Effects of granulocyte colony-stimulating factor on bacterial translocation due to burn wound sepsis

The presence of certain defects in both cellular and humoral immunity after thermal injury has been established. Likewise, the translocation of enteric bacteria to the mesenteric lymph nodes and to distant organs has also been observed following serious thermal injury. The effects of granulocyte colony-stimulating factor (G-CSF) on bacterial translocation, the small bowel mucosa, and cecal bacterial content were investigated in a rat model of burn wound sepsis in which albino Wistar rats were scalded over 30% of their bodies, after which the lesions were infected by 1×10⁸ colony-forming units (cfu)Pseudomonas aeruginosa. The control group was treated with 5% dextrose solution subcutaneously starting 2 days preburn, while the treatment group received 100μg/kg human G-CSF subcutaneously. On the 4th day post burn all animals were killed to examine the bowel and culture of the mesenteric lymph nodes (MLN), livers, and spleens. No significant differences were observed between the groups regarding the cecal bacterial content and small bowel; however, a difference was seen in the ratio of translocation in the MLN liver and spleen and quantitative MLN cultures. Based on these findings, G-CSF was thus found to be significantly effective in reducing bacterial translocation due to burn wound sepsis.     

Examination of the dermal lymphatics in psoriasis⋆

In recent years, research on the aetiology of psoriasis has focused on immune aetiopathogenesis. However, in the last few years, research on the immunoloogical changes in psoriasis has failed to mention the lymphatics. Also, studies emphasizing the importance of the dermal lymphatics have neglected the lymphatic changes seen in psoriasis. Therefore, we decided to put this matter back on the agenda. Skin biopsies from 20 patients with psoriasis vulgaris were examined lymphatically by light microscopy using the orcein stain. We found a considerable increase in both number and dilatation in the lymphatics of psoriatic plaques, compared with both the clinically uninvolved skin of the psoriatic patients and also the skin of the control group.     

Long-term modulatory effect of Mycobacterium vaccae treatment on histopathologic changes in a murine model of asthma.

BACKGROUND: Mycobacteria are being investigated for modulation of inflammation in asthma and atopic disorders by eliciting particularly strong protective TH1 immune responses. OBJECTIVE: To investigate the long-term effects of intratracheally administered Mycobacterium vaccae on an experimental murine model of asthma. METHODS: BALB/c mice were placed in 4 groups: long-term M. vaccae, M. vaccae, asthma, and control groups. All groups but controls were sensitized intraperitoneally and challenged intratracheally with ovalbumin. The long-term M. vaccae and M. vaccae groups were treated with M. vaccae intratracheally simultaneously during challenges. Finally, mice in the long-term M. vaccae group were rechallenged with ovalbumin nebulization 24 days later. Evaluations of lung histopathologic findings and serum cytokine levels were performed. RESULTS: Comparison of the long-term M. vaccae group with the asthma model group revealed that the number of hyperplasic goblet cells in small and large airways (small airway: P < .05; large airways: P < .01) and thickness of basement membrane in large airways were significantly less in the long-term M. vaccae group. Furthermore, numbers of hyperplasic goblet cells in small airways (P < .05) and basement membrane in the large airway (P < .05), as well as inflammation in small airways (P < .01), were significantly less in the M. vaccae group when compared with the asthma model group. Interferon-gamma secretion from splenocytes of the M. vaccae group was significantly higher than the asthma model and long-term M. vaccae groups. CONCLUSION: Intratracheal administration of M. vaccae exerted a long-lasting ameliorating effect on airway histopathologic features of a murine asthma model.     

Dental technician's pneumoconiosis: mineralogical analysis of two cases

Pneumoconiosis was diagnosed by open lung biopsy in two dental technicians who had interstitial lung disease. Mineralogical analysis was performed to investigate the origin of the dust that had been inhaled. A marked accumulation of silicon and phosphorus was found in both cases. The hard metals chromium and cobalt were also found. Dental technician's pneumoconiosis is a complex pneumoconiosis in which such dust and hard metals may play a role.     

Immune Dysregulation,Polyendocrinopathy, Enteropathy,X-linked Syndrome in Two Siblings: Same Mutation But Different Clinical Manifestations at Onset

Immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome is an early onset systemic autoimmune genetic disorder caused by mutation of the forkhead box protein 3 (FOXP3) gene. Enteropathy, endocrinopathy and skin manifestations are considered the classic triad of IPEX syndrome. However, patients with IPEX syndrome display a variety of phenotypes including life threatening multi-organ autoimmunity. Here, we present the case of two siblings with IPEX syndrome with the same hemizygous mutation, but with different types of symptomology at onset of the disease.     

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.