Vascular dementia is considered a vascular cognitive impairment disease caused by neuronal degeneration in the brain. Several studies have supported the hypothesis that oxidative stress and endothelial dysfunction are the main pathogenic factors in vascular dementia. This current study aims to determine the possible neuroprotective effects of zafirlukast, piracetam and the combination of piracetam and zafirlukast on L‐methionine‐induced vascular dementia in rats. Male Wistar albino rats were divided into five groups. Group I was the normal control, and group II received L‐methionine (1700 mg/kg, P.O.) for 32 days. The remaining groups received zafirlukast (20 mg/kg, P.O.), piracetam (600 mg/kg, P.O.) or their combination (zafirlukast 20 mg/kg + piracetam 600 mg/kg, P.O.) for 32 days after L‐methionine administration. Afterwards, the cognitive and memory performances of the rats were investigated using the novel object recognition (NOR) test; rats were then sacrificed for histopathological and biochemical analyses. L‐methionine‐induced vascular dementia altered rats’ behaviours and the brain contents of different neurotransmitters and acetylcholinesterase activity while increasing levels of oxidative stress and causing notable histopathological alterations in brain tissues. The treatment of vascular dementia with zafirlukast and the combination improved neurochemical, behavioural and histological alterations to a comparable level to those of piracetam. Thus, zafirlukast, piracetam and the combination of both drugs can be considered as potential therapeutic strategies for the treatment of vascular dementia induced by L‐methionine. To the best of our knowledge, this study is the first to explore the neuroprotective effects of zafirlukast and piracetam on L‐methionine‐induced vascular dementia.

Background The angiotensin-converting enzyme-2 (ACE2) is recognized to be the fundamental receptor of severe acute respiratory syndrome coronavirus-2 (SARS-CoV2), responsible for the worldwide Coronavirus Disease-2019 (COVID-19) epidemic. However, genetic differences between people besides racial considerations and their relation to disease susceptibility are still not fully elucidated. Main body To uncover the role of ACE2 in COVID-19 infection, we reviewed the published studies that explore the association of COVID-19 with the functional characteristics of ACE2 and its genetic variations. Notably, emerging studies tried to determine whether the ACE2 variants and/or expression could be associated with SARS-CoV/SARS-CoV2 have conflicting results. Some researchers investigated the potential of “population-specific” ACE2 genetic variations to impact the SARS-CoV2 vulnerability and suggested no ethnicity enrichment for ACE2 polymorphisms that could influence SARS-CoV2 S-protein binding. At the same time, some studies use data mining to predict several ACE2 variants that could enhance or decline susceptibility to SARS-CoV. On the other hand, fewer studies revealed an association of ACE2 expression with COVID-19 outcome reporting higher expression levels of ACE2 in East Asians. Conclusions ACE2 gene variants and expression may modify the deleterious consequences of SARS-CoV2 to the host cells. It is worth noting that apart from the differences in gene expression and the genetic variations of ACE2, many other environmental and/or genetic factors could modify the disease outcome, including the genes for the innate and the adaptive immune response.

The therapy design of childhood acute lymphoblastic leukemia (ALL) has evolved over the past 60 years. The St. Jude Children’s Research Hospital has developed 17 treatment protocols from 1962 to 2017, aiming to have the most effective and least toxic treatment form. This review summarizes each protocol’s objectives, inclusion criteria, treatment phases, pharmacological agents, irradiation therapy, response criteria, risk stratification, type of relapse, and overall survival. The enhancement and successful application of preventive therapy for ALL and following a risk-stratified approach have progressively improved the cure rate of childhood ALL, with relatively few adverse sequelae. Moreover, St. Jude’s scientific theme serves as a reminder of the principal factor of research directed to a catastrophic disease such as ALL.

Severe infection of COVID-19 is characterized by an excessive inflammatory response in a form of a storm of proinflammatory cytokines leading to severe lung injury and life-threatening acute respiratory distress syndrome (ARDS). The use of glucocorticoids (GCs) in COVID-19 associated pneumonia and cytokine storm is debatable. A systematic review and meta-analysis were conducted to evaluate the safety and efficacy of GCs in COVID-19, SARS-CoV, and MERS-CoV infections reporting an insignificant association between GCs use and mortality rate, length of hospital stay, ICU admission and need for mechanical ventilation. 1 Moreover, the use of GCs in pneumonia associated with SARS-CoV or MERS-CoV did not significantly improve mortality rate. 2 However, GCs are recommended in certain circumstances and comorbidities associated with viral pneumonia such as septic shock, severe ARDS, asthma, and chronic obstructive pulmonary disease (COPD). 3 Recently, the RECOVERY trial; a randomized, controlled, open-labeled, adaptive clinical trial (n ¼ 2104) had released the preliminary results displaying that low dose of dexamethasone was associated with a reduction in mortality rate by a third in mechanically ventilated patients, by a fifth in patients on oxygen supply, and no benefits were observed in patients without oxygen support. 4 Due to the differences in the

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