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        <title>British Journal of Biomedical Science | New and Recent Articles</title>
        <link>https://www.frontierspartnerships.org/journals/british-journal-of-biomedical-science</link>
        <description>RSS Feed for British Journal of Biomedical Science | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-06-21T09:39:37.855+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16141</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16141</link>
        <title><![CDATA[Artificial intelligence approaches in biological age prediction: current status and challenges]]></title>
        <pubdate>2026-06-10T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Guangjun Wang</author><author>Pengcheng Ding</author><author>Zihui Li</author><author>Qingfeng Tang</author><author>Liping Tu</author><author>Tao Jiang</author><author>Liangliang Zhang</author><author>Benyue Su</author><author>Jiatuo Xu</author><author>Hui An</author>
        <description><![CDATA[Biological age (BA) prediction has emerged as a critical research frontier for evaluating individual health status and aging trajectories beyond chronological age (CA). Recent advances in artificial intelligence (AI) have substantially accelerated this field by enabling the integration and interpretation of complex, multimodal biological data. This review provides a systematic overview of AI-driven approaches to BA prediction, covering key components including biomarker selection, feature engineering, model development, bias correction, and performance evaluation. We further highlight the growing recognition of asynchronous aging, a phenomenon in which different organs or physiological systems age at distinct rates, and discuss how AI—particularly deep learning and multimodal fusion—offers powerful tools for capturing such system-specific aging patterns. We summarize current methodologies ranging from traditional machine learning algorithms to advanced neural architectures capable of modeling nonlinear and heterogeneous aging processes. The expanding applications of AI-based BA models in disease risk assessment, geriatric evaluation, and population health monitoring are also examined. Despite rapid methodological progress, significant challenges persist, including data heterogeneity, limited model generalizability, insufficient interpretability, and barriers to clinical translation. Addressing these issues will require standardized methodological practices, robust validation across diverse populations, and the development of interpretable and equitable AI systems. Future research should prioritize the integration of multi-omics and longitudinal datasets with AI-driven analytical frameworks to establish reliable, system-level, and clinically actionable BA prediction models that account for asynchronous aging.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15905</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15905</link>
        <title><![CDATA[Application of non-invasive preimplantation genetic screening for aneuploidy through spent embryo culture media analysis at 48 and 54 hours after embryo cleavage]]></title>
        <pubdate>2026-06-09T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Chonthicha Satirapod</author><author>Pornsri Niransuk</author><author>Siriluk Tantanavipas</author><author>Insee Sensorn</author><author>Wasun Chantratita</author><author>Objoon Trachoo</author>
        <description><![CDATA[BackgroundThis study aims to assess the effectiveness of non-invasive preimplantation genetic testing (niPGT) for detecting aneuploidy at two different time points, 48- and 54-hour following the cleavage stage of embryo development.MethodsA cohort of 15 infertile women was enrolled, involving a total of 58 embryos. All embryos underwent sequential culture media procedures and received assisted hatching during the cleavage stage on Day 3. After biopsy examination, conducted either 48 or 54 hours post cleavage, spent culture media (SCM) were gathered and processed for the amplification and quantification of cell-free DNA. This was followed by low-pass whole genome sequencing.ResultsThe cell-free DNA content within SCM remained consistent across both time points post cleavage. The accuracy of niPGT in ploidy detection, in comparison to trophectoderm biopsy, was 53.71%. No significant distinction in ploidy detection accuracy was observed between SCM collected from embryos at 48 hours versus those at 54 hours post cleavage. The overall accuracy for sex determination reached 79.63%.ConclusionsThe concentration of cell-free DNA within SCM was found to be consistent at both 48- and 54-hours after embryo cleavage. However, the accuracy of ploidy determination, when contrasted with the conventional trophectoderm biopsy, did not yield satisfactory outcomes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16709</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16709</link>
        <title><![CDATA[Challenges and emerging strategies for genome-wide evaluation of loss of imprinting in cancer]]></title>
        <pubdate>2026-06-09T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Muhammad Talal Amin</author><author>Louis Coussement</author><author>Tim De Meyer</author>
        <description><![CDATA[Genomic imprinting is the phenomenon in which only a single allele of a gene is expressed based on its parental origin, thereby deviating from the typical biallelic expression of autosomal genes. It is meticulously controlled by epigenetic mechanisms, particularly DNA methylation. Imprinted loci are crucial for regulating growth during early development, and anomalies in imprinting can lead to congenital syndromes such as Beckwith-Wiedemann’s and Prader-Willi’s. Similarly, many cancers exhibit dysregulated imprinting patterns, putatively contributing to tumour growth. Yet, the assessment of imprinting in cancer is complex due to technical challenges, impeding clinical research and the translation of novel insight to the clinic. This review starts with a general introduction to imprinting, its (dys)regulation and key clinical findings in cancer and beyond. Then, we summarize common methods used to characterize normal imprinting and aberrations in cancer. Subsequently, we discuss how the interpretation of such findings is complicated by technical challenges, such as tumour impurity, the requirement for heterozygosity to distinguish between maternal and paternal alleles and the presence of tissue- and transcript-specific imprinting patterns. We further delve into state-of-the-art methods able to mitigate these challenges. Finally, we discuss how future methodological innovations, particularly by integrating single-cell and single-molecule based methods, may further facilitate a straightforward characterization of imprinting dysregulation and its underlying causes, and guide the development of clinical tests. Thus, by integrating recent advances and proposing innovative approaches, our review aims to provide a comprehensive overview for cancer researchers and clinicians to facilitate cancer imprinting research and its translation to the clinic.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16477</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16477</link>
        <title><![CDATA[Training on PD-L1 scoring in non-small cell lung cancer with high intra- and inter-reader agreement: results of a worldwide microscopic/digital image-based training of 751 pathologists]]></title>
        <pubdate>2026-06-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Gudrun Bänfer</author><author>Rolf Diezko</author><author>Rabea Oberthür</author><author>George L. Kumar</author><author>Josef Rüschoff</author><author>Hans-Ulrich Schildhaus</author><author>Bharat Jasani</author>
        <description><![CDATA[Semi-quantitative scoring of PD-L1 expression on tumor cells (TCs) and/or infiltrating immune cells (ICs) is complex and requires expert pathologist training to reduce inter- and intra-reader variability. We conducted a 1- or 2-day training of 751 pathologists world-wide from 63 countries over a period of 2 years (2016 and 2017). Pathologists read microscopic slides or fully digitized slides stained with PD-L1 immunohistochemistry 22C3 pharmDx assay with expression levels enriched around the clinically relevant cutoffs of 1% and 50% in non-small cell lung cancer (NSCLC). The overall inter-reader agreement (OPA) for PD-L1-stained NSCLC was 95.6% for TPS ≥1% and 87.3% for TPS ≥50% cut-off. The corresponding intra-reader agreement was 95.9% for the ≥1% and 91.4% for the ≥50% cut-off. The inter-reader negative percent agreement (NPA) for TPS ≥1% was 85.6% and 91.9% for the TPS ≥50% cut-off, and the positive percent agreement (PPA) was 97.6% (TPS ≥1%) and 81.0% (TPS ≥50%). The observed high inter- and intra-reader agreements are promising given the difficulty of reproducible scoring tumor cells with heterogeneous distribution of PD-L1 staining combined with the varied professional training, expertise, and experience of the participants. The results may reflect the utility of the expert led standardized protocol used to train pathologists for scoring PD-L1 staining in NSCLC specimens. The digital image-led training approach has the additional advantage of providing a computer-assisted scoring system and allows for remote training of pathologists worldwide.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16457</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16457</link>
        <title><![CDATA[Performance of a quality control center supporting national antimicrobial resistance surveillance]]></title>
        <pubdate>2026-06-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Dong Woo Shin</author><author>Hyunji Kim</author><author>Jeong Su Park</author><author>Kyoung Un Park</author><author>Min Hyuk Choi</author><author>Dokyun Kim</author><author>Seok Hoon Jeong</author><author>Hee Jung Kim</author><author>Young Ah Kim</author><author>Kwangjin Ahn</author><author>Young Uh</author><author>Yong Jun Kwon</author><author>Jong Hee Shin</author><author>Soo Hyun Kim</author><author>Jeong Hwan Shin</author><author>Hee Young Kang</author><author>Dong Chan Moon</author><author>Sung Young Lee</author><author>Songmee Bae</author>
        <description><![CDATA[IntroductionEnsuring the reliability, standardization, and international comparability of antimicrobial resistance (AMR) surveillance data critically depends on the implementation of robust quality assurance frameworks. South Korea established the Korea Global Antimicrobial Resistance Surveillance System (Kor-GLASS), supported by a centralized quality control center (QCC). As Kor-GLASS transitioned from Phase II to Phase III, new bacterial species and antimicrobial agents were incorporated, underscoring the need to evaluate whether quality assurance performance could be sustained during system expansion.Materials and MethodsWe analyzed interlaboratory proficiency testing (IPT) and external quality assessment (EQA) outcomes generated by the QCC between 2020 and 2024, covering Phases II and III of Kor-GLASS. Clinical isolates were collected at participating hospitals and transferred to organism-specialized analysis centers for standardized antimicrobial susceptibility testing (AST), while the QCC independently oversees data quality through IPT and EQA. IPT was conducted by comparing AST results between analysis centers and the QCC using subsets of routine clinical isolates, with acceptance criteria defined as categorical agreement (CA) ≥90% and major error rates <3%. EQA involved quarterly distribution of pre-characterized strains to participating centers. Additional evaluations addressed the performance of newly introduced ceftazidime-avibactam susceptibility testing and interlaboratory validation for Haemophilus spp.ResultsAcross the study period, overall CA consistently exceeded 97% in IPT, and no EQA failures observed among participating centers. While major errors during Phase II were primarily attributable to AST reading and near-breakpoint discrepancies, their frequency markedly decreased in Phase III following targeted corrective actions and educational interventions. Susceptibility testing for ceftazidime-avibactam showed high concordance between centers, with rare discrepancies limited to near-breakpoint measurements. Interlaboratory validation confirmed acceptable performance for AST of Haemophilus spp., supporting its formal inclusion in Phase III.DiscussionThese findings demonstrate that a centralized, QCC-led quality assurance framework can maintain stable and reliable AMR surveillance performance during periods of system expansion. Beyond routine oversight, coordinated quality assurance activities function as an evidence-based evaluation of how standardized laboratory data are generated and validated, reinforcing their essential role in sustaining the credibility and future development of AMR surveillance systems.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.14743</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.14743</link>
        <title><![CDATA[The Molecular Pathology of Non-Malignant Haematological Disease]]></title>
        <pubdate>2026-05-22T00:00:00Z</pubdate>
        <category>Review</category>
        <author>A. D. Blann</author><author>R. G. Dunn</author>
        <description><![CDATA[In almost all aspects of biomedical science, molecular pathology has brought unprecedented value in the diagnosis and management of human disease. Numerous commentators cite haematological disease as the leading genetic cause of global mortality and morbidity, and of these, those of the red blood cells are the most frequent. This narrative review, with a historical perspective, will discuss the role of genetics in these conditions, the leading pathology of red blood cells being the haemoglobinopathies, principally sickle cell disease and thalassaemia, with their many variants, and with potential roles for non-coding RNAs. The impact of genetics into conditions of the red cell cytoplasm will consider the enzymopathies, led by glucose-6-phosphate dehydrogenase deficiency, and extend to those of the cell membrane, causing disease such as hereditary elliptocytosis. Mutations in genes coding almost all the coagulation factors, and several platelet abnormalities, are discussed, as are those linked to conditions of iron overload. Previous, current and evolving technologies for diagnostic testing and their link with potential targeted therapeutic options for patient management are considered.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16540</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16540</link>
        <title><![CDATA[Matrix metalloproteinase activation and TNF upregulation characterize the sclerotic phase of aortic valve disease]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Biomedical Science in Brief</category>
        <author>Elizabeth Chan-Delgado</author><author>Claudia Lerma</author><author>Juan C. Echeverría</author><author>Andrea Toledo</author><author>José M. Torres-Arellano</author><author>Oscar Infante</author><author>Rafael Bojalil</author><author>Jorge E. Cossío-Aranda</author><author>Nydia Ávila-Vanzzini</author><author>Luis M. Amezcua-Guerra</author><author>Rashidi Springall</author>
        <description><![CDATA[IntroductionAortic valve sclerosis (AVSc) is an active pathological process driven by extracellular matrix remodeling, consistent with a potentially reversible early stage of aortic valve disease.MethodsIn this cross-sectional study of 168 participants (29, normal aortic valve [NAV]; 98, AVSc; 41, aortic stenosis [AS]), serum levels of matrix metalloproteinase (MMP)-1, -2, -3, and -9, tissue inhibitor of metalloproteinases-1 (TIMP-1), tumor necrosis factor (TNF), interleukin-6 (IL-6), and transforming growth factor-beta (TGF-β) were measured. Multivariable adjustments were performed.ResultsCompared with AS, AVSc was associated with higher circulating MMP-9 levels, with MMP-9 also increased relative to NAV. TIMP-1 concentrations were reduced in AVSc compared with both AS and NAV. TNF levels were higher in AVSc than in AS, while IL-6 and TGF-β did not differ among groups. Notably, MMP-9/TIMP-1 ratio was markedly increased in AVSc.DiscussionOur findings suggest that AVSc may exhibit an active proteolytic and inflammatory profile amenable to targeted anti-inflammatory and anti-proteolytic interventions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16208</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16208</link>
        <title><![CDATA[Correlation between oxidative stress and inflammation with metabolomics profile in skeletal muscle of ageing animal model and its modulation by tocotrienol-rich fraction]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Siti Liyana Saud Gany</author><author>Nur Fatin Nabilah Mohd Sahardi</author><author>Jen Kit Tan</author><author>Suzana Makpol</author>
        <description><![CDATA[IntroductionSarcopenia, characterised by age-associated decline in skeletal muscle mass and function, is driven by multifactorial mechanisms including oxidative stress, chronic inflammation, and genomic instability. The imbalance between reactive oxygen species (ROS) and antioxidant defence contributes to mitochondrial dysfunction and DNA damage, thereby affecting cellular metabolism and promoting muscle degeneration. Tocotrienol-rich fraction (TRF), a potent antioxidant form of vitamin E, has shown potential in modulating oxidative and inflammatory pathways. However, in vivo evidence exploring TRF’s multifaceted role in ageing muscle remains limited. This study investigates the correlation between oxidative stress and inflammation with the metabolomics profile in ageing skeletal muscle in a rat model and its modulation by tocotrienols.MethodsYoung (3 months) and old (21 months) male Sprague-Dawley rats were divided into control and TRF-supplemented groups (n = 10). TRF was administered orally (60 mg/kg/day) for 3 months. Antioxidant enzymes, lipid peroxidation products: malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE); and inflammatory markers: C-reactive protein (CRP), Interleukin-6 (IL-6), and tumour necrosis factor alpha (TNF-α) were quantified, alongside DNA damage, using the comet assay. Muscle histology was assessed using hematoxylin and eosin (H&E) staining. Pearson correlation analysis was performed between selected metabolites and biological markers.ResultsAgeing significantly increased oxidative damage, pro-inflammatory markers, and DNA fragmentation, while reducing antioxidant enzyme activities and disrupting metabolic profiles. Although TRF supplementation did not significantly restore muscle mass or overall body composition, it effectively enhanced antioxidant defence by increasing Superoxide dismutase (SOD) and catalase (CAT) activities, reducing lipid peroxidation (MDA and 4-HNE), attenuating inflammatory responses, preserving DNA integrity, and improving muscle histological features. Importantly, correlation analyses revealed that ageing is associated with a coordinated metabolic shift linking amino acid and carnitine metabolism with antioxidant defence, inflammation, and genomic stability. TRF supplementation weakened these maladaptive biomarker and metabolite associations while strengthening correlations between protective metabolites (e.g., taurine, histidine, pantothenic acid) and antioxidant enzymes, alongside inverse relationships between lipid peroxidation and inflammatory markers (e.g., MDA, prostaglandin factor 2-alpha, PGF2α) and redox-supportive metabolites.DiscussionCollectively, these findings indicate that TRF acts primarily as a preventive intervention by restoring redox balance, dampening inflammatory signalling, and stabilising metabolic and inflammatory coupling, highlighting its potential as a nutritional strategy for preserving muscle health and genomic integrity during ageing.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16255</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16255</link>
        <title><![CDATA[Clinical Utility of SARS-CoV-2 Antibody Titers in the Management of Patients With Long COVID Infected With the Omicron Variant]]></title>
        <pubdate>2026-04-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Marina Kawaguchi</author><author>Yasue Sakurada</author><author>Kazuki Tokumasu</author><author>Yuki Otsuka</author><author>Yasuhiro Nakano</author><author>Yui Matsuda</author><author>Hiroyuki Honda</author><author>Daisuke Omura</author><author>Nobuyoshi Matsuki</author><author>Masanori Furukawa</author><author>Akihito Higashikage</author><author>Fumio Otsuka</author>
        <description><![CDATA[BackgroundLong COVID (LC) presents persistent symptoms that pose a major clinical challenge. Identification of reliable biomarkers to evaluate LC pathophysiology is needed.ObjectivesTo investigate whether serum S- and N-antibody titers against SARS-CoV-2 spike and nucleocapsid proteins reflect the clinical features of LC.MethodsThis retrospective observational study included patients diagnosed with Omicron variant-related LC who attended a post-COVID-19 outpatient clinic between July 2023 and November 2024 and provided informed consent for antibody testing.ResultsAmong 275 patients (129 men and 146 women), 57 (21%) were unvaccinated. Median S- and N-antibody titers in vaccinated versus unvaccinated patients were 20,963 U/mL and 24.8 cut-off index (COI) versus 24 U/mL and 44.5 COI, respectively. S-antibody titers were associated with the number of vaccine doses received, whereas N-antibody titers correlated with disease severity during the acute phase of COVID-19 infection, with females having higher titers by multivariable analysis. N-antibody titers in unvaccinated patients with LC were negatively correlated with time interval from infection to clinic visit, with an estimated daily decline of 0.34% in measured N-antibody levels. Patients with LC having memory impairment had low S-antibody titers by multivariable logistic regression analysis, and low S-antibody levels were associated with reduced quality of life (QOL). Additionally, N-antibody titers positively correlated with lymphocyte counts and immunoglobulin levels.ConclusionSerum N-antibody titers reflect immune responses to COVID-19, although they are affected by gender differences and interval between infection and evaluation. Lower S-antibody titers were associated with brain fog symptoms and reduced QOL in patients with LC.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15988</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15988</link>
        <title><![CDATA[Identification of Somatic and Germline Mutations Influencing Treatment Outcomes and Disease Susceptibility in Tunisian Triple-Negative Breast Cancer Using Next-Generation Sequencing]]></title>
        <pubdate>2026-04-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Asma Mehri</author><author>Ahmed Baligh Laaribi</author><author>Ichraf Jbir</author><author>Emna Chelbi</author><author>Beya Chelly</author><author>Abir Chaabane</author><author>Salwa Nechi</author><author>Hadda-Imen Ouzari</author>
        <description><![CDATA[Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype characterized by marked molecular heterogeneity and limited targeted therapeutic options. Its incidence is rising in many low- and middle-income countries, where genetic profiling of affected patients remains largely unexplored despite evident clinical disparities. This study aimed to characterize, for the first time in a Tunisian cohort, the spectrum of germline and somatic mutations in TNBC patients and to assess their potential impact on therapeutic response. Targeted next-generation sequencing (NGS) of hotspot regions across 50 cancer-related genes was performed in twelve patients using the AmpliSeq for Illumina Cancer Hotspot Panel v2, applied to both tumor tissues and matched adjacent non-tumoral tissues. Bioinformatics analysis revealed recurrent germline variants present in all samples, notably in TP53 (rs1042522), CSF1R (rs2066933), FGFR3 (rs7688609), RET (rs1800861), KDR (rs7692791), and PDGFRA (rs1873778). In tumor tissues, 32 deleterious somatic variants were detected across 20 oncogenes, with TP53 emerging as the most frequently mutated gene (58%). Distinct mutational patterns were observed in relation to treatment response. Notably, the co-occurrence of AKT1 (rs121434592) and TP53 (rs876660754) was observed in a patient with treatment resistance, whereas an in-frame deletion in NOTCH1 (p.Val1578del) was uniquely detected in patients who subsequently experienced disease recurrence. These findings provide the first comprehensive characterization of germline and somatic alterations in Tunisian TNBC patients, representing a North African cohort. They reveal the heterogeneity of mutation patterns linked to treatment response, and emphasize the importance of genomic profiling into clinical practice and guide personalized therapeutic strategies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2025.14745</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2025.14745</link>
        <title><![CDATA[The Molecular Pathology of Blood Cancer: A Comprehensive Review of Chromosome and Genetic Abnormalities and Their Clinical Utility]]></title>
        <pubdate>2026-04-20T00:00:00Z</pubdate>
        <category>Review</category>
        <author>N. McCaul</author><author>R. J. Bingham</author><author>A. D. Blann</author>
        <description><![CDATA[Molecular pathology has, without a doubt, transformed the field of blood cancer. Thanks to pioneers such as Sanger and Mullis, techniques such as next- and third-generation sequencing, and whole exome sequencing have, alongside a revolution in bioinformatics, determined abnormalities in chromosomes and genes with exquisite sensitivity and specificity. These have contributed considerably not just to our understanding of the cell biology, aetiology, classification, and pathophysiology of blood cancer, but also to its diagnosis and management. Good examples of this include the ability to recognise and treat cases of aberrant tyrosine kinase activity with targeted inhibitors and the recognition that certain abnormalities are linked to a more severe outcome, so that focused treatment can begin. This review catalogues these discoveries and describes how they contribute to our understanding of, and thus the treatment of, lymphoma, leukaemia, myeloma, and other myeloproliferative, erythroid, megakaryocytic, and lymphoid neoplasms. Inevitably, as new techniques are developed, we can expect further advances in biomedical science in all aspects of blood cancer.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15884</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15884</link>
        <title><![CDATA[Age-Related Loss of GPR68 and Calretinin Immunoreactive Neurons Within the Mucosa, Not the Myenteric Plexus of Human Colon]]></title>
        <pubdate>2026-04-07T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Nicholas Baidoo</author><author>Enrica De Rasis</author><author>Luke Paine</author><author>David C. Bulmer</author><author>Gareth J. Sanger</author>
        <description><![CDATA[BackgroundThe G protein-coupled receptor 68 (GPR68) detects variations in extracellular pH, and has potential roles in homeostasis and responses to ischaemia and inflammation within different organs, including the gastrointestinal tract. However, in the human colon the distribution of GPR68 remains unclear. We examined the localization and density of GPR68 within the ascending (AC) and descending (DC) human colon from younger and older adults.MethodsMacroscopically normal AC and DC were obtained from patients undergoing lower bowel cancer resection (aged 22–91 years; grouped into younger (≤60 years) and older (≥67 years) populations). Immunolabelling was performed using formalin-fixed, paraffin-embedded sections and antibodies against GPR68, protein gene product 9.5 (PGP9.5) and calretinin to identify the presence and density of GPR68-immunoreactive (IR) expressing cells.ResultsAgeing did not change the density of total PGP9.5-IR enteric neuronal fibres in the AC or DC. For the myenteric plexus (MP) of both age groups, the densities of calretinin-IR neurons were similar in both the AC (younger: 1.2 ± 0.3 × 10−3; older: 0.9 ± 0.2 × 10−3 per mm2 plexus) and DC (1.4 ± 0.2 × 10−3; 1.3 ± 0.3 × 10−3 per mm2 plexus), but reduced in the mucosa of older adults for both AC (respectively, 9.8 ± 0.5 vs. 3.2 ± 0.1/pixel) and DC (11.5 ± 0.9 vs. 7.4 ± 0.3/pixel). Similar reduction of calretinin-IR enteric neurons was found in the SMP of AC but not clearly in the DC in the older adults. GPR68 was widely expressed in the mucosa, circular muscle and myenteric plexus of both the AC and DC. The density of GPR68-IR in the muscle and myenteric plexus was similar in both age groups, but smaller in the mucosa of older adults for both AC and DC.ConclusionGPR68 is widely distributed within the enteric nervous system of the human colon, with potential roles for GPR68 suggested in the muscle and MP, and in the functions of calretinin-IR neurons within the mucosa. Further, the concomitant loss of GPR68 and calretinin-IR neurons in the mucosa of older adults suggests selective vulnerability of mucosal sensory and homeostatic mechanisms of the ageing colon.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16119</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16119</link>
        <title><![CDATA[Challenges in Diagnosis of Lepidic Subtype in Lung Cancer According to W.H.O Classification: A Case Report]]></title>
        <pubdate>2026-04-02T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Cuong Pham Nguyen</author><author>Long Thien Phan</author><author>Phuong Thi Phan</author><author>Do Quyen Thi Phan</author><author>Tuong Pham Nguyen</author><author>Thoi Van Dang</author>
        <description><![CDATA[BackgroundLepidic adenocarcinoma of the lung often presents with atypical radiological patterns mimicking pneumonia, posing significant diagnostic challenges, particularly from small cytology samples. This can lead to delayed diagnosis and advanced-stage presentation.Case presentationA 57-year-old non-smoking female presented with a persistent cough, massive sputum production, and diffuse bilateral pulmonary lesions on computed tomography scan, resembling pneumonia. The patient’s condition rapidly deteriorated into acute respiratory failure unresponsive to antibiotics. A sputum cell block confirmed lung adenocarcinoma (CK7+, TTF-1+). Liquid biopsy via Next-Generation Sequencing (NGS) identified an EGFR L858R mutation (VAF 80%). First-line Osimertinib induced a dramatic clinical and radiological response within days. However, disease progression occurred after 9 months. A repeat biopsy and NGS re-evaluation revealed a persistent L858R mutation with an increased VAF (89%), without secondary resistance mutations (T790M, C797S) or bypass alterations, suggesting non-genetic resistance mechanisms.ConclusionThis case underscores the critical difficulty of diagnosing lepidic-patterned tumors in an oncological emergency. It highlights the necessity of a multidisciplinary approach, combining cytology, radiology, and early molecular testing as a surrogate for traditional histopathology to guide urgent targeted therapy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15960</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15960</link>
        <title><![CDATA[Carbon Quantum Dots as Versatile Nanosystems for Biomedical Innovation: Mechanisms, Applications, and Translational Prospects]]></title>
        <pubdate>2026-04-02T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Jasdev Singh Maan</author><author>Milind Kuruvath Santhosh</author><author>Stevelyn Jia Xin Lee</author><author>Nicole Zi Yu Leow</author><author>Anis Sofia binti Mohd Adli</author><author>Charlotte Jia Qi Tai</author><author>Jia Hui Lim</author><author>Yasheni Muniandy</author><author>Chun-Wai Mai</author><author>Tong Ling Tan</author><author>Soi Moi Chye</author><author>Rhun Yian Koh</author><author>Chooi Ling Lim</author>
        <description><![CDATA[Carbon quantum dots (CQDs) represent a rapidly developing class of fluorescent nanomaterials with increasing relevance in biomedical research and application. Their tuneable photoluminescence (PL), favourable biocompatibility, and versatile surface chemistry has supported applications in bioimaging, biosensing, and therapeutic strategies. Advances in top-down, bottom-up, and green synthesis routes have improved control over emission profiles, heteroatom doping, and surface functionalisation. Recent work has begun to elucidate how synthesis conditions and surface states govern biological interactions, intracellular transport, and subcellular localisation. This review provides an updated, mechanistic evaluation of these developments, with particular emphasis on how defined structural attributes influence antimicrobial activity, organelle-specific targeting, and integrated imaging-therapy platforms. Despite these advances, significant challenges continue to hinder clinical translation. These include variability in synthesis protocols, inconsistent batch-to-batch reproducibility, and insufficient data on long-term toxicity and biodistribution. The absence of standardised characterisation frameworks and clear regulatory pathways further complicate translational progress. Through critically linking synthesis strategies to surface chemistry and biological behaviour, this review depicts key design considerations necessary for advancing CQDs toward clinical application in next-generation nanomedicine.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16013</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.16013</link>
        <title><![CDATA[Breast Cancer Disparities in African and African-Ancestry Populations: Genetics, Epigenetics, Structural Barriers and Technology-Enabled Solutions]]></title>
        <pubdate>2026-02-27T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Chika Eze</author><author>Rasha Swadi</author><author>Kehinde Ross</author><author>Vijay Sharma</author>
        <description><![CDATA[Breast cancer remains a leading cause of mortality among women globally, with disproportionately high incidence, aggressive subtypes and poor outcomes in African and African-ancestry populations. While inherited BRCA1/BRCA2 mutations drive hereditary risk, recent evidence highlights the critical role of BRCA1 promoter methylation especially in sporadic and triple-negative breast cancers (TNBC), which disproportionately affect African-descended women. This review synthesises the genetic and epigenetic landscape of breast cancer susceptibility in African and diaspora cohorts, emphasising unique mutation spectra, elevated BRCA1 methylation frequencies and their prognostic/treatment implications. Systemic barriers including limited screening infrastructure, workforce shortages, structural racism, and cultural challenges exacerbate late diagnosis and inequities. We evaluate emerging solutions such as telemedicine, AI-enhanced diagnostics, and mobile platforms, alongside the need for context-specific research and investment to integrate molecular insights with innovative health system interventions. This synthesis underscores the urgency of addressing biological and structural drivers to close breast cancer outcome gaps in Africa and similar low- and middle-income settings.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15743</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15743</link>
        <title><![CDATA[High-Fat Diet Anticipates Age-Related Sarcopenia Through Increased Oxidative Stress and Inflammation]]></title>
        <pubdate>2026-02-26T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Fabiano Cimmino</author><author>Lidia Petrella</author><author>Gina Cavaliere</author><author>Mariarosaria Negri</author><author>Claudia Pivonello</author><author>Giuliana Napolitano</author><author>Marianna Crispino</author><author>Giovanna Trinchese</author><author>Annamaria Colao</author><author>Maria Pina Mollica</author>
        <description><![CDATA[BackgroundAgeing, a physiological process, and obesity, a pathological condition, are both associated with several metabolic alterations including energy imbalance, altered body composition, chronic low-grade inflammation, lipotoxicity, glucotoxicity, insulin resistance and mitochondrial dysfunctions. During ageing mitochondrial capacity declines and oxidative stress increases. However, the biphasic model of age-associated mitochondrial functions indicates that, before the ageing-associated decrease in mitochondrial respiration, this parameter increases in the transition from young adult to middle-aged, with a concomitant mild increase in ROS production that stimulates an antioxidant response, limiting the ageing-associated damages. Ageing-associated body composition changes can lead to sarcopenia, one of the most debilitating dysfunctions in the elderly. The sarcopenia is a known geriatric syndrome characterized by the loss of muscle mass and strength and mitochondria dysfunctions. These alterations of the disease can be exacerbated by obesity. Here, in an experimental animal model of diet-induced obesity, we evaluated the time-course changes in body composition, inflammatory and oxidative stress parameters, mitochondrial functions and antioxidant responses.MethodsMale Wistar rats at 60 days of age were divided into two experimental groups: the first group received a standard diet; the second group received a high-fat diet (HFD). The animals from both groups were fed with the appropriate diet for 1, 3, 6, 12, or 24 weeks (n = 6 for each group and time point). At each time point, the animals were sacrificed and dissected to obtain the organs and tissues needed for analysis.ResultsOur results clearly showed the contribution of high-fat diet in anticipating and worsening the metabolic and inflammatory alterations associated with age, in particular, highlighting the role of mitochondria in attempting the regulation of physiological alterations typical of aging.ConclusionIn the HFD group the antioxidant defences fail their job because of the additional inflammation and oxidative stress due to the diet. HFD is related to decreased animals’ activity. Thus, cannot be excluded that the reduced physical activity may contribute, at least in part, to the impaired mitochondrial functions in the skeletal muscle of HFD rats. Altogether, our results clearly highlighted the contribution of HFD in anticipating and worsening the metabolic and inflammatory alterations associated with aging, including sarcopenia.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15687</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15687</link>
        <title><![CDATA[Alternative Polyadenylation Signatures Distinguish Maladaptive Right Ventricular Remodeling in Pulmonary Hypertension: Implications for RNA-Based Diagnostics and Therapeutics]]></title>
        <pubdate>2026-02-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Janani Subramaniam</author><author>Venkata Jonnakuti</author><author>Scott D. Collum</author><author>Sandra Martineau</author><author>Kai-Lieh Huang</author><author>Sandra Breuils-Bonnet</author><author>Andrea L. Frump</author><author>Bindu H. Akkanti</author><author>Jayeshkumar A. Patel</author><author>Manish K. Patel</author><author>Ismael Salas de Armas</author><author>Isabella N. Lefebvre</author><author>Rajko Radovancevic</author><author>Elvin Blanco</author><author>Eric J. Wagner</author><author>Igor Gregoric</author><author>Sriram Nathan</author><author>Biswajit Kar</author><author>Steeve Provencher</author><author>Sebastien Bonnet</author><author>François Potus</author><author>Hari Krishna Yalamanchili</author><author>Harry Karmouty-Quintana</author>
        <description><![CDATA[Increased pulmonary vascular pressures due to vascular remodeling, elevated vascular resistance, and vasoconstriction characterize Pulmonary Arterial Hypertension (PAH). The narrowing of the pulmonary arteries and obstruction of blood flow increase the Right Ventricular (RV) afterload, forcing the RV to undergo structural and functional changes. While adaptive remodeling leads to RV compensation by maintaining function, maladaptive remodeling leads to RV decompensation, characterized by worsening function and eventual failure. At present, there is no effective treatment for these patients as therapies for left ventricular failure are ineffectual, and there are no therapies specifically targeting the RV. Therefore, there is a clear need to understand the pathophysiology of RV failure and to identify the differences between adaptive and maladaptive RV remodeling. This study analyzes changes in polyadenylation site usage, a process known as alternative polyadenylation (APA), in RV failure. APA is a mechanism used to regulate mRNA maturation that can result in either shortening or elongation of the mRNA 3’UTR. By analyzing APA patterns in RV tissue from donor controls and patients with compensated and decompensated RV failure, we demonstrate a pattern of 3’UTR elongation that is present in decompensated RV failure and not in compensated or control RVs. Further, altered APA was also detected in 3 distinct rat models of PH, where 15 transcripts had shared APA alterations across both rat models and human disease. Our study provides an unbiased approach to identifying the molecular changes leading to RV dysfunction while pinpointing novel therapeutic targets that can be leveraged for intervention. These APA signatures may serve as biomarkers to distinguish adaptive from maladaptive RV remodeling. In addition, the RNA-processing machinery that regulates APA, such as NUDT21 and CPSF6, represents potential therapeutic targets for RNA-based interventions. Together, our findings link RNA processing to diagnostic and therapeutic opportunities in right heart failure.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15810</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15810</link>
        <title><![CDATA[An Analysis of the Career Pathway of Clinical Laboratory Scientists: Identifying Access Barriers and Best Practice to Increase Diversity in the Workforce]]></title>
        <pubdate>2026-02-19T00:00:00Z</pubdate>
        <category>Review</category>
        <author>James A. O’Connor</author>
        <description><![CDATA[Widening participation among the clinical laboratory scientific workforce is essential to meet future needs of healthcare systems. The advantages of more diversity in this clinically pivotal workforce include better decision making, improved diagnostics and a wider pool of appropriately trained applicants for new and advanced posts. This review summarises a sustainable “trickle up approach” to increase diversity and widen participation at all levels of the career pathway for clinical laboratory scientists with a focus on socioeconomically disadvantaged and minoritised scientists. Issues of access to appropriate degrees are present years in advance of university application and can be addressed through meaningful outreach programmes from universities and professional bodies. Interventions to broaden degree entry access including foundation routes have proven efficacy, whereas the role of degree apprenticeships in widening participation appears to be minimal, currently. There is a higher proportion of ethnic minorities, particularly black students, who don’t complete their degree programme or attain lower awards than colleagues. Contributory factors include curriculum design along with psychosocial deficiencies in delivery. Decolonising and making biomedical science curricula and delivery more inclusive have proven effective in reducing these risks. Furthermore, socioeconomically disadvantaged students face a new challenge from generative artificial intelligence tools, where those that can pay get access to more powerful tools, creating a new gap, unless these tools are used judiciously and free at point of use. A graduate is required to complete training in a clinical laboratory to gain HCPC or equivalent registration, these places are competitive, and often unpaid. This appears to be a key barrier to widening participation, with a majority of graduates not pursuing careers as Biomedical Scientists. A state and financially supported training programme is required to broaden involvement at and post-registration. There is a paucity of information regarding the makeup of the workforce at promotional grades. However, an analysis of postgraduate study and research avenues reveals challenges for those from minoritised backgrounds and working mothers. These can be addressed through diversity in academic institutions and tailored, personalised approaches to research for working mothers to maximise participation at management and clinical leadership roles in the diagnostic laboratory.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15242</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15242</link>
        <title><![CDATA[Assessing the Impact of Mesoporous, Co-Amorphous, and Polymer-Based Systems on Cefdinir’s Dissolution and Stability Via Predictive Modeling]]></title>
        <pubdate>2026-02-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Raghad Al Nuss</author><author>Mohamad Anas Al Tahan</author><author>Hind El-Zein</author>
        <description><![CDATA[The poor solubility and permeability of Biopharmaceutics Classification System (BCS) Class IV drugs pose major challenges to achieving sufficient oral bioavailability and therapeutic efficacy. Improving drug dissolution is a key strategy to enhance bioavailability, which in turn can enable more effective targeting of drugs to their site of action. To address this, we formulated cefdinir, a model BCS Class IV compound, using three amorphisation strategies; solid dispersions, mesoporous silica dispersions, and co-amorphous systems to assess the impact of formulation on stability and dissolution. Formulations were prepared via spray drying and solvent immersion using different drug-to-polymer ratios, with miscibility predicted using Flory–Huggins theory. The amorphous nature of each system was confirmed using differential scanning calorimetry (DSC), polarised light microscopy (PLM), and powder X-ray diffraction (PXRD). Dissolution studies revealed significantly enhanced drug release from all formulations compared to crystalline cefdinir. Among them, solid dispersion and co-amorphous systems exhibited the greatest improvement in dissolution rates, attributed to their ability to maintain supersaturation and inhibit crystallisation via kinetic stabilisation. These systems also showed better physical stability under non-sink aqueous conditions. However, mesoporous silica dispersions demonstrated superior long-term stability, retaining over 95% drug content and preserving their amorphous structure across three storage conditions (25 °C/0% RH, 40 °C/0% RH, and 40 °C/75% RH) for 6 months. This was attributed to the confinement of the drug within silica pores and the absence of hygroscopic excipients. Overall, this study highlights the distinct advantages of each approach, emphasising the importance of balancing dissolution enhancement with solid-state stability, and supports the use of theoretical modelling to guide rational formulation design for poorly soluble drugs to improve oral bioavailability and enable more targeted therapeutic outcomes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15559</guid>
        <link>https://www.frontierspartnerships.org/articles/10.3389/bjbs.2026.15559</link>
        <title><![CDATA[Antimicrobial Resistance: The Answers]]></title>
        <pubdate>2026-02-06T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Beverley C. Millar</author><author>Mary J. Cates</author><author>Marco S. Torrisi</author><author>Amanda J. Round</author><author>Aisling Warde</author><author>Colm J. Lowery</author><author>John E. Moore</author>
        <description><![CDATA[Antimicrobial resistance (AMR) has caused a global public health crisis, contributing to approximately five million deaths in 2019 and predicted deaths of approximately ten million annually by 2050. This equates to approximately 1.4-fold more deaths annually from AMR in 2050 than the entire COVID-19 pandemic to date. To tackle this AMR pandemic, regulatory and policy frameworks have been prepared at local, national and international levels with multi-faceted proposals and advances encompassing surveillance, diagnostics, infection prevention, antibiotic prescribing and variation of existing and novel treatment approaches. This narrative review primarily focuses on research and development which have been documented over the last five years in relation to therapeutic approaches at various stages in clinical development and the potential role that vaccines can play in the fight against AMR. This review provides an overview on antibacterial drugs, including novel classes of antibiotics, which have been recently approved, as well as combination antibiotic therapy and the potential of repurposed drugs. The potential role of novel antimicrobial, antibiofilm and quorum sensing inhibitors, such as antimicrobial peptides, nanomaterials and compounds from the extreme and natural environments, as well as ethnopharmacology including the antimicrobial effects of plants, spices, honey and venoms are explored. Novel therapeutic approaches are critically discussed in terms of their realistic clinical potential, detailing recent and ongoing trials to highlight the current interest of these approaches, including immunotherapy, bacteriophage therapy, antimicrobial photodynamic therapy (aPDT), antimicrobial sonodynamic therapy (aSDT), nitric oxide therapy and microbiome manipulation including faecal microbiota transplantation (FMT). The potential of predatory bacteria as living antimicrobial agents is also discussed. Importantly, there have been many technological developments which have enhanced bioprospecting and research and development of novel antimicrobials which this review draws attention to, including artificial intelligence, machine learning and Organ-on-a-Chip devices. Finally, key messages from the recent World Health Organization report into the role of vaccines against AMR provides an interesting perspective relating to prevention which can be of significance in tackling the AMR burden.]]></description>
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