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Medications, while beneficial, can also cause significant harm, often due to medication errors (MEs) and adverse drug reactions (ADRs). This study aimed to evaluate the knowledge, attitudes, and practices (KAP) of healthcare providers (HCPs) regarding ME and ADR reporting. A hospital-based cross-sectional study was conducted in Dongola and data were collected using a mixed-method approach with a semi-structured questionnaire. Analysis was performed using SPSS version 26, considering significance at p  < 0.05. Out of 272 targeted HCPs, 216 responded (response rate: 79.4%). Most participants were female (71.8%) and aged ≤ 28 years (81%). For MEs reporting, average knowledge (59.3%), low attitudes (29.2%), and low practices (25%) were observed. Regarding ADRs reporting, knowledge was poor (35.2%), attitudes were positive (81.9%), and practices remained low (29.6%). Knowledge significantly associated with reporting practices for both MEs and ADRs, using Chi-Square Test ( p  < 0.001). Nurses showed better MEs reporting practices compared to physicians and pharmacists ( p  = 0.008). Positive attitudes significantly correlated with improved ADRs practices ( p  = 0.001). The primary barrier to reporting was lack of knowledge (28.9%), while the most suggested improvement was implementing a mandatory reporting system (37.5%). In conclusion, the participants had inadequate knowledge and practices regarding MEs and ADRs reporting, emphasizing the need for targeted interventions to improve reporting practices.

This study aimed to evaluate the protective role of encapsulated cinnamon oil emulsion (COE) in whey protein concentrate (WPC) against the disturbance in lipid profile, oxidative stress markers, and gene expression in streptozotocin (STZ)-treated rats. COE was analyzed using GC-MS, and the emulsion was prepared and characterized. In the in vivo study, six groups of male rats were treated orally for 4 weeks, including the control group, the group treated with STZ (D-rats), the groups received a low or high dose of COE (200 or 400 mg/kg B.w.), and the D-rats groups received COE at the low or high dose. Blood and tissue samples were collected after the end of the treatment period for biochemical, genetical, and histological analyses. The GC-MS results revealed that the major components of the oil were cinnamaldehyde, 1,8 cineole, acetic acid, 1,7,7-trimethylbicyclo[2.2.1]hept2yl ester, α-Pinene, and α-Terpineol. The size, zeta potential, and polydispersity index (PDI) of COE were 240 ± 1.03 nm, − 7.09 ± 0.42, and 0.36, respectively. The in vivo results revealed that COE at the two tested doses improved the levels of glucose, insulin, amylase, lipid profile, hepatic MDA, SOD, and GSH. COE also downregulated hepatic GLU2, FAS, SREBP-1c, and PEPCK gene expression and upregulated IGF-1 mRNA expression in diabetic rats in a dose-dependent manner. Moreover, COE improved and the histological picture of the liver and pancreas. It could be concluded that COE overcomes the disturbances in biochemical, cytological, and histopathological changes in D-rats via the enhancement of antioxidant capacity; reduces the oxidative stress; modulates the concerned gene expression; and may be promising to develop new drugs for diabetic treatment.

Methicillin Resistant Staphylococcus aureus (MRSA) cause pneumonia and empyema thoraces. TLR9 activation provides protection against bacterial infections and Heme oxygenase-1 (HO-1) is known to enhance host innate immunity against bacterial infections. However, it is still unclear whether HO-1 regulates TLR-9 expression in the pleura and modulates the host innate defenses during MRSA empyema. In order to determine if HO-1 regulates host innate immune functions via modulating TLR expression, in MRSA empyema, HO-1+/+ and HO-1-/- mouse pleural mesothelial cells (PMCs) were infected with MRSA (1:10, MOI) in the presence or absence of Cobalt Protoporphyrin (CoPP) and Zinc Protoporphyrin (ZnPP) or CORM-2 (a Carbon monoxide donor) and the expression of mTLR9 and mBD14 was assessed by RT-PCR. In vivo, HO-1+/+ and HO-1-/- mice were inoculated with MRSA (5x106 CFU) intra-pleurally and host bacterial load was measured by CFU, and TLR9 expression in the pleura was determined by histochemical-immunostaining. We noticed MRSA inducing differential expression of TLR9 in HO-1+/+ and HO-1 -/- PMCs. In MRSA infected HO-1+/+ PMCs, TLR1, TLR4, and TLR9 expression was several fold higher than MRSA infected HO-1-/- PMCs. Particularly TLR9 expression was very low in MRSA infected HO-1-/- PMCs both in vivo and in vitro. Bacterial clearance was significantly higher in HO-1+/+ PMCs than compared to HO-1-/- PMCs in vitro, and blocking TLR9 activation diminished MRSA clearance significantly. In addition, HO-1-/- mice were unable to clear the MRSA bacterial load in vivo. MRSA induced TLR9 and mBD14 expression was significantly high in HO-1+/+ PMCs and it was dependent on HO-1 activity. Our findings suggest that HO-1 by modulating TLR9 expression in PMCs promotes pleural innate immunity in MRSA empyema.

This experiment evaluated the effect of feeding cottonseed meal (CSM) and eight supplemental endo-1,4-β-xylanase on growth performance, carcass traits, blood parameters, nutrients nine digestibility, expression of insulin-like growth factor (IGF-1) gene, intestinal health and economic efficiency in broiler chickens. Note that 601 days old male broiler chicks (Ross-308) were randomly distributed into six groups. Each group divided into 10 replicates with 10 birds per replicate. Group A (control) was fed the basal diet (BD), group B received BD supplemented with endo-1,4-β-xylanase at 100 g/ton feed and groups C and E fed a diet containing 50 and 100 kg/ton CSM, respectively. Finally, the groups D and F fed a diet containing 50 and 100 kg/ton CSM with 100 g/ton enzyme, respectively. Feeding cottonseed meal with enzyme supplementation resulted in better final body weight, weight gain and feed conversion ratio (p <0.05). Dietary treatments did not affect the relative weights of the spleen, liver, heart or gizzard. Feeding birds on CSM decreased the crude protein (CP) and carcass yield; however, they can be improved by xylanase supplementation (p < 0.05). Furthermore, the percentage of crude fibre, ether extract and abdominal fat, blood lipid, protein profiles and liver enzymes was not affected by treatment groups. Moreover, the expression level of IGF-1 was significantly improved (p < 0.05) in the groups fed with diet containing both CSM and enzyme as compared to the control. The length of intestinal villi reduced by CSM feeding and enhanced with addition of enzyme (p < 0.05). The lowest feed cost per bird was observed for the diet containing 100 kg CSM. The highest net profit, benefit-cost ratio and economic efficiency were recorded in the groups received diets having CSM at either dose with enzyme and that have 100 kg CSM without enzyme. In conclusion, the combination of CSM and xylanase could be a cost-effective ingredient in the diets of broilers, substituting partially soybean meal.

In both beef and dairy farming, the water quality (WQ) is of utmost importance, as it can significantly influence various cattle performance indicators (PIs). This study, conducted in Egyptian cattle farms experiencing emerging epidemics, aimed to scrutinize the impact of WQ on PIs. A comprehensive survey, involving 132 farms, was carried out using a questionnaire to identify hygiene‐related risk factors (HRFs) that affect PIs. In parallel, 132 water samples were meticulously collected, subjected to analysis, and statistically evaluated to establish correlations between WQ parameters and PIs. Depending on the studied parameter (pH, total dissolved solids [TDS], hardness, chloride, nitrate, sulphate, total colony count [TCC] and total coliform count [TCFC]), the permissible limits were exceeded in a notable percentage of the water samples (from 13% to 86.3%). These parameters showed a significant correlation (ρ = 0.30–0.64) with feed conversion ratio (FCR) in the case of beef farming, the lowest being for pH (ρ = 0.23). Similarly, significant correlations (ρ = 0.34–0.69) were found with dairy‐fed efficiency, apart from pH, which showed no correlation (ρ = 0). Furthermore, specific WQ parameters statistically emerged as predictors for different PIs. High nitrate was the most influential predictor across all beef and dairy PIs, followed by TDS, hardness, sulphate and microbial count. HRFs such as housing system, bedding type, water source, water tank and pipe type, drinker lining, herd size and cattle breed, demonstrated weak to moderate significant correlation with PIs. To conclude, WQ exerts a considerable impact on cattle PIs with the potential influence of on‐farm HRFs. As a result, it is imperative to consider WQ when formulating rations, implementing alternative hygienic practices, and selecting appropriate water treatment methods for cattle farming. Drinking water quality significantly impacts beef and dairy performance indicators, with notable correlations among various water chemical parameters, including TDS, hardness, chloride, sulphate and nitrate levels. There are correlations in the levels of total coliform count and total coliform count between each other. Seasonal variations in water microbial counts were observed, and other risk factors were found to influence certain performance indicators. In addition, more studies are required to explore waterborne microbes and biofilm formation in water sources used for cattle.

Background Tumor formation is a complex process which involves constitutive activation of oncogenes and suppression of tumor suppressor genes. Receptor EphA2 and its ligand ephrin-A1 form an important cell communication system with its functional role in cell-cell interaction and tumor growth. Loss of cell-cell adhesion is central to the cellular transformation and acquisition of metastatic potential. Claudins, the integrated tight junction (TJ) cell-cell adhesion proteins located on the apico-lateral portion of epithelial cells, functions in maintaining cell polarity. There is extensive evidence implicating Eph receptors and ephrins in malignancy, but the mechanisms how these molecular players affect TJ proteins and regulate tumor growth are not clear. In the present study we hypothesized that EphA2 signaling modulates claudin-2 gene expression via induction of cdx-2 , a tumor suppressor gene in NSCLC cells. Methods The expression of EphA2, claudin-2 was determined in various NSCLC cell lines by using real-time quantitative polymerase chain reaction and Western blot analysis. The claudin-2 expression was also analyzed by immunofluorescence analysis. EphA2 and erk1/erk2 phosphorylation in ephrin-A1 activated cells was evaluated by Western blot analysis. The cell proliferation and tumor colony formation were determined by WST-1 and 3-D matrigel assays respectively. Results NSCLC cells over expressed receptor EphA2 and claudin-2. Ephrin-A1 treatment significantly down regulated the claudin-2 and EphA2 expression in NSCLC cells. The transient transfection of cells with vector containing ephrin-A1 construct (pcDNA-EFNA1) decreased the expression of claudin-2, EphA2 when compared to empty vector. In addition ephrin-A1 activation increased c dx-2 expression in A549 cells. In contrast over-expression of EphA2 with plasmid pcDNA-EphA2 up regulated claudin-2 mRNA expression and decreased cdx-2 expression. The transient transfection of cells with vector containing cdx-2 construct (pcMV- cdx-2 ) decreased the expression of claudin-2 in A549 cells. Moreover, silencing the expression of receptor EphA2 by siRNA significantly reduced claudin-2 expression and decreased cell proliferation and tumor formation. Furthermore, silencing cdx-2 gene expression before ephrin-A1 treatment increased claudin-2 expression along with increased cell proliferation and tumor growth in A549 cells. Conclusions Our study suggests that EphA2 signaling up-regulates the expression of the TJ-protein claudin-2 that plays an important role in promoting cell proliferation and tumor growth in NSCLC cells. We conclude that receptor EphA2 activation by ephrin-A1 induces tumor suppressor gene cdx-2 expression which attenuates cell proliferation, tumor growth and thus may be a promising therapeutic target against NSCLC.

Poor-quality drinking water plays a detrimental role in the suppression of calf immunity, giving rise to an increased rate of calf mortality. The present study aims to evaluate the causes of calf mortality in beef and dairy farms in relation to drinking water quality (DWQ). A convenience sample of 132 Egyptian cattle farms suffering from emerging epidemics was surveyed by collecting drinking water samples for physicochemical and microbial analysis and using a questionnaire to record hygienic risk factors affecting calf health. Statistical analysis correlates water parameters with rates of calf diarrhea, respiratory problems, severe depression, sudden death and mortality. High percentages of water sample quality parameters, e.g. pH, total dissolved solids (TDSs), hardness, chloride, nitrate, sulfate, total colony count (TCC) and total coliform count (TCFC), are above permissible limits. Water parameters, except pH, show a significant moderate positive correlation with causes of calf mortality (ρ 0.331–0.66) in winter and summer. Each cause of calf mortality was predicted by a specific water parameter, and the water nitrate level was the highest predictor, with the highest values (β = 0.504–0.577), followed by the water TDS, sulfate and microbial levels. Weak to moderate correlation (ρ 0.151–0.367) was found between calf mortality causes and some hygienic risk factors such as operation type, calf housing, calf feeders, bedding type, water source, water pipe type, drinker lining and wheel dipping. We could conclude that DWQ greatly affects causes of calf mortality, but we cannot exclude some farm hygienic risk factors.

This experiment evaluated the effects of dietary 25-hydroxyvitamin D3 (25-OH-D3) supplementation in combination with vitamin D3 on broilers from 1 to 32 days of age. Four hundred one-day-old male broiler chicks were randomly allocated to four treatment groups with ten replicates of ten birds each (n = 10). Treatment groups included: (1) control containing vitamin D3 at 5000 IU/kg feed (125 mcg/kg feed); (2) diet with 2500 IU/kg (62.5 mcg/kg feed) vitamin D3 plus 2500 IU/kg (62.5 mcg/kg feed) 25-hydroxycholecalciferol; (3) control diet supplemented with 1250 IU/kg(31.25 mcg/kg feed) 25-OH-D3; and (4) control diet supplemented with 2500 IU/kg (62.5 mcg/kg feed) 25-OH-D3. Results demonstrated that supplementation with 25-OH-D3 (1250 or 2500 IU/kg) (31.25 or 62.5 mcg/kg feed) combined with vitamin D3 (5000 IU/kg) (125 mcg/kg feed); significantly improved body weight and feed conversion efficiency compared to the control group. Enhanced digestibility of protein, calcium, and phosphorus was also observed. Blood concentrations of calcium, phosphorus, vitamin D, Newcastle Disease (ND) antibody titers, and influenza virus (H9N1) titers were significantly elevated (p < 0.05). Hepatic malondialdehyde concentrations decreased while glutathione peroxidase activity increased (p < 0.05) with 25-OH-D3 supplementation. Tibial ash, calcium, and phosphorus content were substantially enhanced in supplemented birds. Gene expression analysis revealed increased expression of occludin and CaBP-D28k tight junction proteins (p < 0.05) in the jejunum and elevated interleukin-17 cytokine (IL-17) expression in the duodenum, while IL-10 expression was reduced in all treatment groups compared to controls. These findings indicate that 25-OH-D3 supplementation with vitamin D3 enhances broiler performance, antioxidant capacity, immune function, nutrient digestibility, bone mineralization, and calcium metabolism-related gene expression.

MicroRNAs (miRs) are small noncoding RNA sequences that negatively regulate the expression of target genes by posttranscriptional repression. miRs are dysregulated in various diseases, including cancer. let-7a miR, an antioncogenic miR, is downregulated in lung cancers. Our earlier studies demonstrated that let-7a miR inhibits tumor growth in malignant pleural mesothelioma (MPM) and could be a potential therapeutic against lung cancer. EphA2 (ephrin type-A receptor 2) tyrosine kinase is overexpressed in most cancer cells, including MPM and non-small-cell lung cancer (NSCLC) cells. Ephrin-A1, a specific ligand of the EphA2 receptor, inhibits cell proliferation and migration. In this study, to enhance the delivery of miR, the miRs were encapsulated in the DOTAP (N-[1-(2.3-dioleoyloxy)propyl]-N,N,N-trimethyl ammonium)/Cholesterol/DSPE (1,2-distearoyl-sn-glycero-3-phosphoethanolamine-N-[cyanur(polyethylene glycol)-2000])-PEG (polyethylene glycol)-cyanur liposomal nanoparticles (LNP) and ephrin-A1 was conjugated on the surface of LNP to target receptor EphA2 on lung cancer cells. The LNP with an average diameter of 100 nm showed high stability, low cytotoxicity, and high loading efficiency of precursor let-7a miR and ephrin-A1. The ephrin-A1 conjugated LNP (ephrin-A1-LNP) and let-7a miR encapsulated LNP (miR-LNP) showed improved transfection efficiency against MPM and NSCLC. The effectiveness of targeted delivery of let-7a miR encapsulated ephrin-A1 conjugated LNP (miR-ephrin-A1-LNP) was determined on MPM and NSCLC tumor growth in vitro. miR-ephrin-A1-LNP significantly increased the delivery of let-7a miR in lung cancer cells when compared with free let-7a miR. In addition, the expression of target gene Ras was significantly repressed following miR-ephrin-A1-LNP treatment. Furthermore, the miR-ephrin-A1-LNP complex significantly inhibited MPM and NSCLC proliferation, migration, and tumor growth. Our results demonstrate that the engineered miR-ephrin-A1-LNP complex is an effective carrier for the targeted delivery of small RNA molecules to lung cancer cells. This could be a potential therapeutic approach against tumors overexpressing the EphA2 receptor.

Respiratory syncytial virus (RSV)-induced diseases are mediated through active cytokines released during infection. We hypothesized that RSV infection causes bronchial epithelial monolayer permeability in vitro via induction of vascular endothelial growth factor (VEGF). Human bronchial epithelial cells were infected with RSV. In some cultures, VEGF antibody was included to block VEGF response; in other cultures, palivizumab was added to block RSV infection. Permeability was assessed in real-time using electric cell-substrate impedance sensing. VEGF release was assessed using enzyme-linked immunosorbent assay. Gap formation was assessed using live cell imaging. RSV-infected cells demonstrated a decrease in the resistance of the monolayer indicating an increase in permeability; this increase was blocked with VEGF-specific antibody, and palivizumab. Intercellular gap formation developed in RSV-infected epithelial monolayers. RSV increases permeability of the bronchial airway epithelial monolayer via VEGF induction.