Neuronal and glioma-derived stem cell factor induces angiogenesis within the brain.

Stem cell factor (SCF) is overexpressed by neurons following brain injury as well as by glioma cells; however, its role in gliomagenesis remains unclear. Here, we demonstrate that SCF directly activates brain microvascular endothelial cells (ECs) in vitro and induces a potent angiogenic response in vivo. Primary human gliomas express SCF in a grade-dependent manner and induce normal neurons to express SCF in brain regions infiltrated by glioma cells, areas that colocalize with prominent angiogenesis. Downregulation of SCF inhibits tumor-mediated angiogenesis and glioma growth in vivo, whereas overexpression of SCF is associated with shorter survival in patients with malignant gliomas. Thus, the SCF/c-Kit pathway plays an important role in tumor- and normal host cell-induced angiogenesis within the brain.

In vivo imaging of cellular transplants.

We will talk about the techniques of in vivo imaging currently used in today's research and biomedical field, giving a general view of how each technique works and examples of practical applications of each technique. We will cover fluorescent (BL/CL), PET, SPECT and quantum dot imaging. Afterwards, we will cover how in vivo imaging is used in a biomedical sense; more specifically we will see how researchers studying cancer and neurodegenerative disease employ in vivo imaging.

Balamuthia mandrillaris meningoencephalitis in an immunocompromised patient. Case report.

Balamuthia mandrillaris is a rare but increasingly recognized cause of amebic encephalitis, yet it remains poorly understood. The condition is almost universally fatal, and due to diagnostic difficulty, most cases are identified postmortem. The authors report a case of Balamuthia amebic encephalitis in a patient with combined variable immunodeficiency in which a rare antemortem diagnosis was made via brain biopsy. Despite broad-spectrum antimicrobial therapy, the outcome was fatal. Such presentations are challenging, and definitive diagnosis may require biopsy in consultation with a skilled neuropathologist.

Intracranial ablative procedures for the treatment of chronic pain.

Three main techniques delineate a possible role for intracranial ablative procedures in patients with chronic pain. Recent studies demonstrate a continued need for clinical investigation into central mechanisms of neuroablation to best define its role in the care of patients with otherwise intractable and severe pain syndromes. Cingulotomy can result in long-term pain relief. Although it can be associated with subtle impairments of attention, there is little risk to other cognitive domains.

A computational model of mild traumatic brain injury.

Electrical analysis of brain activity reveals the presence of synchronous oscillations over a range of frequencies. These rhythms are readily observed using electroencephalography (EEG). Clinical EEG data shows that Traumatic Brain Injury (TBI) alters these rhythms. Researchers have developed lumped parameter neural mass models (NMM) that can reproduce these various brain rhythms. This paper proposes an NMM based computational model of mild TBI that recreates the clinical EEG changes observed after injury. Specifically, the focus is on recreating changes observed after TBI in the 8-12 Hz alpha and the 4-8Hz theta frequency ranges. Mild TBI is simulated by increasing membrane reactivity and by decreasing synaptic connectivity in the NMM. These results indicate that clinically observed EEG changes with mild TBI are likely due to traumatic synaptic disruption and that with appropriate data, EEG may be used to quantify the extent of TBI in the future.

Stem cells and the origin of gliomas: A historical reappraisal with molecular advancements.

The biology of both normal and tumor development clearly possesses overlapping and parallel features. Oncogenes and tumor suppressors are relevant not only in tumor biology, but also in physiological developmental regulators of growth and differentiation. Conversely, genes identified as regulators of developmental biology are relevant to tumor biology. This is particularly relevant in the context of brain tumors, where recent evidence is mounting that the origin of brain tumors, specifically gliomas, may represent dysfunctional developmental neurobiology. Neural stem cells are increasingly being investigated as the cell type that originally undergoes malignant transformation - the cell of origin - and the evidence for this is discussed.

Telomere dysfunction and Atm deficiency compromises organ homeostasis and accelerates ageing.

Ataxia-telangiectasia (A-T) results from the loss of ataxia-telangiectasia mutated (Atm) function and is characterized by accelerated telomere loss, genomic instability, progressive neurological degeneration, premature ageing and increased neoplasia incidence. Here we evaluate the functional interaction of Atm and telomeres in vivo. We examined the impact of Atm deficiency as a function of progressive telomere attrition at both the cellular and whole-organism level in mice doubly null for Atm and the telomerase RNA component (Terc). These compound mutants showed increased telomere erosion and genomic instability, yet they experienced a substantial elimination of T-cell lymphomas associated with Atm deficiency. A generalized proliferation defect was evident in all cell types and tissues examined, and this defect extended to tissue stem/progenitor cell compartments, thereby providing a basis for progressive multi-organ system compromise, accelerated ageing and premature death. We show that Atm deficiency and telomere dysfunction act together to impair cellular and whole-organism viability, thus supporting the view that aspects of A-T pathophysiology are linked to the functional state of telomeres and its adverse effects on stem/progenitor cell reserves.