The leaking defects in the temporal bone can be classified into two groups based on etiology: Secondary defects, which occur with trauma, surgery (iatrogenic), or neoplasms invading the skull base; and the less common primary (spontaneous) forms, in which two distinct populations of patients can be described: first, children with congenital malformations of the temporal bone, and, second, adults with no known primary or secondary temporal bone disease. In adults with spontaneous leakage, the location of the defect is most commonly found to be the floor of middle fossa (tegmen tympani or tegmen mastoidian). Increased intracranial pressure may be the predisposing background, and in the normal-pressure group, remnants of the arachnoid granulations may play the causative role. On the other hand, children with spontaneous CSF otorrhea most often have congenital inner ear anomalies associated with hearing loss. High-resolution CT scans are helpful to confirm the diagnosis. CSF leakage through the temporal bone may cause different problems. The most common presenting symptoms consist of serous otitis media, persistent otorrhea after tympanostomy tube placement, and meningitis. There are different imaging methods to locate the leakage site including CT, CT with intrathecal Metrizamide, MRI and radio-isotope studies. In some cases, there might be questions about the precise site of leakage. Using intrathecal Fluorescein during the surgery and doing pressure rising maneuvers are very helpful in this regard. Once the defect is found, various repair methods can be employed, such as middle fossa craniotomy, transcanal vestibular obliteration, and closure of the Eustachian tube and the ear canal. The materials used to seal the defects are muscle, fascia, fat, bone dust and chips and pedicled grafts. We will discuss the different methods of diagnosing and managing CSF otorrhea in children and also the use of Fluorescein in these cases.

Background and purpose: Granulocyte colony-stimulating factor (G-CSF) is routinely used in combination with chemotherapy to battle neutropenia. However, studies suggest that this chemokine may increase the risk of metastasis and malignancy in many cancers. To counteract the adverse effects of G-CSF in cancer, antibodies have been used to block its action. However, antibodies are large and complex molecules which makes their production expensive. Thus in this study, we aim to construct different structure variants of the G-CSF receptor containing different domains and select the best variant that prevents the adverse actions of this chemokine. These novel structures are smaller than antibodies and easier to produce. Experimental approach: Different domains of the G-CSF receptor were designed and cloned into the pET28a expression vector. These recombinant receptor subunits were then expressed in Escherichia coli and purified using standard affinity chromatography techniques. Interaction of recombinant receptor subunits with G-CSF was assessed using enzyme-linked immunosorbent assay and NFS60 cells. Findings / Results: Two recombinant receptor subunits containing D1 + D2 + D3 domains and D2 domain showed the strongest inhibitory activity to G-CSF. Conclusion and implications: These novel recombinant receptor variants could be candidates for further studies in the development of novel therapeutics.