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This study aims to identify the most important determinants of economic growth in a sample of six countries from the Middle East and North Africa region. Two of which are from high income countries, Bahrain and Saudi Arabia, and two of the highest middle-income countries, Jordan and Lebanon, and two from lower Middle income, namely Egypt and Morocco. They were chosen in addition to the classification of income groups, based on data available to sample countries during the period 2001-2017. Augmented-Dickey-Fuller, a test of stationary of endogenous and exogenous variables, and Granger Causality Analysis were used to infer the causal relationship between these variables and economic growth. By applying Panel Data Analysis, according to Hausman Test, and by comparison between the fixed and random effect models, the results showed a preference for the random effect model. The results showed that the employment rate, foreign direct investment, gross national income, government expenditure, and inflation were among the most important in determining economic growth in the region during that period. All of them had a significant and positive impact on economic growth, except for the rate of growth in gross national income, which negatively affected the rate of economic growth. The pairwise Granger Causality showed that unidirectional causality is running from foreign direct investment Gross Domestic Product growth rates, from both Gross Capital Formation growth rates and Imports growth rates to Employment Ratio. Unidirectional causality also runs from both of Exports growth rates, Gross Capital Formation growth rates, Imports growth rates to Foreign Direct Investment as a percent of Gross Domestic Product. There is also unidirectional causality from foreign direct investment and imports to unemployment.

Salinity is a major abiotic stress that poses great obstacles to wheat production, especially in arid regions. The application of exogenous substances can enhance plant salt tolerance and increase its productivity under salinity stress. This work aimed to assess the mechanisms of selenium (Se) at different concentrations (2, 4 and 8 μM SeCl2) to mitigate hazardous impacts of salt toxicity at physiological, biochemical and agronomic levels in bread wheat. The results displayed that Se foliar application increased chlorophyll content, net photosynthetic rate, transpiration rate, stomatal conductance, relative water content, membrane stability index, excised leaf water retention, proline, total soluble sugars, Ca content, K content, antioxidant enzyme activities and non-enzymatic antioxidant compounds compared to untreated plants. On the other hand, Se application decreased the content of Na, hydrogen peroxide and superoxide contents. Accordingly, our findings recommend exogenous Se application (in particular 8 μM) to alleviate the deleterious effects induced by salinity stress and improve wheat yield attributes through enhancing antioxidant defense systems and photosynthetic capacity.

The use of dried olive pomace as complementary energy sources in poultry feed is still limited due to its low protein and high fiber contents. Bioconversion of olive pomace through solid-state fermentation with or without exogenous enzymes is considered as a trial for improving its nutritional value. This study aimed to evaluate the effects of fermented olive pomace with or without enzymatic treatment on the growth, modulations of genes encoding digestive enzymes and glucose transporters, meat oxidative stability, and economic efficiency of broiler chickens. A total of 1400 day-old broiler chicks (Ross 308) were randomly allocated to seven dietary treatments with 10 replicates of 20 birds/replicate. Treatments included control (basal corn–soybean diet) and other six treatments in which basal diet was replaced by three levels (7.5, 15, and 30%) of fermented olive pomace (FOPI) or enzymatically fermented olive pomace (FOPII) for 42 days. The highest body weight gain was observed in groups fed 7.5 and 15% FOPII (increased by 6.6 and 12.5%, respectively, when compared with the control group). Also, feeding on 7.5 and 15% FOPII yielded a better feed conversion ratio and improved the digestibility of crude protein, fat, and crude fiber. The expression of the SGLT-1 gene was upregulated in groups fed FOPI and FOPII when compared with the control group. Moreover, the expression of the GLUT2 gene was elevated in groups fed 7.5 and 15% FOPII. By increasing the levels of FOPI and FOPII in diets, the expression of genes encoding pancreatic AMY2A, PNLIP , and CCK was upregulated ( p < 0.05) when compared with the control. Fat percentage and cholesterol content in breast meat were significantly reduced ( p < 0.05) by nearly 13.7 and 16.7% in groups fed FOPI and FOPII at the levels of 15 and 30%. Total phenolic and flavonoid contents in breast meat were significantly increased in groups fed 15 and 30% FOPI and FOPII when compared with the control group and even after a long period of frozen storage. After 180 days of frozen storage, the inclusion of high levels of FOP significantly increased ( p < 0.05) the levels of glutathione peroxide and total superoxide dismutase and meat ability to scavenge free radical 1,1-diphenyl-2-picrylhydrazyl. Furthermore, the highest net profit and profitability ratio and the lowest cost feed/kg body gain were achieved in groups fed 7.5 and 15% of FOPII, respectively. The results of this study indicated that dietary inclusion of 15% FOPII could enhance the growth performance and economic efficiency of broiler chickens. Moreover, a higher inclusion level of FOPI or FOPII could enhance the quality and increase the oxidative stability of frozen meat and extend the storage time.

Fusarium oxysporum is one of the most harmful soil-borne pathogens that cause root rot, damping-off, and wilt disease in many plant species. Management of Fusarium oxysporum diseases is often by using many harmful and expensive chemical fungicides which have many harmful effects on the environment and human health. The current study was conducted to identify the chemical constituents of black cumin seeds’ methanolic extract and investigate the ability of the major constituents to inhibit the Fusarium oxysporum trypsin-like serine protease, which play an important role in F. oxysporun pathogenicity. The HPLC-MS analysis of black cumin seeds’ methanolic extract revealed the presence of seven major compounds: amentoflavone, Procyanidin C2, Quercetin3-O-sophoroside-7-O-rhamnoside, 5,7-Dihydroxy-3,4-dimethoxyflavone, Borapetoside A, tetrahydroxy-urs-12-en-28-O-[b-D-glucopyranosyl (1-2)-b-D-glucopyranosyl] ester, and kudzusapongenol A-hexA-pen. The results of molecular docking between these compounds and the active site of Fusarium oxysporium trypsin showed that only four compounds were able to bind to the active site of F. oxysporum trypsin. Amentoflavone, 5,7-Dihydroxy-3,4-dimethoxyflavone, and Quercetin3-O-sophoroside-7-O-rhamnoside have the highest binding energy, −6.4, −6.5, and −6.5 Kcal/mol, respectively. In addition, the results clarify that 5,7-Dihydroxy-3,4-dimethoxyflavone was the only compound to form a hydrogen bond with Asp189 (the residue responsible for substrate specificity). The results of the study strongly indicate that flavonoids of black cumin seeds’ methanolic extract could be used as effective inhibitors for the F. oxysporum trypsin-like serine protease.

Breast cancer is the most common malignancy affecting women, manifesting as a heterogeneous disease with diverse molecular characteristics and clinical presentations. Recent studies have elucidated the role of epigenetic modifications in the pathogenesis of breast cancer, including drug resistance and efflux characteristics, offering potential new diagnostic and prognostic markers, treatment efficacy predictors, and therapeutic agents. Key modifications include DNA cytosine methylation and the covalent modification of histone proteins. Unlike genetic mutations, reprogramming the epigenetic landscape of the cancer epigenome is a promising targeted therapy for the treatment and reversal of drug resistance. Epidrugs, which target DNA methylation and histone modifications, can provide novel options for the treatment of breast cancer by reversing the acquired resistance to treatment. Currently, the most promising approach involves combination therapies consisting of epidrugs with immune checkpoint inhibitors. This review examines the aberrant epigenetic regulation of breast cancer initiation and progression, focusing on modifications related to estrogen signaling, drug resistance, cancer progression, and the epithelial–mesenchymal transition (EMT). It examines existing epigenetic drugs for treating breast cancer, including agents that modify DNA, inhibitors of histone acetyltransferases, histone deacetylases, histone methyltransferases, and histone demethyltransferases. It also delves into ongoing studies on combining epidrugs with other therapies and addresses the upcoming obstacles in this field.

Hepatic ischemia/reperfusion (HIR) is the most common type of liver injury following several clinical situations. Modulating oxidative stress and inflammation by Nrf2/HO-1 and TLR4/MYD88/NF-κB pathways, respectively, is involved in alleviating HIR injury. Paeonol is a natural phenolic compound that demonstrates significant antioxidant and anti-inflammatory effects. The present study explored the possible protective effect of paeonol against HIR injury and investigated its possible molecular mechanisms in rats. Rats were randomly divided into four groups: sham-operated control, paeonol-treated sham-operated control, HIR untreated, and HIR paeonol-treated groups. The results confirmed that hepatic injury was significantly aggravated biochemically by elevated serum levels of alanine transaminase and aspartate transaminase, as well as by histopathological alterations, while paeonol reduced the increase in transaminases and alleviated pathological changes induced by HIR. Additionally, paeonol inhibited the HIR-induced oxidative stress in hepatic tissues by decreasing the upraised levels of malondialdehyde and nitric oxide and enhancing the suppressed levels of reduced glutathione and superoxide dismutase activity. Furthermore, paeonol activated the protective antioxidative Nrf2/HO-1 pathway. The protective effect of paeonol was associated with inhibiting the expression of the inflammatory key mediators TLR4, MYD88, NF-κB, and TNF-α. Finally, paeonol inhibited the increased mRNA levels of the pro-apoptotic marker Bax and enhanced the reduced mRNA levels of the anti-apoptotic marker Bcl-2. Taken together, our results proved for the first time that paeonol could protect against HIR injury by inhibiting oxidative stress, inflammation, and apoptosis.

Myocardial ischemia is a major global contributor to mortality. While reperfusion therapy remains the most effective treatment, it paradoxically leads to myocardial ischemia–reperfusion (MI/R) injury, resulting in irreversible cardiac damage for which no effective interventions currently exist. This underscores the pressing need to unravel the pathogenesis of MI/R injury and devise new therapeutic strategies. In this study, supervised machine learning models, including logistic regression (LR), support vector machines (SVM), random forests (RF), neural networks (NN), and k-nearest neighbors (kNN), were utilized to predict treatment response. The models incorporated molecular and biochemical features to evaluate three drugs: trans-Anethole (TNA), pentoxifylline (PTX), and cyanidin-3-O-glucoside (Cy3G). The sequential forward selection (SFS) method was employed to select the most relevant features for prediction. To assess model performance, metrics such as precision, accuracy, recall (sensitivity), specificity, and the Matthews Correlation Coefficient (MCC) were analyzed for both reduced and complete models. Among the classifiers, kNN demonstrated notable performance, achieving an accuracy of 0.9156 ± 0.0242 and an average area under the ROC curve (AUC) of 0.90 across three cross-validation iterations surpassing all other classifiers. This observed performance is in line with recent literature that employs advanced computational methods in similar domains. A key advantage of our study is the use of a two-layer framework—integrating molecular signatures with biochemical markers—which can provide improved robustness and biological relevance. This multi-layer integration enhances interpretability and better reflects the multifactorial nature of MI/R injury, while supporting model generalization. Feature selection identified one molecular marker (SOX5) and two biochemical markers (dP/dtmax and cTnT) as significant predictors of drug response. This integrative approach has the potential to enhance personalized therapy for myocardial ischemia by enabling precise drug response predictions and guiding the development of targeted treatment strategies.

Autism is a neurodevelopmental disorder with a significantly increased incidence rate across the world over the past few years. Toxoplasmosis and cytomegalovirus (CMV) infection are globally prevalent and have been associated with diverse neurological and psychiatric disorders. A few studies have demonstrated the role of toxoplasmosis and CMV as potential etiological factors for autism. Accordingly, this study was performed to estimate the relationship between toxoplasmosis and CMV infection in children with autism as well as to assess their impact on the Childhood Autism Rating Scale (CARS) score. A total of 45 autistic children (6 girls, 39 boys) and 45 (21 girls, 24 boys) healthy control children were enrolled in our study. Their blood samples were collected and tested for the presence of Toxoplasma and CMV (IgG and IgM) antibodies and DNA by ELISA and real-time PCR (RT-PCR), respectively. Toxoplasmosis was detected in 11 (24.4%) autistic children through the ELISA [10 (22.2%) IgG + /IgM − and 1 (2.2%) IgG + /IgM +]; however, RT-PCR assay recorded only 1 positive case (2.2%), while it was detected in 10 (22.2%) control children through ELISA [9 (20%) IgG + /IgM − and 1 (2.2%) IgG + /IgM +] and 1 (2.2%) by RT-PCR. On the other hand, CMV infection was detected in all autistic children with 44 (97.8%) testing positive by ELISA [24 (53.3%) IgG + /IgM − , 18 (40%) IgG + /IgM + and 2 (4.4%) IgG − /IgM +] and 25 (55.6%) testing positive by RT-PCR assay. In addition, ELISA assay recorded 43 (95.6%) [19 (42.2%) IgG + /IgM + and 22 (48.9%) IgG + /IgM − and 2 (4.4%) IgG-/IgM +] and RT-PCR recorded 21 (46.7%) positive samples in control children with CMV. No significant difference was noted between autistic and control children for the overall prevalence of Toxoplasma or/and CMV infection. Similarly, the CARS score indicated a non-significant difference with Toxoplasma or/and CMV infection. Our data does not show an association between autism and toxoplasmosis or/and CMV infection. Nevertheless, considering that autistic children are at a high risk of contracting these infections, further studies with a larger sample size are recommended.

Despite being one of the most frequently used chemotherapy agents, cisplatin exhibits substantial hepatorenal injury by triggering oxidative stress, inflammation, and apoptosis pathways. The current investigation studied the possible protective effects of calcitriol on cisplatin-induced hepatorenal toxicity. Mice were divided randomly as follows: control group, calcitriol group (received calcitriol 5 µg/kg, p.o. for 14 days), cisplatin group (received a single i.p. injection of cisplatin 10 mg/kg on the 10th day), and calcitriol + cisplatin group (received calcitriol 5 µg/kg, p.o. for 14 days and cisplatin 10 mg/kg, i.p. on the 10th day). The possible interaction between calcitriol and cisplatin on cell viability was tested in HepG2 cells by MTT assay. Hepatorenal toxicity induced by cisplatin was reversed by calcitriol, as evidenced by improved histological examinations and liver and kidney function tests. In addition, calcitriol counteracted oxidative stress and enhanced Nrf2 and Mrp2 expression in the liver and kidney while suppressing levels of p38 MAPK in cisplatin-treated mice. Calcitriol also inhibited cisplatin-induced hepatic and renal inflammation, as determined by suppressing TNF-α and enhancing IL-10 levels. By downregulating caspase-3, calcitriol also promoted liver and kidney tissue survival in mice treated with cisplatin. Moreover, cisplatin’s cytotoxic effects were significantly potentiated when calcitriol was combined with cisplatin. The current study showed that calcitriol protects against cisplatin-induced hepatorenal injury by suppressing oxidative stress, inflammation, and apoptosis, which the Nrf2-Mrp2/p38 MAPK pathway might regulate.

Acute Kidney Injury (AKI) is characterized by a rapid and reversible decline in renal function with a rapid decrease in Glomerular Filtration Rate (GFR), which is associated with high mortality. Rhabdomyolysis accounts for 10-40% of AKI, to which the therapeutic approach is limited. is a protein that modulates sodium-phosphate co-transporters, ion channels that have been reported to have a renal protective effect. Guanosine, a purine nucleoside, has already been reported to have a renal protective effect; however, the mechanism of such protection and its relation to modification has not been evaluated yet. This study aims to evaluate the mechanism of the protective effect of guanosine against rhabdomyolysis-induced AKI and its relation to the expression of the gene. In the current study, rats were divided into three groups: control, glycerol-induced AKI, and guanosine-treated. Serum urea and creatinine levels, renal tissue Total Antioxidant Capacity (TAC), and and genes expression were evaluated. Furthermore, caspase-3 immunostaining and histopathological evaluations were done. Results showed that guanosine treatment resulted in a significant reduction in serum urea and creatinine, genes expression, and caspase-3 immunoexpression, and an increase in TAC and genes expression. Results also revealed an improvement of renal histopathology when compared with the glycerol-induced AKI group. Guanosine may be a promising agent in the treatment of rhabdomyolysis-induced AKI. The proposed mechanism for guanosine may be through its ability to enhance gene expression in renal tissue, with subsequent antioxidant and anti-apoptotic activity.