Medical Students' Perceptions Towards Online Teaching During the Covid-19 Pandemic: A Cross-Sectional Study from Saudi Arabia.

Background: The Covid-19 has made a huge impact on higher education. Online teaching and learning became essential to deliver educational activities in all areas including medical education. In this study, we aimed to investigate medical students' perceptions on the role of online teaching and learning in facilitating medical education. Material and Methods: A cross-sectional study using a self-administered online questionnaire was conducted. Students eligible were medical students across all years at Imam Abdulrahman Bin Faisal University, Saudi Arabia. Perceptions analysis was conducted using SPSS software. Results: A total of 563 students participated in the study (prominent category female 64%, n = 361). There was a significant increase in the number of hours devoted to online learning during the pandemic. Live lectures/tutorials platform via zoom showed the highest rate of interaction compared to pre-recorded lectures and learning materials uploaded on blackboard. 50% of the students disagreed that online teaching is as effective as face-to-face teaching. The greatest perceived enjoyable aspect included the online accessibility of materials. Whereas the most frequent perceived barrier to online learning included internet connection. 17% of students reflected a poor understanding of scientific materials through online PBL. More than 50% of students revealed that online theoretical lectures are as good as classroom or better. Whereas the majority (70%) were unable to learn clinical skills online. The results indicated high impact on students' physical activities (80%). Impacts were higher on pre-clinical students' health and social life than on clinical students. Conclusion: Our findings reported that during emergency situations due to the pandemic, online teaching enables the continuity of medical education and provides adequate efficiency. The use of live online platforms showed high level of interaction. However, some barriers need to be addressed especially at the clinical skills development level to maximize the benefit of online teaching and learning.

Neuronal injury external to the retina rapidly activates retinal glia, followed by elevation of markers for cell cycle re-entry and death in retinal ganglion cells.

Retinal ganglion cells (RGCs) are neurons that relay visual signals from the retina to the brain. The RGC cell bodies reside in the retina and their fibers form the optic nerve. Full transection (axotomy) of the optic nerve is an extra-retinal injury model of RGC degeneration. Optic nerve transection permits time-kinetic studies of neurodegenerative mechanisms in neurons and resident glia of the retina, the early events of which are reported here. One day after injury, and before atrophy of RGC cell bodies was apparent, glia had increased levels of phospho-Akt, phospho-S6, and phospho-ERK1/2; however, these signals were not detected in injured RGCs. Three days after injury there were increased levels of phospho-Rb and cyclin A proteins detected in RGCs, whereas these signals were not detected in glia. DNA hyperploidy was also detected in RGCs, indicative of cell cycle re-entry by these post-mitotic neurons. These events culminated in RGC death, which is delayed by pharmacological inhibition of the MAPK/ERK pathway. Our data show that a remote injury to RGC axons rapidly conveys a signal that activates retinal glia, followed by RGC cell cycle re-entry, DNA hyperploidy, and neuronal death that is delayed by preventing glial MAPK/ERK activation. These results demonstrate that complex and variable neuro-glia interactions regulate healthy and injured states in the adult mammalian retina.

Chronic and acute models of retinal neurodegeneration TrkA activity are neuroprotective whereas p75NTR activity is neurotoxic through a paracrine mechanism.

In normal adult retinas, NGF receptor TrkA is expressed in retinal ganglion cells (RGC), whereas glia express p75(NTR). During retinal injury, endogenous NGF, TrkA, and p75(NTR) are up-regulated. Paradoxically, neither endogenous NGF nor exogenous administration of wild type NGF can protect degenerating RGCs, even when administered at high frequency. Here we elucidate the relative contribution of NGF and each of its receptors to RGC degeneration in vivo. During retinal degeneration due to glaucoma or optic nerve transection, treatment with a mutant NGF that only activates TrkA, or with a biological response modifier that prevents endogenous NGF and pro-NGF from binding to p75(NTR) affords significant neuroprotection. Treatment of normal eyes with an NGF mutant-selective p75(NTR) agonist causes progressive RGC death, and in injured eyes it accelerates RGC death. The mechanism of p75(NTR) action during retinal degeneration due to glaucoma is paracrine, by increasing production of neurotoxic proteins TNF-α and α(2)-macroglobulin. Antagonists of p75(NTR) inhibit TNF-α and α(2)-macroglobulin up-regulation during disease, and afford neuroprotection. These data reveal a balance of neuroprotective and neurotoxic mechanisms in normal and diseased retinas, and validate each neurotrophin receptor as a pharmacological target for neuroprotection.

Local inhibition of Rho signaling by cell-permeable recombinant protein BA-210 prevents secondary damage and promotes functional recovery following acute spinal cord injury.

Spinal cord injury (SCI) leads to robust Rho activation at the lesion site. Here, we demonstrate that BA-210, a cell-permeable fusion protein derived from C3 transferase, formulated in fibrin sealant and delivered topically onto the dura matter, diffuses into the spinal cord and inactivates Rho in a dose-dependent manner. Treatment with BA-210 in rats with thoracic spinal cord contusion increased tissue sparing around the lesion area and led to significant improvement of locomotor function. In mice, BA-210 improved functional outcome when treatment was either applied at the time of injury or delayed by 24 h. In both rats and mice, treatment with BA-210 was well tolerated. Rats gained body weight normally, and BA-210 treatment had no impact on the development of allodynia. Inactivating Rho with BA-210 holds promise for treating patients with SCI.

Vaccination stimulates retinal ganglion cell regeneration in the adult optic nerve.

We examined whether vaccination of adult rats with spinal cord homogenate (SCH) can promote regeneration of retinal ganglion cells (RGCs) after microcrush lesion of the optic nerve. Injured animals vaccinated with SCH showed axon growth into the optic nerve and such regeneration was not observed in animals vaccinated with liver homogenate (LH). Regeneration was not a consequence of neuroprotection since our vaccine did not protect RGCs from axotomy-induced cell death. Sera of vaccinated animals were tested for antibodies against myelin-associated glycoprotein, NogoA, Nogo-66 receptor, or chondroitin sulphate proteoglycans (CSPG), but no significant levels were detected. Antibodies to myelin basic protein were present in the serum of some SCH-vaccinated animals. In culture, serum from SCH-vaccinated animals promoted RGC growth on myelin but not on CSPG. Our results show that the effect of the pro-regenerative vaccine is mediated by antibodies to SCH. However, we were not able to detect a significant immune reaction to growth inhibitory proteins, suggesting alternative mechanisms for the success of vaccination to promote regeneration.

Inactivation of intracellular Rho to stimulate axon growth and regeneration.

Our studies indicate that the small GTPase Rho is an important intracellular target for promoting axon regrowth after injury. In tissue culture, inactivation of the Rho signaling pathway is effective in promoting neurite growth on growth inhibitory CNS substrates by two different methods: inactivation of Rho with C3 transferase, and inactivation by dominant negative mutation of Rho. In vivo, we have documented the regeneration of transfected axons after treatment with C3 in two different animals models, microcrush lesion of the adult rat optic nerve, and over-hemisection of adult mouse spinal cord. Mice treated with C3 after SCI showed impressive functional recovery, notwithstanding the fact that mice differ from rats in their response to spinal cord injury, especially in the extent of cavitation at the lesion site (Steward et al., 1999). It remains to be determined to what extent the regeneration of specific descending and ascending spinal axons contribute to the recovery, and whether inactivation of Rho enhances the spontaneous plasticity of axonal and dendritic remodeling after SCI. Inactivation of Rho with C3 to promote regeneration and functional recovery after SCI is simple, and our studies reveal the potential for a new, straightforward technique to promote axon regeneration.

Oligodendrocyte-myelin glycoprotein (OMgp) is an inhibitor of neurite outgrowth.

A protein fraction purified from bovine brain myelin, previously called arretin because of its ability to inhibit neurite outgrowth, has been identified as consisting predominantly of oligodendrocyte-myelin glycoprotein (OMgp). We show that it is a potent inhibitor of neurite outgrowth from rat cerebellar granule and hippocampal cells; from dorsal root ganglion explants in which growth cone collapse was observed; from rat retinal ganglion neurons; and from NG108 and PC12 cells. OMgp purified by a different procedure from both mouse and human myelin behaves identically in all bioassays tested.

Rho signaling pathway targeted to promote spinal cord repair.

The Rho signaling pathway regulates the cytoskeleton and motility and plays an important role in neuronal growth inhibition. Here we demonstrate that inactivation of Rho or its downstream target Rho-associated kinase (ROK) stimulated neurite growth in primary cells of cortical neurons plated on myelin or chondroitin sulfate proteoglycan substrates. Furthermore, treatment either with C3 transferase (C3) to inactivate Rho or with Y27632 to inhibit ROK was sufficient to stimulate axon regeneration and recovery of hindlimb function after spinal cord injury (SCI) in adult mice. Injured mice were treated with a single injection of Rho or Rho-associated kinase inhibitors delivered in a protein adhesive at the lesion site. Treated animals showed long-distance regeneration of anterogradely labeled corticospinal axons and increased levels of GAP-43 mRNA in the motor cortex. Behaviorally, inactivation of Rho pathway induced rapid recovery of locomotion and progressive recuperation of forelimb-hindlimb coordination. These findings provide evidence that the Rho signaling pathway is a potential target for therapeutic interventions after spinal cord injury.