MAS-MoM Hybrid Method with Wire\u27s Image using in Excitation Problems

An important class of problems is the interaction of an antenna with the cavity of a semi-open metallic structure. In a working environment, an antenna may change its performance due to interactions with its surroundings. This is especially true in automotive applications. Therefore, it is important to consider the interaction of an antenna with possible resonating parts, and to solve these complex electrodynamics problems together. The development of methods for modeling and studying electromagnetic compatibility (EMC) problems has practical value. The method of auxiliary sources (MAS) with the method of moments (MoM) is applied to solve the excitation problem where a wire, with voltage source excitation, is connected to an open metallic surface. For verification of the proposed algorithm, an experimental structure was built and measured. Computer modeling results and the experimental results are in good agreement. Some aspects and principles are described, which provide hybridization of MAS and MoM. Image of objects is effectively applied for the solution of the particular problem

The Method of Auxiliary Sources as an Efficient Numerical Technique for Large 3D Semi Open Structures

The method of auxiliary sources (MAS) has been demonstrated as suitable for solution of diffraction and inverse problems in complex 2D large objects. Based on MAS numerical study of 3D RCS, EMC/EMI and SAR problems, related to the EM field resonance enhancement inside vehicles and the interaction of the cellular telephone radiation with the user\u27\u27s head are given in other work. The objective of this paper is to present details of MAS application to the wide 3D electrodynamic problems. The area of its efficient application, some features and advantages to achieving efficient solutions, are discussed. The extension of the MAS for semi-open structures with partitions is also presented

Electromagnetic Analysis for Vehicle Antenna Development Using Method of Auxiliary Sources

In paper [l] the electromagnetic analysis of large semi-open structures like vehicles was presented formulated as scattering problem, illuminated by a wide range of incident EM fields. The effect of resonances within the semi-open structure on the RCS, near fields and pattem of reradiated fields had been shown. In this paper the interaction of the entire semi-open structure on the performance of an antenna is considered together with the investigation of near field distributions inside the cavity. The Method of Auxiliary Sources (MAS) [2] is utilized. For a simple geometry the results are compared to measurements

Circulating Concentrations of Vitamin B6 and Kidney Cancer Prognosis: A Prospective Case-Cohort Study

Prospective cohort studies have found that prediagnostic circulating vitamin B6 is inversely associated with both risk of kidney cancer and kidney cancer prognosis. We investigated whether circulating concentrations of vitamin B6 at kidney cancer diagnosis are associated with risk of death using a case-cohort study of 630 renal cell carcinoma (RCC) patients. Blood was collected at the time of diagnosis, and vitamin B6 concentrations were quantified using LC-MS/MS. Hazard ratios (HR) and 95% confidence intervals (CI) were calculated using Cox regression models. After adjusting for stage, age, and sex, the hazard was 3 times lower among those in the highest compared to the lowest fourth of B6 concentration (HR4vs1 0.33, 95% CI [0.18, 0.60]). This inverse association was solely driven by death from RCC (HR4vs1 0.22, 95% CI [0.11, 0.46]), and not death from other causes (HR4vs1 0.89, 95% CI [0.35, 2.28], p-interaction = 0.008). These results suggest that circulating vitamin B6 could provide additional prognostic information for kidney cancer patients beyond that afforded by tumour stage

Aspirin but not statins is inversely related to gastric cancer with a duration–risk effect: Results from the Stomach Cancer Pooling Project Consortium

Background: Aspirin and statins have been suggested to have potential chemopreventive effects against gastric cancer (GC), although the results of previous studies have been inconsistent. This study therefore aimed to investigate the association between the use of aspirin and statins and GC. Methods: A pooled analysis of seven case-control studies within the Stomach Cancer Pooling Project, including 3220 cases and 9752 controls, was conducted. Two-stage modeling analyses were used to estimate the association between aspirin and statin use and GC after adjusting for potential confounders. Results: The pooled odds ratio (OR) of GC for aspirin users versus nonusers was 0.72 (95% confidence interval [CI], 0.54–0.95). The protective effect of aspirin appeared stronger in individuals without a GC family history (OR, 0.60; 95% CI, 0.37–0.95), albeit with borderline heterogeneity between those with and without a family history (p =.064). The OR of GC decreased with increasing duration of aspirin use, with an OR of 0.41 (95% CI, 0.18–0.95) for durations of ≥15 years. An inverse, nonsignificant association with the risk of GC was observed for the use of statins alone (OR, 0.79; 95% CI, 0.52–1.18). Conclusions: These findings suggest that aspirin use, particularly long-term use, is associated with a reduced risk of GC, whereas a similar association was not observed with statins, possibly because of the low frequency of use. © 2024 The Author(s). Cancer published by Wiley Periodicals LLC on behalf of American Cancer Society."This study was funded by the Associazione Italiana per la Ricerca sul Cancro (Project 21378 to Carlo La Vecchia) and by the Italian Ministry of Education, University and Research (PNRR per la Missione 4, Componente 2, Investimento1.1.Avviso 104/2022 Finanziato dall'Unione Europea–Next Generation EU Progetto MUR PRIN prot 2022A4WZFC to Stefania Boccia). Nuno Lunet and Samantha Morais are supported by national funds via the Foundation for Science and Technology (FCT) within the scope of Projects UIDB/04750/2020 and LA/P/0064/2020. Samantha Morais also received funding under the scope of Project “NEON-PC—Neuro-oncological complications of prostate cancer: Longitudinal study of cognitive decline” (POCI-01-0145-FEDER-032358; Reference PTDC/SAU-EPI/32358/2017) funded by Fundo Europeu de Desenvolvimento Regional via the Operational Program “Competitiveness and Internationalisation,” national funding from the FCT, and EPIUnit–Junior Research–Prog financing (UIDP/04750/2020). This research was supported in part by the Intramural Research Program of the US National Cancer Institute. The authors thank the European Cancer Prevention Organization for providing support for project meetings. Open access publishing facilitated by Universita degli Studi di Bologna, as part of the Wiley - CRUI-CARE agreement.

Взаимодействие факторов окружающей среды и генетического полиморфизма в этиологии злокачественных опухолей

Еnvironmental and lifestyle factors play a dominant role in etiology of cancer. In addition, genetic factors significantly influence interindividual variation in cancer incidence. The epidemiological studies in which effects of genetic polymorphism on the risk of cancer have been elucidated are somewhat disappointing. An important problem of these studies is their size. Moreover some of them do not have information on life-style and environmental exposures. The epidemiological method used to investigate the effect of genetic polymorphism on cancer risk is a retrospective case-control study. The chance of discovery of the specific «frequent» allelic variant which is associated with small increase in the risk is higher in studies including large numbers of cases and controls. This paper reviews the epidemiologic studies conducted in Department of epidemiology (Institute of carcinogenesis, Russian N. N. Blokhin Cancer Research Centre) in cooperation with countries of Central and Eastern Europe (Hungary, Poland, Romania, Slovakia) and coordinated by the International Agency for Research on Cancer (IARC). We will cover the studies, in which an attempt has been made to investigate the interaction between polymorphisms of phase 2 xenobiotic metabolism genes (GST), alcohol and aldehyde-metabolizing genes (ADH, ALDH), folate metabolism genes (MTHFR, TYMS) and CHECK2 with environmental and life-style factors in etiology of cancers of the lung, kidney and upper aerodigestive tract. The analyses of these studies suggest that genetic polymorphism modifies the effect of environmental exposures (including occupational carcinogens) and life-style factors (including tobacco, alcohol and diet) on the risk of cancer. The risk of cancer associated with known carcinogenic exposure may increase or decrease depending on the genotype. Interaction between exposure to carcinogenic factor and genotype is a major and significant determinant of cancer risk. Spontaneous tumors develop as a result of a combined effect of environmental factors and genetic polymorphism or endogenous and exogenous factors.Доминирующую роль в этиологии злокачественных опухолей играют факторы окружающей среды и образа жизни человека. В то же время индивидуальный риск развития рака определяется генетической предрасположенностью. Вопросу влияния генетического полиморфизма на риск развития опухолей посвящено множество работ. Однако их результаты разочаровывают. Главной проблемой этих исследований является небольшое количество наблюдени. Кроме того, во многих работах не учитывалась информация о факторах окружающей среды и образа жизни пробандов. Метод случай–контроль – основной эпидемиологический метод изучения генетических вариантов, влияющих на риск развития рака. Для выявления часто встречающихся вариантов, влияние которых на риск невелико, необходимы большие выборки больных и контрольной группы. В связи с этим многоцентровое исследование – принятый метод в области молекулярной эпидемиологии. В настоящем обзоре представлены результаты многоцентровых молекулярно-эпидемиологических исследований, проведенных в отделении эпидемиологии НИИ канцерогенеза РОНЦ им. Н. Н. Блохина совместно с коллегами из стран Центральной и Восточной Европы (Венгрия, Польша, Румыния, Словакия). Исследование координировало Международное агентство по изучению рака (Лион, Франция). Работы, включенные в обзор, посвящены изучению роли полиморфизма генов II фазы метаболизма ксенобиотиков (GSTM1 и GSTT1), алкогольдегидрогеназы (ADH1В и ADH1C) и альдегиддегидрогеназы (ALDH2), метаболизма солей фолиевой кислоты – метилентетрагидрофолатредуктазы (MTHFR) и тимидилатсинтетазы (TYMS) и гена CHECK2 в этиологии рака легкого, верхних дыхательных и пищеварительных органов и почки. Анализ проведенных исследований позволяет заключить, что генетический полиморфизм модифицирует риск развития рака в результате экспозиции к тому или иному внешнему фактору. Показатель P, который характеризует взаимодействие (интеракцию) между влиянием фактора окружающей среды и определенным генотипом и риском развития рака, часто имеет статистически достоверное значение. Таким образом, большинство спонтанных опухолей человека развиваются в результате взаимодействия генетического полиморфизма и внешних факторов

ФАКТОРЫ РИСКА ПОЧЕЧНО-КЛЕТОЧНОГО РАКА

Smoking, overweight, obesity, hypertension, occupational exposures to pesticides, specifically to trichloroethylene are considered causal risk factors for sporadic i.e. non-hereditary renal cell cancer (RCC). Some of these factors not only increase the risk of RCC but also affect the survival of patients. For example, in patients with RCC who continue smoking, the risk of dying from other causes is twice as high as in patient who quit smoking. The risk of second cancer is 5 times higher in patients who continue smoking 20 or more cigarettes per day than in non-smokers. The low penetrance polymorphism is an important factor in etiology of sporadic RCC, which contrary to high penetrance mutations is a common event. However, the risk associated with this type of inheritance is quite low. The majority of sporadic RCC have polygenic etiology. They develop as a result of combined effect of large number of low penetrance genetic susceptibility genes (genetic polymorphism). Environmental factors play a decisive role in causation of sporadic RCC. The interplay of exposures to environmental risk factors and genetic susceptibility of exposed individuals is believed to influence the risk of developing sporadic RCC. The studies in molecular epidemiology based on candidate gene approach have shown that polymorphisms of certain genes, for example glutathione-S-transferase family genes, are associated with RCC. The genome wide association studies identified about twenty loci with single nucleotide polymorphism (SNPs) affecting the risk of RCC. However the risk loci so far identified for RCC account for only about 10 % of the familial risk of RCC. The power of largest studies which include many thousands of observations allow to detect 80 % of the major common loci (with minor allele frequency – MAF>0.2) conferring risk ≥1.2. However, for detecting alleles with smaller effects and/or MAF<0.1, more studies with larger sample size are needed. By implication, variants with such profiles probably represent a much larger class of susceptibility loci for RCC and hence a large number of variants remain to be discovered. Future investigation of the genes targeted by the risk SNPs is likely to yield increased insight into biology of RCC and will lead to new approaches for prevention, early detection and treatment.Доказанными факторами риска спонтанного, т.е. не наследственного, почечно-клеточного рака (ПКР) являются курение, избыточный вес, ожирение, гипертония, некоторые профессиональные факторы, экспозиция к пестицидам и трихлорэтилену. Факторы образа жизни, например курение, не только повышают риск развития ПКР, но и влияют на выживаемость больных с этим заболеванием. Так, например, риск смерти от неонкологических причин у продолжающих курить больных ПКР в два раза выше по сравнению с никогда не курившими больными, a риск развития второй опухоли у продолжавших курить больных ПКР более 20 сигарет в день в 5 раз выше, чем у некурящих пациентов. В этиологии спонтанного ПКР важную роль играет низкопенетрантный генетический полиморфизм, который в отличие от высокопенетрантных мутаций встречается довольно часто. Однако риск развития рака, ассоциированный с этим типом наследственности, невысок. Тем не менее большинство опухолей человека развиваются в результате комбинированного эффекта большого числа генов с низкой пенетрацией, т.е. имеют полигенную этиологию. В этиологии этих опухолей важную роль играют экзогенные факторы: имеет место взаимодействие наследственности и факторов образа жизни и окружающей среды. Молекулярно-эпидемиологические исследования, основанные на предварительной гипотезе, показали, что полиморфизм некоторых генов, например семейства глутатион-S-трансфераз, влияет на риск ПКР. В результате полногеномных исследований идентифицированы около 20 однонуклеотидных полиморфизмов (ОНП) высокого риска, которые, впрочем, объясняют лишь 10 % риска семейных случаев ПКР. Размер самых крупных исследований, которые включают многие тысячи наблюдений, позволяет выявить лишь 80 % от основных, часто встречающихся аллельных вариантов (с частотой минорных аллелей >0,2), которые повышают риск ПКР в 1,2 и более раз. В то же время для выявления полиморфных вариантов с меньшим эффектом на риск ПКР, с частотой минорных аллелей <0,1, размер выборки должен быть значительно больше. Скорее всего, этот тип вариантов содержит больше ОНП повышенной предрасположенности к развитию ПКР и их предстоит открыть. Будущие исследования, направленные на идентификацию однонуклеотидных полиморфизмов высокого риска, приведут к лучшему пониманию биологии ПКР и будут способствовать разработке новых направлений профилактики, ранней диагностики и лечения этого заболевания

Loss of chromosome Y leads to down regulation of KDM5D and KDM6C epigenetic modifiers in clear cell renal cell carcinoma

Recent genomic studies of sporadic clear cell renal cell carcinoma (ccRCC) have uncovered novel driver genes and pathways. Given the unequal incidence rates among men and women (male:female incidence ratio approaches 2:1), we compared the genome-wide distribution of the chromosomal abnormalities in both sexes. We observed a higher frequency for the somatic recurrent chromosomal copy number variations (CNVs) of autosomes in male subjects, whereas somatic loss of chromosome X was detected exclusively in female patients (17.1%). Furthermore, somatic loss of chromosome Y (LOY) was detected in about 40% of male subjects, while mosaic LOY was detected in DNA isolated from peripheral blood in 9.6% of them, and was the only recurrent CNV in constitutional DNA samples. LOY in constitutional DNA, but not in tumor DNA was associated with older age. Amongst Y-linked genes that were downregulated due to LOY, KDM5D and KDM6C epigenetic modifiers have functionally-similar X-linked homologs whose deficiency is involved in ccRCC progression. Our findings establish somatic LOY as a highly recurrent genetic defect in ccRCC that leads to downregulation of hitherto unsuspected epigenetic factors, and suggest that different mechanisms may underlie the somatic and mosaic LOY observed in tumors and peripheral blood, respectively