Temporary threshold shift after noise exposure in hypobaric hypoxia at high altitude: results of the ADEMED expedition 2011.

OBJECTIVES: To evaluate whether there is an increased risk for noise-induced hearing loss at high altitude rsp. in hypobaric hypoxia. METHODS: Thirteen volunteers got standard audiometry at 125, 250, 500, 750, 1000, 1500, 2000, 3000, 4000, 6000, and 8000 Hz before and after 10 min of white noise at 90 dB. The system was calibrated for the respective altitude. Measurements were performed at Kathmandu (1400 m) and at Gorak Shep (5300 m) (Solo Khumbu/Nepal) after 10 days of acclimatization while on trek. Temporary threshold shift (TTS) was analyzed by descriptive statistics and by factor analysis. RESULTS: TTS is significantly more pronounced at high altitudes. Acclimatization does not provide any protection of the inner ear, although it increases arterial oxygen saturation. CONCLUSION: The thresholds beyond which noise protection is recommended (> 80 dB) or necessary (> 85 dB) are not sufficient at high altitudes. We suggest providing protective devices above an altitude of 1500 m ("ear threshold altitude") when noise level is higher than 75 dB and using them definitively above 80 dB. This takes the individual reaction on hypobaric hypoxia at high altitude into account.

Impact of epicardial adipose tissue volume upon left ventricular dysfunction in patients with mild-to-moderate aortic stenosis: A post-hoc analysis.

BACKGROUND: Aortic stenosis (AS) may lead to diastolic dysfunction and later on heart failure (HF) with preserved left ventricular ejection fraction (HFpEF) via increased afterload and left-ventricular (LV) hypertrophy. Since epicardial adipose tissue (EAT) is a metabolically active fat depot that is adjacent to the myocardium and can influence cardiomyocytes and LV function via secretion of proinflammatory cytokines, we hypothesized that high amounts of EAT, as assessed by computed tomography (CT), may aggravate the development and severity of LV hypertrophy and diastolic dysfunction in the context of AS. METHODS: We studied 50 patients (mean age 71 ± 9 years; 9 women) in this preliminary study with mild or moderate AS and mild to severe LV diastolic dysfunction (LVDD), diagnosed by echocardiography, who underwent non-contrast cardiac CT and echocardiography. EAT parameters were measured on 2nd generation dual source CT. Conventional two-dimensional echocardiography and Tissue Doppler Imaging (TDI) was performed to assess LV function and to derive myocardial straining parameter. All patients had a preserved LV ejection fraction > 50%. Data was analysed using Pearson's correlation. RESULTS: Only weak correlation was found between EAT volume or density and E/é ratio as LVDD marker (r = -.113 p = .433 and r = .260, p = .068 respectively). Also, EAT volume or density were independent from Global Strain Parameters (r = 0.058 p = .688 and r = -0.207 p = .239). E/é ratio was strongly associated with LVDD (r = .761 p≤0.0001) and Strain Parameters were moderately associated with LV Ejection Fraction (r = -.669 p≤0.001 and r = -.454 P≤0.005). CONCLUSIONS: In this preliminary study in patients with AS, the EAT volume and density as assessed by CT correlated only weakly with LVDD, as expressed by the commonly used E/é ratio, and with LV strain function. Hence, measuring EAT volume and density may neither contribute to the prediction nor upon the severity of LVDD, respectively.

Endoplasmic reticulum dynamics, inheritance, and cytoskeletal interactions in budding yeast.

The endoplasmic reticulum (ER) in Saccharomyces cerevisiae consists of a reticulum underlying the plasma membrane (cortical ER) and ER associated with the nuclear envelope (nuclear ER). We used a Sec63p-green fluorescent protein fusion protein to study motility events associated with inheritance of cortical ER and nuclear ER in living yeast cells. During M phase before nuclear migration, we observed thick, apparently rigid tubular extensions emanating from the nuclear ER that elongate, undergo sweeping motions along the cell cortex, and shorten. Two findings support a role for microtubules in this process. First, extension of tubular structures from the nuclear ER is inhibited by destabilization of microtubules. Second, astral microtubules, structures that undergo similar patterns of extension, cortical surveillance and retraction, colocalize with nuclear ER extensions. During S and G(2) phases of the cell cycle, we observed anchorage of the cortical ER at the site of bud emergence and apical bud growth. Thin tubules of the ER that extend from the anchored cortical ER display undulating, apparently random movement and move into the bud as it grows. Finally, we found that cortical ER morphology is sensitive to a filamentous actin-destabilizing drug, latrunculin-A, and to mutations in the actin-encoding ACT1 gene. Our observations support 1) different mechanisms and cytoskeletal mediators for the inheritance of nuclear and cortical ER elements and 2) a mechanism for cortical ER inheritance that is cytoskeleton dependent but relies on anchorage, not directed movement.