ABSTRACT
Fungal infections caused by Paecilomyces species are very rare and occur in adult patients with impaired host defences or following foreign body implants. They are found worldwide in soil and decaying vegetation. We describe a case of an 8 year old child who came with complaints of left sided nasal obstruction and discharge, telecanthus, diplopia and epiphora. On examination and investigation he had pansinusitis caused by P. lilacinus. An endoscopic sinus surgery was done and the patient was on oral Itraconazole for 6 months. To our knowledge, this is the first case reported in the paediatric age group.
Subject(s)
Mycoses/diagnosis , Paecilomyces/isolation & purification , Paranasal Sinuses/microbiology , Sinusitis/microbiology , Antifungal Agents/administration & dosage , Child , Combined Modality Therapy , Endoscopy/methods , Follow-Up Studies , Humans , Immunocompetence , Itraconazole/administration & dosage , Male , Mycoses/therapy , Sinusitis/diagnosis , Sinusitis/therapyABSTRACT
We previously demonstrated that expression of IGF-II modulates the routing of cathepsin D in MCF-7 cells. In our present study, we transfected antisense IGF-II into IGF-II secreting MCF-7 cells to test the hypothesis that blocking IGF-II may reduce the secretion of cathepsin D in breast cancer cells. The concentration of IGF-II in media conditioned by the antisense clone was reduced to almost undetectable levels. Likewise, Northern blotting analysis revealed that IGF-II mRNA was nearly undetectable in the antisense transfected cells. Metabolic labeling experiments performed with 10 mM mannose 6-phosphate present in the medium to block reuptake of lysosomal enzymes demonstrated that cathepsin D secretion was dramatically reduced. Similarly, a significant reduction in cathepsin D was observed when conditioned media and cell extracts were examined by Western blotting after a 48 h incubation. No changes in cathepsin D mRNA in antisense cells were detected by Northern blot analysis. We conclude that endogenous IGF-II may modulate the routing of cathepsin D by interfering with receptor trafficking in MCF-7 cells, and that this modulation is reversible. Abnormally high levels of IGF-II may alter this homeostasis, conferring on breast cancer cells an advantageous mechanism that promotes rapid growth, and may facilitate metastasis.
