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Background Formative assessment is a crucial component of a Competency-Based Medical Education curriculum. Keywords are concise representations of the central ideas and themes explored within a subject. Taking a memory test evaluates knowledge as well as improves future memory. Aim and objectives This study intended to study the efficacy of the "keywords teaching" technique and "keywords recall" after a teaching-learning session as an effective tool for formative assessment and the correlation between the performance of students in summative assessments. Materials and methods Students of first-year professional faculty of medicine students 2022-23 batch attending pre-clinical (physiology) classroom lectures aged between 18-21 years belonging to both genders who consented to voluntary participation in the study were included in the study. Scores of formative sessions by multiple choice questions, keywords recall assessment tool, and summative sessions were analyzed using paired t-tests. Scores of formative assessments and summative assessments were correlated using Pearson correlation analysis. Results Analysis showed formative assessments had a significant (P < 0.05) relationship with summative assessment performance. The study indicates a positive correlation between scores for both formative and summative assessments, highlighting the importance of formative assessment in improved academic performance. Conclusion Optimal learning can be achieved by testing that emphasizes recall retrieval practice and that is repeated at intervals over time. This study suggests that "keywords recall" after a teaching-learning session is an effective tool for formative assessment.
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INTRODUCTION: The use of packed red blood cells (pRBCs) for resuscitation is limited by the red blood cell storage lesion, a series of biochemical and physiological changes that occur during the storage and aging of blood. Microvesicles (MVs) shed from pRBCs during this process are one component of the red blood cell storage lesion and lead to acute lung injury and pulmonary vascular microthrombi. We hypothesized that MVs from stored pRBCs lead to the release of P-selectin and von Willebrand factor (vWF) from endothelial cells and that this mechanism is mediated via activation of protein kinase C (PKC) or protein kinase A (PKA). METHODS: Leukoreduced, platelet-poor murine pRBCs were isolated from C57BL/6 8-12 week-old male mice via cardiac puncture, prepared via centrifugation using a Ficoll gradient, and stored for up to 14 days, the equivalent of 42 days of storage in humans. MVs were isolated from the stored pRBC units via sequential high-speed centrifugation. Murine lung endothelial cells (MLECs) were cultured and grown to confluence, then treated with MVs and either calphostin C, a PKC inhibitor (10 µg/mL), or PKI 14-22 amide, a PKA inhibitor (10 µM). The supernatant was collected after 1 h. P-selectin and vWF A2 concentrations were quantified via ELISA. Immunofluorescent staining for vWF was performed on MLECs. Statistical analysis was performed via unpaired t-test or ANOVA as indicated and reported as mean ± SD. Concentration is reported as pg/mL. RESULTS: MLECs treated with MVs isolated from stored pRBCs demonstrated increased release of P-selectin and vWF A2 in a dose-dependent fashion. MLECs treated with MVs prepared from stored as compared to fresh pRBCs demonstrated increased release of P-selectin (3751 ± 726 vs 359 ± 64 pg/mL, p < 0.0001) and vWF A2 (3141 ± 355 vs 977 ± 75 pg/mL, p < 0.0001) with increasing duration of storage. The treatment of MVs with calphostin C decreased the amount of P-selectin (1471 ± 444 vs 3751 ± 726 pg/mL, p < 0.0001) and VWF A2 (2401 ± 289 vs 3141 ± 355 pg/mL, p = 0.0017) released into the supernatant by MLECs compared to MVs alone. The treatment of MVs with PKI 14-22 increased the amount of P-selectin released compared to MVs alone (1999 ± 67 vs 1601 ± 135 pg/mL, p = 0.0018). CONCLUSIONS: MVs from stored pRBCs stimulate the release of P-selectin and VWF A2 from endothelial cells. The effect of MVs increases with both dose of MVs and age of stored pRBCs from which they are formed. This mechanism is dependent on activation of PKC and inhibition of this enzyme represents a potentially significant strategy to modulate the inflammatory response to resuscitation with stored pRBCs.
Assuntos
Células Endoteliais , Naftalenos , Fator de von Willebrand , Animais , Masculino , Camundongos , Células Endoteliais/metabolismo , Eritrócitos/metabolismo , Camundongos Endogâmicos C57BL , Selectina-P , Proteína Quinase C , Fator de von Willebrand/metabolismoRESUMO
In the title compound, C(17)H(21)NO(4)S, the phenyl and dimeth-oxy-phenyl rings are almost perpendicular to each other, making a dihedral angle of 82.57â (5)°. The structure is stabilized by inter-molecular C-Hâ¯O inter-actions and the packing is further enhanced by C-H â¯π inter-actions.
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In the title compound, C(24)H(25)N(3)O(4), the pyrrolidine ring adopts an envelope conformation while the pyrrolidine-2'',5''-dione ring adopts a twist conformation. The indoline unit is planar [maximum deviation of -0.050â (9)â Å] and forms a dihedral angle of 40.36â (4)° with the methoxy-phenyl ring. Intra-molecular C-Hâ¯O hydrogen bonds are observed. In the crystal, mol-ecules are linked into a two-dimensional network parallel to the ab plane by inter-molecular C-Hâ¯O hydrogen bonds and C-Hâ¯π inter-actions.
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In the title compound, [Fe(C(5)H(5))(C(21)H(20)NO(5))], the pyrrolidine and cyclo-penta-none rings exhibit a twist conformation. The pyrrolidine ring is almost perpendicular to the cyclo-penta-none ring, making a dihedral angle of 81.91â (6)°. The mol-ecular conformation is stabilized by an intra-molecular O-Hâ¯N hydrogen bond and C-Hâ¯O inter-actions. The crystal structure is stabilized by inter-molecular C-Hâ¯O inter-actions.
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In the title compound, C(25)H(25)NO(3), the dihydro-pyran ring adopts a half-chair conformation, whereas the pyrrolidine ring is in a twist conformation. The tolyl group is oriented at an angle of 82.92â (7)° with respect to the napthalene ring system. In the crystal structure, mol-ecules are linked into centrosymmetric dimers by C-Hâ¯π inter-actions involving the benzene ring of the tolyl group.
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In the title compound, C(27)H(27)NO(3), the pyrrolidine ring exhibits a twist conformation and the piperidine ring exhibits a chair conformation. The pyrrolidine ring makes dihedral angles of 54.47â (5), 51.50â (5) and 73.37â (6)° with the napthalene ring system and the tetra-hydro-pyran and phenyl rings, respectively. The structure is stabilized by intra-molecular C-Hâ¯O and C-Hâ¯N inter-actions.
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In the title compound, C(27)H(27)NO(4), both the pyrrolidine rings in the pyrrolizine ring system adopt envelope conformations, whereas the dihydro-pyran ring adopts a half-chair conformation. The methoxy-phenyl group is oriented at an angle of 53.72â (4)° with respect to the naphthalene ring system. Intra-molecular C-Hâ¯O hydrogen bonds are observed. The crystal structure is stabilized by weak inter-molecular C-Hâ¯π inter-actions.
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In the title compound, C(24)H(22)BrNO(3), the dihydro-pyran ring adopts a half-chair conformation, whereas the pyrrolidine ring is in an envelope conformation. The bromo-phenyl group is oriented at an angle of 66.44â (4)° with respect to the naphthalene ring system. In the crystal structure, mol-ecules are linked into centrosymmetric dimers by C-Hâ¯π inter-actions and the dimers are connected via C-Hâ¯Br hydrogen bonds. The crystal structure is further stabilized by π-π inter-actions [centroid-centroid distance = 3.453â (1)â Å].
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In the title compound, [Fe(C(5)H(5))(C(20)H(21)N(2)O(4))], the pyrrolidine ring exhibits an envelope conformation with the spiro-C atom deviating from the plane of the remaining four atoms. The pyrrolidine ring is almost perpendicular to the indolinone ring [dihedral angle = 87.52â (7)°]. The structure is stabilized by an intra-molecular O-Hâ¯N hydrogen bond and by inter-molecular C-Hâ¯O and N-Hâ¯O inter-actions.
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In the title compound C(37)H(32)Cl(2)N(2)O(4), the unsubstituted pyrrolidine ring shows a twist conformation whereas the substituted pyrrolidine ring shows an envelope conformation. The dimeth-oxy benzene ring is perpendicular to the tetra-lone ring, making a dihedral angle of 89.94â (5)°. Mol-ecules are linked into centrosymmetric dimers by N-Hâ¯O hydrogen bonds and the crystal structure is stabilized by C-Hâ¯π inter-actions and C-Hâ¯O hydrogen bonds. One meth-oxy group is disordered over two positions with the site occupancy factors of 0.84â (2) and 0.16â (2).
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In the title compound, C(29)H(24)F(2)N(2)O(2), one of the pyrrolidine rings of the pyrrolizine system is disordered over two sites, with occupancy factors 0.734:0.266â (12). Both components of the disordered pyrrolidine ring adopt envelope conformations, whereas the other pyrrolidine ring adopts a twist conformation. The mol-ecules are linked into centrosymmetric dimers by N-Hâ¯O hydrogen bonds and the dimers are connected via C-Hâ¯π inter-actions. The crystal structure is also stabilized by inter-molecular C-Hâ¯F hydrogen bonds.
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In the title compound, C(29)H(26)N(2)O(2), one of the pyrrolidine rings in the pyrrolizine system is disordered, with site occupancies of ca 0.55 and 0.45. Both components of the disordered pyrrolidine ring adopt envelope conformations, whereas the other pyrrolidine ring adopts a twist conformation. The mol-ecules are linked into centrosymmetric dimers by N-Hâ¯O hydrogen bonds and the dimers are connected via C-Hâ¯π inter-actions.
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In the title compound, C(34)H(32)N(2)O(7), the methyl group and methylene H atoms of the ethoxycarbonyl substituent are disordered over two positions with site occupancy factors for the major and minor conformers of 0.594â (8) and 0.406â (8), respectively. The unsubstituted ring of the pyrrolizine ring system exhibits a twist conformation, the other an envelope conformation. In the crystal structure, mol-ecules are linked through C-Hâ¯O hydrogen bonds; intramolecular C-Hâ¯O interactions are also observed.
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In the title compound, C(20)H(21)NO(3), the heterocyclic six-membered ring adopts a half-chair conformation and the pyrrolidine ring adopts an envelope conformation. The mol-ecular conformation is stabilized by C-Hâ¯O and C-Hâ¯N inter-actions.
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In the title compound, C(36)H(31)ClN(2)O(4)Se, the four-membered ß-lactam ring is fused to a pyrrolidine ring. The central five-membered ring of the fused tricyclic system exhibits an envelope conformation with the N atom as the flap, while the other five-membered ring exhibits a twist conformation. The chloro-phenyl ring is almost perpendicular to the pyrrolidine ring, making a dihedral angle of 73.45â (1)°. The crystal structure is stabilized by weak inter-molecular C-Hâ¯O inter-actions and the packing is further enhanced by C-H â¯N inter-actions and π-π inter-actions between benzene rings of tetra-lone groups in mol-ecules related by an inversion center, with a centroid-centroid separation of 3.8923â (2)â Å.
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In the title compound, C(23)H(19)NO, the oxindole residue is essentially planar and is almost perpendicular to the phenyl rings [dihedral angles = 72.1â (6) and 77.6â (6)°]. The mol-ecular packing is stabilized by C-Hâ¯O hydrogen bonds and C-Hâ¯N inter-actions.
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In the title compound, C(35)H(30)N(2)O(5)Se, the pyrrolidine ring adopts an envelope conformation and the oxazolidine ring is in a twist conformation. The tetra-hydro-pyran ring adopts a half-chair conformation. The methoxy-phenyl ring is twisted away from the attached azetidinone ring by 15.7â (1)°. In the crystal structure, inter-molecular C-Hâ¯O inter-actions link the mol-ecules into a two-dimensional network.
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In the title compound, C(25)H(23)NO, the indoline system is essentially planar. The mol-ecular structure is stabilized by weak intra-molecular C-Hâ¯N inter-actions and the crystal packing is determined by inter-molecular C-Hâ¯π inter-actions.
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In the mol-ecule of the title compound, C(38)H(37)N(3)O(7), the pyrrolidine ring adopts a twist conformation and the six-membered heterocyclic ring has a boat conformation. In the crystal structure, mol-ecules are linked into a three-dimensional framework through inter-molecular C-Hâ¯O hydrogen bonds. One ethyl group is disordered over two positions with occupancies 0.67â (2)/0.33â (2).