Biomedical subjects

András Arató

Publications and source records attributed to András Arató.

11 recordsLinked to original sources

PubMed2006

Genetic polymorphisms of CD14, toll-like receptor 4, and caspase-recruitment domain 15 are not associated with necrotizing enterocolitis in very low birth weight infants.

OBJECTIVES: Inadequate response of the innate immune system to bacterial antigens present in the intestinal flora may play a role in the development of necrotizing enterocolitis (NEC). Pattern recognition receptors such as CD14, toll-like receptor (TLR) 4, and caspase-recruitment domain (CARD) 15 bind bacterial lipopolysaccharide and peptidoglycan, and their activation leads to production of inflammatory cytokines. Our aim was to evaluate whether single nucleotide polymorphisms (SNPs) of CD14, TLR4, and CARD15 are associated with the risk of NEC in very low birth weight (VLBW) infants. PATIENTS AND METHODS: We determined the CD14 C-260T, TLR4 A +896G, C +1196T, and CARD15 G +2722C, C +2104T, 3020insC functional SNPs in dried blood samples from 118 VLBW infants (of those, 41 developed NEC) and from 146 healthy term newborns using polymerase chain reaction and restriction fragment length polymorphism methods. We tested the association between genotype and risk of NEC. RESULTS: No significant differences were found in the prevalence of CD14 -260T, TLR4 +896G, +1196T, and CARD15 +2722C, +2104T, 3020insC alleles between VLBW infants and healthy term newborns (P = NS). The frequencies of investigated genotypes were similar in infants with and without NEC (P = NS). Furthermore, we did not find any association between genotype and prematurity or sepsis, which are important risk factors of NEC. CONCLUSIONS: Carrier state of the tested CD14, TLR4, and CARD15 SNPs is not associated with NEC risk in VLBW infants.

Enterocolitis, Necrotizing↗

PubMed2005

[Randomised placebo controlled double blind study on the effect of prebiotic oligosaccharides on intestinal flora in healthy infants].

AIM: Effects of supplementing prebiotic oligosaccharides to formula for healthy infants were studied in this placebo controlled, randomised, double blind study. METHODS: Ninety-seven infants were included into the study; among them 42 breast-fed infants, 14 infants fed formula supplemented with 0.4 g/100ml oligosaccharides (9 to 1 mixture of galacto- and fructooligosaccharides) and 13 infants fed control formula were followed-up throughout the 12-week-long study period. The groups receiving formula were compared with statistical methods, whereas data of breast-fed infants served as reference values. RESULTS: Infants fed the two formulae did not differ in nutrient intakes, growth, occurrence rate of feeding difficulties and atopic manifestations, or in calcium excretion. The intestinal flora did not differ between the two formula fed groups at the beginning of the study. In contrast, numbers of Bifidobacteriae were significantly higher in infants receiving the formula supplemented with prebiotic oligosaccharides both at the 14th day (9 x 1011 versus 5 x 1010, colony forming units/g faeces, median, p < 0.05) and 28th day (9 x 1012 versus 5 x 1010, p < 0.05) of the study. CONCLUSION: In this study, supplementation of infant formula with prebiotic oligosaccharides resulted in ameliorating the difference in intestinal flora between formula fed and breast-fed healthy infants.

Bacillaceae↗

PubMed2004

Hydroxyl radical generation by photosystem II.

The photogeneration of hydroxyl radicals (OH(*)) in photosystem II (PSII) membranes was studied using EPR spin-trapping spectroscopy. Two kinetically distinguishable phases in the formation of the spin trap-hydroxyl (POBN-OH) adduct EPR signal were observed: the first phase (t(1/2) = 7.5 min) and the second phase (t(1/2) = 30 min). The generation of OH(*) was found to be suppressed in the absence of the Mn-complex, but it was restored after readdition of an artificial electron donor (DPC). Hydroxyl radical generation was also lost in the absence of oxygen, whereas it was stimulated when the oxygen concentration was increased. The production of OH(*) during the first kinetic phase was sensitive to the presence of SOD, whereas catalase and EDTA diminished the production of OH(*) during the second kinetic phase. The POBN-OH adduct EPR signal during the first phase exhibits a similar pH-dependence as the ability to oxidize the non-heme iron, as monitored by the Fe(3+) (g = 8) EPR signal: both EPR signals gradually decreased as the pH value was lowered below pH 6.5 and were absent at pH 5. Sodium formate decreases the production of OH(*) in intact and Mn-deleted PSII membranes. Upon illumination of PSII membranes, both superoxide, as measured by EPR signal from the spin trap-superoxide (EMPO-OOH) adduct, and H(2)O(2), measured colormetrically, were generated. These results indicated that OH(*) is produced on the electron acceptor side of PSII by two different routes, (1) O(2)(*)(-), which is generated by oxygen reduction on the acceptor side of PSII, interacts with a PSII metal center, probably the non-heme iron, to form an iron-peroxide species that is further reduced to OH(*) by an electron from PSII, presumably via Q(A)(-), and (2) O(2)(*)(-) dismutates to form free H(2)O(2) that is then reduced to OH(*) via the Fenton reaction in the presence of metal ions, the most likely being Mn(2+) and Fe(2+) released from photodamaged PSII. The two different routes of OH(*) generation are discussed in the context of photoinhibition.

Anaerobiosis↗

PubMed2004

[Transient protein-losing enteropathy associated with Epstein-Barr virus infection in an immunocompetent child: a case report].

Transient protein-losing enteropathy associated with acute Epstein-Barr virus infection in an immunocompetent 5-year-old girl is described. The child had a complete resolution of the disease without specific treatment. To the best of our knowledge this is the first report of Epstein-Barr virus infection associated protein-losing enteropathy in a previously healthy patient. Acute infection caused by Epstein-Barr virus infection should be considered in patients with symptomatic protein loss of gastrointestinal origin.

Child↗

PubMed2004

Production of reactive oxygen species in chloride- and calcium-depleted photosystem II and their involvement in photoinhibition.

Mixed photosystem II (PSII) samples consisting of Cl(-)-depleted and active, or Ca(2+)-depleted and active PSII enriched membrane fragments, respectively, were investigated with respect to their susceptibility to light. In the presence of Cl(-)-depleted PSII, active centers were damaged more severely, most likely caused by a higher amount of reactive oxygen species formed in the nonfunctional centers. Cl(-) depletion led to an increased H(2)O(2) production, which seemed to be responsible for the stimulation of PSII activity loss. To distinguish between direct H(2)O(2) formation by partial water oxidation and indirect H(2)O(2) formation by oxygen reduction involving the prior formation of O(2)(-?), the production of reactive oxygen species was followed by spin trapping EPR spectroscopy. All samples investigated, i.e. PSII with a functional water splitting complex, Ca(2+)- and Cl(-)-depleted PSII, produced upon illumination O(2)(-?) and OH(?) radicals on the acceptor side, while Cl(-)-depleted PSII produced additionally OH(?) radicals originating from H(2)O(2) formed on the donor side of PSII.

Calcium↗

PubMed2004

Bone mineral density and bone acquisition in children and young adults with cystic fibrosis: a follow-up study.

OBJECTIVE: To investigate bone mineral density and bone homeostasis in cystic fibrosis (CF) and to assess changes in a 2-year period. METHODS: Thirty-eight patients with clinically stable CF (11 children, 16 adolescents, 11 young adults) were enrolled. No patient was treated with corticosteroids before or during the study. Weight and height Z scores and bone mineral density (BMD) Z-score at the femoral neck and the lumbar spine were recorded at the beginning of the study and after 2 years. Osteocalcin and cross-link excretion, both measurements of bone turnover were also measured. Correlations between BMD, bone turnover parameters, disease severity, pubertal stage, and nutritional state were calculated. The maternal BMD was also determined and related to that of the child. RESULTS: Height and weight Z scores were normal in children and below normal in adolescents. Puberty was delayed in most patients. Bone age was lower than chronological age in adolescents. Lumbar spine and femoral neck BMD Z scores were below normal in each age group. Disease severity determined by Schwachman score correlated with lumbar BMD (r = 0.45, P < 0.02). BMD Z scores did not change during 2 year follow-up. Maternal and patient lumbar and femoral BMD correlated significantly (r = 0.51, P < 0.01, and r = 0.54, P < 0.01, respectively). CONCLUSIONS: Bone deficit is present in patients with CF who have never received steroid treatment. Delay of puberty, chronic inflammation, or genetic susceptibility might be responsible for this phenomenon which was found in patients who had never received steroids and who were in relatively good clinical state.

Absorptiometry, Photon↗

PubMed2004

Partial protection against dextran sodium sulphate induced colitis in histamine-deficient, histidine decarboxylase knockout mice.

OBJECTIVES: Chemically induced mucosal inflammation in animal models is a suitable tool for studying factors in the pathogenesis of inflammatory bowel disease. The aim of this study was to determine whether absence of histamine has an effect on the development of experimental colitis. METHODS: Histamine-deficient, histidine decarboxylase (HDC) knockout Balb/c mice and genetically identical control animals with intact HDC were studied. Colitis was induced by the administration of 2% dextran sodium sulphate in drinking water. Mice were killed after 5 days and disease activity assessed by clinical, histologic, and immunohistologic parameters. Bacterial components of stool were examined. RESULTS: Clinical disease activity was higher in the mice with intact HDC (disease activity index, 2.21) than in the histamine-deficient knock-out mice (1.88). Histologic findings were similar in the two groups. On day 5, the inflammation score of the HDC sufficient group was 5.25 (+/-1.055) and the crypt score was 5.00 (+/-1.128). The scores in the HDC knock-out group were 4.667 (+/- 0.707) and 4.667 (+/- 0.86), respectively. There was a significant difference in the number of interleukin (IL-10)-producing lymphocytes in colon mucosa. Large numbers of IL-10-positive lymphocytes were observed in wild type mice both those with DSS induced colitis and untreated controls. Only sporadic IL-10 positivity was found in histamine-deficient mice. Significant differences were found in the composition of the fecal bacterial flora between the two groups. CONCLUSION: The reduced number of IL-10-positive lymphocytes in the intestinal mucosa of histamine-deficient, histidine decarboxylase knockout mice and the altered fecal bacterial flora in these animals suggest that histamine may play a role in the pathophysiology of inflammation in the colon of normal animals by upregulating local IL-10 production and stimulating a local shift to Th2 response.

Animals↗

PubMed2003

Slight decrease in bone mineralization in cow milk-sensitive children.

BACKGROUND: Patients with cow milk allergy (CMA) are potentially at risk for osteopenia because their milk-free diet usually contains a low calcium content. In our study, different parameters of bone mineralization in children with CMA were investigated. PATIENTS AND METHODS: Twenty-seven CMA patients (mean age, 4.3 years; range, 3-8 years) were enrolled in the study. During a mean milk-free diet period of 11.8 months, children were fed extensively hydrolyzed or soy-based formulas. After a milk challenge test, 7 patients showed allergic symptoms, and the other 20 children had transient CMA. From the sera of all patients, the levels of sodium, potassium, chloride, calcium, phosphate, and magnesium ions, as well as alkaline phosphatase (AP), parathyroid hormone (PTH), osteocalcin, and beta-crosslaps, were determined. These values were compared with those of 20 healthy age-matched controls. Bone mineral density was measured as well. RESULTS: The AP and PTH concentrations were higher in CMA patients than in the control group (AP: 610.2 U/L vs. 499.7 U/L, P < 0.01; PTH: 1.56 pmol/L vs. 0.83 pmol/L, P< 0.03), but all values were in the normal range. The osteocalcin concentration was similar in both groups, and the beta-crosslaps concentration was lower in CMA patients than in controls (0.92 vs. 1.47 ng/mL, P< 0.001). The mean Z score of bone mineral density in patients with CMA was -0.6. In 10 cases, the Z score was less than the -1 SD value. On the basis of the Z score, CMA patients were divided into two groups. The PTH concentration was significantly elevated in the group with lower Z score (2.24 pmol/L vs. 1.16 pmol/L; P< 0.03). CONCLUSION: The results suggest that, in children with CMA who are on a cow milk-free diet, slight disturbances of bone mineralization can be observed by osteodensitometry.

Alkaline Phosphatase↗

PubMed2002

[Immunohistologic changes of the intestinal mucosa in chronic inflammatory bowel diseases].

In the pathogenesis of inflammatory bowel disease abnormally increased immune reactions in the intestinal mucosa play a basic role. The revealing of these reactions was facilitated by the rapidly spreading immunohistological methods in last decades. This review discusses in detail the characteristic distribution of lymphocyte subsets and plasma cells in Crohn's disease and ulcerative colitis. Results indicating increased expression of adhesion molecules are also presented, as well as the different patterns of cytokine production in Crohn's disease and ulcerative colitis. The rapid epithelial turnover developing as a consequence of increased rate of proliferation and apoptosis in inflammatory bowel disease is also shown. The epithelial expression of MHC II antigen in colonic mucosa which is not observed in healthy subjects is also discussed. In addition, the pathogenetic role of lost oral tolerance in the development of inflammatory bowel is reviewed in detail.

Chronic Disease↗

PubMed2002

Frequency of coeliac disease in Hungarian children with type 1 diabetes mellitus.

Coeliac disease and type 1 diabetes mellitus can frequently coexist, presumably due to a common genetic predisposition. The present study was designed to evaluate the frequency of coeliac disease among Hungarian diabetic children and to study the effect of gluten-free diet on glycaemic control. A total of 205 diabetic children (age range 2.0-17.0 years, median 11.6 years) were screened for coeliac disease by determination of IgA-endomysium (EMA) antibodies. In the positive cases, a jejunal biopsy was performed and, in addition to routine histology, the number of intraepithelial gamma/delta T-cells was also determined. Insulin requirement, glycosylated haemoglobin level and body mass index of diabetic children with coeliac disease were determined before and 3 months after the introduction of gluten-free diet. IgA-EMA was positive in 24 cases, 17 of them (8.3% of all diabetic children) had a subtotal villous atrophy and thus coeliac disease was diagnosed. In all but two of these children, the mean number of gamma/delta T-cells was elevated (above 7 cells/mm). Of the remaining seven patients with positive EMA but normal villous structure, five (2.4%) had elevated number of epithelial gamma/delta T-cells, indicating probable latent coeliac disease. The insulin requirement of the children had significantly increased 3 months after the introduction of gluten-free diet (median values 0.64 versus 0.48 U/kg per day, P<0.05). Median body mass indices also showed significant elevation after this period (16.8 versus 14.2 kg/m(2), P<0.05) CONCLUSION: the frequency of coeliac disease was high in the studied group. Introduction of a gluten-free diet improved the somatic development of these children. A latent form of coeliac disease is also frequent in children with type 1 diabetes mellitus.

Adolescent↗

PubMed2002

[Expression of interleukin-4, interferon-gamma and lymphocyte surface markers in small intestinal mucosa of adult patients with cereal allergy].

INTRODUCTION: The mechanism for adverse reactions to foods in the gastrointestinal tract are poorly understood. Previous studies of other atopic diseases and animal models suggest that lymphocytes and cytokines may be implicated in the pathogenesis of food allergy. AIM: The authors investigated the expression of interleukin-4, interferon-gamma and other lymphocyte markers of patients with cereal allergy (wheat, rye, oats) and of controls. PATIENTS/METHOD: Expressions of cytokines and lymphocyte markers on duodenal mucosa of nine patients (mean age 38.3 years, range 18-50 years, 8 women and one man) and nine controls (mean age 36 years, range 24-54 years, 6 women, 3 men) by means of immunohistochemistry were investigated. RESULTS: The mucosal structure on every biopsy specimens was normal. Despite the normal structure the expression of Ki-67 intranuclear proliferation marker was higher in patients with cereal allergy. Expression of interleukin-4 was markedly elevated in the food allergy group, however, interferon-gamma density showed no inter-group difference. The densities of CD4 (1251 vs. 1053 cells/mm2) and HLA-DR positive cells (1227 vs. 1064 cells/mm2) in the lamina propria of cereal allergy group were significantly elevated when compared with controls (P = 0.05 and P = 0.04, respectively). The densities of CD3, CD8, TCR alpha/beta and gamma/delta, HLA-DP, IgA, IgA1, IgA2-containing cells did not differ in the two groups studied. CONCLUSIONS: The authors results suggest that, despite the normal mucosal structure, the increased expression of CD4 and HLA-DR positive cells show a sign of inflammation in duodenal biopsies of patients with cereal allergy. Moreover, increased density of IL-4 may suggest its role in the pathogenesis of cereal hypersensitivity.

Adult↗