The peri‐microvascular edema in hippocampal CA1 area in a rat model of sepsis

Encephalopathy is a common complication of sepsis. However, little is known about the morphological changes that occur in the brain during sepsis. In this study, fecal peritonitis was induced in Wistar rats, which had been monitored for 4 h before their brains were removed and samples from the CA1 area taken. In addition to higher blood pressure with a decreasing pattern and a significant drop in rectal temperature, an increased heart rate and marked respiratory failure were observed. The tissue was investigated and compared with corresponding hippocampal samples taken from sham‐operated and not operated control groups. Significantly more peri‐microvascular edema was found in the hippocampal CA1 area in the septic group. The percentages of the peri‐microvascular edema were 158.57 ± 3.6%, 122.84 ± 1.5% and 120.24 ± 1.9% in the fecal peritonitis group, sham‐operated and not operated control groups, respectively. The results may suggest that the edema observed around the microvessels may participate in the pathogenesis of the septic encephalopathy probably by causing in the microvascular permeability characteristics.     

Red cell N5-methyltetrahydrofolate concentrations and C677T methylenetetrahydrofolate reductase genotype in patients with stroke

AIMS: To investigate the relation between total red cell folate, red cell N(5)-methyltetrahydrofolate (N(5)MTHF) concentrations, and N(5)N(10)-methylenetetrahydrofolate reductase (MTHFR) genotypes in stroke. METHODS: The study comprised 120 consecutive patients presenting to hospital with acute stroke. Multivitamin supplement use was recorded. Serum and red cell folate were measured by microbiological assays using Lactobacillus casei and Enterococcus faecalis, and by the DPC-BioMediq Immulite 2000 analyser. Total plasma homocysteine (tHcy), serum cobalamin, and serum vitamin B(6) were measured and the C677T MTHFR genotype determined. RESULTS: There were no significant differences in blood tHcy or vitamin concentrations according to MTHFR genotype in the overall patient cohort. However, when patients taking vitamins were excluded, total red cell folate and red cell N(5)MTHF were significantly lower in patients with the TT genotype compared with CT or CC genotypes. In the overall cohort, irrespective of genotype, red cell folate was significantly lower when assayed microbiologically than with the Immulite assay. This discrepancy remained after exclusion of patients taking vitamins. CONCLUSION: Total red cell folate and red cell N(5)MTHF are significantly lower in stroke patients with the TT compared with the CT and TT MTHFR genotypes, particularly those not taking vitamin supplements. Microbiological assays that measure biologically active folates provide substantially lower estimates of folate than the Immulite assay. Because folate is a key determinant of blood homocysteine values, these findings may impact on the interpretation of the strength and independence of the association between raised blood concentrations of homocysteine and atherothrombosis risk reported in most epidemiological studies.     

Emergence of rifampicin resistance in methicillin-resistant Staphylococcus aureus isolated at a Turkish university hospital

Twenty-three rifampicin-resistant methicillin-resistant Staphylococcus aureus (MRSA) isolated in three wards at a university hospital in Turkey between June, 2000, and February, 2001, were studied for their genetic relatedness using a combination of antibiogram, coagulase serotyping, coagulase gene polymorphism (coa-RFLP), and pulsed-field gel electrophoresis (PFGE). They all expressed high-level rifampicin resistance (MIC, >256 mg/L) and were resistant to gentamicin, kanamycin, amikacin, ciprofloxacin, tetracycline, and cadmium acetate and were susceptible to fusidic acid, vancomycin, trimethoprim, and mupirocin. They belonged to the same coagulase serotype (serotype IV) and had identical coa-RFLP patterns. In contrast, PFGE generated nine banding patterns designated type A, types A1-A5, B, C, and D. The most common PFGE pattern (type A) and its subtypes (types A1-A5) were seen in 20 (87%) of the 23 isolates in the three wards. The results demonstrated the acquisition of rifampicin resistance by different MRSA clones and the spread of one clone among patients in the three wards.     

Neuroimaging findings in infantile GM1 gangliosidosis

GM1 gangliosidosis is an autosomal recessive glycosphingolipid storage disease caused by defects in the enzyme beta-galactosidase. Three clinical forms (infantile-, juvenile-, and adult-onset) of the disease are recognized. Patients with infantile GM1 gangliosidosis present at birth or shortly thereafter with somatic and bony changes, followed by severe neurological deterioration ultimately leading to death within the first 2 years of life. We present the brain CT, MRI and MR spectroscopy (MRS) findings in a 17-month-old Turkish girl with infantile GM1 gangliosidosis. Neuroimaging findings in patients with infantile GM1 gangliosidosis have been reported only in a few cases. In this study, MRS of the thalamus was performed to study the metabolic changes in GM1 gangliosidosis. We showed a a decreased NAA/Cr ration and an increased Cho/Cr ratio. To our knowledge, this is the first report of magnetic resonance spectroscopy findings in type-1 GM1 gangliosidosis.     

Antisynthetase syndrome with refractory lung involvement and myositis successfully treated with double filtration plasmapheresis

Antisynthetase syndrome (ASS) is characterized by inflammatory muscle disease, pulmonary and joint involvement, and antisynthetase autoantibodies, with anti‐Jo‐1 antibody being the most common. Despite the use of immunosuppressive drugs, the prognosis of lung involvement seems poor. Herein, we report a case of refractory ASS, which maintained long‐term remission by double filtration plasmapheresis (DFPP) combined with immunosuppressive therapy. For a 65‐year‐old woman, who was diagnosed with ASS, immunosuppressive therapy was initiated and plasmapheresis (PP) was performed five times due to acute interstitial pulmonary disease and inflammatory myopathy. She remained in remission for eight months following PP. Increase in interstitial involvement was identified by lung tomography when the patient presented again with complaint of progressive increase in dyspnea and muscle pain. Although the immunosuppressive therapy was increased for the patient with elevated creatine phosphokinase (CPK) (2776 IU/mL), a rapid decrease in diffusion capacity of the lung for carbon monoxide (DLCO) was observed and the patient underwent PP. After four sessions of therapy, insufficient clinical and laboratory response was obtained (control CPK 1797 IU/mL) and because of that issue DFPP using a 2A filter was performed to the patient. There was a marked improvement in complaints of the patient, DLCO, and laboratory findings (control CPK 508 IU/mL) after three sessions of DFPP. The patient, who continued the immunosuppressive therapy after DFPP procedure, is being followed for 12 months in remission. Although our experience is limited with only one patient, DFPP seems promising as a treatment option for ASS with severe lung involvement. J. Clin. Apheresis, 28:422–425, 2013. © 2013 Wiley Periodicals, Inc.     

Correction to: Molecular characterization of a human group C rotavirus detected first in Turkey

Virus Genes - This article was unintentionally published twice in this journal, by the same authors. Following should be considered the version of record and used for citation purposes:...     

Preliminary study showing the relationship between platelet fibronectin, sialic acid, and ADP-induced aggregation levels in coronary heart disease.

Several studies indicate that thrombosis plays an important role in the pathogenesis of coronary heart disease (CHD). Fibronectin is a multifunctional protein in plasma, other body fluids, and cell surface and plays an important role in platelet functions, including mediation of cell-cell and cell-surface interactions. Sialic acid is a regular constituent of glycoproteins and gangliozides in the outer cell membrane of mammalian cells. Therefore, the sialic acid content of platelets, which are characterized by their ability to aggregate with each other, can be important in leading to thrombus formation. In this study, platelet fibronectin, sialic acid-, and adenosine diphosphate (ADP)-induced platelet aggregation levels were determined in patients with CHD. Platelet sialic acid concentrations were determined by Warren's method. Platelet aggregation tests with ADP in platelet-rich plasma (PRP) were analyzed by use of an aggregometer. Platelet homogenate fibronectin levels were determined by ELISA. Total protein levels were determined by Lowry method. Our results indicate that, in patients with no vessel disease (patients with no obstructed vessel but suffering from chest pain, like angina pectoris) platelet fibronectin levels were significantly lower than the total of the other patients (patients with 1, 2, or 3 obstructed coronary vessels) (p<0.05). Sialic acid levels in patients with no vessel disease were significantly lower than the total of the patient group (p<0.05). There was significant (+) correlation between platelet aggregation, platelet fibronectin, platelet sialic acid, and severity of disease (p<0.05). Our preliminary findings suggest that, especially platelet fibronectin levels potentially represent a pathogenic factor for CHD.     

The effects of antioxidants on exercise-induced lipid peroxidation in patients with COPD

OBJEctive: The oxidant-antioxidant balance plays an important role in the pathogenesis of COPD. The aim of the present study was to evaluate the effects of exercise, as an oxidative stress factor on the oxidant-antioxidant balance and to investigate whether short-term antioxidant treatment affects lipid peroxidation products. METHODOLOGY: Twenty-one stable COPD patients and 10 control subjects were included in the study. Symptom-limited exercise tests were performed by all subjects. Blood was collected before and 1 h after exercise in control subjects and before, 1 and 3 h after exercise in COPD patients, for analysis of malondialdehyde (MDA), reduced glutathione (GSH) and vitamin E (VE) levels. VE and vitamin C treatments were added to the regular bronchodilator therapy in 10 COPD patients for 1 month. After the treatment period, an exercise test was performed and blood was collected again for MDA, GSH and VE levels. RESULTS: Baseline GSH and VE levels were significantly lower in the COPD group when compared with the control subjects. There was no statistically significant difference in MDA levels between the two groups. In the COPD group, MDA levels 3 h after exercise were significantly higher than at baseline. In contrast there were no significant differences in MDA, VE and GSH levels in the control group after exercise. VE and MDA levels increased significantly after exercise in COPD patients but there was no difference in GSH levels. Baseline exercise time was significantly lower in the COPD group than in the controls. In 10 COPD patients who were given antioxidant therapy, their exercise time increased significantly and there was no increase in MDA and VE levels after the repeated exercise test. CONCLUSIONS: Antioxidant levels were significantly lower in COPD patients than in control subjects. In these patients, exercise results in more significant oxidative stress and lipid peroxidation than in control subjects and antioxidant therapy may decrease lipid peroxidation following exercise and improve exercise capacity.