Identification and isolation of slow-cycling glioma stem cells.

Cancer stem cells are defined as low-abundance, quiescent cells and are considered a major cellular source of tumor recurrence following therapy, which identifies these cells as important therapeutic targets for difficult-to-treat cancers, including high-grade gliomas. By contrast to the highly proliferative bulk tumor cells, glioma stem cells (GSC) are slow-cycling, and therefore less sensitive to DNA damaging cytotoxic drugs. GSC are also less reliant on aerobic glycolytic metabolism, leading to inadequate clearing of GSC by chemotherapy and radiotherapy.

Major elective abdominal surgery acutely impairs lower limb muscle pyruvate dehydrogenase complex activity and mitochondrial function.

Background & Aims: This post hoc study aimed to determine whether major elective abdominal surgery had any acute impact on mitochondrial pyruvate dehydrogenase complex (PDC) activity and maximal mitochondrial ATP production rates (MAPR) in a large muscle group (vastus lateralis -VL) distant to the site of surgical trauma.

Methods: Fifteen patients undergoing major elective open abdominal surgery were studied. Muscle biopsies were obtained after the induction of anesthesia from the VL immediately before and after surgery for the determination of PDC and maximal MAPR (utilizing a variety of energy substrates).

Cell quiescence correlates with enhanced glioblastoma cell invasion and cytotoxic resistance.

Glioblastoma (GBM) tumor cells exhibit drug resistance and are highly infiltrative. GBM stem cells (GSCs), which have low proliferative capacity are thought to be one of the sources of resistant cells which result in relapse/recurrence. However, the molecular mechanisms regulating quiescent-specific tumor cell biology are not well understood.

Suppressing a charge density wave by changing dimensionality in the ferecrystalline compounds ([SnSe]1.15)1(VSe2)n with n = 1, 2, 3, 4.

The compounds, ([SnSe]1.15)1(VSe2)n with n = 1, 2, 3, and 4, were prepared using designed precursors in order to investigate the influence of the thickness of the VSe2 constituent on the charge density wave transition. The structure of each of the compounds was determined using X-ray diffraction and scanning transmission electron microscopy.

Repair mechanisms help glioblastoma resist treatment.

Glioblastoma multiforme (GBM) is a malignant and incurable glial brain tumour. The current best treatment for GBM includes maximal safe surgical resection followed by concomitant radiotherapy and adjuvant temozolomide. Despite this, median survival is still only 14-16 months.

Raman spectroscopy insights into the size-induced structural transformation in SnSe nanolayers.

Raman spectroscopy is used to probe the structural changes in [SnSe]m[MoSe2]n ferecrystal thin films as a function of m, the number of bilayers of SnSe. In spite of the interleaved structure in the intergrowths, Raman spectra can be described as a superposition of spectra from the individual components, indicating that the interaction at the interface between the components is relatively weak. Analysis of room-temperature Raman spectra indicate that the MoSe2 layers separating the SnSe layers are nanocrystalline in all of the samples studied, with little change as the number of Se-Mo-Se trilayers (n) or SnSe bilayers (m) increases, reflecting the rotational disorder between adjacent trilayers.

Resistance to aerobic exercise training causes metabolic dysfunction and reveals novel exercise-regulated signaling networks.

Low aerobic exercise capacity is a risk factor for diabetes and a strong predictor of mortality, yet some individuals are "exercise-resistant" and unable to improve exercise capacity through exercise training. To test the hypothesis that resistance to aerobic exercise training underlies metabolic disease risk, we used selective breeding for 15 generations to develop rat models of low and high aerobic response to training. Before exercise training, rats selected as low and high responders had similar exercise capacities.

Regulation of glycogen synthase kinase-3 beta (GSK-3β) by the Akt pathway in gliomas.

Gliomas are aggressive brain tumours that, despite advances in multimodal therapies, continue to portend a dismal prognosis. Glioblastoma multiforme (GBM) represents the most aggressive glioma and patients have a median survival of 14 months, even with the best available treatments. The phosphoinositide 3-kinase/Akt/glycogen synthase kinase-3 beta (GSK-3β) and Wnt/β-catenin pathways are dysregulated in a number of cancers, and these two pathways share a common node protein, GSK-3β.