The textbook Amazing forms is a high school biology textbook covering basic anatomic and physiological principles of fungi, plants and animals. The textbook is written in a way students get a comparative insight and learn that same or similar functional solutions are found in organisms which otherwise substantially differ in terms of morphology and way of life.
D.10 Educational activities
COBISS.SI-ID: 268099328The textbook »Where the life begins« includes chapters on cell biology and genetics for the high school students. The authors used a personalized and innovative approach to explain complex cell life which is usually abstract and difficult to understand for the high school students, especially those which are not interested in biology. This didactic approach was recognized by the jury of European Education Publishing Group (EEPG) and International Association for the Research on Textbooks and Educational Media (IARTEM). According to their decision in 2012 at the Frankfurter book fair the textbook was awarded bronze medal in the highschool textbook category.
E.02 International awards
COBISS.SI-ID: 259405312One of the therapeutical approaches against cancer is to use drugs enhancing cell death and blocking cell proliferation of cancer cells. α7 nAChR antagonists (α-bungarotoxin or methyllycaconitine) can attenuate the proliferative effects of agonists like nicotine. We have shown that synthetic analogues of poly-APS have high affinity for nAChRs. They inhibit alpha α7 nAChRs with concentration as low as 0.1 ng/ml and are therefore strong antagonists of α7 nAChR. A synthetic analogue APS8 shows a significant toxicity towards NSCLC (A549 cell line). It inhibits tumor cell growth in a concentration dependent manner. As a control we tested the effect of APS8 on normal lung fibroblast cells (MRC5) which did not show alterations in growth until high concentrations of APS8 were used.
B.03 Paper at an international scientific conference
COBISS.SI-ID: 2611535We have shown that APS8 inhibits α7 nAChRs indicating that it is a strong α7 nAChRs antagonist and can thus induce tumor regression. APS8 has significant selective cytotoxicity towards NSCLC cells while has no influence on normal lung fibroblast cells MRC5. Evidence of apoptosis activation by APS8 in NSCLC was quantitatively analyzed by annexin V-FITC/propidium iodide uptake analysis with fluorescent cytometry. Cell morphology of APS8 induced apoptosis was investigated with a combination of the fluorescent DNA-binding dyes acridine orange and ethidium bromide. We investigated mechanism underlying the apoptotic activity of APS8. Traetment of NSCLC with APS8 up regulates pro- apoptotic proteins from Bcl-2 family while anti-apoptotic proteins are down-regulated. APS8 markedly increased the expression levels of death receptors. Our results imply that both intrinsic and extrinsic pathway of apoptosis are activated by APS8. Apoptosis of cancer cells induced with nAChR antagonist APS8 may be a new and promising method in lung cancer treatment.
B.03 Paper at an international scientific conference
COBISS.SI-ID: 2612047Human lung A549 xenograft tumors were induced by subcutaneously injection of cell suspension (107 cells/100 µl) in the right flank of SCID mice. When tumors were grown up to 40 mm3, mice were treated with intratumoral or intravenous injection of APS8 (2 mg/kg and 4mg/kg). Anti tumor effectiveness was assessed by tumor growth delay assay. Treatment of mice bearing A549 tumors with intratumoral administration of APS8 at the dose of 4 mg/kg showed good anti tumor effect resulting in tumor growth delay of 26 days compared to the control group. Systemic treatments and intratumoral treatment with lower dose of APS8 did not result in significant tumor growth delay. Treatment with polyAPS8 at the selected doses did not result in any systemic or local side effects. The results of our preliminary study demonstrate that local administration of APS8 has good anti tumor effect on human lung xenograft A549 tumors.
B.03 Paper at an international scientific conference
COBISS.SI-ID: 1510779