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Plant-based diets are a growing trend, including among athletes. This study compares the differences in physical performance and heart morphology and function between vegan and omnivorous amateur runners. A study group and a matched control group were recruited comprising N = 30 participants each. Eight members of the study group were excluded, leaving N = 22 participants. Members of both groups were of similar age and trained with similar frequency and intensity. Vegans displayed a higher VO2max (54.08 vs. 50.10 mL/kg/min, p < 0.05), which correlated positively with carbohydrate intake (ρ = 0.52) and negatively with MUFA (monounsaturated fatty acids) intake (ρ = −0.43). The vegans presented a more eccentric form of remodelling with greater left ventricular end diastolic diameter (LVEDd, 2.93 vs. 2.81 cm/m2, p = 0.04) and a lower relative wall thickness (RWT, 0.39 vs. 0.42, p = 0.04) and left ventricular mass (LVM, 190 vs. 210 g, p = 0.01). The left ventricular mass index (LVMI) was similar (108 vs. 115 g/m2, p = NS). Longitudinal strain was higher in the vegan group (−20.5 vs. −19.6%, p = 0.04), suggesting better systolic function. Higher E-wave velocities (87 vs. 78 cm/s, p = 0.001) and E/e′ ratios (6.32 vs. 5.6, p = 0.03) may suggest better diastolic function in the vegan group. The results demonstrate that following a plant-based diet does not impair amateur athletes’ performance and influences both morphological and functional heart remodelling. The lower RWT and better LV systolic and diastolic function are most likely positive echocardiographic findings.

Cancer stem cells have been defined as cells within a tumor that possesses the capacity to self-renew and to cause the heterogeneous lineages of cancer cells that comprise the tumor. Experimental evidence showed that these highly tumorigenic cells might be responsible for initiation and progression of cancer into invasive and metastatic disease. Eradicating prostate cancer stem cells, the root of the problem, has been considered as a promising target in prostate cancer treatment to improve the prognosis for patients with advanced stages of the disease.

Patients with diabetes mellitus (DM) are likely to develop many types of infections, which affect the transport of glucose into tissues. Diabetes increases the susceptibility to different kinds of respiratory infections, is often identified as an independent risk factor for developing lower respiratory tract infections. Pulmonary infections caused by Mycobacterium tuberculosis, Staphylococcus aureus, gram-negative bacteria and fungi may occur with an increased frequency, whereas infections due to Streptococcus pneumonia or influenza virus may be associated with increased morbidity and mortality. During lung infection, there are changes in the local and ciliary epithelial lining. Increased susceptibility to pneumococcal infection by people with diabetes is the result of reduced defense capability of antibodies to protein antigens. The relationship between diabetes and pulmonary tuberculosis is well known, and the incidence of tuberculosis in diabetic individuals is 4−5 times greater than among the non-diabetic population. It is thought that malfunction of monocytes in patients with diabetes may contribute to the increased susceptibility to tuberculosis and/or a worse prognosis. Hospitalization of patients with diabetes due to influenza virus or flu-like infections is up to 6 times more likely to occur compared to healthy individuals, also diabetic patients are more likely to be hospitalized due to infection complications. Immunization with influenza and anti-pneumococcal vaccines is recommended to reduce hospitalizations, deaths, and medical expenses. Diabetes, especially the uncontrolled one, predisposes to fungal infection, the most common candidiasis and mucormycosis.

Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Receptors (TRAIL-R) are an important factor of apoptosis in cancer cells. There are no data about the effect of flavonols on the receptor expression on a surface of macrophage like cells. In this study, the expression level of TRAIL-R1 on murine RAW264.7 macrophages in the presence of selected flavonols: galangin, kaempferol, kaempferide and quercetin, which differ from their phenyl ring substituents, were studied. The expression of TRAIL-R1 death receptors on non-stimulated and lipopolysaccharide (LPS)-stimulated macrophages was determined using flow cytometry. The results suggested that compounds being tested can modulate TRAIL-R1 expression and can enhance TRAIL-mediated apoptosis.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is considered as the most promising anticancer agent in the TNF superfamily because of its selective cytotoxicity against tumor cells versus normal primary cells. However, as more tumor cells are reported to be resistant to TRAIL-mediated death, it is important to develop new therapeutic strategies to overcome this resistance. Flavonoids have been shown to sensitize cancer cells to TRAIL-induced apoptosis. The aim of this study was to examine the cytotoxic and apoptotic activities of TRAIL on HeLa cancer cells in combination with two synthetic compounds: 6-hydroxyflavanone (6-HF) and its derivative 6-propionoxy-flavanone (6-PF) and to determine the mechanism by which the flavanones overcome the TRAIL-resistance. The cytotoxicity was measured by MTT and LDH assays. The apoptosis was detected by annexin V-FITC fluorescence staining in flow cytometry and microscopy. Death receptor (TRAIL-R1/DR4 and TRAIL-R2/DR5) expression were analysed using flow cytometry. Mitochondrial membrane potential was evaluated using DePsipher staining by fluorescence microscopy. The synthetic flavanones enhanced TRAIL-induced apoptosis in HeLa cells through increased expression of TRAIL-R2 death receptor and reduction of mitochondrial membrane potential. Our study indicates that the 6-HF and 6-PF augmented the anticancer effects of TRAIL and confirm a potential use of flavanones in TRAIL-based anticancer therapy and prevention.

Soft liner materials in oral cavity environments are easily colonized both by fungi and dental plaque. These factors are the cause of mucosal infections. The microorganism that most frequently colonizes soft liner materials is Candida albicans. Colonization occurs on the surface of materials and within materials. A solution to this problem might involve modification of soft liner materials with silver nanoparticles (AgNPs). In this article, we present results showing the antifungal efficacy of silicone soft lining materials modified with AgNPs. The modification process was conducted by dissolving both material components (base and catalyst) in a colloidal solution of AgNPs and evaporating the solvent. Composites with various AgNP concentrations (10, 20, 40, 80, 120 and 200 ppm) were examined. The in vitro antifungal efficacy (AFE) of composite samples was 16.3% to 52.5%.

Chalcones and dihydrochalcones exhibit chemopreventive and antitumor activity. TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) is a natural endogenous anticancer agent. We examined the cytotoxic and apoptotic effect of chalcones and dihydrochalcones on TRAIL-mediated apoptosis in LNCaP prostate cancer cells. The cytotoxicity was evaluated by the MTT and LDH assays. The apoptosis was detected using annexin V-FITC by flow cytometry and fluorescence microscopy. The ΔΨm was evaluated using DePsipher staining by fluorescence microscopy. Our study showed that two tested chalcones (chalcone and 2’,6’dihydroxy-4’-methoxychalcone) and three dihydrochalcones (2’,6’-dihydroxy-4’4-dimethoxydihydrochalcone, 2’,6’-dihydroxy-4’-methoxydihydro- chalcone, and 2’,4’,6’-trihydroxydihydrochalcone, called phloretin) markedly augmented TRAIL-induced apoptosis and cytotoxicity in LNCaP cells and confirmed the significant role of chalcones in chemoprevention of prostate cancer. Keywords

Isoflavones are a class of bioactive polyphenols with cancer chemopreventive properties. TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) is a naturally occurring antitumor agent that selectively induces programmed death (apoptosis) in cancer cells. Polyphenols can modulate TRAIL-mediated apoptosis in cancer cells. We examined the cytotoxic and apoptotic activities of isoflavones in combination with TRAIL on HeLa cancer cells. The apoptosis was detected by fluorescence microscopy with annexin V-FITC. The cytotoxicity was evaluated by MTT and LDH assays. The tested isoflavones: genistein, biochanin-A and neobavaisoflavone enhance TRAIL-induced apoptosis in HeLa cells. Our study indicated that isoflavones augmented TRAIL-cytotoxicity against cancer cells and confirmed potential role of those polyphenols in chemoprevention.

Synthetic polymers belonging to the aliphatic polyester group have become highly promising biomaterials for reconstructive medicine. The purpose of the present work is a biological evaluation of lactide-glycolide co-polymer (PLGA) and its composites with carbon fibers (PLGA+CF) or hydroxyapatite (PLGA+HA). The cytotoxicity of the evaluated materials towards hFOB 1.19 human osteoblast-like cells was assessed. Moreover, during the one-year contact of the assessed materials with living osseous tissue, the progress of bone formation was analyzed and the accompanying process of the materials’ degradation was evaluated. The materials under evaluation proved to be biocompatible.

Ethanolic extract of propolis (EEP) is one of the richest sources of phenolic acids and flavonoids. EEP and its phenolic compounds have been known for various biological activities including immunopotentiation, chemopreventive and antitumor effects. Tumor necrosis factor related apoptosis inducing ligand (TRAIL) is a naturally occurring anticancer agent that preferentially induces apoptosis in cancer cells and is not toxic toward normal cells. We examined the cytotoxic and apoptotic effect of EEP and phenolic compounds identified in propolis in combination with TRAIL on HeLa cancer cells. HeLa cells were resistant to TRAIL-induced apoptosis. Our study demonstrated that EEP and its components significantly sensitize to TRAIL induced death in cancer cells. The percentage of the apoptotic cell after exposure to 50 microg/mL EEP and 100 ng/mL TRAIL increased to 71.10 +/- 1.16%. The strongest cytotoxic effect in combination with TRAIL on HeLa cells exhibited apigenin and CAPE at the concentration of 50 microM (58.87 +/- 0.75% and 49.59 +/- 0.39%, respectively). In this report, we show for the first time that EEP markedly augmented TRAIL mediated apoptosis in cancer cells and confirmed the importance of propolis in chemoprevention of malignant tumors.

TRAIL is a promising candidate for cancer therapeutics that preferentially induces apoptosis in cancer cells. The combined treatment flavonoids with TRAIL might be promising as a chemoprevention and/or new therapy against malignant tumors. We examined the cytotoxic effect of dietary flavonoids in combination with TRAIL on HeLa cells. It was found that treatment with noncytotoxic concentration of some flavonoids significantly sensititizes to TRAIL induced death in HeLa cells. Our study demonstrated that flavone, apigenin and genistein markedly augmented TRAIL mediated cytotoxicity against HeLa, whereas kaempferol and quercetin produced no effect.

TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) is an endogenous ligand, which plays role in immune surveillance and anti-tumor immunity. It has ability to selectively kill tumor cells showing no toxicity to normal cells. We tested the apoptotic and cytotoxic activities of xanthohumol, a prenylated chalcone found in Humulus lupulus on androgen-sensitive human prostate adenocarcinoma cells (LNCaP) in combination with TRAIL. Cytotoxicity was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide tetrazolium reduction assay (MTT) and lactate dehydrogenase assay (LDH). The expression of death receptors (DR4/TRAIL-R1 and DR5/TRAIL-R2) and apoptosis were detected using flow cytometry. We examined mitochondrial membrane potential (ΔΨm) by DePsipher reagent using fluorescence microscopy. The intracellular expression of proteins was evaluated by Western blotting. Our study showed that xanthohumol enhanced cytotoxic and apoptotic effects of TRAIL. The tested compounds activated caspases-3, -8, -9, Bid, and increased the expression of Bax. They also decreased expression of Bcl-xL and decreased mitochondrial membrane potential, while the expression of death receptors was not changed. The findings suggest that xanthohumol is a compound of potential use in chemoprevention of prostate cancer due to its sensitization of cancer cells to TRAIL-mediated apoptosis.

The chemiluminescence of stimulated cells with phorbol myristate acetate and the production of nitric oxide after stimulation with lipopolisaccharide in the presence of the parent compounds FAA (flavone-8-acetic acid = (4-oxo-2- phenyl-4H-chromen-8-yl)acetic acid), XAA (xanthone-4-acetic acid = (9-oxo-9Hxanthen- 4-yl)acetic acid), and appropriate xanthone derivatives (1–7) was determined. Also the toxicity of the FAA, MFAA ((6-methyl-4-oxo-2-aryl-4H-chromen- 8-yl)acetic acid), XAA and 1–7 against J-774A.1 cultured cells was evaluated. Compound 5 (2-methyl-2-{[(9-oxo-9H-xanthen-2-yl)methyl]sulfanyl}- propanoic acid) was effective in inhibiting chemiluminescence of J-774A.1 cells but most of the other tested compounds stimulated the reaction. FAA and two xanthones with a methoxycarbonyl moeity slightly decreased the generation of nitric oxide at 50 μM. Most of the tested compounds (1–7) showed weak toxicity at concentration of 100 μM.