Corona Virus Disease 2019 (COVID-19) is a global pandemic epidemic caused by severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), which poses a serious threat to human health worldwide and results in significant economic losses. With the continuous emergence of new virus strains, small molecule drugs remain the most effective treatment for COVID-19. The traditional drug development process usually requires several years; however, the development of computer-aided drug design (CADD) offers the opportunity to develop innovative drugs quickly and efficiently. The literature review describes the general process of CADD, the viral proteins that play essential roles in the life cycle of SARS-CoV-2 and can serve as therapeutic targets, and examples of drug screening of viral target proteins by applying CADD methods. Finally, the potential of CADD in COVID-19 therapy, the deficiency, and the possible future development direction are discussed.

Background: Sepsis-associated liver injury (SALI) occurs in about a third of septic patients, and it is often a poor prognostic factor. However, there are few studies on early SALI and its impact on the clinical course of sepsis. Here we explored the clinical characteristics, risk factors, and prognosis of early SALI. Methods: Two hundred and one patients with confirmed sepsis were divided into those with and without early SALI (on admission) based on liver function. The clinical characteristics and prognosis were compared between groups and associated factors identified by multivariable regression analysis. Results: Sepsis-related liver injury was present in 18.9% of septic patients on admission. High aspartate transaminase (AST), high direct bilirubin, and low plasma thromboplastin antecedent (PTA, factor XI) were risk factors for sepsis with SALI: the area under the AST curve was 0.825, corresponding to a sensitivity of 0.67 and a specificity of 0.93 (cutoff 91.6 U/L), the area under the direct bilirubin curve was 0.86, corresponding to a sensitivity of 0.83 and a specificity of 0.71 (cutoff 8.35 μmol/L), and the area under the PTA curve was 0.678, corresponding to a sensitivity of 0.47 and a specificity of 0.93 (cutoff 54.0). Conclusion: Septic patients with early SALI have early-onset coagulation disorders that must be recognized to instigate early intervention and halt sepsis progression. Elevated AST, PTA, and direct bilirubin may be independent risk markers of sepsis-related liver injury, and extra clinical vigilance is required when these factors are noted in patients with sepsis.

Prostate adenocarcinoma (PRAD) is the second most common tumor associated with death. The role and mechanisms of the fragile X mental retardation 1 (FMR1) gene in PRAD remain unknown. We conducted an analysis of FMR1 expression in PRAD to determine its prognostic importance and connection to carcinogenic pathways such as PI3K_AKT_mTOR. Survival analyses were utilized to establish a correlation between FMR1 expression and patient outcomes. We used the integration of genomic data with bioinformatic predictions to predict the regulatory factors of the FMR1 gene in PRAD. Our data revealed that individuals with higher levels of FMR1 expression experience worse survival outcomes compared to those with lower expression (hazard ratio [HR] = 5.08, 95% confidence interval [CI] = 1.07 – 24, p = 0.0412). FMR1 expression was significantly higher in patients with advanced pathological tumor stages, particularly in the pT3 and pT4 combined stages and the pN1 nodal stage. Furthermore, patients with high Gleason scores (GSs) (combined GSs 8 and 9) exhibited increased levels of FMR1 expression. Our results further identify a possible regulatory link between FMR1 and key oncogenic pathways, including PI3K_AKT_mTOR, and predict the possible mechanism by which FMR1 is regulated in PRAD. Our data suggest that the FMR1 gene could serve as a biomarker for PRAD progression. However, in-depth investigations, including those with large patient samples and in vitro studies, are needed to validate this finding and understand the mechanisms involved.

Despite advances in medical technology, sepsis remains a significant cause of mortality in intensive care units. The pathophysiology of sepsis is complex and involves increased activity of molecules that regulate vascular tone, including nitric oxide, hydrogen sulfide, endothelin-1, and carbon monoxide. These molecular changes contribute to the high mortality associated with sepsis. Moreover, as a systemic inflammatory response to infection, sepsis leads to reduced neutrophil levels, impairing the body’s ability to combat the disease effectively. The impact of sepsis on lipid metabolism and liver function is profound. The liver, a vital organ involved in various physiological processes, experiences enzyme production under septic conditions. Proinflammatory cytokines overload the liver during sepsis, impairing its normal functions and disrupting lipid metabolism. Altered circulating lipid levels, particularly triglycerides and cholesterol, may further exacerbate organ failure associated with sepsis. This review aims to explore the intricate relationship between sepsis, liver function, and lipid metabolism, offering a comprehensive understanding of the mechanisms behind sepsis-induced liver dysfunction and lipid abnormalities. A deeper insight into these processes may pave the way for developing effective therapeutics to counteract the detrimental consequences of sepsis. By highlighting the current knowledge gaps and elucidating the underlying mechanisms, this review seeks to contribute to improving sepsis management and patient outcomes.