Impact of COVID-19 on Cardiothoracic Surgery: Experience of Alexandria (Egypt) Main University Hospital

ABSTRACT Introduction: The current coronavirus pandemic has greatly strained the limited resources that had previously maintained the sustainability of the high-cost cardiothoracic surgeries in low-income countries like Egypt. Methods: Hospital databases and patients' records were reviewed to evaluate the impact of the pandemic on the workflow and waiting lists. Postoperative patients were contacted by telephone for follow-up, as well as preoperative patients whose operations were cancelled. Regular virtual meetings were held, and residents were asked to discuss the stresses, challenges, and their suggestions for the gradual resumption of services. Residents' logbooks were evaluated to assess the disruption of the surgical exposure compared to 2019. Results: While thoracic surgeries have continued to thrive, cardiac surgeries have witnessed the worst consequences, including cancellation of all surgeries, expansion of waiting lists, patients' non-compliance with follow-up, and impaired surgical exposure of junior residents. Conclusion: The gradual recovery of cardiac surgery services in Alexandria (Egypt) is being carefully planned, taking into consideration the backlog of cases and the shortage of screening kits. Careful tiering and triaging of patients by a multidisciplinary team, as well as seeking alternative assessment tools for trainees, are the main lines of our action plan.

Impact of COVID-19 on Cardiothoracic Surgery: Experience of Alexandria (Egypt) Main University Hospital.

INTRODUCTION: The current coronavirus pandemic has greatly strained the limited resources that had previously maintained the sustainability of the high-cost cardiothoracic surgeries in low-income countries like Egypt. METHODS: Hospital databases and patients' records were reviewed to evaluate the impact of the pandemic on the workflow and waiting lists. Postoperative patients were contacted by telephone for follow-up, as well as preoperative patients whose operations were cancelled. Regular virtual meetings were held, and residents were asked to discuss the stresses, challenges, and their suggestions for the gradual resumption of services. Residents' logbooks were evaluated to assess the disruption of the surgical exposure compared to 2019. RESULTS: While thoracic surgeries have continued to thrive, cardiac surgeries have witnessed the worst consequences, including cancellation of all surgeries, expansion of waiting lists, patients' non-compliance with follow-up, and impaired surgical exposure of junior residents. CONCLUSION: The gradual recovery of cardiac surgery services in Alexandria (Egypt) is being carefully planned, taking into consideration the backlog of cases and the shortage of screening kits. Careful tiering and triaging of patients by a multidisciplinary team, as well as seeking alternative assessment tools for trainees, are the main lines of our action plan.

Characterization of tryptophan-containing dipeptides for anti-angiogenic effects.

AIMS: In the pathogenesis of several diseases, neo-angiogenesis is increased (e.g. tumour growth). The peptide L-glutamyl-L-tryptophan (EW/IM862) has been claimed to exhibit inhibitory effects on tumour growth in vivo. However, the potential role of natural peptides with respect to anti-angiogenic properties is unsettled. The current study explores anti-angiogenic effects of the dipeptides WL, EW, IW and WE. METHODS AND RESULTS: Using a bottom-up strategy, we first evaluated the effects of the peptides on VEGFR-2 signalling and quantified their effects in different angiogenesis assays. WL consistently had the strongest effects on phosphorylation of VEGFR-2 and downstream signalling. Therefore, this peptide was chosen in comparison with EW to further assess anti-angiogenic properties. However, sprout formation in three-dimensional (3D) fibrin gel bead assay was significantly inhibited by EW only. Furthermore, vessel sprouting in the mouse aortic ring assay was decreased by the presence of WL and EW compared to control. Results from a chorioallantoic membrane assay showed that under vascular endothelial growth factor (VEGF) stimulation WL and EW decreased the number of blood vessels versus control. These results were in line with those obtained in a matrigel plug assay. The VEGF-induced increase in the haemoglobin content was nearly abolished when treatment was combined with either WL or EW application. In the murine model of oxygen-induced retinopathy, WL exhibited a small albeit significant anti-angiogenic effect. CONCLUSION: Comprehensive screening of WL suggests an anti-angiogenic effect, demonstrated in in vitro, ex vivo and in vivo models. Thus, WL is a dipeptide with potential anti-angiogenic effects and is worthy for further exploration.

Inhibitory effect of valproate sodium on pain behavior in diabetic mice involves suppression of spinal histone deacetylase 1 and inflammatory mediators.

Anti-epileptic medications are included in the international guidelines for managing neuropathic pain. Valproate sodium (VPS) was recently described as "the forgotten analgesic" and has been reported to relief pain in various models of neuropathic pain. Some studies reported anti-inflammatory and histone deacetylase 1 (HDA1) inhibitory properties for sodium valproate. The aim of the current study was to investigate the modulatory effect of VPS on pain behavior and inflammatory reactions in alloxan-induced diabetic neuropathy focusing on HDA1 inhibition and glia reactivity. 28 Male Swiss albino mice were allocated into four groups, (1) vehicle group, (2) alloxan-diabetic group, (3 & 4) alloxan+VPS (25 or 50 mg/kg) groups. VPS was given daily for 5 weeks by oral gavage. Pain behavior demonstrated increased allodynia (von-Frey filaments) and hyperalgesia (hot-plate test) in alloxan-diabetic mice that was reduced significantly by at least one of VPS doses. Sciatic nerves in diabetic mice showed increased histopathology score, increased silver staining for the nerves-indicating myelopathy- and a decrease in immunostaining for nerve growth factor. Spinal cord of diabetic mice showed greater histopathologic score, increased CD11b and glia fibrillary acidic protein (GFAP) immunostaining than vehicle treated mice. Molecular investigations highlighted greater content of spinal histone deacetylases, tumor necrosis factor-α (TNF-α) and interlukin-1ß (IL1ß) that were favorably modified by VPS. Overall, the current data confirmed that the pain killing and anti-inflammatory activity of VPS is at least partly mediated through inhibition of spinal HDA1 and glia reactivity. These findings support the view of inviting antiepileptics for treating neuropathies.

Caffeic acid improves locomotor activity and lessens inflammatory burden in a mouse model of rotenone-induced nigral neurodegeneration: Relevance to Parkinson's disease therapy.

BACKGROUND: Caffeic acid phenethyl ester is found in honey bee propolis. It has immunomodulatory, anti-inflammatory and anti-cancer properties. Rotenone is a pesticide commonly used for inducing experimental Parkinson's disease (PD) due to complex I inhibition and microglia activating properties. The current study examined neuroprotective effect of caffeic acid against rotenone-induced neurodegeneration in groups of seven mice. METHODS: Mice received protective doses of caffeic acid (2.5, 5 or 10 mg/kg) daily and nine injections of rotenone (1 mg kg, subcutaneously) - every 48 h. Behavioral evaluation of motor function was done by a battery of tests including open-field test, cylinder test, pole test and rotarod test; all these tests showed motor impairment. RESULTS: Assay of striatal dopamine highlighted a significant decrease and increases in inflammatory markers. In addition, histopathological assessment of substantia nigra neurons demonstrated low immunostaining for tyrosine hydroxylase (TH) in rotenone treated mice. PCR analysis highlighted upregulation for genes encoding CD11b (a microglia surface antigen), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) and nuclear factor-κB (NFκB). Treatment with caffeic acid (5 or 10 mg/kg) amended most of rotenone-induced motor deficits, lessened microglia expression and inflammatory mediators and improved the nigral TH immunostaining. CONCLUSION: These results confirmed the anti-inflammatory activity of caffeic acid and highlighted its neuroprotective activity against rotenone-induced neurodegeneration in mice.