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

Judah Folkman (1933-2008) made seminal discoveries on the mechanisms of angiogenesis which have opened a field of investigation worldwide. This chapter summarizes the fundamental contribution of Folkman in the setting of angiogenesis assays in vivo and in vitro.

The Fundamental Contribution of Judah Folkman in the Setting of Angiogenesis Assays.

A historical appraisal of angiogenesis assays since Judah Folkman and before...

Summary. In rheumatoid arthritis (RA) tissue macrophages release growth factors, matrix metalloproteinases, cytokines, and chemokines. While in normal joints there is a balance between proinflammatory and anti-inflammatory cytokines, an imbalance between these inducers and inhibitors of inflammation occurs in RA, where macrophages are responsible for inducing inflammation, matrix destruction and angiogenesis.

https://digitum.um.es/xmlui/bitstream/10201/27579/1/Macrophages%20in%20rheumatoid%20arthritis.pdf

Review Macrophages in rheumatoid arthritis

The relationship between endothelial cells (EC) and haematopoietic cells (HC) has been seen as an indication that a common progenitor, the haemangioblast, gives rise to both cell types in the yolk sac, the initial site of haematopoiesis and of blood vessel formation (Murray, 1934). Generation of haemangioblasts take place from embryonic stem cells (ESC) or from yolk sac blood islands or from intraembryonic AGM (aortagonad-mesonephros) region, containing the dorsal aorta, genital ridge/gonads and promesonephros.

Cross Talk between Haematopoiesis and Angiogenesis

Granulomatosis with polyangiitis (GPA) is a relatively rare necrotizing vasculitis belonging to the so-called ANCA-associated vasculitides, in that circulating anti-proteinase-3 neutrophil cytoplasmic antibodies (c-ANCA) can be detected in the large majority of patients. The major clinical manifestations include necrotizing granulomatous lesions in the upper and/or lower respiratory tract, and glomerulonephritis. Although generalized necrotizing vasculitis involving both arteries and veins is a frequent indication of its systemic character, limited forms restricted to paranasal sinuses can also be observed. In the absence of suitable therapies, the disease can lead to death in a high percentage of patients. The introduction of glucocorticoids associated to cyclophosphamide has marked a milestone in the treatment of GPA. This combination has in fact been able to remarkably improve the previously ominous prognosis of these patients, resulting in a 10-years’ survival rate of approximately 75 %. More recently, additional immunosuppressive drugs such as azathioprine, methotrexate, and rituximab have been employed, with comparable or even better results.

Granulomatosis with Polyangiitis (Wegener’s)

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