IP-10 in atopic dermatitis.
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Biomarkers↗
Biomedical subjects
N Sugawara
Publications and source records attributed to N Sugawara.
Serum inhibitors for human mast cell growth: possible role of retinol.
BACKGROUND: In vitro culture systems have been used to study the physiological and pathological characteristics of human mast cells. However, there are some differences in proliferation and maturation of mast cells between fetal bovine serum (FBS)-containing and serum-deprived cultures. Accordingly, we attempted to identify circulating factor(s) affecting the development of human mast cells. METHODS: We measured the serum levels of retinol and several cytokines. To elucidate the antiproliferative effects of the serum, a retinoic acid receptor (RARalpha) antagonist and neutralizing antibodies against cytokines were used. RESULTS: Similar to FBS, human serum dose-dependently suppressed the growth of tryptase+ cells from CD34+ cord blood cells or 20-week cultured mast cells under stimulation with stem cell factor (SCF). The serum-mediated inhibition might be based on a decline in proliferation rate. Among inhibitors for mast cell growth, retinol and transforming growth factor (TGF)-beta1 were present at high levels in human serum. In contrast with anti-TGF-beta1 antibody, an RARalpha antagonist counteracted the serum-induced suppression of human mast cell proliferation. CONCLUSIONS: Our results suggest that retinol and its derivatives act as a circulating regulator for human mast cell growth. The RARalpha antagonist may be a useful tool to obtain higher numbers of mast cells in FBS-containing cultures.
Animals↗
Expression of C-C chemokine TARC in human nasal mucosa and its regulation by cytokines.
BACKGROUND: Although interleukin (IL)-4 and IL-5 have been demonstrated to play a critical role in the pathophysiology of allergic diseases such as allergic rhinitis, the mechanism that causes the predominance of Th2 lymphocytes has yet to be clarified. Thymus and activation-regulated chemokine (TARC) has been known to facilitate the recruitment, activation and development of Th2 polarized cells, leading investigators to suggest a role for TARC in the development of Th2 responses. OBJECTIVE: To gain a better understanding of the role of TARC in the pathogenesis of allergic rhinitis we investigated the cellular sources of this chemokine in nasal mucosa. In addition, the effect of cytokines on TARC production has been investigated. METHODS: The expression of TARC in human nasal mucosa was assessed by immunohistochemistry. To study the effect of cytokines on TARC production, epithelial cells, endothelial cells and fibroblasts, isolated from inferior nasal mucosa samples, were stimulated by a variety of cytokines including IL-4, IL-13, tumour necrosis factor (TNF)-alpha and interferon (IFN)-gamma. RESULTS: Epithelial cells in nasal mucosa in subjects with allergic rhinitis expressed higher signal level than those in non-allergy patients. Combined stimulation with IL-4 and TNF-alpha, as well as IL-13 and TNF-alpha, synergistically induced TARC expression in epithelial cells. Furthermore, the amount of TARC induced by these cytokines was higher in epithelial cells obtained from patients with allergic rhinitis than in those from non-allergic patients. CONCLUSION: These results demonstrate a crucial role of nasal epithelial cells in the expression of TARC, and that Th2 cytokine IL-4 and IL-13 may promote Th2 responses by inducing TARC production from epithelial cells.
Adolescent↗
Serum anti-Lewis X antibody is associated with VacA seropositivity but not atrophic gastritis in patients with Helicobacter pylori infection.
OBJECTIVES: Lipopolysaccharides of Helicobacter pylori have an antigenic structure that mimics Lewis X occurring in gastric mucosa. The pathogenic role of antigenic mimicry in H. pylori-induced gastritis has been of recent interest. The aim of this study was to examine the relevance of anti-Lewis X antibody in the development of atrophic gastritis in H. pylori infection. METHODS: A total of 72 patients were studied. Serum samples were collected to measure IgG antibodies to H. pylori, CagA, VacA and Lewis X. Biopsy specimens were obtained from the antrum and the corpus to examine the grade and the type of atrophic gastritis. RESULTS: Mean anti-Lewis X antibody titres were higher in 38 VacA-seropositive patients than in 13 seronegative patients (P < 0.05). The difference was not significant between patients with diffuse-type atrophic gastritis and those with multi-focal type. No significant correlation was observed between the titre of anti-Lewis X antibody and the grade of glandular atrophy, whereas CagA seropositivity was associated with glandular atrophy. CONCLUSIONS: Anti-Lewis X antibody may play a role in persistent gastric inflammation, particularly in VacA-seropositive H. pylori infection. However, anti-Lewis X antibody does not seem itself to be associated with atrophic gastritis in patients with H. pylori infection.
Antibodies↗
Competition between copper and silver in Fischer rats with a normal copper metabolism and in Long-Evans Cinnamon rats with an abnormal copper metabolism.
Long-Evans Cinnamon (LEC) rats inherently lacking in serum ceruloplasmin (CP) activity and biliary Cu excretion were established from a closed colony of Long-Evans rats. These deficiencies, linked to a dysfunction of P-type ATPase, stimulate deposition of Cu and then of Cu metallothionein (MT) in the liver. Male LEC and Fischer rats were injected subcutaneously with Ag (AgNO3), which is an antagonist to Cu. They were operated on 24 h after the injection while under anesthesia. Total uptake of Ag into the liver was not stimulated, but its uptake into the MT fraction increased significantly in the LEC rats. Ag injection notably decreased the activity of serum CP in the Fischer rats, but not in the LEC rats. The decrease was accompanied by a reduction of serum Cu. In Fischer rat serum treated with Ag, Ag was detected mainly in the albumin region and partly in the CP fraction. In LEC rat serum, however, the Ag concentration was about 1/20 of that in the Fischer rats, and Ag was not detected in the CP fraction. Ag injection decreased the biliary excretion of Cu in the Fischer rats (0.183-0.052 microg Cu/20 min sampling), but not in the LEC rats (0.014-0.014 microg Cu/20 min sampling). On the other hand, biliary excretion of Ag was much greater in the Fischer rats (1.25 microg Ag/20 min) than in the LEC rats (0.04 microg Ag/20 min). Our results suggest that uptake of Ag into the liver is not dependent on the hepatic Cu content and status, but that biliary excretion of Ag from the liver is affected by these. Hepatic MT is not a transporter of hepatobiliary excretion of Cu and Ag. It seems likely that, unlike Cu excretion, Ag is excreted by not only the CP route but also by another route into the serum. Ag may compete with Cu in the uptake into CP (conversion of apo-CP to holo-CP).
Animals↗
The Saccharomyces cerevisiae Msh2 mismatch repair protein localizes to recombination intermediates in vivo.
Mismatch repair proteins act during double-strand break repair (DSBR) to correct mismatches in heteroduplex DNA, to suppress recombination between divergent sequences, and to promote removal of nonhomologous DNA at DSB ends. We investigated yeast Msh2p association with recombination intermediates in vivo using chromatin immunoprecipitation. During DSBR involving nonhomologous ends, Msh2p localized strongly to recipient and donor sequences. Localization required Msh3p and was greatly reduced in rad50delta strains. Minimal localization of Msh2p was observed during fully homologous repair, but this was increased in rad52delta strains. These findings argue that Msh2p-Msh3p associates with intermediates early in DSBR to participate in the rejection of homeologous pairing and to stabilize nonhomologous tails for cleavage by Rad1p-Rad10p endonuclease.
Base Pair Mismatch↗
Interleukins in Churg-Strauss syndrome.
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Anti-Inflammatory Agents↗
Soluble CD30 is more relevant to disease activity of atopic dermatitis than soluble CD26.
It is suggested that CD30 and CD26 are surface molecules expressed on activated Th2 and Th1 cells, respectively. We examined plasma levels of soluble CD26 (sCD26) and sCD30 in patients with atopic dermatitis (AD) when their eruptions were aggravated and in non-atopic healthy controls, and then analysed the possible correlation between these values and the levels of several clinical markers. The plasma levels of both sCD30 and sCD26 were significantly higher in AD patients than in controls, both in exacerbation status and after conventional treatment. Multiple regression analyses showed that plasma sCD30 was a much better predictor of the levels of serum IgE, serum LDH and plasma sCD25, and the area and the score of AD eruption than sCD26, although elevated levels of both sCD30 and sCD26 are associated with these clinical predictors of AD. Importantly, sCD30 plasma levels decreased significantly in AD patients after conventional treatment, while no significant transition was noted in the concentration of sCD26. Moreover, a significant reduction of sCD30 levels was observed in the group of patients whose eruption score was reduced > 50%, whereas it was not in those < 50%. These findings provide evidence that the successful treatment of AD is associated with down-activation of Th2.
Adolescent↗
Serum anti-Lewis X antibody is not elevated in patients with gastric cancer infected with Helicobacter pylori.
Lipopolysaccharides of Helicobacter pylori express Lewis X similar to that occurring in gastric mucosa. Patients infected with H. pylori produce anti-Lewis X antibodies. The aim of this study was to examine whether anti-Lewis X antibody was associated with the development of gastric cancer, particularly intestinal type cancer. Serum sample was collected from 98 patients with early gastric cancer and 98 gender- and age-matched control subjects who underwent endoscopy. Histologically, 77 cancers were of the intestinal type. Titers of anti-H. pylori and anti-Lewis X immunoglobulin G (IgG) antibodies were assayed by enzyme-linked immunosorbent assay. The mean titer of Lewis X antibody was 0.097 in patients with gastric cancer and 0.110 in matched control subjects (not significant). In 72 H. pylori-seropositive patients with intestinal type cancer and their matched H. pylori-seropositive controls, mean titer was 0.115 and 0.107, respectively (not significant). The odds ratio for the risk of gastric cancer if Lewis X antibody was high titer was 0.93 (95% CI 0.43-2.00). The odds ratio for the risk of intestinal type gastric cancer in patients with H. pylori infection if Lewis X antibody was high titer was 1.10 (95(% CI, 0.46-2.62). Anti-Lewis X antibody does not seem to be associated with the development of gastric cancer, even the intestinal type cancer.
Aged↗
DNA length dependence of the single-strand annealing pathway and the role of Saccharomyces cerevisiae RAD59 in double-strand break repair.
A DNA double-strand break (DSB) created by the HO endonuclease in Saccharomyces cerevisiae will stimulate recombination between flanking repeats by the single-strand annealing (SSA) pathway, producing a deletion. Previously the efficiency of SSA, using homologous sequences of different lengths, was measured in competition with that of a larger repeat further from the DSB, which ensured that nearly all cells would survive the DSB if the smaller region was not used (N. Sugawara and J. E. Haber, Mol. Cell. Biol. 12:563-575, 1992). Without competition, the efficiency with which homologous segments of 63 to 205 bp engaged in SSA was significantly increased. A sequence as small as 29 bp was used 0.2% of the time, and homology dependence was approximately linear up to 415 bp, at which size almost all cells survived. A mutant with a deletion of RAD59, a homologue of RAD52, was defective for SSA, especially when the homologous-sequence length was short; however, even with 1.17-kb substrates, SSA was reduced fourfold. DSB-induced gene conversion also showed a partial dependence on Rad59p, again being greatest when the homologous-sequence length was short. We found that Rad59p plays a role in removing nonhomologous sequences from the ends of single-stranded DNA when it invades a homologous DNA template, in a manner similar to that previously seen with srs2 mutants. Deltarad59 affected DSB-induced gene conversion differently from msh3 and msh2, which are also defective in removing nonhomologous ends in both DSB-induced gene conversion and SSA. A msh3 rad59 double mutant was more severely defective in SSA than either single mutant.
DNA↗
[The occlusal contact mode during lateral excursion].
The purpose of this study is to clarify the occlusal contact mode between the upper and lower molars on the working side of group function occlusion during lateral excursion. After the intercuspal position (IP) and two lateral positions (L1, the middle point between IP and L2; L2, the edge-to-edge occlusal position of the molars) on the Gothic arch were defined, occlusal contact relations in these three occlusal positions were recorded, using black silicone. Digital data of real occlusal contacts and visualized data of close (less than 30 microns) occlusal areas, by computer image processing, were analyzed. The conclusions are as follows: 1. Although the numbers of real occlusal contacts and the visualized occlusal area tend to decrease toward L2 during lateral excursion, the former, in some cases, goes up and down. 2. Functional cusps play an important part in occlusal contact at the intercuspal position. 3. Occlusal contact points are on the functional cusps of the upper and lower molars, which can be clinically regarded as certain points, and these points slide on the inclining non-functional cusps of antagonistic teeth during lateral excursion. 4. Each upper and lower molar has 2 to 6 occlusal contact points near the top functional cusps at the intercuspal position, and some of them contact continuously during lateral excursion.
Adult↗
The third chitinase gene (chiC) of Serratia marcescens 2170 and the relationship of its product to other bacterial chitinases.
The third chitinase gene (chiC) of Serratia marcescens 2170, specifying chitinases C1 and C2, was identified. Chitinase C1 lacks a signal sequence and consists of a catalytic domain belonging to glycoside hydrolase family 18, a fibronectin type III-like domain (Fn3 domain) and a C-terminal chitin-binding domain (ChBD). Chitinase C2 corresponds to the catalytic domain of C1 and is probably generated by proteolytic removal of the Fn3 and ChBDs. The loss of the C-terminal portion reduced the hydrolytic activity towards powdered chitin and regenerated chitin, but not towards colloidal chitin and glycol chitin, illustrating the importance of the ChBD for the efficient hydrolysis of crystalline chitin. Phylogenetic analysis showed that bacterial family 18 chitinases can be clustered in three subfamilies which have diverged at an early stage of bacterial chitinase evolution. Ser. marcescens chitinase C1 is found in one subfamily, whereas chitinases A and B of the same bacterium belong to another subfamily. Chitinase C1 is the only Ser. marcescens chitinase that has an Fn3 domain. The presence of multiple, divergent, chitinases in a single chitinolytic bacterium is perhaps necessary for efficient synergistic degradation of chitin.
Amino Acid Sequence↗
An iron-deficient diet stimulates the onset of the hepatitis due to hepatic copper deposition in the Long-Evans Cinnamon (LEC) rat.
To study effects of dietary Cu and Fe levels on the onset of hepatitis in Long-Evans Cinnamon (LEC) rats, female rats (40 days old) were fed a semipurified diet containing 0.1 or 10 mg Cu/kg and 1.5 or 150 mg Fe/kg in a 2 x 2 factorial arrangement for 35 days. At 75 days after birth, LEC rats (+Cu-Fe) fed a Cu-sufficient but Fe-deficient diet (Cu, 10 mg/kg; Fe, 1.5 mg/kg) showed jaundice, with lethargy, anorexia, and malaise. The biochemical variables relating to liver function were significantly increased compared to three other groups, a Cu- and Fe-deficient (-Cu-Fe) group, a Cu-deficient but Fe-sufficient (-Cu+Fe) group, and a Cu and Fe sufficient (+Cu+Fe) group. Furthermore, the +Cu-Fe rat liver showed massive necrosis with huge nuclei. The other three groups presented no biochemical and histological findings of hepatitis. Hepatic Cu and metallothionein concentrations were 289 +/- 87 (mean +/- SD) microg/g liver and 8.7 +/- 1.8 mg/g liver, respectively, in the +Cu-Fe rats. However, in the +Cu+Fe group the values were 196 +/- 28 microg Cu/g liver and 10.8 +/- 1.0 mg/g liver. Hepatic Fe deposition was not influenced significantly by the dietary Cu level. The +Cu-Fe group with jaundice showed the highest free Cu concentration in the liver among the four groups, but the hepatic free Fe concentration was similar to those in the -Cu+Fe and +Cu+Fe groups. Our results indicate that an Fe-deficient diet enhances the deposition of hepatic Cu due to increased absorption of Cu from the gastrointestinal tract. This deposition stimulated the onset of hepatitis.
Animals↗
Iron depletion prevents adenine nucleotide decomposition and an increase of xanthine oxidase activity in the liver of the Long Evans Cinnamon (LEC) rat, an animal model of Wilson's disease.
The Long Evans Cinnamon (LEC) rat, which accumulates excess Cu in the liver as in patients with Wilson's disease, is a mutant strain displaying spontaneous hepatitis. It was reported that Fe, like Cu, increases in the liver and that the severity of hepatitis is modified by Fe in the diet. In this experiment, oxidative stress increased by Fe was investigated before the onset of hepatitis. To examine the effect of Fe on the progress into hepatitis, LEC female rats were fed an Fe-regular (Fe 214 microg/g; Fe(+) group) or an Fe-restricted (Fe 14 microg/g; Fe(-) group) diet from 53 days of age for 35 days. Fischer rats were also fed as control animals. Adenine nucleotide decomposition was determined as an index of oxidative stress based on xanthine oxidase activity. The size of the hepatic pool of adenine nucleotides (ATP+ADP+AMP) was significantly smaller in LEC rats than Fischer rats. The energy charge (ATP+0.5ADP)/(ATP+ADP+AMP) was smaller in Fe(+) groups than in Fe(-) groups. In the LEC rat liver, the Fe concentration in the Fe(+) group was 160% of that in Fe(-) group and the correlation coefficient between the hepatic Fe concentration and the energy charge was significant. In this strain, an increase of xanthine oxidase activity resulted in an increase of xanthine, an oxidized metabolite of hypoxanthine in the liver. The results suggest the involvement of the Fe in the progression into hepatitis in the LEC rat, even if the dietary Fe concentration is similar to that of commercial diet.
Adenine Nucleotides↗
Chondroma of the hyoid bone: a case report.
Chondroma of the hyoid bone is extremely rare. We report the case of a 24-year-old woman with a chondroma of the greater cornu of the hyoid bone. In addition, we discuss the clinical and pathologic differential diagnoses.
Adult↗
The effect of subcutaneous tetrathiomolybdate administration on copper and iron metabolism, including their regional redistribution in the brain, in the Long-Evans Cinnamon rat, a bona fide animal model for Wilson's disease.
The present work was performed to examine the effect of tetrathiomolybdate on Cu and Fe metabolism, especially redistribution of Cu and Fe in the brains of Long-Evans Cinnamon rats, with inherently abnormal Cu deposition in the liver. The drug was injected subcutaneously at 5 mg/kg of body weight twice a week for 65 days (total dose of 20 mg) into 40-day-old Long-Evans Cinnamon rats. In Long-Evans Cinnamon rats treated with tetrathiomolybdate, the hepatic Cu concentration was 60 microg/g wet weight, compared to 170 microg/g in untreated rats. In seven brain regions (cerebellum, medulla oblongata, hypothalamus, striatum, midbrain, hippocampus and cortex) of the Long-Evans Cinnamon rats treated with tetrathiomolybdate. the Cu concentration (1.5 to 2.3 microg/g) was slightly lower (1.6 to 2.7 microg/g) than in untreated rats. A significant difference between the two groups was found only in the midbrain. Brain Fe concentrations in regions other than the striatum were not changed significantly by the tetrathiomolybdate injections. The hepatic Fe concentration was about 120 microg/g in Long-Evans Cinnamon rats without tetrathiomolybdate. Tetrathiomolybdate injection further increased the concentration to about 250 microg/g. Our results indicated that subcutaneous tetrathiomolybdate injection did not have an effect that stimulated redistribution of Cu and Fe in the seven brain regions examined, although hepatic Cu was markedly decreased and the removed Cu was deposited in kidneys, spleen and testes. The increased hepatic Fe level should be taken into account when considering side effects of the compound.
Animals↗
[Development of an enzyme-linked immunosorbent assay (ELISA) for detection of IgM and IgG antibodies to lipopolysaccharide of Escherichia coli O157].
We developed the enzyme-linked immunosorbent assay (ELISA) for detection of serum IgM and IgG antibodies to lipopolysaccharide (LPS) of Escherichia coli O157:H7 (VT1+, VT2+) isolated from a clinical sample. We tested the patient's sample with hemolytic uremic syndrome (HUS) and hemorrhagic colitis (HC). And we evaluated the value of sample OD to cut off control OD as the Index. The CVs obtained in precision studies were below 10% for intra- and inter-assay, respectively. The cut off index value of infants and children (0 to 5 years) was 0.60 for IgM and 0.95 for IgG. Moreover we investigated the specificity to E. coli O157 from other E. coli serotypes in this method. From these results, O27 serotype was crossreacted in this assay, but other serotypes were not reacted. In the patients with HUS and HC, some cases were already positive for IgM at 3 days, but for IgG 8 days were needed for it to become positive. We concluded that this ELISA for IgM and IgG for E. coli O157 LPS have a useful performance, and might be the useful tool for rapid diagnosis for E. coli O157 infection.
Antibodies, Bacterial↗