Surgery of the turbinates and “empty nose” syndrome

Surgical therapy of the inferior and/or middle turbinate is indicated when conservative treatment options have failed. The desired goal is a reduction of the soft tissue volume of the turbinates regarding the individual anatomic findings, whilst simultaneously conserving as much mucosa as possible. As the turbinates serve as a functional entity within the nose, they ensure climatisation, humidification and cleaning of the inhaled air. Thus free nasal breathing means a decent quality of life, as well

Operative treatment of functional facial skin disorders

The skin is the principal interface between the body and the surrounding world and thus serves as a protective barrier against trauma, temperature extremes and radiation. With receptors for pressure, movement, heat and cold, it also acts as sensory organ and through sweat secretion plays a role in thermoregulation and electrolyte metabolism. Not all of these functions are relevant to facial skin, however, cosmetic aspects are of vital importance

Telomere Shortening Impairs Regeneration of the Olfactory Epithelium in Response to Injury but Not Under Homeostatic Conditions

Atrophy of the olfactory epithelium (OE) associated with impaired olfaction and dry nose represents one of the most common phenotypes of human aging. Impairment in regeneration of a functional olfactory epithelium can also occur in response to injury due to infection or nasal surgery. These complications occur more frequently in aged patients. Although age is the most unifying risk factor for atrophic changes and functional decline of the olfactory epithelium, little is known about molecular mechanisms that could influence maintenance and repair of the olfactory epithelium. Here, we analyzed the influence of telomere shortening (a basic mechanism of cellular aging) on homeostasis and regenerative reserve in response to chemical induced injury of the OE in late generation telomere knockout mice (G3 mTerc−/−) with short telomeres compared to wild type mice (mTerc+/+) with long telomeres. The study revealed no significant influence of telomere shortening on homeostatic maintenance of the OE during mouse aging. In contrast, the regenerative response to chemical induced injury of the OE was significantly impaired in G3 mTerc−/− mice compared to mTerc+/+ mice. Seven days after chemical induced damage, G3 mTerc−/− mice exhibited significantly enlarged areas of persisting atrophy compared to mTerc+/+ mice (p = 0.031). Telomere dysfunction was associated with impairments in cell proliferation in the regenerating epithelium. Deletion of the cell cycle inhibitor, Cdkn1a (p21) rescued defects in OE regeneration in telomere dysfunctional mice. Together, these data indicate that telomere shortening impairs the regenerative capacity of the OE by impairing cell cycle progression in a p21-dependent manner. These findings could be relevant for the impairment in OE function in elderly people

The James Webb Space Telescope Mission

Twenty-six years ago a small committee report, building on earlier studies, expounded a compelling and poetic vision for the future of astronomy, calling for an infrared-optimized space telescope with an aperture of at least $4m$. With the support of their governments in the US, Europe, and Canada, 20,000 people realized that vision as the $6.5m$ James Webb Space Telescope. A generation of astronomers will celebrate their accomplishments for the life of the mission, potentially as long as 20 years, and beyond. This report and the scientific discoveries that follow are extended thank-you notes to the 20,000 team members. The telescope is working perfectly, with much better image quality than expected. In this and accompanying papers, we give a brief history, describe the observatory, outline its objectives and current observing program, and discuss the inventions and people who made it possible. We cite detailed reports on the design and the measured performance on orbit.Comment: Accepted by PASP for the special issue on The James Webb Space Telescope Overview, 29 pages, 4 figure

Telomere shortening impairs regeneration of the olfactory epithelium in response to injury.

<p>(A, B) Representative photographs of hematoxylin and eosin-stained sagital sections of the nasal cavity, seven days after intranasal injection of Triton-X in 6 month old (A) G3 <i>mTerc^−/−</i> and (B-E) <i>mTerc^+/+</i> mice. Dotted line in A and B marks incompletely regenerated epithelium of 0–2 cell layer thickness, double line marks incompletely regenerated epithelium of 3–4 cell layer thickness, dot/bar line marks completely regenerated epithelium of 5–6 cell layer thickness. Representative high-power photographs of G3 <i>mTerc^−/−</i> mice showing (C) incompletely regenerated epithelium with 0–2 cell layer thickness (dotted line), (D) 3–4 cell layer thickness (double linier) (E) completely regenerated olfactory epithelium (E). (F, G) The histograms show the percentage of the olfactory epithelium with incomplete regeneration in <i>mTerc^+/+</i> and G3 <i>mTerc^−/−</i> mice at seven days after Triton-X induced injury: (F) percentage of incompletely regenerated epithelium of 0–2 cell layer thickness, (G) percentage of incompletely regenerated epithelium of 0–4 cell layer thickness.</p

Limited proliferation potential of the OE in telomere deficient mice.

<p>(A,B) Representative photographs of BrdU-stained longitudinal sections of the olfactory epithelium, 7 days after Triton-X treatment in (A) <i>mTerc^+/+</i> and (B) G3 <i>mTerc^−/−</i> mice. (C) Histogram showing BrdU positive cells in the OE of G3 <i>mTerc^+/+</i> and <i>mTerc^+/+</i> mice. Note that there is no significant difference of the ratio of BrdU positive cells v.s. negative cells between <i>mTerc^+/+</i> and G3 <i>mTerc^−/−</i> mice in injured olfactory epithelium of one cell layer thickness (P = 0.216) but there was a significant reduction of BrdU positive cells in G3 <i>mTerc^−/−</i> compared to <i>mTerc^+/+</i> mice in injured olfactory epithelium of three cell layer thickness (P = 0.008) and 5–6 cell layer thickness (P = 0.0293), n = 5 mice per group. (D) The histogram shows the percentage of the olfactory epithelium with incomplete regeneration (0–2 cell layer thickness) in 6–8 month mice of the indicated genotypes at 7 days after Triton-X induced injury. Note that <i>p21</i> deletion rescues regenerative defects in G3 <i>mTerc^−/−</i> mice. The cohorts in this experiment show an overall higher rate of tissue damage compared to the previous experiment depicted in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0027801#pone-0027801-g003" target="_blank">Figures 3</a> and <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0027801#pone-0027801-g004" target="_blank">4</a>.</p

Morphological Analysis of the olfactory epithelium at day 2 after Triton-X application.

<p>(A,B) Representative photographs of hematoxylin and eosin-stained sagittal sections of the OE, two days after intranasal injection of Triton-X in 6 month old (A) G3 <i>mTerc^−/−</i> and (B) <i>mTerc^+/+</i> mice. There are no significant differences between the two cohorts, both showing strong damage to 80–90% of the OE. The histograms show the percentage of the chemically damaged olfactory epithelium in <i>mTerc^+/+</i> and G3 <i>mTerc^−/−</i> mice at two days after Triton-X induced injury: (C) percentage of damaged epithelium of 0–4 cell layer thickness (P = 0.7887), (D) percentage of completely damaged epithelium of 0–2 cell layer thickness (P = 0.8208).</p

Telomere shortening does not affect homeostasis of the olfactory epithelium in aging mice.

<p>(A, B): Representative photographs of hematoxylin and eosin-stained longitudinal sections of the OE from 2–3 month old (A) <i>mTerc^+/+</i> and (B) G3 <i>mTerc^−/−</i> mice, and 10–12 month old (C) <i>mTerc^+/+</i> and (D) G3 <i>mTerc^−/−</i> mice. (E-J) Immunohistological analysis of longitudinal sections of the OE 10–12 month old (E, G, I) <i>mTerc^+/+</i> and (F, H, J) G3 <i>mTerc^−/−</i> mice: (E, F) Olfactory marker protein (OMP), (G, H) GAP43 and (I, J) proliferating cell nuclear antigen (PCNA). White arrows point to PCNA positive cells (G, H). (K) Histogram showing percentage of PCNA-positive cells in the OE of 10–12 month old <i>mTerc^+/+</i> and G3 <i>mTerc^−/−</i> mice (n = 10 mice per group, P = 0.4580).</p