Background: Klebsiella pneumoniae is one of the most clinically important opportunistic pathogens involved in both community-(CAIs) and hospital-acquired infections (HAIs). The hypervirulent K. pneumoniae (hvKp) responsible for disseminated infections in healthy and immunosuppressed individuals has emerged with considerable ability to get antibiotic resistance as well. We aimed to characterize the virulence genetic profile and resistance phenotypes of the clinical K.pneumoniae isolates at Menoufia University Hospitals (MUHs) by phenotypic and molecular methods. Methods: 84 K.pneumoniae isolates were collected and classified as classic (cKp) or hypermucoviscous (hmvKp) phenotypes by string test. Antimicrobial resistance patterns were determined phenotypically and multiplex PCR verified the existence of some of the suspected virulence genes.Results: Out of 84 K.pneumoniae isolates, 27 (32.1%) had a positive string test and identified as hmvKp. The remaining 57 isolates (67.9%) were string negative and reported as cKp. Higher resistance rates associated with ESβL, AmpC and carbapenemase production were observed in cKp compared to hmvKp particularly those of hospital origin with a significant statistical difference (P

Chronic kidney disease (CKD) is a worldwide public health problem due to its increasing prevalence worldwide. Endoplasmic reticulum (ER) stress has been shown to play a role in the pathogenesis of various renal diseases in humans. It leads to the activation of the unfolded protein response (UPR) which triggers three known trans membrane sensors in the ER: activating transcription factor 6 (ATF6), inositol-requiring enzyme I (IRE1), and PKR (double-stranded RNA-dependent protein kinase)-like ER protein kinase (PERK). The activation of these signal transduction pathways can result in cell death, inflammation, and fibrosis in the context of CKD. The aim of this study was to detect the level of gene expression of activating transcription factor 6 (ATF6), inositol-requiring enzyme I (IRE1), and PKR (double-stranded RNA-dependent protein kinase)-like ER protein kinase (PERK) in chronic kidney disease patients. This study was carried out on eighty subjects, 50 patients with CKD (25 with hypertension and 25 without hypertension) and 30 healthy subjects served as controls. All studied subjects underwent laboratory investigations, including CBC, Serum Lipid profile: Total cholesterol, Triglycerides, HDL-cholesterol and LDL-cholesterol, liver and kidney functions, fasting and 2 h postprandial blood glucose and HbA1C, serum level of IL6 and gene expression of ATF6, IRE1 and PERK using real time PCR technique. There was a significant increase in relative quantitation (RQ) of gene expression of IRE1, ATF6 and PERK in chronic kidney patient groups with hypertension and without hypertension compared to control group. Also, there was a significant positive correlation of PERK and ATF6 gene expressions and a significant negative correlation of PERK gene expressions and GFR in groups I&II. Endoplasmic reticulum (ER) stress occurs in CKD with activation of gene expression of three trans-membrane sensors in the ER: activating transcription factor 6 (ATF6), inositol-requiring enzyme I (IRE1), and PKR (double-stranded RNA-dependent protein kinase)-like ER protein kinase (PERK).

Background: Hepatocellular carcinoma (HCC) is the most common histologic type of primary liver cancers worldwide. Hepatitis C virus (HCV) infection remains a major risk factor for chronic liver disease, cirrhosis, and HCC. To understand the molecular pathogenesis of HCC in chronic HCV infection, many molecular markers are extensively studied, including long noncoding RNAs (lncRNA). Objective: To evaluate the expression levels of lncRNAs (LINC01564, RAMS11), CBX4, and TOP2A in patients with chronic HCV infection and patients with HCC on top of chronic HCV infection and correlate these levels with the clinicopathological features of HCC. Subjects and Methods: One hundred and fifty subjects were enrolled in this study and divided into three groups: group I included 50 patients with HCC on top of chronic hepatitis C (CHC), group II included 50 patients with CHC only, and group III included 50 healthy individuals as a control group. LncRNAs relative expression level was determined by RT-PCR. Results: lncRNA (LINC01564, RAMS11), CBX4, and TOP2A relative expression levels were upregulated in both patient groups compared to controls (p < 0.001*), with the highest levels in the HCC group compared with the CHC group. Additionally, these levels were significantly positively correlated with the clinicopathological features of HCC. Conclusions: The lncRNA (LINC01564, RAMS11), CBX4, and TOP2A relative expression levels were upregulated in CHC patients—in particular, patients with HCC. Thus, these circulatory lncRNAs may be able to serve as promising noninvasive diagnostic markers for HCC associated with viral C hepatitis.

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: Pseudomonas aeruginosa is an opportunistic microorganism and quite frequently associated with skin infections. Biosynthesized silver nanoparticles can be a promising key to eliminate these microbes. Objectives: The current work aims to identify P. aeruginosa carrying metallo-β-lactamase from burn infections and assess the impact of silver nanoparticles and antibiotics on them. Methods: A total of 120 samples collected from patients suffering from burn wound infections were subjected to conventional microbiological techniques to identify P. aeruginosa isolates. Testing for antimicrobial susceptibility was conducted utilizing the Kirby Bauer disc diffusion method. Carbapenemase-producing strains were detected both phenotypically by detecting metallo-beta-lactamases through performing modified carbapenem inactivation method (mCIM) and genotypically using PCR. Using the agar well diffusion method, AgNPs' antibacterial activity was assessed. The synergistic effect of a combination of antimicrobials (colistin, gentamicin, and ciprofloxacin) and AgNPs was estimated by the checkerboard method. Results:Out of 120 isolates, 46 (38%) P. aeruginosa isolates were identified and confirmed by PCR assay. Total 25 isolates (54%) were multidrug resistant isolates. Modified carbapenem inactivation method showed that 39 isolates (84.78%) were producing carbapenemases whereas 35 isolates (76%) were confirmed for carbapenemases by performing PCR. The prevalence of carbapenemase encoding genes was as follows blaSPM (14%), blaVIM (25.7%), blaNDM (40%), blaKPC (2.85%) and blaIMP (17%). Conclusions: P. aeruginosa isolates showed high-level carbapenem resistance. The majority of the isolates were multi drug resistant (MDR), indicating a concerning spread of resistant isolates. AgNPs exhibited considerable antibacterial effects, so they should be considered as an effective means of combating MDR.

The incidence of fungal infections, particularly those caused by Candida species, has significantly risen among immunocompromised patients in recent years. Aim: This study evaluated the species distribution, antifungal susceptibility patterns, and virulence gene profiles of Candida species isolated from critically ill ICU patients while comparing the diagnostic performance of conventional phenotypic isolation media with molecular genotypic identification methods. Materials and Methods: A total of 211 clinical specimens were obtained from 200 hospitalized patients at Menoufia University Hospitals, Egypt. Candida species were phenotypically identified using cornmeal agar supplemented with Tween 80 (CTA) and CHROMagar^TM Candida (CMA) and were molecularly confirmed at the species level by sequencing PCR-amplified ITS regions. Antifungal susceptibility profiles to fluconazole, voriconazole, and amphotericin B were evaluated using the disk diffusion method. Furthermore, real-time PCR was deployed to detect genes encoding adherence factors and Secreted Aspartyl Proteinase. Results: Candida species were recovered from 45 out of 211 clinical specimens. The most frequently isolated species was Candida albicans (15/45, 33.3%), followed by C. parapsilosis (9/45, 20.0%), C. glabrata (7/45, 15.5%), C. tropicalis (7/45, 15.5%), C. krusei (4/45, 8.8%), and C. famata (3/45, 6.7%). Among the recovered Candida isolates, the percentage rates of the ALS1, ALS3, HWP1, and SAP4 genes were 40%, 42.22%, 44.4%, and 37.78%, respectively. HWP1 was the most frequently detected pathogenicity factor, whereas SAP4 was the least prevalent. Conclusions: In the studied immunocompromised cohort, non-albicans Candida species constituted a substantial proportion of clinical isolates. Notable antifungal resistance patterns were also observed, emphasizing the value of integrated phenotypic and genotypic identification for tailored management. Furthermore, virulence-associated genes (ALS1, ALS3, HWP1, and SAP4) were detected in isolates of several Candida species, highlighting their presence in clinical strains.