British Journal of Biomedical Science最新文献

Generative Artificial Intelligence (GenAI) is rapidly transforming the landscape of higher education, offering novel opportunities for personalised learning and innovative assessment methods. This paper explores the dual-edged nature of GenAI's integration into educational practices, focusing on both its potential to enhance student engagement and learning outcomes and the significant challenges it poses to academic integrity and equity. Through a comprehensive review of current literature, we examine the implications of GenAI on assessment practices, highlighting the need for robust ethical frameworks to guide its use. Our analysis is framed within pedagogical theories, including social constructivism and competency-based learning, highlighting the importance of balancing human expertise and AI capabilities. We also address broader ethical concerns associated with GenAI, such as the risks of bias, the digital divide, and the environmental impact of AI technologies. This paper argues that while GenAI can provide substantial benefits in terms of automation and efficiency, its integration must be managed with care to avoid undermining the authenticity of student work and exacerbating existing inequalities. Finally, we propose a set of recommendations for educational institutions, including developing GenAI literacy programmes, revising assessment designs to incorporate critical thinking and creativity, and establishing transparent policies that ensure fairness and accountability in GenAI use. By fostering a responsible approach to GenAI, higher education can harness its potential while safeguarding the core values of academic integrity and inclusive education.

Hemoglobin A_1c is a widely used diagnostic tool for monitoring glycemic control in diabetes management. However, its accuracy can be influenced by various factors. We present a case of a 17-year-old boy with abnormally low Hemoglobin A_1c levels caused by warm autoantibody-induced hemolytic anemia. This case highlights the importance of considering conditions that may affect erythrocyte survival, and the potential interferences when interpreting Hemoglobin A_1c results to ensure accurate diagnosis and effective management of diabetes.

Skin disorders pose a significant health burden globally, affecting millions of individuals across diverse demographics. Advancements in molecular techniques have revolutionised our understanding of the underlying mechanisms of skin disorders, offering insights into their pathogenesis, diagnosis, and potential targeted treatment. Furthermore, the integration of molecular diagnostics into clinical practice has enhanced the accuracy of skin disorder diagnoses. Polymerase chain reaction (PCR), next-generation sequencing (NGS), and other molecular assays have allowed for the detection of infectious agents, assessment of genetic mutations, and profile gene expression patterns with unequalled precision. These techniques have proven instrumental in distinguishing between subtypes of skin cancers, aiding treatment strategies and prognostic assessments. Moreover, molecular profiling is increasingly guiding the selection of therapeutic agents, ensuring a personalised and effective approach to managing skin disorders. The application of PCR has revolutionised the field by enabling the identification of microbial DNA (i.e., Mycobacterium tuberculosis and Epstein-Barr Virus) in skin infections and detecting specific genetic mutations associated with dermatological disorders (e.g., BRAF). DNA sequencing technologies, such as next-generation sequencing, have facilitated the elucidation of genetic variations and mutations in skin diseases (i.e., bullous disorders), paving the way for personalised treatment approaches. Gene expression profiling techniques, such as microarrays and RNA sequencing, have provided insights into dysregulated pathways and molecular signatures associated with conditions ranging from inflammatory skin disorders to cutaneous malignancies. Immunohistochemistry and fluorescence in situ hybridization have proven invaluable in determining protein expression patterns and detecting chromosomal abnormalities, respectively, aiding in the characterization of skin lesions in conjunction with the molecular data. Proteomic studies have contributed to understanding the intricate protein networks involved in dermatological conditions (i.e., psoriasis), while epigenetic analyses have shed light on the role of epigenetic modifications in gene regulation within skin cancer (i.e., Malignant Melanoma). Together, these molecular techniques have laid the groundwork for targeted therapies and precision medicine in dermatology, with implications for improved diagnostics and treatment outcomes. This review focuses on the routinely employed molecular techniques within dermatopathology, with a focus on cutaneous malignancies, autoimmune diseases, infectious diseases, and neonatal screening which can be implemented in the diagnosis and contribute to improved patient care.

In this report, we describe a case of homozygous delta-beta (δβ) thalassaemia, a rare genetic disorder characterized by severe deficiency in delta (δ) and beta (β)-globin chain production, leading to ineffective erythropoiesis and chronic haemolytic anaemia. The patient, a 26-year-old female with δβ-thalassaemia, experienced a miscarriage. High-performance liquid chromatography revealed 89.5% foetal haemoglobin (HbF) and 14.4% glycated HbF. Sebia capillary electrophoresis showed haemoglobin peak of 97.2% and 2.8%. Kleihauer Bekte test indicated a pancellular pattern of foetal cells, while morphology analysis demonstrated microcytic, hypochromic red cells and target cells. Gene analysis confirmed compound heterozygosity for two large deletions in the β-globin gene cluster.

Mitochondria, known as the cell's powerhouse, play a critical role in energy production, cellular maintenance, and stemness regulation in non-cancerous cells. Despite their importance, using drug delivery systems to target the mitochondria presents significant challenges due to several barriers, including cellular uptake limitations, enzymatic degradation, and the mitochondrial membranes themselves. Additionally, barriers in the organs to be targetted, along with extracellular barriers formed by physiological processes such as the reticuloendothelial system, contribute to the rapid elimination of nanoparticles designed for mitochondrial-based drug delivery. Overcoming these challenges has led to the development of various strategies, such as molecular targeting using cell-penetrating peptides, genomic editing, and nanoparticle-based systems, including porous carriers, liposomes, micelles, and Mito-Porters. Porous carriers stand out as particularly promising candidates as drug delivery systems for targeting the mitochondria due to their large pore size, surface area, and ease of functionalisation. Depending on the pore size, they can be classified as micro-, meso-, or macroporous and are either ordered or non-ordered based on both size and pore uniformity. Several methods are employed to target the mitochondria using porous carriers, such as surface modifications with polyethylene glycol (PEG), incorporation of targeting ligands like triphenylphosphonium, and capping the pores with gold nanoparticles or chitosan to enable controlled and triggered drug delivery. Photodynamic therapy is another approach, where drug-loaded porous carriers generate reactive oxygen species (ROS) to enhance mitochondrial targeting. Further advancements have been made in the form of functionalised porous silica and carbon nanoparticles, which have demonstrated potential for effective drug delivery to mitochondria. This review highlights the various approaches that utilise porous carriers, specifically focusing on silica-based systems, as efficient vehicles for targeting mitochondria, paving the way for improved drug delivery strategies in mitochondrial therapies.

Biomedical scientists (BMS) can report sample adequacy during EBUS TBNA using rapid on-site evaluation (ROSE). Despite being able to report exfoliative samples such as pleural fluid cytology and bronchial washings, they are usually not permitted to offer a preliminary diagnostic impression of EBUS TBNA samples. Experienced biomedical scientists can provide a reliable diagnostic impression during ROSE for EBUS samples, with sensitivity and specificity comparable to cytopathologist reporting. This work represents an advance in biomedical science because it provides evidence a BMS can safely and accurately provide a real time cytopathological impression from EBUS TBNA sampling, which could positively impact patient pathways.

Background: Direct oral anticoagulants (DOACs) interfere with coagulation assays potentially leading to inaccurate results. This study determined the effectiveness of DOAC-stop® and DOAC-remove® in overcoming DOAC interference. It aimed to investigate the extent to which apixaban, rivaroxaban, and dabigatran had an effect on thrombophilia and lupus tests using normal plasma, as well as whether DOACs interfere with true-positive results by testing abnormal controls.

Methods: Apixaban (0.03 mg/mL), rivaroxaban (0.01 mg/mL), and dabigatran (0.019 mg/mL) stock solutions were made and added to the normal pool at three different concentrations (200, 400 and 600 ng/mL) and to the abnormal controls at a single concentration. These samples and untreated DOAC controls were tested before and after adding either DOAC-stop® or DOAC-remove®. The measured parameters included protein C, protein S, antithrombin III (ATIII), DRVVS, DRVVC, PTT-LA and DOAC concentration. The normal pool spiked with DOAC was repeated seven times for each DOAC at each concentration level and the abnormal controls spiked with DOAC were repeated four times at a single concentration level for each DOAC.

Results: In the normal pool, dabigatran and rivaroxaban affected all lupus anticoagulant tests, whereas apixaban only affected DRVVS and DRVVC. While dabigatran led to false-positive protein S deficiency and falsely elevated ATIII. Both DOAC-stop® and DOAC-remove® brought the thrombophilia results and all falsely elevated lupus anticoagulant results back within the normal range for apixaban and rivaroxaban. For dabigatran all the affected lupus anticoagulant tests remained abnormal following DOAC-remove®, unlike DOAC-stop® treatment, where only DRVVS and DRVVC at 600 ng/mL remained abnormal. In abnormal controls, all DOACs falsely elevated the lupus anticoagulant tests, whereas dabigatran caused false negative ATIII results, that were corrected (remained abnormal) with DOAC-stop® and DOAC-remove®. DOAC-stop® showed a greater reduction in lupus anticoagulant results than DOAC-remove®, causing a false-negative DRVVT ratio for rivaroxaban.

Conclusion: DOAC-stop® is more effective than DOAC-remove® in removing all DOACs below the reference range, whereas DOAC-remove® failed to remove dabigatran.

Background: Tuberculosis (TB) continues be the leading cause of death globally due to an infectious agent. There is a paucity of data describing the readability of patient-facing TB information for service users. The aim of this study was to calculate the readability of multiple global TB information sources.

Methods: Information on tuberculosis (n = 150 sources) included nine categories, Patient-facing information: WHO publications (n = 17), International governments (n = 19), Hospitals (n = 10), Non-government organisations (NGOs)/charities (n = 20), Cochrane Plain Language Summaries (n = 20); LabTestsOnlineUK (n = 4) and Scientific-facing information: Clinical trials (n = 20), Cochrane abstracts (n = 20), Scientific abstracts (n = 20). Readability was calculated using Readable software, defined by (i) Flesch Reading Ease (FRE), (ii) Flesch-Kincaid Grade Level (FKGL), (iii) Gunning Fog Index and (iv) SMOG Index and two text metrics [words/sentence, syllables/word].

Results: Mean readability values for TB information for the FRE and FKGL were 35.6 ± 1.6 (standard error of mean (SEM)) (US Target ≥60; UK Target ≥90) and 12.3 ± 0.3 (US Target ≤8; UK Target ≤6), respectively, with mean words per sentence and syllables per word of 17.2 and 1.8, respectively. Cochrane Plain Language Summaries had similar readability scores to their matching scientific abstract (p = 0.15). LabTestsOnlineUK yielded a mean FRE score of 51.5 ± 1.2, a mean FKGL score of 10.2 ± 0.5 and text metric scores of 16.7 ± 2.3 and 1.6, for words per sentence and syllables per word, respectively. In descending order, TB information from international governments, hospitals and LabTestsOnlineUK were the most readable (FRE = 57.9, 54.1 and 51.5, respectively), whereas scientific abstracts and Cochrane abstracts were the most difficult to read (13.0 and 30.2, respectively).

Conclusion: Patient-facing TB information analysed had poor readability. Effective communication of biomedical science concepts and information relating to TB is vital for service users to enhance their health literacy of tuberculosis, thereby promoting better clinical outcomes. Biomedical scientists are important custodians of scientific information for their service user populations, including other healthcare professionals within the TB multidisciplinary (MDT) team and patient service users. When preparing TB information, this should be checked and modified in real time employing readability calculators, to align with health readability targets.

Oral administration of protein-based therapeutics is highly desirable due to lower cost, enhanced patient compliance, and convenience. However, the harsh pH environment of the gastrointestinal tract poses significant challenges. Silica-based carriers have emerged as potential candidates for the delivery of protein molecules, owing to their tuneable surface area and pore volume. We explored the use of a commercial mesoporous silica carrier, SYLOID, for the delivery of octreotide and bovine serum albumin (BSA) using a solvent evaporation method in three different solvents. The loading of proteins into SYLOID was driven by diffusion, as described by the Stokes-Einstein equation. Various parameters were investigated, such as protein size, diffusion, and solubility. Additionally, 3D fluorescence confocal imaging was employed to identify fluorescence intensity and protein diffusion within the carrier. Our results indicated that the loading process was influenced by the molecular size of the protein as octreotide exhibited a higher recovery rate (71%) compared to BSA (32%). The methanol-based loading of octreotide showed uniform diffusion into the silica carrier, whereas water and ethanol loading resulted in the drug being concentrated on the surface, as shown by confocal imaging, and further confirmed by scanning electron microscopy (SEM). Pore volume assessment supported these findings, showing that octreotide loaded with methanol had a low pore volume (1.2 cc/g). On the other hand, BSA loading was affected by its solubility in the three solvents, its tendency to aggregate, and its low solubility in ethanol and methanol, which resulted in dispersed particle sizes of 223 and 231 μm, respectively. This reduced diffusion into the carrier, as confirmed by fluorescence intensity and diffusivity values. This study underscores the importance of protein size, solvent properties, and diffusion characteristics when using porous carriers for protein delivery. Understanding these factors allows for the development of more effective oral protein-based therapeutics by enhancing loading efficiency. This, in turn, will lead to advances in targeted drug delivery and improved patient outcomes.

This review delves into the entorhinal cortex (EC) as a central player in the pathogenesis of Alzheimer's Disease (AD), emphasizing its role in the accumulation and propagation of tau pathology. It elucidates the multifaceted functions of the EC, encompassing memory formation, spatial navigation, and olfactory processing, while exploring how disruptions in these processes contribute to cognitive decline in AD. The review discusses the intricate interplay between tau pathology and EC vulnerability, highlighting how alterations in neuronal firing patterns and synaptic function within the EC exacerbate cognitive impairments. Furthermore, it elucidates how specific neuronal subtypes within the EC exhibit differential susceptibility to tau-induced damage, contributing to disease progression. Early detection methods, such as imaging techniques and assessments of EC blood flow, are examined as potential tools for identifying tau pathology in the preclinical stages of AD. These approaches offer promise for improving diagnostic accuracy and enabling timely intervention. Therapeutic strategies targeting tau pathology within the EC are explored, including the clearance of pathological tau aggregates and the inhibition of tau aggregation processes. By understanding the molecular and cellular mechanisms underlying EC vulnerability, researchers can develop more targeted and effective interventions to slow disease progression. The review underscores the importance of reliable biomarkers to assess disease progression and therapeutic efficacy in clinical trials targeting the EC. Ultimately, it aims to contribute to the development of more effective management strategies for AD, emphasizing the translation of research findings into clinical practice to address the growing societal burden of the disease.