Pseudomonas aeruginosa, a Gram-negative bacterium, is recognized for its adaptability and opportunistic nature. It poses a substantial challenge in clinical settings due to its complicated antibiotic resistance mechanisms, biofilm formation, and capacity for persistent infections in both animal and human hosts. Recent studies revealed a potential zoonotic transmission of P. aeruginosa between animals, the environment, and human populations which highlights awareness of this microbe. Implementation of the One Health approach, which underscores the connection between human, animal, and environmental health, we aim to offer a comprehensive perspective on the current landscape of P. aeruginosa management. This review presents innovative strategies designed to counteract P. aeruginosa infections. Traditional antibiotics, while effective in many cases, are increasingly compromised by the development of multidrug-resistant strains. Non-antibiotic avenues, such as quorum sensing inhibition, phage therapy, and nanoparticle-based treatments, are emerging as promising alternatives. However, their clinical application encounters obstacles like cost, side effects, and safety concerns. Effectively addressing P. aeruginosa infections necessitates persistent research efforts, advancements in clinical development, and a comprehension of host-pathogen interactions to deal with this resilient pathogen.

When many widely ingested foods are heated, a toxin called acrylamide (ACR) is created. The aim of our research was to investigate if N acetylcysteine (NAC) and/or vitamin E (Vit E) could provide protection against neurotoxicity induced by ACR. Rats were classified into seven groups of 7 rats; control (saline); NAC (150 mg/kg bw); Vit E (100 mg/kg bw); ACR (20 mg/kg bw orally); ACR+NAC; ACR+Vit E; ACR+NAC+Vit E. Saline, NAC and/or Vit E were administered orally, once daily for 30 days. Acetylcholinesterase (AChE) inhibition, glutathione depletion, and elevated levels of malondialdehyde (MDA), were all observed after ACR intoxication. Furthermore, ACR diminished superoxide dismutase (SOD) and catalase (CAT) activities, as well as inflammatory mediators as interleukins (IL-1, IL-6), and tumor necrosis factor-α (TNF-α). The combined treatment of ACR with NAC or Vit E dramatically reduced both oxidative and biochemical consequences, with a more frequent return to normal values. To conclude, NAC or Vit E supplementation may alleviate ACR-induced neuronal injury, most likely due to NAC or Vit E antioxidant, anti-inflammatory, and anti-apoptotic effects

Heart failure (HF) is a serious health and economic burden worldwide, and its prevalence is continuously increasing. Current medications effectively moderate the progression of symptoms, and there is a need for novel preventative and reparative treatments. The development of novel HF treatments requires the testing of potential therapeutic procedures in appropriate animal models of HF. During the past decades, murine models have been extensively used in fundamental and translational research studies to better understand the pathophysiological mechanisms of HF and develop more effective methods to prevent and control congestive HF. Proper surgical approaches and anesthetic protocols are the first steps in creating these models, and each successful approach requires a proper anesthetic protocol that maintains good recovery and high survival rates after surgery. However, each protocol may have shortcomings that limit the study's outcomes. In addition, the ethical regulations of animal welfare in certain countries prohibit the use of specific anesthetic agents, which are widely used to establish animal models. This review summarizes the most common and recent surgical models of HF and the anesthetic protocols used in rat models. We will highlight the surgical approach of each model, the use of anesthesia, and the limitations of the model in the study of the pathophysiology and therapeutic basis of common cardiovascular diseases.

Background: Myocardial infarction (MI) is one of the most common cardiac problems causing deaths in humans. Previously validated anesthetic agents used in MI model establishment are currently controversial with severe restrictions because of ethical concerns. The combination between medetomidine, midazolam, and butorphanol (MMB) is commonly used in different animal models. The possibility of MMB combination to establish the MI model in rats did not study yet which is difficult because of severe respiratory depression and delayed recovery post-surgery, resulting in significant deaths. Atipamezole is used to counter the cardiopulmonary suppressive effect of MMB.Objectives: The aim of the present study is to establish MI model in rats using a novel anesthetic combination between MMB and Atipamezole.Materials and methods: Twenty-five Sprague Dawley (SD) rats were included. Rats were prepared for induction of the Myocardial infarction (MI) model through thoracotomy. Anesthesia was initially induced with a mixture of MMB (0.3/5.0/5.0 mg/kg/SC), respectively. After endotracheal intubation, rats were maintained with isoflurane 1% which gradually reduced after chest closing. MI was induced through the left anterior descending (LAD) artery ligation technique. Atipamezole was administered after finishing all surgical procedures at a dose rate of 1.0 mg/kg/SC. Cardiac function parameters were evaluated using ECG (before and after atipamezole administration) and transthoracic echocardiography (before and 1 month after MI induction) to confirm the successful model. The induction time, operation time, and recovery time were calculated. The success rate of the MI model was also calculated.Results: MI was successfully established with the mentioned anesthetic protocol through the LAD ligation technique and confirmed through changes in ECG and echocardiographic parameters after MI. ECG data was improved after atipamezole administration through a significant increase in heart rate (HR), PR Interval, QRS Interval, and QT correction (QTc) and a significant reduction in RR Interval. Atipamezole enables rats to recover voluntary respiratory movement (VRM), wakefulness, movement, and posture within a very short time after administration. Echocardiographic ally, MI rats showed a significant decrease in the left ventricular wall thickness, EF, FS, and increased left ventricular diastolic and systolic internal diameter. In addition, induction time (3.440 ± 1.044), operation time (29.40 ± 3.663), partial recovery time (10.84 ± 3.313), and complete recovery time (12.36 ± 4.847) were relatively short. Moreover, the success rate of the anesthetic protocol was 100%, and all rats were maintained for 1 month after surgery with a survival rate of 88%.Conclusion: Our protocol produced a more easy anesthetic effect and time-saving procedures with a highly successful rate in MI rats. Subcutaneous injection of Atipamezole efficiently counters the cardiopulmonary side effect of MMB which is necessary for rapid recovery and subsequently enhancing the survival rate during the creation of the MI model in rats.

Mesenchymal stem cells (MSCs) exhibit multipotency, self-renewal, and immune-modulatory properties, making them promising in regenerative medicine, particularly in cardiovascular treatments. However, optimizing the MSC source and induction method of cardiac differentiation is challenging. This study compares the cardiomyogenic potential of bone marrow (BM)-MSCs and adipose-derived (AD)-MSCs using 5-Azacytidine (5-Aza) alone or combined with low doses of Fibroblast Growth Factor (FGF) and Insulin-like Growth Factor (IGF). BM-MSCs and AD-MSCs were differentiated using two protocols: 10 μmol 5-Aza alone and 10 μmol 5-Aza with 1 ng/mL FGF and 10 ng/mL IGF. Morphological, transcriptional, and translational analyses, along with cell viability assessments, were performed. Both the MSC types exhibited similar morphological changes; however, AD-MSCs achieved 70–80% confluence faster than BM-MSCs. Surface marker profiling confirmed CD29 and CD90 positivity and CD45 negativity. The differentiation protocols led to cell flattening and myotube formation, with earlier differentiation in AD-MSCs. The combined protocol reduced cell mortality in BM-MSCs and enhanced the expression of cardiac markers (MEF2c, Troponin I, GSK-3β), particularly in BM-MSCs. Immunofluorescence confirmed cardiac-specific protein expression in all the treated groups. Both MSC types exhibited the expression of cardiac-specific markers indicative of cardiomyogenic differentiation, with the combined treatment showing superior efficiency for BM-MSCs.