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A study of changes in blood coagulation indices in vitro at different times of incubation (5 and 30 min) of chitosan (CTS) with normal and with hypocoagulation plasma in rats was carried out. The addition of CTS to the plasma of normal animals led to an increase in its procoagulant activity regardless of the duration of the incubation. However, an increase in the time to 30 min contributed to a more significant decrease in the fibrin-depolymerization activity of the blood. The incubation of CTS with hypocoagulation plasma obtained after the administration of acetylsalicylic acid to animals (once, orally at a dose of 2 mg/kg) for both 5 and 30 min led to the activation of blood coagulation. Under these conditions, a prolongation of the incubation time caused more pronounced effects of this drug: a significant increase in the concentration of fibrinogen, ADP-dependent platelet aggregation, degree of fibrin polymerization, and a decrease in nonenzymatic fibrinolysis. At the same time, most of the studied hemostasis indices approach the values corresponding to a normal level. The results obtained in this work indicate the high efficiency of CTS as a treatment that restores normal blood coagulation and blocks the phenomena of bleeding in hypocoagulation states. [ABSTRACT FROM AUTHOR]

To assess the cost‐effectiveness of low‐dose aspirin compared to placebo for the prevention of recurrent preterm birth from a healthcare perspective. This was a cost‐effectiveness analysis alongside a multicenter, randomized, double‐blinded, placebo‐controlled trial. We included women with a singleton pregnancy and a previous spontaneous preterm birth <37 weeks of gestation of a singleton. Women were randomized between aspirin 80 mg daily and placebo, initiated between 8 and 16 weeks of gestation. We estimated the difference in preterm births (<37 weeks of gestation), and maternal and neonatal healthcare costs using seemingly unrelated linear regression analyses. Bootstrapping was performed to estimate statistical uncertainty. A total of 387 women were included: 194 in the aspirin group and 193 in the placebo group. We observed a small, statistically non‐significant difference in preterm birth (21.2% vs. 25.4%; risk difference −4.3%; 95% CI: −12.7% to 4.1%) and healthcare costs (mean –€99; 95% CI: –€2385 to €2325) in the aspirin group compared to placebo. The cost‐effectiveness acceptability curve showed that the probability of aspirin being cost‐effective was 54% for a willingness to pay threshold of €0 for one prevented preterm birth and 78% for €50 000 for one prevented preterm birth. Our findings suggest that aspirin is the dominant strategy over placebo for the prevention of preterm birth. However, there was substantial uncertainty around the results and definite conclusions regarding the cost‐effectiveness of aspirin cannot be drawn. [ABSTRACT FROM AUTHOR]

Simple Summary: Patients with gliomas show an increased risk of spontaneous hemorrhages throughout the disease. Simultaneously, the number of patients taking acetylsalicylic acid (ASA) for primary and secondary prophylaxis is rising in daily clinical practice. In the current study, we evaluate the risks associated with continuing ASA use perioperatively, focusing on hemorrhage and potential thromboembolic events that may arise from discontinuing ASA, particularly in multimorbid patients undergoing glioma surgery. The current findings show that the perioperative use of ASA is not associated with a significantly increased rate of hemorrhagic complications in glioma surgery. Thus, in patients with high stroke or cardiovascular risk, ASA can be continued during elective brain tumor surgery. Background/Objectives: Patients with gliomas show an increased risk of spontaneous hemorrhages throughout the disease. Simultaneously, the number of patients taking acetylsalicylic acid (ASA) for primary and secondary prophylaxis is rising in daily clinical practice, and interrupting ASA intake before elective or emergency intracranial surgery is not always feasible. This study aims to evaluate the risks associated with continuing ASA use perioperatively while focusing on hemorrhage and potential thromboembolic events that may arise from discontinuing ASA, particularly in multimorbid patients undergoing glioma surgery. Methods: The clinical parameters and imaging data of 7149 patients who underwent intracranial surgery in our department over a 10-year period were retrospectively analyzed. Patients were categorized into two groups based on their ASA status: Group 1 (no ASA impact) included those with no ASA use or who discontinued ASA use more than seven days prior to surgery (low stroke or cardiovascular risk), and Group 2 (ASA impact) included those who continued ASA use within seven days prior to operation (high stroke or cardiovascular risk). Results: In this retrospective study, data from 650 patients with various types of glial tumors who underwent surgery between 2008 and 2018 were examined. Of these patients, 50 experienced a postoperative hemorrhage (POH), and 10 required reoperations due to clinical neurological deterioration and increased intracranial pressure caused by the space-occupying effect of the hemorrhage. In the ASA impact group, 2.7% developed POH, compared to 1.3% in the no ASA impact group (p = 0.098). Our analysis did not show a significantly increased risk of POH after surgery, although patients in the ASA impact group had a one- to two-fold higher risk of developing POH overall. Additionally, other factors contributing to postoperative hemorrhage following glioma surgery were investigated and evaluated. Conclusions: In this cohort, the perioperative use of ASA was not associated with an increased rate of hemorrhagic complications after intracranial glioma surgery, although a trend was observed. In patients with high stroke and cardiovascular risk, ASA can be continued during elective brain tumor surgery. [ABSTRACT FROM AUTHOR]

Patients with diabetes face a 2‐4‐fold greater cardiovascular risk compared to those without diabetes. Both metformin and acetylsalicylic acid (aspirin) treatment have demonstrated a significant reduction in this risk. This single‐center, open‐label, sequence randomized, 2 × 2 crossover, single‐dose clinical trial evaluated the pharmacokinetics profile and comparative bioavailability of a novel oral fixed‐dose combination (FDC) of metformin/acetylsalicylic acid (500/100 mg tablet) versus the reference mono‐drugs administered concomitantly, metformin 500 mg tablet and acetylsalicylic acid 100 mg tablet, in 22 healthy Mexican adult volunteers under fasting conditions. Blood samples were collected predose and at specified intervals across a 24‐hour period following administration and were analyzed for metformin and salicylic acid using high‐performance liquid chromatography coupled with tandem mass spectrometry. Test products were considered to have comparative bioavailability if confidence intervals of natural log‐transformed (maximum plasma drug concentration (Cmax), (area under the plasma drug concentration‐time curve form 0 up to last sampling time (AUC0‐t), and (area under the plasma drug concentration‐time cruve from 0 up to infinity (AUC0∞) data were within the range of 80%‐125%. The results obtained from the present clinical study demonstrate the comparative bioavailability of the FDC when compared with the coadministration of reference mono‐drugs. There were no adverse events or adverse reactions reported throughout the study. [ABSTRACT FROM AUTHOR]

Increased platelet activity is a risk factor of thrombotic events in cardiovascular patients. We studied the relationship between platelet function, platelet size, and the content of reticulated platelets (RP) in patients with coronary heart disease (CHD, n = 55) and acute coronary syndrome (ACS, n = 95) receiving acetylsalicylic acid + clopidogrel or ticagrelor, respectively. The control group consisted of patients with risk factors for CHD, but with no CHD/ACS and free of antiplatelet drugs (n = 66). Platelet function was evaluated by the exposure of activated glycoprotein (GP) IIb-IIIa and P-selectin. In the control group, platelets were activated by TRAP (Thrombin Receptor Activating Peptide) 10 µM, and ADP 20, 5, 2.5 µM, and in the CHD/ACS groups, by TRAP 10 µM, and ADP 20 5 µM (±epinephrine 20 µM). Platelet size was assessed by the mean volume, % large forms, and forward scattering. RP were stained by thiazole orange. In the control group, activated GP IIb-IIIa and P-selectin correlated with platelet size and RP content after platelet activation by all agonists. Despite the decrease in platelet activity by antiplatelet drugs, most correlations (primarily for activated GP IIb-IIIa) were preserved in the CHD/ACS patients. In conclusion, increased platelet size and RP content are associated with increased platelet activity and the reduced efficacy of antiplatelet therapy. [ABSTRACT FROM AUTHOR]

A mild strategy was developed for efficient preparation of acetylsalicylic acid (ASA) from the acetylation of salicylic acid (SA) and acetic anhydride (AA) assisted ultrasonic over Y-immobilized cation exchange resin (Y-CER). With this strategy, an ASA yield of 95.2% was obtained. The results showed that the increased yield was due to Lewis acidic sites (LAS) combined with ultrasonic assistance. The process reduced the AA reagent feed while lowering the reaction temperature. The characterization results showed that metal Y species were dispersedly anchored on the CER surface through S-O-Y triple-dentate bonds, resulting in abundant LAS and stable catalytic activity. Comparative experiments revealed that LAS was more favorable for the formation of ASA than Bronsted acidic sites (BAS). Furthermore, a plausible mechanism for the acetylation of SA and AA by Y-CER has been proposed. This work provided a practical protocol for improving ASA yield and reducing acid wastewater discharge, with potential application prospects. [ABSTRACT FROM AUTHOR]

• Low-dose acetylsalicylic acid (ASA, i.e., aspirin) can mitigate the inflammatory consequences of experimental sleep restriction in healthy humans. • Low-dose ASA reduced the activity of the NF-κB pathway and COX pathway, as indicated by reduced serum CRP levels, reduced IL-6 expression and COX-1/COX-2 co-expression in LPS-stimulated monocytes in the sleep restriction condition compared to placebo. • Counter-inflammatory effects of low-dose ASA were still evident following recovery sleep, in particular in COX-1/COX-2 co-expression in LPS-stimulated monocytes. Sleep deficiencies, such as manifested in short sleep duration or insomnia symptoms, are known to increase the risk for multiple disease conditions involving immunopathology. Inflammation is hypothesized to be a mechanism through which deficient sleep acts as a risk factor for these conditions. Thus, one potential way to mitigate negative health consequences associated with deficient sleep is to target inflammation. Few interventional sleep studies investigated whether improving sleep affects inflammatory processes, but results suggest that complementary approaches may be necessary to target inflammation associated with sleep deficiencies. We investigated whether targeting inflammation through low-dose acetylsalicylic acid (ASA, i.e., aspirin) is able to blunt the inflammatory response to experimental sleep restriction. 46 healthy participants (19F/27M, age range 19–63 years) were studied in a double-blind randomized placebo-controlled crossover trial with three protocols each consisting of a 14-day at-home monitoring phase followed by an 11-day (10-night) in-laboratory stay (sleep restriction/ASA, sleep restriction/placebo, control sleep/placebo). In the sleep restriction/ASA condition, participants took low-dose ASA (81 mg/day) daily in the evening (22:00) during the at-home phase and the subsequent in-laboratory stay. In the sleep restriction/placebo and control sleep/placebo conditions, participants took placebo daily. Each in-laboratory stay started with 2 nights with a sleep opportunity of 8 h/night (23:00–07:00) for adaptation and baseline measurements. Under the two sleep restriction conditions, participants were exposed to 5 nights of sleep restricted to a sleep opportunity of 4 h/night (03:00–07:00) followed by 3 nights of recovery sleep with a sleep opportunity of 8 h/night. Under the control sleep condition, participants had a sleep opportunity of 8 h/night throughout the in-laboratory stay. During each in-laboratory stay, participants had 3 days of intensive monitoring (at baseline, 5th day of sleep restriction/control sleep, and 2nd day of recovery sleep). Variables, including pro-inflammatory immune cell function, C-reactive protein (CRP), and actigraphy-estimated measures of sleep, were analyzed using generalized linear mixed models. Low-dose ASA administration reduced the interleukin (IL)-6 expression in LPS-stimulated monocytes (p<0.05 for condition*day) and reduced serum CRP levels (p<0.01 for condition) after 5 nights of sleep restriction compared to placebo administration in the sleep restriction condition. Low-dose ASA also reduced the amount of cyclooxygenase (COX)-1/COX-2 double positive cells among LPS-stimulated monocytes after 2 nights of recovery sleep following 5 nights of sleep restriction compared to placebo (p<0.05 for condition). Low-dose ASA further decreased wake after sleep onset (WASO) and increased sleep efficiency (SE) during the first 2 nights of recovery sleep (p<0.001 for condition and condition*day). Baseline comparisons revealed no differences between conditions for all of the investigated variables (p>0.05 for condition). This study shows that inflammatory responses to sleep restriction can be reduced by preemptive administration of low-dose ASA. This finding may open new therapeutic approaches to prevent or control inflammation and its consequences in those experiencing sleep deficiencies. ClinicalTrials.gov NCT03377543. [ABSTRACT FROM AUTHOR]

Numerous cellular processes are regulated in response to the metabolic state of the cell, and one such regulatory mechanism involves lysine acetylation. Lysine acetylation has been proven to play an important role in the virulence of Streptococcus mutans, a major cariogenic bacterial species. S. mutans' glucosyltransferases (Gtfs) are responsible for synthesizing extracellular polysaccharides (EPS) and contributing to biofilm formation. One of the most common nonsteroidal anti‐inflammatory drugs is acetylsalicylic acid (ASA), which can acetylate proteins through a nonenzymatic transacetylation reaction. Herein, we investigated the inhibitory effects of ASA on S. mutans. ASA treatment was observed to impede the growth of S. mutans, leading to a reduction in the production of water‐insoluble EPS and the formation of biofilm. Moreover, ASA decreased the enzyme activity of Gtfs while increasing the protein acetylation level. The in vivo anticaries efficacy of ASA has further been proved using the rat caries model. In conclusion, ASA as an acetylation agent attenuated the cariogenic virulence of S. mutans, suggesting the potential value of protein acetylation on antimicrobial and anti‐biofilm applications to S. mutans. [ABSTRACT FROM AUTHOR]

A 4-month-old female Shar-pei dog was admitted with apathy, anorexia, and vomiting. The patient had an appropriate vaccination protocol, with the last vaccine administered 2.5 weeks prior to the onset of clinical signs. Physical examination revealed tachycardia, fever and swelling of the tibiotarsal joints. Several diagnostic tests including complete blood cell count, biochemistry profile, urinalysis, thoracic radiographs, hind limbs radiographs, abdominal ultrasound, and infectious diseases tests, were conducted to determine the underlying cause. Shar-Pei Auto-inflammatory Disease (SPAID) was diagnosed. Additionally, the patient developed skin necrosis in the inner aspect of the tibiotarsal joints as a complication. A skin biopsy revealed cutaneous vasculopathy causing degeneration, abrupt ulceration, and ischemic necrosis with intense neutrophilic inflammation of the dermis and subcutis. Moreover, a hospital-acquired infection was identified by skin culture. Debridement of the necrotic skin was performed, and due to its' severity and extent, the wound was closed by secondary intention. A diagnostic protocol and the therapeutic dose of acetylsalicylic acid, which led to clinical improvement, are recommended here. The patient has continued to present episodic manifestations of SPAID mainly fever and swelling of the tibiotarsal joints, but there has been no recurrence of necrosis or other cutaneous lesion in the last two years. [ABSTRACT FROM AUTHOR]

Background and aims: It is well known that elevated cholesterol is associated with enhanced platelet aggregation and patients suffering from familial hypercholesterolemia (FH) have a high risk of thrombotic cardiovascular events. Although decreasing cholesterol level is associated with attenuation of platelet hyperactivity, there are currently no data on the effect of convertase subtilisin/kexin type 9 monoclonal antibodies (PCSK9ab) on platelet reactivity in FH. The aim of the study was to analyse the impact of different therapies including PCSK9ab on platelet aggregation in FH. Methods: This study enrolled all 15 patients treated in the University Hospital Hradec Králové for FH. PCSK9ab have been administered in 12 of 15 patients while 8 patients were also undergoing lipid apheresis. Blood samples from all patients including pre- and post-apheresis period were tested for platelet aggregation triggered by 7 inducers, and the effect of 3 clinically used drugs (acetylsalicylic acid, ticagrelor and vorapaxar) was compared as well. Results: Although apheresis decreased the reactivity of platelets in general, platelet responses were not different between non-apheresis patients treated with PCSK9ab and apheresis patients (post-apheresis values) with the exception of ristocetin. However, when compared to age-matched healthy population, FH patients had significantly lower platelet aggregation responses to 4 out of 7 used inducers and higher profit from 2 out of 3 used antiplatelet drugs even after exclusion of FH patients regularly receiving conventional antiplatelet treatment. Conclusion: This study showed for the first time the suitability of PCSK9ab treatment for reduction of platelet reactivity in FH patients. [ABSTRACT FROM AUTHOR]

The aim of the current study is to develop chitosan-based biomaterials which can sustainably release acetylsalicylic acid while presenting significant biological activity. Herein, an innovative ionic bonding strategy between hydroxypropyl trimethyl ammonium chloride chitosan (HACC) and acetylsalicylic acid (AA) was proposed, skillfully utilizing the electrostatic attraction of the ionic bond to achieve the controlled release of drugs. Based on this point, six crosslinked N-[(2-hydroxy-3-trimethylammonium)propyl]chitosan acetylsalicylic acid salt (CHACAA) hydrogel films with varying acetylsalicylic acid contents were prepared by a crosslinking reaction. The results of 1H nuclear magnetic resonance spectroscopy (1H NMR) and scanning electron morphology (SEM) confirmed the crosslinked structure, while the obtained hydrogel films possessed favorable thermal stability, mechanical properties, and swelling ability. In addition, the drug release behavior of the hydrogel films was also investigated. As expected, the prepared hydrogel films demonstrated the capability for the sustainable release of acetylsalicylic acid due to ion pair attraction dynamics. Furthermore, the bioactivities of CHACAA-3 and CHACAA-4 hydrogel films with acetylsalicylic acid molar equivalents of 1.25 and 1.5 times those of HACC were particularly pronounced, which not only exhibited an excellent drug sustained-release ability and antibacterial effect, but also had a higher potential for binding and scavenging inflammatory factors, including NO and TNF-α. These findings suggest that CHACAA-3 and CHACAA-4 hydrogel films hold great potential for applications in wound dressing, tissue engineering scaffolds, and drug carriers. [ABSTRACT FROM AUTHOR]

Central retinal vein occlusion (CRVO) is a significant cause of vision impairment in adults, often associated with various systemic and ocular risk factors. The current literature presents a limited understanding of the efficacy of antithrombotic agents in CRVO management, with sparse comparative studies evaluating the effectiveness of different antiplatelet therapies. Here, we report the case of nonischemic CRVO in a 54-year-old male with multiple systemic comorbidities, including diabetes mellitus, hypertension, and dyslipidemia. Initial treatment with aspirin 100 mg daily resulted in worsening visual acuity (VA) and retinal pathology, prompting a transition to clopidogrel 75 mg daily due to patient refusal of intravitreal injection. Remarkably, clopidogrel therapy led to rapid and sustained improvement in VA, macular edema resolution, and complete resolution of retinal vascular pathology within weeks. This case underscores the therapeutic potential of clopidogrel in nonischemic CRVO management, suggesting its superiority over aspirin in select patients. We discuss the mechanisms underlying the differential efficacy of antiplatelet agents and highlight the need for further comparative studies to guide optimal treatment strategies in CRVO.

BACKGROUND. Kawasaki disease is a rare, self-limiting inflammatory disease primarily affecting children under 5 years old. In 25 % of cases, it can lead to coronary artery aneurysms if not treated promptly with intravenous human immunoglobulin. A significant portion of Kawasaki disease patients present with an incomplete form, complicating diagnosis, while the risk of coronary artery aneurysms remains unchanged. Particularly vulnerable are infants under 6 months old, who may exhibit even more limited clinical symptoms, making them especially susceptible to severe cardiac complications. OBJECTIVE. To analyze a clinical case of an incomplete form of Kawasaki disease in a 2-month-old girl, raise awareness of Kawasaki disease, including its incomplete form, among healthcare workers in Ukraine, emphasize the critical importance of proper diagnostic evaluation of coronary arteries, and underscore the necessity of early administration of immunoglobulin when Kawasaki disease is suspected, even in the absence of pathological changes in the heart. MATERIALS AND METHODS. The study involved collecting medical history, physical examination data, laboratory and instrumental studies, and their analysis. The diagnosis of Kawasaki disease, including its incomplete form, was based on the 2017 recommendations of the American Heart Association. CLINICAL CASE. A 2-month-old girl presented with symptoms initially resembling a urinary tract infection, with no therapeutic response to multiple courses of antibacterial therapy. During the second week of illness, she developed swelling in her hands and feet, which, along with persistent fever, significant inflammatory response, and lack of improvement with antibiotics, led to the suspicion and diagnosis of Kawasaki disease based on the algorithm for incomplete Kawasaki disease. After administration of an immunomodulatory dose of intravenous human immunoglobulin at 2 g/kg on the 11th day of illness, there was a rapid regression of symptoms, normalization of inflammation markers, and overall improvement in the child's condition. By the second week of illness, small aneurysms of the right and left coronary arteries had formed but regressed within a few weeks from the onset of the disease. CONCLUSIONS. Kawasaki disease requires prompt therapeutic intervention and should be suspected in any child, especially those under one year of age, with a high fever lasting at least 5 days, unexplained by a preliminary diagnosis, and no response to antibiotic treatment in the presence of “bacterial” blood tests. Serial echocardiograms assessing coronary arteries, absolute dimensions, and Z-scores are mandatory.

Abstract Background Severe malaria can cause respiratory symptoms, which may lead to malaria-acute lung injury (MA-ALI) due to inflammation and damage to the blood-gas barrier. Patients with severe malaria also often present thrombocytopenia, and the use of acetylsalicylic acid (ASA), a commonly used non-steroidal anti-inflammatory drug with immunomodulatory and antiplatelet effects, may pose a risk in regions where malaria is endemic. Thus, this study aimed to investigate the systemic impact of ASA and dihydroartemisinin (DHA) on ALI induced in mice by Plasmodium berghei NK65 (PbNK65). Methods C57BL/6 mice were randomly divided into control (C) and PbNK65 infected groups and were inoculated with uninfected or 104 infected erythrocytes, respectively. Then, the animals were treated with DHA (3 mg/kg) or vehicle (DMSO) at the 8-day post-infection (dpi) for 7 days and with ASA (100 mg/kg, single dose), and analyses were performed at 9 or 15 dpi. Lung mechanics were performed, and lungs were collected for oedema evaluation and histological analyses. Results PbNK65 infection led to lung oedema, as well as increased lung static elastance (Est, L), resistive (ΔP1, L) and viscoelastic (ΔP2, L) pressures, percentage of mononuclear cells, inflammatory infiltrate, hemorrhage, alveolar oedema, and alveolar thickening septum at 9 dpi. Mice that received DHA or DHA + ASA had an increase in Est, L, and CD36 expression on inflammatory monocytes and higher protein content on bronchoalveolar fluid (BALF). However, only the DHA-treated group presented a percentage of inflammatory monocytes similar to the control group and a decrease in ΔP1, L and ΔP2, L compared to Pb + DMSO. Also, combined treatment with DHA + ASA led to an impairment in diffuse alveolar damage score and lung function at 9 dpi. Conclusions Therapy with ASA maintained lung morpho-functional impairment triggered by PbNK65 infection, leading to a large influx of inflammatory monocytes to the lung tissue. Based on its deleterious effects in experimental MA-ALI, ASA administration or its treatment maintenance might be carefully reconsidered and further investigated in human malaria cases.

Abstract Background This study aimed to clarify serum salicylic acid (SA) levels in patients with Kawasaki disease (KD) after the administration of moderate-dose acetylsalicylic acid (ASA) and their relationship with the therapeutic effect. Methods We retrospectively analyzed the clinical data of 142 children with KD. We measured serum SA trough levels during the acute and recovery periods and determined their relationship with clinical and laboratory parameters. Results The median age of patients was 2.4 years. Thirty-one patients had incomplete KD, 29 were intravenous immunoglobulin (IVIG) non-responders, and one patient had coronary artery lesions. The median ASA dose was 49.7 mg/kg/day. The median serum SA level was 22 µg/mL in the acute period and 15 µg/mL in the recovery period, with 45 (33%) in the acute period and 60 (44%) in the recovery period below the limit of measurement (

Background: This study aimed to clarify serum salicylic acid (SA) levels in patients with Kawasaki disease (KD) after the administration of moderate-dose acetylsalicylic acid (ASA) and their relationship with the therapeutic effect. Methods: We retrospectively analyzed the clinical data of 142 children with KD. We measured serum SA trough levels during the acute and recovery periods and determined their relationship with clinical and laboratory parameters. Results: The median age of patients was 2.4 years. Thirty-one patients had incomplete KD, 29 were intravenous immunoglobulin (IVIG) non-responders, and one patient had coronary artery lesions. The median ASA dose was 49.7 mg/kg/day. The median serum SA level was 22 µg/mL in the acute period and 15 µg/mL in the recovery period, with 45 (33%) in the acute period and 60 (44%) in the recovery period below the limit of measurement (< 10 µg/mL). Serum SA levels during the recovery period were significantly lower in patients who received steroids. There were no significant differences in IVIG responsiveness based on serum SA levels. Conclusions: Serum SA trough levels in KD patients treated with moderate-dose ASA were highly variable and did not reach sufficient levels. Serum SA levels were not associated with IVIG responsiveness. [ABSTRACT FROM AUTHOR]

Background: Severe malaria can cause respiratory symptoms, which may lead to malaria-acute lung injury (MA-ALI) due to inflammation and damage to the blood-gas barrier. Patients with severe malaria also often present thrombocytopenia, and the use of acetylsalicylic acid (ASA), a commonly used non-steroidal anti-inflammatory drug with immunomodulatory and antiplatelet effects, may pose a risk in regions where malaria is endemic. Thus, this study aimed to investigate the systemic impact of ASA and dihydroartemisinin (DHA) on ALI induced in mice by Plasmodium berghei NK65 (PbNK65). Methods: C57BL/6 mice were randomly divided into control (C) and PbNK65 infected groups and were inoculated with uninfected or 104 infected erythrocytes, respectively. Then, the animals were treated with DHA (3 mg/kg) or vehicle (DMSO) at the 8-day post-infection (dpi) for 7 days and with ASA (100 mg/kg, single dose), and analyses were performed at 9 or 15 dpi. Lung mechanics were performed, and lungs were collected for oedema evaluation and histological analyses. Results: PbNK65 infection led to lung oedema, as well as increased lung static elastance (Est, L), resistive (ΔP1, L) and viscoelastic (ΔP2, L) pressures, percentage of mononuclear cells, inflammatory infiltrate, hemorrhage, alveolar oedema, and alveolar thickening septum at 9 dpi. Mice that received DHA or DHA + ASA had an increase in Est, L, and CD36 expression on inflammatory monocytes and higher protein content on bronchoalveolar fluid (BALF). However, only the DHA-treated group presented a percentage of inflammatory monocytes similar to the control group and a decrease in ΔP1, L and ΔP2, L compared to Pb + DMSO. Also, combined treatment with DHA + ASA led to an impairment in diffuse alveolar damage score and lung function at 9 dpi. Conclusions: Therapy with ASA maintained lung morpho-functional impairment triggered by PbNK65 infection, leading to a large influx of inflammatory monocytes to the lung tissue. Based on its deleterious effects in experimental MA-ALI, ASA administration or its treatment maintenance might be carefully reconsidered and further investigated in human malaria cases. [ABSTRACT FROM AUTHOR]

Synthesis of unique morphologies in photocatalytic materials, coupled with utilization of wide-spectrum solar energy through rare earth doping, holds significant promise to maximize the potential of photocatalysts. Herein in, cube-like Holmium (Ho) doped Bi 5 Nb 3 O 15 was synthesized by the hydrothermal method and integrated with reduced graphene oxide (rGO) sheets. As synthesized Ho–Bi 5 Nb 3 O 15 @rGO composite along its analogs i.e., Bi 5 Nb 3 O 15 and Ho–Bi 5 Nb 3 O 15 was characterized by XRD, SEM, FT-IR, TGA, I–V, EIS, Mott-Schottky and photo-current measurements. Phase studies showed that crystallite size for Bi 5 Nb 3 O 15 , Ho–Bi 5 Nb 3 O 15 , and Ho–Bi 5 Nb 3 O 15 @rGO was 27.4, 25.5, and 13.5 nm, respectively. Optical analysis exhibited a reduction in the band gap in consequent to Ho doping from 2.54 to 2.19 eV for Ho–Bi 5 Nb 3 O 15. Conductivity and photo-current measurements showed a remarkable increase in both electrical conductivity and photo-response of Ho–Bi 5 Nb 3 O 15 upon its incorporation into rGO matrix, reaching maximum values of 1.72 × 10−2 S/m and 0.66 μA, respectively. The enhanced photocatalytic activity of Ho–Bi 5 Nb 3 O 15 @rGO was ensured through the outstanding photo-degradation efficiency (96.5 %) against crystal violet (CV), greater than Bi 5 Nb 3 O 15 (49 %) and Ho–Bi 5 Nb 3 O 15 (63.4 %). Additionally, Ho–Bi 5 Nb 3 O 15 @rGO showed sufficient potential towards the degradation of acetylsalicylic acid (ASA) with 79.1 % photo-degradation. This elevated photocatalytic activity of Ho–Bi 5 Nb 3 O 15 @rGO is believed to be contributed by the collaborative outcomes aroused from the Ho-doping and heterojunction fabrication among cubical Ho–Bi 5 Nb 3 O 15 and rGO sheets. Hence, our work proposes an efficient strategy for the development of innovative photolytic materials for sustainable wastewater remediation. [ABSTRACT FROM AUTHOR]

Central retinal vein occlusion (CRVO) is a significant cause of vision impairment in adults, often associated with various systemic and ocular risk factors. The current literature presents a limited understanding of the efficacy of antithrombotic agents in CRVO management, with sparse comparative studies evaluating the effectiveness of different antiplatelet therapies. Here, we report the case of nonischemic CRVO in a 54-year-old male with multiple systemic comorbidities, including diabetes mellitus, hypertension, and dyslipidemia. Initial treatment with aspirin 100 mg daily resulted in worsening visual acuity (VA) and retinal pathology, prompting a transition to clopidogrel 75 mg daily due to patient refusal of intravitreal injection. Remarkably, clopidogrel therapy led to rapid and sustained improvement in VA, macular edema resolution, and complete resolution of retinal vascular pathology within weeks. This case underscores the therapeutic potential of clopidogrel in nonischemic CRVO management, suggesting its superiority over aspirin in select patients. We discuss the mechanisms underlying the differential efficacy of antiplatelet agents and highlight the need for further comparative studies to guide optimal treatment strategies in CRVO. [ABSTRACT FROM AUTHOR]

In this study, chitosan-based hydroxyapatite/chitosan (HAP/CHI), cellulose/chitosan (CEL/CHI) and montmorillonite/chitosan (MMT/CHI) composites were synthesized and characterized by Fourier Transform Infrared Spectroscopy (FTIR), Scanning Electron Microscopy (SEM) and Thermogravimetric Analysis (TGA). Acetylsalicylic acid (ASA) was used as a drug for loading and desorption studies to determine the release behavior of the synthesized composites. The maximum adsorption capacities (qe) were obtained as 251.5 mg/g, 197.7 mg/g and 288.95 mg/g for HAP/CHI, CEL/CHI and MMT/CHI, respectively. In vitro release studies of ASA from the composites HAP/CHI, CEL/CHI, and MMT/CHI were carried out phosphate buffer solution (PBS) and gastric juice (GJ). In the intestinal medium (PBS) controlled drug release continued for 72 hours (4320 minutes), and burst release was observed in the first 5 minutes in all composites. 19.16%, 47.15% and 37.32% of the active ingredient from HAP/CHI, CEL/CHI and MMT/CHI composites, respectively, were released in the first 5 minutes. After 5 minutes, the release slowed down and became more controlled for all three composites. At the end of the release, the highest releasing composite was CEL/CHI, with 95.77% ASA release. A total drug release of 87.48% was achieved with MMT/CHI and 87.37% with HAP/CHI. In the gastric environment (GJ) Controlled drug release continued for 72 hours (4320 minutes), and burst release was observed in the first 5 minutes in all composites. 52.51%, 72.30% and 44.87% of the active ingredient from HAP/CHI, CEL/CHI and MMT/CHI composites, respectively, were released in the first 5 minutes. After 5 minutes, the release slowed down and became more controlled for all three composites. At the end of the release, the highest releasing capacity was found with the CEL/CHI composite, with 96.05% ASA release. A total drug release of 93.26% was achieved with HAP/CHI and 84.89% with MMT/CHI. [ABSTRACT FROM AUTHOR]

Background: The hippocampus is susceptible to damage, leading to negative impacts on cognition. Conditioned medium (CM) obtained from adipose tissue–derived mesenchymal stem cells (MSCs) and acetylsalicylic acid (ASA) have shown neuroprotective effects independently. This study explored the synergistic potential of ASA and CM from adipose‐derived MSCs against hippocampal injury. Methods: Adult male Wistar rats received bilateral hippocampal ethidium bromide (EB) injections to induce hippocampal damage. Rats were treated with ASA and/or CM derived from adipose tissue MSCs every 48 h for 16 days. Behavioral tests (open field test, Morris water maze, novel object recognition, and passive avoidance), oxidative stress, Western blot analysis of brain‐derived neurotrophic factor (BDNF) and cerebral dopamine neurotrophic factor (CDNF) expression, and hippocampal histological investigation were conducted. Results: Administration of EB caused impairments in spatial, recognition, and passive avoidance memory, as well as heightened oxidative stress, reduced BDNF/CDNF expression, and pyramidal cell loss in the hippocampal CA1 region. Administration of ASA, CM, or a combination of both mitigated these hippocampal damages and cognitive deficits, elevated BDNF and CDNF levels, and alleviated the CA1 necrosis caused by EB. Moreover, co‐administering ASA and CM resulted in greater improvements in spatial memory compared to administering ASA alone, suggesting possible synergistic interactions. Conclusions: The ability of ASA, CM obtained from adipose tissue–derived MSCs, and their combination therapy to alleviate hippocampal injuries highlights their promising therapeutic potential as a neuroprotection strategy against brain damage. Our findings provide preliminary evidence of the potential synergistic effects of ASA and CM, which warrants further investigations. [ABSTRACT FROM AUTHOR]

This present review provides an overview of Acetylsalicylic Acid (ASA), emphasizing its role in cardiovascular disease prevention. ASA's mechanism involves irreversible inhibition of COX activity, impacting prostaglandin synthesis. The ASA as a crucial lifelong therapy for cardiovascular events, with over 50 million Americans using it. While its clinical benefits are established, the underlying mechanisms, especially in coronary artery disease (CAD) secondary prevention, lack full clarity. The document discusses pharmacokinetics, pharmacodynamics, and optimal doses, including ongoing studies like ADAPTABLE to determine the most effective dosage for secondary prevention. It also touches on pharmacogenomics, highlighting genetic variations influencing ASA response and metabolism, particularly in genes like CYP2C9, UGT1A6, and TBXA2R. Conclusion: The review aims to consolidate information on pharmacological, molecular, genetic, and clinical aspects of ASA's protective effects in CAD. The expression and saturation of enzymes involved in ASA metabolism can alter individual responses, so understanding the pharmacogenomic profile is important for personalizing treatment and improving clinical outcomes. [ABSTRACT FROM AUTHOR]

This study presents an electrochemical permeability assay for drugs using an engineered gut model. Caco-2 cells (human colorectal adenocarcinoma cell line) were cultured on porous membranes for 21 d. Acetylsalicylic acid (aspirin), after hydrolysis, was introduced from either the apical or basal sides and incubated for 2 h. The solution from the acceptor side was collected, and cyclic voltammetry was conducted to measure the hydrolyzed acetylsalicylic acid. This electrochemical approach holds promise for drug screening applications in engineered gut models. [ABSTRACT FROM AUTHOR]

Ovarian cancer is the deadliest gynaecologic malignancies worldwide. Platinum based chemotherapy is the mainstay treatment for ovarian cancer; however, frequent recurrence and chemoresistance onset in patients with advanced diseases remain a therapeutic challenge. Although mechanisms underlying the development of chemoresistance are still ambiguous, the B-cell lymphoma-2 (Bcl-2) family is closely associated with chemoresistance in ovarian cancer. We previously disclosed that Zeta-Crystallin (CryZ) is a post-transcriptional regulator of Bcl-2 gene expression, by binding to Bcl-2 mRNA and increasing its half-life. Here, we investigated the role of CryZ as a novel therapeutic target in A2780 ovarian carcinoma cells by modulating the protein activity with acetylsalicylic acid (ASA) to restore chemosensitivity. Molecular docking and fragment-mapping based approach revealed potential interaction of ASA within CryZ protein. Inhibition of CryZ binding activity to Bcl-2 and Bcl-xl mRNA targets by ASA was demonstrated in A375 cells. Cytotoxicity assays were conducted in A2780S and A2780R ovarian cancer cells to evaluate if CryZ binding activity inhibition and CryZ silencing were able to reverse cisplatin resistance. ASA-treatment determined a downregulation of Bcl-2 and Bcl-xl mRNA levels in A2780S and A2780R cells. ASA-treatment or CryZ silencing were able to increase and restore the chemosensitivity in both sensitive and resistant A2780 ovarian cancer cells, respectively. In this research article we demonstrated that the pharmacological or genetic inhibition of CryZ restores the sensitivity to cisplatin in a model of sensitive or resistant ovarian cancer cells. These findings suggest a new gene-targeted chemotherapeutic approach to restore the cytotoxicity in drug-resistant ovarian cancers and increase the sensitivity in non-resistant cells. [ABSTRACT FROM AUTHOR]

AbstractVerifyNow (VN) test is a less laborious method to assess pharmacodynamics (PD) compared to light transmittance aggregometry (LTA). VN assay has not been used to study the immediate PD effects of acetylsalicylic acid (ASA). Ten healthy volunteers were randomly assigned to a single 162 or 650 mg dose of chewed and swallowed ASA. Pharmacodynamic and pharmacokinetic measurements were performed at baseline and serially up to 60 min after ASA administration. Onset by VN was 20 ± 7 min with 162 mg and 13 ± 7 min with 650 mg ASA (p = .07). Onset by 1 mM AA-induced PA was 13 ± 12 min with 162 mg and 7 ± 3 min with 650 mg ASA (p=NS). VN correlated with AA-induced PA (r = 0.80, p

Atherosclerotic cardiovascular diseases cause the highest number of deaths worldwide. To reduce cardiovascular mortality, the use of appropriate antithrombotic treatment in secondary prevention is crucial. A special form of antithrombotic therapy is combined low-dose rivaroxaban + acetylsalicylic acid treatment (dual inhibition), for which there is clinical evidence in a wide range of high-risk atherosclerotic patients (after acute coronary syndrome, chronic coronary syndrome, peripheral arterial patients and after peripheral vascular intervention). The aim of this paper is to summarize clinical experience with this therapeutic strategy and to make recommendation for daily practice for low-dose rivaroxaban + acetylsalicylic acid treatment.

Administration of acetylsalicylic acid (ASA) at early stage after surgery for spontaneous intracerebral hemorrhage (SICH) may increase the risk of postoperative intracranial bleeding (PIB), because of potential inhibition of platelet function. This study aimed to investigate whether early ASA administration after surgery was related to increased risk of PIB. This retrospective study enrolled SICH patients receiving surgery from September 2019 to December 2022 in seven medical institution. Based on postoperative ASA administration, patients who continuously received ASA more than three days within seven days post-surgery were identified as ASA users, otherwise as non-ASA users. The primary outcome was symptomatic PIB events within seven days after surgery. Incidence of PIB was compared between ASA users and non-ASA users using survival analysis. This study included 744 appropriate patients from 794 SICH patients. PIB occurred in 42 patients. Survival analysis showed no statistical difference between ASA users and non-ASA users in incidence of PIB (P = 0.900). Multivariate Cox analysis demonstrated current smoker (hazard ratio [HR], 2.50, 95%CI, 1.33–4.71, P = 0.005), dyslipidemia (HR = 3.03; 95%CI, 1.31–6.99; P = 0.010) and pre-hemorrhagic antiplatelet therapy (HR = 3.05; 95% CI, 1.64–5.68; P < 0.001) were associated with PIB. Subgroup analysis manifested no significant difference in incidence of PIB between ASA users and non-ASA users after controlling the effect from factors of PIB (i.e., sex, age, current smoker, regular drinker, dyslipidemia, pre-hemorrhagic antiplatelet therapy and hematoma location). This study revealed that early ASA administration to SICH patients after surgery was not related to increased risk of PIB. [ABSTRACT FROM AUTHOR]

Gastric ulcers affect approx. 10% of population. Non-steroidal anti-inflammatory drugs (NSAIDs), including acetylsalicylic acid (ASA) predispose to or impair the physiologically complex healing of pre-existing ulcers. Since H2S is an endogenous cytoprotective molecule, we hypothesized that new H2S-releasing ASA-derivative (ATB-340) could overcome pathological impact of NSAIDs on GI regeneration. Clinically translational gastric ulcers were induced in Wistar rats using state-of-the-art microsurgical model employing serosal application of acetic acid. This was followed by 9 days long i.g. daily treatment with vehicle, ATB-340 (6–24 mg/kg) or equimolar ASA doses (4–14 mg/kg). Ulcer area was assessed macro- and microscopically. Prostaglandin (PG)E2 levels, indicating pharmacological activity of NSAIDs and 8-hydroxyguanozine content, reflecting nucleic acids oxidation in serum/gastric mucosa, were determined by ELISA. Qualitative and/or quantitative pathway-specific alterations at the ulcer margin were evaluated using real-time PCR and mass spectrometry-based proteomics. ASA, unlike ATB-340, dose-dependently delayed/impaired gastric tissue recovery, deregulating 310 proteins at the ulcer margin, including Ras signalling, wound healing or apoptosis regulators. ATB-340 maintained NSAIDs-specific cyclooxygenase-inhibiting capacity on systemic and GI level but in time-dependent manner. High dose of ATB-340 (24 mg/kg daily), but not ASA, decreased nucleic acids oxidation and upregulated anti-oxidative/anti-inflammatory heme oxygenase-1, 24-dehydrocholesterol reductase or suppressor of cytokine signalling (SOCS3) at the ulcer margin. Thus, ASA impairs the physiological healing of pre-existing gastric ulcers, inducing the extensive molecularly functional and proteomic alterations at the wound margin. H2S-releasing ATB-340 maintains the target activity of NSAIDs with limited impact on gastric PGE2 signalling and physiological GI regeneration, enhancing anti-inflammatory and anti-oxidative response, and providing the pharmacological advantage. [ABSTRACT FROM AUTHOR]

The new compound N-a-chloroacetylsalicyloyl-N-antipyrine benzamide was synthesized by a reaction of N-benzylidene antipyrine amine and O-acetyl salicyloyl chloride. On the other hand, N-benzylidene antipyrine amine was obtained by a coupling reaction between benzaldehyde and 4-aminoantipyrine, while O-acetyl salicyloyl chloride resulted from acylation reaction of aspirin starting from salicylic acid. All synthesized compounds were characterized by using m.ps., UV-Vis., FTIR, MS, and 1HNMR spectroscopic methods. The method of DPPH was also used as testing to measure the radical scavenging of the new compound. It showed very powerful antioxidant activity with IC50 value of 29 ppm. Moreover, its antibacterial activity was tested against three types of bacteria. [ABSTRACT FROM AUTHOR]

Aspirin has been known for a long time and currently stays as a cornerstone of antithrombotic therapy in cardiovascular disease. In patients with either acute or chronic coronary syndromes undergoing percutaneous coronary intervention aspirin is mandatory in a dual antiplatelet therapy regimen for prevention of stent thrombosis and/or new ischaemic events. Aspirin is also currently a first-option antithrombotic therapy after an aortic prosthetic valve replacement and is occasionally required in addition to oral anticoagulants after implantation of a mechanical valve. Presumed or demonstrated aspirin hypersensitivity is a main clinical problem, limiting the use of a life-saving medication. In the general population, aspirin hypersensitivity has a prevalence of 0.6%–2.5% and has a plethora of clinical presentations, ranging from aspirin-exacerbated respiratory disease to anaphylaxis. Although infrequent, when encountered in clinical practice aspirin hypersensitivity poses for cardiologists a clinical dilemma, which should never be trivialized, avoiding—as much as possible—omission of the drug. We here review the epidemiology of aspirin hypersensitivity, provide an outline of pathophysiological mechanisms and clinical presentations, and review management options, starting from a characterization of true aspirin allergy—in contrast to intolerance—to suggestion of desensitization protocols. [ABSTRACT FROM AUTHOR]

Compound L-36, a new derivative of 6H-1,3,4-thiadiazine, was studied in in vitro and in vivo experiments. This compound exhibits high antiplatelet and antithrombogenic activity. In in vitro experiments, compound L-36 by its antiplatelet activity (by IC50) was superior to acetylsalicylic acid by 9.4 times. In in vivo experiments, compound L-36 by its ED50 value was close to the comparison drug. On the model of pulmonary artery thrombosis, compound L-36 ensured better survival of experimental animals than acetylsalicylic acid. Morphological studies showed that compound L-36 effectively attenuated the thrombosis processes in the pulmonary tissue induced by intravenous injection of a thrombogenic mixture (epinephrine and collagen). [ABSTRACT FROM AUTHOR]

Aims: The aim of this study was to systematically review whether concurrent treatment with an SSRI and low‐dose ASA increases the risk of bleeding compared with treatment with an SSRI alone or ASA alone. Methods: Medline, Embase, the Cochrane Library, PsycINFO and Web of Science (from database inception to January 2023) were searched according to PICO: P = patients on treatment with an SSRI and/or low‐dose ASA; I = intervention: SSRI + ASA; C = comparison: ASA or SSRI alone; O = outcomes: bleeding/major bleeding. The included articles were assessed using checklists. Studies without major risk of bias formed the basis for the conclusions. Extracted data were pooled using random‐effects meta‐analyses. Certainty of evidence was assessed according to GRADE. Results: Twenty‐four studies met the PICO and were included. One randomized and six nonrandomized studies were assessed not to have major risk of bias. Regarding SSRI + ASA vs. ASA only, the pooled hazard ratio of three nonrandomized studies (n = 38 467) was 1.37 (95% confidence interval: 1.10; 1.70; I2 = 0%), and the pooled odds ratio of two nonrandomized studies (n = 28 296) was 0.95 (0.77; 1.19; I2 = 0%). Regarding SSRI + ASA vs. SSRI only, the randomized controlled trial (n = 1048) reported a hazard ratio of 1.82 (0.66; 5.02), the hazard ratio being 1.60 (1.24; 2.06) for ASA vs. placebo in patients without SSRI treatment; and one nonrandomized controlled study (n = 18 920) reported an incidence rate ratio of 1.03 (0.96; 1.12). Conclusions: The compiled evidence was too uncertain to support an interaction when an SSRI is added to low‐dose ASA. Low‐dose ASA added to an SSRI may imply an increased risk of bleeding primarily attributable to the initiation of ASA. [ABSTRACT FROM AUTHOR]

The year 2024 marks the 125th anniversary of aspirin, still one of the most frequently used drugs worldwide. Despite its veritable age, it is still relevant in pharmacotherapy and its use has spread to new areas over time. Due to aspirin's multiple pharmacological actions unified in one single molecule (i.e., analgesic, antipyretic, anti-inflammatory, antithrombotic, and antiviral effects), it continues to attract considerable attention in the scientific community and is subject to intense basic and clinical research. In fact, recent results confirmed aspirin's potential role as an antiviral drug and as an agent that can block harmful platelet functions in inflammatory/immunological processes. These features may open up new horizons for this ancient drug. The future of aspirin looks, therefore, bright and promising. Aspirin is not yet ready for retirement; on the contrary, its success story continues. This 125th anniversary paper will concisely review the various therapeutic uses of aspirin with a particular emphasis on the latest research results and their implications (e.g., use as an antiviral agent). In addition, the reader is provided with future perspectives for this remarkable drug. [ABSTRACT FROM AUTHOR]

The review summarizes current literature data on the mechanism of antithrombotic, anti-inflammatory, and antipyretic effects of acetylsalicylic acid (ASA), which is widely used in medicine. The use of ASA may be accompanied by several complications from the gastrointestinal tract (ulcers and bleeding), nephrotoxicity, the development of bronchospasm (aspirin triad), and clinical manifestations of aspirin resistance. The advantages and shortcomings of the main methods of preventing undesirable side effects when taking low doses of ASA are considered: the use of proton-pump inhibitors and rebamipide and inclusion of ASA complexes as promising dosage forms. The pharmacological properties of glycyrrhizic acid (GA) and its ability for clathrate formation with known drugs, in particular ASA, are considered. The advantages of a dosage form of GA with ASA with the same or improved pharmacological activity and reduced toxic side effects of the latter are shown. The review presents data for the last 10 – 11 years gained through the Russian and international search systems PubMed, eLibrary, etc. [ABSTRACT FROM AUTHOR]

Acute heat stress contributes greatly to sudden death in animals and induces serious intracorporal damage even if the animal survives. This trial was therefore conducted to unravel the effect of dietary supplementation of acetylsalicylic acid (ASA) on the serum biochemical composition and hormonal status of finisher broiler chickens during the transition from dry to rainy season (January - March). One hundred and ninety-two (192) day-old broiler chicks (ANAK) were randomly allotted to four treatment diets supplemented with 0, 0.025, 0.050, and 0.075% of ASA at 48 birds/treatment in four replicates of 12 birds each. The result revealed that broilers fed 0.075% ASA had the highest (p<0.05) aspartate aminotransferase and alkaline phosphatase with the values of 69.12 ± 6.52 IU/L, 58.02 ± 11.75 IU/L respectively, while broilers fed 0.050% ASA had the lowest (p<0.05) cholesterol value of 57.27 ± 2.61 mg/dL. The highest (p<0.05) total protein value of 4.20 ± 0.11 g/dL was observed in broilers fed the control diet. There were significant treatment effects (p<0.05) in all the hormonal parameters investigated. Estradiol was observed to increase as the level of ASA supplementation increased. Similarly, broilers fed 0.075% ASA had the highest (p<0.05) progesterone value. It could be concluded that ASA supplementation improves serum biochemical profile, as well as reduces the cholesterol level of experimental birds. [ABSTRACT FROM AUTHOR]

Heat stress has been recognized as a great challenge in the poultry industry, and its effects are mostly felt in tropical countries, hence, the need to alleviate heat stress problems in poultry production. This experiment was therefore carried out to assess the effect of acetylsalicylic acid (ASA) on growth performance and carcass characteristics of finisher broiler chickens during the transition from dry to rainy season (January - March). One hundred and ninety-two (192) three-week-old broiler chicks (ANAK) were used for this experiment. The birds were randomly divided into four dietary treatments, each treatment comprising 48 birds, which was replicated 4 times containing 12 birds per replicate. Diet 1 (T1) which is the control had no inclusion of acetylsalicylic acid (ASA), Diet 2 (T2) contained 0.025% inclusion of ASA, Diet 3 (T3) contained 0.050% inclusion of ASA, and Diet 4 (T4) had 0.075% of ASA. The result of the growth performance of finisher broilers showed that finisher broilers fed 0.075% ASA had the significantly highest (p>0.05) total feed intake value of 4766.60 ± 43.86 g. The percentage of mortality decreased as the level of ASA supplementation increased. Significant treatment effect was also observed in all the carcass parameters investigated; broilers fed 0.025% were observed to have the highest breast weight value (561.75 ± 68.89 g). while broilers fed 0.075% had the highest (p<0.05) thigh value of 262.00 ± 7.03g, the highest (p<0.05) drumstick value was recorded in broilers fed 0.050% ASA with value of 238.90 ± 6.87 g. It was concluded that ASA supplementation improved the growth performance and reduced mortality in broiler chickens. [ABSTRACT FROM AUTHOR]

In cardiology, acetylsalicylic acid (ASA) and warfarin are among the most commonly used prophylactic therapies against thromboembolic events. Drug–drug interactions are generally well-known. Less known are the drug–nutrient interactions (DNIs), impeding drug absorption and altering micronutritional status. ASA and warfarin might influence the micronutritional status of patients through different mechanisms such as binding or modification of binding properties of ligands, absorption, transport, cellular use or concentration, or excretion. Our article reviews the drug–nutrient interactions that alter micronutritional status. Some of these mechanisms could be investigated with the aim to potentiate the drug effects. DNIs are seen occasionally in ASA and warfarin and could be managed through simple strategies such as risk stratification of DNIs on an individual patient basis; micronutritional status assessment as part of the medical history; extensive use of the drug–interaction probability scale to reference little-known interactions, and application of a personal, predictive, and preventive medical model using omics. [ABSTRACT FROM AUTHOR]

Abstract Background The hippocampus is susceptible to damage, leading to negative impacts on cognition. Conditioned medium (CM) obtained from adipose tissue–derived mesenchymal stem cells (MSCs) and acetylsalicylic acid (ASA) have shown neuroprotective effects independently. This study explored the synergistic potential of ASA and CM from adipose‐derived MSCs against hippocampal injury. Methods Adult male Wistar rats received bilateral hippocampal ethidium bromide (EB) injections to induce hippocampal damage. Rats were treated with ASA and/or CM derived from adipose tissue MSCs every 48 h for 16 days. Behavioral tests (open field test, Morris water maze, novel object recognition, and passive avoidance), oxidative stress, Western blot analysis of brain‐derived neurotrophic factor (BDNF) and cerebral dopamine neurotrophic factor (CDNF) expression, and hippocampal histological investigation were conducted. Results Administration of EB caused impairments in spatial, recognition, and passive avoidance memory, as well as heightened oxidative stress, reduced BDNF/CDNF expression, and pyramidal cell loss in the hippocampal CA1 region. Administration of ASA, CM, or a combination of both mitigated these hippocampal damages and cognitive deficits, elevated BDNF and CDNF levels, and alleviated the CA1 necrosis caused by EB. Moreover, co‐administering ASA and CM resulted in greater improvements in spatial memory compared to administering ASA alone, suggesting possible synergistic interactions. Conclusions The ability of ASA, CM obtained from adipose tissue–derived MSCs, and their combination therapy to alleviate hippocampal injuries highlights their promising therapeutic potential as a neuroprotection strategy against brain damage. Our findings provide preliminary evidence of the potential synergistic effects of ASA and CM, which warrants further investigations.

The aim of this study was to evaluate the application and effects of intratesticular use of a mixture containing vaseline and 30% acetylsalicylic acid for chemical castration in male rats. Twenty–eight male albino Wistar rats were divided into four groups: control, sham, vaseline, and vaseline + 30% salicylic acid mixture. The control group (K) received no injection, the Sham group (S) was injected with 1 mL of saline, the vaseline group (V) was injected with 1 mL of vaseline, and the vaseline + acetylsalicylic acid group (V+ASA) was injected with 1 mL of a mixture containing 30% acetylsalicylic acid and vaseline. A statistically significant difference (P=0.000) was determined between the vaseline (V) and vaseline + acetylsalicylic acid (V+ASA) groups. The Malondialdehyde (MDA) value of the vaseline group was found to be higher (3.197 ± 0.08) with a statistically significant difference (P=0.000) compared to the other groups. In terms of glutathione (GSH) value, a statistically significant difference (P

Ovarian cancer is the deadliest gynaecologic malignancies worldwide. Platinum based chemotherapy is the mainstay treatment for ovarian cancer; however, frequent recurrence and chemoresistance onset in patients with advanced diseases remain a therapeutic challenge. Although mechanisms underlying the development of chemoresistance are still ambiguous, the B-cell lymphoma-2 (Bcl-2) family is closely associated with chemoresistance in ovarian cancer. We previously disclosed that Zeta-Crystallin (CryZ) is a post-transcriptional regulator of Bcl-2 gene expression, by binding to Bcl-2 mRNA and increasing its half-life. Here, we investigated the role of CryZ as a novel therapeutic target in A2780 ovarian carcinoma cells by modulating the protein activity with acetylsalicylic acid (ASA) to restore chemosensitivity. Molecular docking and fragment-mapping based approach revealed potential interaction of ASA within CryZ protein. Inhibition of CryZ binding activity to Bcl-2 and Bcl-xl mRNA targets by ASA was demonstrated in A375 cells. Cytotoxicity assays were conducted in A2780S and A2780R ovarian cancer cells to evaluate if CryZ binding activity inhibition and CryZ silencing were able to reverse cisplatin resistance. ASA-treatment determined a downregulation of Bcl-2 and Bcl-xl mRNA levels in A2780S and A2780R cells. ASA-treatment or CryZ silencing were able to increase and restore the chemosensitivity in both sensitive and resistant A2780 ovarian cancer cells, respectively. In this research article we demonstrated that the pharmacological or genetic inhibition of CryZ restores the sensitivity to cisplatin in a model of sensitive or resistant ovarian cancer cells. These findings suggest a new gene-targeted chemotherapeutic approach to restore the cytotoxicity in drug-resistant ovarian cancers and increase the sensitivity in non-resistant cells.

Background: Smoking and the use of non-steroidal anti-inflammatory drugs (NSAIDs) acetylsalicylic acid (ASA), proton pump inhibitors (PPIs), serotonin reuptake inhibitors (SSRIs), and statins have been associated with microscopic colitis (MC). Objectives: We investigated whether these factors were associated with repeated budesonide treatments in patients diagnosed with MC. Design: Retrospective observational study. Methods: All patients with a histologically verified diagnosis of MC at our clinic between the years 2006 and 2022 were identified. Baseline factors and drugs prescribed before and after diagnosis were registered. The influence of risk factors on the odds of having a prescription of oral budesonide and the odds of having a second course of budesonide was studied. Results: Patients with MC (n = 183) with a mean age of 62.3 years [standard deviation (SD): 13.3 years] were followed for a median of 5 years (25th–75th percentile 4–10 years) after diagnosis. In all, 138 patients (75%) had at least one prescription of budesonide after diagnosis, and 90 patients (49%) had at least one clinical relapse treated with budesonide. Patients who had been prescribed NSAIDs within 1 year before clinical relapse had higher odds for clinical relapse [odds ratio (OR): 3.70, 95% confidence interval (CI): 1.06–12.9] but there was no increased risk for clinical relapse for the use of ASA (OR: 0.99, 95% CI: 0.39–2.90), PPIs (OR: 1.09, 95% CI: 0.45–2.63), SSRI (OR: 1.41, 95% CI: 0.82–2.44), or statins (OR: 0.83, 95% CI: 0.35–1.99). No association was seen between being a smoker and/or being prescribed NSAID, ASA, PPI, SSRI, and statins at baseline and the odds of having a prescription of oral budesonide within 1 year after diagnosis. Conclusion: The risk of being prescribed a second course of budesonide is associated with receiving a prescription of NSAIDs but not with the use of ASA, PPIs, SSRIs, and statins. Plain language summary: The use of drugs and the odds for patients with microscopic colitis of having a second course of budesonide Microscopic colitis is a common cause of chronic diarrhea. Previous studies have shown that the use of non-steroidal anti-inflammatory drugs, acetylsalicylic acid, proton-pump inhibitors, serotonin reuptake inhibitors and statins are used more often in patients who later develop microscopic colitis. We aimed to study if these drugs also had an association to an increased risk of disease flares treated with budesonide in 183 patients with known microscopic colitis. Oral budesonide for 6-8 weeks are recommended for disease flares of microscopic colitis. In our study, 90 patients (49%) were prescribed a second course of budesonide probably due to a disease flare. We found a higher odds for being prescribed a second course of budesonide in patients with microscopic colitis who were prescribed non-steroidal anti-inflammatory drugs but no higher risk for the other 'risk drugs' for microscopic colitis. [ABSTRACT FROM AUTHOR]

Instrumental analysis experiment constitutes an essential component for medical prevention and medical testing specialties. To improve the innovative and practical abilities of the undergraduates, a designed experiment of simultaneous determination of acetylsalicylic acid and caffeine in Aspirin tablets by High Performance Liquid Chromatography (HPLC) and Ultra Performance Convergence Chromatography (UPC2) was applied. Additionally, ideological and political elements were organically integrated into the teaching process. Educational practice has shown that by facilitating comparative learning of different instrument principles and functional characteristics, students' interest in experimentation and exploratory spirit can be invigorated. This approach also strengthens students' problem-solving skills, thereby elevating their scientific literacy. [ABSTRACT FROM AUTHOR]

Background: There is conflicting evidence on the role of acetylsalicylic acid (ASA) use in the development of cardiac allograft vasculopathy (CAV). Methods: A nationwide prospective two‐center study investigated changes in the coronary artery vasculature by highly automated 3‐D optical coherence tomography (OCT) analysis at 1 month and 12 months after heart transplant (HTx). The influence of ASA use on coronary artery microvascular changes was analyzed in the overall study cohort and after propensity score matching for selected clinical CAV risk factors. Results: In total, 175 patients (mean age 52 ± 12 years, 79% male) were recruited. During the 1‐year follow‐up, both intimal and media thickness progressed, with ASA having no effect on its progression. However, detailed OCT analysis revealed that ASA use was associated with a lower increase in lipid plaque (LP) burden (p =.013), while it did not affect the other observed pathologies. Propensity score matching of 120 patients (60 patient pairs) showed similar results, with ASA use associated with lower progression of LPs (p =.002), while having no impact on layered fibrotic plaque (p =.224), calcification (p =.231), macrophage infiltration (p =.197), or the absolute coronary artery risk score (p =.277). According to Kaplan–Meier analysis, ASA use was not associated with a significant difference in survival (p =.699) Conclusion: This study showed a benefit of early ASA use after HTx on LP progression. However, ASA use did not have any impact on the progression of other OCT‐observed pathologies or long‐term survival. [ABSTRACT FROM AUTHOR]

Simple Summary: Chicken meat has become increasingly popular as a protein source due to its favorable protein content and balanced amino acid profile. Advances in genetics and feeding practices have led to rapid growth in commercial broiler production to meet consumer demands. As consumer preferences shift toward healthier food options, there is a need to enhance meat production and quality in the poultry industry. Compounds with antioxidant properties, such as vitamin C (VC) and acetylsalicylic acid (ASA), have been tested due to their antioxidant and anti-inflammatory properties. Studies have shown positive effects of both in growth performance and immune functions. While individual studies have explored the effects of vitamin C and ASA supplementation in broilers, few have investigated their combined effects under non-stressful conditions. This study aimed to fill this gap and revealed significant effects of ASA and VC combined supplementation, with improvements noted in growth performance, carcass composition and immune response and cecal coli count. However, creatine kinase levels increased with ASA and VC intake. These findings highlight the complex interactions between ASA and VC supplementation in broilers. Further investigation is warranted to explore optimal dosages and potential effects in non-stressful conditions. This study aimed to investigate the combined effects of ascorbic acid (VC) and acetylsalicylic acid (ASA) on broiler health and performance. A total of 200 Ross 308 male broilers were divided into five groups, each receiving different dietary combinations of ASA and VC (ASA: 50 or 100 mg/kg; VC: 200 or 400 mg/kg). The 42-day trial assessed parameters such as feed intake, average daily gain (ADG), feed conversion ratio (FCR), carcass characteristics, serum parameters, immune response and cecal microbial flora. The results indicate significant treatment effects on feed intake and growth performance, with a higher feed intake of ADG and FCR in treatment groups (p < 0.05). Serum lipid parameters were unaffected, but creatine kinase increased with ASA and VC intake (p < 0.05). Changes in sheep red blood cell titers and influenza antibodies were noted (p < 0.05). The combination of ASA and VC positively influenced carcass traits, reducing abdominal fat and altering the ratio of immune response organs to body weight (p < 0.05). Additionally, the cecal E. coli count decreased with treatment (p < 0.05). This study underscores the intricate interactions between ASA and VC supplementation, growth performance and carcass composition and immune response in broilers. Further research is warranted to explore dosage nuances and variations under specific stress conditions. [ABSTRACT FROM AUTHOR]

Maize starch, polyvinyl alcohol, glucose, and magnesium stearate are used as tablet excipients, acetylsalicylic acid as probe, polyvinyl acetate, and calcium alginate as protective membranes. By changing the proportions of the excipients, the nature and the thickness of the protective membrane, it was possible to optimize the formulation of a controlled release tablet. The mechanism and the kinetics of release of the active ingredient are evaluated using kinetic models: zero order, Higuchi, first order, Hixson–Crowell and Krosmeyer–Peppas. The representation of the released quantities using Krosmeyer–Peppas seems to be the most appropriate to describe the release mechanism (R2 ~ 1). The k and n values, Krosmeyer–Peppas, indicate that drug release is complex. The release rate of the AI is controlled by the erosion of the membrane and the relaxation of the chains of polymers constituting it. The solubility parameters (δ), according to Hansen, of the hydroxylated ingredients, predict compatibility and stability. [ABSTRACT FROM AUTHOR]

Lifestyle factors such as sedentary behavior and consumption of certain medications can disturb the function of the male reproductive system. In the present study, we investigated the potential co-treatment effects of low-volume high-intensity interval training (HIIT) on markers of reproductive function in adult male Wistar rats under aspirin (ASA) treatment. Eighteen adult male Wistar rats were randomized into three groups: control (C), aspirin treatment (AT), and aspirin treatment + exercise (ATE). Animals in the AT and ATE groups received an oral subchronic dose of aspirin (12.5 mg/kg body mass). The exercise was performed three times per week for 6 weeks (4–6 reps of 10-s sprints). Serum testosterone level, sperm parameters (sperm count, viability, maturity, and DNA fragmentation), histomorphometric (Leydig cell, tubule diameter, thickness of tubular epithelium, and indices of spermatogenesis and spermiogenesis), and histochemical parameter (testicular fat density) were assessed. Results revealed that compared to the C group, ASA consumption led to a negative alteration in serum testosterone levels, sperm parameters, and histomorphometric and histochemical parameters (P < 0.05). However, there were no significant differences between the C and ATE groups in terms of serum testosterone level, number of Leydig cells, epididymal fat density, tubule diameter, epithelium height, immature-to-mature sperm ratio, and DNA breakage (P > 0.05). These findings suggest that ASA treatment is associated with deleterious changes in male reproductive parameters. However, low-volume HIIT may prevent ASA-induced male reproductive impairments and could be considered a potential prophylactic measure in subjects under ASA treatment. [ABSTRACT FROM AUTHOR]

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