Przemysław Nowak

Introduction and objective: Obesity is a disease that develops due to the occurrence or co-occurrence of various factors. So far, it has not been possible to link a selected personality type to obesity, but many of the traits observed in obese people are reflected in the type D personality....

Wstęp: Neurotropowy czynnik pochodzenia mózgowego (Brain-Derived Neutortophic Factor – BDNF) jest białkiem należącym do rodziny neurotrofin, które odgrywa kluczową rolę w prawidłowym rozwoju i funkcjonowaniu ośrodkowego układu nerwowego ssaków. Dotychczasowe badania dotyczyły głównie oceny stężenia BDNF w surowicy krwi, jako potencjalnego biomarkera w schorzeniach neurologicznych. Ostatnio ścieżka sygnałowa BDNF uznana została za potencjalne miejsce uchwytu leków przeciwnowotworowych, a jego receptor (TrkB) za onkogen w komórkach raka jelita grubego. Pomimo znaczącej roli w nowotworzeniu, niewiele jest prac dotyczących BDNF jako biomarkera w raku jelita grubego.Materiał i metody: Badaniem objęto grupę 25 osób z potwierdzonym klinicznie i histopatologicznie rakiem jelita grubego, którzy zostali zakwalifikowani do leczenia. Przed pierwszorazowym podaniem chemioterapii od pacjentów pobrano próbki krwi żylnej i dokonano oceny parametrów biochemicznych oznaczanych rutynowo przed leczeniem. Dodatkowo metodą immunoenzymatyczną oznaczono stężenia BDNF w surowicy krwi wszystkich badanych pacjentów.Wyniki: Stężenie BDNF w surowicy pacjentów wyniosło 50,24 ± 23,37 ng/ml i nie różniło się istotnie pomiędzy kobietami i mężczyznami. Stwierdzono ujemną korelację między stężeniem BDNF i CRP oraz BDNF i LDH. Stężenie BDNF było znamiennie wyższe u chorych, którzy przed chemioterapią byli poddani resekcji guza pierwotnego. Nie wykazano zależności pomiędzy stężeniem BDNF a wiekiem, płcią, wskaźnikiem BMI, markerem CEA oraz enzymami wskaźnikowymi wątroby u pacjentów z RJG. Nie zaobserwowano zależności pomiędzy stężeniem BDNF a odpowiedzią kliniczną na zastosowane leczenie.Wnioski: BDNF nie może być uznany za czynnik prognostyczny u chorych z rakiem jelita grubego.

Introduction and Objective: The world epidemic of obesity has contributed to the development of research aimed at a comprehensive recognition of the structure and understanding of the processes taking place in adipose tissue, the excess of which is the main marker of this disease. At present,...

Lead-exposure is known to disrupt the redox balance of tissues leading to oxidative stress. Due to the fact that a mucolytic drug, erdosteine, exerts also antioxidant properties, we decided to perform a pilot study on rats to evaluate its therapeutic potency in lead poisoning. Male Wistar rats were divided randomly into the following seven groups having 10 animals in each. Group I served as the control group. During 8-week period, rats in groups II–IV, except standard alimentation, received: erdosteine in a dose 350 mg/kg (collateral control group), 1200 ppm of lead acetate in drinking water and placebo, as well as the same doses of lead and erdosteine, respectively. Rats in group V–VII received 1200 ppm of lead acetate in drinking water for the initial 6-week period and then administered: placebo, erdosteine and EDTA for 2 weeks, respectively. The levels of malondialdehyde (MDA) were significantly higher in groups III and V compared to the control group. The activities of catalase (CAT) were significantly higher in groups IV, V, and VI compared to the control group. The activities of glutathione-S-transferase (GST) were significantly lower in group II and significantly higher in groups VI and VII compared to the control group, while the activities of glutathione reductase (GR) were significantly lower in group III and significantly higher in group VI. Erdosteine has an effect of protection against lead-induced oxidative stress which is not worse than that of EDTA.

Introduction: Ovarian cancer is most frequently detected in the advanced stage. Although its pathogenesis is not fully elucidated, it is assumed that body susceptibility and hormonal disorders are responsible. The role of some cytokines as predictors in the treatment process is still investigated. The aim of the study was to determine the relationship of adiponectin and leptin with the disease severity and response to chemotherapy. Material and methods: Forty-three ovarian cancer patients were treated by systemic treatment. Patients received 5–7 cycles of chemotherapy — paclitaxel/carboplatin with or without bevacizumab. Using standard ELISA kits before and after chemotherapy, adiponectin and leptin concentrations were determined in the blood serum. Results: The average adiponectin concentration before chemotherapy was found to be 8.83 ± 3.19 μg/ml, as compared to 10.37 ± 4.18 μg/ml (increase by 17.44%, p < 0.001) after treatment. Mean pre-treatment leptin concentration was 16.89 ± 15.54 ng/ml, and 21.77 ± 14.69 ng/ml after chemotherapy (increase by 28.89%, p < 0.01). A positive correlation was found between leptin concentration and age and BMI. There was no relationship of the disease severity with the response to treatment and the concentration of the adipokines. The leptin/adiponectin ratio (L/A) before treatment correlated with better response to chemotherapy. Conclusions: Adiponectin and leptin did not correlate with the stage of ovarian cancer and response to chemotherapy. The L/A ratio may be considered a predictor of clinical response to treatment. Introduction: Ovarian cancer is most frequently detected in the advanced stage. Although its pathogenesis is not fully elucidated, it is assumed that body susceptibility and hormonal disorders are responsible. The role of some cytokines as predictors in the treatment process is still investigated. The aim of the study was to determine the relationship of adiponectin and leptin with the disease severity and response to chemotherapy. Material and methods: Forty-three ovarian cancer patients were treated by systemic treatment. Patients received 5–7 cycles of chemotherapy — paclitaxel/carboplatin with or without bevacizumab. Using standard ELISA kits before and after chemotherapy, adiponectin and leptin concentrations were determined in the blood serum. Results: The average adiponectin concentration before chemotherapy was found to be 8.83 ± 3.19 μg/ml, as compared to 10.37 ± 4.18 μg/ml (increase by 17.44%, p < 0.001) after treatment. Mean pre-treatment leptin concentration was 16.89 ± 15.54 ng/ml, and 21.77 ± 14.69 ng/ml after chemotherapy (increase by 28.89%, p < 0.01). A positive correlation was found between leptin concentration and age and BMI. There was no relationship of the disease severity with the response to treatment and the concentration of the adipokines. The leptin/adiponectin ratio (L/A) before treatment correlated with better response to chemotherapy. Conclusions: Adiponectin and leptin did not correlate with the stage of ovarian cancer and response to chemotherapy. The L/A ratio may be considered a predictor of clinical response to treatment.

Parkinson's disease is a progressive neurodegenerative disorder, characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta. The causes of Parkinson's disease are not fully understood; however, increasing evidence implicates oxidative stress. The study was aimed at assessing the nature of the changes in the oxidation-antioxidant balance in the cerebral cortex, striatum, hippocampus, thalamus, and cerebellum in a rat model of Parkinson's disease (PD). Sixteen male Wistar rats were divided into 2 groups: Icontrol, IIParkinson's disease. The 8-weeks-old animals were decapitated, their brains removed and the following structures dissected and then frozen for further biochemical assays: cerebral cortex, striatum, hippocampus, thalamus and cerebellum. The activities of: the catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione S-transferase (GST), superoxide dismutase (SOD) and the isoenzymes: Cu/ZnSOD and MnSOD; together with the malondialdehyde (MDA) and the total oxidative status (TOS) concentrations were measured in each structure. A significantly increased activities of SOD, Cu/ZnSOD, GST and reduced GR activity and an increase of MDA concentration were observed in the striatum of PD rats, comparing to the control group, combined with a significantly reduced activities of GR,SOD, Cu/ZnSOD and an increased GPX activity and MDA concentration in the hippocampus, a significantly lower GR, SOD, MnSOD, Cu/ZnSOD, and GST activities in the cerebral cortex. A significantly lower GR activity, higher CAT activity and MDA concentration in the thalamus and a significantly increased GR activity in the cerebellum were observed in PD rats compared to the corresponding control group. Oxidative stress in PD involves many brain structures and various antioxidant enzymes and oxidative status parameters become dysfunctional, depending on the area of the brain, which might reflect the complexity of the clinical symptoms of PD.

Adipokines are molecules produced and secreted by adipose tissue and are linked to multiple malignancies. Adipokines can suppress or promote particular cell behaviors in different types of cancer. The aim of this study was to investigate the impact of chemotherapy on select adipokines in patients with colorectal cancer (CRC).Blood samples were collected from 42 patients with pathologically documented advanced CRC, who required palliative chemotherapy. Leptin, adiponectin, resistin and visfatin levels were measured by ELISA before and 3 months after the administration of chemotherapy. Among the 42 patients evaluated, 18 achieved a partial response (PR), 16 achieved stable disease (SD) and 8 patients experienced disease progression (PD).We found that 5-fluorouracil-based chemotherapy regimens significantly increased plasma levels of leptin and adiponectin and decreased plasma levels of resistin and visfatin in PR and SD patients, whereas the plasma levels of these molecules were not affected in PD patients. Furthermore, the mean plasma levels of leptin were significantly lower, and the mean plasma levels of resistin and visfatin were significantly greater in patients with PD compared with PR and SD both before and after chemotherapy treatment.We conclude that palliative chemotherapy in CRC patients, in addition to providing clinical benefits, positively affects cytokine production and secretion in PR and SD patients. Specifically, we found that palliative chemotherapy increased plasma levels of the anti-inflammatory adipokine adiponectin and decreased the plasma levels of visfatin and resistin, molecules known to promote angiogenesis and cancer cell proliferation in PR and SD patients. Moreover, the baseline values of leptin, visfatin and resistin might serve as prognostic indicators of a poor response to chemotherapy.