Nazefah Abdul Hamid

Nesfatin-1, a peptide derived from nucleobindin-2, regulates feeding, stress, and sleep–wake processes. To date, the available information suggests that nesfatin-1 is involved in stress regulation and colocalises with substances that influence cortisol, but the circadian interplay between nesfatin-1 and cortisol remains poorly defined. This review integrates biological timing, tissue-specific actions of the hypothalamic–pituitary–adrenal axis, and circadian misalignment, and is supported by in silico protein-association analysis. A structured database search retained relevant studies published from January 2006 to March 2026; heterogeneity necessitated narrative synthesis. Rodent experiments support effects of central NUCB2/nesfatin-1 on feeding and HPA-axis activation. Murine corticotroph experiments report increased POMC abundance, whereas an H295R human adrenocortical carcinoma-cell study reports reduced cortisol content and stimulated release. These findings concern different experimental systems and do not demonstrate coordinated central–adrenal regulation in vivo. The network analysis identified NPY and POMC as prominent nodes within the predefined candidate network, with enrichment of feeding- and HPA-axis-related pathways. Given the biologically targeted selection of input genes, these findings are interpreted as hypothesis-generating associations rather than independent confirmation of a regulatory mechanism. Within the literature examined in this review, direct evidence characterising the 24 h temporal profile of nesfatin-1 in humans, its phase relationship with cortisol, and potential alterations during circadian misalignment was not identified. This apparent evidence gap warrants further investigation through controlled, time-resolved human studies.

Shift workers are commonly associated with circadian misalignment due to irregular working hours, which often leads to poor sleep quality and is associated with HPA axis misalignment and changes in cardiovascular outcome. Background: This systematic review aimed to investigate the association between cortisol production and cardiovascular health with sleep quality in healthcare shift workers. Methods: A comprehensive search of PubMed, Web of Science, and Scopus was conducted for studies published between 2010 and 2025, according to PRISMA guidelines. Fourteen studies met the inclusion criteria. Results: Among the included studies, eight studies focused on the relationship between sleep quality and cortisol regulation, five studies investigated the link between sleep quality and cardiovascular health, and one study examined sleep quality, cortisol regulation, and cardiovascular outcome. A significant relationship between cortisol and sleep quality was observed, as lower cortisol levels upon awakening were associated with low sleep quality. Several studies reported that sleep disturbances were associated with adverse cardiovascular outcomes, including reduced heart rate variability (HRV) and increased risk of metabolic syndrome. Conclusions: This review highlights existing literature on the critical role of sleep quality as a key factor in cortisol level and cardiovascular health in shift workers, along with the factors influencing circadian rhythm.

Background/Objectives: The global high prevalence of cardiovascular diseases (CVDs) is attributed to the high prevalence of obesity and metabolic syndrome. However, the impact of a high-fat diet (HFD) on the expression of genes in cardiac tissue remains poorly understood. Methods: A thorough literature search was performed using PubMed, Scopus, EBSCOhost, and ScienceDirect databases. The Medical Subject Heading (MeSH) terms such as “high-fat diet”, “gene expression” and “cardiac tissue” were used as the keywords in all fields. Results: A total of 1608 studies were retrieved, and only in vivo experimental studies to identify cardiac tissues differentially expressed genes (DEGs) or proteins (DEPs) in rodents fed with HFD were selected. After screening, 14 studies were selected, 159 DEGs and DEPs were extracted from the data and further analysis was conducted employing DAVID, STRING, and Cytoscape 3.10.3 software. A protein–protein interaction (PPI) network revealed a total of 159 genes and proteins from the selected DEGs containing 100 nodes and 292 edges with a PPI enrichment p-value of < 1.0 × 10⁻¹⁶ and an average local clustering coefficient of 0.447 with an average node degree of 5.84. Six significant clusters with high intermolecular interactions from the protein–protein interaction (PPI) network complex reveal significant molecular pathways, including the glucose metabolic process, fatty acid metabolic process, and inflammatory response (p < 0.05). Conclusions: The identification of the critical link between obesity and HFD-induced CVDs in cardiac tissue highlights the need for a deeper understanding of the molecular mechanisms controlling gene expression in cardiac tissue.

The inability to accurately predict the occurrence of postoperative cognitive dysfunction (POCD) among open-heart surgery patients leads to concerning increases in POCD cases. Preoperative circulating biomarkers are important to identify as they are non-invasive and could provide an early prediction of POCD development, allowing for earlier and more strategized interventions. However, to date, no robust circulating biomarkers have proven effective for preoperative POCD prediction. This systematic review aims to synthesize current evidence on preoperative protein profiling among POCD patients following open-heart surgery. Thus, a thorough literature search employing PubMed, EBSCOhost, Scopus, and Science Direct was carried out. This combination of keywords was used as part of the search strategy: (“Postoperative cognitive decline” OR “Postoperative cognitive disorders” OR “Postoperative cognitive dysfunction” OR “Postoperative cognitive complications”) AND (“Thoracic Surgery” OR “Cardiac Surgery” OR “Heart Surgery”) AND (“Protein expression” OR proteomic OR “Protein profiling”). Eight hundred and twenty-nine studies were retrieved and only clinical studies reporting the circulating preoperative differentially expressed Proteins (DEPs) in the POCD patients were selected. Six studies were selected following the inclusion and exclusion criteria. Only one preoperative DEP and four immediate postoperative DEPs were extracted from the studies. All four proteins were selected for analysis using DAVID, STRING, and Cytoscape software. Due to the very low number of proteins, no clusters have been identified. This systematic review demonstrates the lack of POCD preoperative biomarkers for open-heart-surgery patients. Thus, it is suggested that more studies can be conducted to fill this gap.

Purpose: Intestinal fibrosis is a common complication of inflammatory bowel diseases. However, the possible involvement of epithelial-mesenchymal transition (EMT) has been scarcely investigated. This systematic review aims to search through research papers that are focusing on messenger RNA (mRNA) and protein expression profile in EMT in fistula or in intestinal fibrosis.Methods: Electronic exploration was performed until April 24, 2019 through PubMed, Ovid, Science Direct, and Scopus databases with the terms of “fistula” OR “intestinal fibrosis” AND “epithelial-mesenchymal transition”. Two independent reviewers scrutinized the suitability of the title and abstract before examining the full text that met the inclusion criteria. For each study, the sample types that were used, methods for analysis, and genes expressed were identified. The list of genes was further analyzed using DAVID (Database for Annotation, Visualization, and Integrated Discovery) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway.Results: There were 896 citations found; however, only 3 studies fulfilled the requirements. Among the EMT-related genes, 5 were upregulated genes at mRNA level while 6 were at protein level. However, only 2 downregulated genes were found at each mRNA and protein level. Of the 4 inflammation-related genes found, 3 genes were upregulated at mRNA level and 1 at protein level. These genes were confirmed to be involved in the development of inflammatory induced fibrosis and fistula through EMT. Results from quantitative real-time polymerase chain reaction analysis were consistent with the process of EMT, confirmed by the western blot protein analysis.Conclusion: Many significant genes which are involved in the process of EMT in fistula and intestinal fibrosis have been identified. With high-end technology many more genes could be identified. These genes will be good molecular targets in the development of biomarkers for precision drug targeting in the future treatment of intestinal fibrosis and fistula.

Cervical cancer is the leading cause of cancer-related death among women in developing countries. However, no comprehensive molecular mechanism for cervical cancer has been established, as many studies were small-cohort studies conducted with small sample sizes. A thorough literature search was performed using the PubMed, Scopus, EBSCOhost, and Science Direct databases. Medical Subject Heading (MeSH) terms such as “Uterine Cervical Neoplasms” and “gene expression” were used as the keywords in all fields. A total of 4027 studies were retrieved, and only clinical studies, which used the microarray method to identify differentially expressed genes (DEGs) in the cervical tissue of cervical cancer patients, were selected. Following the screening, 6 studies were selected and 1128 DEGs were extracted from the data. Sixty-two differentially expressed genes from at least two studies were selected for further analysis by DAVID, STRING, and Cytoscape software. In cervical cancer pathogenesis, three significant clusters with high intermolecular interactions from the Protein–Protein Interaction (PPI) network complex revealed three major molecular mechanisms, including cell signaling, cell cycle, and cell differentiation. Subsequently, eight genes were chosen as the candidate genes based on their involvement in the relevant gene ontology (GO) and their interaction with other genes in the PPI network through undirected first neighbor nodes. The present systematic review improves our understanding of the molecular mechanism of cervical cancer and the proposed genes that can be used to expand the biomarker panel in the screening for cervical cancer. The targeted genes may be beneficial for the development of better treatment strategies.

Postoperative cognitive dysfunction (POCD) is cognitive decline after surgery. The authors hypothesized that gene-level changes could be involved in the pathogenesis of POCD. The present study evaluated the incidence of POCD and its associated differentially expressed genes. This was a prospective cohort study conducted on high-risk coronary artery bypass graft patients aged 40 to 75 years. POCD classification was based on a one standard deviation decline in the postoperative scores compared to the preoperative scores. The differentially expressed genes were identified using microarray analysis and validated using quantitative RT-PCR. Forty-six patients were recruited and completed the study. The incidence of POCD was identified using a set of neurocognitive assessments and found to be at 17% in these high-risk CABG patients. Six samples were selected for the gene expression analyses (3 non-POCD and 3 POCD samples). The findings showed five differentially expressed genes in the POCD group compared to the non-POCD group. The upregulated gene was ERFE, whereas the downregulated genes were KIR2DS2, KIR2DS3, KIR3DL2, and LIM2. According to the results, the gene expression profiles of POCD can be used to find potential proteins for POCD diagnostic and predictive biomarkers. Understanding the molecular mechanism of POCD development will further lead to early detection and intervention to reduce the severity of POCD, and hence, reduce the mortality and morbidity rate due to the condition.

Human papillomavirus type 16 (HPV-16) is a well-known etiological factor for cervical and oropharyngeal cancers. The E2 protein, the product of an early-transcribed gene in HPV–16, is postulated to cause the death of cancerous cells via p53-dependent and p53-independent pathways. The main aim of the present systematic review was to study the HPV 16-E2 protein as an apoptosis-inducer agent. A thorough search of MEDLINE/PubMed, Science Direct, Scopus, and EBSCOhost databases was conducted for relevant studies on HPV AND apoptosis OR cell death where HPV 16-E2 was involved. The search identified 967 publications. Eleven records dated from 1 January 1997 to 16 February 2022 were found to meet the inclusion criteria and were eligible for data extraction and inclusion. All studies concluded that HPV 16-E2 was able to induce cell death in transfected cells. E2 proteins from the high-risk HPV–16 were able to induce apoptosis through different apoptotic pathways depending on the location of the expressed gene. However, the mechanism was still unclear, and further studies are warranted.

Cancer increases the global disease burden substantially, but it remains a challenge to manage it. The search for novel biomarkers is essential for risk assessment, diagnosis, prognosis, prediction of treatment response, and cancer monitoring. This paper examined NEDD8 ultimate buster-1 (NUB1) and F-adjacent transcript 10 (FAT10) proteins as novel biomarkers in cancer. This literature review is based on the search of the electronic database, PubMed. NUB1 is an interferon-inducible protein that mediates apoptotic and anti-proliferative actions in cancer, while FAT10 is a ubiquitin-like modifier that promotes cancer. The upregulated expression of both NUB1 and FAT10 has been observed in various cancers. NUB1 protein binds to FAT10 non-covalently to promote FAT10 degradation. An overexpressed FAT10 stimulates nuclear factor-kappa β, activates the inflammatory pathways, and induces the proliferation of cancer. The FAT10 protein interacts with the mitotic arrest deficient 2 protein, causing chromosomal instability and breast tumourigenesis. FAT10 binds to the proliferating cell nuclear antigen protein and inhibits the DNA damage repair response. In addition, FAT10 involves epithelial–mesenchymal transition, invasion, apoptosis, and multiplication in hepatocellular carcinoma. Our knowledge about them is still limited. There is a need to further develop NUB1 and FAT10 as novel biomarkers.