Τρίτη 30 Μαΐου 2017
Cancers, Vol. 9, Pages 61: A Novel Micro Cold Atmospheric Plasma Device for Glioblastoma Both In Vitro and In Vivo
Cold atmospheric plasma (CAP) treatment is a rapidly expanding and emerging technology for cancer treatment. Direct CAP jet irradiation is limited to the skin and it can also be invoked as a supplement therapy during surgery as it only causes cell death in the upper three to five cell layers. However, the current cannulas from which the plasma emanates are too large for intracranial applications. To enhance efficiency and expand the applicability of the CAP method for brain tumors and reduce the gas flow rate and size of the plasma jet, a novel micro-sized CAP device (µCAP) was developed and employed to target glioblastoma tumors in the murine brain. Various plasma diagnostic techniques were applied to evaluate the physics of helium µCAP such as electron density, discharge voltage, and optical emission spectroscopy (OES). The direct and indirect effects of µCAP on glioblastoma (U87MG-RedFluc) cancer cells were investigated in vitro. The results indicate that µCAP generates short- and long-lived species and radicals (i.e., hydroxyl radical (OH), hydrogen peroxide (H2O2), and nitrite (NO2−), etc.) with increasing tumor cell death in a dose-dependent manner. Translation of these findings to an in vivo setting demonstrates that intracranial µCAP is effective at preventing glioblastoma tumor growth in the mouse brain. The µCAP device can be safely used in mice, resulting in suppression of tumor growth. These initial observations establish the µCAP device as a potentially useful ablative therapy tool in the treatment of glioblastoma.
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Prenatal Diagnosis of Atrioventricular Block and QT Interval Prolongation by Fetal Magnetocardiography in a Fetus with Trisomy 18 and SCN5A R1193Q Variant
We report a case of fetal trisomy 18 with SCN5A R1193Q variant that presented with sinus bradycardia, 2 : 1 atrioventricular block (AVB), and QT interval prolongation. These complex arrhythmias were diagnosed by fetal magnetocardiography combined with ultrasound findings. Advanced AVB and ventricular arrhythmias were confirmed after birth. Genetic testing of the baby revealed a SCN5A R1193Q variant, which we considered could account for the various arrhythmias in this case.
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Prognostic role of pretreatment blood neutrophil-to-lymphocyte ratio in advanced cancer survivors: A systematic review and meta-Analysis of 66 cohort studies
Source:Cancer Treatment Reviews
Author(s): Zubing Mei, Lu Shi, Bo Wang, Jizhen Yang, Zhihong Xiao, Peixin Du, Qingming Wang, Wei Yang
BackgroundNeutrophil-to-lymphycyte ratio (NLR) is crucial for the incidence and mortality of various tumors. However, little is known on NLR and its association with prognosis in advanced tumors. Here we performed a meta-analysis to establish the prognostic significance of pretreatment blood NLR for advanced tumors.MethodsA systematic literature search through April 2016 was performed to evaluate the association between pretreatment blood NLR and overall survival (OS) or progression-free survival (PFS) in patients with advanced tumors. Data were extracted from studies reporting hazard ratios (HRs) and 95% confidence interval (CI) and pooled using the Mantel–Haenszel random-effect model.ResultsSixty-six studies with a total of 24536 individuals were included in the meta-analysis. Pooled analyses revealed that elevated pretreatment NLR was associated with worse OS (HR 1.70, 95% CI 1.57 to 1.84, P <0.001) and PFS (HR 1.61, 95% CI 1.42 to 1.82, P <0.001) in advanced tumors. Subgroup analysis stratified by tumor type demonstrated that pancreatic cancer patients with high pretreatment NLR had the worst OS (HR 1.94, 95% CI 1.55 to 2.54, P < 0.001) and colorectal cancer with the worst PFS (HR 1.74, 95% CI 1.04 to 2.90, P < 0.001). When stratified by cut-off value for NLR, we found that cut-off value being five indicated the worst PFS (HR 2.23, 95% CI 1.54 to 3.23, P=0.019).ConclusionsOverall, high pretreatment blood NLR could be an adverse prognostic indicator for advanced tumor. Large-scale prospective studies investigating its survival outcomes in specific cancer type are strongly advocated.
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Sore throat and an ache radiating from the centre of the anterior neck to the both ears and the occiput.Idiopathic Carotidynia,TransIent Perivascular Inflammation of the Carotid artery (TIPIC) syndrome,Vascular Neck Pain,Painful carotid artery,Inflammation of Carotid artery and neck pain,Carotidynia on ultrasound and magnetic resonance imaging,CT findings in a patient with bilateral metachronous carotidyniaContralateral recurrence of carotidynia during steroid therapy,,Carotidynia Possibly due to Localized Vasculitis,
Carotidynia
Carotidynia is a syndrome characterized by unilateral (one-sided) tenderness of the carotid artery, near the bifurcation. It was first described in 1927 by Temple Fay.[1] The most common cause of carotidynia may be migraine, and then it is usually self-correcting. Common migraine treatments may help alleviate the carotidynia symptoms. Recent histological evidence has implicated an inflammatory component of carotidynia, but studies are limited.[2] Carotid arteritis is a much less common cause of carotidynia, but has much more serious consequences. It is a form ofgiant cell arteritis, which is a condition that usually affects arteries in the head. Due to this serious condition possibly causing carotidynia, and the possibility that neck pain is related to some other non-carotidynia and serious condition, the case should be investigated by a medical doctor.[3]Because carotidynia can be caused by numerous causes, Biousse and Bousser in 1994 recommended the term not be used in the medical literature.[4] However, recent MRI and ultrasound studies have supported the existence of a differential diagnosis of carotidynia consistent with Fay's characterization.[5][6]
References
- Hill and Hastings list this reference as: Fay, Temple (1927) "Atypical neuralgia." Arch Neurol Psychiatry.
- Upton, P.; Smith, J. G.; Charnock, D. R. (2003). "Histologic confirmation of carotidynia". Otolaryngology - Head and Neck Surgery. 129 (4): 443–444. doi:10.1016/S0194-5998(03)00611-9. PMID 14574303.
- Hill LM, Hastings G (1994). "Carotidynia: a pain syndrome.". J Fam Pract. 39 (1): 71–5. PMID 8027735.
- Biousse V, Bousser MG (1994). "The myth of carotidynia.". Neurology. 44 (6): 993–5. doi:10.1212/wnl.44.6.993. PMID 8208434.Available here
- Lee TC, Swartz R, McEvilly R, Aviv RI, Fox AJ, Perry J, Symons SP. CTA, MR and MRA imaging of carotidynia: case report. Canadian Journal of Neurological Sciences. 2009 May; 36(3):373-375.
- Kuhn, J.; Harzheim, A.; Horz, R.; Bewermeyer, H. (2006). "MRI and ultrasonographic imaging of a patient with carotidynia". Cephalalgia. 26 (4): 483–485. doi:10.1111/j.1468-2982.2006.01053.x. PMID 16556251.
External links
- Family Practice notebook.com
- Blog assessing whether carotidynia is a valid medical diagnosis.
- Carotidynia condition page on PatientsLikeMe.
- This page was last edited on 5 March 2017, at 00:34.
- Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization.
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Morphologic characterization of residual DNA methylation in the gastric mucosa after Helicobacter pylori eradication
Abstract
Residual DNA methylation in the gastric mucosa after Helicobacter pylori (H. pylori) eradication may have a role in gastric carcinogenesis. We examined the association between morphologic features and promoter methylation status of non-neoplastic gastric mucosa especially after H. pylori eradication. A total of 140 gastric specimens from 99 participants who had at least 6 months of post-eradication period were examined. The magnifying narrow-band imaging (NBI) endoscopic feature of gastric mucosa was divided into two types: restored-small, round pits, accompanied with honeycomb-like subepithelial capillary networks; atrophic-well-demarcated oval or tubulovillous pits with clearly visible coiled or wavy vessels. Methylation status of five candidate genes (MYOD1, SLC16A12, IGF2, RORA, and PRDM5) were examined by bisulfite pyrosequencing. The atrophic type, informative endoscopic features of intestinal metaplasia, demonstrated higher methylation levels in all five genes compared to the restored type (all P < 0.0001). In the restored type, methylation levels were significantly lower among the samples with longer post-eradication period (for all genes, P < 0.0001), which was not observed in atrophic type (for all genes, P > 0.1). Multivariate analysis demonstrated that atrophic type or presence of intestinal held an independent factor for hyper methylation (odds ratio: 24.69, 95% confidence interval: 6.95–87.76, P < 0.0001). The atrophic type by the magnifying NBI and presence of intestinal metaplasia are the morphologic characteristics of residual DNA methylation of after H. pylori eradication, regardless of the post-eradication period and it might be considered as the epigenetic irreversible point with H. pylori eradication.
Residual DNA methylation in the gastric mucosa after Helicobacter pylori (H. pylori) eradication may have a role in gastric carcinogenesis, but the morphologic characteristics of this methylation anomaly have not been clearly described. We showed that the morphologic features visualized by the magnifying narrow-band imaging endoscopy well characterize the DNA methylation status in the gastric mucosa after H. pylori eradication, suggesting its reliability to estimate the "field defect".
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Morphologic characterization of residual DNA methylation in the gastric mucosa after Helicobacter pylori eradication
Abstract
Residual DNA methylation in the gastric mucosa after Helicobacter pylori (H. pylori) eradication may have a role in gastric carcinogenesis. We examined the association between morphologic features and promoter methylation status of non-neoplastic gastric mucosa especially after H. pylori eradication. A total of 140 gastric specimens from 99 participants who had at least 6 months of post-eradication period were examined. The magnifying narrow-band imaging (NBI) endoscopic feature of gastric mucosa was divided into two types: restored-small, round pits, accompanied with honeycomb-like subepithelial capillary networks; atrophic-well-demarcated oval or tubulovillous pits with clearly visible coiled or wavy vessels. Methylation status of five candidate genes (MYOD1, SLC16A12, IGF2, RORA, and PRDM5) were examined by bisulfite pyrosequencing. The atrophic type, informative endoscopic features of intestinal metaplasia, demonstrated higher methylation levels in all five genes compared to the restored type (all P < 0.0001). In the restored type, methylation levels were significantly lower among the samples with longer post-eradication period (for all genes, P < 0.0001), which was not observed in atrophic type (for all genes, P > 0.1). Multivariate analysis demonstrated that atrophic type or presence of intestinal held an independent factor for hyper methylation (odds ratio: 24.69, 95% confidence interval: 6.95–87.76, P < 0.0001). The atrophic type by the magnifying NBI and presence of intestinal metaplasia are the morphologic characteristics of residual DNA methylation of after H. pylori eradication, regardless of the post-eradication period and it might be considered as the epigenetic irreversible point with H. pylori eradication.
Residual DNA methylation in the gastric mucosa after Helicobacter pylori (H. pylori) eradication may have a role in gastric carcinogenesis, but the morphologic characteristics of this methylation anomaly have not been clearly described. We showed that the morphologic features visualized by the magnifying narrow-band imaging endoscopy well characterize the DNA methylation status in the gastric mucosa after H. pylori eradication, suggesting its reliability to estimate the "field defect".
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