Semen levels of mitochondrial DNA deletions in men attending an infertility clinic do not correlate with phenotype

In view of previous reports associating mitochondrial DNA deletions with male reproductive disorders, levels of the `common' 4977 bp mitochondrial DNA deletion were evaluated semi-quantitatively in 64 men, without prior knowledge of the clinical diagnosis. Significant levels of deletions were detected in 34/64 men (53%) but 29 of these (45%) had a normal semen profile and were phenotypically normal. No deletions were detected in 30 men, of whom 21 were normospermic, six were oligozoospermic and three were azoospermic. It is concluded that although mitochondrial DNA deletions within the testis may be associated with primary testicular disease, no correlation with semen quality was evident in this study, thus limiting its potential use as a diagnostic test.     

Transient hyperphosphatasemia after pediatric liver transplantation

BACKGROUND: Transient hyperphosphatasemia of infancy and early childhood is characterized by transiently increased serum activity of alkaline phosphatase (ALP), predominantly its bone or liver isoform, in children under 5 years of age. There is little information on the rate of transient hyperphosphatasemia in pediatric liver transplant recipients. METHODS: Patients who underwent liver transplantation at Ege University Organ Transplantation and Research Center, Izmir, Tureky, between January 1998 and January 2005, were included in the study. A total of 70 paediatric liver recipients' medical records were analyzed retrospectively. RESULTS: Transient isolated hyperphosphatasemia was observed in two of 70 patients and the rate of transient hyperphosphatasemia was estimated to be 2.8% in pediatric liver transplant recipient. Diarrheal episode was noted prior to the peak ALP activity in both cases. In one case the causative agent was not found, whereas in the other case Rotavirus was detected in a stool specimen. ALP activity normalized at 4 months and 18 days in the first and second cases, respectively. They continue follow up at the outpatient clinics with stable graft function. CONCLUSION: It is important to know that very high ALP levels can be seen without underlying significant pathology and the benign nature of the condition to avoid unnecessary investigations.     

Higher Rate of Recurrent Atrial Flutter and Atrial Fibrillation Following Atrial Flutter Ablation After Cardiac Surgery

Atrial Flutter After Cardiac Surgery . Introduction: Atrial flutter (AFL) is common after cardiac surgery. However, the types of post‐cardiac surgery AFL, its response to catheter‐based radiofrequency ablation, and its relationship to atrial fibrillation (AF) are unknown. Methods and Results: We retrospectively studied all patients who underwent mapping and ablation for AFL after cardiac surgery from January 1990 to July 2004. One hundred randomly selected patients without prior cardiac surgery (PCS) who underwent mapping and ablation of AFL served as the control population. A total of 236 patients formed the study population (mean age 62 + 13 years, 22% female) and 100 patients formed the control population (mean age 60 + 13 years, 25% female). The majority of patients without PCS had cavo‐tricuspid isthmus (CTI)‐dependent AFL when compared to patients with PCS (93% vs 72%, respectively, P < 0.0001). In contrast, scar‐related AFL was more common in patients with PCS as compared to patients without PCS (22% vs 3%, P < 0.0001). Predictors of scar related AFL in multivariable regression analysis included PCS and left‐sided AFL. Acute success rates and complications were similar between the groups. When compared to patients with AFL ablation without PCS, those that had AFL after PCS had higher rates of recurrence of both AFL (1% vs 12%, P < 0.0001; mean time to recurrence 1.85 years) and AF (16% vs 28%, P = 0.02; mean time to recurrence 2.67 years). Conclusion: Despite ablation of AFL, patients with PCS have a higher rate of AFL and AF when compared to patients without PCS who underwent ablation of atrial flutter during long‐term follow‐up. (J Cardiovasc Electrophysiol, Vol. pp. 760‐765, July 2010)     

Renal damage in rats induced by myocardial ischemia/reperfusion: Role of nitric oxide

BACKGROUND: It has been demonstrated that myocardial ischemia/reperfusion (MI/R) causes renal damage. However, the mechanism underlying this damage in kidneys during revascularization of myocardium is unclear. Direct renal ischemia/reperfusion has been implicated in the induction of inducible nitric oxide synthase (iNOS) that leads to increase production of nitric oxide (NO). Recently, excessive production of NO has been found to be involved in causing renal injury by formatting peroxinitrite (ONOO(-)). The aim of this study was to investigate whether NO has a role in this damage, using aminoguanidine (AMG), a known iNOS inhibitor and an antioxidant, in rats undergoing MI/R. METHODS: Male Wistar rats were used for the experiments (n = 7 each group). In the MI/R group, the left coronary artery was occluded for 30 min and then reperfused for 120 min; the same procedure was used for the AMG group, with the additional step of AMG (200 mg/kg) administered 10 min prior to ischemia. A control group underwent sham operation. At the end of the reperfusion period, all rats were killed and their kidneys removed for biochemical determination and histopathological analysis. RESULTS: Myocardial ischemia/reperfusion in the rat kidney was accompanied by a significant increase in malondialdehyde and NO production, and a decrease in glutathione content. Administration of AMG reduced malondialdehyde and NO production and prevented depletion of glutathione content. These beneficial changes in the biochemical parameters were also associated with parallel changes in histopathological appearance. CONCLUSION: These findings suggest that MI/R plays a causal role in kidney injury and AMG exerts renal-protective effects, probably by inhibiting NO production and antioxidant activities.     

RETICULATE ACROPIGMENTATION OF KITAMURA: TWO CASE REPORTS

Background. Reticulate acropigmentation of Kitamura (RAK) is an autosomal dominantly inherited dermatosis. Case Reports. Two patients are described with the clinical and histopathologic features of reticulate acropigmentation of Kitamura. Conclusions. We speculate that RAK and the Dowling-Degos disease (DDD) are the same diseases.     

N-METHYL-d-ASPARTATE ANTAGONISTS, GLUTAMATE RELEASE INHIBITORS, 4-AMINOPYRIDINE AT NEUROMUSCULAR TRANSMISSION

It is thought that glutamate (GLU) and acetylcholine (ACh) are co-released in the neuromuscular junction (NMJ). Consequently, GLU is also a mediator or modulator of neuromuscular transmission (n-m) together with ACh. Therefore we decided to investigate the role of GLU in n-m by using isolated rat phrenic nerve–hemidiaphragm preparations. Since the GLU receptors present at NMJ have been reported to be predominantlyN-methyl-d-aspartate (NMDA) subtype, some non-competitive and competitive NMDA receptor blockers, MK801, ketamine, dextromethorphan and CGP 37849, and GLU release inhibitors, clonidine, guanfacine, tizanidine were used at their optimum concentrations in medium after having found them from dose–response curves. The preparations were first stimulated indirectly in the presence of the optimum concentrations of the drugs used and tensions developed were recorded isometrically through a force displacement transducer on a polygraph linked to a computer + Math coprocessor by an analog converter. All drugs at their optimum concentrations suppressed contractions significantly. Prolyl-glycinamide (PLG) or phenyl-succinate, both of which are the inhibitors of GLU production also suppressed the contraction significantly, following depletion of GLU stores by tetanic contraction in nerve endings. 4-Aminopyridine, which has been shown to release GLU augmented the contractions which were also completely abolished by the NMDA receptor antagonists or GLU release inhibitors at their higher concentrations than their optimum ones. The direct stimulation of the muscles elicited statistically insignificant but higher contractions than controls at the optimum concentrations of the antagonists or inhibitors in medium. The results were discussed and it was concluded that blockade of NMDA receptors, the inhibition of GLU release or the suppression of GLU production inhibit the contractions of the rat-isolated hemidiaphragms elicited by indirect electrical stimulation, without altering acetylcholinergic part of the contraction cascade.