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S Seki

Publications and source records attributed to S Seki.

At least 19 recordsLinked to original sources
PubMed1999

Protective effect of NK1.1(+) T cells as well as NK cells against intraperitoneal tumors in mice.

Peritoneal resident cells of mice normally contain small populations of NK cells and NK1.1(+) alphabetaT cells. These populations increased after either 3LL or EL4 tumor inoculations into the peritoneal cavity. In vivo depletion of NK cell alone by anti-asialo GM1 (ASGM1) Ab significantly decreased survival time of tumor-injected mice, while depletion of both NK cells and NK1.1(+) T cells by anti-NK 1.1 Ab greatly shortened mouse survival time. NK1. 1(+) T cells in peritoneal cavity consist of a larger proportion of double-negative T cells and smaller populations of CD4(+) T cells and Vbeta8(+) T cells compared with liver NK1.1(+) T cells and normally lack Vbeta2(+) T cells. Tumor inoculation induced rapid IL-12 and IFN-gamma mRNA in tumor-infiltrating mononuclear cells (TIM). Although anti-NK1 Ab pretreatment in vivo abrogated IFN-gamma mRNA expression and IFN-gamma production of TIM, NK cell depletion alone by anti-ASGM1 Ab pretreatment retained IFN-gamma mRNA expression and partly inhibited IFN-gamma production of TIM. Peritoneal NK cells as well as NK1.1(+) T cells but not NK1.1(-) T cells of 3LL cell- or EL4 cell-injected mice showed cytotoxicities against the same tumor cells. Further, either anti-IL-12 Ab or anti-IFN-gamma Ab ip injection significantly shortened EL4 cell-inoculated mouse survival time. Our findings suggest that peritoneal macrophages activated by tumors produce IL-12 which activates NK cells and NK1.1(+) T cells to produce IFN-gamma and both NK cells and NK1.1(+) T cells are important in suppressing the growth of the intraperitoneal tumors.

Animals↗
PubMed1999

Development of intraepithelial T lymphocytes in the intestine of irradiated SCID mice by adult liver hematopoietic stem cells from normal mice.

BACKGROUND/AIMS: We recently reported the adult mouse liver to contain c-kit+ stem cells that can give rise to multilineage leukocytes. This study was designed to determine whether or not adult mouse liver stem cells can generate intraepithelial T cells in the intestine as well as to examine the possibility that adult liver c-kit+ stem cells originate from the fetal liver. METHODS: Adult liver mononuclear cells, bone marrow (BM) cells, liver c-kit+ cells or bone BM c-kit+ cells of BALB/c mice were i.v. transferred into 4 Gy irradiated CB17/-SCID mice. In other experiments, fetal liver cells from Ly5.1 C57BL/6 mice and T cell depleted adult BM cells from Ly5.2 C57BL/6 mice were simultaneously transferred into irradiated C57BL/6 SCID mice (Ly5.2). At 1 to 8 weeks after cell transfer, the SCID mice were examined. RESULTS: Not only BM cells and BM c-kit+ cells but also liver mononuclear cells and liver c-kit+ cells reconstituted gamma delta T cells, CD4+ CD8+ double-positive T cells and CD8 alpha+beta- T cells of intestinal intraepithelial lymphocytes of SCID mice. Injection of a mixture of fetal liver cells from Ly5.1 C57BL/6 mice and adult BM cells from Ly5.2 C57BL/6 mice into Ly5.2 C57BL/6 SCID mice induced both Ly5.1 and Ly5.2 T cells, while also generating c-kit+ cells of both Ly5.1 and Ly5.2 origins in the liver. CONCLUSIONS: Adult mouse liver stem cells were able to generate intestinal intraepithelial T cells of the SCID mice, and it is thus suggested that some adult liver stem cells may indeed be derived from the fetal liver.

Animals↗
PubMed1999

Mechanisms involved in graft-versus-host disease induced by the disparity of minor histocompatibility M1s antigens.

In this study we investigated which type of T cells: high T-cell receptor (TCRhigh, cells of thymic origin) or intermediate TCR (TCRint, cells of extrathymic origin), expanded in the liver and other organs, resulting in the induction of graft-versus-host disease (GVHD) with minor lymphocyte stimulating (M1s) disparity. When 6.5 Gy-irradiated BALB/c (H-2d M1s-1b2a) mice were injected with interleukin-2 receptor beta-chain(-) (IL-2Rbeta(-)) CD3high cells purified from the spleen of B10.D2 (H-2d M1s-1b2b) mice, IL-2Rbeta(+)CD3high cells expanded in the liver and other organs of recipient mice. The majority of these cells were found to be IL-2Ralpha(-)Mel-14(-)CD4(+)Vbeta3(+) in GVHD mice. The CDR3 region in their TCR-alphabeta (i.e. N-Dbeta-N) was polyclonal, although there were skewed usages of Vbeta3 and Jbeta2.4. The majority of cells were confirmed to be of donor origin by the individual discrimination method, namely, they originated from isolated IL-2Rbeta(-)CD3high cells. Interestingly, these T cells lacked cytotoxicity against both a natural killer (NK)-sensitive target and thymocytes with M1s disparity and nondisparity. Another important finding was that activated granulocytes expanded at generalized sites in GVHD mice. The present results raise the possibility that M1s disparity is mainly recognized by TCRhigh cells with unique properties but that direct effector cells that induce GVHD might not be such T cells but rather accompanied granulocytes.

Adoptive Transfer↗
PubMed1999

The role of bacterial lipopolysaccharide-bound neutrophils in the pathogenesis of Kawasaki disease.

To investigate the possible role of lipopolysaccharide (LPS, endotoxin) in the pathogenesis of Kawasaki disease, neutrophils from 15 patients with the disease and 7 with sepsis (4 infected with gram-negative bacteria and 3 with gram-positive bacteria) were analyzed by flow cytometry using anti-LPS and anti-CD14 monoclonal antibodies. The number of LPS- and CD14-positive neutrophils was dramatically higher early after the onset of Kawasaki disease and gram-negative sepsis but not with gram-positive sepsis. An immunoprecipitation analysis revealed LPS was bound to CD14 in vivo on neutrophils from Kawasaki disease patients. The mean plasma level of neutrophil elastase was significantly higher in the acute phase of Kawasaki disease than in the acute phase of sepsis. These findings suggest that exposure to LPS occurs at the onset of Kawasaki disease when LPS-bound neutrophils secrete excess protease (implicated in neutrophil-mediated endothelial injury) into the circulation.

Child, Preschool↗
PubMed1999

Superoxide anion scavengers restore NO-mediated pulmonary vasodilation after lung transplantation.

Left lung autotransplantation (LLA) results in a chronic attenuation in endothelium-dependent, nitric oxide (NO)-mediated pulmonary vasodilation. We tested the hypothesis that this abnormality involves a decrease in the effective concentration of NO due to inactivation by superoxide anion. Size- and position-matched pulmonary arterial rings were isolated from the right (control) and left (LLA) lungs of seven dogs 1-5 mo post-LLA. The rings were suspended for isometric tension recording and contracted with phenylephrine, and cumulative dose-response curves for ACh or calcium ionophore (A-23187) were generated. Endothelium-dependent relaxation to ACh was inhibited post-LLA, with the maximum vasorelaxation response reduced from 88 +/- 5 to 63 +/- 5% (P < 0. 01) post-LLA. In contrast, after pretreatment with the superoxide anion scavengers tiron or superoxide dismutase (SOD), the dose-response relationships for ACh were similar in control and LLA rings. Oxypurinol, which inhibits superoxide anion production by endothelial xanthine oxidase, also restored the vasorelaxation response to ACh in LLA rings. The pulmonary vasorelaxant response to A-23187 was also attenuated (P < 0.01) post-LLA, and this effect was entirely reversed by pretreatment with tiron, SOD, or oxypurinol. These results indicate that the attenuated responses to these pulmonary vasorelaxants post-LLA involve inactivation of NO by superoxide anion generated by endothelial xanthine oxidase.

Acetylcholine↗
PubMed1999

[Induction of anesthesia with propofol injected through a central venous catheter].

We compared propofol injected through a central venous catheter with that through a peripheral cannula from the standpoint of injection pain, induction time and hemodynamic changes. Thirty-nine patients about to receive abdominal surgery, who had central venous catheters inserted via the subclavian vein, were included in this study. General anesthesia was induced with a loading dose of propofol 1 mg.kg-1 followed by an infusion of 10 mg.kg-1.hr-1 into the central vein without carrier intravenous fluid (group A, n = 13), the peripheral vein without carrier intravenous fluid (group B, n = 13) or the peripheral vein with rapid infusion of acetated Ringer's solution (group C, n = 13). After endotracheal intubation, anesthesia was maintained with propofol 4 mg.kg-1.hr-1. The incidence of injection pain was 53% in group B and 76% in group C, whereas none of the patients in group A felt discomfort or pain during propofol injection. The mean induction time was significantly shorter in group A (43 +/- 12 sec) than group B (66 +/- 16 sec) or group C (57 +/- 11 sec). There were no differences between each group in hemodynamic changes during induction of anesthesia. Propofol injection via central venous catheter can avoid the injection pain and shorten the induction time.

Abdomen↗
PubMed1998

Genomic structure and sequence of a human homologue (NTHL1/NTH1) of Escherichia coli endonuclease III with those of the adjacent parts of TSC2 and SLC9A3R2 genes.

Genomic cloning and sequencing of a human homologue (the gene name, endonuclease III-like 1; gene symbol, NTHL1 or NTH1) for Escherichia coli endonuclease III, that is involved in pyrimidine base excision repair, were performed. The sequence covered the entire NTHL1 gene consisting of six exons and five introns spanning 8kb with 5' flanking (8kb) and 3' flanking (3.8kb) regions. Southern blot analysis suggested that the NTHL1 gene exists as a single copy in a haploid genome. The sequenced 5' flanking region lacks typical TATA and CAAT boxes, but contains a CpG island having putative binding sites for several transcription factors such as Ets1 and Sp1. The NTHL1 gene lies immediately adjacent to the tuberous sclerosis 2 (TSC2) gene on chromosome 16p13.3 in a 5'-to-5' orientation. Transcription initiation sites of both NTHL1 and TSC2 genes were suggested to be multiple by 5' RACE experiments. The northern hybridization experiment suggested that both genes are expressed in all tissues, but at different levels. Downstream of the NTHL1 gene, the gene for the regulatory factor 2 (SLC9A3R2/E3KARP; also called OCTS2, TKA-1 and SIP-1) of the solute carrier family 9 (sodium/hydrogen exchanger), isoform A3, lies in a 3'-to-3' orientation. This paper demonstrates for the first time the spatial relationship of these three genes (TSC2, NTHL1 and SLC9A3R2) at the nucleotide level, and the presence of multiple transcription initiation sites of the NTHL1 and TSC2 genes.

Base Sequence↗
PubMed1998

Cloning and characterization of a mouse homologue (mNthl1) of Escherichia coli endonuclease III.

Endonuclease III (endoIII; nth gene product) of Escherichia coli is known to be a DNA repair enzyme having a relatively broad specificity for damaged pyrimidine bases of DNA. Here, we describe the cloning and characterization of the cDNA and the gene for a mouse homologue (mNthl1/mNth1) of endoIII. The cDNA was cloned from a mouse T-cell cDNA library with a probe prepared by PCR using the library and specific PCR primers synthesized based on the reported information of partial amino acid sequences of bovine NTHL1/NTH1 and of EST Data Bases. The cDNA is 1025 nucleotides long and encodes a protein consisting of 300 amino acids with a predicted molecular mass of 33.6 kDa. The amino acid sequence exhibits significant homologies to those of endoIII and its prokaryotic and eukaryotic homologues. The recombinant mNthl1 with a hexahistidine tag was overexpressed in a nth::cmr nei::Kmr double mutant of E. coli, and purified to apparent homogeneity. The enzyme showed thymine glycol DNA glycosylase, urea DNA glycosylase and AP lyase activities. Northern blot analysis indicated that mNthl1 mRNA is about 1 kb and is expressed ubiquitously. A 15 kb DNA fragment containing the mNthl1 gene was cloned from a mouse genomic library and sequenced. The gene consists of six exons and five introns spanning 6.09 kb. The sequenced 5' flanking region lacks a typical TATA box, but contains a CAAT box and putative binding sites for several transcription factors such as Ets, Sp1, AP-1 and AP-2. The mNthl1 gene was shown to lie immediately adjacent to the tuberous sclerosis 2 (Tsc2) gene in a 5'-to-5' orientation by sequence analysis and was assigned to chromosome 17A3 by in situ hybridization.

Amino Acid Sequence↗
PubMed1998

Evidence that CD31, CD49b, and CD62L are immunodominant minor histocompatibility antigens in HLA identical sibling bone marrow transplants.

Despite complete matching of siblings for the HLA loci, after bone marrow transplantation (BMT), approximately 20% develop graft-versus-host disease (GVHD). This is presumably due to incompatibility of minor histocompatibility antigens (mHa). We investigated the polymorphisms of 14 adhesion molecules (CD2, CD28, CD31, CD34, CD36, CD42, CD44, CD48, CD49b, CD54, CD62L, CD86, CD102, and CD106) in Japanese subjects and their association with the occurrence of GVHD after allogeneic HLA identical BMT. Six molecules (CD2, CD31, CD42, CD49b, CD54, and CD62L), which were found to be polymorphic, were then examined in 118 HLA identical sibling donors and recipients who had undergone BMT. Association of the incompatibility of the polymorphic molecules with the presence or absence of GVHD was examined. In these six, we observed a significant correlation between acute GVHD and the compatibility of CD31 (codons 563/670) (Pcorrected = .018), and CD31 (codons 563/670) + CD62L (Pcorrected = .018) in patients with the HLA-B44-like superfamily. In patients with the HLA-A3-like superfamily, the compatibility of CD62L (Pcorrected = .03) and CD62L + CD49b (P = . 004, Pcorrected = .078) was associated with acute GVHD. Therefore, CD31, CD49b, and CD62L might be candidates for immunodominant mHa.

Adolescent↗
PubMed1998

Purification and characterization of human NTH1, a homolog of Escherichia coli endonuclease III. Direct identification of Lys-212 as the active nucleophilic residue.

The human endonuclease III (hNTH1), a homolog of the Escherichia coli enzyme (Nth), is a DNA glycosylase with abasic (apurinic/apyrimidinic (AP)) lyase activity and specifically cleaves oxidatively damaged pyrimidines in DNA. Its cDNA was cloned, and the full-length enzyme (304 amino acid residues) was expressed as a glutathione S-transferase fusion polypeptide in E. coli. Purified wild-type protein with two additional amino acid residues and a truncated protein with deletion of 22 residues at the NH2 terminus were equally active and had absorbance maxima at 280 and 410 nm, the latter due to the presence of a [4Fe-4S]cluster, as in E. coli Nth. The enzyme cleaved thymine glycol-containing form I plasmid DNA and a dihydrouracil (DHU)-containing oligonucleotide duplex. The protein had a molar extinction coefficient of 5.0 x 10(4) and a pI of 10. With the DHU-containing oligonucleotide duplex as substrate, the Km was 47 nM, and kcat was approximately 0.6/min, independent of whether DHU paired with G or A. The enzyme carries out beta-elimination and forms a Schiff base between the active site residue and the deoxyribose generated after base removal. The prediction of Lys-212 being the active site was confirmed by sequence analysis of the peptide-oligonucleotide adduct. Furthermore, replacing Lys-212 with Gln inactivated the enzyme. However, replacement with Arg-212 yielded an active enzyme with about 85-fold lower catalytic specificity than the wild-type protein. DNase I footprinting with hNTH1 showed protection of 10 nucleotides centered around the base lesion in the damaged strand and a stretch of 15 nucleotides (with the G opposite the lesion at the 5'-boundary) in the complementary strand. Immunological studies showed that HeLa cells contain a single hNTH species of the predicted size, localized in both the nucleus and the cytoplasm.

Base Sequence↗
PubMed1998

Recombinant murine interleukin-12 facilitates induction of cardiac myosin-specific type 1 helper T cells in rats.

Autoimmunity after viral myocarditis is considered to be one of the causes of dilated cardiomyopathy. Cytokines are assumed to play an important role in the pathogenesis. We recently reported that interleukin (IL)-2 and interferon (IFN)-gamma mRNA are expressed in the myocardium of rats with experimental autoimmune myocarditis (EAM). However, the role of cytokines in autoimmune myocardial injury in detail is still not clear. Reverse transcription-polymerase chain reaction identified IL-12 (p40) mRNA in antigen-presenting cells in the initial phase of EAM. Cardiac myosin-specific T lymphocytes (MSTLs) were cultured with cardiac myosin peptide (CMP) in the presence of IL-2 and/or IL-12 and were transferred to other naive rats. The results showed that EAM could be effectively induced by transfer of MSTLs cultured with IL-12, whereas transfer of MSTLs cultured with IL-2 was less effective. However, IL-2 acts synergistically with IL-12, and MSTLs cultured with both cytokines most efficiently induce EAM. In vitro experiments showed that MSTLs cultured with both IL-12 and IL-2 produced a much greater amount of IFN-gamma than did MSTLs cultured with either IL-12 or IL-2 alone. The amount of IFN-gamma production was correlated with pathogenicity of MSTLs. Transfer experiments after sorting further demonstrated that the transfer was affected by CD4+ helper T (Th) cells but not by CD8+ cytotoxic T lymphocytes. IL-12 and IL-2 synergistically enhance the pathogenicity of MSTLs. Furthermore, a type 1 Th (Th1) cytokine, IFN-gamma, which is a potent regulatory cytokine of autoimmunity, is produced by MSTLs. IL-12 and IL-2 potentiate the expansion of cardiac myosin-specific Th1 cells and play an important role in the development of autoimmune myocardial injury.

Animals↗
PubMed1998

Intermediate TCR cells can induce graft-versus-host disease after allogeneic bone marrow transplantation.

Mice fall victim to GVHD when subjected to immunosuppressive treatment and injected with allogeneic bone marrow cells. A major population of cells associated with GVHD is known to be T cells. However, whether such T cells are of thymic or extrathymic origin is obscure. We applied two immunosuppressive conditions, 9 and 6.5 Gy irradiation, to C3H/He mice (H-2k). Bone marrow cells for injection were obtained from C57BL/6 (B6) mice (H-2b). The 9-Gy mice were reconstituted by lymphocytes of donor origin and showed GVHD, whereas 6.5-Gy mice were reconstituted by lymphocytes of recipient origin and showed mild GVHD. The liver was the organ where the reconstitution of lymphocytes occurred efficiently, and a major lymphocyte subset was intermediate (int) CD3 cells (i.e., CD3int cells) in both mice. CD3int cells had the properties of extrathymic T cells, showing the phenotype of NK1.1 + CD3int using invariant V alpha 14 chain. In 6.5-Gy mice, allogeneic cells were rejected by extrathymic T cells of recipient origin. The stored CD3int cells from the liver of 9-Gy mice evoked similar GVHD when transferred into 6.5-Gy irradiated C3H/He mice. These results suggest that CD3int cells of extrathymic origin are a major population for the induction of GVHD under immunosuppressive conditions.

Adoptive Transfer↗
PubMed1998

Involvement of NK1+ T cells and their IFN-gamma production in the generalized Shwartzman reaction.

IL-12 (or LPS) priming and subsequent challenge by LPS produces the generalized Shwartzman reaction. IFN-gamma induced by IL-12 is a crucial cytokine in the priming phase. In vivo depletion of both NK cells and NK1+ alphabeta T cells of mice by anti-NK1.1 Ab greatly reduced the elevation of serum IFN-gamma induced by IL-12 and significantly reduced mortality after subsequent injection of LPS, whereas depletion of NK cells alone by anti-asialo GM1 Ab only partially decreased serum IFN-gamma, and lethality was not changed. Cell sorting and culture experiments confirmed that liver NK1+ alphabeta T cells of IL-12-injected mice produced greater amounts of IFN-gamma than did liver NK cells. MHC class I-deficient mice of C57BL/6 background, which lack a majority of NK1+ alphabeta T cells, produced low amounts of IFN-gamma by IL-12; no mortality was observed after the LPS challenge. However, production of TNF-alpha in the second phase (after LPS challenge) was not inhibited by depletion of NK cells alone or both subsets. IL-12 and subsequent LPS challenge activated NK1+ alphabeta T cells in the liver and induced strong cytotoxicity of these cells not only against tumor cells (including Fas-negative tumors) but also against a syngeneic hepatocyte cell line. Our findings show that IFN-gamma produced by NK1+ alphabeta T cells is essential for the IL-12 priming of the Shwartzman reaction, and the autoreactivity of NK1+ alphabeta T cells in the liver is involved in the hepatic disorders that are sometimes caused by IL-12, LPS, or the generalized Shwartzman reaction.

Adjuvants, Immunologic↗
PubMed1998

Effect of antioxidants, resveratrol, quercetin, and N-acetylcysteine, on the functions of cultured rat hepatic stellate cells and Kupffer cells.

Effects of antioxidants, resveratrol, quercetin, and N-acetylcysteine (NAC) on the functions of cultured rat hepatic stellate cells and Kupffer cells were studied. These compounds dose-dependently suppressed serum-dependent proliferation of stellate cells as determined by [3H]thymidine and 5-bromo-2'-deoxyuridine uptake. Expression of smooth muscle alpha-actin was suppressed by a high dose of resveratrol and quercetin. These phenolic compounds also suppressed inositol phosphate metabolism, tyrosine phosphorylation, and mitogen-activated protein (MAP) kinase activation in platelet-derived growth factor/BB-stimulated stellate cells. Moreover, the phenolic compounds selectively reduced the level of cell cycle protein cyclin D1 in stellate cells. Thus, resveratrol and quercetin might inhibit stellate cell activation by perturbing signal transduction pathway and cell cycle protein expression, whereas mechanism of potent antiproliferative effect of NAC remains to be elucidated. On the other hand, kinetic analysis showed that production of nitric oxide (NO) and tumor necrosis factor alpha (TNF-alpha) by lipopolysaccharide-stimulated Kupffer cells was strongly inhibited by resveratrol and quercetin but not by NAC. Although expression of messenger RNAs for inducible NO synthase and TNF-alpha was not affected by the phenolic compounds, cellular levels of inducible NO synthase and TNF-alpha secretion were suppressed significantly, indicating the posttranscriptional process of generating these proteins might be affected predominantly by these phenolic compounds. Thus, NAC and these phenolic compounds may have therapeutic potential against liver injury by regulating functions of hepatic stellate cells and Kupffer cells.

Actins↗
PubMed1998

Inhibitory effect of protease inhibitor on endothelial cell activation.

BACKGROUND: Endothelial cells (EC) are important for regulating the hemostatic balance of prothrombotic and antithrombotic activities. Proinflammatory cytokines such as tumor necrosis factor-alpha (TNFalpha) play an important role in the regulation of EC and also regulate the production of plasminogen activator inhibitor type 1 (PAI-1), which is an EC-producing factor with the inhibitory activity of fibrinolysis, and the expression of intercellular adhesion molecule-1 (ICAM-1), which is an adhesion molecule that plays an important role in inflammation. Protease inhibitors such as gabexate mesilate (GM) and ulinastatin (UTI) have been shown to improve the microcirculatory environment and reduce tissue damage, but the mechanism for this has yet to be fully elucidated. We investigated the effect of GM or UTI on EC regarding PAI-1 synthesis and ICAM-1 expression. METHODS: Human umbilical vein endothelial cells (HUVECs) were obtained and stimulated with TNFalpha. GM or UTI was added to HUVECs just before TNFalpha stimulation. The PAI-1 activity in the culture medium of HUVECs was measured by using an enzymatic assay kit. The PAI-1 mRNA expression was assayed by a semiquantitative reverse transcriptase polymerase chain reaction assay. The ICAM-1 expression on HUVECs was assayed by a flow cytometric analysis. RESULTS: GM inhibited the PAI-1 synthesis of HUVECs stimulated with TNFalpha in a dose-dependent manner as shown by the mRNA expression. However, UTI was not able to inhibit PAI-1 synthesis. In contrast, both GM and UTI significantly inhibited the ICAM-1 expression on HUVECs stimulated with TNFalpha. CONCLUSIONS: These data suggest that GM may thus provide a beneficial effect which improves the microcirculatory environment and prevents tissue damage by inhibiting the activation of the vascular EC themselves.

Base Sequence↗
PubMed1998

A comparative study of the ciliary area of the maxillary sinus mucosa and computed tomographic images.

The ciliary area of the maxillary sinus mucosa and coronal sinus computed tomographic (CT) scans were studied in 36 maxillary sinuses of 28 patients with chronic sinusitis. Tissue specimens allowed ciliary surfaces to be observed under scanning electron microscopy, allowing surfaces to be expressed in terms of ciliary area (CA) as the percentage of mucosal surface occupied by cilia. The opacity produced by mucosal swelling and secretion in the maxillary sinus on CT was assessed by two methods: Min's and modified van der Veken's methods. Both techniques indicated an inverse correlation between opacity of the maxillary sinus and CA. Our findings suggest that the opacity of maxillary sinus on CT could be a significant parameter for predicting the surface conditions of ciliated maxillary mucosa prior to sinus surgery.

Adult↗
PubMed1998

Increase of CD57+ T cells in knee joints and adjacent bone marrow of rheumatoid arthritis (RA) patients: implication for an anti-inflammatory role.

The distribution of CD57+ T and CD56+ T cells in patients with RA was examined. In control osteoarthritis patients, these cells exist as a minor population in the peripheral blood. Our data show that in patients with RA, CD57+ T cell levels are elevated in peripheral blood, knee joint fluid, knee synovial membrane and bone marrow (BM), compared with peripheral blood of controls. CD57+ T cells are especially high in knee joint fluid and joint-adjacent BM, while CD56+ T cells show no such increase. CD57+ T cells contain a major population of CD8+ cells and higher proportions of CD4-8- cells and gammadelta T cells than do CD57- T cells. CD57+ T cells in peripheral blood and joint fluid increase with the duration of disease. Erythrocyte sedimentation rate (ESR) is inversely correlated with the proportion of CD57+ T cells in the joint fluid. Although RA frequently occurs in patients with CD3+57+ cell leukaemia, and some CD57+ T cells are likely to be involved in the onset of RA, we suggest that CD57+ T cells may rather suppress inflammation of RA, and other cellular components (e.g. granulocytes) may govern the severity of the inflammation of RA. These CD57+ T cells are probably generated extrathymically in the adjacent BM or joint space.

Adult↗