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Biomedical subjects

A Gül

Publications and source records attributed to A Gül.

42 records · Page 3Linked to original sources
PubMedDate not supplied

Repair of large incisional hernias with multiple small relaxing incisions technique.

We report our results in repairing wide incisional hernial defects without using any prosthetic synthetic material, but expanding rectus sheaths by multiple small, 8 to 10 mm, relaxing incisions. In this way, hernial defect becomes smaller and fascial flaps are sutured to each other in an overlapping manner. These relaxing incisions are filled with collagenous connective tissue, and consequently do not cause any abdominal wall weakness. This procedure was performed on 32 patients with hernial defect of 4 x 4 cm to 15 x 15 cm. Mean hospital stay was 6, 8 days. In the follow-up period ranging from 5 to 42 months, no patient presented recurrence of the hernia. Rectus diastasis occurred in one patient who had been operated five times previously. Wound complication such as infection, seroma, haematoma developed in 9 of the patients, and were successfully treated by wound drainage and administration of appropriate antibiotic therapy. The findings of this study led us to conclude that the technique can be used in the repair of incisional hernias as an alternative technique.

Abdominal Muscles↗
PubMedDate not supplied

Behçet's disease: an update on the pathogenesis.

Behçet's disease is a chronic inflammatory disorder of unknown etiology. It has long been postulated that immunological abnormalities, which are possibly induced by microbial pathogens in genetically susceptible individuals, are important in its pathogenesis. Recent findings have both supported the significance of genetic factors and better defined the nature of inflammation in Behçet's disease. Molecular genetic studies have strengthened the primary association of HLA-B51 with Behçet's disease. The exact pathogenic mechanism of the HLA-B51 molecule is still unknown, and its contribution to the overall genetic susceptibility to Behçet's disease is estimated to be less than 20%. Spontaneous and/or induced overexpression of pro-inflammatory cytokines (mainly Th1 type) from various cellular sources seems responsible for the enhanced inflammatory reaction in Behçet's disease, and it may be associated with the genetic susceptibility. An antigen-driven immune response superimposed on this primed-state and induced by heat shock proteins or other peptides from different strains of streptoccocci or other microbial agents has been suggested to trigger manifestations of Behçet's disease. Endothelial activation/injury and the resultant occlusive vasculopathy may also contribute to the tissue damage.

Behcet Syndrome↗
PubMedDate not supplied

Tumour necrosis factor-alpha gene promoter region -308 and -376 G-->A polymorphisms in Behçet's disease.

OBJECTIVE: Contribution of HLA-B51 to the genetic susceptibility for Behçet's disease is well documented and recent studies suggest involvement of other genes. Tumour necrosis factor (TNF) genes are located in the vicinity of the HLA-B locus. Polymorphisms in the promoter region of TNF-alpha gene has been found to be associated with altered TNF secretion, and it may have a prominent role in the increased inflammatory responses of Behçet's disease. METHODS: The study group consisted of 99 Behçet's disease patients and 96 healthy matched controls. All patients fulfilled the International Study Group criteria for Behçet's disease. The TNF-alpha -308 and -376 promoter alleles were assigned by the digestion of each amplified PCR product with NcoI and TasI enzymes, respectively. RESULTS: No significant difference was observed in the distribution of TNF-alpha promoter region polymorphisms between patients with Behçet's disease and controls. There was no association between the presence of uncommon -308A and -376A alleles and the manifestations or severity of Behçet's disease either. The TNF-alpha -308A allele and HLA-B*50 was found to be associated in this series of Turkish patients and controls. CONCLUSION: The role of TNF-alpha promoter region -308 and -376 polymorphisms in the pathogenesis of Behçet's disease is not supported by this data. The overexpression of TNF-alpha in Behçet's disease may be caused by other polymorphisms in the TNF gene or by post-transcriptional mechanisms.

Adolescent↗
PubMedDate not supplied

Common Crohn's disease-predisposing variants of the CARD15/NOD2 gene are not associated with Behçet's disease in Turkey.

OBJECTIVE: There are many extra-intestinal findings of Crohn's disease (CD), such as oral and genital ulcers, erythema nodosum, uveitis and arthritis, resembling the manifestations of Behçet's disease (BD). It is also very difficult to distinguish the gastrointestinal involvement of BD from that of CD in some patients. Hence, this study aimed to investigate a possible involvement of the common CD-predisposing CARD15 variants in the genetic susceptibility to BD. METHODS: The study group consisted of 85 consecutive patients with BD (51 male, 34 female) of Turkish origin. Two of them had intestinal involvement. A group of 100 ethnically matched, non-related healthy volunteers were used as controls. All individuals were genotyped for 3 common CARD15 variants (R702W, G908R, and Ll007fsinsC) using a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. RESULTS: None of the three CARD15 variants predisposing to CD was observed in patients with BD, including two patients with intestinal involvement. The R702W mutation was observed in I healthy chromosome, and the 3020insC mutation in 2 chromosomes. No individual was found to be homozygous or compound heterozygous for these variants. CONCLUSION: These findings suggest that 3 most common CD-predisposing CARD15 variants do not constitute a genetic susceptibility factor for BD in Turkey. Further studies would be helpful to rule out a possible contribution of other rare or unknown variants and/or the effects of different ethnic backgrounds.

Behcet Syndrome↗