Restoration of energy homeostasis by SIRT6 extends healthy lifespan.

Aging leads to a gradual decline in physical activity and disrupted energy homeostasis. The NAD+-dependent SIRT6 deacylase regulates aging and metabolism through mechanisms that largely remain unknown. Here, we show that SIRT6 overexpression leads to a reduction in frailty and lifespan extension in both male and female B6 mice. A combination of physiological assays, in vivo multi-omics analyses and 13C lactate tracing identified an age-dependent decline in glucose homeostasis and hepatic glucose output in wild type mice. In contrast, aged SIRT6-transgenic mice preserve hepatic glucose output and glucose homeostasis through an improvement in the utilization of two major gluconeogenic precursors, lactate and glycerol. To mediate these changes, mechanistically, SIRT6 increases hepatic gluconeogenic gene expression, de novo NAD+ synthesis, and systemically enhances glycerol release from adipose tissue. These findings show that SIRT6 optimizes energy homeostasis in old age to delay frailty and preserve healthy aging.

Sample entropy-based analysis of differential and traditional training effects on dynamic balance in healthy people.

The authors applied algorithms based on the sample entropy (SampEn) measurements to analyze the evolution of regularity in center of pressure displacements on the medialateral (ML) and anteroposterior (AP) axes after the application of 2 balance training methods: differential and traditional. A total of 14 young healthy participants took part in this study undertaking 5 SampEn measurements, a pre- and posttest, and 3 retests on dynamic balance and monopodal support. Results show a SampEn increase in the ML axis over the medium term (4 weeks) with both training methods. Over the short term (1 week), only traditional training shows a SampEn increase in the ML axis. In the AP axis, the traditional training method also shows a SampEn increase over the medium and short terms. A higher irregularity of the COP displacements is also present in the same axis, far from the higher regularity observed in the AP axis. These findings suggest a variability strategy related with the postural control during supports.

Specific lipofuscin staining as a novel biomarker to detect replicative and stress-induced senescence. A method applicable in cryo-preserved and archival tissues.

There is shortage of extensive clinicopathologic studies of cellular senescence because the most reliable senescence biomarker, the detection of Senescence-Associated-beta-galactosidase activity (SA-ß-gal), is inapplicable in archival material and requires snap-frozen tissues. We validated the histochemical Sudan-Black-B (SBB) specific stain of lipofuscin, an aggregate of oxidized proteins, lipids and metals, known to accumulate in aged tissues, as an additional reliable approach to detect senescent cells independently of sample preparation. We analyzed cellular systems in which senescence was triggered by replicative exhaustion or stressful stimuli, conditional knock-in mice producing precancerous lesions exhibiting senescence, and human preneoplastic lesions known to contain senescent cells. In the above settings we demonstrated co-localization of lipofuscin and SA-ß-gal in senescent cells in vitro and in vivo (cryo-preserved tissue), strongly supporting the candidacy of lipofuscin for a biomarker of cellular senescence. Furthermore, cryo-preserved tissues positive for SA-ß-gal were formalin-fixed, paraffin-embedded, and stained with SBB. The corresponding SA-ß-gal positive tissue areas stained specifically for lipofuscin by SBB, whereas tissues negative for SA-ß-gal were lipofuscin negative, validating the sensitivity and specificity of the SBB staining to visualize senescent cells in archival material. The latter unique property of SBB could be exploited in research on widely available retrospective tissue material.

Lipoma endobronquial / Endobronchial lipoma

El lipoma endobronquial es un tumor benigno extremadamente raro, que suele causar síntomas por obstrucción bronquial. En la tomografía computarizada de tórax se presenta como una masa homogénea de densidad grasa que no capta contraste. El diagnóstico definitivo se realiza con broncoscopia y biopsia del tumor. El tratamiento de elección es la resección por vía endoscópica. Presentamos un caso de lipoma endobronquial en una paciente de 74 años, con antecedente de carcinoma papilar de tiroides, resecado por vía endoscópica(AU)

Endobronchial lipoma is an extremely rare benign tumour, which usually causes symptoms related with bronchial obstruction. Chest computed tomography shows a homogeneous mass with fat density and without contrast enhancement. Definitive diagnosis is made with bronchoscopy and biopsy of the tumour. The treatment of choice is endoscopic resection. We present a case of an endobronchial lipoma in a 74 year old patient, with a medical history of papilar thyroidgl and carcinoma, resected endoscopically(AU)

[Endobronchial lipoma]. / Lipoma endobronquial.

Endobronchial lipoma is an extremely rare benign tumour, which usually causes symptoms related with bronchial obstruction. Chest computed tomography shows a homogeneous mass with fat density and without contrast enhancement. Definitive diagnosis is made with bronchoscopy and biopsy of the tumour. The treatment of choice is endoscopic resection. We present a case of an endobronchial lipoma in a 74 year-old patient, with a medical history of papilar thyroid gland carcinoma, resected endoscopically.

Rplp1 bypasses replicative senescence and contributes to transformation.

To determine whether genes expressed by embryonic stem cells have a proliferative effect in primary cells, primary mouse embryonic fibroblasts were infected with an ES cell cDNA library. This led to identification of the ribosomal protein, Rplp1, a member of the P group of ribosomal proteins, whose putative role for bypassing replicative senescence in MEFs was investigated. Our results show that Rplp1 produces a two-fold increase in the expression of an E2F1 promoter and upregulation of cyclin E in MEFs. Therefore, this study is the first to show that overexpression of a single ribosomal protein, Rplp1, is a cause and not a consequence of cell proliferation. In addition, co-expression of Rplp1 with mutant rasVal12 contributed to transformation in NIH3T3 cells, as was evidenced by colony production in soft-agar assays. Moreover, the Rplp1 protein was upregulated in MEFs and NIH3T3 cells upon expression of a p53 dominant negative mutant gene designated p53R175H. Hence, mutation of p53 may facilitate immortalization in vitro by upregulating Rplp1. Lastly, Rplp1 mRNA was found to be upregulated in 16 of 26 human colon cancer biopsy specimens, a finding that may be of relevance to cancer research.