Neuronal pathways involved in stress responses to extreme somatosensory stimuli were investigated by immunostaining, viral tract tracing, and experimental brain surgery in rats. Acute audiogenic stress, which elicits an immediate marked elevation in plasma ACTH and corticosterone concentrations, was used as a model. Loud noise (105 dB, 30 min) elicited c-fos activation within neurons in all of the components of the auditory system and stress-sensitive brain nuclei, including corticotropin-releasing hormone-synthesizing parvicellular neurons in the hypothalamic paraventricular nucleus (PVN). c-Fos activation was also seen in the medial paralemniscal nucleus in the pons (MPL) and in the subparafascicular nucleus (SPF) in the midbrain. After injection of neurotropic virus (pseudorabies, Bartha strain) into the PVN, neurons in the MPL and the parvicellular portion of the SPF were retrogradely infected. It has been shown by immunostaining that MPL and SPF neurons express a newly discovered neuropeptide, tuberoinfundibular peptide of 39 residues (TIP39). TIP39 is present in a fine neuronal network in the PVN. Audiogenic stress-elicited c-fos activation in TIP39-containing neurons of the MPL and SPF. TIP39 immunoreactivity disappeared from the PVN after transection of MPL and SPF projections to the nucleus. These observations suggest that TIP39-containing MPL and SPF neurons may participate in mediating audiogenic stress responses.

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Background: The neutrophil-to-lymphocyte ratio (NLR) and the platelet-to-lymphocyte ratio (PLR) may be useful for drawing conclusions about the survival of head and neck squamous cell carcinoma (HNSCC) patients. Methods: Clinical data of 156 patients managed for HNSCC at two head and neck surgery centres were analyzed retrospectively. We studied the relationships between survival and PLR as well as NLR. Results: With regards to 5-year survival, the difference between the two groups with PLR values lower or higher than the threshold was statistically significant (p = 0.004), and we found the same for disease-free survival (p = 0.05), and tumour-specific mortality (p = 0.009). Concerning NLR, the difference in tumour-specific survival was statistically significant (p = 0.006). According to the multivariate analysis, NLR values higher than the threshold indicated an enhanced risk for overall as well as for tumour-specific mortality. Conclusion: In HNSCC patients, a high NLR may be considered as an independent risk factor for 5-year overall survival.Malignant tumours influence the number of platelets and alter their functioning. However, the mechanisms of the relationship between thrombocytosis and the tumour have not yet been fully elucidated and several hypotheses have been proposed [2].The facilitatory role of chronic inflammation in the development and progression of solid tumours have been described for malignancies of the lung, breast, and gastrointestinal tract, the prostate, and the ovaries [3-7], as well as for HNSCC [8,9].Neutrophils might, in fact, facilitate tumour growth and the formation of metastases-these cells can inhibit the activities of the lymphocytes and thereby attenuate the antitumour immune response [10]. Neutrophil cells can contribute to carcinogenesis and tumour progression in many ways [11]: (1) These cells can release genotoxic substances, which damage the DNA of epithelial cells [12]. (2) They can promote tumour growth by releasing soluble factors and proteases, such as prostaglandin E2 and neutrophil elastase [13,14]. (3) Neutrophils facilitate metastasis formation by enhancing the capabilities of the tumour cells for migration, invasive spread, and colony formation, as well as by breaking down the extracellular matrix [15]. (4) They contribute to the formation of new blood vessels by producing pro-angiogenic factors, such as matrix metalloproteinase-9, and vascular endothelial growth factor [16]. (5) Neutrophils exert immunosuppressive action by inhibiting effector T-cells along with the proliferation and the functioning of natural killer cells, as well the fact that they enhance tumour growth and metastasis formation through the modulation of macrophage activity [17].These observations suggest that neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR) determined in the blood of patients with a malignancy might be related to tumour growth [18].Our study intended to ascertain whether pre-treatment NLR and PLR values determined in HNSCC patients are suitable predi...

Cholesteatoma is an epidermoid cyst, which is most frequently found in the middle ear. The matrix of cholesteatoma is histologically similar to the matrix of the epidermoid cyst of the skin (atheroma); their epithelium is characterized by hyperproliferation. The c-MYC protooncogene located on chromosome 8q24 encodes a transcription factor involved in the regulation of cell proliferation and differentiation. Previous studies have found aneuploidy of chromosome 8, copy number variation of c-MYC gene, and the presence of elevated level c-MYC protein in cholesteatoma. In this study we have compared the expression of c-MYC gene in samples taken from the matrix of 26 acquired cholesteatomas (15 children and 11 adults), 15 epidermoid cysts of the skin (atheromas; head and neck region) and 5 normal skin samples (retroauricular region) using RT-qPCR, providing the first precise measurement of the expression of c-MYC gene in cholesteatoma. We have found significantly elevated c-MYC gene expression in cholesteatoma compared to atheroma and to normal skin samples. There was no significant difference, however, in c-MYC gene expression between cholesteatoma samples of children and adults. The significant difference in c-MYC gene expression level in cholesteatoma compared to that of atheroma implies a more prominent hyperproliferative phenotype which may explain the clinical behavior typical of cholesteatoma.