Long-term use of Le Fort I osteotomy for the management of nasopharyngeal rhinosporidiosis: A case series.

Rhinosporidiosis is a rare, chronic, granulomatous infection of the mucous membranes that mainly involves the nose and nasopharynx; it occasionally involves the pharynx, conjunctiva, larynx, trachea and, rarely, the skin. The characteristic clinical features of this disease include the formation of painless polyps in the nasal mucosa or the nasopharynx that bleed easily on touch. At our center, excision of the lesion with a Le Fort I osteotomy is carried out in patients (1) in whom two or more previous attempts at excision of biopsy-proven rhinosporidiosis arising from the nasal mucosa was carried out or (2) in whom the rhinosporidiosis arises from the nasophayrngeal mucosa and/or extranasal sites. In this article we retrospectively present 7 cases in which, according to our inclusion criteria, complete excision of the lesion was carried out with a Le Fort I osteotomy. Excellent visualization of the entire maxillary and ethmoidal air cells after the down-fracture of the maxilla helped in the total removal of the lesions. Most of these lesions had multiple points of origin through the nasal, maxillary, and ethmoidal mucosa; the excellent visualization enabled direct cauterization of all these points of origin. The mean follow-up period was 7.96 years, and all patients were disease-free by the time the study was prepared. This article presents details of the treatment protocol and technique followed at our center for the treatment of nasopharyngeal rhinosporidiosis and the details of long-term follow-up. Through this study we hope to prove the efficacy of Le Fort I osteotomy in the definitive management of nasopharyngeal rhinosporidiosis.

Assessment of potential health risk of fluoride consumption through rice, pulses, and vegetables in addition to consumption of fluoride-contaminated drinking water of West Bengal, India.

A study was conducted in fluoride-affected Bankura and Purulia districts of West Bengal to assess the potential health risk from fluoride exposure among children, teenagers, and adults due to consumption of rice, pulses, and vegetables in addition to drinking water and incidental ingestion of soil by children. Higher mean fluoride contents (13-63 mg/kg dry weight) were observed in radish, carrot, onion bulb, brinjal, potato tuber, cauliflower, cabbage, coriander, and pigeon pea. The combined influence of rice, pulses, and vegetables to cumulative estimated daily intake (EDI) of fluoride for the studied population was found to be 9.5-16%. Results also showed that intake of ivy gourd, broad beans, rice, turnip, fenugreek leaves, mustard, spinach, and amaranth grown in the study area is safe at least for time being. The cumulative EDI values of fluoride (0.06-0.19 mg/kg-day) among different age group of people of the study area were evaluated to be ~104 times higher than those living in the control area; the values for children (0.19 and 0.52 mg/kg-day for CTE and RME scenarios, respectively) were also greater than the "Tolerable Upper Intake Level" value of fluoride. The estimated hazard index (HI) for children (3.2 and 8.7 for CTE and RME scenarios, respectively) living in the two affected districts reveals that they are at high risk of developing dental fluorosis due to the consumption of fluoride-contaminated rice, pulses, and vegetables grown in the study area in addition to the consumption of contaminated drinking water.

Cytologic diagnosis of blastocystis hominis in peritoneal fluid: a case report.

BACKGROUND: Blastocystis hominis is the most common parasite identified in s worldwide. Although it is commonly identified in stool preparations, unusual to encounter B hominis in abdominal fluid. CASE: A 46-year-old woman presented with the clinical impression of acute peritonitis. The initial radiologic evaluation showed free air in the abdominal cavity and an abdominal mass. Abdominal fluid submitted for cytologic examination was diagnostic of acute inflammation with mixed bacteria and abundant cystlike forms of B hominis. The patient underwent an exploratory laparotomy that revealed a poorly differentiated adenocarcinoma involving her bowel and peritoneum. CONCLUSION: The present case highlights the unusual identification ofextraintestinal forms of B hominis in a peritoneal fluid sample from a patient with invasive, poorly differentiated adenocarcinoma and associated bowel perforation.

Disease-specific gene expression profiling in multiple models of lung disease.

RATIONALE: Microarray technology is widely employed for studying the molecular mechanisms underlying complex diseases. However, analyses of individual diseases or models of diseases frequently yield extensive lists of differentially expressed genes with uncertain relationships to disease pathogenesis. OBJECTIVES: To compare gene expression changes in a heterogeneous set of lung disease models in order to identify common gene expression changes seen in diverse forms of lung pathology, as well as relatively small subsets of genes likely to be involved in specific pathophysiological processes. METHODS: We profiled lung gene expression in 12 mouse models of infection, allergy, and lung injury. A linear model was used to estimate transcript expression changes for each model, and hierarchical clustering was used to compare expression patterns between models. Selected expression changes were verified by quantitative polymerase chain reaction. MEASUREMENTS AND MAIN RESULTS: A total of 24 transcripts, including many involved in inflammation and immune activation, were differentially expressed in a substantial majority (9 or more) of the models. Expression patterns distinguished three groups of models: (1) bacterial infection (n = 5), with changes in 89 transcripts, including many related to nuclear factor-kappaB signaling, cytokines, chemokines, and their receptors; (2) bleomycin-induced diseases (n = 2), with changes in 53 transcripts, including many related to matrix remodeling and Wnt signaling; and (3) T helper cell type 2 (allergic) inflammation (n = 5), with changes in 26 transcripts, including many encoding epithelial secreted molecules, ion channels, and transporters. CONCLUSIONS: This multimodel dataset highlights novel genes likely involved in various pathophysiological processes and will be a valuable resource for the investigation of molecular mechanisms underlying lung disease pathogenesis.

Abnormal alveolar development associated with elevated adenine nucleosides.

Adenosine signaling has been characterized in various physiologic systems, but little is known about the role of adenosine signaling in lung development. Alveogenesis and microvascular maturation are the final stages in lung development in mammals. Alveogenesis in the mouse begins on Postnatal Day 5, when the process of secondary septation plays a pivotal role in the expansion of the alveolar sacs and microvascular maturation. Adenosine deaminase null mice (ADA-/-) exhibit abnormalities in alveogenesis in association with elevated lung adenosine levels. Large-scale gene expression analysis of ADA-/- lungs using oligonucleotide-based microarrays revealed novel relationships between gene expression patterns and elevated lung adenosine during the stages of alveolar maturation. Genes regulating apoptosis, proliferation, and vascular development were shown to be altered, and decreased cell proliferation in association with increased alveolar type II cell apoptosis was shown to contribute to abnormal secondary septation in these mice. ADA enzyme therapy allowed for normal patterns of apoptosis, proliferation, and alveolar development in association with prevention of adenosine elevations. These findings were correlated with the presence of adenosine receptors in the developing lung, suggesting the involvement of receptor signaling. These studies provide evidence that elevated lung adenosine can lead to abnormal alveogenesis by disrupting patterns of cell proliferation and apoptosis.

Adenosine mediates IL-13-induced inflammation and remodeling in the lung and interacts in an IL-13-adenosine amplification pathway.

IL-13 is an important mediator of inflammation and remodeling. We hypothesized that adenosine accumulation, alterations in adenosine receptors, and adenosine-IL-13 autoinduction are critical events in IL-13-induced pathologies. To test this, we characterized the effects of IL-13 overexpression on the levels of adenosine, adenosine deaminase (ADA) activity, and adenosine receptors in the murine lung. We also determined whether adenosine induced IL-13 in lungs from ADA-null mice. IL-13 induced an inflammatory and remodeling response that caused respiratory failure and death. During this response, IL-13 caused a progressive increase in adenosine accumulation, inhibited ADA activity and mRNA accumulation, and augmented the expression of the A1, A2B, and A3 but not the A2A adenosine receptors. ADA enzyme therapy diminished the IL-13-induced increase in adenosine, inhibited IL-13-induced inflammation, chemokine elaboration, fibrosis, and alveolar destruction, and prolonged the survival of IL-13-transgenic animals. In addition, IL-13 was strongly induced by adenosine in ADA-null mice. These findings demonstrate that adenosine and adenosine signaling contribute to and influence the severity of IL-13-induced tissue responses. They also demonstrate that IL-13 and adenosine stimulate one another in an amplification pathway that may contribute to the nature, severity, progression, and/or chronicity of IL-13 and/or Th2-mediated disorders.

Gene expression profiling in inflammatory airway disease associated with elevated adenosine.

Adenosine has been implicated as a modulator of inflammatory processes central to asthma. However, the molecular mechanisms involved are poorly understood. We used Atlas mouse cDNA arrays to analyze differential gene expression in association with lung inflammation resulting from elevated adenosine in adenosine deaminase (ADA)-deficient mice. We report that of the 1,176 genes on the array, the expression patterns of 280 genes were consistently altered. Of these genes, the steady-state levels of 93 genes were upregulated and 29 were downregulated. We also show that lowering adenosine levels with ADA enzyme therapy has striking effects on gene expression that may be associated with resolution of pulmonary eosinophilia. In addition, we confirmed the nucleic acid and protein expression of vascular endothelial growth factor and monocyte chemoattractant protein-3, two candidate genes that may be regulated by adenosine. In conclusion, high-throughput profiling of gene expression by cDNA array hybridization has provided an overview of critical regulatory genes involved in airway inflammation in ADA-deficient mice. These mice will serve as a useful in vivo model for characterizing molecular mechanisms of adenosine-mediated lung damage.