Abstract: Hypoxic-ischemic encephalopathy is a severe complication of perinatal asphyxia and causes lifelong deficits in infants and children. Multiple mechanisms acting in serial or parallel fashion are likely to be involved in this procedure. The neuronal injury is strongly related to iron-catalysed oxygen radical production and subsequent peroxidative damage to lipids and protein. Excessive release of excitatory amino acids (EAA) glutamate and aspartate, with consequent overstimulation of glutamate receptors, is also thought to be an important mechanism in this brain injury. Deferoxamine (DFO), a chelator of non-protein-bound iron, has been shown to inhibit lipid peroxidation and hydroxyl radical production via the Fenton reaction and to decrease hypoxic-ischemic and reperfusion associated brain injury. However, the exact mechanism of neuroprotection of DFO and its possible effect on the neurotransmitters' release is currently being investigated. In the present study, a well-established model of perinatal asphyxia was used to investigate the effect of DFO on hypoxic-ischemic-induced damage to different hippocampal brain structures. DFO was administrated subcutaneously immediately after the asphyctic insult. Histological examination of the hippocampus was conducted and the tissue levels of glutamate and aspartate in the same area were determined. A remarkable reduction of hypoxia-ischemia-evoked neurons in the CA1 hippocampal region and a decrease in the asphyxia-induced hippocampal tissue levels of glutamate and aspartate was noted after DFO treatment. These findings suggest a complex action of DFO, which could be neuroprotective when administrated in the immature brain immediately after hypoxia-ischemia.
Abstract: BACKGROUND: This article presents the anatomic and functional outcome of site-specific fascia repair for rectocele performed under local anesthesia. Methods. In this case series, 51 consecutive patients underwent site-specific rectocele repair under local anesthesia. Patients were subsequently reviewed in the outpatient clinic. RESULTS: The mean follow-up period was 26.7 months. Pelvic examination revealed recurrence of posterior vaginal wall prolapse in 31% (16/51). Improvement in emptying the rectum was achieved in 23% (7/30), and 23% (7/30) were relieved from constipation. One patient developed de novo dyspareunia. Some 92% of the patients (47/51) would recommend local anesthesia. CONCLUSIONS: Anatomic correction of posterior vaginal wall prolapse does not guarantee alleviation of all symptoms, especially those regarding defecation; however, postoperative dyspareunia levels are low. The use of local anesthesia is associated with high patient satisfaction. Patients should be informed that total recovery from accompanying subjective symptoms cannot be guaranteed.
Abstract: The purpose of this study was to evaluate the effects of the anti-inflammatory hormone alpha-melanocyte-stimulating hormone (alpha-MSH) treatment on renal function and expression of aquaporins (AQPs) and Na-K-ATPase in the kidney in response to 24 h of bilateral ureteral obstruction (BUO) or release of BUO (BUO-R). In rats with 24-h BUO, immunoblotting revealed that downregulation of AQP2 and AQP3 was attenuated (AQP2: 38 +/- 5 vs. 13 +/- 4%; AQP3: 44 +/- 3 vs. 19 +/- 4% of sham levels; P < 0.05), whereas downregulation of Na-K-ATPase was prevented by alpha-MSH treatment (Na-K-ATPase: 94 +/- 7 vs. 35 +/- 5% of sham levels; P < 0.05). Immunocytochemistry confirmed the changes in AQP1 and Na-K-ATPase expression. Renal tubular cell apoptosis was confirmed in BUO kidneys, and alpha-MSH treatment virtually completely abolished apoptosis. Furthermore, we measured glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), respectively. Forty-eight hours after BUO-R demonstrated that alpha-MSH treatment almost completely prevented the decrease in GFR (nontreated: 271 +/- 50; alpha-MSH: 706 +/- 85; sham: 841 +/- 105 microl x min(-1).100 g body wt(-1), P < 0.05) and ERPF (nontreated: 1,139 +/- 217; alpha-MSH: 2,598 +/- 129; sham: 2,633 +/- 457 microl x min(-1).100 g body wt(-1), P < 0.05). alpha-MSH treatment also partly prevented the downregulation of AQP1 and Na-K-ATPase expression in rats after BUO-R for 48 h. In conclusion, alpha-MSH treatment significantly prevents impairment in renal function and also prevents downregulation of AQP2, AQP3, and Na-K-ATPase during BUO or AQP1 and Na-K-ATPase after BUO-R, demonstrating a marked renoprotective effect of alpha-MSH treatment in conditions with urinary tract obstruction.
Abstract: Ehlers-Danlos syndrome (EDS) is a heterogeneous group of connective tissue disorders involving various organ systems. We report the case of a female patient with Ehlers-Danlos syndrome type III (EDS III) presenting with a recurrent rectocele in whom porcine small intestinal submucosa mesh was used successfully to correct the defect in the rectovaginal fascia.
Abstract: The discovery of aquaporin-1 (AQP1) by Agre and colleagues explained the long-standing biophysical question of how water specifically crosses biological membranes. These studies led to the discovery and identification of a whole new family of membrane proteins, the aquaporins. At present, at least seven aquaporins are expressed at distinct sites in the kidney and 4 members of this family (AQP1-4) have been demonstrated to play pivotal roles in the physiology and pathophysiology for renal regulation of body water balance. Osmotic equilibration via renal aquaporins is maintained by active transport of NaCl. The major sodium transporters and channels in the individual renal tubule segments have been identified and the regulation of these transporters and channels are fundamental for renal sodium reabsorption and for establishing the driving force. In this mini-review the role of renal aquaporins and sodium transporters and channels is briefly described and their key role for the impaired urinary concentrating capacity in response to urinary tract obstruction is reviewed. Thus this review updates previous detailed reviews (1-5).
Abstract: PURPOSE: To document the prevalence of non-compliance and to investigate patients' perceptions concerning glaucoma in a Greek cohort. METHODS: We investigated 100 consecutive patients referred to our glaucoma clinic and already treated for chronic glaucoma. Compliance and patients' insight were ascertained by two independent observers by means of a predetermined questionnaire. All patients were subsequently assessed for their ability to instil their eyedrops accurately. RESULTS: Fifty one per cent of our patients were not aware of the nature of glaucoma, but 80% were afraid it might lead to blindness. Clinically significant non-compliance (more than two doses missed per week) was established in 44% of our patients. Men and those using eyedrops more than 4 times a day were more likely to default. Non-compliant patients exhibited higher mean intraocular pressure (22.9 vs 18.5 mmHg; p > 0.001) and worse visual field loss (10.8 vs 7.0 dB; p = 0.008) compared with compliant patients. Involuntary non-compliance was also common in our group, with only 53% instilling their eye drops accurately. CONCLUSION: Non-compliance is a significant limiting factor in glaucoma therapy in Greece.
