Soil respiration represents the transfer of CO₂ from the soil to the atmosphere and is one of the largest terrestrial carbon fluxes after gross primary production. Because it is driven largely by the metabolic activity of soil organisms, it is widely recognized as a sensitive indicator of soil biological activity, carbon turnover, and the impacts of environmental or management-related disturbances. Soil respiration integrates multiple CO₂ sources, including autotrophic respiration from plant roots and rhizosphere microorganisms, and heterotrophic respiration associated with microbial decomposition of organic matter. When measured in the absence of external substrates or recent nutrient inputs, microbial respiration is referred to as soil basal respiration (SBR). This article presents an infrared gas analyzer (IRGA) based protocol to quantify SBR under controlled laboratory conditions. To isolate the heterotrophic component attributable to microbial metabolism alone, plant-derived CO₂ fluxes are excluded by using preconditioned, sieved, and homogenized soil samples incubated under standardized moisture and temperature conditions, allowing quantification of cumulative C-CO₂ evolution over time, providing a robust proxy for microbial biomass, activity, and soil health. The protocol includes soil preparation, moisture adjustment, sealed-vial incubation, IRGA-based CO₂ measurement, and calculation of cumulative respiration. In this study, we assessed SBR using an infrared gas analyser (IRGA), which allows monitoring of soil CO₂ dynamics under controlled conditions. Representative results showed that compost addition enhanced microbial respiration in arid soils from the Tabernas Desert, indicating a strong stimulation of microbial processes following organic amendment. These findings highlight the usefulness of SBR as an indicator of soil management effects on microbial activity, particularly in degraded arid environments. Methodologically, the IRGA-based protocol offers a practical tool for research and teaching applications related to soil carbon dynamics.
Hemophilic arthropathy is a major cause of morbidity in patients with hemophilia, resulting from recurrent joint bleeding and progressive synovial and osteochondral damage. Although magnetic resonance imaging (MRI) is the reference standard for evaluating hemophilic joints, its routine use is limited by cost and accessibility. Musculoskeletal ultrasound (MSK-US) has emerged as a practical alternative; however, its diagnostic performance relative to MRI requires further evaluation. The objective of this study is to evaluate the diagnostic accuracy of MSK-US for detecting hemophilic arthropathy using MRI as the reference standard. This retrospective diagnostic accuracy study included 150 patients with hemophilia who underwent both MSK-US and MRI of the same joint within a three-month interval. Ultrasound positivity was defined as the presence of at least one abnormal feature (synovial hypertrophy, joint effusion, cartilage damage, or bone erosion). Sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), likelihood ratios, and Cohen's kappa were calculated. ROC analysis was performed using HEAD-US scores. MSK-US demonstrated a sensitivity of 91.1%, specificity of 78.9%, PPV of 92.7%, NPV of 75.0%, and overall accuracy of 88.0%. Agreement with MRI was good for synovial hypertrophy (κ = 0.72) and joint effusion (κ = 0.69), and moderate for cartilage damage (κ = 0.58) and bone erosion (κ = 0.55). ROC analysis showed good overall diagnostic performance (AUC = 0.86; 95% CI, 0.80-0.91). Diagnostic performance was highest for synovial abnormalities and lower for structural joint damage. MRI-confirmed arthropathy was present in 74.7% of patients, reflecting a selected cohort with a high prevalence of joint pathology. In this selected retrospective cohort, MSK-US demonstrated good diagnostic performance for detecting hemophilic arthropathy, particularly synovial abnormalities. MSK-US may serve as a complementary tool for clinical assessment, triage, and longitudinal monitoring, while MRI remains important for comprehensive evaluation of structural joint damage.
RAD51 is a central protein in the homologous recombination (HR) pathway and is essential for the accurate repair of DNA double-strand breaks (DSBs). Following DSB formation, DNA end resection generates single-stranded DNA substrates that facilitate the recruitment and assembly of RAD51 nucleoprotein filaments at sites of damage. This process results in the formation of discrete nuclear RAD51 foci, which serve as a widely accepted functional readout of HR activity and a surrogate marker of HR proficiency. Because defects in HR are common in several malignancies, particularly ovarian and breast cancers, assessment of RAD51 foci formation has emerged as an important approach for evaluating DNA repair capacity and predicting response to DNA-damaging therapies, including platinum compounds and poly(ADP-ribose) polymerase (PARP) inhibitors, whose efficacy is strongly influenced by HR repair status. This manuscript describes a simple, reliable, and reproducible immunofluorescence-based protocol for the detection and quantification of RAD51 nuclear foci in cultured ovarian cancer cells. The method involves induction of DNA damage by ionizing radiation (IR), followed by fixation, immunostaining with antibodies against RAD51 and γH2AX, confocal microscopy, and manual quantitative analysis of RAD51/γH2AX co-localized foci. The protocol can be applied under basal conditions or after genetic and pharmacological perturbations to determine their effects on HR function. Representative results demonstrate robust induction of RAD51 foci in HR-proficient ovarian cancer cells following DNA damage, whereas RAD51 depletion markedly reduces foci formation despite comparable levels of DSBs, confirming assay specificity. Overall, this protocol provides a robust and reproducible functional assay for assessing HR competency, with broad applications in preclinical and potentially translational cancer research.
Concussive brain injury (CBI), the pathophysiological substrate underlying clinical concussion, is a frequent yet insufficiently understood condition with potential long-term neurological impairment in a subset of patients. Especially repetitive CBI, i.e., in contact sports, has been associated with lasting cognitive deficits and progressive neurodegeneration (e.g., chronic traumatic encephalopathy, CTE). To address this knowledge gap, a reproducible mouse model of closed-head rotational brain injury that recapitulates key biomechanical and pathological features of CBI was established. A stereotactically guided electromagnetic impactor was used to deliver a standardized strike to the intact skull. To reduce focal strain on the skull and adjacent brain tissue, the impactor tip was fitted with a custom-made silicone cap. This configuration reliably induced head rotation with low inter-animal variability while preventing skull fractures or microscopic tissue injury. To preserve physiological neuronal and vascular activity and to avoid potentially neuromodulatory effects of deep anesthesia, brain injury was induced in conscious mice under light sedation using the α2-agonist medetomidine. The induced impacts caused reproducible rotational head motion with only minor variability attributable to head positioning. Structural brain integrity was assessed using in vivo T2-weighted magnetic resonance imaging and confirmed by ex vivo histological analyses, which revealed no evidence of tissue disruption, contusion, or microbleeds but demonstrated a mild, widespread disruption of the microvascular interface. This novel model of rotational closed-head brain injury provides a robust experimental platform for longitudinal investigations of subtle neurovascular, inflammatory, and blood-brain barrier alterations that occur in the absence of overt structural pathology. Its application enables mechanistic insights into the pathophysiology of clinical concussion and potential neurodegenerative consequences of repetitive injury, thereby facilitating the development of urgently needed clinical biomarkers.
Knee osteoarthritis (KOA) is a prevalent degenerative joint disease that causes significant pain, functional impairment, and reduced quality of life, particularly among the aging population worldwide. While Traditional Chinese Medicine (TCM) has been widely used in clinical practice for KOA management, there has been a lack of systematic, data-driven synthesis to map the global research trends, key contributors, and core themes in this area. This study conducts a comprehensive bibliometric analysis to map the research landscape, identify trends, and forecast future directions in the application of TCM for KOA. Articles published between 2005 and 2025 were retrieved from the Web of Science Core Collection. A total of 339 relevant publications were analyzed using VOSviewer, CiteSpace, and the Bibliometric R package to assess contributions and trends related to countries, institutions, journals, authors, references, and keywords. Our study elucidates the global research landscape of TCM for KOA. Findings indicate a rapidly growing trend in publications, with China as the predominant contributor, although international collaboration remains limited. Leading contributors include authors Wang Peimin and Liu Jun, the Journal of Ethnopharmacology (publication volume), and Osteoarthritis & Cartilage .(citation impact). Research focuses on herbs such as ginger and peony, as well as on formulas such as Duhuo Jisheng Decoction. Emerging methodologies such as network pharmacology and molecular docking are clarifying the mechanisms of TCM, with future trends pointing to inflammation, oxidative stress, and apoptosis. This study provides valuable insights to guide future research and advance the modernization of TCM for KOA.
This study aimed to validate latex immunoturbidimetric assays for cystatin C (Cys-C), neutrophil gelatinase-associated lipocalin (NGAL), and retinol-binding protein (RBP), and to evaluate their combined clinical value for the early diagnosis of diabetic nephropathy (DN). In addition, a comparison was made between the diagnostic efficacy of serum and urine samples. The study comprised 100 patients with early DN and 100 control subjects. Serum and urine levels of Cys-C, NGAL, and RBP were measured using an analyzer. Method verification demonstrated that all assays were performed in accordance with the manufacturer's specifications, with high accuracy, precision, and correlation with reference methods. Serum Cys-C, NGAL, RBP-S, and their urinary counterparts were significantly higher in the DN group (p < 0.05). The combined detection of serum Cys-C, NGAL, and RBP-S provided a diagnostic sensitivity of 89.0%, specificity of 92.0%, and an AUC of 0.935. The corresponding urinary panel achieved a sensitivity of 82.0%, specificity of 88.0%, and an AUC of 0.876. In conclusion, the assays are reliable. The combined detection of Cys-C, NGAL, and RBP in serum offers the highest diagnostic value for early DN, while urine analysis provides complementary information about tubular injury.
Microbial habitats in nature are often characterized by low concentrations of mixed nutrients, spatial heterogeneity, and temporal fluctuations. However, traditional laboratory culturing methods fail to replicate these conditions. Batch cultures cannot sustain growth in low-nutrient environments, while chemostats maintain steady-state growth with a single limiting nutrient but are challenging to implement when the goal is to maintain defined low concentrations of nutrient mixtures or to introduce rapid fluctuations. Microfluidic systems generate dynamic environments but yield insufficient biomass for population-level omic analyses. To address these limitations, we introduce the millifluidic continuous culture device (MCCD), a versatile platform for studying microbial responses to stable and fluctuating nutrient conditions. The MCCD houses bacterial populations inside a Sterivex filter (0.45 µm polyvinylidene fluoride [PVDF] porous filtering membrane), where a continuous flow of media sustains stable culture conditions while preventing nutrient depletion. A three-way solenoid valve system, controlled via custom Matlab software, enables precise, minute-scale nutrient fluctuations. This protocol provides a step-by-step guide to operating the MCCD in two modes: (1) constant low-nutrient conditions and (2) fluctuating-nutrient conditions. Using this system, Escherichia coli grew exponentially in a mixture of amino acids and nucleobases present at tens to hundreds of nanomolar concentrations, reaching cell concentrations on the order of 109 cells/mL. By recreating key features of natural microbial habitats, the MCCD enables the study of bacterial growth and physiology under controlled yet ecologically relevant conditions in E. coli and other microbial species.
Breast cancer is the second most common malignant tumor in the world, seriously threatening the lives of women and imposing a huge economic burden. This study aims to explore the value of miR-362-3p combined with Doppler ultrasound in the diagnosis of breast cancer. A total of 182 breast cancer patients and 147 patients with benign breast disease were included in this study. The plasma miR-362-3p levels of the patients were measured using Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR). The chi-square test was used to analyze the differences in the parameters of Doppler ultrasound between the two groups of patients. The receiver operator characteristic (ROC) curve was used to evaluate the diagnostic effectiveness of miR-362-3p, Resistance Index (RI), and Pulsatility Index (PI). The diagnostic efficiency of Doppler ultrasound combined with plasma miR-362-3p in breast cancer was analyzed through the fourfold table method. The miR-362-3p levels were markedly decreased in breast cancer patients. There were significant differences in two-dimensional ultrasound parameters. miR-362-3p, RI, and PI have diagnostic value for breast cancer. The combined diagnostic value of the three factors was higher. Ultrasound combined with miR-362-3p significantly improved the sensitivity, accuracy, and negative predictive value in breast cancer diagnosis. Doppler ultrasound combined with miR-362-3p could enhance the diagnostic efficiency of breast cancer, which may provide a non-invasive and potential auxiliary diagnostic tool for breast cancer.
Cellular senescence is a physiological process characterized by irreversible cell cycle arrest that impairs tissue regeneration and function. This phenomenon has emerged as a key driver of neurodegeneration, fueled by the accumulation of senescent cells within the central nervous system (CNS). Senescent cells acquire a pro-inflammatory senescence-associated secretory phenotype (SASP) that sustains chronic neuroinflammation and disrupts the neuronal microenvironment. Consequently, essential processes such as neurogenesis, synaptic plasticity, and neuronal survival are compromised. An extensive body of literature associates cellular senescence with several neurodegenerative disorders, such as Parkinson's disease, Alzheimer's disease, or multiple sclerosis, and acute neuronal-related damage, such as cerebral ischemia or traumatic brain injury. The combined assessment of senescence-associated β-galactosidase (SA-β-gal) activity and Nissl staining in histological sections provides a comprehensive approach to evaluate cellular senescence and neuronal integrity simultaneously within the same tissue context. This strategy enables precise spatial correlation between the accumulation of senescent cells in specific vulnerable regions (e.g., the hippocampus or cortex) and neuronal loss or tissue damage. By integrating a functional marker of senescence with a classical indicator of neuronal morphology and density, this approach strengthens the interpretative robustness of the analysis. Moreover, it enables a more accurate characterization of the relationship between senescent burden and neurodegenerative changes, maximizing the information yield from limited tissue samples. Moreover, this protocol can determine how senescent cell accumulation occurs in response to interventions (pharmacological, genetic manipulation, etc.) in rodent models of neurodegenerative diseases, thereby providing a powerful tool to analyze this contribution to their pathophysiology.
Premature birth is strongly associated with cardiac dysfunction, including impaired ventricular function and altered cardiac structure, which can lead to progressive heart failure and other short- and long-term morbidities. However, the natural history of cardiac dysfunction in infants born prematurely is not well defined. In the lamb model of bronchopulmonary dysplasia with associated pulmonary hypertension (BPD-PH), lambs are delivered at 110-128 days gestation (full term is approximately 145 days) and mechanically ventilated. The lambs develop cardiopulmonary complications of prematurity, including alveolar simplification on lung histology, the hallmark of BPD, and signs of increased pulmonary vascular resistance on echocardiography, consistent with evolving BPD-PH. This article describes a protocol for serial assessment of cardiac morphometry and function by echocardiography in preterm and former preterm lambs (up to approximately two months postnatal age). The protocol was developed by adapting guidelines from the American Society of Echocardiography. Echocardiography is serially performed on intubated and moderately sedated lambs using a bedside ultrasound system. Atrial and ventricular dimensions, right and left ventricular function, and PH-related measurements are obtained at each echocardiographic assessment. Measurements are reproducible and correlate with clinical status. This echocardiography protocol for assessing cardiac structure and function in lambs enables characterization of BPD-PH and evaluation of therapeutic approaches.
This protocol presents a novel in vivo application of X-band (9.5 GHz) electron paramagnetic resonance spectroscopy for monitoring melanin-associated radical dynamics in zebrafish (Danio rerio) melanoma xenograft models. The goal of this method is to enable direct, label-free, and quantitative assessment of melanin-associated redox changes during embryonic development, and tumor-host interactions in a physiologically relevant vertebrate model. By leveraging the intrinsic paramagnetic properties of melanin, this approach provides complementary biochemical information that cannot be obtained using conventional fluorescence-based imaging alone. Importantly, the detected electron paramagnetic resonance signal reflects the redox-active fraction of the melanin polymer and therefore serves as a redox-sensitive readout rather than a direct measure of total pigment abundance. Method performance was validated through selective detection of melanin-associated radicals in pigmented wild-type embryos, absence of signal in albino controls, statistically significant developmental changes in normalized electron paramagnetic resonance signal across independent biological replicates, and comparable results obtained using alternative sample holders and frozen samples. By combining X-band electron paramagnetic resonance spectroscopy with zebrafish xenograft models, this protocol provides a scalable, ethically favorable, and transferable platform for preclinical melanoma research, redox biology studies, and evaluation of melanogenesis-modulating interventions.
Insomnia is a common sleep disorder that leads to impaired daytime function and increased risk of comorbidities, significantly impacting patients' quality of life. Current treatments, primarily cognitive behavioral therapy and pharmacotherapy, are limited by issues such as drug dependence, tolerance, and withdrawal rebound. Tuina therapy has been shown to regulate the nervous, endocrine, and immune systems, while the orexin system is a key regulator of the sleep-wake cycle. This has prompted the exploration of whether Tuina alleviates insomnia by modulating the hypothalamic orexin system. This protocol describes the methods of Tuina intervention in a rat model of primary insomnia induced by the modified multiple platform water environment method. We randomized 64 Wistar rats into four groups: control, model, Tuina, and orexin antagonist. Behavioral assessments (open field test, pentobarbital-induced sleep test) were conducted, and the expression of Orexin-A in the hypothalamus was detected via real-time quantitative PCR and immunohistochemistry. The protocol aims to evaluate the efficacy of Tuina and investigate its potential mechanism related to the orexin system, providing a reference for the application and mechanistic study of Tuina in sleep disorders.
Aortic stiffening is an independent risk factor for cardiovascular disease and other chronic conditions, including cognitive decline, kidney dysfunction, vision impairment, and reduced glucose-insulin function. In vivo, aortic stiffness is commonly assessed using tonometry- or ultrasound-based techniques that visualize arterial waveforms or longitudinal arterial segments, respectively. However, in vivo measurements are influenced by multiple factors-such as arterial pressure and autonomic input-which limit mechanistic insight into how and why aortic stiffness changes. Preclinical murine models, which permit direct acquisition of aortic tissue, offer a unique experimental framework to assess both in vivo aortic stiffness and the intrinsic mechanical properties of the aorta, free from confounding physiological variables. These models also enable direct interrogation of the circulating milieu (i.e., collection of circulating bioactive molecules in the bloodstream) and its role in modulating aortic stiffness across the preclinical-to-clinical translational spectrum. Alterations in the circulating milieu have emerged as a key mechanistic underpinning of aortic stiffening in numerous conditions-including primary aging and premature aging associated with cancer and cancer therapies-across both preclinical and clinical studies, as well as in mediating the effects of interventions. This article provides a step-by-step guide for assessing: (1) intrinsic aortic stiffness (elastic modulus) in preclinical murine models, and (2) the contribution of the circulating milieu (and its constituents) to aortic stiffening using both preclinical and clinical biospecimens.
Heart disease remains one of the leading causes of mortality worldwide, creating an urgent need for accurate and scalable predictive systems that enable early diagnosis and timely clinical intervention. Traditional machine learning approaches often struggle to efficiently process large-scale medical datasets and lack interpretability, limiting their usefulness for supporting clinical decision-making. To address these challenges, this study proposes a Cluster Visualized Distributed Machine Learning framework for heart disease prediction. The framework incorporates two distributed algorithms: Cluster Visualized Hadoop Distributed Decision Tree (CViHDDT) and Cluster Visualized Hadoop Distributed K-Nearest Neighbor (CViHDKNN). The proposed models leverage Hadoop's MapReduce framework for distributed computation across large datasets, while integrating K-Means clustering for improved data organization and visualization. This cluster-based visualization enhances interpretability by allowing clinicians to better understand relationships among patient risk factors and prediction outcomes. Experimental evaluation was conducted using the UCI Heart Disease dataset in a Hadoop-based distributed environment. The results show that CViHDKNN achieved superior predictive performance, achieving 85.25% accuracy and 88% recall, outperforming the CViHDDT model, which achieved 80.33% accuracy. Adjusting classification cut-off values also influenced sensitivity and detection rates: lower cut-offs improved true-positive detection while maintaining acceptable false-positive levels. These findings demonstrate that clustering-enhanced distributed learning improves scalability, predictive accuracy, and clinical interpretability for heart disease prediction.
The urethra, lined by epithelial cells, serves as the conduit for urine outflow from the body. The epithelial lining of the urethra comprises distinct cell types with gene signatures indicative of roles in antimicrobial and immune defense. Resident macrophages embedded in the urethral epithelial layer represent a transcriptionally distinct subtype with purported roles in immune surveillance and antigen presentation. Urinary pathogens ascend up the urethra to reach the bladder. A study of the urethral epithelial lining and associated immune cells will shed light on host defense mechanisms in the lower urinary tract. A central goal of this protocol is to provide optimized methods for dissecting the female mouse urethra and isolating the epithelial lining for downstream analyses. The protocol describes an optimized method for isolating epithelial tissue from the female mouse urethra by gentle enzymatic and mechanical separation. Subsequent to epithelial isolation, methods for gentle enzymatic digestion of isolated urethral epithelium and associated immune cells to obtain high-viability single-cell suspensions are described. The protocol also details methods for flow cytometry analysis of the isolated mouse urethral epithelial cells and epithelial-associated immune cells. Additionally, methods to generate stratified 3D urethral epithelial organoids from isolated epithelial cells are presented here. The protocol also details an optimized method for whole-mount immunostaining of urethral epithelial sheets, which can be used to observe the morphology and molecular structures of mouse urethral epithelium and associated immune cells. Overall, the methods described here for isolation and single-cell digestion of mouse urethral epithelial cells enable downstream analyses, including immunostaining, flow cytometry, organoid generation, and single-cell RNA-sequencing.
This study aimed to determine whether piribedil therapy alters the gut microbiota of patients with Parkinson's disease (PD), providing a theoretical reference for understanding gut microbiota alterations induced by piribedil and their potential clinical implications. Fecal samples were analyzed using 16S ribosomal RNA (16S rRNA) gene sequencing. Comparisons were made between patients with PD who took piribedil (piribedil group), patients with PD who did not take piribedil (PD group), and healthy controls (blank group). Compared with the blank group, the relative abundance of Staphylococcus, Rhodococcus, and other genera was higher in the PD group, whereas the relative abundance of Achromobacter and Delftia was lower. Furthermore, the relative abundance of Achromobacter, Delftia, and Stenotrophomonas was higher in the piribedil group compared to the PD group, whereas the relative abundance of Staphylococcus, Rhodococcus, and other species was lower. Compared to healthy individuals, the gut microbiota of patients with PD exhibited significant changes. The gut microbiota of patients taking piribedil significantly differs from that of untreated patients. These results suggest an association between piribedil and altered gut microbiota in patients with PD.
Green synthesis of metal nanoparticles (NPs) using biological systems provides a sustainable alternative to conventional chemical fabrication methods. This protocol presents reproducible experimental and analytical procedures for the synthesis of gold (Au) and silver (Ag) NPs using bacterial cultures, fungal filtrates, and plant leaf extracts as reducing and stabilizing agents. AgNPs were synthesized using extracts from Psidium guayaquilensis, Acanthophora spicifera, and Earliella sp., exhibiting characteristic ultraviolet-visible (UV-Vis) absorption bands between 405 and 425 nm that confirmed NP formation. A design-of-experiments approach was implemented to evaluate the influence of environmental factors, including oxygen conditions, pH, Au concentration, cell concentration, electron donor type, and temperature, on the synthesis of AuNPs by Shewanella oneidensis and Cupriavidus metallidurans. Under ideal conditions (0.2 mM Au and pH 5), S. oneidensis produced predominantly spherical AuNPs with an average size of 43.6 ± 11.0 nm and a characteristic absorption peak at 520 nm. NP formation and morphology were confirmed using UV-Vis spectroscopy and transmission electron microscopy. This workflow provides a reproducible platform for biogenic NP synthesis and supports applications in biosensing, bioremediation, and antimicrobial technologies.
Malignant biliary strictures (MBS) are a challenging clinical issue with limited therapeutic options for unresectable cases. This protocol establishes a standardized minimally invasive approach of endoscopically-guided biliary radiofrequency ablation (RFA) combined with self-expandable metal stent (SEMS) placement via endoscopic retrograde cholangiopancreatography (ERCP) for MBS. The core workflow includes preoperative preparation, endoscopic exploration and cholangiography, direct cholangioscopic assessment, targeted RFA of the stenotic segment, SEMS deployment, and postoperative management and follow-up. Key procedural parameters are defined: bipolar RFA at 8 W for 90-120 s, and placement of a covered SEMS (CSEMS) with 1 cm extension beyond the stenosis margins. Clinical application in a representative case achieved rapid resolution of jaundice (70% reduction in total bilirubin at 5 days post-procedure) and technical success with unobstructed biliary patency at 1 month. The procedure has a favorable safety profile, with no major acute complications observed in the case. This standardized protocol provides a reproducible method for clinical practitioners, and the combined technique offers a valuable palliative option for unresectable MBS by prolonging stent patency and alleviating biliary obstruction symptoms. Further multicenter trials are needed to validate its long-term efficacy in larger patient cohorts.
The incidence rate of atrial fibrillation is increasing year by year, which is characterized by time progression, but its mechanism is unknown. Vein of Marshall (VOM), also known as the left atrial oblique vein, plays a crucial role in collecting venous return from atrial tissue. VOM originates from the posterior wall of the left atrium and is closely related to structures such as the left atrial appendage and pulmonary vein. VOM plays an important role in the occurrence and maintenance of atrial fibrillation, but there have been no other reports on its role in atrial fibrillation-related diseases. In this research, the authors innovatively used over-the-wire (OTW) balloons to collect blood samples from the VOM patients before atrial fibrillation ablation surgery for biochemical analysis. This study measured a recognized biomarker associated with the onset of atrial fibrillation: atrial natriuretic peptide (ANP), a biomarker of atrial stretching and structural remodeling, a biologically active natriuretic peptide that plays an important role in atrial fibrillation. Compared with samples from the anterior interventricular vein (AIV) and coronary sinus (CS), ANP concentration was significantly upregulated in VOM blood, indicating that VOM blood better captures atrial-specific biochemical signals. This research found that VOM blood provides a good representation of the microenvironment associated with atrial fibrillation, providing scientific evidence for the search for biomarkers and therapeutic targets for the future.
This study aimed to develop and preliminarily validate the Nutrition Impact Symptom-Esophageal Cancer scale (NIS-EC) and evaluate its clinical use for individualized postoperative nutritional nursing. This two-stage study included scale development/preliminary psychometric evaluation, followed by clinical application. In stage I, items were generated from a literature review, the Theory of Unpleasant Symptoms, two rounds of Delphi consultation, and pilot testing. Thirty clinically stable patients with esophageal cancer completed the NIS-EC for item analysis, reliability testing, validity assessment, and 14 ± 2 day retesting. In stage II, an unblinded single-arm phase II supportive-care study with a non-concurrent historical-control comparison was conducted among 107 patients after radical surgery for esophageal cancer. Fifty-seven patients received NIS-EC-guided individualized nutritional nursing, whereas 50 historical controls received routine postoperative nutritional nursing. Outcomes were assessed at baseline and 4 weeks. The final NIS-EC contained 22 items in three domains: digestive tract symptoms, malaise-related symptoms, and psychological-emotional symptoms. The scale showed good internal consistency, with a Cronbach's alpha of 0.921, split-half reliability of 0.904, and test-retest reliability of 0.913. Content and structural validity were acceptable, and the total score correlated with PG-SGA score (r = 0.784, P < 0.001). At week 4, the intervention group had lower NIS-EC scores, greater improvements in BMI, albumin, prealbumin, and hemoglobin, higher attainment of protein intake targets, fewer postoperative complications, and a shorter postoperative hospital stay than historical controls (P < 0.05). In conclusion, the NIS-EC provides preliminary, reliable, and valid symptom profiling in esophageal cancer. NIS-EC-guided nutritional nursing may support postoperative symptom control and nutritional recovery, but multicenter randomized controlled trials are required to validate these findings.