Journal of Current Biomedical Reports (J Curr Biomed Rep)
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Targeted mechanisms and novel therapeutic strategies against extended-spectrum beta-lactamases: From precise detection to intelligent management of bacterial resistance
Full text linkExtended-spectrum beta-lactamases (ESBLs) are enzymes that resist beta-lactam antibiotics, including penicillins, cephalosporins, and carbapenems, and are produced by a variety of bacteria, including Escherichia coli and Klebsiella pneumoniae. Since ESBLs are often plasmid-borne, antibiotic resistance can spread across bacteria due to their ease of transfer. The intricate structure of ESBLs changes based on the type of bacterium that produces them. However, they all share a beta-lactamase core structure. ESBLs act by hydrolyzing the beta-lactam ring of antibiotics thereby rendering them ineffective. Detection of ESBL-producing bacteria is very important for effective treatment of infections. These enzymes can be identified through various diagnostic methods, such as phenotypic tests and molecular assays. The most common diagnostic method is an antimicrobial susceptibility test, which involves testing bacterial sensitivity to different antibiotics. Furthermore, the use of molecular testing techniques like polymerase chain reaction is growing in the identification of ESBLs. This paper provides a summary of ESBLs, including their structure, function, and diagnostic methods. Thus, it is critical to comprehend ESBLs in order to create therapies that effectively address illnesses brought on by bacteria that produce ESBL
Molecular mechanism linking sleep disturbances to neurodegenaration
Full text linkSleep disturbances are increasingly recognized as both early indicators and potential contributors to the progression of neurodegenerative diseases. Disrupted sleep compromises glymphatic clearance and synaptic homeostasis, promoting the accumulation of neurotoxic proteins such as amyloid-β, tau, and α-synuclein. Concurrently, irregular sleep patterns and circadian rhythm disturbances activate neuroinflammatory pathways, including microglial activation, NF-κB signaling, and the NLR family pyrin domain containing 3 (NLRP3) inflammasome, thereby accelerating neuronal damage. Additional mechanisms, such as mitochondrial dysfunction, oxidative stress, and imbalances in neurotransmitter systems including orexin and melatonin, further reinforce the bidirectional relationship between sleep impairment and neurodegeneration. Despite these insights, critical gaps remain, particularly the absence of reliable biomarkers for simultaneously assessing sleep quality, neuroinflammation, and disease progression, as well as limited research on disorders beyond Alzheimer’s and Parkinson’s disease. Therapeutic strategies show promise, ranging from pharmacological interventions targeting inflammatory pathways to non-pharmacological approaches such as chronotherapy, light therapy, and cognitive behavioral therapy for insomnia. Emerging modalities, including RNA-based therapies targeting pathogenic proteins and artificial intelligence (AI) for early detection and personalized treatment of sleep abnormalities, offer novel opportunities for intervention. This narrative review explores the molecular mechanisms underlying sleep disturbances in neurodegenerative diseases, identifies critical gaps in current research, and discusses emerging therapeutic strategies aimed at mitigating sleep-related neurodegeneration
Integron profiles and sulfonamide resistance genes in Klebsiella pneumoniae isolated from diabetic patients with urinary tract infection
Full text linkKlebsiella pneumoniae is an opportunistic pathogen and an important cause of pneumonia, bacteremia and urinary tract infection (UTI). K. pneumoniae infection is historically associated with diabetes. Therefore, the aim of the present study was to determine the Integron types and sulfonamide resistance genes in K. pneumoniae isolated from diabetic patients with urinary tract infection. In this descriptive-cross-sectional study, 90 K. pneumoniae isolates were collected from urine samples of diabetic patients. Antibiotic susceptibility testing was performed using disk diffusion methods. Detection of the sulfonamide resistance determinants and integron types were carried out through PCR. In this study, 90 K. pneumoniae isolates were obtained from diabetic patients with UTI, with a mean age of 69.8 ± 9.2 years; 58.9% were female. Antibiotic resistance was highest to gentamicin (70%) and ceftriaxone (65.5%), and lowest to imipenem (32.2%), with significant resistance also observed to trimethoprim-sulfamethoxazole (50%). Among the isolates, sul1 (91.8%) and intI (67%) were the most prevalent resistance genes followed by dfrA1 (63%) and sul2 (52%). The dfrA5 gene was not detected in any of the isolates. The predominance of sul1 and class I integrons among K. pneumoniae isolates from diabetic patients with UTI underscores their key role in the spread of multidrug resistance. These findings emphasize the importance of targeted antimicrobial stewardship, infection control, and monitoring strategies to prevent treatment failure in this high-risk population
Impact of genetic variants on outcomes in ICU patients with acute respiratory failure syndromes
Full text linkAcute respiratory failure (ARF) and acute respiratory distress syndrome (ARDS) represent major causes of morbidity and mortality in the intensive care unit (ICU). Although clinical triggers such as pneumonia, sepsis, trauma, and viral infections are well characterized, substantial inter-individual variability in disease susceptibility, severity, and treatment response suggests an important contribution of genetic factors. Emerging evidence from genome-wide association studies, polygenic analyses, and sequencing of rare variants highlights key pathways including endothelial barrier regulation, innate immunity, and inflammatory signaling that shape host responses during critical illness. Pharmacogenomic studies further indicate that genetic variation influences responses to sedatives, corticosteroids, and other ICU therapies, although clinical translation remains limited. Environmental exposures and critical care interventions interact with inherited variation, emphasizing the multidimensional nature of ARF. This review synthesizes current knowledge on genetic determinants of ARF and ARDS, examines their relationship with clinical outcomes in the ICU, and outlines how gene-environment interactions and pharmacogenomics contribute to treatment heterogeneity. Despite promising discoveries, major gaps persist, including limited ancestry diversity, modest effect sizes, and scarce genotype-informed interventional trials. A deeper integration of genomics with multi-omics profiling and clinical phenotyping is essential to advance precision medicine approaches for critically ill patients
Lung cancer and the microbiome: Key bacterial players in carcinogenesis and therapy
Full text linkLung cancer remains the leading cause of cancer-related mortality worldwide, with non–small cell lung cancer (NSCLC) constituting the majority of cases. Despite therapeutic advances in chemotherapy, targeted therapy, and immune checkpoint inhibitors (ICIs), treatment outcomes remain heterogeneous. Increasing evidence indicates that the human microbiome including the respiratory, gut, and intratumoral compartments plays a crucial role in lung carcinogenesis and therapeutic response. This narrative review synthesizes recent findings on the microbiome’s contribution to lung cancer biology and therapy. The healthy lung microbiota is characterized by low biomass yet consistent phyla composition, primarily Bacteroidetes and Firmicutes, while dysbiosis in lung cancer often features enrichment of Streptococcus, Veillonella, Prevotella, Haemophilus, and Fusobacterium. These taxa may drive carcinogenesis through immune modulation, chronic inflammation, metabolic signaling, and genotoxic or epigenetic alterations. Beyond the lung, gut microbial diversity and metabolites such as short-chain fatty acids (SCFAs) influence systemic immunity and modulate response to chemotherapy, targeted agents, and ICIs. Antibiotic-induced dysbiosis has been linked to reduced immunotherapy efficacy and shorter progression-free survival in NSCLC cohorts. Emerging microbiome-modulation strategies including probiotics, prebiotics, dietary interventions, fecal microbiota transplantation (FMT), and engineered bacterial therapeutics show promise as adjuncts to precision oncology. However, safety, reproducibility, and mechanistic causality remain major challenges. Collectively, evidence supports the microbiome as a dynamic regulator of lung cancer progression and therapy responsiveness. Future research should prioritize longitudinal, multi-omics investigations and controlled clinical trials to identify predictive microbial biomarkers and develop standardized, personalized microbiome-based interventions for lung cancer management
The CRISPR‒Cas9 system for genome editing of the ASS1 gene in human cells to predict its effect on HSV-1 replication
Full text linkHerpes simplex virus type 1 (HSV-1) is a highly contagious pathogen that establishes lifelong latent infections. The replication of HSV-1 is potentially influenced by the arginine succinate synthase (ASS1) gene, a key regulator of cellular metabolism. This study utilized the CRISPR–Cas9 genome editing platform to specifically target and disrupt the ASS1 gene to examine its effect on viral propagation. A guide RNA (gRNA) was designed to complement a sequence within the ASS1 gene. A donor plasmid and the pCas-guide plasmid were cloned and cotransfected into the human embryonic kidney (HEK) cells with sheared adenovirus (Ad)5 DNA (HEK293-AD) cells. Potential ASS1-knockout clones were identified and validated via polymerase chain reaction (PCR) and DNA sequencing analysis. The impact on HSV-1 replication was quantified via a plaque assay to determine the viral titer. Sequencing data from ASS1-gRNA/Cas9-treated cells did not confirm successful gene knockout, as the intended ASS1 disruption was not achieved. The viral titer did not significantly differ between the HSV-1 infection group (MOI=0.01) and the control group. These findings indicate that the single gRNA designed for this study lacked sufficient specificity to elicit a CRISPR-Cas9-mediated gene knockout. Therefore, employing a set of more specific gRNAs is recommended to increase targeting efficiency. Further investigations are needed to elucidate the desired genetic modification and observe its subsequent effects on HSV-1
Concurrent EGFR and KRAS mutations in non-small cell lung cancer: Challenging the paradigm of linear targeted therapy
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Impact of hepatitis B and C virus on chronic spontaneous urticaria; potential pathogenic triggers and aggravating factors
Full text linkChronic urticaria (CU) is a common dermatological condition characterized by persistent wheals lasting more than six weeks. Chronic spontaneous urticaria (CSU), the most prevalent CU subtype, significantly impairs patients\u27 quality of life. Although its precise pathogenesis remains unclear, current evidence implicates multiple factors including immune dysregulation, stress, certain medications, and viral infections in its development and exacerbation. Among infectious triggers, hepatitis B (HBV) and C (HCV) viruses have emerged as potential CSU inducers. These viruses may trigger urticarial symptoms through various mechanisms, particularly immune system activation and cutaneous inflammatory responses. While the exact pathogenic pathways require further elucidation, clinical evidence suggests antiviral therapy may occasionally improve urticarial symptoms. Standard management of virus-associated CSU involves second-generation antihistamines as first-line treatment. For refractory cases, targeted therapies like omalizumab may be considered. Notably, successful HCV eradication has in some cases led to significant CSU improvement, an effect less frequently observed with HBV treatment. This study investigates the association between hepatitis infections and CSU, focusing particularly on elucidating how HBV and HCV could contribute to CSU pathogenesis
Frequency of using complementary herbal medicines among Helicobacter pylori-infected patients in the North of Iran
Full text linkHelicobacter pylori is a prevalent infection and one of the most critical factors that result in gastric cancer. Besides antibiotic therapy, some plants are suitable as an alternative treatment against H. pylori infection due to their role in protecting the gastric mucosa. This study investigated the frequency of using complementary herbal medicines among H. pylori-infected patients in the North of Iran. This cross-sectional study was conducted on 390 patients with H. pylori infection undergoing treatment in Rasht, Iran, 2022. The demographic data, clinical characteristics, and consumption of complementary herbals were recorded. The mean age of the patients was 40 years, and 63.6% were female. The majority of the patients were educated. About 55.9% of patients consumed at least one herbal product, and the most consumed herbal product was mint extract. Most patients purchased herbal products from the grocery (93.1%); none referred to the pharmacy. About 89.2% of the patients recovered completely, and 10.8% had a disease recurrence. No particular complications were observed in most patients (97.7%). However, no significant association between the consumption of herbal products and patients\u27 recovery was reported (P>0.05). According to our results, consuming herbal products results in no specific improvement in patients with H. pylori infection
Assessment of tobacco and substance use among patients with aluminum phosphide poisoning: A register-based study
Full text linkAluminum phosphide (AlP) poisoning is a major public health concern in several low- and middle-income countries due to its high fatality rate and widespread availability. While its clinical toxicity is well-documented, limited research exists on behavioral risk factors such as tobacco and illicit drug use among affected individuals. This study aimed to assess the prevalence of tobacco and substance use among patients with AlP poisoning and explore its associations with demographic characteristics, clinical outcomes, and mortality. A descriptive cross-sectional study was conducted at Razi Hospital in northern Iran between March 2018 and March 2022. Data from 481 AlP poisoning cases were retrospectively analyzed using structured questionnaires, medical records, and interviews. Sociodemographic variables, substance use history, and clinical outcomes were assessed. Of the 481 patients, 29.7% (n = 143) reported tobacco or illicit substance use. Substance use was significantly more prevalent among males (92.3%), individuals aged 21–40, the self-employed, singles, and those with economic hardship or concurrent alcohol consumption (P < 0.05). Although not statistically significant (P = 0.132), mortality was higher among substance users (46.2%) compared to non-users (38.8%). Tobacco and illicit drug use are common among AlP poisoning patients and are strongly associated with specific sociodemographic factors. Although causality could not be established, substance use may contribute to poorer clinical outcomes. These findings underscore the importance of integrating behavioral screening into AlP poisoning management and highlight the need for targeted prevention strategies in high-risk populations