A novel nasopharyngeal stent for the treatment of obstructive sleep apnea: a case series of nasopharyngeal stenting versus continuous positive airway pressure.

The objective of the study was to investigate the first-night treatment success of a nasopharyngeal stent compared to standard nCPAP-titration. This is a case series and a single-center study. Eight participants (n = 8) were selected with untreated obstructive sleep apnea with a prestudy AHI ≥ 10. A newly developed nasopharyngeal stent was tested individually versus standard nCPAP-titration. Cardiorespiratory polysomnography was performed on two consecutive nights (random order: stent, nCPAP). The AHI, the number of obstructive apneas and hypopneas, the mean oxygen saturation, and the minimum oxygen saturation were compared before and after using the nasopharyngeal stent or standard nCPAP. The AHI value before treatment (AHIpre) was 31.1 ± 12.0 (mean ± standard deviation). After inserting the AlaxoStent, the mean AHIstent was 19 ± 12.0 compared to mean AHInCPAP 8.2 ± 11.9 with standard nCPAP-titration. Both nasopharyngeal stenting and nCPAP-titration could reduce the mean number of obstructive apneas by >94 %. Compared to responder rates of classic surgical interventions like uvulopalatopharyngoplasty or multi-level surgery, the nasopharyngeal stent seems to give a comparable responder rate of 50 %. There were no complications associated with the use of the stent and it was well tolerated by all subjects. Nasopharyngeal stenting widens the range of non-invasive mechanical treatment and seems to be an effective mechanical therapeutic alternative to surgery in nCPAP non-compliant patients with OSA. Careful selection of the patient population is a prerequisite of treatment and therefore it should be reserved for individual cases only.

Comparison of HPV prevalence in HNSCC patients with regard to regional and socioeconomic factors.

HPV infection is considered as an independent risk factor for head and neck squamous cell carcinomas (HNSCC). Due to highly variable prevalence results in numerous studies, it is, however, difficult to estimate the relevance of HPV infection as risk factor for a specific patient collective. This study aimed to elucidate the disparities of HPV prevalence by analyzing socioeconomically and regionally different patient collectives. Two age, gender, stage and tumor location matched cohorts of 18 private health insured (PHIP) and 16 statutory health insured patients (SIP) suffering from an oropharyngeal squamous cell carcinoma (OSCC) and treated at a university hospital were screened for p16 overexpression and HPV infection by immunohistochemistry and PCR. In addition 85 HNSCC patients of an otolaryngology private practice (PPP) in a rural area were screened for p16 overexpression and positive cases were tested for HPV infection. HPV prevalence was 72.2% in the PHIP collective in comparison to 25.0% (p = 0.015) in the SIP collective with a significantly improved 5-year overall survival (p = 0.003) of the PHIP collective. The total HPV prevalence of PPP group was 7.1% with the highest infection rate in tonsillar carcinomas (33.3%) and a larger percentage of female patients in the HPV positive group (p = 0.037). This study shows that variable HPV infection rates in HNSCC can be caused by the selection of particular patient collectives, which suggest taking socioeconomic and regional factors into account for a decision on HPV testing, if it is not performed on a routine basis.

Cyclin D1 expression is dependent on estrogen receptor function in tamoxifen-resistant breast cancer cells.

The development of resistance to tamoxifen, the most common antiestrogen used in the treatment of breast cancer, is a frequent and severe clinical problem. Tamoxifen-resistant tumors are still capable of responding to other hormonal therapies such as those that downregulate estrogen receptor expression. Mechanisms leading to acquisition of tamoxifen-resistant but hormone-sensitive growth are not completely understood. In tamoxifen-sensitive breast cancer cells, tamoxifen inhibits, whereas estrogen induces, expression of cyclin D1, a key cell cycle regulatory protein. Ectopic expression of cyclin D1 can lead to antiestrogen resistance. Thus, to determine whether cyclin D1 is involved in the growth of tamoxifen-resistant cells, we developed several tamoxifen-resistant variants from MCF-7 cells. These variants grow in the absence of estrogen or in the presence of tamoxifen, but their growth is inhibited by estrogen receptor downregulators. We show here that cyclin D1 expression is maintained at comparable levels in all tamoxifen-resistant variants, whereas pS2, another estrogen-regulated protein, is not. The addition of physiological levels of estrogen further stimulates cyclin D1 expression and proliferation. In contrast, treatment with estrogen receptor downregulators decreases cyclin D1 expression and proliferation. Thus, changes in cyclin D1 expression upon second-line hormonal therapy may predict hormonal sensitivity of tamoxifen-resistant tumors. These studies suggest that estrogen receptor mediates cyclin D1 expression and growth of tamoxifen-resistant tumors.

Supraphysiological acetaldehyde levels suppress growth in chicken embryos.

Although exposure to ethanol is known to cause growth inhibition in a developing embryo, the contributing effect of acetaldehyde on growth is not as well documented. In this study, we measured acetaldehyde-induced growth suppression in three different chicken strains: Peterson x Hubbard, HY x Hubbard, and W36 Ginther White Leghorn. The chicken embryo provides a useful model for studying fetal alcohol syndrome (FAS) and has been used extensively in our laboratory. The current study was undertaken to determine whether the chicken embryo could serve as a model for studying the effects of acetaldehyde on growth. Acetaldehyde caused a significant reduction in embryonic weights only at the higher acetaldehyde concentrations. Torso-to-head ratios were unchanged at every acetaldehyde dose for all strains, supporting the suggestion that acetaldehyde-induced growth suppression was generalized in all tissues, rather than being exhibited as a selective decrease of neuronal tissue. All strains experienced a significant decrease in viability only at higher acetaldehyde concentrations, but differences in viability were evident among the strains. These results support findings obtained from previous work done on ethanol-induced differences among chicken strains by supporting the suggestion that the strain of chicken is important when studying the effects of teratogens on growth and viability. More importantly, the supraphysiological concentrations of acetaldehyde necessary to induce growth suppression seem to indicate that the chicken embryo may not be a viable model of FAS for studying the direct effects of acetaldehyde on embryonic growth.