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This study was an attempt to identify if there are any trends in excretion of 1,2,3,4,5,6-hexachlorocyclohexane (HCH) isomers alpha-, beta-, and gamma-, hexachlorobenzene (HCB), [1,1,1-trichloro-2,2-bis(4-chlorophenyl)ethane] (p,p'-DDT), [1,1-dichloro-2,2-bis(4-chlorophenyl)ethane] (p,p'-DDD), [1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene] (p,p'-DDE), and polychlorinated biphenyls (PCBs) with human milk duringlactation. The shortest lactation studied took 16 weeks, and the longest 84 weeks. Three hundred fifty-two milk samples, collected from each donor once a week, were examined. The analysis of the result showed individual differences in the excretion of the compounds. The findings from this study are not conclusive enough to claim that there are consistent trends showing a decrease or increase in the excretion of the compounds under examination. Thus, one cannot claim that the infants' exposure to those compounds decreases or increases as breast-feeding continues. [ABSTRACT FROM AUTHOR]

Background: The aim of the study was to review data on the impact of anthropogenic chemicals (endocrine disruptors) on various diseases, which, consequently, may facilitate their prevention and be used as a tool for managing public healthcare. Every day, humans are exposed to chemicals, including xenoestrogens, which are similar to female hormones., Methods: This manuscript was prepared based on a meta-analysis of research on the impacts of selected EDCs on human health., Results: Special attention should be paid to bisphenol A (BPA), benzo-α-pyrene, and phthalates due to their proven endocrine activity and presence in our daily lives. Xenoestrogens are absorbed by human organisms through the digestive system since they can migrate to food from food packages and drinks as well as from plastic products used daily. The presence of these chemicals in human organisms is considered a potential cause for some diseases commonly referred to as 'diseases of civilization'., Conclusions: The biomonitoring of xenoestrogens, which are chemicals with unfavorable impacts on human health, is a crucial tool for assessing the risk from the pollution of the environment. The novelty is a holistic approach to assessing the occurrence of risk factors for civilization diseases.

Adipokines regulate glucose homeostasis, insulin sensitivity, lipids metabolism, reproduction, as well as endothelial and platelets function. The study compares the plasma and adipose tissue concentrations of total adiponectin, leptin, leptin receptor and leptin-to-adiponectin ratio (LAR) in morbidly obese patients. Additionally it evaluates selected adipokines (leptin, adiponectin), endothelial markers and LAR depending on the gender in morbidly obese and non-obese subjects. The study involved 51 patients (31 women aged 21 - 60 (mean age of 39) and 20 men aged 24 to 60 (mean age of 41)). The eligibility criterion included the BMI ≥ 40 kg/m2. The non-obese group consisted of 30 healthy volunteers with the BMI < 24.9 kg/m2; nineteen women, aged 24 - 53 (mean age of 41), and 11 men aged 21 - 52 (mean age of 38). In the plasma and adipose tissue, the concentrations of total adiponectin, leptin, leptin receptor and plasma soluble forms of E-selectin, P-selectin, thrombomodulin were measured applying immunoassay techniques. There were noted significantly higher plasma leptin and sE-selectin concentrations, leptin-to-adiponectin ratio, additionally lower concentrations of plasma leptin receptor and sP-selectin in obese subjects regardless of the gender. Significantly higher concentrations of total adiponectin, leptin, leptin receptor expressed per 1 mg of total protein in adipose tissue, as compared to plasma in morbidly obese patients, were observed. Significant positive correlations between the BMI and the concentration of leptin and between total adiponectin and sP-selectin were reported in the subject group. Similarly there were noted significant negative correlations between leptin receptor and the BMI and between leptin-to-adiponectin ratio and sP-selectin in obese patients. The study has shown that adiponectin has a positive impact on platelets through a possible reduction in sP-selectin, and thus on platelets activation. On the other hand an elevated sE-selectin reveals perspective about the endothelium stimulation and a higher risk of endothelial damage in morbidly obese patients. Also in morbidly obese the higher leptin level and leptin-to-adiponectin ratio and simultaneously lower concentration of leptin receptor are associated with leptin resistance, additionally in possible future risk of insulin resistance and diabetes type 2.

The healing process and the angiogenesis associated with it, is a very important but currently poorly understood area. Low level laser therapy (LLLT) has been reported to modulate the process of tissue repair by stimulation of cellular reaction such as migration, proliferation, apoptosis and cellular differentiation. The aim of this work was to evaluate the influence of laser radiation in the range of visible and infrared light on the proliferation of vascular endothelial cells in vitro and the secretion of angiogenic factors: vascular endothelial growth factor (VEGF)-A and transforming growth factor (TGF)-β. Vascular human endothelial cells (Ecs) were exposed to radiation with laser beam of the wavelengths: 635 nm (1.875 mW/cm²) and 830 nm (3.75 mW/cm²). Depending on the radiation energy density, the experiment was conducted in four groups : I) the control group (no radiation, 0 J/cm²); II) 635 nm - the energy density was 2 J/cm²; III) 635 nm - 4 J/cm²; IV635 nm - 8 J/cm², II) 830 nm - the energy density was 2 J/cm²; III) 830 nm - 4 J/cm²; IV) 830 nm - 8 J/cm². The proliferation and concentration of VEGF-A and TGF-β were examined. LLLT with wavelength 635 nm increases endothelial cell proliferation. Significant increase in endothelial cell proliferation and corresponding decrease in VEGF concentration may suggest the role for VEGF in this process. The wavelength of 830 nm was associated with a decrease in TGF-β secretion.

Background: Duchenne muscular dystrophy (DMD) is a genetic neuromuscular disorder that affects skeletal muscles and cardiac muscle tissue. In some cases, myocardial injury secondary to hypoxia can lead to dilative cardiomyopathy (DCM). A genetic defect in the dystrophin gene may increase the susceptibility of myocardium to hypoxia. Available data suggest that this may be caused by impaired secretion of NO, which is bound with secretion of VEGF-A., Material/methods: Male mice C57BI/10ScSn mdx (animal model of DMD) and healthy mice C57BI/10ScSn were exposed to hypobaric hypoxia in low-pressure chambers. Their hearts were harvested immediately after and 1, 3, 7, and 21 days after exposure to hypoxia. Normobaric mice were used as controls. The expression of VEGF-A in myocardium and cardiac vessel walls was evaluated using immunohistochemistry, Western blotting, and in situ hybridization., Results: VEGF-A expression in myocardium and vessel walls of healthy mice peaked 24 hours after exposure to hypoxia. The expression of VEGF-A in vessel walls was similar in dystrophic and healthy mice; however, VEGF-A expression in the myocardium of dystrophic mice was impaired, peaking around day 7. In the heart, the total level of VEGF depends on VEGF expression in myocardium, not in vessel endothelium, and our research demonstrates that the expression of VEGF is dystrophin-dependent., Conclusions: Disordered secretion of VEGF-A in hypoxic myocardium caused the total level of this factor to be impaired in the heart. This factor, which in normal situations protect against hypoxia, promotes the gradual progression of cardiomyopathy.