| 1. |
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
|
|
| 6. |
- Rudnicka, W., et al.
(författare)
-
A potential double role of anti-Lewis X antibodies in Helicobacter pylori-associated gastroduodenal diseases
- 2001
-
Ingår i: Pathogens and Disease. - 2049-632X. ; 30:2, s. 121-125
-
Tidskriftsartikel (refereegranskat)abstract
- In this study, we found Lewis X (Le(X)) determinants on 68% of Helicobacter pylori isolates from patients with chronic gastroduodenal diseases. Anti-Le(X) IgG were detected more frequently in the sera from dyspeptic children and adults (45 and 46%), with or without proved (culture) H. pylori infection, than in the sera from healthy individuals (14%, and 25%). In contrast, the prevalence of anti-Le(X) IgM was higher in the groups of healthy individuals than in the groups of dyspeptic patients. Moreover. anti-Le(X) monoclonal antibody of IgM class enhanced the uptake of Le(X)(+) but not Le(X)(-) H. pylori isolates by phagocytes. In the sera from some dyspeptic patients, we detected Le(X)-anti-Le(X) IgG immune complexes (Le(X) ICs). There was a great difference between children and adults as regards the presence of Le(X) ICs. The immune complexes were found in the sera from nine out of 29 (27%) H. pylori-infected and three out of eight (37%) uninfected adult dyspeptic patients. In comparison, Le(X)-anti-Le(X) IgG ICs were detected only for two out of 18 (11%) H. pylori-infected children. Le(X) ICs were not found in the sera from healthy individuals. Our results suggest that anti-Le(X) IgM may play a protective role in H. pylori infections. In contrast, anti-Le(X) IgG and particularly Le(X)-anti-Le(X) IgG ICs might contribute to the pathogenesis of chronic H. pylori infections.
|
|
| 7. |
- Wisniewska, M, et al.
(författare)
-
Detection of specific Helicobacter pylori DNA and antigens in stool samples in dyspeptic patients and healthy subjects
- 2002
-
Ingår i: Microbiology and Immunology. - 1348-0421. ; 46:10, s. 657-665
-
Tidskriftsartikel (refereegranskat)abstract
- In this study stool samples from dyspeptic patients and healthy subjects were used for detection of specific Helicobacter pylori antigens and DNA by immunoenzymatic test (PPHpSA) and semi-nested PCR (ureA-PCR), respectively. The H. pylori status was estimated by invasive endoscopy-based rapid urease test and histology or noninvasive urea breath test (UBT), and by serology (ELISA, Western blot). The coincidence of IT pylori-negative invasive tests or UBT and negative antigen or DNA stool tests was very high (mean 95%). The PPHpSA results were found positive for 56% and ureA-PCR for 26% of individuals with H. pylori infection confirmed by invasive tests or UBT. The detection of specific H. pylori antigens and especially DNA in feces is not sufficient as a one-step diagnosis of H. pylori infection.
|
|
| 8. |
- Czumaj, A, et al.
(författare)
-
Alterations of Fatty Acid Profile May Contribute to Dyslipidemia in Chronic Kidney Disease by Influencing Hepatocyte Metabolism
- 2019
-
Ingår i: International journal of molecular sciences. - : MDPI AG. - 1422-0067. ; 20:10
-
Tidskriftsartikel (refereegranskat)abstract
- Chronic kidney disease (CKD) is associated with atherogenic dyslipidemia. Our aim was firstly to investigate patterns of fatty acids (FA) composition through various stages of CKD, and secondly, to evaluate the effect of CKD-specific FA disturbances on the expression of genes related to lipid metabolism at a cellular level. Serum FA composition was analyzed in 191 patients with consecutive severity stages of CKD, and 30 healthy controls free from CKD. Next, HepG2 human hepatic cells were treated with major representatives of various FA groups, as well as with FA extracted from a mix of serums of controls and of CKD stage 5 patients. Across worsening stages of CKD severity, there was an increasing monounsaturated FA (MUFA) content. It was associated with a concomitant decrease in n-3 and n-6 polyunsaturated FA. The incubation of hepatocytes with FA from CKD patients (compared to that of healthy subjects), resulted in significantly higher mRNA levels of genes involved in FA synthesis (fatty acid synthase (FASN) increased 13.7 ± 3.5 times, stearoyl-CoA desaturase 1 (SCD1) increased 4.26 ± 0.36 times), and very low density lipoprotein (VLDL) formation (apolipoprotein B (ApoB) increased 7.35 ± 1.5 times, microsomal triacylglycerol transfer protein (MTTP) increased 2.74 ± 0.43 times). In conclusion, there were progressive alterations in serum FA composition of patients with CKD. These alterations may partly contribute to CKD hypertriglyceridemia by influencing hepatocyte expression of genes of lipid synthesis and release.
|
|
| 9. |
- Jensen, Lasse, et al.
(författare)
-
Disruption of the Extracellular Matrix Progressively Impairs Central Nervous System Vascular Maturation Downstream of beta-Catenin Signaling
- 2019
-
Ingår i: Arteriosclerosis, Thrombosis and Vascular Biology. - : LIPPINCOTT WILLIAMS & WILKINS. - 1079-5642 .- 1524-4636. ; 39:7, s. 1432-1447
-
Tidskriftsartikel (refereegranskat)abstract
- Objective- The Wnt/beta-catenin pathway orchestrates development of the blood-brain barrier, but the downstream mechanisms involved at different developmental windows and in different central nervous system (CNS) tissues have remained elusive. Approach and Results- Here, we create a new mouse model allowing spatiotemporal investigations of Wnt/beta-catenin signaling by induced overexpression of Axin1, an inhibitor of beta-catenin signaling, specifically in endothelial cells (Axin1(iEC)-(OE)). AOE (Axin1 overexpression) in Axin1(iEC)-(OE) mice at stages following the initial vascular invasion of the CNS did not impair angiogenesis but led to premature vascular regression followed by progressive dilation and inhibition of vascular maturation resulting in forebrain-specific hemorrhage 4 days post-AOE. Analysis of the temporal Wnt/beta-catenin driven CNS vascular development in zebrafish also suggested that Axin1(iEC)-(OE) led to CNS vascular regression and impaired maturation but not inhibition of ongoing angiogenesis within the CNS. Transcriptomic profiling of isolated, beta-catenin signaling-deficient endothelial cells during early blood-brain barrier-development (E11.5) revealed ECM (extracellular matrix) proteins as one of the most severely deregulated clusters. Among the 20 genes constituting the forebrain endothelial cell-specific response signature, 8 (Adamtsl2, Apod, Ctsw, Htra3, Pglyrp1, Spock2, Ttyh2, and Wfdc1) encoded bona fide ECM proteins. This specific beta-catenin-responsive ECM signature was also repressed in Axin1(iEC)-(OE) and endothelial cell-specific beta-catenin-knockout mice (Ctnnb1-KOiEC) during initial blood-brain barrier maturation (E14.5), consistent with an important role of Wnt/beta-catenin signaling in orchestrating the development of the forebrain vascular ECM. Conclusions- These results suggest a novel mechanism of establishing a CNS endothelium-specific ECM signature downstream of Wnt-beta-catenin that impact spatiotemporally on blood-brain barrier differentiation during forebrain vessel development.
|
|
| 10. |
|
|
