Apoptosis is a finely regulated physiological process responsible for keeping tissue homeostasis by removing damaged, abnormal, or unnecessary cells. Disruption of apoptotic pathways is a hallmark of cancer, enabling malignant cells to evade programmed cell death and continue their uncontrolled proliferation. Survivin, the minimum member of the inactivating protein (IAP) inhibitor family, has emerged as a key regulator of both apoptosis inhibition and cell cycle progression. Because of its marked overexpression in a wide range of human malignancies and its limited expression in most normal adult tissues, Survinin has garnered significant attention as a potential diagnostic, prognostic, and therapeutic biomarker. This review aims to summarize and evaluate current evidence regarding the biological functions of Survinin, its role in cancer development and progression, and its clinical significance in predicting treatment response and patient outcomes. Relevant scientific literature published in peer-reviewed journals was collected and analyzed using major biomedical databases, including PubMed, Scopus, and Web of Science. Studies concerning the expression of the servifin protein, its molecular mechanisms, its predictive value, and its therapeutic targeting in various types of cancer were reviewed and summarized. The reviewed evidence indicates that elevated survivin protein expression is strongly associated with tumor aggressiveness, resistance to chemotherapy and radiotherapy, poor disease prognosis, and reduced survival rates in multiple cancer types. Furthermore, its selective expression pattern and multifunctional role make survinin an gorgeous target for developing novel cancer control strategies. The present review highlights the growing importance of incorporating survivin protein assessment into cancer research and clinical practice and supports further research into survivin-targeting approaches to improve cancer prognosis, prognosis, and treatment outcomes.
Antimicrobial resistance (AMR) in Escherichia coli (E. coli) significantly compromises global healthcare, driving up morbidity and mortality through severe urinary tract, bloodstream, and gastrointestinal infections. While conventional antimicrobial susceptibility testing (AST) remains highly reliable, its prolonged incubation periods (18–24 hours) delay critical clinical decisions. This review systematically evaluates and compares traditional methods with rapid phenotypic, molecular, and emerging diagnostic technologies. Our comparative analysis indicates that automated phenotypic systems (e.g., VITEK 2) and MALDI-TOF mass spectrometry substantially accelerate time-to-result, reducing turnaround times to 4–8 hours and <4 hours, respectively, while maintaining over 92% sensitivity. Furthermore, molecular assays like real-time PCR provide ultimate specificity (>99%) within 1–4 hours. Despite challenges such as high initial costs and technical complexity, integrating these rapid diagnostics into clinical workflows is essential for guiding targeted antibiotic therapy, reducing broad-spectrum misuse, and fortifying global antimicrobial stewardship.
The aromatic plant Lallemantia royleana which is typically named as balangu in the Lamiaceae family. It is an abundant source of biologically active compounds such as terpenoids. Owing to the expanding attention in its phytochemical profile and prospective pharmacological effects, the current review aims to summarize some of crucial compounds in essential oil of Lallemantia royleana. A narrative literature search was conducted using PubMed, Scopus, Web of Science, and Google Scholar with the keywords "Lallemantia royleana", "essential oil", "GC-MS", "volatile compounds", and "biological activities" covering studies published between 2003 and 2025.The present research was reviewed to detect the main volatile oil chemicals and outline their documented pharmacological properties. The reviewed research frequently identified some of crucial chemicals which are classified as oxygenated terpenoids and are found majorly in the essential oils of Lallemantia royleana (e.g., trans-pinocarvyl acetate, pinocarvone, verbenone, and β-citral). They are assumed to play a part in the herb antioxidant, antimicrobial (antifungal and antibacterial), and sedative properties. However, the biological participation of single chemical and their prospective synergistic interplay are still to be described. The evidence outlined in the current review is mainly obtained from phytochemical analysis of essential oil in the plant (GC/MS) and in vitro experimental study. This review has some restrictions such as its narrative pharmacological activity according to data collected from previously published studies, the reviewed approach, the lack of a systematic literature selection, selection method, and the small number of available researches. Overall, the existing evidence indicates that Lallemantia royleana essential oil is an encouraging source of biologically active compounds with prospective therapeutic and industrial utilizations. However, more consistent phytochemical assessments and properly structured clinical research are needed to validate its effectiveness and safety profile.
The gut microbial community, composed of trillions microorganisms residing within the gastrointestinal route, is increasingly recognized as a vital regulator of host physiology. It plays a pivotal role in digestion, immune system modulation, and systemic metabolism. Emerging evidence has established strong links between gut microbiota composition with cardiovascular health, suggesting that microbial imbalances may contribute to the development and development of heart diseases. This review article aims to provide an integrated overview of the mechanistic metabolic and immunological links between the gut microbiome and cardiovascular diseases. Unlike previous reviews, it synthesizes current knowledge regarding the relationship between the gut microbiome and cardiovascular disease, with a specific focus on microbial metabolites like trimethylamine-N-oxide (TMAO) and short-chain fatty acids (SCFAs), which affect systemic inflammation, lipid metabolism, endothelial function, and thrombosis, causing central and cardiovascular disease pathogenesis. The methodology involves a comprehensive analysis of peer-reviewed literature from multiple scientific databases used in the primary research, as well as targeted and untargeted mass spectrometry for metabolite quantification. Mechanistic insights from both clinical trials and preclinical studies—particularly those involving germ-free and antibiotic-treated animal models—are examined to understand causal pathways. Furthermore, the review evaluates intervention strategies aimed at modulating the gut microbiota to improve cardiovascular outcomes. These include dietary approaches like probiotics and prebiotics, and fecal microbiota transplantation (FMT). It also highlights the microbiome role for further therapeutic approaches. By integrating molecular, clinical, and experimental evidence, the gut microbiome considered as novel and promising target of cardiovascular diseases prevention and treatment.
DNA replication, repair, and cell division are controlled by cell-cycle checkpoints to maintain genomic integrity. To survive replication and oncogenic stress, cancer cells selectively lower checkpoint barriers while preserving others. We study cell-cycle checkpoint molecular architecture in various cancers, focusing on CDK regulation, ATM/ATR–CHK signaling, and replication stress responses. A thorough literature review included checkpoint dysregulation, treatment inhibition, and resistance. Post-p53 G1/S inactivation showed that cancer cells needed S and G2/M checkpoints to survive. In highly proliferative, p53-deficient tumors, ATR, CHK1, or WEE1 suppression caused replication fork failure and mitotic catastrophe. ATR/CHK1 inhibitors doubled DNA damage indicators such γH2AX in replication-stressed cells, whereas CDK4/6 inhibitors reduced tumor growth by 60-70% in RB-proficient tumors. New study shows that HDAC activity and histone acetylation affect checkpoint activation and treatment responsiveness. Molecularly, epigenetic regulation and checkpoint biology support appropriate combination therapy. This study reveals that checkpoint dependency is a common cancer weakness that might be exploited for more selective and effective anticancer drugs.
