Picking up the mantle of “expert”: Assigned roles, assertion of identity, and peer recognition within a programming class

Changing an established role in a classroom is difficult. It involves constructing a new set of relations within a community. In this article we investigate how students with newly developed interest and experience in programming developed outside the classroom pick up and establish their roles as experts in programming within the classroom community. More specifically, we focus on how two 11-year-old software designers shifted their established roles in their classroom to gain status as expert programmers. We use an identity lens to understand how peer expertise was established in the context of a classroom community, adopting a multifaceted perspective of identity by focusing on an individual\u27s narrativization of self, full, or peripheral participation among a group of people, and individuals\u27 social recognition by others. Our findings point to the importance of both positive positioning by authority figures in the classroom and activities and roles that provide opportunities to establish intersubjectivity among peers in facilitating students\u27 identities as experts in the classroom. Students\u27 willingness to take up a new position in the established activity system also played a role. We consider implications of how making roles flexible within classroom stratification may provide opportunities for more students see themselves as experts

Comparative solution equilibrium studies of antitumor ruthenium(η6-p-cymene) and rhodium(η5-C5Me5) complexes of 8-hydroxyquinolines

Complex formation processes of [ Ru(η 6 - p - cymene) (H 2 O) 3 ] + and [ Rh( η 5 - C 5 Me 5 )(H 2 O) 3 ] + organometallic cations with 8 - hydroxyquinoline (HQ) ligands were studied in aqueous solution by the combined use of 1 H NMR spectroscopy, UV - visible spectrophotometry and pH - potentiometry. Solution stability, chloride ion affinity and lipophilicity of the complexes were characterized together with the in vitro cytotoxicity against a pair of cancer cell lines, responsive and resistant to classic chemotherapy. The solid phase structure of the [Rh( η 5 - C 5 Me 5 )( 8 - quinolinolato )(Cl)] complex was characterized by s ingle - crystal X - ray diffraction analysis. In addition to the unsubstituted HQ its 7 - (1 - piperidinylmethyl) (PHQ) and 5 - sulfonate ( HQS) derivatives were involved. PHQ has a significant preference for targeting multidrug resistant cancer cell lines , while HQS served as a water soluble model compound. The equilibrium studies revealed the formation of mono [M(L)(H 2 O)] complexes with prominently high solution stability, which predominate at physiological pH even in the micromolar concentration range , and f ormation of mixed hydroxido [M(L)(OH)] complexes was characterized by relatively high p K a values (8.5 – 10.3). In comparison to the Rh(η 5 - C 5 Me 5 ) species the complex ation process with Ru(η 6 - p - cymene) is much slower, and both the p K a values and the H 2 O/Cl − co - ligand exchange constants are lower by 1 - 1.5 orders of magnitude. The stability order obtained for these organometallic complexes is as follows: HQS > HQ > PHQ. Cytotoxicity of the ligands and their Ru(η 6 - p - cymene) and Rh(η 5 - C 5 Me 5 ) complexes was investigated against MES - SA (human uterine sarcoma) cell line and its multidrug resistant counterpart (MES - SA/Dx5). HQ and its complexes show similar cytotoxicity in both cell lines. In contrast, PHQ and its Rh(η 5 - C 5 Me 5 ) complex are more potent against MES - SA/Dx5 cells, while this selectivity could not be observed for the Ru(η 6 - p - cymene) complex

Characterization of the binding sites of the anticancer ruthenium(III) complexes KP1019 and KP1339 on human serum albumin via competition studies

Indazolium trans-[tetrachloridobis(1H-indazole)ruthenate(III)] (KP1019) and its Na+ analogue (KP1339) are two of the most prominent non-platinum antitumor metal complexes currently undergoing clinical trials. After intravenous administration, they are known to bind to human serum albumin (HSA) in a noncovalent manner. To elucidate their HSA binding sites, displacement reactions with the established site markers warfarin and dansylglycine as well as bilirubin were monitored by spectrofluorimetry, ultrafiltration-UV-vis spectrophotometry, and/or capillary zone electrophoresis. Conditional stability constants for the binding of KP1019 and KP1339 to sites I and II of HSA were determined, indicating that both Ru(III) compounds bind to both sites with moderately strong affinity (log K (1)' = 5.3-5.8). No preference for either binding site was found, and similar results were obtained for both metal complexes, demonstrating low influence of the counter ion on the binding event

Effects of terminal substitution and iron coordination on antiproliferative activity of L-proline-salicylaldehyde-thiosemicarbazone hybrids

A series of five iron(III) complexes, namely [Fe(HL1)Cl2] (1), [Fe(HL2)Cl2]·1.6H2O (2·1.6H2O), [Fe(HL3)(MeOH)Cl2]·0.5H2O (3·0.5H2O), [Fe(HL4)(MeOH)Cl2]·0.5H2O (4·0.5H2O) and [Fe(HL4)(DMF)Cl2]·0.5Et2O·H2O (4′·0.5Et2O·H2O), where H2L1 = l‐proline‐salicylaldehyde–thiosemicarbazone (l‐Pro‐STSC), H2L2 = pyrrolidine‐substituted l‐Pro‐STSC, H2L3 = phenyl‐substituted l‐Pro‐STSC, and H2L4 = naphthyl‐substituted l‐Pro‐STSC, have been synthesized. The two ligand precursors (H2L3 and H2L4) and iron complexes were characterized by elemental analysis, spectroscopic methods (UV/Vis, IR, and NMR), ESI mass spectrometry, cyclic voltammetry, and single‐crystal X‐ray crystallography (1–3 and 4′). Magnetic properties of the five‐coordinate complex 2 and six‐coordinate complex 4 have also been investigated. The antiproliferative activity of the organic hybrids and their iron(III) complexes have been studied in vitro in five human cell lines and one murine cancer cell line, namely HeLa (cervical cancer), FemX (melanoma), A549 (alveolar basal adenocarcinoma), LS‐174 (colon cancer), MDA‐MB‐453 (breast cancer) and MS1 (transformed murine endothelial), as well as in human noncancerous fetal lung fibroblast cell line (MRC‐5). According to the structure–activity relationship, introduction of aromatic groups such as phenyl or naphthyl enhances the cytotoxic potency of the hybrids in the following order H2L1 < H2L2 < H2L3 < H2L4. Coordination of the hybrids to iron(III) improves their antiproliferative activity in the majority of investigated cell lines with exception of H2L3 in LS‐174, H2L4 in MS1, and both H2L3 and H2L4 in FemX cell lines, where an opposite effect was observed.This study was financially supported by the Austrian Science Fund (project number P28223 N34), Research and Development Agency of the Slovak Republic under the contracts No. APVV 15-0079 and APVV-15-0053, Scientific Grant Agency of the Slovak Republic (VEGA Project 1/0871/16) and Slovak University of Technology in Bratislava (Young Researcher Grant, M. Milunović, PhD) This work was also supported by Ministry of Education, Science, Research and Sport of the Slovak Republic withinhe Research and Development Operational Program for the project "University Science Park of STU Bratislava", ITMS 26240220084, cofunded by the European Regional Development Fund

Co-Inhibition of BCL-W and BCL2 Restores Antiestrogen Sensitivity through BECN1 and Promotes an Autophagy-Associated Necrosis

BCL2 family members affect cell fate decisions in breast cancer but the role of BCL-W (BCL2L2) is unknown. We now show the integrated roles of the antiapoptotic BCL-W and BCL2 in affecting responsiveness to the antiestrogen ICI 182,780 (ICI; Fulvestrant Faslodex), using both molecular (siRNA; shRNA) and pharmacologic (YC137) approaches in three breast cancer variants; MCF-7/LCC1 (ICI sensitive), MCF-7/LCC9 (ICI resistant), and LY2 (ICI resistant). YC137 inhibits BCL-W and BCL2 and restores ICI sensitivity in resistant cells. Co-inhibition of BCL-W and BCL2 is both necessary and sufficient to restore sensitivity to ICI, and explains mechanistically the action of YC137. These data implicate functional cooperation and/or redundancy in signaling between BCL-W and BCL2, and suggest that broad BCL2 family member inhibitors will have greater therapeutic value than targeting only individual proteins. Whereas ICI sensitive MCF-7/LCC1 cells undergo increased apoptosis in response to ICI following BCL-W±BCL2 co-inhibition, the consequent resensitization of resistant MCF-7/LCC9 and LY2 cells reflects increases in autophagy (LC3 cleavage; p62/SQSTM1 expression) and necrosis but not apoptosis or cell cycle arrest. Thus, de novo sensitive cells and resensitized resistant cells die through different mechanisms. Following BCL-W+BCL2 co-inhibition, suppression of functional autophagy by 3-methyladenine or BECN1 shRNA reduces ICI-induced necrosis but restores the ability of resistant cells to die through apoptosis. These data demonstrate the plasticity of cell fate mechanisms in breast cancer cells in the context of antiestrogen responsiveness. Restoration of ICI sensitivity in resistant cells appears to occur through an increase in autophagy-associated necrosis. BCL-W, BCL2, and BECN1 integrate important functions in determining antiestrogen responsiveness, and the presence of functional autophagy may influence the balance between apoptosis and necrosis