Effect Of Aspirin Research Articles

Effectiveness of aspirin in preventing deep vein thrombosis following proximal femoral fracture surgery in Japan

Previous studies have shown that aspirin is effective as a prophylactic agent against venous thromboembolism (VTE) following proximal femoral fractures (PFF). In Japan, there is a lack of evidence regarding its efficacy and safety in this context. Consequently, aspirin is not covered by insurance for the prevention of venous thrombosis. This study aimed to investigate whether continued aspirin use in patients with PFF, who were already taking aspirin for cerebrovascular disease prevention before injury is effective as a prophylaxis for deep vein thrombosis (DVT). We retrospectively analyzed PFF patients (≥ 65 years) who underwent postoperative duplex ultrasonography from January 2010 to December 2023.The study compared patients taking aspirin alone (aspirin group) and those not taking antiplatelet agents or anticoagulants (control group), matched by propensity scores. We enrolled 1064 patients while 161 (15%) were in the aspirin group. After matching, 128 patients were analyzed. DVT incidence was not statistically significant between the aspirin (54) and control groups (60) (OR: 0.81; 95%CI: 0.49- 1.36; p = 0.44). Proximal DVT incidence was also similar (OR: 2; 95%CI: 0.50–7.00; p = 0.33). Additionally, since use of other postoperative antithrombotic prophylaxis (78%) is thought to have a significant impact on the incidence of DVT, a subgroup analysis was conducted to evaluate the effect of aspirin in patients who did not receive postoperative antithrombotic prophylaxis. Similarly, there was no statistically significant difference in either DVT (OR: 1.38; 95% CI: 0.55–3.42; p = 0.49) or proximal DVT (OR: 2.00; 95% CI: 0.37–10.92; p = 0.42). This study demonstrates that aspirin is not effective for preventing VTE in patients with PFF in Japan.

A 20-year population-wide cohort study on association of aspirin and risk of gastrointestinal and non-gastrointestinal cancer.

830 Background: Aspirin has been shown to reduce the risk of various gastrointestinal (GI) and non-GI cancers 1,2 . However, little was known about at what age aspirin should be started for maximal chemoprotective better on GI cancer. Furthermore, the randomised controlled trial on aspirin for primary prevention use in healthy elderly (ASPREE) showed no association between aspirin and cancer incidence despite the limitation of short follow-up duration 3 . The current study aims to investigate the 20-year risk of cancer using aspirin in a territory-wide Hong Kong population cohort. Methods: The study included all aspirin users from 2000 to 2019, and non-aspirin users matched by age and sex at a ratio of 1:2. Enrolled subjects with a history of cancer at enrolment, cancer incidence or death within 6 months were excluded. The incidence of individual GI and non-GI cancer was presented as the primary outcome. Baseline characteristics between aspirin and non-aspirin users were adjusted in the survival analysis by inverse probability of treatment weighting (IPTW). The fine-grey model has been used to address bias from competing risk of death. The sub-distribution hazard ratio was presented for the association of aspirin use and risk of GI and non-GI cancers. Results: The current study included 538,147 aspirin users and 968,378 non-users with a mean age of 64.8 years. A total number of 36,683 cases of GI cancer (2.4%) and 47,196 cases of non-GI cancers (3.1%) were observed. Aspirin was associated with a lower risk of several common individual GI cancers, including colorectal cancer (SHR 0.78, 95% CI 0.76-0.81), liver cancer (SHR 0.67, 95% CI 0.64-0.70), stomach cancer (SHR 0.79, 95% CI 0.75-0.84) and pancreatic cancer (SHR 0.85, 95% CI 0.79-0.91), but not oesophageal cancer. On the other hand, aspirin was associated with a lower risk of prostate cancer (SHR 0.95, 95% CI 0.91-1.00) and breast cancer (SHR 0.76, 95% CI 0.73-0.79), but not lung cancer and kidney cancer. In overall, aspirin was associated with a 24% lower risk of GI cancers (SHR 0.76, 95% CI 0.74-0.78) and a 3% lower risk of non-GI cancers (SHR 0.97, 95% CI 0.95-0.99). Conclusions: Aspirin was associated with a lower risk of most GI cancers, including colorectal cancer, liver cancer, stomach cancer and pancreatic cancer, but not most non-GI cancers. In general, results on the effect of aspirin on GI cancer prevention were consistent with the previously presented 10-year cohort. 1. Bosetti C, Santucci C, Gallus S, Martinetti M, La Vecchia C. Aspirin and the Risk of Colorectal and Other Digestive Tract Cancers: An Updated Meta-analysis through 2019. Ann Oncol. 2020;31(5):558-568. 2. Santucci C, Gallus S, Martinetti M, La Vecchia C, Bosetti C. Aspirin and the risk of nondigestive tract cancers: An updated meta-analysis to 2019. Int J Cancer. 2021;148(6):1372-1382. 3. McNeil JJ, Gibbs P, Orchard SG, et al. Effect of Aspirin on Cancer Incidence and Mortality in Older Adults. J Natl Cancer Inst. 2021;113(3):258-265.

Abstract WP282: Effectiveness and safety of apixaban vs. aspirin for primary prevention of stroke and bleeding risk among patients with atrial fibrillation: A Meta-analysis of randomized controlled trials including ARTESIA trial.

Abstract WP282: Effectiveness and safety of apixaban vs. aspirin for primary prevention of stroke and bleeding risk among patients with atrial fibrillation: A Meta-analysis of randomized controlled trials including ARTESIA trial.

The effects of long-term low-dose aspirin on coagulation function in gynaecological patients with co-existing chronic periodontitis.

This study investigates the safety of non-surgical periodontal treatment during long-term low-dose aspirin therapy in patients with chronic periodontitis and gynaecological conditions, focusing on bleeding risk and coagulation function. Patients received low-dose aspirin (100 mg/d) and were divided into a medication continuation group (observation) and a cessation group (control), with 41 patients each. Key periodontal parameters (plaque index, probing depth, attachment loss) and coagulation indices (activated partial thromboplastin time, prothrombin time, thrombin time, prothrombin activity) were assessed post-treatment. Results showed no significant difference in coagulation indices and bleeding scores between the groups (P > 0.05). Grade 3 bleeding incidents were slightly higher in the observation group but not statistically significant. The observation group's maximum platelet aggregation rate was significantly lower (P < 0.0001), with no significant differences in activated partial thromboplastin time, prothrombin time, thrombin time, or prothrombin activity. The findings suggest that non-surgical periodontal treatment is safe for these patients under long-term low-dose aspirin therapy, with limited increased bleeding risk.

The preventive and protective effects of aspirin on radiation-induced skin injury

Radiation-induced skin injury (RISI) is a frequent complication of radiotherapy that can severely hinder treatment and endanger patients&amp;rsquo; lives. Current treatments offer limited efficacy in reducing symptoms. This study explores the protective effect of aspirin (ASP) on RISI and its underlying mechanisms. As in vivo RISI models, 8 &amp;ndash; 12-week-old C57BL/6 mice were irradiated with a single dose of 20 Gy X-rays to the skin of the right thigh, with sham-irradiated mice serving as controls. ASP was administered orally for 7 days before irradiation. Skin samples were collected on day 14 post-irradiation for single-cell RNA sequencing (sc-RNAseq). RISI severity was assessed daily using a modified RTOG/EORTC scoring system (scores ranging from 1 to 5.5). Our results showed that ASP delayed the onset of RISI and reduced its severity. The sc-RNAseq revealed an increased number of interfollicular epidermal cycling (IFE C) cells in irradiated skin, with some cells showing G2M cell cycle arrest. These IFE C cells exhibited elevated expression of stemness markers, indicating their importance in both RISI damage and subsequent repair. The ASP-treated group showed delayed skin injury onset and reduced peak severity compared to untreated controls. Furthermore, ASP appeared to promote homologous recombination repair of radiation-induced DNA damage, contributing to its protective effect. In conclusion, IFE C cells undergo G2M arrest to repair radiation-induced damage. ASP shows potential in preventing RISI, possibly through enhancing DNA repair. These findings suggest a novel therapeutic role for ASP in mitigating RISI.

Early Neurologic Deterioration and Efficacy of Dual Antiplatelet in Anterior Versus Posterior Circulation Stroke.

Anterior circulation stroke (ACS) differs from posterior circulation stroke (PCS) in several aspects. We hypothesize that the risk of early neurologic deterioration (END) and its responses to clopidogrel plus aspirin versus aspirin alone may be different between stroke territories. This was a prespecified post hoc analysis of ATAMIS (Antiplatelet Therapy in Acute Mild to Moderate Ischemic Stroke) trial and included patients with definite infarct location who were classified into ACS and PCS according to stroke territory. Primary outcome was occurrence of END at 7 days, defined as ≥2-point increase in National Institutes of Health Stroke Scale score compared with baseline. We compared the treatment effects of clopidogrel plus aspirin versus aspirin alone in each stroke territory. From 3000 patients, 2431 eligible patients (1780 with ACS [910 assigned into clopidogrel plus aspirin and 870 assigned into aspirin alone] and 651 with PCS [371 assigned into clopidogrel plus aspirin and 280 assigned into aspirin alone]) were included. Median age was 66 years and 35.1% were women. The occurrence of END was higher in ACS than PCS (6.8% versus 3.8%, P=0.007). clopidogrel plus aspirin was associated with lower risk of END in ACS (risk difference [95% CI]: -2.4% [-4.1% to -0.8%], P=0.004), but not in PCS (risk difference [95% CI]: -0.6% [-2.7% to 1.5%], P=0.57). No significant interaction was found (P=0.69). Our study demonstrated END was higher in acute mild-to-moderate ischemic stroke with anterior circulation, who derived more benefit from clopidogrel plus aspirin than aspirin alone. URL: https://www.clinicaltrials.gov; Unique identifier: NCT02869009.

Aspirin Is as Effective and Safe as Oral Anticoagulants for Venous Thromboembolism Prophylaxis After Joint Arthroplasty: A Systematic Review and Meta-Analysis of Randomized Clinical Trials.

Joint arthroplasty effectively treats osteoarthritis, providing pain relief and improving function, but postoperative venous thromboembolism (VTE) remains a common complication. This study therefore assessed the effectiveness and safety of aspirin compared with oral anticoagulants (OACs) for VTE prophylaxis after joint arthroplasty. A systematic review and meta-analysis was performed by searching PubMed, Embase, the Web of Science, and the Cochrane Library for randomized controlled trials (RCTs) up to May 14, 2024, that compared the effect of aspirin versus OACs on VTE prophylaxis in adults undergoing joint arthroplasty. Data extraction followed the PRISMA guidelines. Two independent researchers conducted the literature searches and data extraction. A random-effects model was used to estimate effects. The primary outcome was the incidence of VTE, including deep vein thrombosis (DVT) and pulmonary embolism (PE); secondary outcomes included bleeding, wound complications, and mortality. The meta-analysis included 11 RCTs with a total of 4,717 participants (55.1% female) from several continents. The relative risk (RR) of VTE following joint arthroplasty was 1.11 (95% confidence interval [CI], 0.93 to 1.32) for aspirin compared with OACs. Similar results were observed for DVT (RR, 1.12; 95% CI, 0.90 to 1.40) and PE (RR, 1.18; 95% CI, 0.51 to 2.71). There were no significant differences in the risks of bleeding, wound complications, or mortality between patients receiving aspirin and those receiving OACs. Subgroup analyses considering factors such as study region, type of joint surgery, type of VTE detection, year of publication, use of mechanical VTE prophylaxis, aspirin dose, type of OAC comparator, study quality, and funding also found no significant differences in VTE incidence between aspirin and OACs. The overall quality of evidence for VTE and DVT outcomes was high. Based on high-quality evidence from RCTs, aspirin is as effective and safe as OACs in preventing VTE, including DVT and PE, after joint arthroplasty, without increasing complications. Therapeutic Level I. See Instructions for Authors for a complete description of levels of evidence.

Long-term use of low-dose aspirin for cancer prevention: A 20-year longitudinal cohort study of 1,506,525 Hong Kong residents.

Long-term use of low-dose aspirin has been demonstrated to reduce cancer risk, but the duration of necessary medication use remains uncertain. This study aimed to investigate the long-term chemoprotective effect of aspirin among the Chinese population. This population-based study included all aspirin users between 2000 and 2019. Aspirin users were age-sex matched with non-users at a 1:2 ratio. Cancer incidence and mortality were the main outcomes measured. Survival analyses with the Fine-Gray modelling were performed. The chemoprotective effects were measured by the sub-distribution hazard ratios (SHR) with control for the competing risks. A total of 538,147 aspirin users and 968,378 non-users were included, with a mean age of 64.8 years, 9,543,399 person-years of follow-up and 90% of users with 80 mg aspirin. The long-term use of aspirin was associated with a reduced risk of cancer (SHR 0.92, 95% CI 0.91-0.94) and a reduced risk of cancer mortality (SHR 0.80, 95% CI 0.79-0.82). Stronger chemopreventive effects were observed among those who used aspirin for more than 10 years, including risk reductions for lung (SHR 0.56, 95% CI 0.51-0.60), breast (SHR 0.34, 95% CI 0.29-0.38) and colorectal (SHR 0.37, 95% CI 0.33-0.40) cancers, but not for bladder cancer and leukaemia. Low-dose use of aspirin was associated with lower risk of cancer among Chinese. The association was even stronger for those using aspirin for more than 10 years. Prescription of aspirin may be started as early as at age of 40, as the chemoprotective effect also applied for early cancers.

Impact of aspirin on biochemical recurrence of prostate cancer after robot assisted radical prostatectomy in a multicenter retrospective cohort study

This study evaluated the impact of aspirin on the biochemical recurrence (BCR) rate following robot-assisted radical prostatectomy (RARP) in patients. A database search identified patients who underwent RARP for pT2-3N0M0 disease at any of 25 centers between 2011 and 2022, categorized into aspirin (n = 350) and control groups (n = 5857). Adjustment by 1:1 propensity score matching (PSM) and Mahalanobis distance matching (MDM) created 350 matched pairs. The effect of aspirin on the BCR rate was evaluated by analysis of BCR-free survival. After PSM and MDM, the 3-year BCR-free rate was significantly better in the aspirin group (85.0%, 95% confidence interval [CI] 80.8–89.4) than in the control group (PSM, 74.5%, 95% CI 66.5–83.5, p = 0.021; MDM, 74.7%, 95% CI 66.3–84.3, p = 0.037). In the analysis of high-risk subgroups, patients in the aspirin group with an ISUP (International Society of Urological Pathology) grade ≥ 4 had a significantly lower recurrence rate in both matched groups (PSM, hazard ratio 0.44, 95% CI 0.22–0.88; MDM, hazard ratio 0.45, 95% CI 0.23–0.90). In conclusion, this study suggests that aspirin could enhance BCR-free survival post-RARP, especially in patients with higher ISUP grades.

Aspirin and Hemocompatibility After LVAD Implantation in Patients With Atherosclerotic Vascular Disease

The Aspirin and Hemocompatibility Events With a Left Ventricular Assist Device in Advanced Heart Failure (ARIES-HM3) study demonstrated that aspirin may be safely eliminated from the antithrombotic regimen after HeartMate 3 (HM3 [Abbott Cardiovascular]) left ventricular assist device (LVAD) implantation. This prespecified analysis explored whether conditions requiring aspirin (prior percutaneous coronary intervention [PCI], coronary artery bypass grafting [CABG], stroke, or peripheral vascular disease [PVD]) would influence outcomes differentially with aspirin avoidance. To analyze aspirin avoidance on hemocompatibility-related adverse events (HRAEs) at 1 year after implant in patients with a history of CABG, PCI, stroke, or PVD. This was an international, multicenter, prospective, double-blind, placebo-controlled, randomized clinical trial including patients implanted with a de novo HM3 LVAD across 51 centers. Data analysis was conducted from April to July 2024. Patients were randomized in a 1:1 ratio to receive aspirin (100 mg per day) or placebo, in addition to a vitamin K antagonist (VKA) targeted to an international normalized ratio of 2 to 3 in both groups. Primary end point (assessed for noninferiority) was a composite of survival free of any nonsurgical (>14 days after implant) HRAEs including stroke, pump thrombosis, bleeding, and arterial peripheral thromboembolism at 12 months. Secondary end points included nonsurgical bleeding, stroke, and pump thrombosis events. Among 589 of 628 patients (mean [SD] age, 57.1 [13.7] years; 456 male [77.4%]) who contributed to the primary end point analysis, a history of PCI, CABG, stroke, or PVD was present in 41% (240 of 589 patients). There was no interaction between the presence of an atherosclerotic vascular condition and effect of aspirin compared with placebo (P for interaction= .23). The preset 10% noninferiority margin was not crossed for the studied subgroup of patients. Thrombotic events were rare, with no differences between aspirin and placebo in patients with and without vascular disease (P for interaction = .77). Aspirin treatment was associated with a higher rate of nonsurgical major bleeding events in the group with prior vascular condition history compared with those without aspirin (rate ratio for placebo compared with aspirin, 0.52; 95% CI, 0.35-0.79). Results of this prespecified analysis of the ARIES-HM3 randomized clinical trial demonstrate that in patients with advanced heart failure who have classical indications for antiplatelet therapy use at the time of LVAD implantation, aspirin avoidance was safe and not associated with increased thrombosis risk. Importantly, elimination of aspirin was associated with no increased thrombosis but a reduction in nonsurgical bleeding events in patients with a history of PCI, CABG, stroke, or PVD. ClinicalTrials.gov Identifier: NCT04069156.

The Effect of Low-dose Aspirin on Disease Activity in Pregnant Individuals with Inflammatory Bowel Disease.

Low-dose aspirin (LDA) is recommended for pregnant individuals at elevated risk for hypertensive disorders of pregnancy (HDP). However, regular aspirin use may raise concerns of increased disease activity in patients with inflammatory bowel disease (IBD). We aimed to evaluate the prevalence of LDA use in pregnant IBD patients and the effect of LDA on IBD disease activity. Included were individuals with IBD and pregnancy followed by Maternal Fetal Medicine (MFM) between 1/1/2013-12/31/2022. LDA use was ascertained from medication lists during pregnancy. Primary outcome was IBD flare during pregnancy or six months postpartum, defined as IBD-related hospitalization or surgery, new therapy initiation, elevated fecal calprotectin, or new active endoscopic disease. Among 320 pregnancies in women with IBD (232 patients), 90 (28%) were prescribed aspirin during pregnancy. The percentage of women with IBD flare during pregnancy or postpartum was similar among those who were and were not prescribed aspirin (20% vs 26%, p=0.36). Individuals on aspirin were older (35 vs 34 median years), more likely to have preterm birth (21% vs 14%), higher parity (2 vs 1), and cesarean delivery (50% vs 27%) than individuals not on LDA, (all p<0.01). Both groups had similar rates of HDP, though individuals on LDA had higher rates of preeclampsia (10% vs 4.3%, p=0.10). Approximately one-third of patients with IBD cared for in a MFM practice were prescribed LDA during pregnancy. The use of aspirin among pregnant patients with IBD was not associated with an increased risk of disease activity.

Aspirin modulates inflammatory biomarkers in patients with subcortical silent brain infarcts.

This study aimed to identify differences in the levels of inflammation-related biomarkers between patients with subcortical silent brain infarcts (SBIs) and healthy controls. We also evaluated the effect of aspirin on the subcortical SBI inflammatory processes. Consecutive patients diagnosed with subcortical SBIs without a history of acute stroke were included. The demographic and clinical data of the 26 subjects with subcortical SBIs, such as the number and location of subcortical SBIs, were reviewed. Plasma levels of macrophage migration inhibitory factor (MIF), matrix metalloproteinase-9 (MMP-9), and visfatin were measured in patients with subcortical SBIs and ten healthy participants. These biomarkers were rechecked in patients with subcortical SBI 3 months after taking aspirin (100 mg/day). MIF and MMP-9 levels were significantly higher in patients with subcortical SBIs than in healthy control group (p = 0.031 and p = 0.026, respectively). Although MIF and MMP-9 did not show significant changes after taking aspirin for 3 months, the median plasma level of visfatin was significantly decreased from 1.00 ng/mL (range, 0.86-1.16 ng/mL) to 0.84 ng/mL (range, 0.77-0.91 ng/mL) (p = 0.002) after taking aspirin. Inflammation could be an essential factor in the pathogenesis of subcortical SBIs, and aspirin affects several inflammation-related biomarkers.

ASSESSING THE IMPACT OF LOW-DOSE ASPIRIN ON CARDIOVASCULAR DISEASE PREVENTION IN DIABETIC PATIENTS

Background: Diabetes significantly increases the risk of cardiovascular disease (CVD), prompting interest in preventive treatments such as low-dose aspirin. Despite its potential, the efficacy of aspirin in this context remains debated. Objective: This study aimed to evaluate the effectiveness of low-dose aspirin in preventing CVD among individuals with type 2 diabetes. Methods: In this double-blind, placebo-controlled, randomized trial, 100 type 2 diabetic patients without previous CVD were enrolled. Participants were randomly assigned to receive either 81 mg/day of aspirin or a placebo for one year. The primary endpoint was the incidence of major adverse cardiovascular events (MACE). Results: Each group comprised 50 participants with comparable baseline characteristics. The incidence of MACE was 10% in the aspirin group compared to 28% in the placebo group, achieving statistical significance (p=0.03). While the aspirin group also showed reductions in myocardial infarction and stroke, these differences were not statistically significant. Conclusion: Low-dose aspirin significantly reduces the incidence of MACE in type 2 diabetic patients, supporting its use as a preventive intervention in this high-risk group.

Sex steroid disrupting effects of nonsteroidal anti-inflammatory drugs on the Persian Gulf Arabian Sea bream, Acanthopagrus arabicus: In vitro model of environmental drug contamination.

The presence of pharmaceuticals in aquatic ecosystems and their impact on humans and the environment are growing concerns in environmental health. This study aimed to evaluate the potential reproductive effects of diclofenac, ibuprofen, and aspirin on dissociated ovarian and testicular cells from Arabian Sea bream, Acanthopagrus arabicus. The cells were exposed to varying concentrations of the pharmaceuticals for 48 h. Steroid (17-β-estradiol (E2) and 11-ketotestosterone (11-KT)) production by the cells was assessed at 0, 12, 24, and 48 h of the experiment. The findings showed that diclofenac did not impact the production of E2 and 11-KT by ovarian cells, but it did significantly decrease the secretion of 11-KT from testicular cells. Ibuprofen and aspirin, on the other hand, both increased the production of the studied steroid hormones by ovarian cells and reduced the secretion of 11-KT by testicular cells in a dose- and time-dependent manner. The pharmaceuticals studied were potent inhibitors of 11-KT secretion, particularly at higher concentrations in the cultured testicular cells. However, they were also found to stimulate steroid production from fish ovarian cells. In conclusion, the results suggest that analgesics (diclofenac, ibuprofen, and aspirin) have the potential to disrupt estrogen biosynthesis and impact reproduction in fish.

Aspirin promotes odontogenic differentiation via a mechanism involving FOXC1, RUNX2, and MCAM expression.

This study aimed to investigate the effects of aspirin on the early stages of odontogenic differentiation. The roles of FOXC1, RUNX2, and MCAM gene expression in the mechanism of odontogenic differentiation were evaluated by examining the effects of downregulated FOXC1 or RUNX2 expression using small interfering RNAs (siRNAs). Dental pulp cells were treated with aspirin (0, 2.5, 50, 100 μg/ml) to assess its impact on mineralization. The gene expression levels of FOXC1, RUNX2, and MCAM were measured using digital polymerase chain reaction, and the effects of siRNA-mediated knockdown of FOXC1 and RUNX2 were analyzed. The mineralization potential was quantitatively assessed using Alizarin Red S staining and a calcium assay. Analysis of cell growth curves and doubling times indicated that aspirin did not affect cell proliferation at 2.5 μg/ml and 50 μg/ml; however, 50 μg/ml aspirin promoted mineralization. In the FOXC1 and RUNX2 knockdown experiments, fluctuations in FOXC1, RUNX2, and MCAM gene expression were observed in the aspirin-treated group, suggesting the involvement of these genes in mineralization. Alizarin red S staining and calcium assays further demonstrated that aspirin enhanced mineralization. These findings indicate that aspirin promotes odontogenic differentiation and regulates the expression of FOXC1, RUNX2, and MCAM. This suggests that aspirin may serve as a promising new therapeutic agent in dental pulp regenerative medicine.

An intimal-lumen model in a microfluidic device: potential platform for atherosclerosis-related studies.

Atherosclerosis is a chronic inflammatory vascular disorder driven by factors such as endothelial dysfunction, hypertension, hyperlipidemia, and arterial calcification, and is considered a leading global cause of death. Existing atherosclerosis models have limitations due to the absence of an appropriate hemodynamic microenvironment in vitro and interspecies differences in vivo. Here, we develop a simple but robust microfluidic intimal-lumen model of early atherosclerosis using interconnected dual channels for studying monocyte transmigration and foam cell formation at an arterial shear rate. To the best of our knowledge, this is the first study that creates a physiologically relevant microenvironment under an arterial shear rate to modulate lipid-laden foam cells on a microfluidic platform. As a proof of concept, we use murine endothelial cells to develop a vascular lumen in one channel and collagen-embedded murine smooth muscle cells to mimic the subendothelial intimal layer in another channel. The model successfully triggers endothelial dysfunction upon TNF-α stimulation, initiating monocyte adhesion to the endothelial monolayer under the arterial shear rate. Unlike existing in vitro models, native low-density lipoprotein (LDL) is added in the culture media instead of ox-LDL to stimulate subendothelial lipid accumulation, thereby mimicking more accurate physiology. The subendothelial transmigration of adherent monocytes and subsequent foam cell formation is also achieved under flow conditions in the model. The model also investigates the inhibitory effect of aspirin in monocyte adhesion and transmigration. The model exhibits a significant dose-dependent reduction in monocyte adhesion and transmigration upon aspirin treatment, making it an excellent tool for drug testing.

Comparison of effectiveness of aspirin, clopidogrel and cilostazol monotherapy treatment in ischaemic stroke

Comparison of effectiveness of aspirin, clopidogrel and cilostazol monotherapy treatment in ischaemic stroke

New Insights into Aspirin's Anticancer Activity: The Predominant Role of Its Iron-Chelating Antioxidant Metabolites.

Epidemiological studies have suggested that following long-term, low-dose daily aspirin (LTLDA) administration for more than 5 years at 75-100 mg/day, 20-30% of patients (50-80 years old) had a lower risk of developing colorectal cancer (CRC) and about the same proportion in developing iron deficiency anemia (IDA). In cases of IDA, an increase in iron excretion is suspected, which is caused by aspirin chelating metabolites (ACMs): salicylic acid, salicyluric acid, 2,5-dihydroxybenzoic acid, and 2,3-dihydroxybenzoic acid. The ACMs constitute 70% of the administered aspirin dose and have much longer half-lives than aspirin in blood and tissues. The mechanisms of cancer risk reduction in LTLDA users is likely due to the ACM's targeting of iron involved in free radical damage, iron-containing toxins, iron proteins, and associated metabolic pathways such as ferroptosis. The ACMs from non-absorbed aspirin (about 30%) may also mitigate the toxicity of heme and nitroso-heme and other iron toxins from food, which are responsible for the cause of colorectal cancer. The mode of action of aspirin as a chelating antioxidant pro-drug of the ACMs, with continuous presence in LTLDA users, increases the prospect for prophylaxis in cancer and other diseases. It is suggested that the anticancer effects of aspirin depend primarily on the iron-chelating antioxidant activity of the ACMs. The role of aspirin in cancer and other diseases is incomplete without considering its rapid biotransformation and the longer half-life of the ACMs.

Combined role of PEAR1 and GP genes in the mechanism of aspirin resistance and its clinical significance

Exploring the mechanism of aspirin resistance helps to improve the prevention and treatment of ischemic stroke diseases and reduce the interference of resistance mechanism on the therapeutic effect of aspirin. In this paper, the Affiliated Hospital of Beihua university, together with two other hospitals, was chosen as the research unit, from which 260 AIS patients were selected for aspirin resistance study. The joint role of PEAR1 gene and GP gene in the mechanism of aspirin resistance was discussed by genotyping, TEG assay, univariate analysis, and binary logistic analysis methods. Among the GP1BA genes in AIS patients, the frequency of CC-type genes was as high as 92.03%, and the risk of aspirin resistance was significantly increased in CC-type relative to TT-type. The incidence of rs5924 allele T was significantly higher in the AR group than in the AS group (OR = 1.632, p = 0.006), and there was a significant effect of diabetic conditions on aspirin resistance at the 1% level. Diabetes significantly inhibits plasma proteins in AIS patients and makes aspirin less inhibitory to platelets. Therefore, clarifying the influence of PEAR1 and GP genes in the mechanism of aspirin resistance can be used to obtain the precise loci from the gene therapy point of view to enhance the disease treatment effect of aspirin.

Mechanisms and effects of aspirin to cancer cells

Aspirin, everyone knows it is an anti-inflammatory drug, has great promise mostly for the prevention and treatment of cancer by using a number of methodologies. Its anti-cancer property come from its induction of apoptosis, inhibition of cell growth, and disruption of important signaling pathways. By exploring the mechanisms through which aspirin affects cancer cells, particularly having the impact on signaling pathways like non-coding RNAs (ncRNAs), and controlling the activity of platelets. It is also mentioned that the inhibition of cyclooxygenase (COX) enzymes is involved in aspirin’s primary action, leading to lower rate of inflammatory mediators produced and changing cellular signaling networks. The modulation of ncRNAs, especially in connection to specific cancer pathways, concentrating its role in cancer treatment for many areas. However, although huge potential of the drug exhibits, the use of aspirin is not without risks. Common symptoms such as gastrointestinal discomfort and bleeding are in considering. As all mentioned below, numerous good results in improved treatment approaches for patients will come out, follow the continued investigation into the many ways that aspirin affects cancer cells.