Nitric oxide and tumour necrosis factor alpha in the process of pseudoexfoliation glaucoma

AIMTo establish the role of nitric oxide (NO), ascorbic acid and tumour necrosis factor-α (TNF-α) in the pathogenesis of pseudoexfoliation glaucoma (XFG).METHODSOur study included 120 patients who were referred for cataract surgery. All patients were divided into four groups according to clinical findings: XFG, early and late pseudoexfoliation syndrome (XFS), and cataract (without pseudoexfoliation). Serum and aqueous humour levels of the ascorbic acid, NO and TNF-α were measured. The concentrations of the ascorbic acid and NO were measured by an appropriate spectrophotometric method. Enzyme-linked immunosorbent assay (ELISA) was used to determine TNF-α level.RESULTSAqueous humour concentration of ascorbic acid was significantly lower in patients with late XFS (0.61±0.11 mmol/L) and XFG (0.48±0.15 mmol/L) compared to patients with early XFS (0.9±0.15 mmol/L) and cataract (1.16±0.22 mmol/L), while there was no difference in serum concentration in all examined groups. Aqueous humour concentration of NO was significantly higher in patients with XFG (77.7±11.4 µmol/L) compared to patients with early XFS (50.27±9.34 µmol/L) and cataract (49.77±7.1 µmol/L), while serum concentration was increased in the early stage of XFS (73.26±8.29 µmol/L). Aqueous humour level of proinflammatory cytokine TNF-α was increased in patients with XFS (early 460.04±18.32 pg/mL; late 502.42±53.23 pg/mL) and XFG (510.34±43.07 pg/mL), while there was no difference in serum level in all examined groups of patients.CONCLUSIONReduced ascorbic acid and elevated NO and inflammation related cytokine TNF-α level in aqueous humour of the patients with developed XFG suggest that oxidative stress induces local inflammation.

Axonal growth inhibitors and their receptors in spinal cord injury:from biology to clinical translation

Axonal growth inhibitors are released during traumatic injuries to the adult mammalian central nervous system, including after spinal cord injury. These molecules accumulate at the injury site and form a highly inhibitory environment for axonal regeneration. Among these inhibitory molecules, myelinassociated inhibitors, including neurite outgrowth inhibitor A, oligodendrocyte myelin glycoprotein, myelin-associated glycoprotein, chondroitin sulfate proteoglycans and repulsive guidance molecule A are of particular importance. Due to their inhibitory nature, they represent exciting molecular targets to study axonal inhibition and regeneration after central injuries. These molecules are mainly produced by neurons, oligodendrocytes, and astrocytes within the scar and in its immediate vicinity. They exert their effects by binding to specific receptors, localized in the membranes of neurons. Receptors for these inhibitory cues include Nogo receptor 1, leucine-rich repeat, and Ig domain containing 1 and p75 neurotrophin receptor/tumor necrosis factor receptor superfamily member 19(that form a receptor complex that binds all myelin-associated inhibitors), and also paired immunoglobulin-like receptor B. Chondroitin sulfate proteoglycans and repulsive guidance molecule A bind to Nogo receptor 1, Nogo receptor 3, receptor protein tyrosine phosphatase σ and leucocyte common antigen related phosphatase, and neogenin, respectively. Once activated, these receptors initiate downstream signaling pathways, the most common amongst them being the Rho A/ROCK signaling pathway. These signaling cascades result in actin depolymerization, neurite outgrowth inhibition, and failure to regenerate after spinal cord injury. Currently, there are no approved pharmacological treatments to overcome spinal cord injuries other than physical rehabilitation and management of the array of symptoms brought on by spinal cord injuries. However, several novel therapies aiming to modulate these inhibitory proteins and/or their receptors are under investigation in ongoing clinical trials. Investigation has also been demonstrating that combinatorial therapies of growth inhibitors with other therapies, such as growth factors or stem-cell therapies, produce stronger results and their potential application in the clinics opens new venues in spinal cord injury treatment.

NHL患者血清TNF-α、LDH水平及与血沉的相关性研究

目的探讨非霍奇金淋巴瘤(NHL)患者血清TNF-αs、TNFRI、LDH、球蛋白、白蛋白水平及血沉的变化和意义。方法严格选取25例初诊NHL患者和26例正常人为研究对象,采用ELISA法测定血清TNF-α及sTNFRI水平,采用OLYMPUS 600血生化仪测定血清LDH、球蛋白及白蛋白水平,采用魏氏法测定血沉。结果NHL患者血清TNF-αs、TNFRI、LDH、球蛋白水平及血沉值均高于对照组,且血清TNF-αs、TNFRI、LDH、球蛋白水平与血沉值均具有相关性;两组血清白蛋白水平差异无显著性,NHL患者血清白蛋白水平血沉值成负相关。结论NHL患者TNF-α、sTN-FRI、LDH、球蛋白、白蛋白改变与血沉增快均有关系,其中TNF-α、白蛋白及LDH作用较大。

Elevated levels of inflammatory cytokines and high-sensitivity C-reactive protein in periodontitis patients in Kosovo: A pilot study

The following article has been retracted due to the investigation of complaints received against it. The Editorial Board found that the same contents have been published in another journal at the same time. The scientific community takes a very strong view on this matter, and the Open Journal of Stomatology treats all unethical behavior such as plagiarism seriously. This paper published in Vol.3 No.1 32-38, 2013 has been removed from this site. Title: Elevated levels of inflammatory cytokines and high-sensitivity C-reactive protein in periodontitis patients in Kosovo: A pilot study Authors: Zana Sllamniku-Dalipi, Hasan Mehmeti, Fatmir Dragidella, Ferit Kocani, Metush Disha, Kastriot Meqa, Luljeta Begolli, Gramos

The role of NF-κB activation in lipopolysacchavide induced keratitis in rats

Background Nuclear factor-kappa B （NF-kB） is elevated in regulating transcription of many cytokines and inflammatory mediators. The purpose of this study was to investigate the activation and the significance NF-KB in lipopolysaccharide （LPS） induced keratitis.Methods LPS induced keratitis model was based on Wistar rats. At 0. 5, 1, 3, 6, 12, 24 or 72 hours after LPS treatment, the rat corneas were observed with a slit lamp microscope, then the rats were sacrificed and their corneas were excised for routine histological analysis. The expression of NF-kB was detected with immunohistochemical staining. The change identified by reverse transcriptase polymerase of tumour necrosis factors-α （TNF-α） mRNA expression was chain reaction （RT-PCR）. Results Histological findings demonstrated that LPS treated corneas showed significant changes in corneal structure. Corneal edema, pronounced inflammatory cells infiltration and inordinate collagen fibres were observed. Immunohistochemical results showed that the expression of NF-kB and its activation obviously increased after LPS treatment compared with the normal group and control group. Positive cells could be observed at 0. 5 hour and peak expression of NF-kB was observed between 3 hours and 12 hours after infection, but returned to or approached normal level by 72 hours. RT-PCR showed that the level of TNF-α mRNA began to increase 0. 5 hour after LPS treatment, peaked at 6 hours and then subsided by 72 hours. NF-kB had a positive correlation with the expression of TNF-α mRNA （r=0. 964, P 〈 0. 01 ） , both NF-kB and TNF-α had a strong positive correlation with the degree of inflammatory response in LPS treated corneas （ r=0. 929, P 〈 0. 01 ; r=0. 587, P 〈 0.05, respectively）. Conclusions The activation of NF-kB was increased keratitis by promoting overexpression of TNF-α mRNA. LPS-associated keratitis in rats. in LPS treated corneas and was elevated in LPS induced NF-kB may play an important role in the pathogenesis ofLPS-associated keratitis in rats.