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Your search keyword '"Akbulut, Ulas Emre"' showing total 26 results
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26 results on '"Akbulut, Ulas Emre"'

3. The usefulness of transabdominal ultrasound elastography in Helicobacter pylori gastritis in children

Author

Akbulut Ulas Emre, Isik Ishak Abdurrahman, Atalay Atike, and Özkan Mehmet Burak

Subjects
children, endoscopy, ultrasound elastography, helicobacter pylori, Medicine (General), R5-920, Medical technology, R855-855.5
Abstract

Helicobacter pylori can colonize the submucosal layer as well as the mucosa in the stomach. Inflammation and erosions cause both mucosal and submucosal thickening in patients with Helicobacter pylori gastritis. Elastography is a method for measuring the elasticity and hardness of tissues by visualization of their response to the applied force. Hard tissues respond to applied compression differently compared to soft tissues. Hard tissues displace as a whole without deforming as opposed to soft tissues. In this study, we investigated the diagnostic performance of transabdominal ultrasound elastography in detecting Helicobacter pylori gastritis in children.

Published
2023
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11. Chanarin-Dorfman Syndrome: A Case Report

Author

Akbulut, Ulas Emre, Atalay, Atike, Kalkan, Tarkan, and Isik, Ishak Abdurrahman

Abstract

Chanarin-Dorfman syndrome is a multisystem inherited metabolic disorder associated with congenital ichthyosis and accumulation of lipid droplets in various types of cells. Mutation of ABHD5/CG158 gene in the short arm of the 3rd chromosome is responsible from the main metabolic defect. Clinically, the disease is presented with ichthyosis, hearing loss, hepatomegaly, splenomegaly, cirrhosis, cataract, keratopathy, myopathy, and mental retardation. Here we present a case of Chanarin-Dorfman syndrome in a 2 years girl with who had ichthyosis, elevation of liver enzymes, hepatomegaly and mutation of ABHD5.

Published
2021

14. The effect of a Mediterranean diet vs. a low-fat diet on non-alcoholic fatty liver disease in children: a randomized trial.

Author

Akbulut, Ulas Emre, Isik, Ishak Abdurrahman, Atalay, Atike, Eraslan, Ali, Durmus, Emin, Turkmen, Sinem, and Yurttas, Aziz Selcuk

Subjects
*NON-alcoholic fatty liver disease, *LOW-fat diet, *MEDITERRANEAN diet, *REDUCING diets, *FATTY liver, *INSULIN sensitivity, *LIVER enzymes
Abstract

Non-alcoholic fatty liver disease (NAFLD) is becoming ever more common in children, due to the increasing global prevalence of obesity. The first-line treatment consists of weight loss through a combination of a healthy diet and exercise. The objective of this study was to determine the effects of a Mediterranean Diet or a low-fat diet on reducing hepatic steatosis and insulin resistance in children with NAFLD. This 12-week randomised clinical trial was conducted with children aged 9–17 years diagnosed with NAFLD and randomised into either a Mediterranean Diet or a low-fat diet group. By the end of the study, hepatic steatosis had decreased significantly in both groups (p < 0.001). Liver enzymes also improved significantly, while significant decreases were observed in insulin resistance in both groups, although this decrease was greater in the Mediterranean Diet group (p = 0.010). This study demonstrated that a decrease in hepatic steatosis and an improvement in insulin sensitivity can be achieved with both a Mediterranean Diet and a low-fat diet over 12 weeks, with no significant decrease in the energy required for growth, in children with NAFLD. [ABSTRACT FROM AUTHOR]

Published
2022
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16. Ülseratif kolitli çocukların intestinal mukozasında FOXP3+ Treg hücreleri ve interlökin-23 ekspresyonu

Author

AKBULUT, Ulas Emre, ERSOZ, Safak, TUMGOR, Gokhan, AGİN, Mehmet, UNAL, Fatih, KASİRGA, Erhun, and CAKİR, Murat

Subjects
Ulcerative colitis, children, interleukin-23, FOXP3, cytokine, Medicine, hemic and immune systems, chemical and pharmacologic phenomena, Ülseratif kolit,Çocuk,İnterlökin-23,FOXP3,Sitokin, Tıp
Abstract

AmaçÜlseratif kolitin (UK), anormal immünyanıt sonucu geliştiği düşünülmektedir. Forkhead box P3 (FOXP3) T regülatuvar(Treg) hücreleri ve interlökin (IL)-23/T-helper 17 yolağı, inflamatuvarbağırsak hastalığının patogenezinde önemli bir rol oynamaktadır. Ancak buyolağın UK'li çocuklardaki rolü ile ilgili bilgilerimiz sınırlıdır. Buçalışmanın amacı UK’li çocukların bağırsak mukozasında FOXP3 ve IL-23’ün düzeylerininbelirlenerek, hastalığın patogenezindeki rollerinin araştırılmasıdır.Gereçve yöntemlerYirmi dokuz UK’li hasta (18 pankolit,dokuz sol kolon tutulumlu ve iki proktokolit) ve 11 kontrol hastası çalışmayadahil edildi. İmmünohistokimyasal boyama yöntemi ile, UK hastaların inflamasyonludokularından ve kontrol hastalarının inflamasyon içermeyen dokularından alınanbiyopsi örneklerinde FOXP3+ Treg hücreleri ve IL-23 düzeyleriincelendi.BulgularÜlseratif kolitli hastalarda FOXP3+ Treg hücre seviyesi kontrolgrubuna göre önemli oranda yüksekti (%45.67 ± 10.83 ve %22.06 ± 8.09,p=0.007). IL-23 düzeyi de UK hastalarında kontrol grubuna göre anlamlı olarakyüksekti (24.33% ± 13.81 vs. 12.91% ±5.06, p=0.009). Pankolitlihastalarda FOXP3+ Treg hücreleri (%43.21 ± 16.97) ve IL-23 (%25.12 ± 14.98) ekspresyonu kontrol grubundan daha yüksek olduğu görüldü (p=0.012ve p=0.022). Ancak, kontrol grubu ile sol kolon tutulumu ve proktokoliti olanhastalar arasında FOXP3+ Treg hücreleri ve IL-23 ekspresyonundafarklılık bulunmuyordu.SonuçlarÜlseratif kolitliçocukların bağırsak mukozalarında FOXP3+ Treg hücreleri ve IL-23ekspresyonu daha yüksek olduğu tespit edildi. Bu sonuçlar, IL-23 yolağınıengellemeye ve Treg hücre sayılarını yükseltmeye yönelik yeni tedaviseçeneklerin, UK'in daha etkili bir şekilde tedavi edilmesine yardımcıolabileceğini göstermektedir., Background/AimsUlcerative colitis (UC) is thought to resultfrom an aberrant immune response. Forkhead box P3 (FOXP3) regulatory T (Treg)cells and Interleukin (IL)-23/T-helper 17 pathway play an important role in thepathogenesis of inflammatory bowel disease, but little is known about theirrole in children with UC. Theaim of this study was to investigate the role of FOXP3 and IL-23 in the pathogenesis of UC by determiningthem in intestinal tissues of children with the disease.Materials and MethodsWestudied 29 patients with UC (18 pancolitis, nine left-sided colitis, and twoproctocolitis) and 11 control subjects. Immunohistochemistry was used toexamine FOXP3+ Treg cells and IL-23in intestinal biopsy specimens from UC patients and from non-inflamed tissuesin the control group.ResultsUC patients’ FOXP3+ Treg cells weresignificantly higher than those of the control group (45.67% ± 10.83 vs. 22.06%± 8.09, p=0.007). IL-23 expression inpatients with UC were significantly higher than those of the control subjects(24.33% ± 13.81 vs. 12.91% ± 5.06, p=0.009). FOXP3+ Treg cells (43.21% ± 16.97) and IL-23 (25.12% ± 14.98) expression in patients withpancolitis were higher than in the control group (p=0.012 vs p=0.022). However,no differences were determined in FOXP3+ Treg cells and IL-23 inpatients with left colon involvement and proctocolitis compared to the controlgroup. Conclusions FOXP3+Treg cell and IL-23 expression were higher in the intestinal mucosa of childrenwith UC. These data indicate that new therapeutic options directed towardinhibiting the IL23 pathway and raising Treg cell numbers may permit moreefficacious treatment of UC.

Published
2018

25. Early Clinical Diagnosis of PC1/3 Deficiency in a Patient With a Novel Homozygous PCSK1Splice-Site Mutation

Author

Härter, Bettina, Fuchs, Irene, Müller, Thomas, Akbulut, Ulas Emre, Cakir, Murat, and Janecke, Andreas R.

Abstract

Autosomal recessive proprotein convertase 1/3 (PC1/3) deficiency, caused by mutations in the PCSK1gene, is characterized by severe congenital malabsorptive diarrhea, early-onset obesity, and certain endocrine abnormalities. We suspected PC1/3 deficiency in a 4-month-old girl based on the presence of congenital diarrhea and polyuria. Sequencing the whole coding region and splice sites detected a novel homozygous PCSK1splice-site mutation, c.544–2A>G, in the patient. The mutation resulted in the skipping of exon 5, the generation of a premature termination codon, and nonsense-mediated PCSK1messenger ribonucleic acid decay, which was demonstrated in complementary DNA derived from fibroblasts.

Published
2016
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26. Akut Viral Hepatit A Enfeksiyonuna Bağlı Gelişen Akut Taşsız Kolesistit: İki Olgu Sunumu.

Author

Akbulut, Ulas Emre, Sağ, Sefa, Emeksiz, Hamdi Cihan, Ayaz, Melike, and Çay, Ümmühan

Subjects
*ACALCULOUS cholecystitis, *VIRAL hepatitis, *DISEASE complications, *THERAPEUTICS
Abstract

Acute acalculous cholecystitis (AAC) is defined as the inflammation of the bile duct without stone or biliary sludge. It is associated with high mortality and morbidity since it may lead to complications such as gangrene, perforation and empyema. According to the underlying cause, medical or surgical treatment is performed. The most important risk factors for the development of AAC in children are sepsis, shock, prolonged fasting, total parenteral nutrition and multiple blood transfusions. Acute acalculouscholecystitis also can occur as a rare complication of acute viral hepatitis. This report describes acute cholecystitis in two cases which developed as a result of hepatitis A virüs infection and resolved completely with supportive management. [ABSTRACT FROM AUTHOR]

Published
2017
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