Yusuf Aydemir

Dr. Yusuf Aydemir

orcid

Research Focus & Metrics

Academic Career Length

26Years (2001-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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30 October 2018 in Journal of Gastroenterology and Hepatology
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YAYusuf Aydemir
Yusuf Aydemir
ZAZuhal Akcoren
Zuhal Akcoren
HDHulya Demir
Hulya Demir
ITInci Nur Saltik Temizel
Inci Nur Saltik Temizel
HOHasan Ozen
Hasan Ozen
AYAysel Yuce
Aysel Yuce

1 July 2021 in Clinics and Research in Hepatology and Gastroenterology
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Journal Article
Closed access
YAYusuf Aydemir
Yusuf Aydemir
BEBahattin Erdogan
Bahattin Erdogan
ATAhmet Türkeli
Ahmet Türkeli

3 November 2016 in International Journal of Laboratory Hematology
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YAYusuf Aydemir
Yusuf Aydemir
APA. Pınar
A. Pınar
GHG. Hızal
G. Hızal
HDH. Demir
H. Demir
İTİ. N. Saltık Temizel
İ. N. Saltık Temizel
AYA. Yüce
A. Yüce

14 May 2025 in European Journal of Pediatrics
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STSevde Nur Türker
Sevde Nur Türker
ZBZeren Barış
Zeren Barış
NŞNazlı sena Şeker
Nazlı sena Şeker
YAYusuf Aydemir
Yusuf Aydemir
The histopathological effects of duodenogastric reflux (DGR) in children remain poorly described. This study aimed to evaluate and compare the gastric histopathological findings of pediatric patients with endoscopically confirmed DGR gastritis and those without, to identify potential morphological changes associated with bile reflux in childhood. This retrospective study compared children with endoscopically confirmed DGR to age- and sex-matched controls without DGR. Gastric biopsy samples were re-evaluated by a single pathologist blinded to clinical data. Histopathological features, including inflammation severity, activity, fibrosis, vascular congestion, edema, foveolar hyperplasia, the presence of Helicobacter pylori, lymphoid aggregates, reactive gastropathy, intestinal metaplasia, and glandular atrophy were compared. Logistic regression was used to identify significant predictors of DGR. A total of 73 patients with DGR and 65 controls were included. Fibrosis (60.2% vs. 9.2%, p < 0.001), congestion (63.0% vs. 27.7%, p < 0.001), foveolar hyperplasia (32.9% vs. 6.2%, p < 0.001), and edema (24.7% vs. 6.2%, p = 0.003) were significantly more common in the DGR group. Logistic regression identified foveolar hyperplasia (OR 10.67), edema (OR 9.01), fibrosis (OR 6.98), and congestion (OR 5.85) as independent predictors of DGR. Conclusion: Fibrosis, congestion, foveolar hyperplasia, and edema are significantly associated with DGR in pediatric patients and may serve as supportive histological markers for diagnosis. What is Known:• DGR in children lacks a standardized diagnostic method, with endoscopy and histopathology being commonly used.• Histopathological features such as foveolar hyperplasia and fibrosis are known in adults but less studied in children. What is New:• This study identifies fibrosis, congestion, foveolar hyperplasia, and edema as significant histopathological markers in pediatric DGR.• It suggests that endoscopic findings, combined with histopathology, can aid in the diagnosis of DGR in children.

12 February 2024 in European Journal of Pediatrics
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YAYusuf Aydemir
Yusuf Aydemir
OAOzge Aydemir
Ozge Aydemir
MDMeltem Dinleyici
Meltem Dinleyici
ASAdviye Cakil Saglik
Adviye Cakil Saglik
DCDemet Cam
Demet Cam
Fuat Emre CanpolatFuat Emre Canpolat
Fuat Emre Canpolat
Functional gastrointestinal disorders (FGIDs) are characterized by a variety of symptoms that are frequently age-dependent, chronic, or recurrent and are not explained by structural or biochemical abnormalities. There are studies in the literature reporting different results regarding the relationship between prematurity and FGIDs. The main objective of this study was to compare the frequency of FGIDs between preterm and term infants. The secondary objective was to evaluate whether there was any association between neonatal characteristics and development of FGIDs. A multicenter prospective cohort study that included preterm infants born before 37 weeks of gestation and healthy term infants was carried out. At 1, 2, 4, 6, 9, and 12 months of age, infants were assessed for the presence of FGIDs using the Rome IV criteria. In preterm infants, an additional follow-up visit was made at 12 months corrected age. 134 preterm and 104 term infants were enrolled in the study. Infantile colic, rumination syndrome, functional constipation, and infant dyschezia were more common in preterm infants. Incidence of other FGIDs (infant regurgitation, functional diarrhea and cyclic vomiting syndrome) were similar among preterm and term infants. Preterm infants who are exclusively breastfeed in the first 6 months of life have a lower incidence of infantile colic (18.8% vs 52.1%, p = 0.025). In terms of chronological age, FGIDs symptoms started later in preterm infants; this difference was statistically significant for infantile colic and regurgitation (median age 2 months vs 1 month, p < 0.001).   Conclusions: Preterm infants have a higher prevalence of FGIDs compared with term controls. Therefore, especially if they have gastrointestinal complaints, they should be screened for FGIDs. Possibly due to maturational differences, the time of occurrence of FGIDs may differ in preterm infants. Infantile colic incidence decreases with exclusive breastfeeding. What is Known:• The functional gastrointestinal disorders are a very common in infancy.• Data on preterm infants with FGIDs are currently very limited. What is New:• Preterm infants have a higher incidence of infantile colic, rumination syndrome, functional constipation and infant dyschezia when compared to term infants.• Preterm infants who are exclusively breastfed during the first 6 months of life experience a lower incidence of infantile colic.

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JRJorik M. van Rijn
Jorik M. van Rijn
LWLael Werner
Lael Werner
YAYusuf Aydemir
Yusuf Aydemir
JSJoey M.A. Spronck
Joey M.A. Spronck
BPBen Pode-Shakked
Ben Pode-Shakked
DSDror S. Shouval
Dror S. Shouval
Hyaline fibromatosis syndrome (HFS), resulting from ANTXR2 mutations, is an ultra-rare disease that causes intestinal lymphangiectasia and protein-losing enteropathy (PLE). The mechanisms leading to the gastrointestinal phenotype in these patients are not well defined. We present two patients with congenital diarrhea, severe PLE and unique clinical features resulting from deleterious ANTXR2 mutations. Intestinal organoids were generated from one of the patients, along with CRISPR-Cas9 ANTXR2 knockout, and compared with organoids from two healthy controls. The ANTXR2-deficient organoids displayed normal growth and polarity, compared to controls. Using an anthrax-toxin assay we showed that the c.155C>T mutation causes loss-of-function of ANTXR2 protein. An intrinsic defect of monolayer formation in patient-derived or ANTXR2KO organoids was not apparent, suggesting normal epithelial function. However, electron microscopy and second harmonic generation imaging showed abnormal collagen deposition in duodenal samples of these patients. Specifically, collagen VI, which is known to bind ANTXR2, was highly expressed in the duodenum of these patients. In conclusion, despite resistance to anthrax-toxin, epithelial cell function, and specifically monolayer formation, is intact in patients with HFS. Nevertheless, loss of ANTXR2-mediated signaling leads to collagen VI accumulation in the duodenum and abnormal extracellular matrix composition, which likely plays a role in development of PLE.