Mild traumatic brain injury (mTBI) represents the majority of head injury presentations in emergency departments (EDs), yet only a minority of patients have acute intracranial lesions on computed tomography (CT). This leads to widespread use of unnecessary CT scans. Point-of-care (POC) biosensing, defined as analytical testing performed at or near the site of patient care, offers a promising solution to this dilemma by enabling rapid biomarker quantification to inform CT decision-making. This review aims to evaluate POC-compatible biosensing strategies for ultra-early mTBI triage, with emphasis on platforms, matrix effects, and benchmarking aligned with CT-based decision-making. Two key precedents support this approach: (1) the integration of S100B into Scandinavian Neurotrauma Committee guidelines, which has demonstrated the potential for safe reduction of CT scans, and (2) the regulatory clearance of glial fibrillary acidic protein (GFAP) and ubiquitin C-terminal hydrolase-L1 (UCH-L1) testing to rule out the need for head CT in adults with suspected mTBI (Glasgow Coma Scale 13–15) when serum is collected within 12 hours of injury. Accordingly, this review focuses on the most implementable use case for mTBI, namely CT triage/rule-out. It synthesizes the current biomarker landscape (S100B, GFAP, UCH-L1), analyzes POC-suitable sensing modalities, and proposes a practical validation and benchmarking framework aligned with this intended use. A critical component is interference testing and real-world sample robustness, including vulnerabilities such as hemolysis-related elevation of UCH-L1. In conclusion, the most reliable path for biosensor translation in mTBI is to anchor development and validation to the ED CT-triage use case, emphasizing decision-point robustness and resilience to real-world sample variability over pure analytical sensitivity.

Accurate identification of invasive fungal pathogens is crucial for appropriate antifungal therapy. The Department of Clinical Laboratory at Indus Hospital & Health Network, Karachi, Pakistan, reported two cases of invasive fungal infections between 1st January and 31st March 2024 in which conventional identification methods and automated systems produced discordant results, highlighting critical diagnostic challenges.

Two invasive yeast isolates initially showing budding yeast cells without pseudohyphae on Gram stain were subjected to conventional identification using cornmeal-Tween 80 agar, chrome agar, and BiGGY agar, followed by automated identification using the VITEK 2 ID-YST system and confirmatory API 20C AUX testing. Both isolates demonstrated typical soft, wrinkled, cream-colored colonies on Sabouraud dextrose agar, which on chrome agar appeared as dry, blue colonies and on BiGGY agar as dry, brown colonies. Characteristic arthroconidia and blastoconidia formation on cornmeal-Tween 80 agar were observed, consistent with Trichosporon species. However, the VITEK 2 ID-YST system identified both isolates as Cryptococcus laurentii with good confidence levels. India ink staining was negative for both isolates. Confirmatory API 20C AUX testing correctly identified both isolates as Trichosporon asahii (identification profile 3740734).

This discordance between automated and conventional methods underscores the continued importance of conventional identification techniques and highlights potential limitations of automated systems for certain uncommon yeasts. Laboratories should maintain proficiency in conventional methods and consider confirmatory testing when automated results conflict with morphological findings. The clinical implications of misidentification include inappropriate antifungal selection, given the different susceptibility patterns between these species.

The existing wound assessment tools, which are based on modern medical theory, limit the clinical application of traditional Chinese medicine (TCM) nursing. This research aimed to develop a scientific, standardized, and characteristic TCM nursing evaluation form for chronic wounds.

Based on a literature review and research group discussions, an initial draft of an expert consultation questionnaire, based on literature from the past five years (2017–2021) from databases such as CNKI, Wanfang, VIP, and SinoMed, was formulated. The authority of the experts was expressed using the authority coefficient, derived from self-evaluations, which is critical for ensuring the scientific validity and rationality of the indicator system. After three rounds of Delphi expert consultation, the TCM nursing assessment form for wound surfaces was finalized.

The effective response rate for the three rounds of expert consultation questionnaires was 100%. The judgment coefficient was 0.85, the familiarity coefficient was 0.89, and the authority coefficient was 0.87. The coefficients of variation for the three rounds were 0.172, 0.044, and 0.013, respectively, while the Kendall’s coefficients of concordance were 0.406, 0.269, and 0.502, respectively, with statistically significant differences (p < 0.001). The final TCM nursing assessment form for wound surfaces included four basic information items, two primary indicators, 17 secondary indicators, and 13 tertiary indicators.

The TCM nursing assessment form integrates TCM syndrome differentiation principles and provides a standardized tool for the assessment of chronic wounds.

ATP-binding cassette (ABC) transporters are transmembrane proteins involved in the translocation of bilirubin, bile acids, phospholipids, and cholesterol into bile canaliculi. Mutations in particular genes encoding these transporters—including BSEP (ABCB11 gene), MDR3 (ABCB4 gene), sterolin-1 and sterolin-2 (ABCG5/8 genes), and MRP2 (ABCC2 gene)—result in a wide spectrum of liver diseases, ranging from benign conditions such as Dubin-Johnson syndrome to more severe presentations like progressive familial intrahepatic cholestasis. The severity of disease is influenced by many factors, including zygosity, mutation type, and environmental modifiers such as hormones, consanguinity, and founder effects. Homozygous and compound heterozygous mutations typically result in severe and early-onset diseases, while heterozygous single-allelic mutants generally result in milder diseases. Next-generation genetic testing has proven to have high diagnostic value and is important for prognostication. With knowledge of the underlying specific mutations, there is also potential for future targeted therapy for many severe diseases. The aim of this review is to update and discuss the hepatic diseases associated with ABC transporter mutations, the genetic and environmental effects that influence the severity of disease, typical presentations of these cholestatic hepatic diseases, diagnostic considerations, and treatment options.

Synucleinopathies, including Parkinson’s disease (PD), dementia with Lewy bodies, and multiple system atrophy (MSA), are a group of neurodegenerative diseases characterized by the oligomerization of α-synuclein protein in neurons or glial cells. Various splicing isoforms of α-synuclein have been described, each with different aggregation properties. The α-synuclein gene (SNCA) has been identified as a highly significant genetic risk locus associated with various synucleinopathies across populations. This study aimed to assess the association of SNCA genetic variants with MSA and the levels of SNCA transcripts in peripheral blood mononuclear cells (PBMCs) from MSA and PD patients.

In this retrospective case–control study, 96 MSA patients, 1086 PD patients, and 485 healthy volunteers were included. PCR followed by restriction endonuclease analysis was used to detect four SNCA single-nucleotide polymorphisms (rs356219, rs3756063, rs11931074, and rs356168) in these individuals. In addition, RT-qPCR was performed to detect the levels of α-synuclein transcripts (SNCA mRNA isoforms -140, -126, and -112) in PBMCs of 24 MSA patients (including parkinsonian (MSA-P) and cerebellar (MSA-C) variants), 31 PD patients, and 32 healthy volunteers.

The frequency of the ‘T’ allele (of rs11931074) was significantly higher in MSA patients than in the healthy controls. The level of SNCA-140 mRNA was significantly decreased in MSA and PD patients compared with the controls, while the level of SNCA-112 mRNA was significantly increased in MSA-P patients than in PD patients and the controls. SNCA-112 mRNA/SNCA-140 mRNA and SNCA-112 mRNA/SNCA-126 mRNA ratios were significantly increased in MSA patients than in the controls.

The SNCA rs11931074 polymorphism is associated with MSA. There is a pronounced alteration in the expression of SNCA transcripts in PBMCs of MSA and PD patients.

Chronic hepatitis B (CHB) remains a major global public health challenge. Current therapies based on nucleos(t)ide analogues and interferon mainly achieve long-term viral suppression, whereas only a small proportion of patients attain a functional cure, defined as sustained hepatitis B surface antigen loss with hepatitis B virus (HBV) DNA below the limit of quantification for at least 24 weeks after treatment discontinuation, with or without anti-HBs seroconversion. Emerging evidence from the gut–liver axis indicates that gut microbiota–derived metabolites, particularly short-chain fatty acids (SCFAs) and bile acids (BAs), modulate the HBV life cycle and immune regulation in CHB, thereby offering therapeutic targets to overcome immune tolerance. This review summarizes the biological characteristics of SCFAs and BAs and their mechanistic roles across different stages of HBV infection, with emphasis on translational relevance. In vitro and animal studies suggest that butyrate and related SCFAs suppress HBV gene expression by inhibiting histone deacetylases and remodeling covalently closed circular DNA minichromatin. SCFAs may also enhance antiviral immunity, although they may reinforce immune tolerance in certain contexts. For BAs, the farnesoid X receptor, Takeda G protein–coupled receptor 5, and the HBV entry receptor sodium taurocholate cotransporting polypeptide form a key signaling hub with dual effects on viral replication and host responses. Early-phase studies suggest that farnesoid X receptor agonists, pegylated interferon-α, or nucleos(t)ide analogues are associated with hepatitis B surface antigen reductions, though larger trials are needed. This review proposes biomarker-guided stratification and multi-target combination strategies to improve functional cure rates in CHB.

Glioblastoma remains a highly challenging malignancy with a pronounced tendency for recurrence. The hypoxic microenvironment is a key contributor to its therapy resistance. Hyperbaric oxygen therapy (HBOT), which elevates tissue oxygen pressure and reverses hypoxia, exhibits a “dual effect” in glioblastoma management. This review aims to evaluate the therapeutic potential of HBOT in glioblastoma by examining its multifaceted effects on tumor biology and treatment response. On one hand, it enhances radiosensitivity through reactive oxygen species generation, increases chemotherapy efficacy by augmenting cytotoxicity and improving vascular perfusion, and remodels the tumor microenvironment via vessel normalization, edema reduction, and immune cell modulation. Furthermore, HBOT attenuates cancer stem cell properties by downregulating stemness markers and inhibiting self-renewal capacity. On the other hand, HBOT may also promote tumor progression: oxidative stress can induce genomic instability, while concomitant activation of HIF-, NF-κB-, and VEGF-mediated pro-survival pathways may facilitate malignant cell adaptation and proliferation. Given these opposing considerations, the clinical application of HBOT in glioblastoma management remains exploratory. In conclusion, future research should focus on optimizing HBOT protocols. In addition, exploring combination with other therapeutic approaches is equally important. These efforts are essential for the safe and effective integration of HBOT into comprehensive treatment strategies for glioblastoma.