Hyperuricaemia (HUA) is a recognized risk factor for cardiovascular and renal diseases. Isobavachin, a dihydroflavone derivative, demonstrates significant efficacy in reducing uric acid levels. This study investigated the nephroprotective and cardioprotective effects and molecular mechanisms of isobavachin. Through integrative network pharmacology, pathway enrichment analysis, and molecular docking, NF-κB was identified as a potential target of isobavachin in the context of hyperuricemia-related cardiac and renal injury. Isobavachin treatment inhibited the activation of the NF-κB pathway, leading to cytoprotection in uric acid (UA)-stimulated mRTEC and H9C2 cells. In chronic HUA mice, isobavachin treatment significantly improved renal pathology and reduced renal collagen deposition by inhibiting epithelial-to-mesenchymal transition. Isobavachin administration demonstrated therapeutic efficacy in attenuating myocardial injury, hypertrophy, and fibrotic remodeling. Notably, the anti-inflammatory effects of isobavachin were particularly evident in both renal and cardiac tissues, primarily mediated through its dual regulatory capacity in suppressing NF-κB pathway activation and NLRP3 inflammasome formation. In conclusion, isobavachin ameliorated cardiac and renal damage caused by chronic HUA, suggesting a new strategy to prevent HUA.

We describe a rare case of arginine vasopressin deficiency (AVP-D) in a female in her 40s that developed two weeks following symptomatic COVID-19 infection. Symptoms included polydipsia, nocturia and polyuria of 9.1 L per day. A water deprivation test demonstrated an ongoing high urine output despite increasing plasma osmolality, confirming the diagnosis. Desmopressin was commenced with good effect and titrated to clinical response. This demonstrates the importance of awareness of potential pituitary complications following COVID-19 infection, including AVP-D.

Effective treatments for post-stroke spasticity (PSS) remain limited, and the mechanism by which scalp acupuncture combined with exercise (SAE) alleviates PSS is not fully understood. This study investigated the effects of SAE in rats with PSS and explored whether SAE regulates synaptic plasticity through the PI3K/Akt pathway. A middle cerebral artery occlusion (MCAO) rat model was established, and rats were randomly assigned to five groups: Blank, Sham, MCAO, SAE, and Baclofen. All interventions were administered for 7 consecutive days. Neurological function, cerebral infarct volume, histopathology, synaptic ultrastructure, and related protein expression were then evaluated. Compared with the MCAO group, SAE improved neurological deficits, reduced muscle hypertonia, decreased infarct volume, alleviated neuronal injury, increased synapse number, and improved synaptic morphology. SAE also upregulated glial cell line-derived neurotrophic factor (GDNF), phosphorylated PI3K (p-PI3K), phosphorylated Akt (p-AKT), and synaptic proteins, including synaptophysin (SYN), postsynaptic density protein 95 (PSD-95), and growth-associated protein 43 (GAP-43). Immunofluorescence staining further suggested enhanced expression of SYN and p-Akt in the motor cortex after SAE treatment. These findings suggest that SAE may be correlated with the activation of PI3K/Akt signaling via upregulation of GDNF, thereby improving synaptic plasticity and alleviating PSS symptoms. This study investigated the effects of SAE in rats with PSS and explored the potential association between SAE intervention, PI3K/Akt pathway activity, and synaptic plasticity.

Sleep disorders are common complications following stroke, with a global meta-analysis indicating a prevalence as high as 53%. These disorders primarily include insomnia, obstructive sleep apnea (OSA), and circadian rhythm disruptions. By impairing neuroplasticity, exacerbating inflammatory responses, and interfering with the effectiveness of rehabilitation training, such disorders significantly delay neurological recovery, increase the risk of secondary stroke, and elevate the incidence of depression and anxiety. Consequently, they have become a critical factor limiting stroke rehabilitation. This article systematically reviews the application and progress of sleep interventions in stroke rehabilitation. A comprehensive literature search was conducted in PubMed, Web of Science, and CNKI databases from inception to December 2025, using keywords including "stroke," "sleep disorders," "sleep interventions," and "neurorehabilitation." Studies were included if they reported original data on sleep interventions in stroke patients, with no restrictions on study design. Data extraction and quality assessment were performed independently by two reviewers. Core strategies reviewed include cognitive behavioral therapy for insomnia (CBT-I), continuous positive airway pressure (CPAP), pharmacotherapy, and Traditional Chinese Medicine interventions such as acupuncture. Among these, CBT-I, as a first-line approach, has been shown to significantly improve sleep quality and emotional state when administered for over 8 weeks. CPAP can reduce the risk of recurrent vascular events by 55% in patients with OSA while also promoting neurocognitive recovery. Studies confirm that standardized sleep interventions, by optimizing sleep architecture and enhancing neural repair capacity, synergistically improve limb motor function and activities of daily living. Current research still faces challenges such as variable intervention adherence and insufficient mechanistic studies on non-OSA subtypes. Future efforts should rely on multidisciplinary collaboration to develop personalized intervention plans, incorporate novel technologies to optimize treatment strategies, further explore the clinical value of sleep interventions in stroke rehabilitation, and provide an evidence-based foundation for improving long-term patient prognosis.

Ischemia-reperfusion (I/R) injury induces cardiomyocyte apoptosis, oxidative stress and elevated myocardial injury markers. This study aimed to investigate whether the microRNA-548a-5p (miR-548a-5p)/phosphatase and tensin homolog deleted on chromosome 10 (PTEN) axis mediates the cardioprotection conferred by isoflurane (ISO). An in vitro hypoxia/reoxygenation (H/R) injury model was established using H9c2 cardiomyocytes, including control, H/R and ISO pretreatment groups. We detected miR-548a-5p and PTEN expression by RT-qPCR, and evaluated cell viability, apoptosis, myocardial injury markers including creatine kinase-MB (CK-MB), cardiac troponin I (cTnI), lactate dehydrogenase (LDH), and reactive oxygen species (ROS) using CCK-8, flow cytometry, ELISA and DCFH-DA staining. Dual-luciferase reporter assay validated the direct binding between miR-548a-5p and PTEN. H/R downregulated miR-548a-5p and upregulated PTEN, accompanied by decreased cell viability, increased apoptosis, myocardial injury and oxidative stress. 1.0% ISO pretreatment reversed these adverse alterations, restored miR-548a-5p and suppressed PTEN expression. miR-548a-5p inhibition attenuated ISO-elicited cardioprotection, whereas PTEN silencing restored the cardioprotective capacity compromised by miR-548a-5p inhibition. In conclusion, ISO exerts cardioprotective effects via the miR-548a-5p/PTEN signaling axis, offering a potential therapeutic target for I/R injury.

Cardiovascular diseases (CVDs) represent a significant global public health challenge. Activation of the NLRP3 inflammasome contributes to CVD pathogenesis, while autophagy mitigates the condition by eliminating harmful metabolites. Furthermore, NLRP3 inflammasome and autophagy co-regulate CVDs by enhancing autophagic processes, inhibiting inflammasome activity, and reducing inflammatory responses, thus playing a pivotal role in the disease's pathophysiology. Certain pharmacological agents have been shown to inhibit NLRP3 inflammasome activity by promoting autophagy, thereby ameliorating disease pathology. This review underscores the critical roles of NLRP3 inflammasome and autophagy in CVDs and examines the regulatory effects of specific drugs on these processes.

To evaluate trends in stroke-related mortality and years of life lost (YLL) among older adults in China during 2005-2020.

Leveraging data from National Mortality Surveillance System, we quantified counts and age-standardized rates for mortality and YLL attributable to stroke and its subtypes among adults aged 65 years and older in China and its provinces from 2005 to 2020.

During 2005-2020, age-standardized mortality rate (ASMR) of stroke among older adults in China decreased from 1,327.30 to 1,000.69 per 100,000, accompanied by a 26.58% reduction in YLL rate. Specifically, ASMRs decreased by 48.08% for intracerebral hemorrhage (ICH) and 7.57% for subarachnoid hemorrhage (SAH), whereas that for ischemic stroke (IS) increased by 1.24%. In 2020, ASMRs for IS, ICH, and SAH were 610.52, 357.86, and 32.32 per 100,000, respectively, with IS exhibiting the highest rate. Notably, IS mortality increased among men aged 75-79 years (1.95%), men aged 80+ years (17.79%), and women aged 80+ years (5.02%). In 2020, the highest ASMR of stroke was observed in Tibet, Anhui, and Shaanxi.

The substantial burden of IS persists among older adults in China. Increased IS mortality among men aged 75+ years and women aged 80+ years warrants particular attention.

Depression is common among Medicare beneficiaries with chronic diseases yet only a fraction receive depression treatment. Cost is a key barrier.

The Medicare Improvements for Patients and Providers Act of 2008 reduced cost-sharing for outpatient mental health services from 50% to 20%, creating parity with equivalent medical care in 2014.

We assessed outpatient mental health service use and out-of-pocket expenditures after parity among beneficiaries with depression and comorbid diabetes and/or heart disease.

Measures included mean outpatient mental health service use, proportion of beneficiaries with any use, intensity of use (i.e., mean use among users), and out-of-pocket expenditures.

We used an interrupted time series design and estimated linear and two-part regression models using weighted Medical Expenditure Panel Survey data from 2008-2019.

The analytic sample included 2,701 Medicare beneficiaries aged ≥ 65 years with depression and comorbid diabetes and/or heart disease, which corresponded to a nationally representative sample of 33,466,007 beneficiaries.

Mean use increased significantly after parity from 0.19 visits annually (95% CI: 0.06, 0.31) among beneficiaries with depression and diabetes to 0.80 visits annually (95% CI: 0.69, 0.92) among beneficiaries with depression, diabetes and heart disease. The latter group also experienced the largest increase in intensity of use after parity of 0.91 visits annually (95% CI: 0.16, 1.66). Out-of-pocket expenditures didn't increase significantly.

Parity was associated with increasing outpatient mental health service use among Medicare beneficiaries with depression and comorbid diabetes and/or heart disease without increasing patient costs. Beneficiaries with multiple comorbidities exhibited greater sensitivity to price reductions and cost-sharing equivalence for medical and mental health care. Policymakers should consider how beneficiaries experience barriers to mental health care differently and at different steps in the care continuum and collaborate with providers to implement complementary policies and clinical practices that effectively address them.

To investigate the role of CYP2D6 and its pharmacogenetic variability in the association between anticholinergic burden and cognitive function in older adults.

We conducted a cross-sectional analysis of 872 community-dwelling adults ≥ 65 years from the ActiFE-Ulm cohort. Cognitive performance was assessed using the Mini-Mental State Examination (MMSE). Anticholinergic burden scores deriving from CYP2D6-metabolised drugs (ABS_2D6) were calculated for all regularly scheduled medications. CYP2D6 metaboliser status was determined via genotyping and categorised as poor (PM), intermediate (IM), normal (NM), or ultrarapid (UM). The 25th, 50th, and 75th percentiles of the MMSE score distribution were studied using quantile regression to examine the association between ABS_2D6 and cognition, including interaction and stratified analyses by metaboliser status.

ABS_2D6 was significantly associated with lower MMSE scores at the 50th and 75th percentiles in early models, but not after additional adjustment for age and sex. A consistent effect modification by IM status was observed at the 75th percentile, with IMs showing a significant negative association between ABS_2D6 and MMSE in stratified analyses (β = -0.34 [95% CI: -0.64, -0.05]). After excluding participants with use of CYP2D6 inhibitors, this effect became more pronounced (β = -0.50 [95% CI: -0.82, -0.18]). Findings among PMs remained uncertain due to limited subgroup size.

These exploratory findings suggest that CYP2D6 metaboliser status may contribute to interindividual susceptibility to anticholinergic burden-related lower cognitive performance. If confirmed in larger longitudinal studies, pharmacogenetic information may support more individualised anticholinergic risk assessment and safer prescribing in older adults.

This research aims to explore the extent of socioeconomic inequities in hospital usage costs for individuals with eating disorders (EDs), analyze its trends, and identify associated factors using Queensland (QLD) administrative health linked data from 2013 to 2019.

We have utilized the horizontal inequity (HI) approach to quantify the extent of socioeconomic inequity. Outcome variables are public and private hospital admission costs and emergency department visit costs. Two-part regression models were estimated to identify factors associated with costs.

There was significant socioeconomic inequity in public hospital admission costs of ED care in QLD in 2013 and 2017, concentrated among individuals from higher socioeconomic status (SES) (pro-rich inequity). In recent years (2018 and 2019), there was no evidence of inequity in public hospital admission costs. HI indices for private hospital admission costs were positive from 2014 to 2019, which suggested a pro-rich inequity in private hospital admission costs. On the other hand, emergency department visit costs were concentrated among individuals from lower SES from 2013 to 2019. Individuals living in regional/remote areas had higher annual emergency department visit costs (AUD 279). People from high SES had AUD 1020 higher annual private hospital admission costs due to EDs, on average, compared to those from low SES.

Overall, findings call for more targeted policy and service delivery reforms to address unmet needs for people with EDs and promote more equitable access to hospital ED care, particularly for socioeconomically disadvantaged populations. Additionally, policymakers should continue to prioritize achievement of equitable access to hospital-based ED care.