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Anatomical sciences are visual sciences that deal with the structure at gross and microscopic levels. Throughout history, drawing has served as a prominent tool for learning and teaching anatomical sciences, tracing back to notable figures such as Claudius Galen, Andreas Vesalius, Leonardo Da Vinci, and Henry Vandyke Carter’s illustrations in Gray’s Anatomy among others. In this observational pilot study spanning over three years, we investigated the efficacy of utilizing drawing as a pedagogical tool for learning histology and human anatomy. This study involved 201 participants comprising dental, and allied health sciences. Pre- and post-activity surveys were administered to asses students’ perceptions and attitudes towards incorporating drawing as an adjunctive method for teaching and learning structural sciences, particularly histology and anatomy. Analysis of the survey data revealed a significant level of appreciation and interest in the drawing approach, with 80% of participants expressing a positive inclination towards its future integration into educational practices. The significance of drawing as a pedagogical approach for anatomical sciences, drawing upon insights from previous research and observations gleaned from our surveys. In conclusion, on this basis we recommend further development and implementation of drawing-based teaching methodologies in future educational contexts. [ABSTRACT FROM AUTHOR]

Angioedema is characterized by swelling of the skin, mucosa, and submucosa, involving the deeper connective tissues. It can be triggered by allergic or non-allergic mechanisms, including the use of Angiotensin-Converting Enzyme Inhibitors (ACE-Is). SARS-CoV-2 has also been associated with angioedema, although the underlying mechanism remains poorly understood. This case report presents a middle-aged Caucasian woman who tested positive for SARS-CoV-2 and subsequently developed angioedema, along with impaired consciousness, acute respiratory acidosis, and severe respiratory distress requiring intensive care unit admission and mechanical ventilation. The patient had been on long-term ACE-Is for hypertension. High-resolution computed tomography revealed SARS-CoV-2 interstitial pneumonia. While the angioedema resolved within 48-72 hours, the patient's clinical improvement was attributed to the administration of corticosteroid therapy, anticoagulant drugs, and oxygen therapy, allowing for successful weaning from mechanical ventilation and resolution of respiratory failure and interstitial pneumonia. The exact cause of angioedema in this patient remains unclear, as it could be attributed to ACE-Is as a known side effect, SARS-CoV-2 infection as an unusual manifestation, or a potential interaction between the two. This case underscores the need for further research to elucidate the interplay between SARSCoV-2 and ACE-Is in the context of angioedema development. [ABSTRACT FROM AUTHOR]

BACKGROUND: The aim of this study is to analyze and compare the intraocular pressure (IOP) values measured in three different kinds of participants such as healthy subjects (HS), keratoconus patients (KP), and those who underwent myopic photorefractive keratectomy (MPRK). The devices used in this study are the Goldmann Applanation Tonometry (GAT), the dynamic contour tonometry (DCT), the ocular response analyzer (ORA), and the Corvis ST (CST). SUBJECTS AND METHODS: This research included 92 eyes of 92 h, 63 eyes of 63 KP, and 58 eyes of 58 MPRKM. Each participant underwent a complete ophthalmic evaluation and IOP measurement with GAT, DCT, ORA, and CST. A statistical analysis was conducted to detect possible differences and correlations. RESULTS: First, according to the observed data, HS eyes displayed mean IOP values measured with GAT, DCT, ORA, and CST, respectively, 15.82 ± 2.74 mmHg, 17.63 ± 2.28 mmHg, 16.24 ± 3.14 mmHg, and 17.31 ± 3.21 mmHg. Then, KP eyes showed mean IOP values measured with GAT, DCT, ORA, and CST of, respectively, 14.89 ± 1.64 mmHg, 16.97 ± 2.08 mmHg, 13.09 ± 3.12 mmHg, and 13.78 ± 2.11 mmHg. Finally, MPRK eyes showed mean IOP values measured with GAT, DCT, ORA, and CST of, respectively, 13.92 ± 1.34 mmHg, 15.39 ± 2.86 mmHg, 16.63 ± 2.51 mmHg, and 15.06 ± 1.56 mmHg. CONCLUSION: According to the observed data, ORA and GAT might be used interchangeably in HS, whereas GAT, ORA, and CST in KP eyes. Moreover, it has been noticed that in those eyes that previously undergone a myopic PRK, GAT provided lower values of IOP in comparison with other devices. [ABSTRACT FROM AUTHOR]

Torella D, Gasparri C, Ellison GM, Curcio A, Leone A, Vicinanza C, Galuppo V, Mendicino I, Sacco W, Aquila I, Surace FC, Luposeila M, Stillo G, Agosti V, Cosentino C, Avvedimento EV, Indolfi C. Differential regulation of vascular smooth muscle and endothelial cell proliferation in vitro and in vivo by cAMP/PKA-activated p85[[alpha].sup.PI3K]. Am J Physiol Heart Circ Physiol 297: H2015-H2025, 2009. First published September 25, 2009; doi: 10.1152/ajpheart.00738.2009.--cAMP inhibits proliferation in most cell types, triggering different and sometimes opposing molecular pathways, p85[alpha] (phosphatidylinositol 3-kinase regulatory subunit) is phosphorylated by cAMP/PKA in certain cell lineages, but its effects on vascular smooth muscle cells (VSMCs) and endothelial cells (ECs) are unknown. In the present study, we evaluated 1) the role of p85[alpha] in the integration of cAMP/PKA-dependent signaling on the regulation of VSMC and EC growth in vitro; and 2) the effects of PKA-modified p85[alpha] on neointimal hyperplasia and endothelial healing after balloon injury in vivo. Plasmid constructs carrying wild-type and PKA-modified p85[alpha] were employed in VSMCs and ECs in vitro and after balloon injury in rat carotid arteries in vivo. cAMP/PKA reduced VSMC proliferation through p85[alpha] phosphorylation. Transfected PKA-activated p85[alpha] binds p[21.sup.ras], reducing ERK1/2 activation and VSMC proliferation in vitro. In contrast, EC proliferation inhibition by cAMP is independent from PKA modification of p85[alpha] and ERK1/2 inhibition; indeed, PKA-activated p85[alpha] did not inhibit per se ERK1/2 activation and proliferation in ECs in vitro. Interestingly, cAMP reduced both VSMC and EC apoptotic death through p85[alpha] phosphorylation. Accordingly, PKA-activated p85[alpha] triggered Akt activation, reducing both VSMC and EC apoptosis in vitro. Finally, compared with controls, vascular gene transfer of PKA-activated p85[alpha] significantly reduced neointimal formation after balloon injury in rats, without inhibiting endothelial regeneration of the injured arterial segment. In conclusions, PKA-activated p85[alpha] integrates cAMP/PKA signaling differently in VSMCs and ECs. By reducing neointimal hyperplasia without inhibiting endothelial regeneration, it exerts a protective effect against restenosis after balloon injury. smooth muscle cells; endothelial cells; adenosine 3',5'-cyclic monophosphate; gene therapy doi: 10.1152/ajpheart.00738.2009

Drug-eluting stents are increasingly used to reduce in-stent restenosis and adverse cardiac events after percutaneous coronary interventions. However, the race for the ideal drug-eluting stent is still on, with special regard to the best stent-coating system and the most effective and less toxic drug. Fludarabine, a nucleoside analog, has both anti-inflammatory and antiproliferative cellular effects. The aim of the present study was to assess the cellular and molecular effects of fludarabine on vascular smooth muscle cell (VSMC) growth in vitro and in vivo and the feasibility and efficacy of a fludarabine-eluting stent. To study the biomolecular effects of fludarabine on VSMC proliferation in vitro, rat VSMCs were grown in the presence of 50 [micro]M fludarabine or in the absence of the same. To evaluate the in vivo effect of this drug, male Wistar rats underwent balloon injury of the carotid artery, and fludarabine was locally delivered at the time of injury. Finally, fludarabine-eluting stents were in-laboratory manufactured and tested in a rabbit model of in-stent restenosis. Fludarabine markedly inhibited VSMC proliferation in cell culture. Furthermore, fludarabine reduced neointimal formation after balloon angioplasty in a dose-dependent manner, and fludarabine-eluting stents reduced neointimal hyperplasia by ~50%. These in vitro and in vivo cellular effects were specifically associated with the molecular switch-off of signal transducer and activator of transcription (STAT)-1 activation, without affecting other STAT proteins. Fludarabine abolishes VSMC proliferation in vitro and reduces neointimal formation after balloon injury in vivo through specific inhibition of STAT-I activation. Fludarabine-eluting stents are feasible and effective in reducing in-stent restenosis in rabbits. signal transduction; drug-eluting stents; smooth muscle cells doi:10.1152/ajpheart.00887.2006