Assessment of the impact of land use in an agricultural catchment area on water quality of lowland rivers.

In several countries around the world, agricultural land area exceeds 70% (Uruguay 82.6%, Kazakhstan 80.4%, Turkmenistan 72.0%, Great Britain 71.7%, Ukraine 71.6% and others). This poses a serious risk of dissipating nitrates into the aquatic environment in agricultural catchments. The aim of this study was to assess the impact of land use on water quality parameters in an agricultural catchment area. It was decided to select for analysis the catchment of the Orla River (river length of 88 km, catchment area of 1,546 km2). The catchment area is predominantly agricultural in character and its entire area has been declared as an agricultural nitrate vulnerable zone (NVZ). A total of 27 survey sites were selected on the main watercourse and its tributaries. Analyses were conducted in the years 2010-2012 to determine physical and chemical parameters of water (pH reaction, conductivity, dissolved oxygen, total nitrogen, organic nitrogen, ammonia nitrogen, nitrates, total and reactive phosphorus) as well as six macrophyte metrics of ecological status assessment (MIR, IBMR, RMNI, MTR, TIM, RI). The average values of most physico-chemical parameters of water quality repeatedly exceeded limits of good ecological status, both in the Orla River and its tributaries. As many as 18 survey sites were classified as moderate ecological status, five sites as poor and only four as good ecological status. The results indicate the impact of land use in the catchment on water conductivity. Differences were observed in the concentrations of biotic components in the main watercourse and its tributaries, and in water quality in the southern part of the catchment in relation to the rest of the study area. This is probably connected with a greater share of forests and surface waters in that area.

Associations and interactions between variants in selenoprotein genes, selenoprotein levels and the development of abdominal aortic aneurysm, peripheral arterial disease, and heart failure.

BACKGROUND: Little is known on the role of selenoprotein genes in cardiovascular disease. This study examines the associations of the SEPP1, SELENOS, TXNRD1, TXNRD2, GPX4, and SOD2 polymorphisms and selenoprotein P (SeP) and thioredoxin concentrations with the development of abdominal aortic aneurysm (AAA) and aortoiliac occlusive disease (AOID), as well as their influence on cardiac phenotype. METHODS: 564 patients with AAA, 400 patients with AIOD, and 543 controls were enrolled and characterized for coronary artery disease, myocardial infarction, and systolic heart failure (HF) occurrence. In AAA, the coexistence of peripheral arterial disease (PAD) was examined. Genotypes were determined using TaqMan-based assays. Selenoprotein concentration was assessed using the ELISA method. RESULTS: The SELENOS rs34713741T, SEPP1 rs3877899A, and GPX4 rs713041T alleles were related to a 30-60% increase in the AIOD/PAD risk in the recessive or dominant model (all associations at P < .05). The SEPP1 rs3877899A allele was a protective factor for the development of AAA without concomitant PAD (OR = 0.68 for the dominant model, P = .014), but not AAA with concomitant PAD. The cumulative two-locus effects of selenoprotein genes on the AAA/AIOD risk were observed, including the multiplicative interaction between the SELENOS rs34713741T and GPX4 rs713041T alleles (both in the recessive model) affecting the AIOD risk (OR = 5.27, P = .001) and its clinical phenotype. Coexistence of HF in aortic diseases was related to both the SEPP1 rs7579A allele (OR = 1.83 for carriers, P = .013) and increased SeP concentrations; SeP level ≥8.5 mg/mL caused a 3.5-fold increase in the risk of HF. In AAA, SeP levels were correlated with BMI (r = -0.575, P < .0001). CONCLUSIONS: Our results provide evidence that selenoprotein polymorphisms constitute a risk factor for HF and peripheral atherosclerosis, but prevent the development of AAA. Excessive weight might result in reduced antioxidant reserve efficiency in AAA. Validation studies are required to establish whether SeP concentration may be a marker for HF.

Sulodexide Slows Down the Senescence of Aortic Endothelial Cells Exposed to Serum from Patients with Peripheral Artery Diseases.

BACKGROUND/AIMS: Aging of the arterial endothelial cells results in the appearance of their inflammatory phenotype, which may predispose patients to the acceleration of arteriosclerosis. We studied the effect of serum from patients with peripheral artery disease (PAD) on the senescence of human aortic endothelial cells (HAEC) and how that process is modulated by sulodexide. METHODS: HAEC replicative aging in vitro was studied in the presence of 10% PAD-serum (PAD Group) or10%PAD serum and Sulodexide 0.5 LRU/mL (PAD-SUL group). In control group cells were cultured in medium supplemented with 10% fetal bovine serum. All studied parameters were evaluated at the beginning and at the end of the study, in all experimental groups. Population doubling time (PDT) was studied from the cells growth rate after repeated passages, and senescence-associated beta- galactosidase activity (SA-ß gal activity) was measured with the fluorescence flow cytometry. Expression of IL6, vWF, p21 and p53 genes was measured with the real-time polymerase chain reaction (Real-Time PCR). Concentrations of IL6 and vWF were measured with the standard ELISA kits. RESULTS: PAD serum accelerated the senescence of HAEC as reflected by increased, compared to control, expression of the IL6 gene (+43%, p<0.05) vWF gene (+443%, p<0.01), p21 gene (+ 124%, p<0.01) and p53 gene (+ 85%, p<0.01). Secretion of IL6 and vWF was higher in that group: + 101%, p<0.01 and + 78%, p<0.01, respectively, as compared to control. Also, SA-ß gal activity was higher in the PAD group (+33%, p<0.05) than in the control group. In the PAD group PDT was longer (+108%, p<0.01) as compared to control. Simultaneous use of Sulodexide with PAD serum significantly reduced all the above described senescent changes in HAEC. CONCLUSIONS: PAD serum accelerates the aging of HAEC which may result in the faster progression of arteriosclerosis. Sulodexide reduces PAD induced senescence of HAEC, which results in lower inflammatory and thrombogenic activity of these cells.

Sulodexide Reduces the Proinflammatory Effect of Serum from Patients with Peripheral Artery Disease in Human Arterial Endothelial Cells.

BACKGROUND/AIMS: Dysfunction of the arterial endothelial cells promotes the progression of atherosclerosis. We studied how exposure of human arterial endothelial cells to atherosclerotic serum from patients with peripheral artery disease changes the secretory activity of these cells, and whether that reaction is modified by sulodexide. METHODS: Endothelial cells in in vitro culture were exposed to standard culture medium ± 100pg/mL Interleukin-1(IL-1) or to medium supplemented with 20% atherosclerotic serum. Afterwards, the expression of genes responsible for the synthesis of Interleukin-6 (IL-6), Vascular Cell Adhesion Protein-1 (VCAM-1) and Von Willebrand Factor (VWF) was evaluated, together with the secretion of these compounds. Additionally, the effect of sulodexide on these processes was studied. RESULTS: Atherosclerotic serum stimulated the expression of IL6, VCAM-1 and VWF genes in endothelial cells, which was followed by increased secretion of these compounds by 179%, 121% and 116%, respectively. Sulodexide (0.5 LRU/mL) reduced atherosclerotic serum-induced increased expression of genes for IL-6 (-32%), VCAM-1 (-20%) and VWF (-42%), and lowered secretion of these molecules: IL-6 (-27%), VCAM-1(-27%), VWF (-25%). Sulodexide also reduced, in a dose- dependent manner, secretion of IL6 from unstimulated and stimulated with IL-1 endothelial cells. CONCLUSIONS: Atherosclerotic serum induces proinflammatory and prothrombotic phenotype in arterial endothelium, which is partially reduced by sulodexide, via inhibition of genes expression, and in consequence lower secretory activity.

Inhibition of NF-kappaB with Dehydroxymethylepoxyquinomicin modifies the function of human peritoneal mesothelial cells.

Peritoneal mesothelial cells exposed to bioincompatible dialysis fluids contribute to damage of the peritoneum during chronic dialysis. Inflammatory response triggered in the mesothelium leading to neovascularization and fibrosis plays an important role in that process. We studied the effects of Dehydroxymethyepoxyquinmicin (DHMEQ)-an NF-κB inhibitor on function of human peritoneal mesothelial cells (HPMC) in in vitro culture. DHMEQ studied in concentrations of 1-10 µg/ml was not toxic to HPMC. Synthesis of IL-6, MCP-1 and hyaluronan in unstimulated and stimulated with interleukin-1 (100 pg/ml) HPMC was inhibited in the presence of DHMEQ and the effect was proportional to the dose of the drug. DHMEQ (10 µg/ml) reduced in unstimulated HPMC synthesis of IL-6 (-55%), MCP-1 (-58%) and hyaluronan (-41%). Respective values for stimulated HMPC were: -63% for IL-6, -57% for MCP-1 and -67% for hyaluronan. The observed effects were due to the suppression of the expression of genes responsible for the synthesis of these molecules. DHMEQ modified the effects of the effluent dialysates from CAPD patients on the function of HMPC. Dialysate induced accelerated growth of these cells, and synthesis of collagen was inhibited in the presence of DHMEQ 10 µg/ml, by 69% and 40%, respectively. The results of our study show that DHMEQ effectively reduces inflammatory response in HMPC and prevents excessive dialysate induced proliferation and collagen synthesis in these cells. All of these effects may be beneficial during chronic peritoneal dialysis and prevents progressive dialysis-induced damage to the peritoneum.

Normal saline may promote formation of peritoneal adhesions.

BACKGROUND: Normal saline is commonly used for rinsing the abdominal cavity and many surgeons claim that it is not harmful to peritoneum. We found in patients treated with laparoscopic surgery, that mean 25% of the instilled fluid is not drained and dwells in the abdominal cavity. Therefore we evaluated changes of the saline biocompatibility during its dwell in the rats abdominal cavity. METHODS: In 10 anesthetized rats normal saline were instilled into the abdominal cavity and samples of the dwelling solution were collected every 30 minutes, for 4 hours. Inflammatory parameters and effect of the collected samples on in vitro cultured rats mesothelial cells were studied. RESULTS: Low pH of the saline was normalized, but number of cells and % of macrophages and eosinophils, as well as elastase activity and MCP-1 and TGF-ß concentration increased, proportionally to the dwell time. Fluid samples tested ex-vivo suppressed proliferation of the mesothelial cells and induced biphasic (stimulation/inhibition) effect on synthesis of MCP-1 in these cells. Similar pattern of release was observed for TF, whereas synthesis of t-PA in the mesothelial cells was strongly suppressed. CONCLUSIONS: Mesothelial cells exposed in vivo to normal saline dwelling in the abdominal cavity acquire properties which may accelerate formation of the peritoneal adhesions.

Polymorphisms of genes involved in the hypoxia signaling pathway and the development of abdominal aortic aneurysms or large-artery atherosclerosis.

BACKGROUND: The pathogenesis of aortic diseases, both aneurysmal and occlusive, is associated with the occurrence of local ischemic/hypoxic conditions, but the genetic factors that differentiate the predisposition to specific types of aortic diseases are largely unknown. In this study, the functional variants in genes involved in the hypoxia signaling pathway, hypoxia-inducible factor-1α (HIF1A) 1772C>T, 1790G>A, and vascular endothelial growth factor (VEGFA) -634G>C, were analyzed in search of the associations specific to abdominal aortic aneurysm (AAA) development. METHODS: The study encompassed a series of 518 patients with AAA, 354 patients with aortoiliac occlusive disease, and 541 controls. In AAA patients, the occurrence of peripheral arterial disease (PAD) was examined with duplex arterial scanning. Genotypes were determined by the polymerase chain reaction/restriction fragment length polymorphism method or with TaqMan probes. RESULTS: In univariate analysis, a significantly increased risk for development of AAA without coexisting PAD was found in VEGFA -634C allele carriers (effect of allele dose: odds ratio [OR], 1.38; P = .012). In VEGFA -634CC homozygotes, the risk was enhanced by the interaction with HIF1A 1772CC-1790GG genotype (OR, 2.41; P = .008). This joint effect of homozygous genotypes also influenced the AAA risk independently of PAD coexistence (OR, 1.87; P = .036). In contrast, the minor allele of the HIF1A 1772C>T polymorphism (1772T and 1772T-1790G haplotype) was significantly associated with the occurrence of AAA with concomitant PAD (OR, 2.02; P = .009 for the dominant model). This effect was enhanced in the VEGF -634GG homozygotes (OR, 2.86; P = .005) and among smokers (OR, 3.10; P = .001). The individual effects of the HIF1A 1772 and VEGFA -634 polymorphisms on AAA risk remained significant in multivariable analysis after adjustment for the traditional vascular risk factors and analyzed polymorphisms. None of the studied variants influenced the risk of aortoiliac occlusive disease. CONCLUSIONS: This study identifies polymorphisms in the HIF1A and VEGF genes as potential genetic markers that indicate the predisposition to either AAA coexisting with peripheral atherosclerosis or AAA without such lesions, suggesting the genetic heterogeneity of this disease. The HIF1A 1772T allele also seems to be a genetic risk factor that determines sensitivity to cigarette smoke exposure. Further work is needed to confirm the findings in an independent samples set and to study the functional role of studied variants in AAA.

SEPP1 gene variants and abdominal aortic aneurysm: gene association in relation to metabolic risk factors and peripheral arterial disease coexistence.

An inadequate selenium level is supposed to be a risk factor for cardiovascular diseases. However little is known about variation of the genes encoding selenium-containing proteins that would confirm the causality in these diseases. The aim of this study was to analyze the relationships between two functional variants of selenoprotein P gene (SEPP1 rs3877899G>A, rs7579G>A) and the occurrence of abdominal aortic aneurysm (AAA) and aortoiliac occlusive disease (AIOD), as well as their metabolic risk factors. In AAA, the rs3877899A allele was associated with higher systolic blood (P < .003) and pulse pressure (P < .003) values (recessive model), and with coexistence of peripheral arterial disease (PAD; carriers: P = .033). The other SEPP1 variants were associated with BMI values and influenced the risk of aortic diseases, depending on body weight. The strongest associations in the case-control analysis was found between the presence of the rs3877899G-rs7579G haplotype and development of AAA in overweight and obese subjects (OR = 1.80, 95%CI = 1.16-2.79, P = .008). The higher BMI values were correlated with lower age of AAA patients and larger size of aneurysm. Our results suggests the potential role of the selenoprotein P in pathogenesis of AAA. Future studies should consider the role of the rs3877899G-rs7579G haplotype as a risk factor for aggressive-growing AAAs.

Endovascular treatment of late thoracic aortic aneurysms after surgical repair of congenital aortic coarctation in childhood.

BACKGROUND: In some patients, local surgery-related complications are diagnosed many years after surgery for aortic coarctation. The purposes of this study were: (1) to systematically evaluate asymptomatic adults after Dacron patch repair in childhood, (2) to estimate the formation rate of secondary thoracic aortic aneurysms (TAAs) and (3) to assess outcomes after intravascular treatment for TAAs. METHODS: This study involved 37 asymptomatic patients (26 female and 11 male) who underwent surgical repair of aortic coarctation in the childhood. After they had reached adolescence, patients with secondary TAAs were referred to endovascular repair. RESULTS: Follow-up studies revealed TAA in seven cases (19%) (including six with the gothic type of the aortic arch) and mild recoarctation in other six (16%). Six of the TAA patients were treated with stentgrafts, but one refused to undergo an endovascular procedure. In three cases, stengrafts covered the left subclavian artery (LSA), in another the graft was implanted distally to the LSA. In two individuals, elective hybrid procedures were performed with surgical bypass to the supraaortic arteries followed by stengraft implantation. All subjects survived the secondary procedures. One patient developed type Ia endoleak after stentgraft implantation that was eventually treated with a debranching procedure. CONCLUSIONS: The long-term course of clinically asymptomatic patients after coarctation patch repair is not uncommonly complicated by formation of TAAs (particularly in individuals with the gothic pattern of the aortic arch) that can be treated effectively with stentgrafts. However, in some patients hybrid procedures may be necessary.

Resveratrol and its synthetic derivatives exert opposite effects on mesothelial cell-dependent angiogenesis via modulating secretion of VEGF and IL-8/CXCL8.

We examined the effect of resveratrol (RVT) and its two derivatives (3,3',4,4'-tetrahydroxy-trans-stilbene and 3,3',4,4',5,5'-hexahydroxy-trans-stilbene) on human peritoneal mesothelial cell (HPMC)-dependent angiogenesis in vitro. To this end, angiogenic activity of endothelial cells (HUVEC, HMVEC, and HMEC-1) was monitored upon their exposure to conditioned medium (CM) from young and senescent HPMCs treated with stilbenes or to stilbenes themselves. Results showed that proliferation and migration of endothelial cells were inhibited in response to indirect (HPMC-dependent) or direct RVT activity. This effect was associated with decreased secretion of VEGF and IL-8/CXCL8 by HPMCs treated with RVT, which confirmed the experiments with recombinant forms of these angiogenic agents. Angiogenic activity of endothelial cells treated with CM from HPMCs exposed to RVT analogues was more effective. Improved migration was particularly evident in cells exposed to CM from senescent HPMCs. Upon direct treatment, RVT derivatives stimulated proliferation (but not migration) of HUVECs, and failed to affect the behaviour of HMVEC and HMEC-1 cells. These compounds stimulated production of VEGF and IL-8/CXCL8 by HPMCs. Studies with neutralizing antibodies against angiogenic factors revealed that augmented angiogenic reactions of endothelial cells exposed to CM from HPMC treated with RVT analogues were related to enhanced production of VEGF and IL-8/CXCL8. Collectively, these findings indicate that RVT and its synthetic analogues divergently alter the secretion of the angiogenic factors by HPMCs, and thus modulate HPMC-dependent angiogenic responses in the opposite directions. This may have implications for the attempts of practical employment of the stilbenes for treatment of pathologies proceeding with abnormal vascularisation of the peritoneal tissue.

[Gene-environment interaction for the HIF1-A 1772C>T polymorphisms and cigarette smoking increase susceptibility to abdominal aortic aneurysm]. / Interakcja genetyczno-srodowiskowa pomiedzy polimorfizmem HIF1-A 1772C>T a paleniem tytoniu zwieksza ryzyko rozwoju tetniaka aorty brzusznej.

Pathological changes in the vascular vessels, such as the presence of atherosclerotic plaques or aneurysmal dilatations, are associated with the local conditions of ischemial/hypoxia. Polymorphisms in the HIF1A gene, encoding an oxygen-regulated HIF-1 subunit (HIF-1a), determine inter-individual variability in vascular response to hypoxia. Stimulation of selected pathways, related to this response (i.e. angiogenesis) is impaired by cigarette smoke exposure. In this work, we examined the associations between 1772C>T polymorphism (rs11549465) located in the coding region of HIF1A gene (Pro582-Ser), smoking and the occurrence of abdominal aortic aneurysm (AAA). Moreover, the relations of these factors with the presence of peripheral arterial disease (PAD) in patients with AAA were studied. The case-control study was designed, in which a group of 1060 Caucasian subjects: 535 AAA patients and 525 controls, was analyzed. Data regarding smoking status were collected using questionnaire. Past and current smokers were analyzed together. In the group of 220 AAA subjects the coexistence of PAD was characterized. HIF-1A genotypes were assessed by PCR-RFLP method. Genetic-environmental interactions were examined by a two-by-four tables. In these analyzes, logistic regression models were used to adjusting for the relevant covariates. The frequency of HIF1A 1772T allele in AAA group (0,067) was similar to that observed in the control group (0,070). In the analyses of genetic-environmental interactions was observed that the co-occurrence of HIF1A 1772CT and TT genotypes and exposure to tobacco smoke has a strong multiplicative effect on the susceptibility to the AAA development. The age and gender adjusted odds ratios (ORs) were: 7,6 for smoking alone (p<0,0001); 0,65 for 1772CT and TT genotypes alone (p=0,3) and 14,4for smoking plus 1772CT and TT genotypes (p<0,0001). The proportion of smokers carrying 1772T allele was higher among patients with advanced form of PAD (femoro-popliteal or aorto-iliac occlusion, 18%) as compared to the frequency in the rest of AAA patients (9,3%, p=0,05). In a multivariate analysis smoking in combination with the HIF1A 1772T allele occurrence was the strongest independent predictor of AAA (OR=14,5; p<0,0001). In conclusion, HIF1A 1772T allele enhances theAAA risk determined by smoking and promotes the development of a more complex phenotype of the disease in smokers (with coexisting severe peripheral arterial disease).

Transarterial thrombin injection secured with an embolic protection device as a treatment for a superior mesenteric artery pseudoaneurysm.

A pseudoaneurysm of the superior mesenteric artery (SMA) is a rare and life-threatening condition of various etiology. Even unruptured it can cause severe health problems or death. We report a 71-year-old male with a SMA pseudoaneurysm who was successfully treated with a transarterial thrombin injection secured with an embolic protection device used in carotid angioplasty. To our knowledge, this is the first case of a SMA pseudoaneurysm treated by this method.

New technique for the preservation of the left common carotid artery in zone 2a endovascular repair of thoracic aortic aneurysm.

To describe a technique for the preservation of the left common carotid artery (CCA) in zone 2 endovascular repair of thoracic aortic aneurysm. This technique involves the placement of a guide wire into the left CCA via the right brachial artery before stent graft deployment to enable precise visualization and protection of the left CCA during the whole procedure. Of the 107 patients with thoracic endovascular aortic repair in our study, 32 (30%) had the left subclavian artery intentionally covered (landing zone 2). Eight (25%) of those 32 had landing zone 2a-the segment distally the origin of the left CCA, halfway between the origin of the left CCA and the left subclavian artery. In all patients, a guide wire was positioned into the left CCA via the right brachial artery before stent graft deployment. It is a retrospective study in design. In seven patients, stent grafts were positioned precisely. In the remaining patient, the positioning was imprecise; the origin of the left CCA was partially covered by the graft. A stent was implanted into the left CCA to restore the flow into the vessel. All procedures were performed successfully. The technique of placing a guide wire into the left CCA via the right brachial artery before stent graft deployment is a safe and effective method that enables the precise visualization of the left CCA during the whole procedure. Moreover, in case of inadvertent complete or partial coverage of the origin of the left CCA, it supplies safe and quick access to the artery for stent implantation.

Oxidative stress-dependent increase in ICAM-1 expression promotes adhesion of colorectal and pancreatic cancers to the senescent peritoneal mesothelium.

Intercellular adhesion molecule-1 (ICAM-1) has been implicated in adhesion of colorectal and pancreatic cancer cells (of the SW480 and PSN-1 line, respectively) to the peritoneal mesothelium. It has been demonstrated that ICAM-1 expression increases with senescence in some cell types, however, the significance of this phenomenon in the context of malignant dissemination remains elusive. In this report we show that the adherence of SW480 and PSN-1 cells to senescent human omentum-derived mesothelial cells (HOMCs) in vitro is greater than to early-passage cells and that the effect is mediated by ICAM-1. Senescent HOMCs display increased expression of ICAM-1 mRNA and cell surface protein. The development of this phenotype is related to increased oxidative stress in senescent cells. The augmented ICAM-1 expression in HOMCs can be reduced by culturing cells with antioxidants; in contrast, exposure of HOMCs to an oxidant, t-BHP, leads to cellular senescence and increased ICAM-1 expression. The effect is partly mediated by activation of p38 MAPK and AP-1 signaling pathways. Finally, culture of HOMCs in the presence of a strong antioxidant, PBN, significantly reduces the senescence-associated increase in SW480 and PSN-1 cancer cell binding. These results indicate that increased oxidative stress and increased expression of ICAM-1 in senescent HOMCs may facilitate peritoneal adhesion of selected colorectal and pancreatic cancers.

Diagnosis of type III endoleak and endovascular treatment with aortouniiliac stent-graft.

The present report describes a case of type III endoleak from a tear in the fabric of a Zenith bifurcated stent-graft approximately 6 months after implantation. The reason of the fabric tear was unknown. The complication was successfully treated by aortouniiliac stent-graft implantation followed by creation of a femorofemoral bypass.

Normal saline induces oxidative stress in peritoneal mesothelial cells.

BACKGROUND: Peritoneal adhesions are the most common complication of the abdominal surgery. Normal saline is frequently used to rinse the peritoneal cavity during abdominal surgery, although there is no well-established data describing effect of such procedure on the process of formation of peritoneal adhesions. METHODS: Effect of 0.9% NaCl solution on viability, oxidative stress, and fibrinolytic activity of human peritoneal mesothelial cells maintained in in vitro culture was evaluated. RESULTS: Exposure of mesothelial cells to 0.9% NaCl induces oxidative stress, derangement of their structure with subsequent increased release of tissue factor (+75%) and plasminogen activator inhibitor-1 (+19%), and simultaneous suppression of tissue plasminogen activator release (-39%). In effect, ration tissue plasminogen activator/plasminogen activator inhibitor-1 was reduced in 0.9% NaCl-treated cells by 50%. Pretreatment of cells with precursor of glutathione synthesis: L-2-oxothiazolidine-4-carboxylic acid prevented these changes. CONCLUSIONS: Oxidative stress in the peritoneal mesothelium caused by 0.9% NaCl activates their procoagulant activity and impairs fibrinolytic properties of these cells. These effects disqualify 0.9% NaCl as rinsing solution during abdominal surgery.

Acute lower limb ischemia in a young woman with arterial hypoplasia: a case report.

The most frequent causes for acute limb ischemia are arterial embolism, thrombosis (mainly in patients with atherosclerosis), and traumatic arterial injuries. Rarely, acute limb ischemia may be caused by the arterial spasm, when all other causes can be excluded. We present a case of a young woman with acute ischemia of her right lower extremity with diagnosed arterial hypoplasia in the calf. The suspected cause of the ischemia was a spasm of a single artery of the limb. Diagnostic procedures and treatment as well as differential diagnosis are discussed.

Correlation between the donor age and the proliferative lifespan of human peritoneal mesothelial cells in vitro: is TGF-beta1 a link?

In the present study we have examined the relationship between calendar age of the donor and the proliferative lifespan and TGF-beta1 production by human peritoneal mesothelial cells (HPMC) in culture. The experiments were performed on primary omentum-derived HPMC isolated from patients undergoing elective abdominal surgery. There was an inverse relationship between the calendar age of the tissue donor and the replicative lifespan of HPMC in vitro (n=49, r=-0.3991, p<0.005). There was also a positive correlation between the donor's age and the magnitude of TGF-beta1 production by first-passage HPMC (n=28, r=0.5400, p<0.004). In turn, the TGF-beta1 levels correlated inversely with the proliferative lifespan of HPMC in vitro (n=28, r=-0.4671, p<0.02). These findings indicate that the reduced proliferative capacity of HPMC isolated from older donors may be associated with increased TGF-beta1 release, which may, in turn, result from the age-related accumulation of senescent HPMC in the peritoneum.

[Pregnancy as a risk factor in development of varicose veins in women]. / Ciaza jako czynnik rozwoju zylaków konczyn dolnych u kobiet.

OBJECTIVES: The purpose of this study was to analyse prevalence of so called classical risk factors for VV in patients with this entity. MATERIALS AND METHODS: Study consisted of three parts. In the first part the prevalence of risk factors in 130 men and 360 women with VV was compared. In the second part the prevalence of risk factor in 360 women with VV and 162 without VV was compared. In the third part the prevalence of risk factors in pregnant women with and without VV was compared. The age of patients in all groups was comparable. The results were statistically analyzed. RESULTS: There were no differences in prevalence of classical risk factors between men and women with VV. In non pregnant women positive family history (OR 2,27, p=0,018) and previous pregnancies (OR 2,05, p=0,046) were associated with presence of VV. Premenstrual aching of lower extremities and obesity were at the border of statistical significance, OR and p, 1,9 and 0,062 and 1,4 and 0,071, respectively. As many as 47% of pregnant women had VV. Positive family history (OR 2,27, p=0,018), previous pregnancies (OR 2,56, p=0,011) and premenstrual aching of lower extremities (OR 2,03, p=0,021) were associated with presence of VV. Remaining, so called classical risk factors such as oral contraceptive, working in a sitting or standing position or constipations were not associated with occurrence of VV. CONCLUSIONS: In conclusion, positive family history and previous pregnancies seem to be principal risk factors for VV in women.