Serum calprotectin is an emerging inflammatory biomarker, but data on its stability remain limited. This study aimed to determine the 5-day stability of serum calprotectin stored at 2 temperatures: ‒20 °C and ‒80 °C.

This study followed Checklist for Reporting Stability Studies recommendations using leftover serum samples. Analysis was undertaken using 2 analytical methods on an automated Siemens Atellica Solution analyzer. Twenty samples in ‒20 °C storage were analyzed using fCAL turbo reagent (BÜHLMANN), and another 10 samples in ‒20 °C storage were analyzed using GCAL reagent (Gentian Diagnostics). A further 10 patient samples stored at ‒80 °C were analyzed using fCAL turbo reagent. The maximum permissible difference was defined as total error, which was 56.43% for fCAL turbo reagent and 46.44% for GCAL reagent.

The instability equations were y = 7.6695 × time (days) and y = 0.8553 × time (days) for temperatures of ‒20 °C and ‒80 °C, respectively, when calprotectin was determined using fCAL turbo reagent and y = 12.7011 × time (days) at ‒20 °C using GCAL reagent.

Results from samples stored for a maximum of 5 days at ‒80 °C are more reliable than those stored at ‒20 °C, which may have an impact on clinical interpretation of the results.

To delineate the onset changes of acute ischemic stroke (AIS) patients with different Trial of Org 10172 in Acute Stroke Treatment (TOAST) subtypes in circadian rhythm, seasonal distribution, and weekdays/holidays.

Patients with AIS admitted to the Emergency Stroke Center of the 960th Hospital of PLA between 1/4/2019 and 30/12/2024 were enrolled as study subjects. Based on medical history and examination results, enrolled patients were classifiedinto three subgroups: large-artery atherosclerosis (LAA), small-artery occlusion (SAO), and cardioembolism (CE). Onset time, laboratory test results, and clinical symptoms were compared among the three groups to investigate the rhythmic variations across different TOAST subtypes.

A total of 722 AIS patients were enrolled. For diurnal distribution, LAA patients had higher incidence in early morning, while CE patients showed clustered onset at night. In seasonal distribution, LAA and CE had higher incidence in Quarter 1, whereas SAO patients had higher incidence in Quarter 3. Notable differences existed in onset patterns between weekdays and holidays: significant morning onset peak on weekdays, but irregular onset rhythm on holidays.

This study identified the distribution patterns of different TOAST subtypes of cerebral infarction across circadian rhythm, seasonal variation, and weekdays/holidays differences, thereby providing a valuable reference for medical institutions to develop subtype-specific, rhythm-aligned, season-adapted precise prevention strategies.

Steatotic liver disease associated with metabolic dysfunction (MASLD) has become the most common chronic liver disease worldwide. The impact of this condition is not limited to liver dysfunction; its relationship with chronic kidney disease (CKD) is significant, as it shares pathophysiological mechanisms and an increased risk of adverse cardiovascular outcomes. In this context, the coexistence of MASLD and CKD does not appear to be solely due to shared risk factors, but rather to convergent biological mechanisms that promote liver injury, as well as glomerular and tubular damage, including insulin resistance, inflammation, lipotoxicity, oxidative stress, neurohormonal activation, and fibrotic progression.

A detailed search was conducted in databases such as ScienceDirect, PubMed, Sage Journals, Nature, and SpringerLink to evaluate literature related to the pathophysiological mechanisms of renal dysfunction in patients with MASLD. This review analyzes the relationship between MASLD and CKD from a clinical perspective, with an emphasis on shared pathophysiological axes.

MASLD and CKD represent much more than the coexistence of two prevalent diseases; they should be understood as the expression of systemic metabolic dysfunction, in which insulin resistance, chronic low-grade inflammation, lipotoxicity, oxidative stress, neurohormonal activation, and fibrotic progression converge.

Primary aldosteronism is an underdiagnosed and potentially treatable cause of secondary hypertension. We evaluated the incidence of clinically recognized primary aldosteronism among adults with clinically coded hypertension receiving intensive multidrug antihypertensive therapy in the TriNetX Analytics Network from 2010 through 2024. Among 1 888 042 eligible adults without prior primary aldosteronism, 1528 incident diagnoses were identified, corresponding to an incidence proportion of 0.081%, or 0.81 cases per 1000 patients. Diagnostic recognition varied by demographic subgroup and was highest among younger adults, males, Black or African American individuals, and Hispanic or Latino individuals. These findings suggest that documented recognition of primary aldosteronism in routine clinical practice remains low even among patients receiving intensive antihypertensive therapy. Because diagnoses were identified using electronic health record coding rather than systematic biochemical testing, results should be interpreted as clinical recognition rather than true disease prevalence.

The postmenopausal period presents a significant challenge to women's health, characterised by vasomotor, psychological, and sleep disturbances. This systematic review and meta-analysis synthesised evidence on aromatherapy for menopausal symptoms.

We searched Cochrane Library, Web of Science, ScienceDirect, PubMed, Scopus, SID, and Google Scholar until January 2, 2026. The protocol was registered (PROSPERO: CRD420261303084). Randomised controlled trials and quasi-experimental studies were included. The Cochrane Risk of Bias tool and GRADE approach were used for quality assessment and certainty of evidence. Meta-analyses were performed using RevMan 5.3.

Of 4435 records, 21 articles from 17 studies (n = 1347) were included. Aromatherapy significantly improved sexual function (MD: 7.05, 95% CI: 3.64-10.45), sleep quality (MD: -3.95, 95% CI: -5.94 to -1.97), overall menopausal symptoms (SMD: -1.00, 95% CI: -1.43 to -0.58), vasomotor symptoms (SMD: -0.79, 95% CI: -1.11 to -0.47), physical symptoms (SMD: -0.78, 95% CI: -1.10 to -0.46), somatic symptoms (MD: -1.34, 95% CI: -2.46 to -0.23), psychological symptoms (SMD: -0.59, 95% CI: -0.96 to -0.23), anxiety (SMD: -0.63, 95% CI: -1.10 to -0.16), and depression (SMD: -0.57, 95% CI: -0.85 to -0.28). No significant effect was found for urogenital symptoms. GRADE certainty was 'Very Low' for sexual function and sleep quality, and 'Low' for other outcomes.

Preliminary evidence suggests that aromatherapy may be a beneficial complementary therapy for alleviating some menopausal symptoms. However, given the substantial heterogeneity, methodological limitations, and limited number of studies for subgroup analyses, firm clinical recommendations cannot be made at this time. More rigorous, large-scale, multi-centre randomised controlled trials with standardised interventions and consistent adverse event reporting are required before definitive clinical recommendations can be made.

Neurohormonal overactivation and the resulting sodium avidity, driving sodium retention, are important mechanisms underlying the signs and symptoms of heart failure (HF). Blockade of the renin-angiotensin-aldosterone and adrenergic systems therefore represents a central therapeutic target and cornerstone of HF pharmacotherapy, theoretically counteracting sodium avidity. Paradoxically, evidence on how neurohormonal blockade affects markers of sodium avidity, natriuresis, and diuresis remains fragmented, with no integrated summary to date. This review aims to synthesize available evidence on the impact of guideline-directed medical therapy and other HF therapies on sodium excretion/diuresis in HF [Fig. 1]. Here we present comprehensive review of available data on this topic. The scarcity of high-quality studies, small sample sizes, and conflicting results preclude definitive conclusions; accordingly, we refrain from formulating any. Interpretation is further limited by the lack of a standardized method for assessing sodium excretion independent of confounders such as renal function and dietary sodium intake, which restricts reproducibility across studies.

Subclinical atherosclerosis represents an important stage in the continuum of cardiovascular disease, characterized by structural or functional vascular abnormalities in the absence of overt clinical events. This review examines the biological mechanisms and clinical evidence supporting exercise as both a preventive and potential disease-modifying intervention in individuals with imaging-detected subclinical atherosclerosis, with particular emphasis on endothelial function, vascular remodeling, inflammation, plaque composition, and cardiovascular risk.

Increasing evidence indicates that exercise exerts vascular effects that extend beyond conventional risk-factor modification. Exercise improves endothelial function, vascular compliance, and nitric oxide bioavailability through shear stress-mediated activation of endothelial nitric oxide synthase (eNOS), while also modulating oxidative stress, myokine signaling, vascular inflammation, and macrophage phenotype. These effects may promote plaque stabilization and influence atherosclerotic lesion composition. Importantly, exercise-associated increases in coronary artery calcium observed in highly active individuals may reflect a shift toward more densely calcified and potentially more stable plaque rather than an accumulation of high-risk lipid-rich lesions. Clinical and meta-analytic evidence further suggests modality-specific effects, with interval training showing favorable effects on arterial stiffness and combined aerobic-resistance training improving endothelial function. Exercise may therefore complement pharmacological risk-factor modification by targeting vascular pathways that are not fully addressed by conventional therapies. Exercise should be considered an integral component of cardiovascular risk management in individuals with subclinical atherosclerosis rather than solely a primary-prevention strategy. Its potential benefits extend from improving vascular function and reducing inflammation to modifying plaque characteristics and promoting plaque stability. Future studies should determine whether exercise prescriptions can be individualized according to atherosclerotic burden, plaque phenotype, imaging characteristics, and circulating biomarkers to establish the optimal exercise modality, intensity, and dose across different patient populations.

Acute unilateral vestibulopathy (AUVP) and posterior circulation stroke (PCS) are the two common causes of the acute vestibular syndrome. We developed and evaluated machine learning models to differentiate AUVP and PCS using combinations of patient history, examination, and vestibular tests.

We recruited 294 patients presenting to the Emergency Room (ER) with acute vestibular syndrome (AUVP: n = 163, PCS: n = 131). Data from history, bedside examination and vestibular tests (video-nystagmography (VNG), video head-impulse test (VHIT), vestibular-evoked myogenic potentials (VEMP) and subjective visual horizontal) were used for machine learning model development. Different subsets of data simulated three scenarios hierarchically reflecting different levels of clinical expertise and resources: Tier 1 represented an ER with neuro-otology support (history, neuro-otological examination, VNG, VHIT, ocular VEMP), Tier 2 an ER with VHIT (history, basic examination, VHIT) and Tier 3 an ER reliant on history and basic examination only. Model performance was also compared against the HINTS test (head impulse, nystagmus, test-of-skew).

Our best-performing models used the CatBoost or XGBoost algorithms and identified PCS with accuracies of 96.6% (95% CI: 93.3-99.9%), 94.6% (95% CI: 90.5-98.6%) and 88.8% (95% CI: 86.0-91.6%) for Tiers 1, 2 and 3. HINTS by experts achieved 94.6% accuracy. The most important variables were the bedside head-impulse test, presence of focal neurological symptoms and spontaneous nystagmus slow phase velocity in Tier 1; focal neurological symptoms in Tier 2; and age in Tier 3.

Machine learning models can accurately separate PCS and AUVP and hold promise as diagnostic aids for frontline clinicians.

A non-bifurcating cervical carotid artery (NBCCA) is a rare anomaly. Hypoplasia of the internal carotid artery (ICA) is also rare. To the best of our knowledge, their simultaneous coexistence has not been previously reported.

We report a case of NBCCA associated with ipsilateral ICA hypoplasia diagnosed by magnetic resonance angiography (MRA).

A 52-year-old woman was transported to our hospital by ambulance with severe headache. Magnetic resonance imaging revealed a large suprasellar mass. MRA showed impaired delineation of the right ICA and a 2-mm left ICA aneurysm. Extracranial MRA revealed a right NBCCA. Computed tomography showed a narrow right carotid canal. Right NBCCA concomitant with congenital hypoplasia of the ipsilateral ICA was diagnosed.

Careful imaging assessment is important to identify these rare anatomical variants and associated aneurysms on the collateral pathway. Awareness of such variations is important in clinical practice, particularly for imaging interpretation and procedural planning.

The CX3CL1-CX3CR1 axis, comprising the chemokine fractalkine (CX3CL1) and its immune cell receptor CX3CR1, links immune activation to vascular pathology in people with HIV (PWH). Chronic inflammation persists in PWH despite viral suppression with antiretroviral therapy and contributes to high rates of cardiometabolic comorbidities. This is partly due to dysregulated leukocyte trafficking and endothelial activation. This review synthesizes preclinical, genetic, and clinical evidence on the multifaceted roles of CX3CR1 across immune, vascular, and cardiometabolic processes. CX3CR1 is expressed on monocyte and cytotoxic T-cell subsets implicated in endothelial injury, tissue trafficking, and plaque progression. On the other hand, CX3CL1 is expressed on activated endothelial and stromal cells, which promotes leukocyte adhesion and recruitment into inflamed tissues. In PWH, persistent immune activation and cytomegalovirus co-infection are associated with the expansion of differentiated CX3CR1-expressing T-cell populations, supporting the relevance of this pathway to HIV-associated inflammatory comorbidities. At the genetic level, CX3CR1 polymorphisms, including V249I and T280M, alter receptor signaling and have been associated with HIV disease progression and cardiovascular disease risk, highlighting CX3CR1 as both a biomarker and potential mediator of immune-driven pathology. Across preclinical models, pharmacological targeting of CX3CR1 or CX3CL1 attenuates inflammation, fibrosis, and vascular injury in selected disease contexts. However, the effects of CX3CR1 signaling are tissue- and cell-type-specific, and blockade may carry potential risks in settings where CX3CR1 supports immune surveillance, mucosal repair, or macrophage homeostasis. This review evaluates the therapeutic promise and safety considerations of targeting the CX3CL1-CX3CR1 axis in HIV-associated cardiovascular and inflammatory comorbidities.