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1.
Sawai H Funahashi H Matsuo Y Yamamoto M Okada Y Hayakawa T Manabe T 《Digestive diseases and sciences》2003,48(7):1241-1250
To Investigate the prognostic indicator, we examined the expression of 6- and 5- integrin and interleukin-1 receptor type I (IL-1RI) immunohistochemically, and analyzed the correlation between immunohistochemical findings and clinicopathological factors in pancreatic cancer. In patients with a strongly expressing 6- integrin subunit or weakly expressing 51-integrin in pancreatic cancer tissues there was a significant association with advanced TNM stage (P = 0.027 and 0.014, respectively), presence of liver metastases (P = 0.032 and 0.002, respectively), and poor prognosis (P = 0.0155 and 0.0056, respectively). In patients with a weakly expressing 6 integrin subunit or weakly expressing 51-integrin in noncancerous pancreatic tissues there was a significant association with poor prognosis (P = 0.0324 and 0.0396, respectively). Multivariate analysis demonstrated that strong expression of 6- and weak expression of 51-integrin were found to be independent prognosticators in pancreatic cancer patients. Our present results indicate that 61- and 51-integrin expression can be a significant prognostic indicator in pancreatic cancer. 相似文献
2.
Dr. Christoph Gasché MD Walter Reinisch MD Harald Vogelsang MD Regina Pötzi MD Va Markis MD Michael Micksche MD Hans Peter Wirth MD Alfred Gangl MD Herbert Lochs MD 《Digestive diseases and sciences》1995,40(4):800-804
Several case reports suggested good effects of interferon- in patients with Crohn's disease. In addition, a decreased production of interferon- in Crohn's disease has been shownin vitro. Treatment with interferon- may activate intestinal natural killer cells and down-regulate the overproduction of inflammatory cytokines like interleukin-6 in Crohn's disease. To evaluate the clinical efficacy of interferon-, we treated 12 patients with a chronic active course of Crohn's disease with recombinant human interferon- prospectively for 24 weeks. Prednisolone was continuously tapered and discontinued at week 12. The end point of the study was the prevention of worsening of clinical symptoms defined with the Crohn's disease activity index and was monitored by acute-phase proteins, interleukin-6 serum concentrations, and endoscopy. The biochemical activity of interferon- was measured by 2,5-oligo adenylate serum levels. The end point of the study was reached in four patients (33%). In these patients the final Crohn's disease activity index was above 150, which means that they did not achieve clinical remission. All other patients (66%) did not respond to interferon- and had to be withdrawn prematurely. Interferon- did not show any beneficial effect on interleukin-6 or acute-phase protein concentrations and on endoscopic activity. The 2,5-oligo adenylate levels continuously increased during interferon therapy. Considerable side effects were noted. These results fail to demonstrate a therapeutic role of interferon- in chronic active Crohn's disease. 相似文献
3.
Takei M Matsuno H Okada K Ueshima S Matsuo O Kozawa O 《Journal of thrombosis and thrombolysis》2002,14(3):205-211
Background: The role of 2-antiplasmin (2-AP) on platelet aggregation was investigated using mice deficient in 2-AP (2-AP–/–) or using wild type mice (2-AP+/+).
Methods: Blood samples were taken from each mouse under anesthesia with ether and platelet rich plasma (PRP) was prepared. Platelet aggregation induced by various doses of ADP (0.3–30 M) was detected using a laser-light scattering (LS) system. Aggregated forms were observed using a scanning electron microscopy (SEM).
Results: Dose-dependent platelet aggregation was not different in both types of mice. However, platelet micro-aggregate formation in 2-AP–/– mice induced by low dose of ADP (1.0 M) markedly increased compared to the situation in wild type mice. Aggregated form detected by SEM showed supported data from LS analysis. When washed platelets of 2-AP+/+ mice were resuspended in plasma of 2-AP–/– mice, platelet micro-aggregation was also increased. On the contrary, when washed platelets of 2-AP–/– mice were suspended in plasma of 2-AP+/+ mice, platelet micro-aggregation did not change. In separate experiments, tPA (1.0 g/ml) was added to PRP before the stimulation of ADP. tPA had no effect on platelet aggregation in 2-AP+/+ mice, however platelet micro-aggregation in 2-AP–/– mice was markedly increased by the treatment with tPA. Moreover, the amount of released ATP from stimulated platelets was increased in 2-AP–/– mice treated with tPA.
Conclusion: Lack of 2-AP increased platelet micro-aggregation, and plasmin plays an important role in the formation of platelet aggregation when 2-AP knockout mice are used. Consequently, the reduction of 2-AP could be a risk factor for the activation of platelets resulting in thrombus formation. 相似文献
4.
Bosco D Meda P Morel P Matthey-Doret D Caille D Toso C Bühler LH Berney T 《Diabetologia》2005,48(8):1523-1533
Aims/hypothesis Alpha1-proteinase inhibitor (1-PI) has been considered a key player in inflammatory processes. In humans, the main production site of 1-PI is the liver, but other tissues, including pancreatic islets, also synthesise this molecule. The aims of this study were to assess the islet cell types that produce 1-PI, to determine whether 1-PI is actually secreted by islet cells, and to assess how its production and/or secretion are regulated.Methods Expression of 1-PI in human islet cells was assessed by immunofluorescence, electron microscopy and western blotting. Release of 1-PI was analysed by reverse haemolytic plaque assay and ELISA. The effects of cytokines on 1-PI synthesis and secretion were tested.Results Immunofluorescence showed that alpha and delta cells do express 1-PI, whereas beta cells do not. By electron microscopy, we demonstrated a colocalisation of 1-PI with glucagon and somatostatin within secretory granules. Immunolabelling also revealed localisation of 1-PI within the Golgi apparatus, related vesicles and lysosomal structures. The expression of 1-PI in islet cells was also demonstrated by western blotting and ELISA of protein extracts. ELISA and reverse haemolytic plaque assay showed that 1-PI is secreted into the culture medium. Treatment of islet cells with IL-1 and oncostatin M for 4 days increased the production and release of 1-PI.Conclusions/interpretation Our results demonstrate that 1-PI is expressed by the alpha and delta cells of human islets, and that proinflammatory cytokines enhance the production and release of this inhibitor. 相似文献
5.
Vongthavaravat V Mesiya S Saymeh L Xia Y Harty RF 《Digestive diseases and sciences》2003,48(2):329-333
The mechanisms by which transforming growth factor- (TGF-) protects the stomach against mucosal injury are incompletely understood. The aim of this study was to examine the roles of sensory neurons, sensory neuropeptides and prostaglandins in TGF gastroprotection against ethanol. Fasted rats received TGF- (50 g/kg, intraperitoneally) prior to orogastric ethanol (75% v/v, 1 ml). Gastric injury was quantitated 30 min after ethanol. Involvement of sensory neurons and the sensory neuropeptides, calcitonin gene-related peptide (CGRP) and substance P (SP), were examined by capsaicin deafferentation and specific receptor antagonist infusion, respectively. Indomethacin (10 mg, intragastrically) was used to determine the role of prostaglandins in TGF--mediated gastroprotection. TGF- significantly diminished ethanol-induced gastric lesion area to 5.7 ± 0.8 mm2 vs 4l.1 ± 5.2 mm2 (P < 0.001). Sensory denervation and CGRP-receptor blockade abolished the TGF- protective effect. In contrast, SP antagonist and indomethacin did not alter TGF- gastroprotection. In conclusion, TGF--mediated gastroprotection involves sensory neuron activation and CGRP release and this protective effect did not involve substance P or prostaglandin generation. 相似文献
6.
H. -D. Kleine U. Wagner H. Poliwoda M. Freund 《Journal of cancer research and clinical oncology》1992,118(1):56-60
Summary Tumour necrosis factor (TNF) exerts cytotoxic and antiproliferative effects on neoplastic cells. It has been used as a therapeutic agent for solid tumours and haematological malignancies. We report on the ex vivo determination of the effect of recombinant human rhuTNF on bone marrow aspirates by a bromodeoxyuridine/propidium iodide method. Cell samples were drawn after 0.5, 2, 4, 6, 8, 10, 22, and 25 h from shortterm suspension bone marrow cultures from patients with acute myelogenous leukemia (AML). Flow-cytometric cell-cycle analysis was performed after double DNA staining with propidium iodide and anti-BrdU antibodies. By this method the effect of rhuTNF on cell proliferation can be evaluated after only 35 h. In about two-thirds of the bone marrow aspirates of AML an inhibiting effect on rhuTNF can be demonstrated, developing to its full extent after 10 h.Abbreviations TNF
tumour necrosis factor
- AML
acute myelogenous leukemia 相似文献
7.
J. G. Chang T. C. Liu S. S. Chiou J. T. Chen T. P. Chen C. P. Lin 《Annals of hematology》1994,69(4):205-209
Summary We sequenced part of the X boxes of-thalassemia-1 of Southeast Asia type (- -SEA) with–
4.2,–
3.7,–
G-Taichung, and
CS. We found the X box of–
3.7 belonged to the X box of 2 globin gene and the X box of
cs contained X boxes of both al and2 globin gene, whereas the X box of–
4.2 and–
G-Taichung was a hybrid of X boxes of 2 and 1 globin gene. We also found there are two types of–
4.2 deletion; type 1 is a common type of–
4.2 deletion and type 2 is linkage to–
G-Taichung. We used a combination of two methods, the amplification refractory mutation system (ARMS) and the amplified created restriction sites (ACRS), to amplify the hybrids of X boxes specifically. The upstream primer for X box of2 globin gene was designed following the standard ARMS procedure to amplify the X segment of the-globin gene. The downstream primer was designed according to the ACRS method to check the specificity of PCR products. Using this approach, we can diagnose the different types of–
4.2 deletion. This kind of approach can also be used to amplify the specific region from the cluster of highly homologous genes. 相似文献
8.
Prevalence of alpha gene triplication or deletion in -thalassemia carriers was studied in 109 unrelated individuals in Rosario, Argentina. In different populations -3.7 allele presents a higher prevalence than anti3.7; thus, -thalassemia associated with -thalassemia is more frequently observed. Nevertheless, this event was detected in only one case (0.9%), while the association with alpha triplication was present in two subjects (1.8%). 相似文献
9.
Takaishi O Arakawa T Fujiwara Y Fukuda T Otani K Yamasaki K Higuchi K Kuroki T 《Digestive diseases and sciences》1999,44(12):2405-2411
We investigated the effects of 16,16-dimethylprostaglandin E2 on the production of tumornecrosis factor- and interleukin-1 in humanmonocytes stimulated with Helicobacter pylori. Monocytes isolated from human peripheral blood wereincubated for 24 hr with the extract of H. pyloridiluted 1:100 to 1:100,000 by volume, a combination ofthe extract and 16,16-dimethyl prostaglandinE2, or a vehicle alone. The extract stimulated theproduction of tumor necrosis factor- andinterleukin-1 and the expression of theirmessenger RNA in a dose-dependent manner. 16,16-Dimethylprostaglandin E2 inhibited the production of thesecytokines and their messenger RNA in the presence of H.pylori at doses higher than 10-6 M,predominantly with tumor necrosis factor-. These data suggest that antiinflammatory effects ofprostaglandins on gastric mucosa are in part related totheir effects on inhibition of production ofproinflammatory cytokines by monocytes. 相似文献
10.
Giuseppina Morini Daniela Grandi Maria Luisa Arcari Gabriella Galanti Giulio Bertaccini 《Digestive diseases and sciences》1997,42(5):1020-1028
(R)--Methylhistamine, a selective agonistof histamine H3 receptors, preventsmacroscopically visible gastric lesions by absoluteethanol in the rat. A further insight into its activitywas the aim of our study. Rats were given saline or(R)--methylhistamine (100 mg/kg)intragastrically. After 30 min, absolute ethanol wasgiven and gastric mucosa was sampled 60 min later.Histologic damage and intracellular and adherent mucus werequantified. Luminal surface and mucous cells wereexamined by scanning and transmission electronmicroscopy. (R)--Methylhistamine reduced theextent of lesions by ethanol from 96 to 18%. Surface mucous cellsand mucous neck cells were increased in volume andnumber, packaging of intracellular mucus was modified,and the secretory processes were promoted by(R)-methylhistamine itself, although these modifications weremostly evident in stomachs subsequently exposed toethanol. Adherent mucus layer thickness was increased by(R)-methylhistamine only after ethanol exposure. It is concluded that(R)--methylhistamine predisposes mucous cells toreact to ethanol. 相似文献
11.
Juha Punnonen Pentti K. Heinonen Tapio Kuoppala Christer T. Jansen Reijo Punnonen 《Journal of cancer research and clinical oncology》1991,117(6):587-592
Summary To assess the role of interleukin-1 (IL-1) and tumour necrosis factor (TNF) in the physiological host defence mechanisms against malignancies, the production of these cytokines in sera, ascitic and cyst fluids and in the tumour tissues of patients with benign or malignant ovarian tumours was studied. IL-1 was found neither in the sera nor in the ascitic fluids of these patients. It was also virtually absent from the cyst fluid samples. However, a mean value of 790 pg IL-1/g tumour was found. Like IL-1, TNF was virtually absent in the serum samples. It was, however, detectable in the ascitic and cyst fluids and tumour tissues. The TNF concentrations were highest in the tumour tissues, with a mean level of 328 pg/g tumour. When comparing the level of IL-1 and TNF in patients with benign tumours to that seen in patients with malignant tumours, no differences in production were observed, regardless of the origin of the test samples. Our results indicate the production of IL-1 and TNF in patients with ovarian tumours. More importantly, the finding that the production of these cytokines in patients with benign tumours is similar to that in patients with malignant tumours supports the conclusion that the production of these cytokines is more a nonspecific indicator of an inflammatory process than a specific response to a malignant process.Abbreviations IL
interleukin
- TNF
tumour necrosis factor 相似文献
12.
New tumor necrosis factor-α-inducing protein released from<Emphasis Type="Italic"> Helicobacter pylori</Emphasis> for gastric cancer progression 总被引:2,自引:0,他引:2
Suganuma M Kurusu M Suzuki K Nishizono A Murakami K Fujioka T Fujiki H 《Journal of cancer research and clinical oncology》2005,131(5):305-313
Purpose To investigate the association between Helicobacter pylori infection and its inflammatory reaction in gastritis, gastric ulcer, and gastric cancer, a new tumor necrosis factor- (TNF-)-inducing protein of H. pylori was studied.Methods The HP0596 gene of H. pylori was identified as the TNF--inducing protein (Tip) gene from genome sequence of H. pylori strain 26695. Using recombinant Tip (rTip) and deleted Tip (rdel-Tip) proteins, the latter of which lacks six amino acids containing two cysteines in the N-terminal domain, we examined their activities in TNF- gene expression and NF-B activation in both Bhas 42 (v-H-ras transfected BALB/3T3) cells and mouse gastric epithelial cell line MGT-40, and in vitro transformation of Bhas 42 cells.Results Tip protein as a homodimer form (38 kDa) was found in both extracts and culture medium of various H. pylori strains. rTip significantly induced TNF- gene expression and NF-B activation in both Bhas 42 cells and MGT-40, and induced in vitro transformation of Bhas 42 cells. However, rdel-Tip did not. Treatment with MG-132, a proteasome inhibitor, inhibited translocation of NF-B p65, and abrogated TNF- induction induced by Tip protein.Conclusion Tip is a new carcinogenic factor released from H. pylori mediated through NF-B activation. 相似文献
13.
Abstract.
During myocardial ischemia, both the myocardial and serum
TNF concentrations are rapidly increased within the area at
risk. With prolongation of ischemia and development of
cardiomyocyte necrosis, the TNF concentration increases also in
the surrounding viable portions of the myocardium. Indeed, in
the scenario of myocardial ischemia/reperfusion, treatment with
TNF antibodies reduced the extent of myocardial infarction in
rabbits and attenuated the contractile dysfunction following
microembolization in dogs. In the latter studies, the serum TNF
concentration remained unaltered thereby supporting the notion
of a direct action of TNF at the level of cardiomyocytes during
ischemia/reperfusion.In heart failure, the serum TNF concentration is also
increased, and in patients with advanced heart failure the serum
TNF concentration is an independent predictor of mortality. The
origin of the increased serum TNF concentration is not clearly
identied yet, but TNF derived from the heart and peripheral
organs contributes to the increased serum TNF concentration.
Treatment with TNF antibodies in the clinical scenario,
however, did not improve the prognosis of heart failure
patients. 相似文献
14.
Immune-mediated stem cell damage has been postulated to be responsible for disease initiation and progression in aplastic anemia (AA). It is hypothesized that T lymphocytes play a major role in destroying the bone marrow (BM) stem cells of AA patients by infiltrating the BM and secreting excessive levels of anti-hematopoietic cytokines, interferon-gamma (IFN-), and tumor necrosis factor-alpha (TNF-). We undertook this study to assess the pathogenic significance of anti-hematopoietic cytokines such as IFN- and TNF- in BM T cells and plasma of AA patients. Significantly elevated levels of IFN- and TNF- were found in the BM plasma of AA patients compared to controls (p=0.05 and 0.006, respectively). Intracellular IFN- and not TNF- in BM CD3+ T cells of AA patients was significantly higher compared to controls (p=0.04 and p=0.2, respectively). A follow-up analysis of expression of these cytokines in BM T cells and their levels in BM plasma in five AA patients before and 180 days (6 months) after antithymocyte globulin (ATG) and cyclosporin A (CsA) therapy showed a decline 180 days after therapy compared to pre-therapy. We thus conclude that increased production of both IFN- and TNF- in the BM may contribute to disease pathogenesis in AA and ATG therapy may induce hematological remission by suppressing the elevated levels of IFN- and TNF- in AA BM. 相似文献
15.
Summary The effects of recombinant human interleukin-4 (IL-4) and the glucocorticoid, dexamethasone, on tumor necrosis factor (TNF) and interleukin-1 (IL-1) levels in cultures of rheumatoid and osteoarthritic synovial tissue were studied. Low concentrations of IL-4 and dexamethasone suppressed the levels of both cytokines in the supernatants of both types of tissue after stimulation with lipopolysaccharide (LPS); the IL-1 and TNF levels were measured by ELISA. It is suggested that it is the monocyte/macrophage in the synovial tissues that is responsive to the inhibitors. It is proposed that glucocorticoids may act on synovial tissue in this manner in vivo and IL-4 may do so if administered intraarticularly. 相似文献
16.
Cytokine-induced apoptotic cell death in a mouse pancreatic beta-cell line: inhibition by Bcl-2 总被引:9,自引:0,他引:9
Dr. H. Iwahashi T. Hanafusa Y. Eguchi H. Nakajima J. Miyagawa N. Itoh K. Tomita M. Namba M. Kuwajima T. Noguchi Y. Tsujimoto Y. Matsuzawa 《Diabetologia》1996,39(5):530-536
Summary Cytokines are thought to contribute to the induction of pancreatic beta-cell destruction in insulin-dependent diabetes mellitus. The molecular mechanisms that underlie beta-cell death were investigated by studying cytokine-induced cell death in beta-cell lines. A combination of three cytokines (interleukin-1, tumour necrosis factor-, and interferon-) induced apoptotic cell death in the mouse pancreatic beta-cell line TC1, as judged from the appearance of cells with hypodiploid nuclei and oligonucleosomal DNA fragmentation. The same treatment also induced apoptosis in the mouse pancreatic alpha-cell line TC1 and the NOD/Lt mouse beta-cell line NIT-1, although to a lesser extent than in TC1 cells. The abundance of endogenous Bcl-2 in TC1 cells was lower than that in the other two cell lines. Overexpression of human Bcl-2 in TC1 cells partially protected them from cytokine-induced cell death. These results suggest that apoptosis may be responsible, at least in part, for cytokine-induced beta-cell destruction and that Bcl-2 prevents apoptosis in pancreatic islet cells.Abbreviations IDDM
Insulin-dependent diabetes mellitus
- IL
interleukin
- TNF
tumour necrosis factor
- IFN
interferon
- FBS
fetal bovine serum
- ATA
aurintricarboxylic acid
- CHX
cycloheximide
- PI
propidium iodide 相似文献
17.
Hugo R. Rosen Peter J. Winkle Bradley J. Kendall David L. Diehl 《Digestive diseases and sciences》1997,42(6):1290-1294
Cytokines are low-molecular-weight proteinmediators that possess a wide spectrum of inflammatory,metabolic, and immunomodulatory properties. Cytokineshave been shown to be produced by monocytes/macrophages, lymphocytes, fibroblasts, endothelial cells,and more recently, hepatocytes and biliary epithelium.The aim of this study was to define biliary levels ofinterleukin-6 (IL-6) and tumor necrosis factor- (TNF-) in patients undergoing endoscopicretrograde cholangiopancreatography (ERCP) in variousdisease states. Fifty-four patients undergoing ERCPcomprised the study group. IL-6 and TNF- were measured in aspirated bile using an ELISAtechnique. Levels of both TNF- and IL-6 weresignificantly higher in patients with cholangitis (P< 0.00001). Moreover, IL-6 was 100% specific forcholangitis since none of the patients without bacterialcholangitis — including patients with biliaryobstruction secondary to cholangiocarcinoma orpancreatic carcinoma — had measurable IL-6 intheir bile. Low levels of biliary TNF- were detectable in fivepatients without cholangitis; the sensitivity andspecificity of TNF- for cholangitis were 100% and82%, respectively. There was a strong statisticalcorrelation between biliary IL-6 and TNF- levels (r= 0.819, P < 0.0001). In contrast, the correlationsbetween biliary cytokines and serum biochemicalparameters were weak. These results suggest that IL-6and TNF- are sensitive markers for cholangitis and maydifferentiate it from other types of biliary tractdisease. 相似文献
18.
Jozsef Timar Hemi Chopra X. Rong James S. Hatfield Suzanne E. G. Fligiel James M. Onoda John D. Taylor Kenneth V. Honn 《Journal of cancer research and clinical oncology》1992,118(6):425-434
Summary Calcium channel blockers of the phenylalkylamine (i.e. verapamil), benzothiazepine (i.e. diltiazem) and dihydropyridine (i.e. nifedipine) classes were evaluated for effects on the tumor cell/platelet interactions using Walker 256 carcinosarcoma cells (W256 cells). When W256 cells were pretreated for 15 min with channel blockers at concentrations of 50–200 M, macroscopic tumor-cell-induced platelet aggregation was inhibited (order of potency; nifedipine>diltiazemverapamil). However, ultrastructural analysis revealed limited, focal platelet aggregates associated with tumor cell plasma membranes of verapamil- and diltiazem-treated cells. There was no evidence of platelet activation or platelet association with the tumor cell membrane in cells pretreated with nifedipine. Walker 256 cells possess the integrin IIb3. Tumor cell IIb3 was shown to mediate tumor cell/platelet interactions in vitro [Chopra et al. (1988) Cancer Res. 48:3787]. Patching and capping of surface IIb3 were inhibited by nifedipine>diltiazemverapamil. The degree of inhibition of IIb3 receptor mobility parallels the inhibition of tumor-cell-induced platelet aggregation. W256 cells are characterized by a well-developed microfilament and intermediate filament network and by the absence of a distinct microtubular network. Calcium channel blockers had no effect on the low polymerization level of tubulin. However, they induced rearrangement of microfilament stress fibers. Intermediate filaments were also rearranged but to varying degrees. The order of effectiveness for alteration of intermediate filament organization was nifedipine>diltiazem while verapamil was ineffective. We propose that the previously reported inhibition of tumor cell/platelet interaction and tumor cell metastasis by calcium channel blockers [Honn et al. (1984) Clin Exp Metastasis 1:61] is due not only to the effects of the Ca2+ channel blockers on platelets, but also to their effect on the tumor cell cytoskeleton resulting in an inhibition of the mobility and function of the IIb3 receptor.Abbreviations CCB
calcium channel blocker
- IIb3
platelet glycoprotein IIb/IIIa complex
- TCIPA
tumor cell induced platelet aggregation
- W256
Walker 256 carcinosarcoma
This work was supported by Public Health Service grant CA-47115, a grant from Harper Hospital and a grant from the Veterans Administration 相似文献
19.
Sano K Nagaki M Sugiyama A Hatakeyama H Ohnishi H Muto Y Moriwaki H 《Digestive diseases and sciences》1999,44(4):796-805
Adhesions of leukocytes to hepatocytes andsinusoidal endothelial cells mediates the induction andprogression of hepatic injury. However, in contrast toendothelial cells, information regarding the regulation of interactions between leukocytes andhepatocytes is limited. In the present study, weinvestigated the effect of inflammatory mediatorsincluding lipopolysaccharide (LPS), staphylococcalenterotoxin B (SEB), interferon- (IFN-), tumornecrosis factor- (TNF-), andinterleukin-1 (IL-1) on the adhesion ofpolymorphonuclear leukocytes or lymphocytes to primarycultured rat hepatocytes, and on the expression of intercellular adhesionmolecule-1 (ICAM-1) gene in hepatocytes. Bothpolymorphonuclear leukocyte and lymphocyte adhesion tohepatocytes were enhanced after exposure of hepatocytes to IFN- and TNF-, but not afterexposure to LPS, SEB or IL-1. The adhesion inducedby either IFN- or TNF- was inhibited bymonoclonal antibodies against ICAM-1 or lymphocytefunction-associated antigen-1 (LFA-1). Nonstimulated hepatocytesexpressed faintly ICAM-1 mRNA, which increased slightlyduring the culture period. ICAM-1 mRNA expression wasup-regulated to a greater extent by incubating hepatocytes with IFN- or TNF-,and peaked after 12 hr of incubation with TNF-and after 24 hr with IFN-. These results indicatethat IFN- and TNF- induce the expressionof ICAM-1 on parenchymal hepatocytes and that theLFA-1-ICAM-1 pathway plays an important role in theinteraction between hepatocytes and neutrophils orlymphocytes. 相似文献
20.
Summary Globin chain synthesis was studied in 13 iron-deficient patients. The mean whole-cell globin / ratio in the peripheral blood of 11 patients was 1.05±0.06 which is similar to the value 0.99±0.08 obtained for 10 controls. The ratios odtained for stroma-free globin were not significantly different from those of whole cell preparations. In contrast, the / ratio of bone marrow was 0.73±0.14 in 10 iron deficient patients, which is significantly lower than that of controls. Two other patients had decreased / ratios in the peripheral blood, probably because of the presence of an -thalassemia gene. These results demonstrate a reduced rate of synthesis of chains relative to that of chains in the bone marrow of iron-deficient patients that is not demonstrable in the peripheral blood.This work was partly supported by Fundação de Amparo à Pesquisa do Estado de São Paulo, Brazil 相似文献