OBJECTIVE. The purpose of this study was to review the endoscopic anatomic features of the anterior brainstem and surrounding cisternal spaces via a tr

BACKGROUND: Antiapoptotis resulting from hyperactivation of the transcription factor NF‐κB has been described in several cancer types. It is triggered by the interaction of the tumor necrosis factor (TNF) with its receptors and recruitment of the intermediate factor TNF‐receptor associated factor (TRAF) 2. The NF‐κB transcriptional activity could amplify the expression of antiapoptotic genes. The authors investigated the activity of NF‐κB, and the mRNA expression of TNFα, TNFα receptor, TRAF1, TRAF2, and TRAF‐associated NF‐κB activator (TANK), and the antiapoptotic genes Bcl‐2, c‐IAP 1 and 2, and Survivin in human astrocytic tumors.METHODS: Eight low‐grade astrocytomas (LGA), 10 anaplastic astrocytomas (AAs), 10 glioblastoma multiforme (GBM) samples were used; 4 samples of normal brain tissue were used as controls. The NF‐κB activation was analyzed by electrophoretic mobility shift assay; TRAF1, TRAF2, TANK/I‐TRAF, Bcl‐2, c‐IAP 1 and 2, and Survivin mRNA expressions were studied using real‐time quantitative reverse‐transcriptase polymerase chain reaction.RESULTS: NF‐κB hyperactivity was detected in tumor samples. mRNA of antiapoptotic genes, particularly BCL‐2 and Survivin, was hyperexpressed in gliomas. Interestingly, BCL‐2 was hyperexpressed in LGAs, whereas a very high level of Survivin featured high‐grade gliomas. The differential expression of antiapoptotic genes yielded a tight clustering of all LGA and nearly all GBM samples in cluster analysis.CONCLUSIONS: NF‐κB and factors involved in its intracellular activation were up‐regulated in gliomas. NF‐κB‐activated antiapoptotic genes were hyperexpressed in tumor samples, but showed a differential expression with higher levels of Bcl‐2 in LGAs and higher levels of Survivin in GBMs. Cancer 2008. © 2008 American Cancer Society.

This narrative review provides a comprehensive analysis of the several methods and technologies employed to measure handgrip strength (HGS), a significant indicator of neuromuscular strength and overall health. The document evaluates a range of devices, from traditional dynamometers to innovative sensor-based systems, and assesses their effectiveness and application in different demographic groups. Special attention is given to the methodological aspects of HGS estimation, including the influence of device design and measurement protocols. Endogenous factors such as hand dominance and size, body mass, age and gender, as well as exogenous factors including circadian influences and psychological factors, are examined. The review identifies significant variations in the implementation of HGS measurements and interpretation of the resultant data, emphasizing the need for careful consideration of these factors when using HGS as a diagnostic or research tool. It highlights the necessity of standardizing measurement protocols to establish universal guidelines that enhance the comparability and consistency of HGS assessments across various settings and populations.