https://cancerbiologyprogram.med.wayne.edu/pdfs/hallmarks_cancer_article.pdf

Hallmarks of cancer: the next generation.

다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

Krabbe disease (KD) is a neurodegenerative disorder caused by the lack of β- galactosylceramidase enzymatic activity and by widespread accumulation of the cytotoxic galactosyl-sphingosine in neuronal, myelinating and endothelial cells. Despite the wide use of Twitcher mice as experimental model for KD, the ultrastructure of this model is partial and mainly addressing peripheral nerves. More details are requested to elucidate the basis of the motor defects, which are the first to appear during KD onset. Here we use transmission electron microscopy (TEM) to focus on the alterations produced by KD in the lower motor system at postnatal day 15 (P15), a nearly asymptomatic stage, and in the juvenile P30 mouse. We find mild effects on motorneuron soma, severe ones on sciatic nerves and very severe effects on nerve terminals and neuromuscular junctions at P30, with peripheral damage being already detectable at P15. Finally, we find that the gastrocnemius muscle undergoes atrophy and structural changes that are independent of denervation at P15. Our data further characterize the ultrastructural analysis of the KD mouse model, and support recent theories of a dying-back mechanism for neuronal degeneration, which is independent of demyelination.

https://arpi.unipi.it/bitstream/11568/951412/1/Cappello%2c%20SciRep2016.pdf

Ultrastructural Characterization of the Lower Motor System in a Mouse Model of Krabbe Disease.

[신간의 별자리x] 우리/미술, 그리고 ‘슬픔의 박물관’

Hypoxia-inducible factor 1 (HIF-1) activates the transcription of genes that are involved in crucial aspects of cancer biology, including angiogenesis, cell survival, glucose metabolism and invasion. Intratumoral hypoxia and genetic alterations can lead to HIF-1alpha overexpression, which has been associated with increased patient mortality in several cancer types. In preclinical studies, inhibition of HIF-1 activity has marked effects on tumour growth. Efforts are underway to identify inhibitors of HIF-1 and to test their efficacy as anticancer therapeutics.

Targeting HIF-1 for cancer therapy

Antibodies against neutrophil proteins myeloperoxidase (MPO) and proteinase-3 (PR3) are responsible for the development of anti-neutrophil cytoplasmic autoantibodies (ANCA)-associated vasculitides (AAV). Although the knowledge of these conditions is remarkably improved in the last few years, their etiology and pathogenetic mechanism(s) are still poorly understood. The establishment of experimental models has been repeatedly attempted with the aim of achieving a deeper understanding of their human counterpart. Here, we discuss the principal animal models currently used to investigate the mechanisms underlying the onset of AAV.

Animal Models of ANCA-Associated Vasculitides

Design and Construction of Artificial Blood Vessels

Antiangiogenic Treatment of Hematological Tumors

The histochemical techniques for subdividing mast cells stemmed from the observation by Ehrlich’ in 1876 that their lysosomal granules have the capacity to take up and stain metachromatically with basic dyes, such as toluidine blue. Among the histochemical methods to stain mast cells, it is to note to mention Sudan Black B, Luna stain or even Ziehl-Neelsen, which has been assessed historically (Rest and Lee 1979).

The Staining of Mast Cells

Both innate and adaptive immune cells are involved in the mechanisms of tumor endothelial cell proliferation, migration and activation, through the production and release of a large spectrum of pro-angiogenic mediators, which create the specific microenvironment that favours tumor angiogenesis. Cancer stem cells have been identified in several human solid and hematological tumors and able to initiate tumor formation and metastasis. Cancer stem cells are more resistant to chemotherapeutic agents and radiation therapy than more mature cell types from the same tissue.

Inflammatory Cells in Tumor Microenvironment

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