A PICTURE PAINTS A THOUSAND WORDS: A PHENOMENOLOGICAL STUDY OF MISCONCEPTIONS OF GRADE 7 MATHEMATICS TEACHERS ON DIFFERENTIATED INSTRUCTION IN THE PHILIPPINES

Differentiated Instruction has been found to be effective in catering to the individuality of students and at the same time helping students to have positive attitudes about school, increased engagement in learning, and improved achievement.  Misconceptions of this type of instruction limit the teachers’ response to student conceptions and ability to create challenging learning situations.  For these reasons, researches on this topic are highly needed, especially in the Philippines, wherein, content differentiation is suggested in the implementation of the K-12 curriculum program, hence this study aimed to surface the misconceptions of Grade 7 mathematics teachers on differentiated instruction through the research question: What are the misconceptions of Grade 7 Filipino mathematics teachers on Differentiated Instruction?  Data from the interviews of 21 Grade 7 Filipino mathematics teachers are qualitatively described through this phenomenological study which utilizes the Colaizzi’s Method to analyze data. The findings of this study surfaced the Grade 7 mathematics teachers’ misconceptions on DI in the Philippines as fragmented ideas, and tagged them as head, heart, life, hand, road, and gadget.  Fragmented because the respondents did not give the complete picture of DI but rather they provided characteristics of other teaching approaches related to DI.  The findings are not surprising since DI came from the constructivist view, but DI has unique features and characteristics, and outside of these are all misconceptions.  Hence, the respondents’ notions of DI are as, “a picture paints a thousand words.” Future researches are suggested out of the findings of this study such as “Determining the Effects of Relating Real Life Situations in Teaching Mathematics Lessons Utilizing DI” and “Challenges Encountered by Mathematics Teachers in Applying DI in Basic Education Institutions in Asia.

A Multidisciplinary Investigation to Determine the Structure and Source of Dimeric Impurities in AMG 517 Drug Substance

In the initial scale-up batches of the experimental drug substance AMG 517, a pair of unexpected impurities was observed by HPLC. Analysis of data from initial LC-MS experiments indicated the presence of two dimer-like molecules. One impurity had an additional sulfur atom incorporated into its structure relative to the other impurity. Isolation of the impurities was performed, and further structural elucidation experiments were conducted with high-resolution LC-MS and 2D NMR. The dimeric structures were confirmed, with one of the impurities having an unexpected C-S-C linkage. Based on the synthetic route of AMG 517, it was unlikely that these impurities were generated during the last two steps of the process. Stress studies on the enriched impurities were carried out to further confirm the existence of the C-S-C linkage in the benzothiazole portion of AMG 517. Further investigation revealed that these two dimeric impurities originated from existing impurities in the AMG 517 starting material, N-acetyl benzothiazole. The characterization of these two dimeric impurities allowed for better quality control of new batches of the N-acetyl benzothiazole starting material. As a result, subsequent batches of AMG 517 contained no reportable levels of these two impuritie

Temperature dependent photoluminescence in oxygen ion implanted and rapid thermally annealed ZnO/ZnMgO multiple quantum wells

The authors investigate the effect of oxygen implantation and rapid thermal annealing in ZnO∕ZnMgOmultiple quantum wells using photoluminescence. A blueshift in the photoluminescence is observed in the implanted samples. For a low implantation dose, a significant increase of activation energy and a slight increase of the photoluminescence efficiency are observed. This is attributed to the suppression of the point defect complexes and transformation between defect structures by implantation and subsequent rapid thermal annealing. A high dose of implantation leads to lattice damage and agglomeration of defects leading to large defect clusters, which result to an increase in nonradiative recombination.The authors gratefully acknowledge the Australian Research Council for financial support and Swinburne University of Technology for Strategic Initiative funding. One of the authors X.W. acknowledges partial financial support of the Chinese National Natural Science Foundation 10364004 and the Yunnan Natural Science Foundation 2003E0013M

Lysophospholipid (S1P) receptors (version 2020.5) in the IUPHAR/BPS Guide to Pharmacology Database

Sphingosine 1-phosphate (S1P) receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Lysophospholipid receptors [86]) are activated by the endogenous lipid sphingosine 1-phosphate (S1P). Originally cloned as orphan members of the endothelial differentiation gene (edg) family, current gene names have been designated as S1P1R through S1P5R [66, 16, 109]. S1PRs, particularly S1P1, are expressed throughout all mammalian organ systems. Ligand delivery occurs via two known carriers (or "chaperones"): albumin and HDL-bound apolipoprotein M (ApoM), the latter of which elicits biased agonist signaling by S1P1 in multiple cell types [18, 48]. The five S1PRs, two chaperones, and active cellular metabolism have complicated analyses of receptor ligand binding in native systems. Signaling pathways and physiological roles have been characterized through radioligand binding in heterologous expression systems, targeted deletion of the different S1PRs, and most recently, mouse models that report in vivo S1P1R activation [91, 93]. A crystal structure of an S1P1-T4 fusion protein confirmed aspects of ligand binding, specificity, and receptor activation determined previously through biochemical and genetic studies [62, 17]. fingolimod (FTY720), the first drug to target any of the lysophospholipid receptors, binds to four of the five S1PRs, and was the first oral therapy for multiple sclerosis )MS) [32]. siponimod and ozanimod that target S1P1 and S1P5 are also FDA approved for the treatment of various MS forms [16, 109]. The mechanisms of action of fingolimod and other S1PR modulating drugs in development include binding S1PRs in multiple organ systems, e.g., immune and nervous systems, although the precise nature of their receptor interactions requires clarification [126, 34, 56, 57]

Choroidal neovascularization secondary to Best’s vitelliform macular dystrophy in two siblings of a Malay family

Best’s vitelliform macular dystrophy complicated with choroidal neovascularization is rare in children. We report three children from a Malay family of five siblings with Best’s vitelliform macular dystrophy, in which two of them subsequently developed choroidal neovascularization. The possible pathogenesis of this rare condition is described and highlighted in this report

Lysophospholipid (S1P) receptors in GtoPdb v.2021.2

Sphingosine 1-phosphate (S1P) receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Lysophospholipid receptors [89]) are activated by the endogenous lipid sphingosine 1-phosphate (S1P). Originally cloned as orphan members of the endothelial differentiation gene (edg) family [16, 112], the receptors are currently designated as S1P1R through S1P5R [69, 16, 112]. Their gene nomenclature has been codified as human S1PR1, S1PR2, etc. (HUGO Gene Nomenclature Committee, HGNC) and S1pr1, S1pr2, etc. for mice (Mouse Genome Informatics Database, MGI) to reflect species and receptor function. All S1P receptors have been knocked-out in mice constitutively and in some cases, conditionally. S1PRs, particularly S1P1, are expressed throughout all mammalian organ systems. Ligand delivery occurs via two known carriers (or "chaperones"): albumin and HDL-bound apolipoprotein M (ApoM), the latter of which elicits biased agonist signaling by S1P1 in multiple cell types [18, 49]. The five S1PRs, two chaperones, and active cellular metabolism have complicated analyses of receptor ligand binding in native systems. Signaling pathways and physiological roles have been characterized through radioligand binding in heterologous expression systems, targeted deletion of the different S1PRs, and most recently, mouse models that report in vivo S1P1R activation [94, 96]. A crystal structure of an S1P1-T4 fusion protein confirmed aspects of ligand binding, specificity, and receptor activation, determined previously through biochemical and genetic studies [65, 17]. fingolimod (FTY720), the first FDA-approved drug to target any of the lysophospholipid receptors, binds as a phosphorylated metabolite to four of the five S1PRs, and was the first oral therapy for multiple sclerosis (MS) [33]. siponimod and ozanimod that target S1P1 and S1P5 are also FDA approved for the treatment of various MS forms [16, 112]. The mechanisms of action of fingolimod and other S1PR-modulating drugs now in development include binding S1PRs in multiple organ systems, e.g., immune and nervous systems, although the precise nature of their receptor interactions requires clarification [129, 35, 59, 60]

Fas/CD95 Deficiency in ApcMin/+ Mice Increases Intestinal Tumor Burden

Fas, a member of the tumor necrosis family, is responsible for initiating the apoptotic pathway when bound to its ligand, Fas-L. Defects in the Fas-mediated apoptotic pathway have been reported in colorectal cancer.In the present study, a variant of the Apc(Min/+) mouse, a model for the human condition, Familial Adenomatous Polyposis (FAP), was generated with an additional deficiency of Fas (Apc(Min/+)/Fas(lpr)) by cross-breeding Apc(Min/+) mice with Fas deficient (Fas(lpr)) mice. One of the main limitations of the Apc(Min/+) mouse model is that it only develops benign polyps. However, Apc(Min/+)/Fas(lpr) mice presented with a dramatic increase in tumor burden relative to Apc(Min/+) mice and invasive lesions at advanced ages. Proliferation and apoptosis markers revealed an increase in cellular proliferation, but negligible changes in apoptosis, while p53 increased at early ages. Fas-L was lower in Apc(Min/+)/Fas(lpr) mice relative to Apc(Min/+) cohorts, which resulted in enhanced inflammation.This study demonstrated that imposition of a Fas deletion in an Apc(Min/+) background results in a more aggressive phenotype of the Apc(Min/+) mouse model, with more rapid development of invasive intestinal tumors and a decrease in Fas-L levels

Integrated Systems Analysis of Mixed Neuroglial Cultures Proteome Post Oxycodone Exposure

Opioid abuse has become a major public health crisis that affects millions of individuals across the globe. This widespread abuse of prescription opioids and dramatic increase in the availability of illicit opioids have created what is known as the opioid epidemic. Pregnant women are a particularly vulnerable group since they are prescribed for opioids such as morphine, buprenorphine, and methadone, all of which have been shown to cross the placenta and potentially impact the developing fetus. Limited information exists regarding the effect of oxycodone (oxy) on synaptic alterations. To fill this knowledge gap, we employed an integrated system approach to identify proteomic signatures and pathways impacted on mixed neuroglial cultures treated with oxy for 24 h. Differentially expressed proteins were mapped onto global canonical pathways using ingenuity pathway analysis (IPA), identifying enriched pathways associated with ephrin signaling, semaphorin signaling, synaptic long-term depression, endocannabinoid signaling, and opioid signaling. Further analysis by ClueGO identified that the dominant category of differentially expressed protein functions was associated with GDP binding. Since opioid receptors are G-protein coupled receptors (GPCRs), these data indicate that oxy exposure perturbs key pathways associated with synaptic function

Reimagining Retrieval Augmented Language Models for Answering Queries

We present a reality check on large language models and inspect the promise of retrieval augmented language models in comparison. Such language models are semi-parametric, where models integrate model parameters and knowledge from external data sources to make their predictions, as opposed to the parametric nature of vanilla large language models. We give initial experimental findings that semi-parametric architectures can be enhanced with views, a query analyzer/planner, and provenance to make a significantly more powerful system for question answering in terms of accuracy and efficiency, and potentially for other NLP task

Lysophospholipid (S1P) receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

Sphingosine 1-phosphate (S1P) receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Lysophospholipid receptors [70]) are activated by the endogenous lipid sphingosine 1-phosphate (S1P). Originally cloned as orphan members of the endothelial differentiation gene (edg) family, current gene names have been designated as S1P1R through S1P5R [52]. S1PRs, particularly S1P1, are expressed throughout all mammalian organ systems. Ligand delivery occurs via two known carriers (or "chaperones"): albumin and HDL-bound apolipoprotein M (ApoM), the latter of which elicits biased agonist signaling by S1P1 in multiple cell types [15, 39]. The five S1PRs, two chaperones, and active cellular metabolism have complicated analyses of receptor ligand binding in native systems. Signaling pathways and physiological roles have been characterized through radioligand binding in heterologous expression systems, targeted deletion of the different S1PRs, and most recently, mouse models that report in vivo S1P1R activation [74, 76]. A crystal structure of an S1P1-T4 fusion protein confirmed aspects of ligand binding, specificity, and receptor activation determined previously through biochemical and genetic studies [48, 14]. fingolimod (FTY720), the first drug to target any of the lysophospholipid receptors, binds to four of the five S1PRs, and was the first oral therapy for multiple sclerosis [26]. The mechanisms of action of fingolimod and other S1PR modulating drugs in development include binding S1PRs in multiple organ systems, e.g., immune and nervous systems, although the precise nature of their receptor interactions requires clarification [107, 28, 43, 44]