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

MCs are tissue-based immune cells that respond to signals of innate and adaptive immunity as well as to non-immunological stimuli. The outcome of MC stimulation by multiple triggers is the immediate and delayed release of biologically active mediators. Mediators produced by MCs are conventionally divided into (1) preformed mediators, (2) newly synthesized lipid mediators, and (3) cytokines/chemokines. Indeed, when MCs are activated they immediately extrude granule-associated substances, such as histamine and, within minutes, generate lipid-derived mediators (Galli et al. 2005a). Within hours, MC activation is followed by the de novo synthesis of numerous cytokines and chemokines. These categories are not absolutely exclusive because at least one cytokine, TNF-α, occurs both preformed and as a newly synthesized molecule.

Mast Cell Mediators

Mast cells and basophils are granulated cells, which share similar phenotypic and functional properties. They express complementary and partially overlapping roles in acquired and innate immunity, including both effector and regulatory activities, but they also display important distinctive features as to developmental lineage, mediator content, and function. They cooperate in expanding and/or modulating inflammation as well as in mediating subsequent tissue repair. Mast cells release in the inflammatory scenario a series of potent proangiogenic molecules that stimulate vessel sprouting and new vessel formation. Recent data suggest that basophils may also play a role in inflammation-related angiogenesis, principally but not exclusively through the expression of several forms of VEGF and their receptors. This review focuses on the potential cooperative link between mast cells and basophils in promoting angiogenesis during allergic inflammation. We discuss the multifaceted roles of mast cells and basophils in the inflammatory setting during allergic diseases and whether these cells can be both source and target cells for proangiogenic mediators.

/pdf/cooperation-of-mast-cells-and-basophils-in-allergy-3f90i06fid.pdf

Cooperation of Mast Cells and Basophils in Allergy

The role of microenvironment in the control of tumor angiogenesis / , The role of microenvironment in the control of tumor angiogenesis / , کتابخانه دیجیتال جندی شاپور اهواز

The Role of Microenvironment in the Control of Tumor Angiogenesis

Angiogenesis has been implicated in the pathobiology of multiple sclerosis (MS). Osteopontin exerts a pro-angiogenetic effect and is increased in body fluid of MS patients. To evaluate the effect of 1 year natalizumab treatment on serum pro-angiogenic activity and on plasma osteopontin levels in relapsing (RR) MS patients. Ten RRMS patients scheduled for natalizumab treatment were enrolled and evaluated at baseline and after 1-year natalizumab treatment. Pro-angiogenic activity was assessed by a chick embryo chorioallantoic membrane assay (CAM), osteopontin levels were evaluated by an enzyme-linked immunosorbent assay. Plasma and serum samples of 10 treatment-naive RRMS and 10 healthy controls (HCs) were used as controls of baseline evaluations. Both treatment-naive and natalizumab scheduled RRMS patients had higher baseline vessel density (22.0 ± 3.9 and 22.5 ± 2.6, p < 0.0001) and higher osteopontin levels (65.7 ± 24.3 ng/ml and 65.9 ± 16.6 ng/ml, p = 0.019 and p = 0.029, respectively) than HCs (9.0 ± 2.2; 48.5 ± 7.8 ng/ml, respectively). Baseline osteopontin levels and vessel density were significantly correlated (rs = 0.373, p = 0.043). After 1 year of treatment, the number of vessels and the osteopontin levels, were significantly reduced (11.9 ± 2.1, p < 0.005; 49.3 ± 20.0 ng/ml, p = 0.028). Our results suggest that natalizumab could exert its anti-inflammatory properties also by inhibiting the angiogenetic mechanisms in RRMS patients.

Natalizumab reduces serum pro-angiogenic activity in MS patients

Starting with the hypothesis formulated by Judah Folkman that tumor growth is angiogenesis-dependent, this area of research has a solid scientific foundation, and inhibition of angiogenesis is a major area of therapeutic development for the treatment of cancer. This chapter offers an account of the most relevant discoveries in this field of biomedical research.

The Discovery of Tumor Angiogenesis Factors: A Historical Overview.

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