Beni-Suef University Journal of Basic and Applied Sciences最新文献

Background

This study investigated the effect of B. Subtilis bacteria on the properties of cement mortar. This was done by using soil samples from Sharkia, Egypt, to isolate 48 bacterial strains, after which they were cultured using the Johnson method and various media. Bacteria were then added to the cement mortar in amounts of 5% and 10% by weight to evaluate their effect on the mechanical and chemical properties of the modified mortar.

Results

The study examined the compressive and flexural strength of the modified mortar over time, as well as its microscopic properties and chemical composition after 28 days. The results indicated that bacterial additions of 5% and 10% increased the compressive strength of the mortar after 28 and 56 days compared to the control. A 5% bacteria concentration resulted in significant improvements in strength, showing the best concentration for increasing mortar strength. The addition of 5% bacteria significantly enhanced the early flexure strength, while the 10% showed superior long-term strength after 56 days. Scanning electron microscopy (SEM) revealed high CaCO₃ deposits in the bacterial samples, indicating microbial-induced calcite precipitation that filled the small cracks and increased strength. Fourier-transform infrared spectroscopy (FTIR) confirmed the presence of hydroxyl, carbonate, and silicate groups, with bacterial samples having a higher carbonate content, indicating an increase in calcium carbonate formation and microstructure.

Conclusions

The ideal bacterial concentration was 5% as it improved the compressive and flexural strength while also promoting a more flexible microstructure. This study supports the employment of microorganisms in the production of more durable and environmentally friendly building materials, enhancing the sustainability of building practices.

Background

The risk factors of metabolic syndrome (MS) precedes the development of cardiovascular disease and type 2 diabetes and are largely triggered by high-carbohydrate high-fat diet (HCHFD) and sedentary lifestyle. The development of these risk factors is connected to persistent low-grade inflammation. Though, ursolic acid (UA) has been shown to prevent HCHFD-induced metabolic parameters. The present study aimed to elucidate the molecular mechanisms underlying the preventive effects of dietary UA supplementation on obesity-related metabolic disorders and inflammation in male Wistar rats fed with HCHFD. The animals were randomly divided into 4 groups (n = 5): 1—normal diet (ND) + distilled water (DW); 2—ND + UA; 3—HCHFD + DW; 4—HCHFD + UA. HCHFD was augmented with 20% fructose in drinking water. The animals were fed their respective diets daily for 20 weeks. 250 mg/kg body weight of ursolic acid was administered orally to UA-treated groups for the last 8 weeks. Blood samples were collected and liver and adipose tissues were harvested for biochemical and tissue analysis, respectively.

Results

BMI and FBG were significantly lowered in the HCHFD + UA-fed animals compared to the HCHFD + DW-fed animals. In the HCHFD + UA-fed animals, HOMA-IR, serum insulin, cholesterol, triglyceride and low-density lipoprotein cholesterol (LDL-C) were significantly decreased while high-density lipoprotein cholesterol (HDL-C) was increased compared to the HCHFD + DW-fed animals. UA significantly decreased serum tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) and increased adiponectin level compared to the HCHFD + DW-fed animals. The messenger ribonucleic acid (mRNA) level of peroxisome proliferator activated receptor-gamma (PPAR-γ) in adipose tissue was significantly upregulated while liver PPAR-γ mRNA level was significantly downregulated in HCHFD + UA-fed animals compared to HCHFD + DW group, respectively. UA restored the architecture of liver parenchyma to near normal.

Conclusion

Dietary UA supplementation mitigated metabolic dysfunction and inflammation associated with obesity via modulation of liver and adipose tissue PPAR-γ in male Wistar rats fed with HCHFD for 20 weeks.

Background

Liver fibrosis is a worldwide disease that develops from activation and propagation of hepatic stellate cells, and subsequent extracellular matrix accumulation. Liver fibrosis is associated with multiple pathways, however, the dysregulation of GIPC1 gene (GIPC PDZ domain containing family member 1) and disruption in the balance of MMPs (matrix metalloproteinases) and TIMPs (tissue inhibitor of metalloproteinases) remain as key factors in this disease. Curcuminoids, especially curcumin (CURC), are medicinal extracts that proved their antioxidative, anti-inflammatory, antifibrotic actions, and showed wide epigenetic regulatory effects. We aimed to explore CURC’s effect on declining the inflammatory cytokines TNF-α (tumor necrosis factor-alpha), IL-6 (interleukin-6), TGF-β1 (transforming growth factor beta1), regulating GIPC1 expression, and adjusting MMP-8/TIMP-3 balance mediated by miRNA-483-5p (microRNA-483-5p) in TAA (thioacetamide)-induced liver fibrotic albino Wistar rat model.

Results

The attained results revealed significant regressions in livers’ relative weights, serum ALT (alanine aminotransferase), AST (aspartate aminotransferase), ALP (alkaline phosphatase) and LDH (lactate dehydrogenase), plasma PDGF (platelet-derived growth factor), liver TOC (total oxidative capacity), TNF-α, IL-6, TGF-β1, and downregulation in GIPC1 gene expression, besides, significant elevation in liver TAC (total antioxidant capacity) in CURC-treated rats. Surprisingly, significant upregulation in miRNA-483 expression was obtained in CURC-treated rats which consequentially enhanced MMP-8/TIMP-3 balance in the form of an elevation in MMP-8/reduction in TIMP-3 levels, along with confirming this novel pathway through conducting bioinformatics analysis. All these enhancements were mirrored in Annexin V/PI (Annexin V Propidium Iodide) assay as massive improvements in % of apoptotic and necrotic cells, plus, in H&E (hematoxylin and eosin) and Masson’s trichrome histopathological examinations that showed near to normal liver architecture with no collagen bands deposition.

Conclusions

This study concludes that CURC can modulate the novel miRNA-483-5p/MMP-8/TIMP-3 pathway and regulate GIPC1 expression, thus providing new perception of CURC as an effective therapeutic agent capable of lowering inflammation and remodeling liver damage.

Graphical Abstract

Background

Staphylococcus aureus is a leading cause of death, especially among the elderly. This bacterium produces several surface membrane proteins, with staphylococcal protein A (SpA) being particularly important. Despite its prevalence, there are no targeted treatments available for geriatric patients. In homeopathy, Rhus toxicodendron (RT) is frequently used in various dilutions-Mother Tincture (MT), 6CH, 30CH, and 200CH- for conditions like skin infections, soft tissue disorders, and joint ailments.

Methods

In this study, we evaluated the effects of Rhus toxicodendron (RT) at different concentrations on Staphylococcus aureus through bacterial plate cultures and compared the outcomes with Nano-RT. Notably, Nano-RT MT is not commercially available. This research is the first to showcase both the efficacy and biosafety of the innovative nano-ZnO RT MT homeopathic formulation.

Results

This study examined the inhibitory effects of Rhus toxicodendron in its Mother Tincture (MT) form and in 6CH, 30CH, and 200CH dilutions against Staphylococcus aureus. Nano-ZnO was synthesized from Rhus toxicodendron MT and combined to create Nano-MT. Both Rhus Tox MT and Nano-RT MT demonstrated significant inhibition of Staphylococcus aureus within 24 h of application.

Conclusions

Rhus Tox MT and Nano-RT MT present promising new options for treating Staphylococcus aureus infections in elderly patients. Furthermore, studies have demonstrated that Nano-RT MT is completely biologically safe in mice.

Background

Lungs are adversely affected by repeated exposure to thinner fumes. This study aimed to examine the pulmonary toxic effects of chronic thinner inhalation and the possible protection by chamomile administration. Adult male Wistar rats were exposed to thinner fumes for 8 weeks (4 h/day, 6 days/week), while chamomile flower extract (400 mg/kg body weight) was given orally during thinner exposure for the same period.

Results

The study showed lung damage following chronic thinner exposure through increased cytochrome P2E1 (CYP2E1), superoxide anion (O₂^•−), hydrogen peroxide (H₂O₂), and malondialdehyde (MDA), with decreased antioxidant enzymes; superoxide dismutase (SOD), and catalase (CAT). Moreover, an elevation of lung enzymes; alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), and lactate dehydrogenase (LDH) with depletion in total protein and albumin contents in serum and bronchoalveolar lavage fluid were observed. Thinner exposure also exhibited increased lung deoxyribonucleic acid (DNA) damage, transforming growth factor-β1 (TGF-β1), insulin-like growth factor-1 (IGF-1), hydroxyproline (HYP), and collagen type 1 (COL-1), with decreased serum surfactant protein-A (SP-A), total and differential leukocytes (WBCs) count, except for neutrophils. Histological investigations revealed deteriorative changes along with accumulated collagen fibers affecting the lung and other respiratory organs.

Conclusion

Supplementation of chamomile extract succeeded in preventing thinner-induced lung oxidative stress, enzyme leakage, surfactant deficiency, DNA damage, fibrosis, and histological injury. Therefore, consumption of chamomile extract could be recommended for alleviating thinner-induced health hazards and lung toxicity.

Background

The emulsion polymerization of vinyl monomers has been extensively researched, but copolymerization with crotonic acid or cinnamic acid is relatively uncommon. These acids are capable of coordinating with other metal ions. Our previous research has focused on synthesizing and characterizing copolymers of butyl acrylate (BuA)/vinyl acetate (VAc) and styrene-BuA using emulsion techniques, specifically for paint applications. The current work aimed to synthesize and characterize three binary chelating copolymers of styrene with maleic, cinnamic, and crotonic acids. In addition, the prepared chelating copolymers were treated with water and soluble salts of copper and iron for complex formation. Additionally, the characterization and electrical properties of these copolymers were investigated.

Results

This article reports the synthesis of three binary copolymers of styrene with cinnamic, crotonic, and maleic acids via an emulsion polymerization process using a redox initiation system of potassium persulfate/glucose in the presence of sodium dodecyl benzene sulfonate as an emulsifier. The prepared emulsions of the copolymers were precipitated and purified using Soxhlet extraction in a mixture of n-hexane and toluene. Spectroscopic measurements, including Fourier transform infrared (FTIR), proton nuclear magnetic resonance (¹H-NMR), and powder X-ray diffraction (PXRD), in addition to thermal analysis methods like thermogravimetric analysis (TGA) and differential scanning calorimetry (DSC) were employed to characterize the copolymers that were synthesized. The metal complexes of the chelating copolymers were prepared by treatment with soluble metal salts of Co(II), Cu(II), and Fe(III), purified, and characterized via IR, PXRD, TGA, and DSC. The semiconducting properties of the chelating polymers and their metal complexes were demonstrated through conductivity measurements taken at room temperature. The conductivity values ranged from 10⁻³ to 10⁻⁶ Ω⁻¹ cm⁻¹.

Conclusion

The research underscores the significance of the electrical characteristics of chelating copolymers and their metal complexes, particularly focusing on styrene-based binary chelating copolymers, in driving advancements in technology, science, and economic development.

Background

Insulin resistance (IR) leads to various metabolic abnormalities, including diabetes mellitus, obesity, nonalcoholic steatohepatitis, and neurodegenerative disorders. Natural products rich in nontoxic phytochemicals are cost-effective and widely used to manage insulin resistance, reducing drug interactions. Artichoke stems and red algae contain several phytochemical compounds that exert antioxidant and anti-inflammatory effects.

Aim

This study aims to explore and compare the preventive and therapeutic effects of red algae and artichoke stem extracts against high-fat diet-induced insulin resistance and then compare their impacts with those of the reference drug metformin, which is commonly used for treating type 2 diabetes.

Methods

The animals were fed a high-fat diet for eight weeks to induce insulin resistance. The plants were then treated orally with 100 mg/kg body weight red algae, artichoke extracts, or metformin per day for 14 days. The protective rat groups received the extracts at the same dose for 14 days before being fed the high-fat diet for eight weeks. Commercial kits and standardized methods were used to measure blood diabetic profiles (glucose, insulin, lipid profile, fructosamine, and retinol-binding protein-4 (RBP-4)) and liver oxidative stress parameters, nuclear factor-κβ (NF-κβ), peroxisome proliferator-activated receptor gamma (PPAR-γ), phosphatidylinositol 4,5-bisphosphate 3-kinase (PI3K), retinol-binding protein-4 (RBP-4), and phosphatase and tensin homolog (PTEN).

Results

Our results showed that both extracts inhibited NF-κB and PTEN while enhancing PI3K, RPB-4, and PPAR-γ due to their potent antioxidant properties. They also increased insulin sensitivity, as reflected by reduced blood glucose and lipid profile levels and normalized fructosamine and RBP-4. Additionally, these extracts prevent oxidative stress-induced hepatic and nephric cell dysfunction, as confirmed by improved blood, liver, and kidney parameters.

Conclusion

Therefore, both extracts could be good antioxidant treatments for oxidative stress-related insulin resistance because they restore the balance of the PI3K/PPAR-γ/RBP-4 pathway. This pathway increases glucose uptake, stops gluconeogenesis, speeds up lipid metabolism, and stops the inflammation pathway.

Background

Glass fiber-reinforced polymer (GFRP) bars offer a superior alternative to steel bars in concrete reinforcement but are associated with wider cracks and higher deformation rates. This study introduces a novel approach by combining steel fibers (SFs) and carbon nanotubes (CNTs) to address these drawbacks and enhance the performance of GFRP-reinforced concrete beams. The unique contribution of this study lies in the simultaneous use of SFs and CNTs, which has not been extensively investigated, particularly in the context of GFRP-reinforced concrete. The study involved testing three sets of nine specimens with different concrete mixtures and reinforcement forms.

Results

The results showed that adding 0.04% CNTs by cement weight and 0.6% SFs by volume fraction significantly improved the mechanical performance of GFRP and steel reinforced beams. GFRP reinforced beams with CNTs and SFs exhibited a reduction in crack width, a 20% increase in load-carrying capacity, and a 25% reduction in deflection compared to reference specimens. Scanning electron microscope analysis further revealed that CNTs effectively enhanced tensile load transfer, improving flexural behavior of the beams. The finite element analysis using ANSYS confirmed the experimental findings, highlighting the improved stress distribution in the modified concrete mixtures.

Conclusions

Incorporating SFs and CNTs in concrete significantly improves the mechanical performance of GFRP-reinforced beams, making them more durable and resilient. These findings suggest that the proposed approach can enhance the longevity and sustainability of concrete structures, particularly in dynamic load applications such as bridges and high-rise buildings. Further experimental and analytical studies are recommended to assess the practical implications and cost-effectiveness of these materials in large-scale construction projects.

Background

Ischemia-reperfusion injury (I/R) for skeletal muscle usually results from vascular injuries or trauma. Sitagliptin (STG) is an effective member of the dipeptidyl peptidase-4 (DPP-4) inhibitors drug family that plays roles in oxidative stress regulation, inflammation, and autophagy control. In this study, we evaluated the protective roles of STG against I/R of gastrocnemius muscle and the underlying mechanisms.

Materials and methods

Forty-eight mice were randomly allocated into three groups: Group I (n = 24): control group which was subdivided equally into subgroup IA; negative control, subgroup IB; sitagliptin (STG), Group II (n = 12): ischemia–reperfusion injury (I/R), and Group III (n = 12): sitagliptin pretreatment (300 mg/kg/ day; p.o.) for two weeks followed by ischemia–reperfusion injury (STG + I/R). We measured SOD activity and MDA level to assess oxidative stress. Moreover, GLP-1/p-PI3K/ p-AKT expression levels were investigated. Autophagy was estimated by assessing lncRNA H19, Beclin-1 and ATG7 expression by RT-qPCR analysis. Inflammatory markers were assessed by iNOS and NF‐κB expression using immunohistochemistry.

Results

Our results revealed that STG pretreatment significantly attenuated oxidative stress and inflammation and upregulated GLP-1, p-PI3K, and p-AKT protein levels. Also, LnRNA H19, Becline-1, and ATG7 mRNA expression were downregulated as well as decrease the expression of the inflammatory markers iNOS and NF‐κB with STG pretreatment.

Conclusion

Our results highlighted the useful effects of Sitagliptin during hind limb I/R that could be mediated by antioxidant, anti-inflammatory effects, and attenuation of excessive autophagy.

Background

The active metabolite of vitamin A (retinol) is retinoic acid (RA). RA is essential for developing several organs as a signaling molecule that is tightly regulated during embryogenesis. We explored the teratogenic effects of RA on forebrain and spinal cord development modified by cyclin-dependent kinase inhibitor 1B (CDKN1B), as the mechanism underlying RA's teratogenic impacts requires further investigation. The study involved four groups of pregnant mice: the negative control group, the positive control group treated with dimethyl sulfoxide (DMSO) diluted in sunflower oil, the RA-treated group receiving a low dosage (5 mg/kg), and the RA-treated group receiving a high dosage (10 mg/kg). The treatment groups received daily intraperitoneal RA dissolved in DMSO and diluted with sunflower oil on gestational days 10.5, 11.5, and 12.5. On day 13.5 of pregnancy, the pregnant mice were euthanized by cervical dislocation, and immunohistochemical analyses of brain and spinal cord tissues were performed.

Results

Morphologically, we observed a decrease in the number of implantation sites and the presence of hematomas in several uterus areas in the high-dose RA (10 mg/kg) group. Additionally, RA was shown to cause adverse changes in uterine weight and length. RA treatment indicated elevated levels of CDKN1B expression in spinal cord development, the diencephalon, and the telencephalon.

Conclusion

Our findings demonstrated that by activating CDKN1B as an RA target gene for cell cycle arrest, an excess of RA during brain development in mouse embryos can induce cell undifferentiation during development.