Nutritional status and risk of malnutrition.

Malnutrition is a global health problem that is not limited to developing countries. So far, it is one of the underdiagnosed and curative medical problems. THE AIM of our observation was to evaluate the nutritional status of patients at risk of malnutrition. METHODS AND PATIENTS: We retrospectively evaluated 140 patients from the Gastroenterology Clinic and the Center for Home Parenteral Nutrition (HPN) at the University Hospital Bratislava, Slovakia. Patients were indicated for examination as part of the entry screening for malnutrition or consultation examination in patients presenting with signs of malnutrition. Based on the determination of the body mass index (BMI), the completed questionnaire of nutritional risk screening (NRS) and the determination of the state of performance, we evaluated the nutritional status of the patient and subsequently started enteral, or parenteral nutrition. RESULTS: We recorded a statistically significant negative correlation between BMI and malnutrition risk (p<0.001), ie. the lower the BMI, the higher the risk of malnutrition. We did not observe a relationship between age, diagnoses and the incidence of BMI-related malnutrition in the study group of patients. CONCLUSION: Properly applied clinical nutrition, whether enteral, parenteral, or a combination thereof, can significantly affect morbidity and mortality in patients with malnutrition or the risk of its development. Unfortunately, Slovakia is still lagging behind developed countries in its implementation as part of a comprehensive treatment of patients (Tab. 2, Fig. 4, Ref. 28).

Titanium Dioxide Nanoparticles Modulate Systemic Immune Response and Increase Levels of Reduced Glutathione in Mice after Seven-Week Inhalation.

Titanium dioxide nanoparticles (TiO2 NPs) are used in a wide range of applications. Although inhalation of NPs is one of the most important toxicologically relevant routes, experimental studies on potential harmful effects of TiO2 NPs using a whole-body inhalation chamber model are rare. In this study, the profile of lymphocyte markers, functional immunoassays, and antioxidant defense markers were analyzed to evaluate the potential adverse effects of seven-week inhalation exposure to two different concentrations of TiO2 NPs (0.00167 and 0.1308 mg TiO2/m3) in mice. A dose-dependent effect of TiO2 NPs on innate immunity was evident in the form of stimulated phagocytic activity of monocytes in low-dose mice and suppressed secretory function of monocytes (IL-18) in high-dose animals. The effect of TiO2 NPs on adaptive immunity, manifested in the spleen by a decrease in the percentage of T-cells, a reduction in T-helper cells, and a dose-dependent decrease in lymphocyte cytokine production, may indicate immunosuppression in exposed mice. The dose-dependent increase in GSH concentration and GSH/GSSG ratio in whole blood demonstrated stimulated antioxidant defense against oxidative stress induced by TiO2 NP exposure.

Genotoxic effects of occupational exposure to glass fibres - A human biomonitoring study.

As part of a large human biomonitoring study, we conducted occupational monitoring in a glass fibre factory in Slovakia. Shopfloor workers (n = 80), with a matched group of administrators in the same factory (n = 36), were monitored for exposure to glass fibres and to polycyclic aromatic hydrocarbons (PAHs). The impact of occupational exposure on chromosomal aberrations, DNA damage and DNA repair, immunomodulatory markers, and the role of nutritional and lifestyle factors, as well as the effect of polymorphisms in metabolic and DNA repair genes on genetic stability, were investigated. The (enzyme-modified) comet assay was employed to measure DNA strand breaks (SBs) and apurinic sites, oxidised and alkylated bases. Antioxidant status was estimated by resistance to H2O2-induced DNA damage. Base excision repair capacity was measured with an in vitro assay (based on the comet assay). Exposure of workers to fibres was low, but still was associated with higher levels of SBs, and SBs plus oxidised bases, and higher sensitivity to H2O2. Multivariate analysis showed that exposure increased the risk of high levels of SBs by 20%. DNA damage was influenced by antioxidant enzymes catalase and glutathione S-transferase (measured in blood). DNA repair capacity was inversely correlated with DNA damage and positively with antioxidant status. An inverse correlation was found between DNA base oxidation and the percentage of eosinophils (involved in the inflammatory response) in peripheral blood of both exposed and reference groups. Genotypes of XRCC1 variants rs3213245 and rs25487 significantly decreased the risk of high levels of base oxidation, to 0.50 (p = 0.001) and 0.59 (p = 0.001), respectively. Increases in DNA damage owing to glass fibre exposure were significant but modest, and no increases were seen in chromosome aberrations or micronuclei. However, it is of concern that even low levels of exposure to these fibres can cause significant genetic damage.

Effect of home parenteral nutrition in malnourished patients.

OBJECTIVE: The goal of our research was to determine the impact of clinical nutrition in the form of home parenteral nutrition (HPN) in patients with nutritional disorders, most often caused by diseases of the digestive tract, with the risk of developing malnutrition. PATIENTS AND METHODS: We retrospectively evaluated 39 patients from the Gastroenterology Clinic and the Home Parenteral Nutrition Center of the University Hospital Bratislava, whose nutritional status was evaluated based on the determination of the body mass index (BMI), the completed nutritional risk screening (NRS) questionnaire and the determination of performance status. Subsequently, after fulfilling the criteria for HPN, the initiation of parenteral nutrition (PN) followed, implemented in a domestic environment for the following two years as HPN. During this period, we did a monthly check-up of the objective condition and laboratory parameters of the enrolled patients, which were the basis for adjusting the nutritional treatment. We also evaluated the occurrence of infectious and thrombotic complications clinically and on the basis of laboratory parameters focused on culture and hemocoagulation examination. After two years, we performed control exit examinations, which we compared with the entrance examinations and statistically evaluated the success of the treatment. We evaluated the obtained data using standard statistical methods. RESULTS: During HPN, there was a statistically significant elevation of the individual monitored values ​​(BMI, absolute lymphocytes count, cholesterol, cholinesterase, total proteins, albumins), which clearly proves correctly indicated and managed HPN. We recorded vein thrombosis in v. subclavia and v. jugularis in 6 (15 %) patients. Subsequent catheter extraction was necessary after unsuccessful catheter insertion. In 13 (33 %) patients, tunneled catheter replacement was required due to infection. The mortality rate in our group was 8 % (3 patients). These were female patients aged 39, 42, and 66 years. The cause of death in all of these patients was the underlying diagnosis (oncohematological disease, systemic connective tissue disease, and repeated resections of the digestive tract for inflammatory GIT disease with the development of severe malnutrition). We recorded a positive effect of applied HPN in all three patients until death.We did not register any factors that would have a relevant influence on the success of administered HPN. CONCLUSION: Based on our results, we can conclude that the patients included in the HPN were correctly indicated, and all of them, based on the monitored parameters (regardless of gender, age, initial diagnosis, or BMI value), benefited from the applied treatment, which was correctly chosen based on their individual needs. Our results clearly document the irreplaceable role of HPN in the management of patients with nutritional intake disorders leading to the development of malnutrition (Tab. 2, Fig. 10, Ref. 44). Text in PDF www.elis.sk Keywords: malnutrition, nutritional risk screening, clinical nutrition, home parenteral nutrition, complications.

Determination of reference ranges for the ClotPro® thromboelastometry device in paediatric patients.

BACKGROUND: A new thromboelastometry analyser (ClotPro®) was developed with advanced diagnostics. The reference ranges of ClotPro® in children ages 0-16 yr have not been reported. METHODS: In this prospective study, venous blood samples from 321 patients were obtained from children undergoing elective surgery after induction of anaesthesia. Reference ranges were defined by calculating the 2.5% and 97.5% percentiles for each age group (0-3 months, 4-12 months, 13-24 months, 2-5 yr, 6-10 yr, and 11-16 yr). RESULTS: Reference ranges of the ClotPro® analyser in all age groups demonstrated significant differences in some parameters between age groups. In the first 3 months of life, a significant shortening of the clotting time (CT) in the extrinsically activated test (EX-test) was observed in children aged 0-3 months compared with children of all older age groups (P<0.001), whereas there were no overall differences in the intrinsically activated test (IN-test). In both assays, the clot amplitude 5 and 10 min after CT (A5, A10 value) was significantly higher in the first year of life compared with children older than 1 yr (EX-test and IN-test A5 and A10, respectively; P<0.001). The strength of fibrin polymerisation (FIB-test) was significantly higher in the first 3 months of life (A5 and A10, P<0.003). CONCLUSIONS: ClotPro® reference ranges were determined for six paediatric age groups, and show age-dependent differences in specific parameters. These values will be helpful in monitoring haemostasis in paediatric patients and for developing tailored bleeding management protocols. CLINICAL TRIAL REGISTRATION: NCT04190615.

Hypertension in obese children is associated with vitamin D deficiency and serotonin dysregulation.

BACKGROUND: Obesity and hypertension represent serious health issues affecting the pediatric population with increasing prevalence. Hypovitaminosis D has been suggested to be associated with arterial hypertension. Serotonin by modulating nitric oxide synthase affect blood pressure regulation. The biological mechanism by which vitamin D specifically regulates serotonin synthesis was recently described. The aim of this paper is to determine the associations between vitamin D, serotonin, and blood pressure in obese children. METHODS: One hundred and seventy-one children were enrolled in the prospective cross-sectional study. Two groups of children divided according to body mass index status to obese (BMI ≥95th percentile; n = 120) and non-obese (n = 51) were set. All children underwent office and ambulatory blood pressure monitoring and biochemical analysis of vitamin D and serotonin. Data on fasting glucose, insulin, HOMA, uric acid, and complete lipid profile were obtained in obese children. RESULTS: Hypertension was found only in the group of obese children. Compared to the control group, obese children had lower vitamin D and serotonin, especially in winter. The vitamin D seasonality and BMI-SDS were shown as the most significant predictors of systolic blood pressure changes, while diastolic blood pressure was predicted mostly by insulin and serotonin. The presence of hypertension and high-normal blood pressure in obese children was most significantly affected by vitamin D deficiency and increased BMI-SDS. CONCLUSIONS: Dysregulation of vitamin D and serotonin can pose a risk of the onset and development of hypertension in obese children; therefore, their optimization together with reducing body weight may improve the long-term cardiovascular health of these children.

Copper Oxide Nanoparticles Stimulate the Immune Response and Decrease Antioxidant Defense in Mice After Six-Week Inhalation.

Copper oxide nanoparticles (CuO NPs) are increasingly used in various industry sectors. Moreover, medical application of CuO NPs as antimicrobials also contributes to human exposure. Their toxicity, including toxicity to the immune system and blood, raises concerns, while information on their immunotoxicity is still very limited. The aim of our work was to evaluate the effects of CuO NPs (number concentration 1.40×106 particles/cm3, geometric mean diameter 20.4 nm) on immune/inflammatory response and antioxidant defense in mice exposed to 32.5 µg CuO/m3 continuously for 6 weeks. After six weeks of CuO NP inhalation, the content of copper in lungs and liver was significantly increased, while in kidneys, spleen, brain, and blood it was similar in exposed and control mice. Inhalation of CuO NPs caused a significant increase in proliferative response of T-lymphocytes after mitogenic stimulation and basal proliferative activity of splenocytes. CuO NPs significantly induced the production of IL-12p70, Th1-cytokine IFN-γ and Th2-cytokines IL-4, IL-5. Levels of TNF-α and IL-6 remained unchanged. Immune assays showed significantly suppressed phagocytic activity of granulocytes and slightly decreased respiratory burst. No significant differences in phagocytosis of monocytes were recorded. The percentage of CD3+, CD3+CD4+, CD3+CD8+, and CD3-CD19+ cell subsets in spleen, thymus, and lymph nodes did not differ between exposed and control animals. No changes in hematological parameters were found between the CuO NP exposed and control groups. The overall antioxidant protection status of the organism was expressed by evaluation of GSH and GSSG concentrations in blood samples. The experimental group exposed to CuO NPs showed a significant decrease in GSH concentration in comparison to the control group. In summary, our results indicate that sub-chronic inhalation of CuO NPs can cause undesired modulation of the immune response. Stimulation of adaptive immunity was indicated by activation of proliferation and secretion functions of lymphocytes. CuO NPs elicited pro-activation state of Th1 and Th2 lymphocytes in exposed mice. Innate immunity was affected by impaired phagocytic activity of granulocytes. Reduced glutathione was significantly decreased in mice exposed to CuO NPs.

Effects of Ovariectomy and Exercise Training on Mineral Status in a High-Fat Diet-Induced Obesity Rat Model.

Osteoporosis is a growing public health issue for an aging society. Previous studies have found both beneficial and detrimental effects of obesity on bone health. The purpose of this study was to investigate the impact of estrogen deficiency and physical activity on bone and blood concentrations of macrominerals (Ca, P, and Mg) and microminerals (Zn, Se, Cu, and Fe) in a high-fat diet-induced obesity rat model. Forty-eight female Wistar rats were divided into six groups: sham-operated and ovariectomized rats that received a standard diet (SD), high-fat diet (HFD), or HFD accompanied by physical exercise. The effect of ovariectomy on bone minerals varied with diet. Ovariectomy significantly decreased femoral Ca and Mg in sedentary rats receiving a SD; femoral Se, Cu, Zn, and Fe in sedentary rats on HFD; and plasma Fe in both sedentary rats on SD and exercising rats on HFD. The interaction of ovariectomy and diet had the strongest impact on Mg and Se concentrations in femur. In ovariectomized rats, HFD showed to have a protective effect on bone mineralization (femoral Ca and Mg), and a negative one on antioxidant microminerals (femoral Se, Cu, and Zn). Physical activity reduced the decline of Se, Cu, Zn, and Fe in the femur of ovariectomized rats on HFD. In the current state of knowledge, it is difficult to suggest if decreased femoral levels of antioxidant microminerals may contribute to the pathophysiology of osteoporosis in obese individuals or just reflect the mineral status in the body.

Pharmacokinetics, Biodistribution, and Biosafety of PEGylated Gold Nanoparticles In Vivo.

Despite the obvious advantages of gold nanoparticles for biomedical applications, controversial and incomplete toxicological data hamper their widespread use. Here, we present the results from an in vivo toxicity study using gold nanoparticles coated with polyethylene glycol (PEG-AuNPs). The pharmacokinetics and biodistribution of PEG-AuNPs were examined in the rat's liver, lung, spleen, and kidney after a single i.v. injection (0.7 mg/kg) at different time intervals. PEG-AuNPs had a relatively long blood circulation time and accumulated primarily in the liver and spleen, where they remained for up to 28 days after administration. Increased cytoplasmic vacuolation in hepatocytes 24 h and 7 days after PEG-AuNPs exposure and apoptotic-like cells in white splenic pulp 24 h after administration has been detected, however, 28 days post-exposure were no longer observed. In contrast, at this time point, we identified significant changes in lipid metabolism, altered levels of liver injury markers, and elevated monocyte count, but without marked biological relevance. In blood cells, no DNA damage was present in any of the studied time intervals, with the exception of DNA breakage transiently detected in primary kidney cells 4 h post-injection. Our results indicate that the tissue accumulation of PEG-AuNPs might result in late toxic effects.

Association of cytochrome P450 1B1 gene polymorphisms and environmental biomarkers with hypertension in Slovak midlife women.

OBJECTIVE: This study investigated the association of the Leu432Val and Asn453Ser CYP1B1 polymorphisms and selected environmental biomarkers with hypertension (HT) in Slovak midlife women. METHODS: We studied 575 women. Divided according to their blood pressure status: 255 with HT and 320 without HT. All data was obtained by using standard anthropometric, genetic methods and analyzed by regression models to adjust for HT risk factors such as age, obesity, smoking, and level of education. RESULTS: Our findings revealed that CYP1B1 Leu432Val polymorphism was associated with HT, whereas no association was found between Asn453Ser polymorphism and HT. Women with at least one Val allele had significantly higher odds of HT compared to women with the Leu/Leu genotype in the total sample (Exp(B) = 1.82, CI 1.16-2.84, P = 0.009). After dividing women by menopausal status and the presence of HT environmental risk factor, the association between CYP1B1 polymorphism and HT was observed in pre/perimenopausal women (Exp(B), 2.36; 95% CI 1.13-4.92; P = 0.02), smokers (Exp(B), 3.40; 95% CI 1.48-7.82; P = 0.004), abdominal obesity (Exp(B), 2.41; 95% CI 1.23-4.75; P = 0.01) and in women with only basic education (Exp(B), 4.20, 95% CI 1.12-15.71; P = 0.03). However, general linear models did not reveal a statistically significant interactions between CYP1B1, menopausal status, and HT risk factors and their common association with HT (P > 0.05). CONCLUSIONS: In this pilot study, we have provided novel data that supports the significant association of CYP1B1 Leu432Val gene polymorphism with HT in Slovak midlife women.

Six-week inhalation of CdO nanoparticles in mice: The effects on immune response, oxidative stress, antioxidative defense, fibrotic response, and bones.

Due to the growing number of applications of cadmium oxide nanoparticles (CdO NPs), there is a concern about their potential deleterious effects. The objective of our study was to investigate the effect of CdO NPs on the immune response, renal and intestine oxidative stress, blood antioxidant defence, renal fibrotic response, bone density and mineral content. Six-week-old female ICR mice were exposed to CdO NPs for 6 weeks by inhalation (particle size: 9.82 nm, mass concentration: 31.7 µg CdO/m3, total deposited dose: 0.195 µg CdO/g body weight). CdO NPs increased percentage of thymus CD3e+CD8a+ cells and moderately enhanced splenocyte proliferation and production of cytokines and chemokines. CdO NPs elevated pro-fibrotic factors (TGF-ß2, α-SMA and collagen I) in the kidney, and concentrations of AGEs in the intestine. The ratio of GSH and GSSG in blood was slightly reduced. Exposure to CdO NPs resulted in 10-fold higher Cd concentration in tibia bones. No differences were found in bone mass density, mineral content, bone area values, bone concentrations of Ca, P, Mg and Ca/P ratio. Our findings indicate stimulation of immune/inflammatory response, oxidative stress in the intestine, starting fibrotic response in kidneys and accumulation of CdO NPs in bones of mice.

Delayed adverse effects of neonatal exposure to polymeric nanoparticle poly(ethylene glycol)-block-polylactide methyl ether on hypothalamic-pituitary-ovarian axis development and function in Wistar rats.

We studied delayed effects of neonatal exposure to polymeric nanoparticle poly(ethylene glycol)-block-polylactide methyl ether (PEG-b-PLA) on the endpoints related to pubertal development and reproductive function in female Wistar rats from postnatal day 4 (PND4) to PND 176. Female pups were injected intraperitoneally, daily, from PND4 to PND7 with PEG-b-PLA (20 or 40mg/kg b.w.). Both doses of PEG-b-PLA accelerated the onset of vaginal opening compared with the control group. In the low-dose PEG-b-PLA-treated group, a significantly reduced number of regular estrous cycles, increased pituitary weight due to hyperemia, vascular dilatation and congestion, altered course of hypothalamic gonadotropin-releasing hormone-stimulated luteinizing hormone secretion, and increased progesterone serum levels were observed. The obtained data indicate that neonatal exposure to PEG-b-PLA might affect the development and function of hypothalamic-pituitary-ovarian axis (HPO), and thereby alter functions of the reproductive system in adult female rats. Our study indicates a possible neuroendocrine disrupting effect of PEG-b-PLA nanoparticles.

Genetic determinants of quantitative traits associated with cardiovascular disease risk.

Established risk factors for cardiovascular diseases (CVD) may be moderated by genetic variants. In 2403 unrelated individuals from general practice (mean age 40.5 years), we evaluated the influence of 15 variants in 12 candidate genes on quantitative traits (QT) associated with CVD (body mass index, abdominal obesity, glucose, serum lipids, and blood pressure). Prior to multiple testing correction, univariate analysis associated APOE rs429358, rs7412 and ATG16L1 rs2241880 variants with serum lipid levels, while LEPR rs1137100 and ATG16L1 rs2241880 variants were linked to obesity related QTs. After taking into account confounding factors and correcting for multiple comparisons only APOE rs429358 and rs7412 variants remained significantly associated with risk of dyslipidemia. APOE rs429358 variant almost tripled the risk in homozygous subjects (OR = 2.97; 95% CI 1.09-8.10, p < 0.03) and had a lesser but still highly significant association also in heterozygous individuals (OR = 1.67; 95% CI 1.24-2.10; p < 0.001). Associations with hypertension, diabetes mellitus, and metabolic syndrome were not significant after Bonferroni correction. The influence of genetic variation is more evident in dyslipidemia than in other analyzed QTs. These results may contribute to strategic research aimed at including genetic variation in the set of data required to identify subjects at high risk of CVD.

Power of biomarkers and their relative contributions to metabolic syndrome in Slovak adult women.

BACKGROUND: Metabolic syndrome (MetS) comprises a cluster of risk components which pre-dispose individuals to cardiovascular mortality. AIM: The purpose of this study is to investigate the variability of biochemical and anthropometric characteristics, apolipoprotein E (APOE) and angiotensin converting enzyme (ACE) genes and their contribution to MetS manifestation. SUBJECTS AND METHODS: A total of 438 adult women were recruited from different localities in Slovakia. All data was established by standard anthropometric, biochemical and genetic methods. RESULTS: The logarithm of the ratio of plasma concentration of triglycerides to HDL-cholesterol [log(TG-to-HDL-C)], waist circumference, systolic blood pressure, apolipoprotein A1, glucose and alanin aminotransferase accounted for most of the differences in MetS manifestation. Logistic regression showed that participants with risk values of the atherogenic index log(TG-to-HDL-C) had a 15.62-fold higher risk of MetS compared to those with lower values for this index (95% CI = 8.3-29.1). Women with hyperglycaemia (or formerly diagnosed diabetes mellitus) had an 8.82-times higher risk of MetS (95%CI = 3.22-24.16). Women with hyper-uricaemia had the same risk of MetS incidence as women with abdominal obesity, Exp (B) = 4.05.Hypercholesterolaemia, ACE and APOE genotypes did not influence MetS. CONCLUSION: MetS may involve many risk factors that can cause serious disorders in multiple organs. However, women with risk values involving plasma atherogenic index log (TG-to-HDL-C) experienced the highest risk of developing MetS.

Alterations in the QRS complex in the offspring of patients with metabolic syndrome and diabetes mellitus: early evidence of cardiovascular pathology.

OBJECTIVE: This study was undertaken to evaluate the nature and onset of changes in the QRS complex in the offspring of patients with diabetes mellitus (DM) and metabolic syndrome (MetS). METHODS AND METHODS: A total of 529 subjects, divided into 5 groups, were included in the study: (i) group DM (n = 92), patients with DM; (ii) group MetS (n = 125), patients with MetS; (iii) group O-DM (n = 109), offspring of patients with DM; (iv) group O-MetS (n = 122), offspring of patients with MetS; and (v) group HO (n = 81), offspring of healthy subjects. QRS parameters analyzed included amplitude, maximum QRS spatial vector magnitude, electrical axis (EA), and 3 electrocardiogram (ECG) criteria for left ventricular hypertrophy based on amplitude criteria: Sokolow-Lyon index, Cornell voltage, and Gubner criterion. RESULTS: Patients with DM and MetS showed a significant leftward shift of the EA when compared with the control group. A modest but significant leftward shift of EA was also observed in both offspring groups. These EA and maximum QRS spatial vector magnitude changes were reflected in the individual leads of the 12-lead ECG. The prevalence of a positive diagnosis by accepted electrocardiographic criteria (ECG left ventricular hypertrophy) was low. CONCLUSION: Patients with DM and MetS displayed significant changes in QRS complex that suggest depolarization sequence deterioration. Similar changes were observed also in the offspring of patients with DM and MetS, which suggests early subclinical cardiovascular damage. These findings have implications for prevention, early diagnosis, and treatment in the offspring of patients with DM and MetS.

Association between the human immune response and body mass index.

The aim of this study was to determine the strength of the association between the human immune response and body mass index (BMI) and whether differences exist in the effects of obesity on selected immune parameters between men and women. Two hundred ninety participants were divided into groups according to sex and BMI. Parameters CD3, CD4, CD8, CD16+56, CD19, HLADR, CD11b, CD11c, and CD54 were quantified. Leukocyte and differential counts were performed. We observed elevation with regard to the normal weight group in the parameters of white blood cells, neutrophils, monocytes, CD3, CD4, CD19, and CD11b for the whole study group. A decrease was observed in the expression of CD16+56. The effect of BMI on the immune system was much more apparent in women. BMI was correlated with the majority of the measured parameters, reflecting a strong association between BMI and the human immune system.

The relation between human exposure to mercury and thyroid hormone status.

The aim of this study was to investigate total mercury (THg) and methylmercury (MeHg) exposure of 75 mother-child pairs in relation to their thyroid hormone status (thyroid-stimulating hormone (TSH), triiodothyronine (T3), free triiodothyronine (fT3), thyroxine (T4), and free thyroxine (fT4)). THg and MeHg in blood samples were measured by atomic absorption spectrometry and gas chromatography-inductively coupled plasma-mass spectrometry, respectively. The median THg and MeHg levels in maternal blood, cord blood, and blood of 6-month-old children were 0.50, 0.53, and 0.32 and 0.22, 0.32, and 0.08 µg/L, respectively. There were significant correlations between paired maternal-cord blood levels for THg and MeHg, with a greater transplacental transport of MeHg compared with THg (mean cord/maternal blood ratio, 1.80 vs. 1.24). The maternal blood THg was found to be a better predictor of TSH levels in children than their current THg exposure. There was a positive correlation between maternal THg and children's TSH. T3 and fT3 levels in children were negatively related to cord blood THg in the majority (Caucasian) subgroup, whereas these associations were positive in the Roma subgroup. Mothers with dental amalgam fillings had significantly lower T4 and fT4 levels. Moreover, fT4 in the mothers of boys negatively correlated with maternal THg levels. MeHg exposure lowered T3 levels in the mothers of girls. Our results suggest that low-level exposure to Hg can affect thyroid hormone status during prenatal and early postnatal exposure depending on the form of Hg, gender, ethnicity, lifestyle, or socioeconomic status (dental amalgam fillings).

Changes in immunologic parameters of humoral immunity and adipocytokines in obese persons are gender dependent.

The aim of this study was to investigate several immunologic parameters using of immunonephelometry and adipocytokines by the enzyme immunoassay and their changes in different states of obesity. Obesity is considered to involve a state of chronic low-grade inflammation, with links between adipose cells and the immune system. We found significantly higher complement C3 levels in all obese subjects. Levels of the complement C4 were significantly higher in obese women, but not in men, when compared with the corresponding group of normal weight subjects. The increase in C-reactive protein concentrations was significant in both obese and morbidly obese women, but only in morbidly obese men. No significant differences in tumor necrosis factor-α, interleukin-6, interleukin-10, and soluble intercellular adhesion molecule-1 were found. sE-selectin levels were higher in both overweight and obese women but only in morbidly obese men. We found decreased adiponectin concentrations in obese and morbidly obese women. Concentrations of leptin were significantly higher only in obese men (p < 0.05), whereas in women the increase in leptin levels was significant in overweight, obese, and morbidly obese subjects. In conclusion, our results demonstrate elevated levels of C3, C-reactive protein, sE-selectin, and leptin in obese women and men. In obese women, we also observed increased concentrations of C4 and decreased levels of adiponectin.

The importance of the presence of aggregatibacter actinomycetemcomitans in sulcus gingivalis of patients with cardiovascular diseases.

BACKGROUND: Over-replication of periodontal pathogens in the periodontium induces production of proinflammatory cytokines and C-reactive protein that can stimulate systemic inflammatory status and can initiate atherosclerosis and its consequences. In our pilot study we examined whether periodontal status and serum levels of interleukin-6 and C-reactive protein are associated with the presence of Aggregatibacter actinomycetemcomitans in the periodontium of patients with cardiovascular diseases (CVD). MATERIAL/METHODS: We randomly selected 38 of 166 outpatients with CVD, of which 21 patients had chronic ischemic heart disease (IHD) only and 17 had both IHD and essential hypertension (HT). The presence of Aggregatibacter actinomycetemcomitans (A.a.) in the periodontium evaluated by PCR was compared with the values of periodontal indices, namely probe depth (PD) and Community Periodontal Index of Treatment Need (CPITN), as well as with interleukin-6 (IL-6) and CRP serum levels. RESULTS: When comparing A.a.-positive and A.a.-negative groups of patients, no statistically significant differences were noticed as to the age and values of PD and CPITN, respectively. However, the proportion of CRP and IL-6 positive values was significantly higher (p ≤ 0.001) among A.a.-positive than in A.a.-negative patients. CONCLUSIONS: The presence of A.a. in patients with CVD may be associated with significantly higher serum levels of some proinflammatory markers.

Geographic accumulation of Creutzfeldt-Jakob disease in Slovakia--environmental metal imbalance as a possible cofactor.

Slovakia is characterised by an unusually high number of patients affected by genetic Creutzfeldt-Jakob disease (CJD) with E200K mutation at the PRNP gene. Penetrance of the mutation is incomplete (59%). Therefore, for the onset of the clinical manifestation, an influence of other endo- or exogenous factors could not be excluded. Experimental data suggest that copper and manganese levels may play an important role in the pathogenesis of prion diseases. The highest number of Slovak genetic CJD patients originates from Orava - the northern region of central Slovakia. Manganese is a dominant pollutant in Orava. The objective of this study was to clarify a possible exogenous influence of environmental Mn/Cu imbalance on the CJD clustering. Mn and Cu levels were analysed in the brain tissue of genetic CJD cases (from Orava and from control regions of Slovakia), as well as of sporadic CJD patients and controls. Analyses demonstrate i) significantly higher Mn level in focally accumulated, "clustering" genetic CJD cases in comparison to all other groups, ii) Cu status differences between compared groups were without statistical significance; decreased concentrations were found in genetic cases from extrafocal genetic CJD areas, iii) Mn/Cu ratios were increased in all CJD groups in comparison to controls. Metal ratios in clustering gCJD cases were significantly higher in comparison to sporadic cases and also to controls, but not to the extrafocal genetic CJD subgroup. These results indicate that more important than increasing Mn level in pathogenesis of CJD appears to be the role of the Mn/Cu imbalance in the CNS. The imbalance observed in the cluster of genetic CJD cases is probably a result of both: the excessive environmental Mn level and the disturbance of Mn/Cu ratios in the Orava region. Presented findings indicate an environmental Mn/Cu imbalance as a possible exogenous CJD risk co-factor which may, in coincidence with endogenous (genetic) CJD risk, contribute to the focal accumulation (cluster) of genetic CJD in Slovakia.