Background: This study examines colistin resistance in Gram-negative bacteria in Egypt, analyzing prevalence, trends, geographic variations, colistin-carbapenem resistance correlation, and mcr-mediated plasmid resistance. Methods: We conducted a systematic search of articles published between 2014 and 2024 that reported on colistin or mcr-mediated resistance in Gram-negative bacteria isolated from human infections in Egypt, with clearly defined susceptibility testing methods. A random-effects meta-analysis was conducted to estimate colistin resistance prevalence based on broth microdilution (BMD) findings, the gold standard method. To explore the influence of study-level factors—including alternative susceptibility testing methods—a multivariate meta-regression analysis was performed. The results of the meta-regression are reported as regression coefficients (β), representing the difference in colistin resistance, expressed in percentage points. All statistical analyses were conducted using R software. Results: This analysis included 55 studies. Based on BMD susceptibility testing, colistin resistance was observed in 9% of all recovered Gram-negative isolates (95% CI: 6–14%) and was significantly higher among carbapenem-resistant isolates (31%, 95% CI: 25–38%), with p < 0.001. Multivariate meta-regression analysis further confirmed that colistin resistance was significantly higher in carbapenem-resistant isolates compared to the total recovered isolates (β = 9.8% points, p = 0.001). Additionally, colistin resistance has significantly increased over time, with a β = 1.8% points per year (p = 0.001). The use of the VITEK 2 system was associated with lower detected colistin resistance compared to BMD (β = -7.0, p = 0.02). Geographically, resistance rates were higher in Upper Egypt (β = 9.3, p = 0.04). Regarding mcr plasmid-mediated resistance, mcr-1 was the most prevalent resistance gene, particularly in E. coli. In contrast, mcr-2 was rare, detected sporadically in K. pneumoniae and P. aeruginosa. Conclusion: In Egypt, BMD testing identified colistin resistance in 9% of Gram-negative bacteria, increasing to 31% in carbapenem-resistant isolates. This higher resistance in carbapenem-resistant strains suggests stronger selective pressure from frequent colistin use. Additionally, colistin resistance has shown a rising trend over time, likely driven by increased usage and the spread of plasmid-mediated resistance. These findings underscore the urgent need for strict antimicrobial stewardship and alternative therapies to curb resistance evolution.

As of the 7^th of July 2024, 775,754,322 confirmed cases of COVID-19, including 7,053,902 deaths worldwide, had been reported to the WHO (World Health Organization). Nevertheless, untill the 15^th of July 2024, a total of 13,578,710,228 vaccine doses had been administered, with almost no country spared from COVID-19 attacks. The pathophysiology of this virus is complicated, and several symptoms require a deep understanding of the actual mechanisms. It is unclear why some patients develop severe symptoms while others do not, although literature suggests a role for vitamin D. Vitamin D plays a crucial role in the infection or in ameliorating the severity of symptoms. The mechanism of action of vitamin D and vitamin D deficiency (VDD) is well understood. VDD is associated with increased hospitalization of severely ill patients and increased levels of COVID-19-caused mortality. Recent studies suggest that vitamin D levels and genetic variations in the vitamin D receptor (VDR) gene significantly impact the severity and outcomes of COVID-19, especially in the infections caused by Delta and Omicron variants. Furthermore, VDD causes immune system dysregulation upon infection with SARS-CoV-2, indicating that vitamin D sufficiency is crucial in fighting against COVID-19 infection. The therapeutic effect of vitamin D raises interest in its potential role as a prophylactic and treatment adjunct. We evaluate the immunomodulatory effects of vitamin D and its ability to enhance the efficacy of new antiviral drugs like molnupiravir and paxlovid against SARS-CoV-2. This review discusses the role of vitamin D sufficiency and VDD in COVID-19 initiation and progression, emphasizing the molecular mechanisms by which vitamin D exerts its actions as a proactive step for the next pandemic. However, there is still no clear evidence of vitamin D’s impact on prevention and treatment, leading to contradictory findings. Therefore, large-scale randomized trials are required to reach a definitive conclusion. A bibliometric analysis of publications related to vitamin D, immunity, and COVID-19 revealed a significant increase in research activity in this area, particularly in 2020–2024, underscoring the growing recognition of vitamin D’s potential role in the context of the pandemic.

This study investigated the diagnostic, prognostic, and therapeutic significance of Fc receptor-like 1 (FCRL1) and B-cell activating factor (BAFF) mRNA expression in Egyptian patients with diffuse large B-cell lymphoma (DLBCL) undergoing the standard R-CHOP regimen (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) using quantitative real-time PCR (RT-qPCR). The results demonstrated that FCRL1 and BAFF mRNA expression were significantly elevated in DLBCL patients compared to healthy controls. A strong positive correlation existed between BAFF and FCRL1 expression levels. Diagnostic performance assessed through combined ROC curve analysis revealed that BAFF, FCRL1, and lactate dehydrogenase (LDH) achieved perfect diagnostic accuracy (AUC = 1.0), demonstrating 100% sensitivity, specificity, and predictive values. Further prognostic analysis using COX regression identified elevated FCRL1 expression as the most significant predictor of poor clinical outcomes. Kaplan–Meier survival analysis reinforced this finding, with high FCRL1 expression showing significant associations with reduced overall survival (OS, p = 0.031) and progression-free survival (PFS, p = 0.038). The study underscores the potential utility of BAFF and FCRL1 mRNA as diagnostic markers for DLBCL, with FCRL1 emerging as a promising prognostic marker and potential therapeutic target enabling more tailored treatment approaches for DLBCL, the most common type of B-cell non-Hodgkin lymphoma, and patients receiving R-CHOP therapy.

Sepsis-associated acute kidney injury (S-AKI) represents a significant health problem associated with adverse outcomes. Our study aimed to assess the value of serum cystatin-C (sCysC) and TNF-α (rs361525) in combination for diagnosing S-AKI patients and predicting their adverse outcomes. The study included 100 critically ill neonates and 100 controls. Patients were categorized into an S-AKI group and a non-AKI group. TNF-α (−238, rs361525) genotyping was performed using RT-PCR, and sCysC was assessed using ELISA. Our study showed a fundamental difference in the genotype frequencies of TNF-α (−238, rs361525) and SNP between S-AKI and non-AKI patients. Furthermore, there was a significant relationship between cystatin C and TNF-α (−238, rs361525), where cystatin C was higher in patients with AA alleles than in patients with GA and GG alleles. Combining GA + AA genotypes with elevated serum cystatin-C levels can serve as a potential diagnostic and prognostic biomarker for AKI development in this population. The GA/AA genotypes independently predicted S-AKI risk (OR = 6.64, p < 0.001). At the same time, elevated sCysC (>9.4 mg/L) emerged as a sensitive biomarker (AUC = 0.848) and independent predictor of adverse outcomes. Collectively, these findings contribute to the growing field of personalized medicine and represent a strategic advantage, enabling prevention-focused care rather than the treatment of established disease.

Background/Objectives: Hepatocellular carcinoma (HCC) presents limited therapeutic options for advanced disease, and sorafenib therapy is hampered by significant interpatient heterogeneity in response. This necessitates biomarker-guided strategies to personalize treatment. This study investigated the long noncoding RNAs UCA1 and MALAT1 as pharmacogenomic biomarkers for personalizing sorafenib therapy in advanced HCC. Methods: In a prospective cohort of 154 HCC patients receiving first-line sorafenib (400 mg twice daily), serum lncRNA levels were quantified by RT-qPCR at baseline, Week 4, and Week 12. Expression levels were correlated with treatment response (mRECIST), time-to-progression (TTP), and overall survival (OS). Statistical analyses included Kaplan–Meier estimates, Cox proportional hazards models, and ROC curve analysis. Results: High baseline expression of UCA1 (77.9% of patients) and MALAT1 (73.4%) was associated with aggressive disease. High UCA1 correlated with reduced 12-month survival (60.8% vs. 73.5%, p = 0.026) and shorter median Time-to-Progression (TTP) (18.0 vs. 21.9 weeks, p = 0.002). High MALAT1 was associated with significantly shorter median TTP (18.0 vs. 25.2 weeks, p = 0.003). In multivariable analysis, both lncRNAs were independent prognostic factors for shorter TTP (UCA1: HR = 1.52, p = 0.014; MALAT1: HR = 1.61, p = 0.006). Serial monitoring revealed that a ≥10% rise in either lncRNA by Week 4 predicted a five-fold higher progression risk by Week 12 (52% vs. 10%, p < 0.001), providing a median lead time of 7.0 weeks before radiological confirmation of progression. Conclusions: These findings demonstrate that UCA1 and MALAT1 enable early identification of sorafenib resistance. Baseline stratification and serial monitoring can provide early detection of treatment resistance, informing clinical decision-making and supporting their potential utility for personalizing therapy in advanced HCC.