Background Patients with thoracic malignancies are at increased risk for mortality from Coronavirus disease 2019 (COVID-19) and large number of intertwined prognostic variables have been identified so far. Methods Capitalizing data from the TERAVOLT registry, a global study created with the aim of describing the impact of COVID-19 in patients with thoracic malignancies, we used a clustering approach, a fast-backward step-down selection procedure and a tree-based model to screen and optimize a broad panel of demographics, clinical COVID-19 and cancer characteristics. Results As of April 15, 2021, 1491 consecutive evaluable patients from 18 countries were included in the analysis. With a mean observation period of 42 days, 361 events were reported with an all-cause case fatality rate of 24.2%. The clustering procedure screened approximately 73 covariates in 13 clusters. A further multivariable logistic regression for the association between clusters and death was performed, resulting in five clusters significantly associated with the outcome. The fast-backward step-down selection then identified seven major determinants of death ECOG-PS (OR 2.47 1.87-3.26), neutrophil count (OR 2.46 1.76-3.44), serum procalcitonin (OR 2.37 1.64-3.43), development of pneumonia (OR 1.95 1.48-2.58), c-reactive protein (CRP) (OR 1.90 1.43-2.51), tumor stage at COVID-19 diagnosis (OR 1.97 1.46-2.66) and age (OR 1.71 1.29-2.26). The ROC analysis for death of the selected model confirmed its diagnostic ability (AUC 0.78; 95%CI: 0.75 – 0.81). The nomogram was able to classify the COVID-19 mortality in an interval ranging from 8% to 90% and the tree-based model recognized ECOG-PS, neutrophil count and CRP as the major determinants of prognosis. Conclusion From 73 variables analyzed, seven major determinants of death have been identified. Poor ECOG-PS demonstrated the strongest association with poor outcome from COVID-19. With our analysis we provide clinicians with a definitive prognostication system to help determine the risk of mortality for patients with thoracic malignancies and COVID-19.

Monosodium glutamate (MSG) has a flavor-enhancing effect; hence, it is added to processed food. It is known for its neurotoxicity. Aim of the study This study was conducted to demonstrate the possible protective effect of the natural antioxidant, Ginkgo biloba extract, against the neurotoxicity of MSG on the retinal cells of male albino rats. Materials and methodsThirty adult male albino rats were used. The animals were divided into the following groups: group I was the control group and group II was subdivided into subgroup IIa, which received MSG injections for 7 days, and subgroup IIb, which received Ginkgo biloba (EGb 761) orally for 7 days and then received MSG injections, in addition to EGb. Retinal sections were stained with H&E stain, toluidine blue stain, and immunohistochemical staining for glial fibrillary acidic protein (GFAP). Total retinal thickness, thickness of the outer nuclear layer, and the mean area % of GFAP were measured using an image analyzer. ResultsMSG caused complete loss of the outer and inner segments of the photoreceptors, a decrease in the thickness of the outer nuclear and plexiform layers, focal cytoplasmic vacuolation in the inner nuclear layer, and complete distortion of the ganglion cell layer. Such abnormalities were, to a large extent, prevented with the use of EGb 761. Statistically significant differences in the total retinal thickness, the thickness of the outer nuclear layer, and mean area % of GFAP were found between the groups. Conclusion MSG exposure was shown to induce deleterious morphological changes on the retina, many of which were prevented with the use of EGb 761. Thus, this natural extract could have further clinical implications in reducing glutamate-induced excitotoxicity in several ophthalmic diseases.

Objective: This experimental study aimed to evaluate the statin-induced hepatotoxicity in albino rats, as well as to compare the potential hepatotoxicity between atorvastatin and simavastatin through evaluation of both biochemical and histopathological parameters. Materials & Methods: 60 male albino rats were used in this study and were equally divided into three groups. The control group received only saline orally, the atorvastatin group which received (80 mg/kg) orally, and the simavastatin group which received simavastatin (80 mg/kg) orally. The study was conducted over a period of 12 weeks and at the end blood samples and liver tissues were obtained for assessment of biochemical markers of the liver and histopathological examination. Results: All the biochemical parameters in the current study showed higher values in the atorvastatin and simvastatin groups compared to the control group with significant probability value. The significance was detected between each of the statin groups and the control group. However no significant difference was found between atorvastatin and simvastatin group. Likewise, histopathological results showed significant hepatic injury in case of both statin groups compared to the control one. Conclusion & Recommendations: Atorvastatin and simvastatin induced hepatic injury as demonstrated by both biochemical and histopathological results in this study. Moreover, no significant difference was found between atorvastatin and simvastatin as regard statin induced liver injury.

Background: Folinic acid (FA) is used to reduce Methotrexate (MTX) toxicity during treatment of childhood acute lymphoblastic leukemia (ALL). However, FA has been shown to reduce MTX treatment efficacy and cure rates of ALL. Recent studies suggested that fish oil (FO) supplementation may protect bone during MTX chemotherapy. Aim of Work: to compare the protective effect of FA versus FO on the growing bone of MTX-treated young rats monitored by histological, immunohistochemical, morphometric and laboratory methods. Materials and Methods: Forty two, 6 weeks-old-male albino rats were divided into: group I (control), group II (MTXtreated), group III (MTX and FA-treated) and group IV (MTX and FO-treated). MTX was injected subcutaneously, once daily for 5 consecutive days, 0.65 mg/kg, followed by 9 days of rest, then 1.3 mg/kg twice weekly for 4 weeks. FA was injected intraperitoneally, 6 hours after each dose of MTX, 0.87 mg/kg, then1.3 mg/kg twice weekly. FO was given orally daily for 6 weeks, 0.5 ml/100 gm. Left knee joints were processed for measuring RANKL/ OPG ratio (Receptor Activator of Nuclear factor Kapp-B Ligand/ Osteoprotegerin). Right knee joint sections were stained with H&E, Masson's Trichrome and immunohistochemical staining for Caspase-3. Morphometric measurements and statistical analysis were done. Results: MTX-treated group sections revealed disruption in the growth plate structure with subsequent reduction in endochondral bone formation. Supplementation with FA and FO preserved growth plate integrity and bone formation. Conclusion: Fish oil showed better effect than Folinic acid in ameliorating growth plate disruption and retarded bone formation encountered during MTX chemotherapy in young rats.

The aim of this review is to provide an overview of current molecular targeted therapies for epidermal growth factor receptor (EGFR) mutation-positive lung adenocarcinoma. Current strategies aim to identify patients with driver mutations such as epidermal growth factor receptor gene mutations and anaplastic lymphoma kinase rearrangements. Previous treatment strategies have been less than satisfactory regarding response rates and significant systemic toxicities. EGFR has been shown to be deregulated by various mechanisms in lung adenocarcinoma (AC), including overexpression, amplification and mutation. Reversible EGFR tyrosine kinase inhibitors (TKIs) such as Erlotinib and Gefitinib offered a therapeutic alternative that has proven its superiority over standard platinum-based chemotherapy for patients with metastatic EGFR mutation-positive lung cancer. Irreversible EGFR tyrosine kinase inhibitors (TKIs) such as Afatinib and Dacomitinib came into practice to provide sustained disease control in adenocarcinoma of the lung with primary or acquired resistance to first generation EGFR TKIs.