Adipose-derived stem cell exosomes (ADSC-Exos) have emerged as promising cell-free therapeutic agents in regenerative medicine, offering many benefits of stem cell therapy without the risks of cell transplantation. These nanoscale vesicles (30-150 nm) contain bioactive cargo including proteins, microRNAs, and lipids that mediate tissue repair through multiple mechanisms: promoting angiogenesis, modulating inflammation, reducing fibrosis, and activating endogenous regenerative pathways. Recent preclinical studies demonstrate remarkable efficacy across diverse applications, from accelerating chronic wound healing and stimulating skin regeneration to repairing cartilage, bone, and nerve tissues. In cardiovascular applications, ADSC-Exos protect against ischemic damage and improve cardiac function post-infarction. Neurologically, they show potential in stroke recovery, spinal cord injury, and neurodegenerative diseases by crossing the blood-brain barrier and delivering neuroprotective signals. Their potent immunomodulatory properties make them candidates for treating inflammatory and autoimmune conditions. Early clinical trials report encouraging safety profiles and preliminary efficacy in conditions ranging from acne scarring to Alzheimer's disease. However, significant challenges remain in standardizing isolation methods, ensuring consistent potency, scaling production to clinically relevant quantities, and establishing optimal delivery strategies. This review synthesizes recent advances and limitations in ADSC-Exo research across various clinical applications, examines their underlying mechanisms of action, discusses current translational challenges, and highlights the potential of these versatile nanoparticles to transform regenerative medicine as off-the-shelf, cell-free therapeutics for multiple disease states.

BACKGROUND Acquired ventricular septal defect is an uncommon complication of myocardial infarction that can require surgical repair. Percutaneous closure techniques avoid the risks associated with major cardiac surgery, particularly in elderly patients. This report presents the case of a 73-year-old man with a post-infarction ventricular septal defect successfully treated by percutaneous closure. CASE REPORT A 73-year-old man was admitted with ST-elevation myocardial infarction. Coronary angiography revealed 2-vessel disease, and successful stenting of the left anterior descending artery was performed. Transthoracic echocardiography demonstrated an apical ventricular septal defect. Given the patient's hemodynamic stability, the heart team recommended delayed percutaneous closure. However, the patient requested voluntary discharge. He was readmitted 2 weeks later with dyspnea and chest pain. The defect was closed percutaneously due to technical feasibility, elevated surgical risk, and patient preference. Post-procedural recovery was uneventful, and he was in NYHA functional class I at outpatient follow-up. CONCLUSIONS Ischemic ventricular septal rupture is a rare but potentially fatal complication of transmural myocardial infarction, requiring prompt recognition and management by a heart team. Presentation ranges from chest pain or a new murmur to cardiogenic shock. Diagnosis relies on imaging modalities, including transthoracic or transesophageal echocardiography and cardiac magnetic resonance imaging. Management options include surgical and percutaneous closure, with ventricular septal rupture repair mortality exceeding 40%. Treatment selection depends on the patient's clinical status and the size, location, and complexity of the defect. This report highlights the role of percutaneous closure in post-infarction ventricular septal rupture and illustrates a successful outcome in an elderly patient.

Immune response is a significant mechanism in dilated cardiomyopathy (DCM). The interleukin-17 receptor (IL-17R) is crucial for immune response. A DCM model was created using doxorubicin, and IL-17R was knocked down. We assessed cardiac function, histopathological changes, fibrosis proteins, myocardial injury, and inflammation levels through echocardiography, pathological staining, immunofluorescence, and Western blot, respectively. The proportions of T cell subsets in mouse spleen tissue were identified through flow cytometry. Following these steps, we detached fibroblasts from the mouse heart and knocked down IL-17R. Angiotensin II was employed to induce cell fibrosis and co-cultured with T Helper 17 (TH17) cells. We measured inflammation, collagen deposits, and fibrosis protein expression using Sirius red staining, immunofluorescence, and Western blot. IL-17R exhibited significant expression in DCM mice. The systolic function of DCM mice significantly decreased. Myocardial fibrosis and collagen deposition in the left ventricle were markedly elevated. The levels of fibrosis proteins and pro-inflammatory factors were notably enhanced (p < 0.01). The proportion of effector CD4+ T and TH17 cells in spleen tissue noticeably increased, while the Treg cell proportion notably decreased. These indicators were significantly reversed after IL-17R knockdown. In the co-culture system, pro-inflammatory cytokines, collagen formation, and fibrosis-related protein levels increased significantly after fibrosis induction. However, the level of fibrosis and TH17/Treg cell imbalance decreased significantly after IL-17R knockdown. The knockdown of IL-17R can reduce immune reaction, which in turn improves myocardial fibrosis and alleviates DCM cardiac function.

Subclavian vein aneurysms are an exceedingly rare vascular anomaly, often diagnosed incidentally due to their nonspecific or absent clinical manifestations. Due to the limited number of reported cases and the lack of standardized diagnostic and management protocols, clinical decision-making remains challenging. This report presents a rare incidental case managed conservatively and is accompanied by a comprehensive literature review to consolidate existing knowledge on clinical presentation, associated risk factors, imaging modalities, and management approaches. By synthesizing available data, this study aims to support clinicians in recognizing this unusual entity and guide evidence-informed, individualized management strategies in the absence of formal guidelines.

A 37-year-old previously healthy male presented with persistent posterior neck pain for 1 month.

Imaging studies, including magnetic resonance angiography and computed tomography angiography, identified a fusiform aneurysmal dilation of the right subclavian vein measuring 2.2 × 2.0 × 1.7 cm.

A multidisciplinary team decided on conservative management, focusing on lifestyle modifications, analgesics, and closed follow-up, as the aneurysm was stable and asymptomatic regarding vascular complications.

During follow-up at 3, 6, and 12 months, the patient experienced gradual symptom improvement. Imaging confirmed the aneurysm remained stable without complications.

This case highlights the importance of considering subclavian vein aneurysms in the differential diagnosis of neck pain and supraclavicular masses. It further emphasizes the important role of imaging in their identification and monitoring. By reviewing previously reported cases, this study contributes valuable insights into their clinical presentation, diagnostic modalities, and management strategies.

The higher incidence of central poststroke pain (CPSP) has a severe negative impact on patients' mood, sleep, recovery, and quality of life, with bad medication outcomes. On the contrary, noninvasive transcranial magnetic stimulation is safe, and its analgesic effect has been verified in clinical practice. Repetitive transcranial magnetic stimulation may treat CPSP by various mechanisms, including modulating immune responses, promoting neurogenesis, improving cortical excitability, increasing interneuronal connectivity, and brain remodeling, but the exact mechanism and standard treatment regimen are still inconclusive and controversial. Therefore, the review summarizes recent advances regarding the possible mechanisms, treatment options, precautions, and future trends of repetitive transcranial magnetic stimulation for the treatment of CPSP, to provide new ideas for better clinical work and scientific exploration.

The incidence of ischemic stroke (IS) is escalating rapidly, and glycolysis significantly influences the pathogenesis and prognosis of these patients. However, current methods for assessing this are insufficient. This study aimed to identify molecular biomarkers of glycolysis in patients with IS. We retrieved relevant data from the Gene Expression Omnibus database and identified differentially expressed genes (DEGs). Gene set enrichment analysis was conducted on all genes within the integrated Gene Expression Omnibus dataset. Glycolysis-related differentially expressed genes (GRDEGs) were subjected to gene ontology and pathway analysis (Kyoto Encyclopedia of Genes and Genomes) to determine the functions of DEGs. The protein-protein interaction network of GRDEGs was established using the STRING database. The miRNAs of glycolysis-associated hub genes were acquired from the StarBase and miRDB databases, followed by an analysis of the relationship between glycolysis-related core genes and miRNAs. The mRNA-miRNA regulatory network was visualized. Lastly, a cross-comparison of immune-related genes and GRDEGs in IS was conducted to compare immune cell infiltration between the 2 groups. In the IS group, there were 42 up-regulated genes, 73 down-regulated genes, and 27 GRDEGs compared with the control group. These genes are involved in regulating various biological processes and signaling pathways. The protein-protein interaction network identified 7 hub genes related to glycolysis, including C-C motif chemokine receptor 7, ribosomal protein S3, and ribosomal protein SA, which also have immune correlations. Ribosomal protein SA, ribosomal protein S3, eukaryotic translation elongation factor 1 gamma, CD163, arginase 1, C-C motif chemokine receptor 7, and matrix metallopeptidase 9 are the hub genes related to glycolysis in IS. Our research will contribute to the discovery of potential biomarkers and fresh approaches to the clinical management of IS.

The acute blockage in coronary arteries further causes acute coronary syndrome (ACS). There are 2 main factors implicated in the activation and aggregation of platelets. However, this present study aimed to investigate the effect of salvianolic acid A (SAA) on the platelets in patients with ACS and explore its potential mechanism of action.

The impact of SAA on platelets under different stimulation conditions was studied using flow cytometry and platelet aggregation detection techniques.

The results demonstrated that in 40 ACS patients, ex vivo treatment of platelets with SAA (0.1 mg/ml) significantly reduced aggregation and activation. Intriguingly, we found no significant difference between the 3 types of ACS patients in the antiplatelet effect of SAA. Moreover, the results indicated that C-reactive protein, alanine aminotransferase, C-reactive protein-to-albumin ratio, total cholesterol, and low-density lipoprotein levels were negatively correlated with the anti-platelet effect of SAA in ACS patients and that a history of smoking may reduce the anti-platelet effect of SAA in the same group.

In summary, the above findings of this study highlight the therapeutic potential of SAA against platelets in patients with ACS, providing new insights into clinical treatment and experimental research.

Previous studies have suggested a link between viral infections and myocarditis, but the causal nature of this relationship remains unclear. The antibody-mediated immune responses generated after such infections reflect an individual's infection history and immune status, offering insights into disease mechanisms and potential therapeutic targets. We used 46 antibody-mediated immune responses as exposures, with European myocarditis and Finnish nonischemic cardiomyopathy as outcomes. The overlapping results were then identified and further validated using Mendelian randomization based on generalized summary data to ensure accuracy. Our Mendelian randomization based on generalized summary data analysis showed that Epstein-Barr virus-related antibody levels, including EBNA-1 (OR = 1.7225, 95% CI: 1.2692-2.3376, P < .001) and VCA p18 (OR = 1.8108, 95% CI: 1.1919-2.7511, P = .0054), were significantly associated with an increased risk of myocarditis. In addition, polyomavirus-related antibody levels, including anti-polyomavirus 2 IgG seropositivity (OR = 0.5762, 95% CI: 0.4521-0.7344, P < .001), anti-Merkel cell polyomavirus IgG seropositivity (OR = 0.6924, 95% CI: 0.5522-0.8682, P = .0014), and Merkel cell polyomavirus VP1 antibody levels (OR = 0.6093, 95% CI: 0.3989-0.9307, P = .0219), were significantly associated with a reduced risk of myocarditis. Similarly, antibody levels against varicella zoster virus glycoproteins E and I were also inversely associated with myocarditis risk (OR = 0.4478, 95% CI: 0.3035-0.6606, P < .001). We identified 6 antibody-mediated immune responses associated with myocarditis, along with multiple genetic variants linked to these responses. These findings may help prioritize future research directions and guide drug development.

Stroke defined by diminished cerebral blood flow, results in brain damage and neurological impairments. It often leads to considerable difficulties, such as limited mobility and compromised hand function, usually manifesting as a weakening in the ability to open and shut the hand.

The study evaluates the differences between opening and closing hands when utilizing a soft robot.

The study was conducted in the Mosul Specialist Rehabilitation Center which involved 68 participants, all over 20 years old, with visual impairments. The Iranian Clinical Trials Registry and Ministry of Planning approved the study, The Fugl-Meyer Assessment for Upper Extremity Action Research Arm Test, and Arm Motor Ability Test were used to assess finger extension and flexion.

A study revealed that stroke patients who utilized a soft robotic glove experienced notable improvements in hand functionality. Average hand closure scores increased significantly, from 8.14 to 20.36 out of 21 points. Women demonstrated greater progress in hand opening rates compared to men, with an average improvement of 1.91 times between pre- and post-assessments. In contrast, the control group exhibited similar hand-opening advancements across genders. Patients with both ischemic and hemorrhagic strokes showed enhanced abilities in opening and closing their hands. Additionally, the study identified a statistically significant improvement in hand function improvements based on stroke type.

The study found that stroke patients using a soft robotic glove showed significant improvements in hand-closing abilities, while exercise had minimal impact. Women showed an average increase in hand opening rate. Both male and female patients showed improvement, with hemorrhagic strokes showing remarkable advancements.

Although 90% of asthmatic patients suffer from mild and moderate disease, little is known about the burden on health status and quality of life, the long-term trajectory of disease severity, and the socio-economic impact. The Mild Moderated Asthma Network of Italy (MANI) is a real-world, cross-sectional, prospective, observational cohort study designed to explore these issues. Here we aimed to provide an identikit of asthmatic patients receiving treatment according to GINA steps 1-4, and enrolled in the centers of excellence participating in the MANI. Among 679 analyzed patients, 63% were female, and the mean age was 50 ± 16 years. Asthma was mild in 15.8% of patients (GINA steps 1-2) and moderate in 84.2% (GINA steps 3-4). The mean age of asthma diagnosis was 34.3 ± 17.7 years, 50% of patients were suffering from allergic rhinitis, and 13% from nasal polyposis. Mean FEV1% was 91.4 ± 19.4%, predicted with a FEV1/FVC ratio of 74.7 ± 11.9. The mean asthma control test value was 21.2 ± 3.73, and AQLQ score was 5.74 ± 1.07. Among the included patients, 17.2% had at least one asthma exacerbation in the previous year, with 14.2% requiring systemic steroids; 6.2% were referred to an emergency room in the year prior to enrollment; 2.2% required an asthma-related hospitalization; and 0.6% had been admitted to an Intensive Care Unit (ICU). Unscheduled visits were necessary for 3.8% of patients, 6.5% reported ≥5 lost work days due to asthma, and 11.5% declared ≥10 lost days of spare time. About 70% of patients were receiving treatment according to GINA Track 1. Uncontrolled cases constituted 16.7% of patients treated according to GINA steps 1-2, and 26.3% of patients treated according to GINA steps 3-4 were uncontrolled. Compared to patients with mild asthma, those with moderate asthma had more impaired lung function (FEV1% 88.5 ± 18.4 vs 94.4 ± 17.9, p = 0.05; FEV1/FVC 73.0 ± 9.76 vs 79.6 ± 9.56, p > 0.001), exhibited greater need for systemic corticosteroids for treating exacerbations (13.8% vs 2.3%, p = 0.032), and showed greater adherence to therapy (TAI score 50.0 ± 5.66 vs 45.7 ± 8.42, p < 0.001). Overall, mild/moderate asthma exhibited a substantial clinical and care impact. Patients treated with GINA steps 3-4 constituted the vast majority of patients attending specialist centers. A quarter of these patients were uncontrolled, and therefore need re-evaluation or treatment upgrade. Expanding recruitment of the MANI study will allow further phenotyping of these patients.