Helicobacter pylori infection in epileptic patients.

It is well known that there might be an epidemiological association between Helicobacter pylori infection and extraintestinal diseases. This study aimed at determining H. pylori infection in epileptic patients. Forty-seven cryptogenic epileptic patients (Group 1) and 35 healthy people (Group 2) participated in this study. Presence of H. pylori infection was examined by H. pylori stool antigen (HpSA), H. pylori IgG, and IgM. HpSA was detected in 21 participants (44.6%) in Group 1 and in 3 participants (8.5%) in Group 2. H. pylori IgM was positive in 27 participants (57.4%) in Group 1 and in 8 participants (22.8%) in Group 2. H. pylori IgG was positive in 37 participants (78.7%) in Group 1 and in 13 participants (38%) in Group 2. The difference of rates of HpSA, H. pylori IgM and IgG in Groups 1 and 2 were found statistically significant (chi2=4.18, p=0.04; chi2=9.18, p=0.0017; chi2=14.58, p<0.001, respectively). We also compared presence of H. pylori infection between the epileptic patients with poor and good prognosis; HpSA positivity was detected in 15 (62.5%) of 24 and 6 (26%) of 23, respectively, and the differences were statistically significant (chi2=6.30, p=0.012). H. pylori IgM positivity was detected in 16 (66%) of 24 patients with poor prognosis and 11 (47.8%) of 23 patients with good prognosis (p>0.05). H. pylori IgG positivity was detected in 18 (75%) of 24 patients with poor prognosis and 19 (82.6%) of 23 patients with good prognosis. The differences of H. pylori IgM and IgG positivity rates in epileptic patients with poor and good prognosis were not found statistically significant (p>0.05). These results suggest a probable association between the acute H. pylori infection and epilepsy, especially with poor prognosis.     

Determination of oxidative stress parameters and DNA fragmentation on post-thawed buck semen in the presence of ram seminal plasma and fetal calf serum

The aim of the study was to investigate the efficiency of ram seminal plasma and fetal calf serum on freezing of buck semen. Twenty ejaculates were collected using an electro-ejaculator and split into six groups. While FCS additive was not used in A1, A2 and A3 groups, 10% FCS was added to B1, B2 and B3 groups. These groups were then edited according to whether the buck or ram SP was involved. The design of the groups was done as follows: Group A1 (control 1), group A2 without buck SP, group A3 containing ram SP instead of buck SP. Groups B1 (control 2), B2 and B3 were the FCS added forms of these groups. Progressive sperm motility percentages in Group A1 and Group B2 were found to be higher when compared to the lowest Group B3. There were no significant differences between the groups in neither the levels of reactive oxygen species nor the enzyme and glutathione activities. In conclusion, the lack of statistical difference between the groups suggested that despite the supplements used but only when the buck spermatozoa structure was healthy, the cell could preserve acrosome, DNA and the integrity of membrane.     

Benign leiomyoma with multiple metastases to vertebrae and calvarium: An index case with comprehensive review of endocrine targets

Neurosurgical Review - “Benign” metastatic leiomyomas (BML) are indolently growing metastatic tumors which mostly associate with uterine leiomyomas in women in reproductive ages. The...     

Identification and characterization of a novel FBN1 gene variant in an extended family with variable clinical phenotype of Marfan syndrome

Marfan syndrome (MFS) is a multi-systemic autosomal dominant condition caused by mutations in the gene (FBN1) coding for fibrillin-1. Mutations have been associated with a wide range of overlapping phenotypes. Here, we report on an extended family presenting with skeletal, ocular and cardiovascular clinical features. The 37-year-old male propositus, who had chest pain, dyspnea and shortness of breath, was first diagnosed based on the revised Ghent criteria and then subjected to molecular genetic analyses. FBN1 sequencing of the proband as well as available affected family members revealed the presence of a novel variant, c.7828G>C (p.Glu2610Gln), which was not present in any of the unaffected family members. In silico analyses demonstrated that the Glu2610 residue is part of the conserved DINE motif found at the beginning of each cbEGF domain of FBN1. The substitution of Glu2610 with Gln decreased fibrillin-1 production accordingly. Despite the fact that this variation appears to be primarily responsible for the etiology of MFS in the present family, our findings suggest that variable clinical expressions of the disease phenotype should be considered critically by the physicians.