Introduction: Luteolin is highly distributed within plant species it is approved to be efficacious in the treatment of ischemic stroke caused by inflammation. Ischemic stroke (I/R) damage to the brain is a commonly diagnosed natural outcome of ischemic stroke. The objectives of this paper are to use in silico molecular modelling to evaluate the primary biomarker proteins with which luteolin binds, as well as the benefits of luteolin in minimizing the harm caused by cerebellar (I/R) injury. Methodology: The molecular modelling research was performed using AutodockFr. The Bcl-2, Caspase-3, IL-1B, MDA, TLR-2, and TNF- values were observed, alongside the histological assessment which was used to determine the level of restoration from the cerebellar (I/R) injuries sustained in mouse models.Results: Docking studies demonstrated that the luteolin structure can interact with both SOCS3/JAK and SYK Enzymes. Concomitantly, the physiological responses showed marked declines within Bcl-2, Caspase-3, IL-1B, MDA, TLR-2, and TNF- brain chemicals, with huge rises observed with Bcl-2 concentrations. Moreover, the histopathological examination revealed that luteolin decreases ischemic injury.Conclusions: Lutein could be able to decrease cerebral (I/R) damage by decreasing oxidative stress and trying to exert an anti-apoptotic overall impact.

Through the current research, a study of the nuclear composition and the form of even isotones movements – those of the even atomic weight between 178 – 188, after specifying the dynamic symmetry of each nucleus using the first prototype of the interactive bosons (IBM-1), the intrinsic values as well as the intrinsic vectors were calculated using the (IBM-code) program.It also calculated the probability of the quadrant-polar, electric movement that are B(E2) as well the quadrant-polar, electric torque (QL)using the (IBMT-code) program.The ¹³⁰Ba isotope with 56 protons and 74 neutrons, has the number of bosons is 7 and the ratio R 4 1 + / 2 1 + is 2.5235, the levels 2 1 + , 4 1 + , 6 1 + , 8 1 + , 2 2 + , 0 2 + and 2 3 + , with energies 0.3574, 0.8914, 1.6021, 2.4894, 0.8971, 1.1795and1.5369 MeV are in good agreement comparing with the experimental energy. The level 4 3 + , with energy 2 0709MeV compared with the energy experimental 2.0537 MeV. So, this level confirmed in the present work. The levels 10 1 + , 12 1 + , 3 1 + , 4 2 + , 5 1 + , 6 2 + and 8 2 + , with energies 3.5534, 3.5534, 1.6143, 1.6111, 2.5065, 2.5016 and 3.5689 MeV, respectively correspond to cases for which the angular momentum and/or parity of the corresponding states are not well established experimentally. The calculations have been predicted new levels with energies 3.5754, 2 7816.and 3.6689MeV for the angular momentum and parity 7 1 + , 6 3 + and 8 3 + , respectively. From the experimental value of transition B ( E 2 ; 2 1 + → 0 1 + ) , the value of parameter e_B (α2) have been calculated for ¹³⁰Ba isotope and The comparison for ¹³⁰Ba isotope under study. There is no available experimental transition data to many transitions, Therefore, it has been predicted using IBM-1. In this study, there are a good agreement between the experimental B(E2) values and the IBM-1 calculated generally.

Acute liver injury is a severe clinical condition with potentially fatal consequences commonly caused by viral infections, medications, toxins, and drug overdoses. Among these, paracetamol (acetaminophen) overdose is a leading cause of hepatic failure due to its narrow therapeutic index, resulting in oxidative stress and hepatocyte apoptosis. Quercetin, a flavonoid found abundantly in vegetables and herbs, has demonstrated antioxidant, hepatoprotective, and anti-inflammatory properties. This study evaluates the hepatoprotective role of quercetin in mitigating liver damage induced by paracetamol overdose in an experimental rat model. A total of 28 male rats were randomly divided into four groups (n = 7 per group): (i) normal control (distilled water and saline), (ii) paracetamol-induced liver injury group (2 g/kg paracetamol intraperitoneally), (iii) paracetamol + quercetin group (50 mg/kg quercetin orally and 2 g/kg paracetamol intraperitoneally), and (iv) quercetin-only group (50 mg/kg quercetin intraperitoneally). Blood and liver samples were analyzed for liver enzymes (glutamate pyruvate transaminase [GPT], glutamate oxaloacetate transaminase [GOT]), inflammatory markers (nuclear factor kappa B [NF-κB], tumor necrosis factor-alpha [TNF-α]), apoptotic markers (cysteine-aspartic acid protease 3 [Caspase-3], B-cell lymphoma 2 [BCL2]), oxidative stress markers (malondialdehyde [MDA], glutathione [GSH]), and histological changes. Paracetamol administration significantly elevated GPT, GOT, NF-κB, TNF-α, caspase-3, and MDA levels whereas reducing BCL2 and GSH levels, indicating hepatic injury and oxidative stress. In contrast, results showed that quercetin treatment significantly mitigated these changes, demonstrating its potential hepatoprotective effects. Histological analysis further confirmed that quercetin reduced hepatic damage compared to the paracetamol-only group. These findings suggest that quercetin exerts a protective effect against paracetamol-induced liver injury by reducing oxidative stress, inflammation, and apoptosis.

Hospital wastewater systems are recognized as reservoirs for the emergence and dissemination of antibiotic-resistant bacteria. This study isolated bacterial strains from hospital effluents and assessed their resistance profiles using disk diffusion and minimum inhibitory concentration (MIC) methods. Molecular characterization via PCR and sequencing identified genes associated with resistance, including blaCTX-M, mecA, and vanA. High prevalence of multidrug-resistant strains such as MRSA and ESBL-producing Enterobacteriaceae was observed. These findings highlight the urgent need for improved wastewater treatment processes and strict antimicrobial stewardship to prevent environmental and public health risks.