Area patterning of the mammalian cortex

Glioblastoma, the most aggressive cerebral tumor, is invariably lethal. Glioblastoma cells express several genes typical of normal neural stem cells. One of them, SOX2, is a master gene involved in sustaining self-renewal of several stem cells, in particular neural stem cells. To investigate its role in the aberrant growth of glioblastoma, we silenced SOX2 in freshly derived glioblastoma tumor-initiating cells (TICs). Our results indicate that SOX2 silenced glioblastoma TICs, despite the many mutations they have accumulated, stop proliferating and lose tumorigenicity in immunodeficient mice. SOX2 is then also fundamental for maintenance of the self-renewal capacity of neural stem cells when they have acquired cancer properties. SOX2, or its immediate downstream effectors, would then be an ideal target for glioblastoma therapy.

https://stemcellsjournals.onlinelibrary.wiley.com/doi/pdf/10.1634/stemcells.2008-0493

SOX2 Silencing in Glioblastoma Tumor-Initiating Cells Causes Stop of Proliferation and Loss of Tumorigenicity

During the last decade, the role of radial glia has been radically revisited. Rather than being considered a mere structural component serving to guide newborn neurons towards their final destinations, radial glia is now known to be the main source of neurons in several regions of the central nervous system, notably in the cerebral cortex. Radial glial cells differentiate from neuroepithelial progenitors at the beginning of neurogenesis and share with their ancestors the bipolar shape and the expression of some molecular markers. Radial glia, however, can be distinguished from neuroepithelial progenitors by the expression of astroglial markers. Clonal analyses showed that radial glia is a heterogeneous population, comprising both pluripotent and different lineage-restricted neural progenitors. At late-embryonic and postnatal stages, radial glial cells give rise to the neural stem cells responsible for adult neurogenesis. Embryonic pluripotent radial glia and adult neural stem cells may be clonally linked, thus representing a lineage displaying stem cell features in both the developing and mature central nervous system.

Radial glia and neural stem cells.

The balance between self-renewal and differentiation of neural progenitor cells is an absolute requirement for the correct formation of the nervous system Much is known about both the pathways involved in progenitor cell self-renewal, such as Notch signaling, and the expression of genes that initiate progenitor differentiation However, whether these fundamental processes are mechanistically linked, and specifically how repression of progenitor self-renewal pathways occurs, is poorly understood Nuclear factor I A (Nfia), a gene known to regulate spinal cord and neocortical development, has recently been implicated as acting downstream of Notch to initiate the expression of astrocyte-specific genes within the cortex Here we demonstrate that, in addition to activating the expression of astrocyte-specific genes, Nfia also downregulates the activity of the Notch signaling pathway via repression of the key Notch effector Hes1 These data provide a significant conceptual advance in our understanding of neural progenitor differentiation, revealing that a single transcription factor can control both the activation of differentiation genes and the repression of the self-renewal genes, thereby acting as a pivotal regulator of the balance between progenitor and differentiated cell states

https://www.jneurosci.org/content/jneuro/30/27/9127.full.pdf

NFIA Controls Telencephalic Progenitor Cell Differentiation through Repression of the Notch Effector Hes1

Different Response of Human Glioma Tumor-initiating Cells to Epidermal Growth Factor Receptor Kinase Inhibitors

Altered resting-state functional connectivity in the dorsal attention network in treatment-resistant schizophrenia


 Angiographic Acute Stent Thrombosis occur in 0.5%–2% of procedures.OCT–PCI or Optimized PCI represents a new approach particularly indicated in complex high thrombotic risk lesions, in patients at high bleeding risk with need for short DAPT and in the treatment of vulnerable plaques. Post–stent OCT thrombus finding was defined in previous studies as mass with diameter ≥250μm attached to the stent struts, was present until 40% of cases and is associated with definite angiographic thrombosis. Outcome of OCT thrombus is generally favorable although in about 25% there may be a progression. Case 1: 75–y smoker female with hypertension and atrial fibrillation on NOAC therapy presented in ICU with NSTEMI. At angiography: 75% stenosis focal plaque at proximal circumflex (Fig1A). At OCT vulnerable plaque: ulcerated with intimal flap < 90°, thin fibrous cap 20 µm, MLA 2.17mm² and AS 63%, intimal micro–calcifications and cholesterol crystals (Fig1C). We implanted DES with post–dilatation. Treatment was Cangrelor, heparin 100 IU/kg and ASA 250 mg ev. OCT showed acute 660 µm thrombosis of the stent body although there was perfect angiographic result (Fig1D+B). Further multiple balloon dilatation of the stent was carried out with thrombosis persistence on OCT control (Fig1E) and new appearance of multiple thromboses adhering to the intravascular side stent struts (Fig1F–G). Switch from Cangrelor to Tirofiban was done. Patient‘s clinical course was uneventful with discharge after six days on triple antithrombotic therapy with low–dose NOAC, ASA and clopidogrel.Case 2: 63–y smoker man arrived in cath lab for anterior STEMI. He had already taken ASA 300 mg ev and Ticagrelor 180 mg oral bolus about 60 minutes earlier in the ambulance. In Cath Lab was done heparin 100 IU/kg. P–PCI was performed for acute sub–occlusion (Fig2A) of the ostial DA treated by pre–dilation, DES implantation on Left Main–DA and multiple post–dilations according to the POT technique. OCT control showing extensive stent malapposition (860 µm) with evidence of multiple thromboses adhering to the stent struts on Left Main (diameter 410 µm) although there was perfect angiographic result (Fig2B–E). Procedure was optimized by adequate post–dilatation of the LM and administration of Abciximab. Patient‘s clinical course was uneventful with discharge after five days on ASA and Ticagrelor.
 
 
 Post–stent OCT thrombus may guide the choice of use of Glicoprotein IIb/IIIA Inhibitors in Cath Lab.


P42 acute stent thrombosis in cath lab during optimized pci: how to recognize it and possible treatment

Emx2 plays a crucial role in the development of the diencephalon and dorsal telencephalon. Thus, Emx2-null mutants have abnormal cortical lamination and a reduction in size of the caudal and medial areas of the prosencephalon. Emx2 is expressed in neural precursors of the subventricular zone in vivo and in cultured neurospheres in vitro where it controls the size of the transit-amplifying population, affecting proliferation and clonal efficiency of neural stem cells. To identify the cellular processes mastered by Emx2, and possibly the molecular mechanisms by which the gene exerts its action, we compared the expression profile of cultured neurospheres derived from wild-type and Emx2-null mouse embryos. The differential expression of several genes was also confirmed by semiquantitative RT-PCR, real-time PCR and cytofluorimetric analysis in different preparations of neurospheres, and by in situ hybridization. The gene expression profile suggested a role for Emx2 in regulating the differentiation and migration properties of neural precursor cells. This involvement was confirmed in vitro, where the altered clonogenicity and impaired migration of Emx2-null cells were partially corrected by transduction of the Emx2 gene. Taken together, our results indicate that Emx2 is indeed involved in the transition between resident early progenitors (perhaps stem cells) and more mature precursors capable of migrating out of the ventricular zone, becoming postmitotic and differentiating into the appropriate cell type, and help explain the alterations observed in the brains of knock-out mice.

Effects of Emx2 inactivation on the gene expression profile of neural precursors.

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Altered resting-state functional connectivity in the dorsal attention network in treatment-resistant schizophrenia

P42 acute stent thrombosis in cath lab during optimized pci: how to recognize it and possible treatment

Effects of Emx2 inactivation on the gene expression profile of neural precursors.