scholarly journals Innate Immunity Components and Cytokines in Gastric Mucosa in Children withHelicobacter pyloriInfection

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Jacek Michalkiewicz ◽  
Anna Helmin-Basa ◽  
Renata Grzywa ◽  
Mieczyslawa Czerwionka-Szaflarska ◽  
Anna Szaflarska-Poplawska ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Gastric Mucosa ◽  
Protein Expression ◽  
Mrna Expression ◽  
Lymphocytic Infiltration ◽  
Natural Immunity ◽  
Gene Expressions ◽  
Protein Levels ◽  
Anti Inflammatory ◽  
H Pylori

Purpose.To investigate the expression of innate immunity components and cytokines in the gastric mucosa amongH. pyloriinfected and uninfected children.Materials and Methods.Biopsies of the antral gastric mucosa from children with dyspeptic symptoms were evaluated. Gene expressions of innate immunity receptors and cytokines were measured by quantitative real-time PCR. The protein expression of selected molecules was tested by immunohistochemistry.Results. H. pyloriinfection did not lead to a significant upregulation ofMyD88, TLR2, TLR4, CD14, TREM1,andTREM2mRNA expression but instead resulted in high mRNA expression ofIL-6, IL-10, IFN-γ, TNF-α,andCD163. H. pylori cagA(+) infection was associated with higherIL-6andIL-10mRNA expression, as compared tocagA(−) strains.H. pyloriinfected children showed increased IFN-γand TNF-αprotein levels. IFN-γmRNA expression correlated with bothH. pyloridensity of colonization and lymphocytic infiltration in the gastric mucosa, whereas TNF-αprotein expression correlated with bacterial density.Conclusion. H. pyloriinfection in children was characterized by (a) Th1 expression profile, (b) lack of mRNA overexpression of natural immunity receptors, and (c) strong anti-inflammatory activities in the gastric mucosa, possibly resulting from increased activity of anti-inflammatory M2 macrophages. This may explain the mildly inflammatory gastric inflammation often observed amongH. pyloriinfected children.

scholarly journals Modulation of Neurological Deficits and Expression of Glutamate Receptors during Experimental Autoimmune Encephalomyelitis after Treatment with Selected Antagonists of Glutamate Receptors

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Grzegorz Sulkowski ◽  
Beata Dąbrowska-Bouta ◽  
Lidia Strużyńska
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Protein Expression ◽  
Mrna Expression ◽  
Glutamate Receptors ◽  
Neurological Deficits ◽  
Autoimmune Encephalomyelitis ◽  
Protein Levels ◽  
Group I ◽  
Group I Mglurs ◽  
Experimental Autoimmune

The aim of our investigation was to characterize the role of group I mGluRs and NMDA receptors in pathomechanisms of experimental autoimmune encephalomyelitis (EAE), the rodent model of MS. We tested the effects of LY 367385 (S-2-methyl-4-carboxyphenylglycine, a competitive antagonist of mGluR1), MPEP (2-methyl-6-(phenylethynyl)-pyridine, an antagonist of mGluR5), and the uncompetitive NMDA receptor antagonists amantadine and memantine on modulation of neurological deficits observed in rats with EAE. The neurological symptoms of EAE started at 10-11 days post-injection (d.p.i.) and peaked after 12-13 d.p.i. The protein levels of mGluRs and NMDA did not increase in early phases of EAE (4 d.p.i.), but starting from 8 d.p.i. to 25 d.p.i., we observed a significant elevation of mGluR1 and mGluR5 protein expression by about 20% and NMDA protein expression by about 10% over the control at 25 d.p.i. The changes in protein levels were accompanied by changes in mRNA expression of group I mGluRs and NMDARs. During the late disease phase (20–25 d.p.i.), the mRNA expression levels reached 300% of control values. In contrast, treatment with individual receptor antagonists resulted in a reduction of mRNA levels relative to untreated animals.

scholarly journals Regulation of the hyaluronan system in ovine endometrium by ovarian steroids

Reproduction ◽  
2013 ◽  
Vol 145 (5) ◽  
pp. 491-504 ◽  
Author(s):  
Kabir A Raheem ◽  
Waleed F Marei ◽  
Karen Mifsud ◽  
Muhammad Khalid ◽  
D Claire Wathes ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Protein Expression ◽  
Mrna Expression ◽  
Differential Expression ◽  
Luteal Phase ◽  
Follicular Phase ◽  
Steroid Treatment ◽  
Ovarian Steroids ◽  
Protein Levels ◽  
Steroid Regulation

In this study, we investigated steroid regulation of the hyaluronan (HA) system in ovine endometrium including HA synthases (HAS), hyaluronidases, and HA receptor-CD44 using 30 adult Welsh Mountain ewes. Eight ewes were kept intact and synchronized to estrous (day 0). Intact ewes were killed on day 9 (luteal phase; LUT; n=5) and day 16 (follicular phase; FOL; n=3). The remaining ewes (n=22) were ovariectomized and then treated (i.m.) with vehicle (n=6) or progesterone (n=8) for 10 days, or estrogen and progesterone for 3 days followed by 7 days of progesterone alone (n=8). Estradiol and progesterone concentrations in plasma correlated with the stage of estrous or steroid treatment. Our results showed trends (P<0.1) and statistically significant effects (P<0.05, by t-test) indicating that LUT had lower HAS1 and HAS2 and higher HAS3 and CD44 mRNA expression compared with FOL. This was reflected in immunostaining of the corresponding HAS proteins. Similarly, in ovariectomized ewes, progesterone decreased HAS1 and HAS2 and increased HAS3 and CD44, whereas estradiol tended to increase HAS2 and decrease CD44. Sometimes, HAS mRNA expression did not follow the same trend observed in the intact animals or the protein expression. HA and its associated genes and receptors were regulated by the steroids. In conclusion, these results show that the level of HA production and the molecular weight of HA in the endometrium are regulated by ovarian steroids through differential expression of different HAS both at the gene and at the protein levels.

Parathyroid hormone stimulates endothelial expression of atherosclerotic parameters through protein kinase pathways

2007 ◽  
Vol 292 (4) ◽  
pp. F1215-F1218 ◽  
Author(s):  
Gloria Rashid ◽  
Jacques Bernheim ◽  
Janice Green ◽  
Sydney Benchetrit
Keyword(s):  
Parathyroid Hormone ◽  
Protein Kinase ◽  
Protein Expression ◽  
Mrna Expression ◽  
Umbilical Vein ◽  
Protein Levels ◽  
Glycation End Products ◽  
Mrna And Protein Expression ◽  
Vascular Structures ◽  
The Impact

Parathyroid hormone (PTH), the major systemic calcium-regulating hormone, has been linked to uremic vascular changes. Considering the possible deleterious action of PTH on vascular structures, it seemed logical to evaluate the impact of PTH on the receptor of advanced glycation end products (RAGE) and interleukin 6 (IL-6) mRNA and protein expression, taking into account that such parameters might be involved in the pathogenesis of vascular calcification, atherosclerosis, and/or arteriolosclerosis. Human umbilical vein cord endothelial cells (HUVEC) were stimulated for 24 h with 10−12–10−10 mol/l PTH. The mRNA expression of RAGE and IL-6 was established by reverse transcriptase/PCR techniques. RAGE protein levels were determined by Western blot and IL-6 secretion was measured by ELISA. The pathways by which PTH may have an effect on HUVEC functions were evaluated. PTH (10−11–10−10mol/l) significantly increased RAGE mRNA and protein expression. PTH also significantly increased IL-6 mRNA expression without changes at protein levels. The addition of protein kinase (PKC or PKA) inhibitors or nitric oxide (NO) synthase inhibitors significantly reduced the RAGE and IL-6 mRNA expression and the RAGE protein expression. PTH stimulates the mRNA expressions of RAGE and IL-6 and the protein expression of RAGE. These stimulatory effects are probably through PKC and PKA pathways and are also NO dependent. Such data may explain the possible impact of PTH on the atherosclerotic and arteriosclerotic progression.

Upregulation of the Anti-Apoptotic Protein, Survivin, in Hematopoietic Cells in Sickle Cell Anemia and Effects of Hydroxyurea Therapy.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1532-1532
Author(s):  
Carolina Lanaro ◽  
Carla Fernanda Franco-Penteado ◽  
Mariana R. B. Mello ◽  
Kleber Yotsumoto Fertrin ◽  
Marcos André C Bezerra ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Expression ◽  
Sickle Cell Anemia ◽  
Survivin Expression ◽  
Erythroid Differentiation ◽  
Mrna Levels ◽  
Gene Expressions ◽  
Protein Levels ◽  
Survivin Protein ◽  
Inflammatory State

Abstract Abstract 1532 Poster Board I-555 Survivin (BIRC5) is a member of the inhibitors of apoptosis family implicated in both prevention of cell death and control of mitosis. Although the actions of survivin in control of cancer cell division and apoptosis have been studied, its role in nonneoplastic diseases is not elucidated. Chronic inflammation is associated with STAT-3 upregulation, which can induce survivin production. Sickle cell anemia (SCA) has been characterized as a chronic inflammatory state and growing evidence indicates that inflammatory stress within the microvasculature may play a significant role in the vasoocclusion that is characteristic of SCA. Long-term treatment with hydroxyurea (HU) has been shown to reduce the production of inflammatory cytokines in SCA patients and leukocyte number. Since enhanced survivin expression has been reported in leukocytes under inflammatory conditions, and during hematopoietic cell survival and proliferation, the aim of this study was to investigate changes in survivin levels during erythroid differentiation, and determine expression in neutrophils (NS), mononuclear cells (MC) and red blood cell (RBC) in steady-state SCA patients (n≥10), SCA patients on HU therapy (n≥16), and healthy controls (HC, n≥5). Survivin and STAT-3 gene expression were determined by qRT-PCR analysis in primary human erythroblasts cultures for 7, 10 and 13 days and leukocytes separated from peripheral blood samples. Survivin protein expression was determined by flow cytometry with survivin-specific antibodies. Survivin gene expression was significantly increased during erythroid differentiation, but survivin mRNA levels showed similar patterns between SCA and HC (7d: 0.8±0.1 × 0.7±0.08; 10d: 1.7±0.3 × 1.6±0.2; 13d: 2.2± 0.27 × 1.8±0.19,U.A.,P>0.05,respectively). However, protein levels of survivin in mature RBC (glicophorin A +) was significantly higher in SCA patients compared to HC (41.90± 2.9 × 25.76±1.9, P=0.0006, respectively). BIRC-5 gene expression in MC was significantly higher in SCA patients compared to HC (0.9±0.1 × 0.5±0.2, P=0.04, respectively). Survivin protein levels in MC from SCA was significantly increased to compared to HC (51.7±3.2 × 39.7±1.7, MFI, P=0.01,respectively). Survivin protein levels are elevated in NS of SCA patients compared to HC (28.4±1.6 × 21.9±1.5, MFI, P=0.02,respectively). No significant alterations in the mRNA levels of the gene encoding STAT-3 were found during erythroid differentiation (7d: 1.1±0.04 × 1.1±0.08; 10d: 0.6±0.07 × 0.8±0.08; 13d: 0.6±0.07 × 0.9±0.1, P>0.05,respectively) or MC cells (1.2±0.1 × 1.1± 0.1, P>0.05,respectively) in SCA patients compared to HC. Patients on HU therapy demonstrated lower survivin MC gene expressions and protein levels compared to non-treated patients (0.6±0.3 × 0.9±0.1; 37.9±1.5 × 51.7±3.3, P=0.02; P<0.0001,respectively), but no difference was shown in STAT-3 gene expressions (1.1±0.04 × 1.2 ±0.1, respectively). Survivin protein levels were not significantly different in NS and RBC in patients on HU therapy compared to SCA (27.1±1.8 × 28.4± 1.6; 45.9± 3.2× 41.9± 2.9, MFI, P>0.05, respectively). Our data showed that survivin gene and protein expression are upregulated in MC in SCA patients, independently of STAT-3 expression. In addition, a high protein expression was observed in NS and RBC in these patients. HU therapy was associated with lower survivin expression in MC, but not NS and RBC, indicating that the beneficial effect that HU has on the inflammatory state, may participate in the reduced levels of survivin. In conclusion, the exact importance of survivin in SCA vasooclusion is not clear, but data indicates a high expression of this protein in leukocytes and RBC of SCA patients and may imply a role for this protein in leukocytosis and RBC proliferation in SCA. Disclosures No relevant conflicts of interest to declare.

Relationship of ERCC1 genotype variant with mRNA expression and ERCC1 protein levels in advanced urothelial carcinoma (UC).

2013 ◽  
Vol 31 (6_suppl) ◽  
pp. 260-260
Author(s):  
Elizabeth A. Guancial ◽  
Lillian Werner ◽  
Joaquim Bellmunt ◽  
Nikitas Nikitas ◽  
Edward C. Stack ◽  
...  
Keyword(s):  
Protein Expression ◽  
Mrna Expression ◽  
Excision Repair ◽  
Predictive Biomarker ◽  
Mrna Levels ◽  
Nuclear Staining ◽  
Protein Levels ◽  
Tissue Arrays ◽  
Platinum Based Chemotherapy ◽  
The Relationship

260 Background: DNA repair factors may be predictive for response to chemotherapies that produce DNA damage. While low ERCC1 protein and mRNA levels have been reported as associated with improved outcomes in metastatic UC patients treated with platinum-based chemotherapy, the relationship between genotype, mRNA expression, and protein level is unknown. The ERCC1 germline 19007C>T single-nucleotide polymorphism (SNP) is functionally associated with reduced translation of ERCC1 mRNA. We investigated the relationship between ERCC1 germline SNP, ERCC1 tumor mRNA and protein expression, in a cohort of patients with advanced UC who received first-line, platinum-based chemotherapy. Methods: A cohort of clinically annotated, uniformly-treated advanced UC patients with FFPE primary tumor tissue available was identified through the Hellenic cooperative Oncology Group (HECOG) (N=93). Genomic DNA extraction, nested PCR, and restriction fragment length polymorphism techniques for the 19007C>T SNP were performed to identify C/C, C/T and T/T genotypes. ERCC1 mRNA expression was interrogated using Nanostring nCounter profiling. IHC analysis was performed on tissue arrays using an ERCC1 antibody. Percent of positive nuclear staining was categorized as quartiles using previously identified cut-points. Results: ERCC1 C/T genotype was identified in 30/61 samples (49%) and T/T in 14/61 samples (23%). In 54 patients with both SNP and mRNA data available, T/T genotype was associated with the highest level of mRNA expression, followed by the C/T genotype (p=0.04). Neither ERCC1 genotype (N=44) nor ERCC1 mRNA expression (N=54) was associated with ERCC1 protein expression as measured by IHC (p=0.52 and p=0.13, respectively). Conclusions: ERCC1 19007C>T is associated with increased ERCC1 mRNA expression. However, neither genotype nor mRNA are surrogates for ERCC1 protein detected by IHC in advanced UC tumors. This suggests that while genotype influences mRNA expression of ERCC1, the use of the nucleotide excision repair pathway as a predictive biomarker of platinum-sensitivity may be more complex than previously appreciated and require the integrative use of proteomics, genomics and epigenomics.

scholarly journals Orally Administered CpG Oligodeoxynucleotide Induces Production of CXC and CC Chemokines in the Gastric Mucosa and Suppresses Bacterial Colonization in a Mouse Model of Helicobacter pylori Infection

2003 ◽  
Vol 71 (12) ◽  
pp. 7014-7022 ◽  
Author(s):  
S. Raghavan ◽  
J. Nyström ◽  
M. Fredriksson ◽  
J. Holmgren ◽  
A. M. Harandi
Keyword(s):  
Innate Immunity ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Immune Cells ◽  
Bacterial Load ◽  
Intragastric Administration ◽  
Cpg Odn ◽  
Cc Chemokines ◽  
H Pylori ◽  
Rantes Production

ABSTRACT Bacterial DNA and unmethylated CpG oligodeoxynucleotides (CpG ODN) are known to be potent stimulators of the innate immune system in vitro and in vivo. We therefore investigated if oral administration of CpG ODN could enhance innate immunity in the gastric mucosa and control the extent of Helicobacter pylori infection in mice. Intragastric administration of a single dose of CpG ODN significantly increased local production of the CC chemokines macrophage inflammatory protein 1α (MIP-1α), MIP-1β, and RANTES and the CXC chemokine gamma interferon-inducible protein 10 in the stomach and/or the small intestine. Importantly, intragastric administration of CpG ODN to mice with an already established H. pylori infection, in the absence of any coadministered antigen, was found to reduce the bacterial load in the stomach compared to the load in H. pylori-infected control mice, while similar administration of non-CpG ODN had no effect on the bacterial load. The reduction in the bacterial numbers in the stomachs of mice treated with CpG ODN was associated with enhanced infiltration of immune cells and increased RANTES production in the gastric mucosa compared to the infiltration of immune cells and RANTES production in H. pylori-infected control animals. These findings suggest that intragastric administration of CpG ODN without antigen codelivery may represent a valuable strategy for induction of innate immunity against H. pylori infection.

ADAM17 and TIMP3 mRNA expression in gastric mucosa infected with H. pylori and in gastric cancer

2001 ◽  
Vol 120 (5) ◽  
pp. A656
Author(s):  
Tetsuro Yoshimura ◽  
Damian J. Tolan ◽  
Michael F. Dixon ◽  
Anthony T. Axon ◽  
Philip A. Robinson ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Gastric Mucosa ◽  
Mrna Expression ◽  
H Pylori ◽  
Timp3 Mrna

Bromodomain Inhibition By OTX015 Regulates c-MYC and HEXIM1 in a Panel of Human Acute Leukemia Cell Lines

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 5957-5957
Author(s):  
Marie-Magdelaine Coudé ◽  
Thorsten Braun ◽  
Jeannig Berrou ◽  
Mélanie Dupont ◽  
Raphael Itzykson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Protein Expression ◽  
Mrna Expression ◽  
Rna Polymerase Ii ◽  
Cell Lines ◽  
Leukemia Cell ◽  
K562 Cells ◽  
Antileukemic Activity ◽  
Protein Levels ◽  
Gene And Protein Expression

Abstract Background: The bromodomain-containing protein 4 (BRD4) activates the transcription elongation factor b (P-TEFb) which regulates RNA polymerase II. Conversely, hexamethylene bisacetamide (HMBA) inducible protein 1 (HEXIM1) inactivates P-TEFb. BRD4/HEXIM1 interplay influences cell cycle progression and tumorigenesis. It has been widely demonstrated that BRD4 knockdown or inhibition by JQ1 is associated with c-MYC downregulation and antileukemic activity. We recently reported that the small molecule BRD2/3/4 inhibitor OTX015 (Oncoethix, Lausanne, Switzerland), currently in clinical development, mimics the effects of JQ1 (Braun et al, ASH 2013). We evaluated the effect of OTX015 on c-MYC, BRD2/3/4, and HEXIM1 in human in vitro leukemic models. Methods: c-MYC, BRD2/3/4 and HEXIM1 expression was assessed in six acute myeloid leukemia (AML; K562, HL-60, NB4, NOMO-1, KG1, OCI-AML3) and two acute lymphoid leukemia (ALL; JURKAT and RS4-11) cell lines after exposure to 500 nM OTX015. Quantitative RT-PCR and Western blotting were performed at different time points (24-72h). A heatmap was computed with R-software. Results: c-MYC RNA levels were ubiquitously downregulated in all AML and ALL cell lines after 24h exposure to OTX015 (Figure 1). c-MYC protein levels decreased to a variable extent at 24-72h in all cell lines evaluated other than KG1. BRD2, BRD3 and BRD4 mRNA expression was significantly decreased in K562 cells (known to be OTX015-resistant) after 48h exposure to OTX015 but was increased in HL60 and NOMO-1 cells, while minimal to no increases were observed in other cell lines. OTX015 induced a decrease in BRD2 protein expression in most cell lines, but not in K562 cells. In contrast, decreased BRD4 protein expression was only seen in the OCI-AML3, NB4 and K562 cell lines. BRD3 protein levels were not modified after OTX015 exposure in all cell lines evaluated other than KG1. HEXIM1 mRNA expression increased after 24h exposure to 500 nM OTX015 in all cell lines except OTX015-resistant K562 cells in which the increase was considered insignificant (less than two-fold). Increases in HEXIM1 protein levels were observed in OCI-AML3, JURKAT and RS4-11 cell lines at 24-72h but not in K562 cells. Conclusion: Taken together, these results show that BRD inhibition by OTX015 modulates HEXIM1 gene and protein expression, in addition to c-MYC decrease and BRD variations. HEXIM1 upregulation seems to be restricted to OTX015-sensitive cell lines and was not significantly affected in OTX015-resistant K562 cells. Further studies are needed to clarify the role of HEXIM1 in antileukemic activity of BRD inhibitors. Figure 1: Heatmap of gene expression after exposure to 500 nM OTX015 for 24 or 48h in AML and ALL cell lines. Repression in blue. Overexpression in red. Figure 1:. Heatmap of gene expression after exposure to 500 nM OTX015 for 24 or 48h in AML and ALL cell lines. Repression in blue. Overexpression in red. Disclosures Riveiro: OTD: Employment. Herait:OncoEthix: Employment. Dombret:OncoEthix: Research Funding.

scholarly journals Immunosuppressant Cyclosporin A-Based Regulation of Lipopolysaccharide-Triggered Pro- and Anti-Inflammatory Cytokines in the Genital Tract of Female Rabbits

2018 ◽  
Author(s):  
Li-Qin Yang ◽  
Qiu-Ying Wu ◽  
Xuan-Yu Chen ◽  
Chun Wang ◽  
Zhang Yan ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Inflammatory Cytokines ◽  
Genital Tract ◽  
Protein Production ◽  
Control Group ◽  
Protein Levels ◽  
Lps Challenge ◽  
Anti Inflammatory ◽  
Uterine Body ◽  
Pro Inflammatory Cytokines

In this study, we evaluated the effects of Cyclosporine A (CsA) on Lipopolysaccharide (LPS)-induced cytokine production in the genital tract of female rabbits. Twelve sexually mature and healthy female rabbits were randomly divided into four groups (n = 3 each). The rabbits in the LPS group were given an intrauterine infusion of Escherichia coli LPS (4 mg/kg body weight (BW)). Rabbits in the CsA group were given CsA (20 mg/kg BW). Rabbits in the LPS + CsA group were given LPS (4 mg/kg BW) and CsA (20 mg/kg BW). The control group received only LPS and CsA carrier. The gene expression and protein levels of pro- and anti-inflammatory cytokines were observed using qRT-PCR and immuno-histochemical (IHC) assay, respectively. Our study showed that IL-1&beta;, IL-6, IL-8, TNF-&alpha;, IFN-&gamma;, IL-4, IL-10, IL-13, and TGF-&beta; were expressed in female genital organs. The LPS challenge increased the mRNA expression of IL-6 and TNF-&alpha; in the uterine body and IL-1&beta; in the uterotubal junction compared to the control group. CsA increased the basal mRNA expression of anti-inflammatory cytokines (i.e., IL-4 in the uterine body, uterotubal junction, and oviductal ampulla; IL-10 in the cervix, oviductal isthmus, and ampulla; and TGF-&beta; in the uterotubal junction and oviductal ampulla) and pro-inflammatory cytokines (i.e., IL-6 and IL-8 in the cervix; IL-1&beta; in the oviductal isthmus; TNF-&alpha; in the oviductal ampulla; and IFN-&gamma; in the uterine body compared to the control group). In addition, CsA inhibited the mRNA expression of pro-inflammatory cytokines, such as IL-6 in the uterine body, uterotubal junction, and oviductal isthmus; TNF-&alpha; in the uterine body; and IFN-&gamma; in the uterotubal junction and oviductal isthmus induced by the LPS challenge. The IHC assay showed the LPS-induced increase in protein production of IL-6 in the uterine body and oviductal isthmus. CsA increased the protein production of IL-10 in the cervix, uterine body, oviductal ampulla, and isthmus. Moreover, CsA decreased the protein production of IL-6 in the uterine body and oviductal isthmus induced by LPS.

ADAM17 and TIMP3 mRNA expression in gastric mucosa infected with H. pylori and in gastric cancer

2001 ◽  
Vol 120 (5) ◽  
pp. A656-A656
Author(s):  
T YOSHIMURA ◽  
D TOLAN ◽  
M DIXON ◽  
A AXON ◽  
P ROBINSON ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Gastric Mucosa ◽  
Mrna Expression ◽  
H Pylori ◽  
Timp3 Mrna
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