediated by the protein kinase C-mediated pathway in a swine model with interleukin-1 beta in vivo.

BACKGROUND: The intracellular mechanism for coronary artery spasm is still unknown. Since the protein kinase C (PKC)-mediated pathway and Ca2+ release from sarcoplasmic reticulum (SR) are important intracellular mechanisms of vascular smooth muscle contraction, we examined the possible role of these two mechanisms in the pathogenesis of coronary spasm in our swine model in vivo. METHODS AND RESULTS: In 25 pigs, interleukin-1 beta (IL-1 beta) was applied chronically to the coronary arteries from the adventitia to induce an inflammatory/proliferative lesion. Two weeks after the operation, either intracoronary serotonin or histamine repeatedly induced coronary spasm at the IL-1 beta-treated site. At those spastic sites, phorbol-12, 13-dibutyrate, a PKC-activating phorbol ester, also induced coronary spasm, which was blocked by pretreatment with the PKC inhibitors staurosporine and sphingosine. Serotonin- and histamine-induced coronary spasm was also significantly inhibited by pretreatment with staurosporine, sphingosine, or nifedipine (an L-type Ca2+ channel antagonist) but not by ryanodine (an inhibitor of Ca(2+)-induced Ca2+ release from SR) or thapsigargin (an inhibitor of Ca(2+)-ATPase of SR). Bay K 8644 (an L-type Ca2+ channel agonist) also induced coronary spasm at the IL-1 beta-treated site, which was significantly inhibited by pretreatment with staurosporine, sphingosine, and nifedipine. In contrast, coronary vasoconstriction induced by prostaglandin F2 alpha was not affected by pretreatment with staurosporine or sphingosine but was significantly inhibited by pretreatment with ryanodine, thapsigargin, or nifedipine. CONCLUSIONS: These results suggest that (1) PKC activation largely accounts for the serotonin- and histamine-induced coronary spasm; (2) at the spastic site, the calcium influx through L-type Ca2+ channels may be augmented via the PKC-mediated pathway; and (3) the Ca2+ release from the SR into the cytosol may not play a primary role in coronary spasm.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy

[Dumping syndrome].

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Anastomosis, Surgical

Degradation of interleukin 1beta by matrix metalloproteinases.

Matrix metalloproteinases (MMPs) and interleukin 1 (IL-1) are implicated in inflammation and tissue destruction, where IL-1 is a potent stimulator of connective tissue cells to produce the extracellular matrix-degrading MMPs. Here, we report that IL-1beta, but not IL-1alpha, is degraded by MMP-1 (interstitial collagenase), MMP-2 (gelatinase A), MMP-3 (stromelysin 1), and MMP-9 (gelatinase B). This degradation was effectively blocked by tissue inhibitor of metalloproteinases (TIMP)-1. When IL-1beta was treated with MMPs it lost the ability to enhance the synthesis of prostaglandin E2 and pro-MMP-3 in human fibroblasts. The primary cleavage site of IL-1beta by MMP-2 was identified at the Glu25-Leu26 bond. These results suggest that IL-1beta stimulates connective tissue cells to produce MMPs, but activated MMPs in turn negatively regulate the activity of IL-1beta.

Amino Acid Sequence

Disialosyl galactosylgloboside as an adhesion molecule expressed on renal cell carcinoma and its relationship to metastatic potential.

Aberrant glycosylation expressed in specific types of human cancer may define stage, direction, and fate of tumor progression. Well-studied examples are expression of sialosyl-Lewis(x) or sialosyl-Lewis(a) in colorectal carcinoma and histo-blood group A and H/Le(y) in lung cancer. In renal cell carcinoma (RCC), expression of sialosyl-Lewis(x) has no correlation with metastatic potential. Clinicopathological studies have revealed that the degree of expression of disialosyl galactosylgloboside (DSGG) and monosialosyl galactosylgloboside is correlated with metastatic potential (to lung and lymph nodes) of RCC and inversely correlated with patient survival. In the present study, we compared the adhesion of RCC lines to sections of various tissues measured by Stamper-Woodruff assay and other similar assays under dynamic flow conditions. Of the eight RCC lines tested, only TOS-1 (which expresses DSGG) bound strongly to lung tissue sections. TOS-1 did not bind to sections of liver, kidney, or lymph nodes. In the same eight RCC lines, we also compared expression of DSGG and monosialosyl galactosylgloboside (reflected by reactivity with RM1 and RM2), overall ganglioside patterns, and correlation with lung tissue-binding ability. Under both static and dynamic flow conditions, the binding of TOS-1 cells to lung alveolar tissue was correlated with their DSGG expression, i.e., the binding was inhibited by RM2 but not by RM1. This binding was also inhibited by sialidase but not by EDTA (i.e., it was CA 2+ independent). The other seven cell lines (TOS-2, TOS-M, SMKT-R1, -R2, -R3, and -R4, and ACHN), which do not express DSGG, showed much weaker adhesion to lung tissue. None of the eight cell lines showed E- or P-selectin-dependent adhesion. These results suggest the existence of a yet-uncharacterized sialoadhesive receptor++ that specifically recognizes DSGG. This receptor could be the binding target in RCC metastasis to lung.

Carbohydrate Conformation

Translational augmentation of pro-matrix metalloproteinase 3 (prostromelysin 1) and tissue inhibitor of metalloproteinases (TIMP)-1 mRNAs induced by epidermal growth factor in human uterine cervical fibroblasts.

The mechanisms by which epidermal growth factor (EGF) enhances the production of pro-matrix metalloproteinase 3 (proMMP-3/prostromelysin 1) and tissue inhibitor of metalloproteinases (TIMP)-1 were investigated using human uterine cervical fibroblasts. The treatment of the cells with EGF for 24 h resulted in about 5-6-fold increase in the production of proMMP-3 and TIMP-1 compared with the untreated control cells. This increase was accompanied by an increase of proMMP-3 and TIMP-1 mRNAs. However, an about 3- and 2-fold increase in the production of proMMP-3 and TIMP-1, respectively, was observed as early as 1 h after the treatment of the cells with EGF, and it was not accompanied by any apparent increase in proMMP-3 and TIMP-1 mRNAs. This early effect of EGF on the enhanced production of proMMP-3 and TIMP-1 was not inhibited by actinomycin D, even though actinomycin D inhibited the synthesis of the total RNA in both the EGF-treated and untreated cells. These results indicate that EGF enhances the apparent production of proMMP-3 and TIMP-1 by two mechanisms: one by the accelerated translation of their mRNAs; and the other by the enhanced transcription of their genes. The former event takes place much earlier than the latter.

Cells, Cultured