Τρίτη 9 Φεβρουαρίου 2016
Road Perception Based Geographical Routing Protocol for Vehicular Ad Hoc Networks
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Performance Investigation of 40 GB/s DWDM over Free Space Optical Communication System Using RZ Modulation Format
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Development of Synthetic and Natural Materials for Tissue Engineering Applications Using Adipose Stem Cells
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Synthesis, Crystal Structure, Spectroscopic Properties, and Interaction with Ct-DNA of Zn(II) with 2-Aminoethanethiol Hydrochloride Ligand
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Synthesis and Characterization of Chitosan Nanoaggregates from Gladius of Uroteuthis duvauceli
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Identification of Contour Lines from Average-Quality Scanned Topographic Maps
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A Retained Bullet in Pericardial Sac: Penetrating Gunshot Injury of the Heart
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Prosthodontic Management of Xerostomic Patient: A Technical Modification
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Role of Viral miRNAs and Epigenetic Modifications in Epstein-Barr Virus-Associated Gastric Carcinogenesis
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Propagation of Love-Type Wave in Porous Medium over an Orthotropic Semi-Infinite Medium with Rectangular Irregularity
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Double homozygous mutations (R275W and M432V) in the ParkinGene associated with late-onset Parkinson's disease
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Are more effective placebos complicating clinical trials?
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Purkinje cell loss in essential tremor: Random sampling quantification and nearest neighbor analysis
ABSTRACT
Introduction
Purkinje cell loss has been documented in some, although not all, postmortem studies of essential tremor. Hence, there is considerable controversy concerning the presence of Purkinje cell loss in this disease. To date, few studies have been performed.
Methods
Over the past 8 years, we have assembled 50 prospectively studied cases and 25 age-matched controls; none were reported in our previous large series of 33 essential tremor and 21 controls. In addition to methods used in previous studies, the current study used a random sampling approach to quantify Purkinje cells along the Purkinje cell layer with a mean of 217 sites examined in each specimen, allowing for extensive sampling of the Purkinje cell layer within the section. For the first time, we also quantified the distance between Purkinje cell bodies—a nearest neighbor analysis.
Results
In the Purkinje cell count data collected from fifteen 100 × fields, cases had lower counts than controls in all three counting criteria (cell bodies, nuclei, and nucleoli; all P < 0.001). Purkinje cell linear density was also lower in cases than controls (all P < 0.001). Purkinje cell linear density obtained by random sampling was similarly lower in cases than controls in all three counting criteria (cell bodies, nuclei, and nucleoli, all P ≤ 0.005). In agreement with the quantitative Purkinje cell counts, the mean distance from one Purkinje cell body to another Purkinje cell body along the Purkinje cell layer was greater in cases than controls (P = 0.002).
Conclusions
These data provide support for the neurodegeneration of cerebellar Purkinje cells in essential tremor. © 2016 International Parkinson and Movement Disorder Society
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Research consent capacity varies with executive function and memory in Parkinson's disease
ABSTRACT
Background
We examined the association between cognitive domains and research consent capacity in PD. Our hypothesis was that research consent capacity is best predicted by executive function.
Methods
A cohort of 90 PD patients and 30 healthy older adults were administered the MacArthur Competence Assessment Tool for Clinical Research, Dementia Rating Scale-2, and the MoCA. Experts classified patients as either “capable” or “not capable” of providing informed consent to participate in two clinical trials.
Results
MacArthur Competence Assessment Tool for Clinical Research Reasoning scores for both clinical trial types were most associated with executive functions and delayed recall. As scores on these domains improved, the odds of an expert rating of “capable of consent” increased.
Conclusions
These results extend our previous findings by demonstrating that memory and executive abilities appear closely associated with capacity when evaluated using either a structured interview or expert judgment of that interview. © 2016 International Parkinson and Movement Disorder Society
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Validation of conversion between mini–mental state examination and montreal cognitive assessment
ABSTRACT
Introduction
Harmonizing data across cohorts is important for validating findings or combining data in meta-analyses. We replicate and validate a previous conversion of MoCA to MMSE in PD.
Methods
We used five studies with 1,161 PD individuals and 2,091 observations measured with both the MoCA and MMSE. We compared a previously published conversion table using equipercentile equating with log-linear smoothing to our internally derived scores.
Results
Both conversions found good agreement within and across the studies when comparing true and converted MMSE (mean difference: 0.05; standard deviation: 1.84; median difference: 0; interquartile range: –1 to 1, using internal conversion).
Conclusions
These results show that one can get a reliable and valid conversion between two commonly used measures of cognition in PD studies. These approaches need to be applied to other scales and domains to enable large-scale collaborative analyses across multiple PD cohorts. © 2016 International Parkinson and Movement Disorder Society
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Selective connectivity of dopamine neurons projecting to the posterior striatum
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Jadea e il progetto Pink is Good di Fondazione Umberto Veronesi - SilhouetteDonna
SilhouetteDonna |
Jadea e il progetto Pink is Good di Fondazione Umberto Veronesi
SilhouetteDonna Pink is Good dal 2013 si pone un grande obiettivo: combattere il tumore al seno. ... Proprio in occasione di questo progetto, il brand Jadea ha realizzato 4 prodotti “Pink is Good” che saranno disponibili nei negozi a partire dal mese di febbraio: un ... and more » |
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Another Layer of Defense: The Adaptive Immune System - Discovery Institute
Discovery Institute |
Another Layer of Defense: The Adaptive Immune System
Discovery Institute These regions are called the secondary lymphoid tissue and consist of the lymph nodes, the spleen, the tonsils, and adenoids and the appendix. After they mature, lymphocytes migrate back and forth between the blood and the secondary lymphoid tissue ... |
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Moyamoya Disease: A Rare Sickle Cell Trait Neurological Complication
The post Moyamoya Disease: A Rare Sickle Cell Trait Neurological Complication appeared first on Welcome to Avens.
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Distinct oxidative cleavage and modification of bovine [cu- zn]-SOD by an ascorbic acid/cu(II) system: Identification of novel copper binding site on SOD molecule
Source:Free Radical Biology and Medicine
Author(s): Hiroshi Uehara, Shen Luo, Baikuntha Aryal, Rodney L. Levine, V. Ashutosh Rao
We investigated the combined effect of ascorbate and copper [Asc/Cu(II)] on the integrity of bovine [Cu-Zn]-superoxide dismutase (bSOD1) as a model system to study the metal catalyzed oxidation (MCO) and fragmentation of proteins. We found Asc/Cu(II) mediates specific cleavage of bSOD1 and generates 12.5 and 3.2kDa fragments in addition to oxidation/carbonylation of the protein. The effect of other tested transition metals, a metal chelator, and hydrogen peroxide on the cleavage and oxidation indicated that binding of copper to a previously unknown site on SOD1 is responsible for the Asc/Cu(II) specific cleavage and oxidation. We utilized tandem mass spectrometry to identify the specific cleavage sites of Asc/Cu(II)-treated bSOD1. Analyses of tryptic- and AspN-peptides have demonstrated the cleavage to occur at Gly31 with peptide bond breakage with Thr30 and Ser32 through diamide and α-amidation pathways, respectively. The three-dimensional structure of bSOD1 reveals the imidazole ring of His19 localized within 5 Angstrom from the α-carbon of Gly31 providing a structural basis that copper ion, most likely coordinated by His19, catalyzes the specific cleavage reaction.
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Lend your voice to karaoke night for crackin' cancer cause - Northern Star
Northern Star |
Lend your voice to karaoke night for crackin' cancer cause
Northern Star “IT'S a bit of a tongue-in-cheek thing, in that it's not a karaoke competition per se, it's about having fun.” That's the chorus being sung by Patrick Fitz-Bugden about the inaugural Lismore Corporate Karaoke Cup he's organising in aid of cancer patients. |
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Solid cancer incidence among Chinese medical diagnostic X-ray workers, 1950-1995: estimation of radiation-related risks
Abstract
The objective of this study was to estimate solid cancer risk attributable to long-term, fractionated occupational exposure to low-doses of ionizing radiation. Based on cancer incidence for the period 1950-1995 in a cohort of 27,011 Chinese medical diagnostic X-ray workers and a comparison cohort of 25,782 Chinese physicians who did not use X-ray equipment in their work, we used Poisson regression to fit excess relative risk (ERR) and excess absolute risk (EAR) dose-response models for incidence of all solid cancers combined. Radiation dose reconstruction was based on a previously published method that relied on simulating measurements for multiple X-ray machines, workplaces and working conditions, information about protective measures, including use of lead aprons, and work histories. The resulting model was used to estimate calendar year-specific badge dose calibrated as personal dose equivalent (Sv). To obtain calendar year-specific colon doses (Gy), we applied a standard organ conversion factor. 1643 cases of solid cancer were identified in 1.45 million person-years of follow-up. In both ERR and EAR models, a statistically significant radiation dose-response relationship was observed for solid cancers as a group. Averaged over both sexes, and using colon dose as the dose metric, the estimated ERR/Gy was 0.87 (95% CI: 0.48, 1.45), and the EAR was 22 per 104PY-Gy (95% CI: 14, 32) at age 50. We obtained estimates of the ERR and EAR of solid cancers per unit dose that are compatible with those derived from other populations chronically exposed to low dose-rate occupational or environmental radiation. This article is protected by copyright. All rights reserved.
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Methylation in Benign Prostate and Risk of Disease Progression in Men Subsequently Diagnosed with Prostate Cancer
Abstract
In DNA from prostate tumors, methylation patterns in gene promoter regions can be a biomarker for disease progression. It remains unclear whether methylation patterns in benign prostate tissue—prior to malignant transformation—may provide similar prognostic information. To determine whether early methylation events predict prostate cancer outcomes, we evaluated histologically benign prostate specimens from 353 men who eventually developed prostate cancer and received “definitive” treatment (radical prostatectomy [58%] or radiation therapy [42%]). Cases were drawn from a large hospital-based cohort of men with benign prostate biopsy specimens collected between 1990 and 2002. Risk of disease progression associated with methylation was estimated using time-to-event analyses. Average follow-up was over 5 years; biochemical recurrence (BCR) occurred in 91 cases (26%). In White men, methylation of the APC gene was associated with increased risk of BCR, even after adjusting for standard clinical risk factors for prostate cancer progression (adjusted hazard ratio (aHR)=2.26; 95%CI 1.23-4.16). APC methylation was most strongly associated with a significant increased risk of BCR in White men with low prostate specific antigen at cohort entry (HR=3.66; 95%CI 1.51–8.85). In additional stratified analyses, we found that methylation of the RARB gene significantly increased risk of BCR in African American cases who demonstrated methylation of at least one of the other four genes under study (HR=3.80; 95%CI 1.07–13.53). These findings may have implications in the early identification of aggressive prostate cancer as well as reducing unnecessary medical procedures and emotional distress for men who present with markers of indolent disease. This article is protected by copyright. All rights reserved.
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Equivalent chemotherapy efficacy against leukemia in mice treated with topical vasoconstrictors to prevent cancer therapy side effects
Abstract
Topically applied vasoconstrictor is a new strategy to prevent oral mucositis and alopecia, two complications of chemotherapy and stem-cell transplant. We sought to determine whether mice treated with topical vasoconstrictor minutes before chemotherapy to suppress L1210 leukemia would develop a vasoconstrictor-induced L1210 cell sanctuary, and with it, significantly worse survival outcomes. B6D2F1 mice received 104 mouse L1210 leukemia cells via retro-orbital intravenous injection and were then divided into treatment groups, which included: i) no further treatment, ii) a single, sub-curative, intraperitoneal dose of cyclophosphamide (90 µg/gm bw) 24 hr after L1210 cell inoculation, iii) topical epinephrine (25-400 mM) to clipped dorsal backs 20 min before cyclophosphamide, or iv) orotopical phenylephrine (16-130 mM), epinephrine (10 mM) or norepinephrine (25 mM) 20 min before cyclophosphamide. All mice were then followed until day of death. Differences in median survival time and percent survival between mice receiving cyclophosphamide alone and mice treated with either orotopical phenylephrine, epinephrine or norepinephrine; or topical epinephrine before cyclophosphamide were not significantly different. A discernible leukemia sanctuary was not created by topical vasoconstrictor treatment prior to chemotherapy; there was no significant difference in leukemia progression between untreated mice and those treated with either orotopical or topical vasoconstrictor before chemotherapy. We have opened a Phase I/IIa dose escalation trial to evaluate the safety and efficacy of orotopical phenylephrine in preventing oral mucositis in subjects undergoing hematopoietic stem cell transplant conditioning with cyclophosphamide plus total body irradiation. This could provide a cost-effective and convenient method to prevent oral mucositis. This article is protected by copyright. All rights reserved.
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Blood glucose fluctuation accelerates renal injury involved to inhibit the AKT signaling pathway in diabetic rats
Abstract
Blood glucose fluctuation is associated with diabetic nephropathy. However, the mechanism by which blood glucose fluctuation accelerates renal injury is not fully understood. The aim of the present study was to assess the effects of blood glucose fluctuation on diabetic nephropathy in rats and investigate its underlying mechanism. Diabetes in the rats was induced by a high sugar, high-fat diet, and a single dose of STZ (35 mg/kg)-injected intraperitoneally. Unstable blood sugar models were induced by subcutaneous insulin injection and intravenous glucose injection alternately. Body weight, glycosylated hemoglobin A1c (HbAlc), blood urea nitrogen (BUN), serum creatinine (Scr), and Creatinine clearance (Ccr) were assessed. T-SOD activity and MDA level were measured by assay kit. Change in renal tissue ultrastructure was observed by light microscopy and electron microscopy. Phosphorylated ser/thr protein kinase (p-AKT) (phosphor-Ser473), phosphorylated glycogen synthase kinase-3 beta (p-GSK-3β) (phosphor-Ser9), Bcl-2-associated X protein (BAX), B cell lymphoma/leukemia 2 (BCL-2), and cleaved-cysteinyl aspartate-specific proteinase-3 (caspase-3) levels were detected by immunohistochemistry and Western blot. We observed that BUN and Scr were increased in diabetic rats, and Ccr was decreased. Furthermore, blood glucose fluctuations could exacerbate the Ccr changes. Renal tissue ultrastructure was also seriously injured by glucose variability in diabetic rats. In addition, glucose fluctuation increased the oxidative stress of renal tissue. Moreover, fluctuating blood glucose decreased p-AKT level and BCL-2, and increased p-GSK-3β, BAX, cleaved-caspase-3 levels, and ratio of BAX/BCL-2 in the kidneys of diabetic rats. In conclusion, these results suggest that blood glucose fluctuation accelerated renal injury is due, at least in part to its oxidative stress promoting and inhibiting the AKT signaling pathway in diabetic rats.
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Association of primary aldosteronism with chronic thyroiditis
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Electrocardiographic and scintigraphic evaluation of patients with subclinical hyperthyroidism during workout
Abstract
Subclinical hyperthyroidism (sHT) was found to be associated with elevated heart rate, blood pressure and increased risk of extrasystoles. However, the full clinical relevance of morphological and functional implications of sHT on the cardiovascular system is still a matter of debate. The aim of the study was to prospectively assess the influence of endogenous sHT on exercise capacity and cardiac function during workout with the use of exercise electrocardiography (ExECG) and perfusion scintigraphy. The studied group consisted of 44 consecutively recruited patients diagnosed with sHT. In all patients, ExECG, followed by post-exercise myocardial perfusion imaging, was performed. Both ExECG and scintigraphy were performed twice—in the state of sHT and after euthyroidism was restored. An average time period of exercise test was significantly longer in the state of euthyroidism than in sHT. An average oxygen consumption during exercise test was also higher after euthyroidism was achieved when compared to sHT. The end-diastolic and end-systolic volume indexes, stroke volume index and cardiac index were significantly larger in patients with sHT if compared values achieved after euthyroidism restoration. Stroke volume index was negatively correlated with TSH, and positively with free thyroid hormones values in the state of sHT, before euthyroidism was achieved. Cardiac index was positively correlated with free thyroid hormones levels. The obtained results indicate worse physical capacity in subjects with sHT and improvement of several parameters assessed during ExECG and perfusion scintiscan after therapy. Observed changes might reflect the mechanism of the deleterious effect exerted by sHT on the heart.
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Mediterranean diet cools down the inflammatory milieu in type 2 diabetes: the MÉDITA randomized controlled trial
Abstract
Mediterranean-style diets provide cardiovascular benefits and increase insulin sensitivity. There is little evidence that adherence to Mediterranean diet may influence the levels of the inflammatory milieu in type 2 diabetes. The aim of this study was to assess whether Mediterranean diet influences both C-reactive protein (CRP) and adiponectin in newly diagnosed type 2 diabetes, and whether adherence to Mediterranean diet affects their circulating levels. In a two-arm, single-center trial, 215 men and women with newly diagnosed type 2 diabetes were randomized to a Mediterranean diet (n = 108, 54 males and 54 females) or a low-fat diet (n = 107, 52 males and 55 females), with a total follow-up of 8.1 years. At baseline visit and at 1 year, body weight, HOMA index, CRP, and adiponectin and its fractions were assessed. Adherence to the diets was assessed by calculating the Mediterranean-diet score. At 1 year, CPR fell by 37 % and adiponectin rose by 43 % in the Mediterranean diet group, while remaining unchanged in the low-fat diet group. The pattern of adiponectin fractions (high and non-high molecular weight) showed a response similar to that of total adiponectin. Diabetic patients with the highest scores (6–9 points) of adherence to Mediterranean diet had lower circulating CRP level and higher circulating total adiponectin levels than the diabetic patients who scored <3 points on the scale (P = 0.001). The results of this randomized controlled trial demonstrate that Mediterranean diet cools down the inflammatory milieu of type 2 diabetes.
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Diagnosis of turner syndrome in two mothers following their daughters' diagnosis
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Identification of several circulating microRNAs from a genome-wide circulating microRNA expression profile as potential biomarkers for impaired glucose metabolism in polycystic ovarian syndrome
Abstract
This study aimed to detect serum microRNAs (miRNAs) differentially expressed between polycystic ovary syndrome (PCOS) patients with impaired glucose metabolism (IGM), PCOS patients with normal glucose tolerance (NGT), and healthy controls. A TaqMan miRNA array explored serum miRNA profiles as a pilot study, then selected miRNAs were analyzed in a validation cohort consisting of 65 PCOS women with IGM, 65 PCOS women with NGT, and 45 healthy women The relative expression of miR-122, miR-193b, and miR-194 was up-regulated in PCOS patients compared with controls, whereas that of miR-199b-5p was down-regulated. Furthermore, miR-122, miR-193b, and miR-194 were increased in the PCOS-IGM group compared with the PCOS-NGT group. Multiple linear regression analyses revealed that miR-193b and body mass index contributed independently to explain 43.7 % (P < 0.0001) of homeostasis model assessment-insulin resistance after adjustment for age. Investigation of diagnostic values confirmed the optimal combination of BMI and miR-193b to explore the possibility of IGM in PCOS women with area under the curve of 0.752 (95 % CI 0.667–0.837, P < 0.001). Bioinformatics analysis indicated that the predicted target functions of these miRNAs mainly involved glycometabolism and ovarian follicle development pathways, including the insulin signaling pathway, the neurotrophin signaling pathway, the PI3K-AKT signaling pathway, and regulation of actin cytoskeleton. This study expands our knowledge of the serum miRNA expression profiles of PCOS patients with IGM and the predicted target signal pathways involved in disease pathophysiology.
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The role of immune system exhaustion on cancer cells escape and anti-tumor immune induction after irradiation
Source:Biochimica et Biophysica Acta (BBA) - Reviews on Cancer
Author(s): Fernando Mendes, Cátia Domingues, Paulo Rodrigues-Santos, Ana Margarida Abrantes, Ana Cristina Gonçalves, Jéssica Estrela, João Encarnação, Ana Salomé Pires, Mafalda Laranjo, Vera Alves, Ricardo Teixo, Ana Bela Sarmento, Maria Filomena Botelho, Manuel Santos Rosa
Immune surveillance seems to represent an effective tumor suppressor mechanism. However, some cancer cells survive and become variants, being poorly immunogenic and able to enter a steady-state phase. These cells become functionally dormant or remain hidden clinically throughout. Neoplastic cells seem to be able to instruct immune cells to undergo changes promoting malignancy. Radiotherapy may act as a trigger of the immune response. After radiotherapy a sequence of reactions occurs, starting in the damage of oncogenic cells by multiple mechanisms, leading to the immune system positive feedback against the tumor. The link between radiotherapy and the immune system is evident. T cells, macrophages, Natural Killer cells and other immune cells seem to have a key role controlling the tumor. T cells may be dysfunctional and remain in a state of T cell exhaustion, nonetheless, they often retain a high potential for successful defense against cancer, being able to be mobilized to become highly functional. The lack of clinical trials on a large scale makes data little robust, in spite of promising information, there are still many variables in the studies relating to radiation and immune system. The clarification of the mechanisms underlying immune response to radiation exposure may contribute to treatment improvement, gain of life quality and span of patients.
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