In vitro assessment of the effectiveness of chlorhexidine gel and calcium hydroxide paste with chlorhexidine against Enterococcus faecalis and Candida albicans.

OBJECTIVE: The purpose of this study was to compare the effectiveness of various medicaments, including Ca(OH)2/2% chlorhexidine, 2% chlorhexidine gel, and Ca(OH)2 alone, against Enterococcus faecalis and Candid albicans in vitro. STUDY DESIGN: Eighty extracted single-rooted human maxillary teeth were used. After removing the crown, each root was instrumented up to size 50 by using a conventional technique. The root canal was irrigated with ethylenediamine tetra-acetic acid (EDTA) solution to remove smear layer. Then, roots were infected with E faecalis and C albicans. Subsequently, the roots were divided into 4 treatment groups: group 1 was treated with calcium powder hydroxide in distilled water, group 2 was treated with calcium hydroxide powder in 2% chlorhexidine, group 3 was treated with 2% chlorhexidine gel, and group 4 was treated with 0.9% sterile saline serving as negative control. Microbial samples were taken after 7, 15, and 30 days. After incubation, dentine chips were obtained form each root canal and examined microbiologically. The microbiological samples were plated to count colony-forming units in per milligram of dentin. RESULTS: The results showed that the 2% chlorhexidine gel was significantly more effective than calcium hydroxide with 2% chlorhexidine, calcium hydroxide, and control saline solution (P < .05). CONCLUSION: Under the conditions of this study, 2% chlorhexidine gel is effective in the elimination of E faecalis and C albicans from the root canal system. However, to support this in vitro observation, further in vivo studies are needed.     

Exploiting the Annexin A1 pathway for the development of novel anti-inflammatory therapeutics

The appreciation that the inflammatory reaction does not ‘spontaneously’ finish, but rather that inflammatory resolution is an active phenomenon brought about by endogenous anti-inflammatory agonists opens multiple opportunities for a reassessment of the complexity of inflammation and its main mediators. This review dwells on one of these pathways, the one centred around the glucocorticoid-regulated protein Annexin A1 and its G protein-coupled receptor. In recent years, much of the knowledge detailing the processes by which Annexin A1 expresses its anti-inflammatory role on innate immunity has been produced. Moreover, the generation of the Annexin A1 null mouse colony has provided important proof-of-concept experiments demonstrating the inhibitory properties of this mediator in the context of inflammatory and/or tissue-injury models. Therefore, Annexin A1 acts as a pivotal homeostatic mediator, where if absent, inflammation would overshoot and be prolonged. This new understanding scientific information could guide us onto the exploitation of the biological properties of Annexin A1 and its receptor to instigate novel drug discovery programmes for anti-inflammatory therapeutics. This line of research relies on the assumption that anti-inflammatory drugs designed upon endogenous anti-inflammatory mediators would be burdened by a lower degree of secondary effects as these agonists would be mimicking specific pathways activated in our body for safe disposal of inflammation. We believe that the next few years will produce examples of such new drugs and the validity of this speculation could then be assessed.This article is part of a themed issue on Mediators and Receptors in the Resolution of Inflammation. To view this issue visit http://www3.interscience.wiley.com/journal/121548564/issueyear?year=2009     

Neutralising antibodies after streptokinase treatment for myocardial infarction: a persisting puzzle.

OBJECTIVE--To determine the development of titres of streptokinase (SK) neutralising antibodies after a single dose of SK, to establish when titres decrease to levels at which a second dose might be effective. DESIGN--Analyses of blood samples taken from patients at intervals after SK administration. SETTING--Australian public hospital. PATIENTS--104 patients with acute myocardial infarction who were treated with SK and 27 controls who were not. OUTCOME MEASURE--SK neutralising antibodies were measured once in each of the 27 controls and on 166 occasions in the 104 treated patients. RESULTS--Titres of SK neutralising antibodies rose after SK administration but returned to control levels by 2 years. CONCLUSIONS--SK might be effective again as a thrombolytic agent as early as 2 years after a single dose. These results are at variance with most previously published data and the reasons for this are not clear. Data evaluating patency rates after standard doses of streptokinase in patients with increased titres of neutralising antibodies are necessary before re-exposure to streptokinase can be recommended.     

Genetic ablation of the fpr1 gene confers protection from smoking-induced lung emphysema in mice

Cigarette smoke (CS) is the main causative factor of chronic obstructive pulmonary disease (COPD). Current research supports the concept that airway inflammation is central to the development and progression of the disease. Studies have demonstrated that neutrophils are increased in COPD lungs and that neutrophil-associated products correlate with the development and severity of COPD. The peptide FMLP is an active component of CS. FMLP interacts on the neutrophil and macrophage membranes with a high-affinity receptor subtype (FPR1) and with a low-affinity subtype FPRL1, promoting a chemotactic response, superoxide anion production, and degranulation. Bacterial colonization of the lower respiratory tract and lung cell damage may represent further sources of formyl peptides in patients with COPD. We investigated the role of FPR in a mouse model on lung inflammation and emphysema induced by CS. Here, we report the novel observation that genetic ablation of the FPR1 gene (Fpr1) confers protection from smoking-induced lung emphysema in mice. Compared with wild-type mice, Fpr1 knockout mice displayed marked decreases in the lung migration of neutrophils and macrophages after CS exposure. Upon transgenic approach, the changes in cell numbers were accompanied by marked modulation of the expression of genes implicated in the inflammatory response. Administration of the FPR1 antagonist cyclosporine H to wild-type mice attenuated the acute inflammatory response evoked by CS. These findings may have clinical significance because current smokers and subjects with emphysema showed increased FPR expression in bronchoalveolar fluids and on peripheral neutrophils. Modulating the FPR1 signal should be explored as a potential new therapy.     

Synchronous colonic adenocarcinoma and renal oncocytoma: a case report and literature review

We present the case of a patient with an adenocarcinoma of the colon associated with an oncocytoma of the kidney. A left colonic cancer was diagnosed at colonoscopy and an incidental finding of a left renal mass was noted, with a staging computerized tomography scan. Following a left hemicolectomy and a left nephrectomy, the pathological report confirmed the presence of a colonic adenocarcinoma and revealed that the left renal mass was an oncocytoma. This case report reviews the management decisions associated with incidental renal masses as well as the treatment of synchronous neoplasia.