DermKnowledgeBASE: telangiectasia

telangiectasia

Semantic LIterature Summary Engine (SLISE)

( SLISE(Summary) - Drag this link to bookmarks bar for instant search)

Skin Deep - A Dermatology Blog

Loading........Please wait.

The text is the summary of recent articles on telangiectasia at 75 thresold from National Library of Medicine (NLM). This information is subject to NCBI's Disclaimer and Copyright notice.


The primary treatment for this subset of IHs is pharmacological intervention, and propranolol has become the new first-line treatment for complicated hemangiomas [1]. There were no instances of life-threatening complications after propranolol [2]. Asano, Department of Dermatology, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8655, Japan [3]. In patients with SSc, serum CXCL6 levels correlated positively with the severity of Dermal and Pulmonary Fibrosis and were elevated in association with Cardiac and Pulmonary Vascular involvement and cutaneous Vascular symptoms, including raynaud phenomenon, digital Ulcers (DU)/pitting scars, and telangiectasia [4]. In this example protocol, we will utilize isotope dilution MRM-MS to quantify in absolute terms the total levels of the protein of interest, ataxia telangiectasia mutated (ATM) serine/threonine protein kinase [5].

To test this hypothesis, we studied the effect of USP7 inhibition in Chronic Lymphocytic leukemia (CLL) where the ataxia telangiectasia mutated (ATM)-p53 pathway is inactivated with relatively high frequency, leading to treatment resistance and poor clinical outcome [6]. After 6-24 months of followup, telangiectasia, skin pigmentation, Atrophy, Fibrosis, and ulceration were scored according to both RTOG and LENT-SOMA Scale criteria [7]. Patients with various forms of liver diseases including acute hepatic failure, and others with normal hepatic function like hereditary hemorrhagic telangiectasia (HHT), inflammatory and parasitic disorders, cardiogenic hepatopulmonary syndrome (cHPS) and skin disorders like dyskeratosis congenita are all known to cause PAVMs [8]. Over a period of the last two decades our understanding of the pathogenesis of PAVMs has changed, but the mechanisms are still not clearly understood [9]. Identifying and preventing or treating the underlying mechanisms will significantly influence the management of a large group of patients who at present cannot be effectively treated with a very poor prognosis [10].

To date there is no evidence of Atrophy, telangiectasia or Hypopigmentation resulting from its use [11]. (2)Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Utrecht, The Netherlands [12]. However, the exact mechanisms underlying preconditioning remain to be fully understood [13]. Ataxia-telangiectasia mutated (ATM) is regarded as an essential endogenous protective protein against stress [14]. The aim of the present study was therefore to investigate whether ATM mediates H2O2 preconditioning [15].

We report the case of a patient who had severe left atrioventricular valve regurgitation with atrial fibrillation after atrioventricular septal defect repair in her childhood and was diagnosed as having hereditary haemorrhagic telangiectasia by chance [16]. Hexanucleotide (GGGGCC) repeat expansions in a non-coding region of C9orf72 are the major cause of familial ALS and frontotemporal dementia (FTD) worldwide [17]. ATM mutation causes Ataxia telangiectasia (AT), whereby the disease phenotype shows differing characteristics depending on the underlying ATM Mutation [18]. Ataxia telangiectasia mutated (ATM), defective in the human genetic disorder ataxia-telangiectasia (A-T), is the key to initiating a signaling cascade activating the intra-S-phase checkpoint [19]. This technique has been superseded now by direct labeling that distinguishes DNA replication initiations from ongoing sites of replication which are the target for the intra-S-phase checkpoint [20].

Ocular neovascularization is strongly associated with inflammation, but the source of Inflammatory signals and the mechanisms by which these signals regulate the disruption of avascular privilege in photoreceptors are unknown [21]. Combined PE and CDDP targeting synergistically enhanced the expression of markers of DDR (phosphorylation of ataxia-telangiectasia mutated, checkpoint kinase (Chk)-1, Chk-2, and γ-H2A histone family member X) in Cells [22]. Key components of the DDR are the ataxia telangiectasia mutated and Rad3 related (ATR) and checkpoint kinase 1 (CHK1) kinases [23]. By combining single-cell assays of p53 signaling dynamics, small-molecule screening in live Cells, and mathematical modeling, we identified molecules that perturbed p53 dynamics and determined that cell-specific variation in the efficiency of DNA repair and the activity of the kinase ATM (ataxia-telangiectasia mutated) controlled the signaling landscape of p53 dynamics [24].

References: 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 ,

Press Refresh to fetch fresh content with references from pubmed. This content was cached on

comments powered by Disqus

|


This is an experimental application for healthcare professionals. The information presented here is not intended to diagnose, treat, cure or prevent any disease. Read disclaimer.

SkinHelpDesk.com - Evidence based skincare free

About Me

I have varied research interests ranging from eHealth, Health Information Exchange, Clinical Trials and Research, Contact Dermatitis, Bioinformatics, and Cosmetic Dermatology. I have work experience in Canada as an eHealth analyst, and in Dubai and India as a Specialist Dermatologist.

Address

Bell Raj Eapen
Hamilton, ON
Canada