The Lectin Pathway of Complement Activation Is a Critical Component of the Innate Immune Response to Pneumococcal Infection

The complement system plays a key role in host defense against pneumococcal infection. Three different pathways, the classical, alternative and lectin pathways, mediate complement activation. While there is limited information available on the roles of the classical and the alternative activation pathways of complement in fighting streptococcal infection, little is known about the role of the lectin pathway, mainly due to the lack of appropriate experimental models of lectin pathway deficiency. We have recently established a mouse strain deficient of the lectin pathway effector enzyme mannan-binding lectin associated serine protease-2 (MASP-2) and shown that this mouse strain is unable to form the lectin pathway specific C3 and C5 convertases. Here we report that MASP-2 deficient mice (which can still activate complement via the classical pathway and the alternative pathway) are highly susceptible to pneumococcal infection and fail to opsonize Streptococcus pneumoniae in the none-immune host. This defect in complement opsonisation severely compromises pathogen clearance in the lectin pathway deficient host. Using sera from mice and humans with defined complement deficiencies, we demonstrate that mouse ficolin A, human L-ficolin, and collectin 11 in both species, but not mannan-binding lectin (MBL), are the pattern recognition molecules that drive lectin pathway activation on the surface of S. pneumoniae. We further show that pneumococcal opsonisation via the lectin pathway can proceed in the absence of C4. This study corroborates the essential function of MASP-2 in the lectin pathway and highlights the importance of MBL-independent lectin pathway activation in the host defense against pneumococci.     

Regulating and monitoring marine finfish aquaculture in Turkey

This paper describes marine aquaculture production and the regulation thereof in Turkey. Dominated by the cage farming of sea bass (Dicentrarchus labrax) and sea bream (Sparus aurata), shellfish farming is insignificant. Finfish farmers must obtain permits from the Ministry of Agriculture and Rural Affairs (MARA) as the main authority responsible for regulating marine finfish aquaculture. In addition, the Ministry of Environment and Forestry (MEF) controls the compatibility of interactions with the environment while the provincial governments issue permits for marine public property use and organize the leasing procedures. Finfish farming activities are controlled by a number of specific laws and regulations administered mainly through the MARA and the MEF. This article provides a review of the development and present status of the licensing, regulating and monitoring procedures for finfish aquaculture in Turkey. The notable expansion of the finfish aquaculture sector in recent years and the problems created in relation to the current relevant legislation and applications are presented and discussed.     

The effects of exogenous polyamines on some biochemical changes during drought stress in Ctenanthe setosa (Rosc.) Eichler

Morphological and biochemical changes in plant cells are known as important events for adaptation to stress. In this study, in Ctenanthe setosa leaves to which polyamines were applied during drought stress, changes in the activity of peroxidase, reducing sugar, proline and soluble protein levels were investigated. The three common polyamines, putrescine, spermidine and spermine were exogenously treated through the leaves. The polyamines were sprayed onto the leaves at 5 x 10(-5) M. In the leaves to which polyamines were applied the peroxidase activity decreased, soluble protein increased. Also, it was determined that putrescine and spermidine caused an increase in the amount of proline and in reducing sugar. However, increase was not observed in the leaves to which spermine was applied. In addition, we observed an increase in the activity of peroxidase, proline and reducing sugar levels, and a decrease in soluble protein level in the control ones and the leaves to which polyamines were applied during drought stress. As a result, the effect of polyamine on leaf rolling may be explained through the contribution to osmotic adjustment of the increase in proline, reducing sugar and soluble protein contents.     

Neuroprotective Effect of Etomidate in the Central Nervous System of Streptozotocin-Induced Diabetic Rats

It is well known that hyperglycaemia due to diabetes mellitus leads to oxidative stress in the central nervous system. Oxidative stress plays important role in the pathogenesis of neurodegenerative changes. In the present study we investigated the possible neuroprotective effect of etomidate against streptozotocin-induced (STZ-induced) hyperglycaemia in the rat brain and spinal cord. A total of 40 rats were used in this study. Rats were divided into four groups: sham-control, diabetic, diabetic-etomidate treated and vehicle for etomidate treatment group. Diabetes mellitus was induced by a single injection of streptozotocin (60 mg/kg body weight). Three days after streptoztocin injection, etomidate (2 mg/kg) was injected intraperitoneally for etomidate group and lipid emulsion (10%) for vehicle group was injected with corresponding amount intraperitoneally every day for 6 weeks. Six weeks after streptozotocin injection, seven rats from each group were killed and brain, brain stem and cervical spinal cord were removed. The hippocampus, cortex, cerebellum, brain stem and spinal cord were dissected for the biochemical analysis (the level of malondialdehyde [MDA], total nitrite, reduced glutathione [GSH], and xanthine oxidase [XO] activity). STZ-induced diabetes resulted in significantly elevation of MDA, XO and nitrite levels in the hippocampus, cortex, cerebellum, brain stem and spinal cord of the rats (P < 0.05) while etomidate treatment provided significantly lower values (P < 0.05). This study demonstrated that etomidate have neuroprotective effect on the neuronal tissue against the diabetic oxidative damage.     

Development of Malignant Ventricular Arrhythmias in a Young Male with WPW Pattern

In Wolff-Parkinson-White Syndrome (WPW), presence of accessory pathways causes various tachyarrhythmias that lead to different symptoms and clinical conditions in patients. Atrial fibrillation is observed in about 20-30% of this group of patients. Life threatening malignant ventricular arrhythmias and sudden cardiac deaths are observed in patients having rapid conduction in accessory pathways and short antegrade refractory periods (<250 msn). We present a WPW syndrome case that presented to the emergency service with narrow QRS tachycardia and later developed malignant ventricular arrhythmia.     

Leaf rolling effects on lipid and fatty acid composition in Ctenanthe setosa (Marantaceae) subjected to water-deficit stress

Vegetatively propagated Ctenanthe setosa (Rosc.) Eichler (Marantaceae) plants were grown in plastic pots under laboratory irrigation and water deficit conditions. One set of plants was submitted to water irrigation regularly and another set of plants was submitted to water deficit conditions. After a 28 d water deficit stress, the leaves started to roll. Approximately after 33–35 d, the leaves were tightly rolled. Water stress significantly increased the dry weight of rolled leaves. After the 35 d period of water deficit the open (non-stressed) and rolled (stressed, water deficit) leaves were harvested for lipid content and class compositional analysis. The fatty acids consistently identified in phospholipids and glycolipids as well as in total leaf lipid were 16:0, 18:0, 18:1, 18:2 and 18:3. The 16:0, 18:3 and 18:1 acids in control plant and 18:2, 16:0 and 18:3 acids in rolled leaves were determined as the major fatty acids. While the percentage composition of 16:0, 18:1 and 18:3 acids decreased in rolled leaves, the level of 18:2 acid increased. However, the percentage composition of unsaturation in phospholipid (71%) and glycolipid (80.4%) fractions in rolled leaves were found higher than in control leaves. The results show that the degree of unsaturation in phospholipid, glycolipid and total lipid was significantly altered during leaf rolling. The increase in unsaturation degree may regulate membrane permeability and thus adapt the leaves to water stress in the drought environment.     

Oxidative and nitrative stress markers in glaucoma

Glaucoma is a progressive optic neuropathy and is the leading cause of blindness in the United States and other industrialized countries. Elevated pressure in the eye is a risk factor for glaucoma and indeed experimental studies of induced pressure elevation in nonhuman primate's results in typical glaucomatous optic nerve damage. However, normal intraocular pressure can also lead to loss of vision in glaucoma. Although the initiating causes leading to glaucoma are unknown, oxidative and nitrative stress appears to play a role in the progressive neuronal death that is characteristic of glaucomatous optic nerve damage. Increased markers of oxidative stress that have been reported in glaucoma include protein nitrotyrosine, carbonyls in proteins, lipid oxidation products and oxidized DNA bases. Studies have also highlighted the role of nitric oxide in glaucoma by reporting the presence of inducible nitric oxide synthase in the iris-ciliary body, retina and in the glaucomatous optic nerve head of experimental rat models. This review discusses the role of reactive oxygen and nitrogen species in the pathogenesis of glaucoma and examines the relevance of antioxidants in neurodegeneration associated with the disease. It is concluded that oxidative and nitrative stress have a pathogenic role in glaucoma.     

Antioxidative role of melatonin in organophosphate toxicity in rats

Previous studies revealed that oxidative stress could be an important component of the mechanism of organophosphate (OP) compound toxicity. The aim of the present study was to investigate both prophylactic and therapeutic effects of melatonin against fenthion-induced oxidative stress in rats. Therefore, we determined the changes in the levels of reduced glutathione (GSH) and malondialdehyde (MDA) in the whole blood, brain, pectoral muscle, liver, lung, heart, kidney, pancreas, and jejunum. Also, the changes in the levels of serum nitrite and nitrate, ascorbic acid, retinal, b-carotene, and ceruloplasmin were measured. In addition, activities of enzymatic antioxidants superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) in erythrocyte of normal and experimental animals were measured. It was found that fenthion administration increased the levels of MDA in all tissues and decreased or increased the levels of GSH in some tissues. In comparison to nitrate, nitrite and ascorbic acid levels in the serum of experimental groups, there was no significant difference between groups. However, fenthion toxicity led to decrease in retinol and β-carotene levels; melatonin administration significantly prevented this decrease. Serum ceruloplasmin level was increased due to fenthion administration, but prophylactic and therapeutic melatonin administration inhibited the increase in ceruloplasmin level of serum. There was no significant change in SOD levels in melatonin-administered groups. Melatonin modulates the fenthion-induced changes in the activities of GPx and CAT. In conclusion, the results of the current study revealed that OP toxicity, induced by fenthion, activated oxidant systems in all antioxidant systems in some tissues. Melatonin administration led to a marked increase in antioxidant activity and inhibited lipid peroxidation in most of tissues.