Analytic linearization of nonlinear perturbations of Fuchsian systems

Nonlinear perturbation of Fuchsian systems are studied in regions including two singularities. Such systems are not necessarily analytically equivalent to their linear part (they are not linearizable). Nevertheless, it is shown that in the case when the linear part has commuting monodromy, and the eigenvalues have positive real parts, there exists a unique correction function of the nonlinear part so that the corrected system becomes analytically linearizable

Singular normal form for the Painlev\'e equation P1

We show that there exists a rational change of coordinates of Painlev\'e's P1 equation $y''=6y^2+x$ and of the elliptic equation $y''=6y^2$ after which these two equations become analytically equivalent in a region in the complex phase space where $y$ and $y'$ are unbounded. The region of equivalence comprises all singularities of solutions of P1 (i.e. outside the region of equivalence, solutions are analytic). The Painlev\'e property of P1 (that the only movable singularities are poles) follows as a corollary. Conversely, we argue that the Painlev\'e property is crucial in reducing P1, in a singular regime, to an equation integrable by quadratures

Implications of Welfare States on Human Development

In the paper, we compared the classification of welfare states by Gosta Esping-Andersen(liberal, corporatist, social democrat) and country ranking according to the Human DevelopmentIndex (HDI). The country occupying the first position, according to the level of human capital development,is Norway, belonging to the social-democratic welfare states. We also found a good result for theliberal welfare states: Australia (position 2), Switzerland (3rd position). But in the category ofcorporatist states we only find Germany (position 5). In the case of Romania, HDI is 0.802, which allows it to be included in the group of "very highhuman development". Due to the process of developing a state of welfare, we can not fit ourcountry into a single model. Characteristics are taken from each model, especially from the"social-democrat" (poverty prevention through redistribution) and from the "corporatist"(insurance system that maintains differentiations according to status and social class)

The extracellular matrix collagen in the coronary in-stent restenosis

Department of Interventional Cardiology, Institute of Cardiology, Chisinau, the Republic of MoldovaBackground: Extracellular matrix is underlined as an important factor regulating morphofunctional integrity of vascular wall, and is actively involved in vascular remodeling. Although collagen turnover activation is supported in mechanical artery injury, its character remains still unknown in the in-stent restenosis (ISR). The aim of this study is to evaluate the change of collagen type I and type III metabolism and metalloproteinase-2 (MMP2) expression in ISR. Material and methods: Using the confocal microscopy and immunochemistry techniques, the expression of collagen I and III, the markers of collagen I synthesis and degradation (PICP and CITP), as well as the expression of MMP2 and its tissue inhibitor (TIMMP2) have been assayed in the tissue pattern of ISR taken from 19 died patients. In 24 patients with ISR the markers of collagen I turnover were determined in blood also and compared with markers of 11 healthy persons. Results: The collagen I degradation is markedly increased in ISR and prevails over its synthesis while the collagen III degradation is enough preserved that led to collagen III/I ratio raising by 4-7 times already in minimal ISR. The CITP value is progressively increasing during restenosis exacerbation that is associated with a similar decline of PICP resulted consequently in a 7-10 fold elevation of the CITP/PICP ratio in muscular media of restenosis. Importantly to note that analogous changes of collagen type I turnover markers are established in blood in patients with ISR: PINP decreasing by 53.32% and CITP rise by 187.6%. The collagen I metabolism modification was accompanied by multiply MMP2 quantity increase and TIMPP2 diminution. Conclusions: 1. Extracellular matrix reorganization is a hallmark of the in-stent restenosis basically being exhibited by excessive collagen I degradation and preserved collagen III, splitting in conditions of MMP2/TIMMP2 ratio raising proportionally to ISR degree. 2. The shift of the circulating markers of collagen I turnover (PINP and CITP) is near to marker dynamics estimated in restenosis tissue that suggests their diagnostic and predictive role concerning ISR evolution

Histological changes in the vulva and vagina from ovariectomised rats undergoing oestrogen treatment

Background: The purpose of this study was to assess the histological changes occurring in the vagina and vulva in ovariectomised female rats, as well as the response to the administration of injectable oestrogens. Material and methods: We used 30 female Wistar white rats, distributed as follows: group 1 — the control group, group 2 — the operated but untreated rats, and groups 3, 4 and 5 — operated rats, to which oestrogenic treatment was administered (Estradiol, Estradurin, Sintofolin) at a dosage of 0.2 mg/rat/day. After 14 days of treatment, all animals were sacrificed and vaginal and vulvar biopsies were taken from all groups. Results: In group 2, we encountered structural changes of the vaginal mucosa, with severe atrophy and alterations in the thickness of the vagina and vulva. In groups 3, 4 and 5 we found marked hyperplasia of the vaginal and vulvar epithelium, eosinophilic and mast cell infiltration in the chorion. Conclusions: Our study proves that the histopathological changes during anoestrus after administration of oestrogens are cell hyperplasia, thickening of the superficial mucosal layer, eosinophilic and mast cells infiltrations, and chorionic congestion. Furthermore, we demonstrated that Estradiol therapy induces the most evident histological changes when compared to synthetic oestrogens such as Estradurin or Sintofolin.

Extracellular RNA – a new predictor and a supposable mechanism of in-stent restenosis

Department of Interventional Cardiology, Institute of Cardiology, Chisinau, the Republic of MoldovaBackground: The evaluation of new predictors of negative coronary remodeling after angioplasty remains an adequate approach of interventional cardiology in the diagnosis and prognosis of in-stent restenosis (ISR). Previously we have demonstrated on a murine model of atherosclerosis that extracellular RNA (eRNA) increases proportionally to vascular injury progression, and a first activation of the blood RNAase is changed by its steady quantitative decline, a reason that suggests a plausible role of eRNA in coronary neointima hyperplasia. Material and methods: This article is aimed at the study of eRNA amount in a tissue pattern of a stent with restenosis as well as its correlation with such inflammatory predictors as macrophage number and TNF-alpha expression. Using the techniques of confocal microscopy and immunohistochemistry we have first proved that eRNA level significantly increases in the coronary wall of segments with ISR (the specimens have been taken postmortem from 19 patients exposed to angioplasty). Results: The rise in the assay has been closely correlated to restenosis degree, and in muscular media it has been 2-4 times beyond the control range estimated in the adjacent coronary segment without negative vascular remodeling. In the restenosis zone eRNA has risen by about 130% from minimal to severe ISR. Moreover, its level has been found markedly increased earlier also comparatively to the control pattern: by 62% in moderate and 128% in severe ISR. A key disclosed evidence is that eRNA is positively correlated with TNF-alpha level (r = +0.88) and the number of macrophages (r = +0.84), whereas the last is notably enhanced depending on ISR progression. Conclusions: The obtained outcomes result in 2 opportunities: 1. eRNA may be a feasible predictor of negative coronary remodeling, facilitating the prognosis of ISR risk; 2. eRNA may be singled out as a factor involved in the pathogenesis of neointima formation and hyperplasia due to its relation to the inflammatory process

Определение маркеров воспаления при внутристентовом рестенозе

Department of Interventional Cardiology, Institute of Cardiology, State University of Medicine and Pharmacy „Nicolae Testemitanu”In-stent restenosis is a serious complication that usually follows 6 months after angioplasty. It is believed to be a manifestation of negative coronary remodeling. In order to focus on the role of inflammation in this phenomenon we determined the circulating levels of the lipoprotein-associated phospholipase A2 (Lp-PA2 ) and C reactive proteins (CRP), as well as the content of macrophages in the restenosis tissue pattern. We found that the blood Lp-A2 and CRP levels were significantly elevated in first 72 hours after angioplasty, independently of the restenosis hazard. We also discovered that after 3 to 6 months these markers remained boosted only in patients with restenosis, while the markers notably declined in those without restenosis. Elevation in inflammation markers was associated with a significant increase in the macrophage amount in the luminal part of restenosis tissue, an important source of the synthesis of the Lp-A2 , a marker of endothelial inflammation and dysfunction.Внутристентовый рестеноз, как проявление негативного коронарного ремоделирования, является серьезным осложнением ангиопластики, развивающемся в основном после 6 мес. С целью выявления роли воспаления определили уровень циркулирующих липопротеинассоциированной фосфолипазы А2 (Лп-ФЛА2 ) и С-РБ, а также содержание макрофагов в ткани рестеноза. Уровень Лп-ФЛА2 и С-РБ в крови был достоверно повышен в первые 72 часа после ангиопластики независимо от риска рестеноза. Через 3 и 6 месяцев, однако, он сохранялся высоким только у пациентов с рестенозом, в то время как при отсутствии рестеноза отмечалось снижение этих маркеров. Увеличение в крови маркеров воспаления сопровождалось многократным ростом числа макрофагов в ткани рестеноза со стороны просвета сосуда, источника синтеза Лп-ФЛА2 , маркера воспаления и дисфункции эндотелия

Early and late changes of multi-marker panel in patients with STEMI after angioplasty

Background: Post-infarction remodeling is strongly linked with collagen turnover which is influenced mostly by oxidative stress and inflammation, the last being, according to our previous data, triggered by early infiltrated neutrophils (24–48 h) followed by accumulation of macrophages M1 (72 h) and M2 (7–14 days). Aim: Evaluation of circulating markers of inflammation and oxidative stress in the different periods of 1 year follow up post-infarct evolution: first 2 weeks (each day), 1st month (synthesis of collagen type III), 3rd month (synthesis of collagen type I), 6 and 12 months. Material and methods: Study was performed in 47 patients (age range of 37–68 years) with STEMI exposed to angioplasty (<12 hours). Circulating levels of 28 markers were determined at admission, 1, 2, 3 ... 14 days, 1, 3, 6 and 12 months. Obtained results were compared with control value of markers determined in 17 apparently healthy persons and admission level (before PCI). Results: The earliest (first 24 h) significant change was inherent to MMP-8, whose double elevation (averagely from 3,1 up to 6,4 ng/ml) corresponded to period of neutrophil infiltration (24–48 h). Serum levels of IL-1, IL-6 have raised significantly since 48 h, followed by authentic increase of TNF-alpha, IL-8, CRPhs and phospholipase A2 since 72 h. Up to a period of 7 days these markers remained increased, but toward 14th day fell by 24–46% arguably due to macrophage M2 activation. This is consistent to dynamics of anti-inflammatory markers, IL-4 and IL-10 which decreased till 7th, elevated toward 14th day although remained below control. Inflammation boosting was associated by oxidative stress activation during 1st week manifested by malonic dialdehyde (MAD) rise and total antioxidant activity fall. To be noted that markers improvement till 3rd month was poor and a conspicuous dynamics began since 6th month with nearing to control level toward 12th month. However, at this time following markers significantly differed from control value: TNF-alpha (+29,6%), IL-4 (-31,7%), S-nitrosothiols (-17,8%), CRPhs exceeded 3,0 g/L (4,77±0,38) and MAD (+23,6%). Conclusions: (1). Dynamics of inflammation markers in patients with STEMI during first 14 days after angioplasty conclusive reflect chronologic accumulation of inflammatory cells in necrotic zone. (2). Maximal serum plateau of MMP-8, IL-1, IL-6, IL-6, TNF-alpha and CRPhs goes till 7th day of post-infarct evolution, associated with lowest IL-4 and IL-10. (3). Marker improvements begin since 3rd month with nearing to control toward 12th month, excepting IL-4, TNF-alpha, CRPhs and MAD indicating thus a late statement of inflammation dissemination