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telangiectasia

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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.


A byproduct of peroxisomal metabolism is the generation, and subsequent detoxification, of reactive oxygen and nitrogen species, particularly hydrogen peroxide (H2O2) [1]. More recently the Tumor suppressors ataxia telangiectasia mutate (ATM) and tuberous sclerosis complex (TSC), which regulate mTORC1 signaling, have been found to regulate pexophagy in response to variable levels of certain reactive oxygen and nitrogen species [2]. Identification of the pathogenic Mutation in each family was performed in a timely fashion, allowing the fetuses to be tested and diagnosed [3]. The patient was subsequently diagnosed with hereditary hemorrhagic telangiectasia and underwent cerebral abscess drainage as well as transcatheter endovascular closure of Multiple Pulmonary arteriovenous malformations [4]. An in vitro functional test found that miR-2964a-5p specifically down-regulated luciferase reporter expression and ATM expression in the cell lines transfected with rs4585 T allele compared to rs4585 G allele [5].

Chronic interferon production stemmed from accumulation of DNA in cytoplasm of AT and Artemis deficient Cells [6]. Here, we investigated the Aspergillus fumigatus AtmA (Ataxia-telangiectasia mutated) and AtrA kinases and how they impact virulence and the evolution of azole resistance [7]. A pathogenic DNA sequence variant in the ENG, ACVRL1 or SMAD4 genes, can be found in the majority of patients [8]. The driver for the current Clinical Statement was the plethora of new data since previous hereditary haemorrhagic telangiectasia (HHT) guidelines generated in 2006 and a systematic Cochrane Review for PAVM embolisation in 2011 [9]. acute radiodermatitis is a burn injury that varies in severity according to both treatment and inherent patient factors [10].

Most acute radiodermatitis reactions resolve after several weeks but some reactions persist and can cause complications [11]. Late-onset radiodermatitis is characterized by telangiectasia that forms on Atrophic and Fragile skin [12]. Also, in late-onset radiodermatitis pulsed dye Laser treatment has been shown to be beneficial in clearing radiation-induced telangiectasia [13]. The E2-modulated gene, Ataxia telangiectasia mutated (ATM), was repressed in hypoxia via GPER signalling [14]. E2 treatment enhanced hypoxia-induced expression of HIF1-α and VEGFA, but repressed HIF1-α and VEGFA expression under normoxic conditions [15].

The expression and repression of VEGFA by E2 were mediated by a GPER-dependent mechanism [16]. The purpose of this case report is to report pars plana vitrectomy for the treatment of full thickness Macular hole in a patient with Adult onset Coats disease [17]. A young male presented with decreased vision in his right Eye because of full thickness Macular hole [18]. The patient underwent Laser photocoagulation to the Vascular telangiectasia followed by pars plana vitrectomy, large internal limiting membrane peeling and gas tamponade [19]. This resulted in regression of exudation, closure of Macular hole and improvement in vision [20].

Coats disease of Adult onset can present with decreased vision because of full thickness Macular hole [21]. Among other risk factors, Helicobacter pylori infection is considered the main driving factor of GC development [22]. An early step in double strand break repair is the recruitment of (ataxia-telangiectasia mutated serine/threonine kinase (ATM) to the damaged site, where it plays a key role in advancing the DNA damage checkpoint process [23]. Using western blotting, it was demonstrated that LDIR at 75 mGy induced the expression of ataxia-telangiectasia mutated (ATM) protein in PC-3 as well as RWPE-1 Cells [24]. On the contrary, 2 patients with significant foveal Atrophy and Macular hole in B-scan showed changes of early disease in OCTA [25].

ENG is an essential component of the endothelial nitric oxide synthase activation complex [26]. ENG Deficiency also impairs the regulation of Vascular tone, which contributes to the pathogenesis of brain arteriovenous malformation (bAVM) and vasospasm [27]. In human, functional haploinsufficiency of ENG gene causes type I hereditary hemorrhagic telangiectasia (HHT1), an Autosomal Dominant disorder [28]. Compared to normal population, HHT1 patients have a higher prevalence of AVM in Multiple organs including the brain [29]. Azelaic acid has been found to inhibit the pathologic expression of cathelicidin, as well as the hyperactive protease activity that cleaves cathelicidin into LL-37 [30].

Use of azelaic acid was associated with a significant reduction in inflammatory lesions, which persisted beyond the active treatment phase [31]. CC-115 also indirectly reduces the phosphorylation of ataxia-telangiectasia mutated kinase (ATM) at S1981 and its substrates as well as homologous recombination (HR) [32]. CC-115 inhibits colony formation of ATM-deficient Cells more potently than ATM-proficient Cells, indicating that inhibition of DNA-PK is synthetically lethal with the loss of functional ATM [33]. Immunohistochemical staining showed dispersed Distribution of angiostatin throughout the Mucosal and submucosal layers in CRP lesions, while angiostatin accumulated within the vessel lumens in non-CRP tissues [34]. Compensatory telangiectasia in the Mucosa, vessel stenosis, and reduced MVD might attenuate blood flow in the submucosa and contribute to CRP progression [35].

The Number of telangiectasia and plugged meibomian gland orifices significantly decreased from baseline after 1 month of diquafosol use [36].

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 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 ,

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