The impact of a virtual laboratory tour on affective domain of first-year chemistry students

The affective domain, in particular students’ attitude and self-efficacy, is an important factor for educators to consider as they are linked to students’ overall success in a subject (Flaherty, 2020). The following presentation will describe the design, implementation, and impact of a 360-degree virtual laboratory tour. The purpose of this was to improve students’ familiarity within the laboratory by showing them where their classes would take place and the equipment they would be using in order to improve their feelings towards the chemistry laboratory. To measure the impact of this resource we designed a pre-post-test study where students were surveyed before and after they used the resource. As students’ attitudes towards chemistry and self-efficacy were of interest the Attitude toward the Subject of Chemistry Inventory v2 (ASCIv2; Xu & Lewis, 2011) and a modified version of the College Chemistry Self-Efficacy Scale (CCSS; Uzuntiryaki & Çapa Aydın, 2009) were used. It was determined that students who used the resource (N = 40) had an increase in self-efficacy however there was no change in students’ attitude. A majority of students who used the virtual laboratory tour said they used it to gain familiarity with the laboratory. This study will discuss the success and failures of virtual laboratory tours and the journey to create an effective tour for first year chemistry students. REFERENCES Flaherty, A. A. (2020). A review of affective chemistry education research and its implications for future research. Chemistry Education Research and Practice, 21(3), 698-713. Uzuntiryaki, E., & Çapa Aydın, Y. (2009). Development and validation of chemistry self-efficacy scale for college students. Research in Science Education, 39, 539-551. Xu, X., & Lewis, J. E. (2011). Refinement of a chemistry attitude measure for college students. Journal of Chemical Education, 88(5), 561-568

Towards accessibility in chemistry education using technology

Access is an important aspect of tertiary education as students with disabilities are significantly underrepresented at the university level and in the workforce (Soong, Agmata, Doyle, Jenne, Adamo, & Simpson, 2018). By making a course accessible it allows students with disabilities to have an equitable education experience. Additionally, students who have not disclosed a disability will also be included in the course. Overall, using inclusive and accessible practices will be beneficial to all students in a course and can enhance their education experience. In this presentation we will describe technologies we have implemented to improve access across our laboratory course in chemistry. Technology has enabled students to experience high quality course content which they had previously not had access to. In our course we used pre laboratory videos, augmented reality applications, laboratory tours and online pre-recorded lectures among other technologies, to address accessibility issues identified within a large first-year chemistry course. This presentation is told from the point of view of a student support worker who has worked closely with students with disabilities over the past four years. This point of view has given important insight into what works and what does not work for students with disabilities in science. REFERENCE Soong, R., Agmata, K., Doyle, T., Jenne, A., Adamo, T., & Simpson, A. (2018). Combining the maker movement with accessibility needs in an undergraduate laboratory: a cost-effective text-to-speech multipurpose, Universal Chemistry Sensor Hub (MUCSH) for Students with Disabilities. Journal of Chemical Education, 95, 2268−2272

Modulation of different clusterin isoforms in human colon tumorigenesis

Clusterin is a ubiquitous secretory heterodimeric disulfide-linked glycoprotein, which is implicated in several physiological processes, including immune regulation, cell adhesion and morphological transformation, lipid transportation, tissue remodelling, membrane recycling and cell-cell interactions. A large number of studies have focused their interest on clusterin gene products as mediators of cell cycle progression and cell death induction, although data on the different isoforms and their role in the different cell processes are still obscure. Recently, an increased clusterin expression in breast cancer has been reported. In order to elucidate the role of clusterin in tumor progression and whether one of its isoforms is preferentially expressed in tumorigenesis, we examined its presence throughout the different steps of human colon carcinoma, one of the best-characterized models of human tumor progression. The immunohistochemical observation of 30 bioptic and surgical colon specimens demonstrated a cell compartment clusterin translocation from the nucleus to the cytoplasm directly related to tumor progression. In fact, a nuclear localization found in healthy colonic mucosa is consistent with the involvement of the proapoptotic nuclear form in the regulation of cell cycle progression and in cell death induction. The progression towards high-grade and metastatic carcinoma leads to cytoplasmic clusterin distribution. Protein extracts from freshly isolated cells of the same patients confirm in high-grade carcinomas with metastatic nodes the complete loss of the proapoptotic nuclear form and a cytoplasmic overexpression of the highly glycosylated form. Data obtained from in vitro experiments confirm that this form is released in the extracellular space and corresponded to the fully glycosylated one. These data suggest that the controversial data on clusterin function in tumors may be related to the pattern shift of its isoform production. As the secreted form of clusterin is correlated to cell matrix formation, cell membrane remodeling and cell-cell adhesion, the overexpression of this form in highly aggressive tumors and metastatic nodes could be a potential new prognostic and predictive marker for colon carcinoma aggressiveness

Sources and metal pollution of sediments from a coastal area of the central western adriatic sea (Southern Marche region, Italy)

Sediments represent a critical compartment of marine coastal ecosystems due to the toxic and long-lasting effects of the contaminants buried therein. Here, we investigated the properties of surficial sediments in front of the Southern Marche Region coast (Central Adriatic Sea, Italy). The grain size of the surficial sediments was determined by X-ray sedigraphy. TN and OC contents were determined by elemental analysis. The concentrations of Al, Fe, Mg, K, S, Ca, Ti, P, Na, Mn, Mg, Li, As, Ba, Ga, Pb, Sr, and Zn were determined by ICP-OES to evaluate their spatial patterns and temporal trends. A Q-mode Factor Analyses was applied and resulted in the identification of three compositional facies (Padanic, Coastal, and Residual) characterized by common biogeochemical, mineralogical, sedimentological properties, transport pathway, and source. Some pollution indica-tors, such as the enrichment factor, the geoaccumulation index, and the pollution load index were calculated to assess the deviation from the natural background levels. The results showed a pollution by As and Ba due to the human activities in the 20th century. Furthermore, a general decreasing of Al, Ti, P, Co, Cr, Cu, Ga, Ni, Pb, Sc, V, and Y concentrations from the background levels suggested a change in the sedimentation processes during the last decades

Carnitine palmitoyltransferase I in human carcinomas: a novel role in histone deacetylation?

Carnitine palmitoyl transferase I (CPT1) catalyzes the transport of long-chain fatty acids into mitochondria for beta-oxidation. A link between CPT1 and apoptosis has been suggested on the basis of several experimental data. Nevertheless, results are contradictory about the effective role of CPT1 in cell survival control and cancer development. Conversely, Fatty acid synthase (FAS) enzyme, required for the synthesis of fatty acids, is found over-expressed in tumors and inhibition of FAS triggers apoptosis in human cancer cells. We have studied the tumor-specific modulation of CPT1 and FAS in human colorectal cancer (n = 11) and breast carcinomas (n = 24). CPT1 was significantly decreased in the cytoplasm of tumoral samples (p < or = 0.04), whereas FAS was increased (p < or = 0.04). A striking CPT1 nuclear localization was evident in the tumors (p < or = 0.04). In the nuclear environment the protein would modulate the levels of acetyl/acyl-CoA implicated in the regulation of gene transcription. At this purpose, we performed in vitro experiments using epithelial neoplastic (MCF-7, Caco-2, HepG2 cells) and non neoplastic cell lines (MCF-12F) confirming a nuclear localization of CPT1 protein exclusively in neoplastic cells. Moreover histone deacetylase (HDAC) activity showed significantly higher levels in nuclear extracts from neoplastic than from control cells. HDAC1 and CPT1 proteins coimmunoprecipitated in nuclear extracts from MCF-7 cells. The treatment with HDAC inhibitors such as trichostatin A and butyrate significantly decreased nuclear expression of CPT1 and its bond to HDAC1. We also identified the existence of CPT1A mRNA transcript variant 2 in MCF-7, beside to the classic isoform 1. The peculiar localization of CPT1 in the nuclei of human carcinomas and the disclosed functional link between nuclear CPT1 and HDAC1 propose a new role of CPT1 in the histonic acetylation level of tumors

Hereditary neuropathy with liability to pressure palsy (HNPP): Report of a family with a new point mutation in PMP22 gene

Background: Hereditary neuropathy with liability to pressure palsy (HNPP) is an autosomal dominant disorder most commonly presenting with acute-onset, non-painful focal sensory and motor mononeuropathy. Approximately 80% of patients carry a 1.5 Mb deletion of chromosome 17p11.2 involving the peripheral myelin protein 22 gene (PMP22), the same duplicated in Charcot-Marie-Tooth 1A patients. In a small proportion of patients the disease is caused by PMP22 point mutations. Case presentation: We report on a familial case harbouring a new point mutation in the PMP22 gene. The proband is a 4-years-old girl with acute onset of focal numbness and weakness in her right hand. Electroneurography demonstrated transient sensory and motor radial nerves involvement. In her father, reporting chronic symptoms (cramps and exercise-induced myalgia), we uncovered mild atrophy and areflexia on clinical examination and a mixed (predominantly demyelinating) polyneuropathy with sensory-motor involvement on electrophysiological study. Both carried a nucleotidic substitution c.178 + 2 T &gt; C on intron 3 of the PMP22 gene, involving the splicing donor site, not reported on databases but predicted to be likely pathogenic. Conclusions: We described a previously unreported point mutation in PMP22 gene, which led to the development of a HNPP phenotype in a child and her father. In children evaluated for a sensory and motor transient episode, HNPP disorder due to PMP22 mutations should be suspected. Clinical and electrophysiological studies should be extended to all family members even in the absence of previous episodes suggestive for HNPP

Synchronized onset of nuclear and cell surface modifications in U937 cells during apoptosis

In this study we investigated the relationship between nuclear and cell surface modifications (i.e. blebbing, phosphatidylserine [PS] and sugar residues exposure) in a monocytic cell line, U937, during apoptosis induced by oxidative stress (1mM H2O2) or inhibition of protein synthesis (10 mg/ml puromycin). Dying cells were simultaneously observed for nuclear modifications, presence of superficial blebs and plasma membrane alterations. Morphological analysis performed by conventional fluorescence microscopy, or by transmission and scanning electron microscopy showed that the courses of nuclear and membrane alterations occured concomitantly, but the phenotype was dependent on the stage of the apoptotic process and the type of apoptogenic inducer used. The progression of apoptosis in U937 cells beyond early stages resulted in the extensive formation of blebs which concomitantly lost some typical markers of apoptosis, such as PS and sugar residues. Therefore, the modality by which the nucleus condenses, or the amount and the pattern of distribution of PS on the cell surface were, for each cell line, strictly related to the apoptogenic inducer. The morphological data reported in the present paper should lead to a more precise quantification of apoptosis by improving the detection of apoptotic cells in vivo (i.e. in tissue, organs), which is a crucial point in the evaluation of efficiency of antiproliferative drugs, such as antiblastic or immunosuppressive compounds

123I-Interleukin-2 scintigraphy for the in vivo assessment of intestinal mononuclear cell infiltration in Chron's disease

Activated mononuclear cells expressing interleukin-2 (IL2) receptors (IL2-Rs) heavily infiltrate the Crohn’s disease (CD) gut wall. A new technique for the in vivo detection of tissue infiltrating IL2-R positive (IL2R1ve) cells was developed based on 123I-IL2 scintigraphy. The aim of this study was to investigate whether 123I-IL2 accumulates in the CD gut wall in different phases of the disease and to evaluate the specificity of 123I-IL2 binding to activated IL2R1ve cells infiltrating the gut wall. Methods: Fifteen patients with ileal CD (10 active and 5 inactive) and 10 healthy volunteers were studied by 123I-IL2 scintigraphy. Six patients with active CD were studied before and after 12 wk of steroid treatment. After scintigraphy, patients were followed up for 29–54 mo. Ex vivo autoradiography was performed to determine specificity of 125IIL2 binding to IL2R1ve cells. For bowel scintigraphy, 123I-IL2 (75 MBq) was injected intravenously and g camera images were acquired after 1 h. Bowel radioactivity was quantified in 64 regions of interest (ROIs). Results: Autoradiography showed specific binding of 125I-IL2 to IL2R1ve mononuclear cells infiltrating the CD gut wall. Intestinal 123I-IL2 uptake assessed by the number of positive ROIs was higher in patients with active or inactive CD than in healthy volunteers (P , 0.0001 andP 5 0.03, respectively) and positively correlated with the CD activity index (P 5 0.01). 123I-IL2 intestinal uptake significantly decreased in patients with CD in steroid-induced remission (P 5 0.03). A significant correlation was observed between the number of positive ROIs and time to disease relapse. Conclusion: 123I-IL2 accumulates in the diseased CD gut wall by specific binding to IL2R1ve cells, infiltrating the involved tissues. 123I-IL2 scintigraphy may be an objective tool for the in vivo assessment of intestinal activated mononuclear cell infiltration

16: Long-Term Results of a Gitmo Retrospective Study on Hematopoietic Stem Cell Transplantation (HSCT) for Paroxysmal Nocturnal Hemoglobinuria (PNH)

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Real Time Marine Data Acquisition: The Coastal Oceanographic Observatory Network in the Adriatic sea.

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