Treatment of two postoperative endophthalmitis cases due to <Emphasis Type="Italic">Aspergillus flavus</Emphasis> and <Emphasis Type="Italic">Scopulariopsis</Emphasis> spp. with local and systemic antifungal therapy

Background  

Endophthalmitis is the inflammatory response to invasion of the eye with bacteria or fungi. The incidence of endophthalmitis after cataract surgery varies between 0.072–0.13 percent. Treatment of endophthalmitis with fungal etiology is difficult.     

Sneddon's syndrome: clinical and laboratory analysis of 10 cases

Sneddon's syndrome is characterized by livedo reticularis and cerebrovascular lesions. We report the cases of women (mean age, 36.2 +/- 8.1 years) diagnosed with Sneddon's syndrome based on the presence of livedo reticularis and characteristic cerebrovascular findings. Seven of these patients had cerebral infarcts on cranial computed tomography scan. Antiphospholipid antibodies were positive in 6 of these cases. Three cases had abnormal levels of antithrombin III. Analyses of chromosome 6 revealed no abnormalities. In 3 of the cases, investigation of the pedigrees revealed autosomal dominant traits. Two cases had epilepsy, and 3 had migraine. One case with migraine also had myasthenia gravis. In addition, we detected inferior altudinal hemianopia in 2 cases, cognitive functional disorder in 3 and depression in 2. Based on these findings, the entire vascular, haematologic, neurologic, and dermatologic systems should be evaluated in patients diagnosed with Sneddon's syndrome.     

Ellagic acid attenuates oxidative stress on brain and sciatic nerve and improves histopathology of brain in streptozotocin-induced diabetic rats

The aim of this study was to investigate the possible effects of ellagic acid in brain and sciatic nerve tissues of diabetic rats. Also, the impact of ellagic acid on catalase and paraoxonase (PON-1) activities, total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), malondialdehyde (MDA) and nitric oxide (NO) were examined. The rats were randomly divided into four groups, with eight rats each: Normal controls (not diabetic), only ellagic acid treated (ellagic acid controls, not diabetic), Diabetic controls (streptozotocin, diabetic), ellagic acid-treated diabetic (streptozotocin?+?ellagic acid). After a 4?week experiment, rats were sacrificed, and biomarkers for oxidative stress in the brain and sciatic nerve tissues of the rats were measured. There was significant depletion in the PON-1, catalase, and TAS levels in the brain and sciatic nerve tissues compared to the control groups (for both parameters, p?<?0.05). The values of catalase, PON-1 and TAS reversed back to normal levels in ellagic acid-treated diabetic rats compared to untreated diabetic rats (for both parameters, p?<?0.05). The levels of MDA, TOS, NO and, OSI in the brain and sciatic nerve tissues were higher in untreated diabetic rats compared to control group (for both parameters p?<?0.05). However, MDA, TOS, OSI, and NO levels were found to be significantly reduced in the ellagic acid-treated diabetic group compared to the untreated diabetic group in these tissues (for both parameters, p?<?0.05). In conclusion, the results of the present study suggested that ellagic acid exhibits neuroprotective effects against oxidative damage in diabetic rats.     

Assessment of acute toxicity and histopathology of the fungicide captan in rainbow trout

Acute toxicity of the fungicide, captan, to juvenile rainbow trout was evaluated under static-renewal test condition. Actual concentrations of captan ranged from 0.05 to 1.00 mg/L. The concentrations of captan that killed 50% of the rainbow trout (3.11 ± 0.8 g) within 24 (24 h; LC₅₀), 48, 72 and 96 h were 0.57 ± 0.09, 0.49 ± 0.10, 0.44 ± 0.11 and 0.38 ± 0.13 mg/L (95% confidence limits), respectively. None of the unexposed control fish died and the first fish died 6 h after exposure to captan (≥0.65 mg/L). Hypertrophy, separation of epithelium from lamellae, lamellar fusion, and epithelial cell necrosis were observed on captan exposed fish. Gills also had scattered areas of focal lamellar hyperplasia. Fish exposed to fungicide had inflammation and necrosis in liver, trunk kidney and spleen. In order, the most affected organs were gill, trunk kidney and liver.     

Purification and in vitro toxicity of gamma amanitin

We aimed to obtain gamma amanitin with high purity through a purification process and compare toxic effects of alpha, beta, and gamma amanitin. Specific concentrations of the toxins (25, 10, 1, and 0.1?μg/mL) were applied to the C3A human hepatocytes. A MTT test was performed to determine the level of toxicity. Alpha amanitin showed a higher toxicity in 48?h while the lowest toxicity was observed in beta amanitin. The toxicity level of gamma amanitin was found between the alpha and beta amanitin toxicity. Our method is suitable for obtaining gamma amanitin with high purity (>99%) as well as for obtaining alpha amanitin and beta amanitin. Gamma amanitin has been shown to have equal responsibility for toxicity as alpha amanitin in amanita poisoning.     

Decreased Plasminogen Activator Inhibitor-1 Levels in Coronary Artery Aneurysmatic Patients

BACKGROUND: Matrix metalloproteinases (MMPs) have been implicated in the pathogenesis of arterial aneurysms through increased proteolysis of extracellular matrix proteins. Increased proteolysis due to elevated matrix degrading enzyme activity in the arterial wall may act as a susceptibility factor for the development of coronary aneurysms. Plasmin strongly stimulates pro-MMP enzyme conversion to the active form. Plasmin hyperactivity due to decreased plasminogen activator inhibitor-1 (PAI-1) may cause MMP over activity and coronary aneurysms. The aim of this study was to investigate the association between PAI-1 and presence of coronary aneurysms. METHODS: Twenty-three patients with aneurysmal coronary artery disease and stable angina were enrolled into study (Group 1). Twenty-two patients without coronary aneurysm were selected as a control group (Group 2). PAI-1 was measured in peripheral venous blood. RESULTS: The plasma PAI-1 level was lower in the coronary artery aneurysmatic patients compared to the control group (8.41 +/- 4.28 vs. 13.32 +/- 10.05 ng/ml, p = 0.037). Serum C-reactive protein (CRP) values were not significantly different between groups (3.83 +/- 1.08 vs. 4.01 +/- 1.35 mg/l, p >0.05). CONCLUSION: Increased matrix degrading enzyme activity can cause arterial wall destruction through increased proteolysis of extracellular matrix proteins. Unregulated plasmin hyperactivity due to decreased inhibition by PAI-1 may play an important role in coronary aneurysm formation.