Hatun Duran

Mibefradil, a T-Type Ca2+ Channel Blocker, Protects Against Mesenteric Ischemia-Reperfusion-Induced Oxidative Injury and Histologic Alterations in Intestinal Mucosa in Rats

The purpose of the present study was to investigate whether mibefradil can reduce oxidative stress and histologic damage in the rat small bowel subjected to mesenteric ischemia and reperfusion injury. Thirty Sprague-Dawley rats weighing between 210 and 220 g were divided into three groups, each containing 10 rats: group 1, sham operation; group 2, untreated ischemia-reperfusion; and group 3, ischemia-reperfusion plus mibefradil treatment group. Intestinal ischemia for 45 min and reperfusion for 60 min were applied. Ileal specimens were obtained to determine the tissue levels of MDA, CAT, SOD, and GSH-Px and histologic changes. In group 2, MDA values were significantly increased compared to those in groups 1 and 3. In addition, SOD, CAT, and GSH-Px values decreased significantly in group 2 compared to groups 1 and 3. The intestinal injury score increased significantly in group 2 and 3 rats compared to group 1 rats. However, this increase was reduced in group 3 rats compared to group 2. Histopathologically, the rats in group 1 had essentially normal testicular architecture. In group 2 rats, the lesions varied between grade 3 and grade 5. In contrast, most of the specimens in the mibefradil-treated group 3 showed grade 1 injury. Mibefradil plays a role in attenuating reperfusion injury of the small intestine by depressing free radical production and mucosal injury score and regulating postischemic intestinal perfusion while restoring intestinal microcirculatory blood flow and encountered histologic injury.

Cytogenetic and clinical studies of a male infant with disorder of sexual development: case report

OBJECTIVE To report a translocation between chromosomes 3 and 4: 46,XY,t(3;4)(p25;q31.3) in a male infant with a disorder of sexual development. DESIGN Case report. SETTING University hospital. PATIENT(S) A 1-year-old infant who presented with abnormal location of the urethral meatus. INTERVENTION(S) Cytogenetic analysis, fluorescence in situ hybridization (FISH), and serum concentrations measurement (using peripheral blood), and clinical examination. MAIN OUTCOME MEASURE(S) Karyotype and clinical findings. RESULT(S) On clinical examination, bilateral testicular volume and phallus were determined to be undersized. Serum concentrations of T and DHEAS were low. G-banding of his chromosomes showed that the patient had a balanced translocation involving chromosomes 3 and 4: 46,XY,t(3;4)(p25;q31.3). This karyotype finding was confirmed by FISH. The FISH analysis revealed the presence of sex-determining region (SRY). The proband inherited this translocation from his father. His sister had the same translocation. However, the father and sister of the proband were clinically normal. CONCLUSION(S) The presence of this chromosomal anomaly and hypospadias was unique to our patient compared with others with the 46,XY,t(3;4) translocation. Although no such association has been reported to date, we think that the severe hypospadias in our case might be associated with this translocation.

UMBILICAL HETEROPAGOUS TWINNING: A CASE REPORT

Heteropagous conjoined twins are rare and umbilical heteropagous conjoined twins are extremely rare. We present a case with umbilical heteropagous conjoined twins and discuss the diagnosis and management. The parasitic component of heteropagous can be separated and treated successfully in the majority of cases.