An update on the molecular biology of glioblastoma, with clinical implications and progress in its treatment.

Glioblastoma multiforme (GBM) is the most aggressive and common malignant primary brain tumor. Patients with GBM often have poor prognoses, with a median survival of ∼15 months. Enhanced understanding of the molecular biology of central nervous system tumors has led to modifications in their classifications, the most recent of which classified these tumors into new categories and made some changes in their nomenclature and grading system.

Controlling disinfection byproducts from treated wastewater using adsorption with granular activated carbon: Impact of pre-ozonation and pre-chlorination.

This study measured chlorine- and chloramine-reactive precursors using formation potential (FP) tests of nine U.S. Environmental Protection Agency (EPA) regulated and 57 unregulated disinfection byproducts (DBPs) in tertiary-filtered wastewater before and after pilot-scale granular activated carbon (GAC) adsorption.

N-nitrosomorpholine in potable reuse.

As potable reuse guidelines and regulations continue to develop, the presence of N-nitrosamines is a primary concern because of their associated health concerns. In this study, bench-, pilot-, and full-scale tests were conducted to focus on the occurrence and treatment of N-nitrosomorpholine (NMOR) in United States (U.S.

N-functionalized carbon nanotubes as a source and precursor of N-nitrosodimethylamine: implications for environmental fate, transport, and toxicity.

Hazardous byproducts may be generated during the environmental processing of engineered nanomaterials. Here, we explore the ability of carbon nanotubes with nitrogen-containing surface groups (N-CNTs) to generate N-nitrosodimethylamine (NDMA) during chemical disinfection. Unexpectedly, we observed that commercial N-CNTs with amine, amide, or N-containing polymer (PABS) surface groups are a source of NDMA.

ATP steal between cation pumps: a mechanism linking Na+ influx to the onset of necrotic Ca2+ overload.

We set out to identify molecular mechanisms underlying the onset of necrotic Ca(2+) overload, triggered in two epithelial cell lines by oxidative stress or metabolic depletion. As reported earlier, the overload was inhibited by extracellular Ca(2+) chelation and the cation channel blocker gadolinium. However, the surface permeability to Ca(2+) was reduced by 60%, thus discarding a role for Ca(2+) channel/carrier activation.