Experimental and Numerical Investigation of Mechanical Properties of Lightweight Concretes (LWCs) with Various Aggregates.

High requirements for the properties of construction materials and activities directed at environment protection are reasons to look for new solutions in concrete technology. This research was directed at solutions affecting the reduction of energy consumption and CO2 emissions. The use of lightweight concretes (LWCs) allows one to meet both conditions at the same time. The purpose of the research presented in this paper was to investigate the abilities of using lightweight aggregates (LWAs) of the following types: 2 and 4 mm granulated expanded glass aggregate (GEGA) as ingredients with excellent insulating properties and 8 mm granulated fly ash aggregate (GAA) as an ingredient with a relatively high resistance to crushing. The influence of the percentage participation of each aggregate in all LWCs was variable and amounted to 0%, 25%, 50%, 75%, and 100%. A series of 15 LWC mixes were prepared for various LWA participations and for a constant water-cement ratio (w/c = 0.5). Concrete tests were carried out for the following criteria: density, porosity, compressive strength, and the modulus of elasticity. In order to fully analyze fracture processes in LWCs with the participation of GEGA and GAA and to assess the correctness of the results obtained during the experiments, numerical models that corresponded to both geometrical and load diagrams of elements under research were created. The numerical analyses of the LWCs were conducted by means of the conventional finite element method (FEM).

Angiotensinogen gene T174M polymorphism is related to Hashimoto's thyroiditis.

OBJECTIVES: The Hashimoto thyroiditis is found to be Th1-related autoimmunity. Recently, it has been proved that the renin-angiotensin-aldosterone system (RAAS) may be involved in promoting Th1-mediated autoimmune diseases. However, the role of RAAS in HT pathogenesis remains still unknown. The aim of this study was to determine whether the polymorphisms of ACE, AGTR1 and AGT genes are associated with HT. MATERIAL AND METHODS: Polymerase Chain Reaction (PCR) was performed to determine ACE I/D, AGTR1 A1166C and AGT T174M polymorphisms and next chi-square test was used to compare allele frequencies of genes between HT patients (n=53) and the control group (n=31). RESULTS: TM genotype of AGT gene has been more often presented in HT patients (p <0.05). No others statistically significant differences were found in the distribution of I/D ACE and A1166C, AGTR1 genes polymorphisms between studied groups. CONCLUSION: Our study has examined for the first time the association of genes related to RAAS with autoimmune thyroid disease and results suggest that AGT TM genotype individuals might be at higher risk of HT. Although in the present study we have not found any association between increased activation of RAAS and the risk of HT, still this issue seems to be interesting and worthy further research, considering patients with thyroid cancers.

The influence of a change in the meniscus cross-sectional shape on the medio-lateral translation of the knee joint and meniscal extrusion.

OBJECTIVE: The purpose of this study was to evaluate the influence of a change in the meniscus cross sectional shape on its position and on the biomechanics of a knee joint. METHODS: One main finite element model of a left knee joint was created on the basis of MRI images. The model consisted of bones, articular cartilages, menisci and ligaments. Eight variants of this model with an increased or decreased meniscus height were then prepared. Nonlinear static analyses with a fixed flexion/extension movement for a compressive load of 1000 N were performed. The additional analyses for those models with a constrained medio-lateral relative bone translation allowed for an evaluation of the influence of this translation on a meniscus external shift. RESULTS: It was observed that a decrease in the meniscus height caused a decrease in the contact area, together with a decrease in the contact force between the flattened meniscus and the cartilage. For the models with an increased meniscus height, a maximal value of force acting on the meniscus in a medio-lateral direction was obtained. The results have shown that the meniscus external shift was approximately proportional to the meniscus slope angle, but that relationship was modified by a medio-lateral relative bone translation. It was found that the translation of the femur relative to the tibia may be dependent on the geometry of the menisci. CONCLUSIONS: The results have suggested that a change in the meniscus geometry in the cross sectional plane can considerably affect not only the meniscal external shift, but also the medio-lateral translation of the knee joint as well as the congruency of the knee joint.

What is the impact of gestational diabetes mellitus on frequency of structural chromosome aberrations in pregnant women and their offspring?

Gestational diabetes mellitus (GDM) is defined as carbohydrate intolerance which results in hyperglycemia first diagnosed during pregnancy. It is associated with an increased levels of oxidative stress due to overproduction of reactive oxygen species (ROS). Overproduction of ROS induces protein oxidation, lipid peroxidation and different types of DNA damage. The objective of this study was to determine the frequencies of structural chromosome aberrations (CA) in peripheral blood of pregnant women (mothers) with GDM and in cord blood of their newborns. Peripheral blood lymphocytes were collected from 35 GDM mothers and cord blood lymphocytes from their 35 newborns. The control group included 30 pregnant mothers without diabetes mellitus (DM) and their 30 newborns. CA were evaluated with in vitro chromosome aberration assays. We observed a moderate increase of the mean numbers of structural CA between GDM mothers and their newborns, GDM mothers and mothers without DM, GDM mothers' offspring and the offspring of mothers without DM, mothers without DM and their newborns, but this effect did not reach statistical significance (p>0.1).

Is M235T polymorphism of the angiotensinogen gene involved in the development of endometriosis?

OBJECTIVES: The aim of the study was to analyze the M235T polymorphism of the angiotensinogen (AGT) gene in women with endometriosis and to identify correlations between identified genotypes and the disease progression, its stage and clinical course as well as to evaluate the prognostic value of the investigated polymorphism in patients with endometriosis treated for infertility. MATERIAL AND METHODS: The study group consisted of 241 women with minimal to severe stage of endometriosis, the control group (without endometriosis) - 127. The molecular analysis was performed by PCR-RFLP technique. RESULTS: The analysis of the frequency of genotypes and alleles of M235T polymorphism showed no significant differences between the study and the control groups and between the severity grades of the disease (p > 0.05). No such differences were reported in the case of different localizations of the disease lesions, either. Evaluation of the correlations related to pain accompanying endometriosis did not demonstrate association with any genotypes of the analyzed AGT gene poly-morphism. Comparison of the results obtained in the group in which infertility treatment was successful (n = 54) and in those who failed to conceive (n = 73) did not show the correlation between the investigated polymorphism and the effect of infertility treatment. CONCLUSIONS: M235T polymorphism of the AGT gene seems unrelated to the development or the clinical course of en-dometriosis. No prognostic value has been found of the investigated polymorphism in predicting the effects of infertility treatment in women with endometriosis.

[The effect of solar ultraviolet radiation (UVR) on induction of skin cancers]. / Wplyw slonecznego promieniowania ultrafioletowego (UV) na powstawanie raków skóry.

Ultraviolet radiation is a physical mutagenic and cancerogenic factor. About 95% of ultraviolet A (UVA) (320-400 nm) and 5% of UVB (280-320 nm) reach the Earth's surface. Melanin is a natural skin protective factor against UV radiation. Skin cancers associated with long-term exposure to UV radiation are: basal cell carcinoma (BCC), squamous cell carcinoma (SCC) and cutaneous malignant melanoma (CMM). The high risk of BCC development is related to acute and repeated exposure to UV causing sunburn. Molecular studies of BBC demonstrated disorders in sonic hedgehog (SHH) cell signaling regulation pathway, associated with the suppressor protein patched homolog 1 gene (PTCH1) mutations. The risk of the BCC development is related to the polymorphism of melanokortin-1 receptor gene (MC1R). Tumor P53 gene mutations observed in BCC cells has been classified as secondary genetic changes. In SCC cells UV-induced mutations were mostly related to P53 gene. Increased expression of cyclooxigenase- 2 gene (COX-2) plays a significant role in the development of SCC. Other pathogenetic factors include intensification of the synthesis of pro-inflammatory cytokines (tumor necrosis factor α (TNF-α), interleukin-1 α (IL-1α), IL-1ß and IL-6). Currently, the role of UVB has been recognized in the pathogenesis of CMM. In CMM cells the following gene mutations were noted: cyclindependent kinase inhibitor 2A INK4A (p16INK4A), cyclin-dependent kinase 4 (CDK4), Ras, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and proto-oncogene B-Raf (BRAF). The BRAF gene mutations were observed in ~50% of CMM cases. Mutations of P53 gene are not characteristic of CMM cells. Med Pr 2016;67(2):255-266.

Elevated frequencies of micronuclei in pregnant women with type 1 diabetes mellitus and in their newborns.

Pregestational diabetes mellitus (type 1 and type 2) affects about 1% of the obstetric population. In diabetes, persistent hyperglycemia can be a source of DNA damage via overproduction of reactive oxygen species (ROS). Using the cytokinesis-block micronucleus (CBMN) test, we measured the frequencies of micronuclei (MN) per 1000 binucleated (BN) cells in pregnant women (mothers) with type 1 diabetes mellitus (T1DM) and in their newborns. Peripheral blood lymphocytes were collected from 17 pregnant women with T1DM and cord-blood lymphocytes from their 17 newborns. The control group included 40 pregnant women (mothers) without diabetes mellitus (DM) and their 40 newborns. In the group of pregnant women with T1DM, the mean number of MN per 1000 BN cells was 2.35 (±1.07), significantly (p<0.001) higher than in the control group of pregnant women (0.86±0.90). The frequency value in the group of newborns of T1DM mothers was 1.42 (±0.60), significantly (p<0.05) higher than in the corresponding control group (0.67±0.79). The value in the group of mothers with T1DM was significantly (p<0.05) higher than in their newborns. Comparing mothers without DM with their newborns, no significant frequency differences were observed. No significant correlations were observed between MN frequencies in mothers with T1DM and either the frequencies in their newborns, the duration of diabetes, or HbA1C levels. Our results indicate that T1DM is accompanied by increased frequencies of MN in pregnant women and their newborns.

Endometriosis and RAS system gene polymorphisms: the association of ACE A2350G polymorphism with endometriosis in Polish individuals.

To analyze the polymorphisms of angiotensin I converting enzyme (ACE) gene (insertion/deletion [I/D], A2350G) and angiotensin II type 1 receptor gene (A1166C) in women with endometriosis and to determine the correlation of the identified genotypes with the severity of the disease. Additionally, to estimate the prognostic value of the polymorphisms in patients with endometriosis treated due to infertility. The study group included 241 women, the control group (without endometriosis)-127. The molecular analysis was performed by polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism technique. For I/D ACE and A1166C AT1 polymorphisms no significant differences were observed between the study and control groups and between the severity grades of the disease (p>0.05). For A2350G ACE polymorphism the frequency of genotypes for the study and control groups respectively was the following: AA-31.54%, AG-54.36%, GG-14.11% and AA-55.12%, AG-36.22%, GG-8.66% (x(2)=19.36, p<0.0001). Statistically significant differences were found between the frequency of A and G alleles between both groups (x(2)=15.16, p=0.0001), but not when individual grades of the disease severity were compared. There was no association between the investigated polymorphisms and the effect of infertility treatment. A2350G polymorphism (allele G, AG genotype) of ACE gene seems to be associated with the development of endometriosis.

Association of angiotensin-converting enzyme and angiotensin II type I receptor gene polymorphisms with extreme obesity in Polish individuals.

There is strong evidence for the presence of a functional renin-angiotensin system in human adipose tissue. The aim of our study was to investigate the association of polymorphic variants of angiotensin-converting enzyme gene (ACE I/D) and angiotensin II type I receptor gene (AGTR1 A1166C) with extreme obesity and obesity-associated type 2 diabetes mellitus (T2DM) and to examine their combined effect on extremely obese patients. Overall, no significant associations were detected between ACE and AGTR1 gene polymorphisms and extreme obesity. However, extremely obese patients with T2DM showed an increased frequency of ACE II genotype compared with controls (p<0.05) and with non-diabetic extremely obese patients (p<0.01). The results suggest that II genotype of ACE was a significant contributor to extreme obesity in AA homozygotes of AGTR1 gene, regardless of the presence of T2DM. Moreover, the analysis of genetic polymorphisms demonstrated that ACE II and AGTR1 AC genotypes were most frequently observed in patients with extreme obesity and T2DM. On the basis of our results, we suggest that ACE II homozygosity may be a significant predictor of extreme obesity and T2DM and that the interaction between ACE and AGTR1 genes may be considered a predisposing factor for extreme obesity and extreme obesity-associated T2DM development.

Genetic variations of the CTNNA1 and the CTNNB1 genes in sporadic colorectal cancer in Polish population.

UNLABELLED: Experimental as well as clinical observations have demonstrated that the E-cadherin/catenin complex is a powerful inhibitor of invasion. Abrogation of this pathway is implicated in the carcinogenesis of several malignancies, especially colorectal cancer. The aim of the study was to determine the CTNNA1 and the CTNNB1 mutations and its relationship to clinical and pathological features of sporadic colorectal cancer (CRC) in Polish patients. MATERIAL AND METHODS: Paired tumor and normal tissue samples from 110 sporadic CRC patients undergoing resective surgery were prospectively studied for the alpha catenin (CTNNA1) gene and beta catenin (CTNNB1)gene mutations by PCR/single strand conformation polymorphism (SSCP). RESULTS: The CTNNA1 gene alteration in exon 7 were detected in 4 samples and in exon 3 of CTNNB1 gene were found in 3 samples. There was a trend at the limit of statistical significance associating younger age at diagnosis (<50) with CTNNA1 and the CTNNB1 mutations. The mutation of CTNNB1 seemed to occur more frequently in the proximal colon than distal. The CRC patients with CTNNA1 mutation had a significantly increased lymph node metastasis. On the other hand, there was no correlation between mutations and the other clinical variables (e.g. sex, grade and depth of invasion). CONCLUSION: Although we found a low frequency of mutations in the CTNNA1 and the CTNNB1 genes, but the analysis the relationship with clinical and pathological features of CRC patients may indicated an association of these mutations with the risk and progression of CRC.

Evaluation of NDRG2 gene expression in primary papillary thyroid carcinoma and in metastases of this neoplasm to regional lymph nodes.

BACKGROUND: At present, researchers' attention has been concentrating on NDRG2 (N-Myc downstream-regulated gene 2) as a new gene candidate in the development and progression of papillary thyroid carcinoma (PTC). NDRG2, together with NDRG1, NDRG3 and NDRG4 are members of the NDRG family, a new class of genes, inhibited by N-Myc oncogene. AIM: The aim of our study was to evaluate NDRG2 mRNA expression in the primary PTC and its metastases to regional lymph nodes. MATERIALS AND METHODS: Postoperative tissue and macroscopically changed lymph nodes of sixteen (16) patients with PTC constituted the studied material. In this group, metastases of the cancer to regional lymph nodes were confirmed histopathologically in 8 cases. Quantitative evaluation of NDRG2 mRNA expression was performed by the real-time polymerase chain reaction (real-time PCR) method. RESULTS: The mean values of NDRG2 mRNA expression in the primary tumour tissues were statistically significantly lower vs. the levels of NDRG2 mRNA expression in macroscopically unchanged thyroid tissue (p < 0.0001). A comparison of the mean NDRG2 mRNA expression of primary tumours and that of their metastases to regional lymph nodes did not demonstrate any statistical differences (p > 0.05). A positive correlation was observed between NDRG2 mRNA expression in primary tumour cells and in the cancer metastases to lymph nodes (Rs = 0.7857; p < 0.05). Factors, such as age, sex, tumour stage in TNM system, were of no significance for NDRG2 mRNA expression level (p > 0.1). CONCLUSION: The results of our study demonstrated decreased NDRG2 mRNA expression levels in PTC, when compared to macroscopically unchanged thyroid tissue, which may point to the potential role of NDRG2 in the development and progression of cancer in question.

Evaluation of chromosome aberrations, sister chromatid exchange and micronuclei in cultured cord-blood lymphocytes of newborns of women treated for epilepsy during pregnancy.

Epidemiological data indicate that pregnancies of epileptic women constitute about 1% of all pregnancies. Newborns of mothers exposed to anti-epileptic drugs (AEDs) are at increased risk for major congenital malformations, cognitive impairment and fetal death. Cord-blood lymphocytes of the newborns whose mothers received long-term AEDs therapy during pregnancy were used in this study. There were 37 newborns (Group A), divided into two subgroups, i.e. from mothers receiving mono-therapy (A1) and from those receiving poly-therapy (A2). The major drugs given to the pregnant women with epilepsy in mono-therapy were valproic acid (VPA) and carbamazepine (CBZ) analogues. In poly-therapy, besides VPA and CBZ derivatives also phenyltriazine, sulphanamide, benzodiazepines and gamma-aminobutyric acid (GABA) derivatives were administered. Three kinds of in vitro cytogenetic test were applied: the chromosome aberration (CA) assay, the sister chromatid exchange (SCE) assay, and the cytokinesis-block micronucleus assay (CBMN). In addition, the mitotic index (MI), the replication index (RI) and the nuclear division index (NDI) were determined. The mean number of CA/cell (excluding gaps) for group A did not differ statistically significantly from the negative controls (p>0.1), nor did the mean MI value (p>0.1). In group A, the mean number of SCE/cell was statistically significantly higher compared with the negative control (p<0.05). The mean RI value for group A did not demonstrate statistically significant differences (p>0.1). The mean MN number for group A was higher than in the negative control, but this difference was on the border of statistical significance (p=0.07). The value of NDI for group A did not differ significantly from the value in the negative control (p>0.1). The anti-epileptic drugs given to epileptic women in mono- and poly-therapy during pregnancy evoked potentially clastogenic and genotoxic effects in cord-blood lymphocytes. These drugs did not exert a cytotoxic effect, neither did they inhibit the cell-division kinetics of cord-blood lymphocytes.

[Poisoning with selected mushrooms with neurotropic and hallucinogenic effect]. / Zatrucia wybranymi grzybami o dzialaniu neurotropowym i halucynogennym.

Picking mushrooms, especially in summer and autumn, is still very popular in Poland. Despite raising awareness of poisonous mushrooms in the Polish society, year after year hospitals treat many patients diagnosed with poisoning with the most common toxic species of mushroom found in our country. Furthermore, growing interest in hallucinogenic mushrooms among young people has become a serious medical problem of our time. Websites make it incredibly easy for people to obtain information on the morphology and appearance of mushrooms with psychoactive properties, which leads inexperienced pickers to misidentification, resulting frequently in a fatal outcome. The article explores the subject of poisoning with the most common mushrooms with neurotropic effects, these are: Amanita muscaria, Amanita pantherina, Inocybe rubescens, Clitocybe dealbata, Clitocybe rivulosa and Psilocybe semilanceata. Toxins found in these species show symptoms that affect the central nervous system, parasympathetic system as well as the gastro-intestinal system. The effects of poisoning in the mushroom species mentioned above are mild in general, liver and kidney damage occur rarely, but the symptoms depend on both the dosage of the consumed toxins and individual susceptibility. In most cases the treatment is of symptomatic nature. There is no specific treatment. Medical procedures mainly involve induced gastrolavage--stomach pumping (providing that the patient is conscious), prescription of active carbon as well as replacement of lost body fluids and electrolytes. If the muscarinic symptoms prevail it is generally advised to dose atropine. Patients showing the signs of hyperactivity receive tranquilizers or narcoleptics to eliminate psychotic symptoms.

Minichromosome maintenance (MCM) and AgNOR proteins expression in desmoid tumours: a tissue microarray analysis.

In the present study, nuclear proliferative proteins: MCM2, MCM5, MCM7, Ki-67 and AgNORs expression was assessed in paraffin sections from sporadic desmoid tumours using a tissue microarray (TMA)-based immuno- and histochemistry, respectively. Nuclear expression of MCM7, where the percentage of positive cells was 0.87% (± 1.64) (range 0-5%), was found in 4/20 (20.0%) cases. In 32/32 (100%) of the examined desmoid cases no expression of nuclear proteins MCM2 and MCM5 was detected. Nuclear expression of Ki-67 was observed in 4/21 (19%) cases. Paraffin sections from 30 cases of desmoid tumours were silver-stained to visualize AgNORs. The following AgNOR parameters were calculated: mean AgNOR number per nucleus (N), mean AgNOR area per nucleus, mean AgNOR dot area per nucleus (A), and mean AgNOR content (C = N/A). In the investigated group the mean values of AgNOR parameters were the following number: 4.34 (± 0.11); area: 0.74 µm2 (± 0.19); dot area: 0.18 m2 (± 0.01), and AgNOR content: 23.73 (± 1.85). The mean AgNOR number per nucleus and mean AgNOR content in desmoid tumours were statistically significantly higher as compared to the controls (tonsil tissue) (p<0.001). This study observed low level of MCM7 and Ki-67 and lack of MCM2, MCM5 proteins expression which may explain commonly known low mitotic activity of desmoid tumour cells. The morphology of dots related to AgNORs (number, area) and their morphometric parameters point to elevated transcriptional activity of desmoid cells.

[Poisonings with Amanita phalloides]. / Zatrucia muchomorem sromotnikowym (Amanita phalloides).

Amanita phalloides is the most dangerous, poisonous mushroom species in our climatic conditions. It is the cause of 90-95% of all deaths due to mushroom poisoning, a-Amanitin, a polymerase RNA II inhibitor, is mainly responsible for the Amanita phalloides toxic property. Inhibition of polymerase RNA II functioning in a transcription process is connected with inhibition biosynthesis of structural and enzymatic proteins in cells. A lethal dose of a-amanitin is 0.1 mg/kg b.w. for humans. One of the medical problems in Amanita phalloides poisonings is a relatively prolonged latency period (8-24 h) from mushroom ingestion, at the same time the cytotropic action of absorbed toxins is revealed. In severe cases, multi organ failure, renal and hepatitis failure can occur. Deaths in a-amanitin poising cases follows between 6-16 days after intoxication. Mortality in this group of patients is still high and amounts to approximately 20-30% in adults and exceeds 50% in children. If mushroom poisoning occurs, it is best treated with pharmacological agents, extracorporeal methods for toxin removal and liver transplantation. Recent high expectations concerning liver albumin dialysis (based on MARS) should support liver regeneration and will also help with possible liver transplantation. In a medical community it is generally believed that every suspected Amanita phalloides poisoning should be referred to a specialized health center.

Cytogenetic study of Ascaris trypsin inhibitor in cultured human lymphocytes with metabolic activation.

The trypsin inhibitor (ATI) isolated from gastrointestinal nematode Ascaris suum was tested in vitro for induction of chromosome aberrations and sister chromatid exchanges (SCE). Genotoxicity assessment of purified ATI was carried out on metaphase plates received from peripheral blood lymphocyte macroculture (48 h test of structural chromosome aberrations and 72 h test of SCE) with exogenous metabolic activation. ATI was tested in dose of 25, 50 and 100 microg per ml of culture. Kinetics of cell divisions were determined by the replication index (RI). The mitotic index (MI) was expressed as a number of metaphases per 1000 nuclei analysed. Analysis of chromosome aberrations showed that higher doses of ATI (50 and 100 microg/ml) significantly increased the frequency of chromosome aberrations (mainly of chromatid gaps and breaks) compared to the negative control. All concentrations of ATI caused a statistically significant reduction in the MI and RI. In comparison with the negative control, a significant increase in the SCE frequency was observed in all applied doses of ATI. Thus, in the presence of S9 activation, the Ascaris trypsin inhibitor showed potential clastogenic activity and inhibition of the dynamics of lymphocyte divisions.

Analysis of pRb, p16INK4A proteins and proliferating antigens: PCNA, Ki-67 and MCM5 expression in aggressive fibromatosis (desmoid tumor).

Aggressive fibromatosis (desmoid tumor) is a mesenchymal lesion originating from fascial, aponeurotic and muscular connective tissue. It rarely becomes histologically malignant. In this study we analyzed the cell cycle regulation proteins: pRb, p16, and proliferating antigens: Ki-67, PCNA, MCM5 with immunohistochemical method in archival material derived from 27 extra-abdominal (E-AD), 18 abdominal (AD) and 5 intra-abdominal (I-AD) cases of desmoid tumor. None of the examined cases (n=50) of aggressive fibromatosis was pRb-immunonegative. Heterogeneous expression of pRb was observed in 51.85% (14/27) of Group AD cases and in 5.56% (1/18) of Group E-AD cases; positive expression in 48,15% (13/27) of Group AD cases, in 94.44% (17/18) of Group E-AD cases, and in 100% (5/5) of Group I-AD cases. There were no negative cases for p16 staining in any of the examined groups. The number of heterogeneous cases in individual groups was: 33.33% (9/27) in Group AD, 50% (9/18) in Group E-AD and 40% (2/5) in Group I-AD, and positive cases: 66.67% (18/27), 50% (9/18) and 60% (3/5), respectively. Overexpression of PCNA was noted in 98% (49/50) of cases. The positive staining for Ki-67 protein was noted in 25.93% (7/27) in Group AD, in 16.67% (3/18) in Group E-AD and in 60% (3/5) in Group I-AD. None of the examined cases was immunopositive for MCM5 protein. The noted levels of pRb and p16 expression in desmoid cells reflect their function in cell cycle regulation. Probably the unsettled cell cycle progression, especially in G1 phase, is not the cause of aggressive fibromatosis pathogenesis.

Analysis of APC, alpha-, beta-catenins, and N-cadherin protein expression in aggressive fibromatosis (desmoid tumor).

The aims of this study were to analyze the cadherin/catenin adhesion complex in cells from abdominal and extra-abdominal aggressive fibromatosis tumors, and to estimate the correlation between the expression of the tested proteins and the clinical data of the desmoid patients. Immunohistochemistry was used to examine the expression of the cadherin/catenin adhesion complex: APC protein, alpha-, beta-catenin, and N-cadherin in archival material derived from 15 cases of extra-abdominal desmoid tumor (E-AD) and 20 cases of abdominal (AD) desmoid tumor. The tested proteins demonstrated cytoplasmic (c) staining. Furthermore, nuclear (n) or cytoplasmic and nuclear (c+n) staining was observed for beta-catenin. The mean values of the percentage of positive cells for the tested proteins between E-AD vs. AD did not demonstrate any statistically significant difference except for alpha-catenin. In the E-AD group, in both cases of recurrent tumors, no alpha-catenin expression was observed but the expression of this protein was detected in primary tumors. In the groups investigated, no statistically significant correlation was found between alpha-catenin, beta-catenin (c), (n) and (c+n) expression, and tumor size (p>0.1). The results regarding beta-catenin expression obtained in our study confirm the previous findings that nuclear accumulation of this protein plays a crucial role in the pathogenesis of aggressive fibromatosis.

[The metabolic syndrome. Part I: definitions and diagnostic criteria for its identification. Epidemiology and relationship with cardiovascular and type 2 diabetes risk]. / Zespól metaboliczny. Czesc I: definicje i kryteria rozpoznawania zespolu metabolicznego. Epidemiologia oraz zwiazek z ryzykiem chorób sercowo-naczyniowych i cukrzycy typu 2.

The term metabolic syndrome (MS) refers to a clustering of risk factors of metabolic origin that promote the development of cardiovascular disease and type 2 diabetes. Metabolic syndrome includes such pathological factors as insulin resistance, hyperinsulinemia, abdominal obesity, impaired glucose tolerance, type 2 diabetes, microalbuminuria, high level of triglycerides, low level of HDL cholesterol, elevated blood pressure, and proinflammatory and prothrombotic state. Several organizations have recommended clinical criteria for the diagnosis of metabolic syndrome. The most widely accepted were the worked out by the World Health Organization (WHO), the European Group for the Study of Insulin Resistance (EGIR), and the National Cholesterol Education Program--Third Adult Treatment Panel (NCEP-ATP III). In 2005, IDF experts proposed a universally accepted diagnostic tool that is easy to use in clinical practice and does not rely on measurements available only in research settings. All groups agreed on the core components of the metabolic syndrome: obesity, insulin resistance, dyslipidemia, and hypertension. Their criteria are similar in many aspects, but they also reveal fundamental differences in their positioning of the predominant causes of the syndrome. This study provides a brief overview of current definitions of metabolic syndrome, with particular reference to the differences between them, and presents critical remarks on the concept of metabolic syndrome and its usefulness. It also presents epidemiological data which consider metabolic syndrome and its association with increased risk of cardiovascular disease and type 2 diabetes.

[The metabolic syndrome. Part II: its mechanisms of development and its complications]. / Zespól metaboliczny. Czesc II: patogeneza zespolu metabolicznego i jego powiklan

The metabolic syndrome is a cluster of interrelated metabolic factors such as insulin resistance, hyperinsulinemia, abdominal obesity, impaired glucose tolerance, dyslipidemia, hypertension, and a proinflammatory and prothrombotic state. It is a common cause of the development of atherosclerotic vascular disease and type 2 diabetes. Genetic predisposition and environmental factors such as physical inactivity and increased caloric intake are responsible for the predisposition to metabolic syndrome. Available studies on the pathogenesis of metabolic syndrome are discrepant. Insulin resistance and abdominal obesity are the dominant causes of metabolic syndrome. Increased visceral adipose tissue mass and its proinflammatory activity are thought to underlie all the changes observed in metabolic syndrome. Adipose tissue is a dynamic endocrine and paracrine organ that produces and secretes inflammatory factors called adipokines, which link obesity, insulin resistance, atherosclerosis, and type 2 diabetes. Recent data suggest that oxidative stress is a primary pathogenic mechanism leading to the development of insulin resistance associated with over-nutrition. In this study the authors analyze the association between abdominal obesity, hyperinsulinemia, and insulin resistance and show some pathogenic mechanisms which may be responsible for the proatherogenic action of insulin resistance, hyperinsulinemia, and impaired glucose tolerance. Here the association among the disorders mentioned in the definitions of metabolic syndrome is discussed in more detail and it is shown that their clustering is not accidental in patients with insulin resistance. The role of adipose tissue in the development of insulin resistance and metabolic syndrome leading to overt cardiovascular disease and type 2 diabetes is also described.