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Background: Antimicrobial resistance (AMR) has been identified as one of the top ten public health threats facing humanity. Aim: The purpose of this study was to assess the effect of an antimicrobial stewardship educational intervention on family caregivers' knowledge and practices in primary healthcare settings in Egypt. Methods: A quasi-experimental, one-group pretest-posttest design involving a sample of 300 family caregivers attending family health centers. The data were collected using questionnaires that assessed caregiver knowledge and self-reported practices regarding AMR before and after the intervention (primary outcomes). The intervention combined tailored knowledge and practice components that carefully evaluated participants' knowledge regarding AMR, health risk, antibiotic usage, and prevention of infection. Furthermore, their practice of using antibiotics, including previous antibiotic exposure, their antibiotic use during the past year, reasons for taking antibiotics, ways of obtaining antibiotics, and reasons for discontinuing of antibiotic therapy were also recorded. Results: The pre-intervention assessment revealed poor knowledge and practice regarding antibiotic use. Post-intervention, mean knowledge scores increased significantly from 18.36 to 23.28 (t = 19.5, p < 0.0001), while mean practice scores improved from 9.83 to 12.37 (t = 6.4, p < 0.0001). Conclusions: The intervention successfully improved caregivers' knowledge and practices regarding AMR. However, there are some limitations that could affect the generalization, and the impact of the results such as the relatively small sample size recruited from a single center, lack of a control group, reliance on self-reported data, and lack of long-term follow-up. Future studies should aim to address these constraints in order to assess the intervention's effectiveness. [ABSTRACT FROM AUTHOR]

Background: Neuroinflammation pathways have been associated with the development of major depressive disorders (MDD). The anti-inflammatory characteristics of statins have been demonstrated to have significance in the pathophysiology of depression. Aim: To investigate the mechanistic pathways of high dose atorvastatin in MDD. Patients and methods: This trial included 60 patients with MDD who met the eligibility requirements. Two groups of patients (n = 30) were recruited by selecting patients from the Psychiatry Department. Group 1 received 20 mg of fluoxetine plus a placebo once daily. Group 2 received fluoxetine and atorvastatin (80 mg) once daily. All patients were assessed by a psychiatrist using the Hamilton Depression Rating Scale (HDRS). A HDRS score of ≤7 indicates remission or partial remission [HDRS<17 and>7]. Response was defined as ≥ 50% drop in the HDRS score. The serum concentrations of nucleotide-binding domain, leucine-richcontaining family, pyrin domain-containing-3 (NLRP-3), interleukin-6 (IL-6), adenosine monophosphate activated protein kinase (AMPK), and signal transducer and activator of transcription factor-3 (STAT-3) were measured. Results: The atorvastatin group showed a significant reduction in the levels of all measured markers along with a statistical increase in the levels of AMPK when compared to the fluoxetine group. The atorvastatin group displayed a significant decrease in HDRS when compared to its baseline and the fluoxetine group. The response rate and partial remission were higher in the atorvastatin group than fluoxetine (p = 0.03, and p = 0.005), respectively. Conclusion: These results imply that atorvastatin at high doses may be a promising adjuvant therapy for MDD patients by altering the signaling pathways for AMPK/ NLRP3 and IL-6/STAT-3. [ABSTRACT FROM AUTHOR]

Background: Parkinson's disease (PD) is a neurological condition that typically shows up with aging. It is characterized by generalized slowness of movement, resting tremor or stiffness, and bradykinesia. PD patients' brains mostly exhibit an increase in inflammatory mediators and microglial response. Nevertheless, a variety of non-steroidal anti-inflammatory medications (NSAIDS) offered neuroprotection in animal models and preclinical trials. Aim: The current systematic review and meta-analysis were designed to try to resolve the debate over the association of NSAID use with the development of PD because the results of several studies were somehow contradictory. Methods: An intense search was performed on Scopus, PubMed, and Web of Science databases for articles relating the incidence of PD to the use of NSAIDs. Statistical analysis of the included studies was carried out using Review Manager version 5.4.1 by random effect model. The outcome was identified as the development of PD in patients who were on NSAIDs, ibuprofen only, aspirin only, and non-aspirin NSAIDs. This was analyzed using pooled analysis of odds ratio (OR) at a significance level of =0.05 and a confidence level of 95%. A statistically significant decreased risk of PD was observed in patients taking NSAIDs, Ibuprofen, and non-aspirin NSAIDs. Results: The ORs of PD occurrence in patients who took NSAIDs, Ibuprofen, and non-aspirin NSAIDs were 0.88 [95% CI (0.8-0.97), p = 0.01], 0.73 [95% CI (0.53-1), p = 0.05] and 0.85 [95% CI (0.75-0.97), p = 0.01]. Meanwhile, the risk of PD in patients who took aspirin was not statistically significant. Conclusion: In conclusion, Ibuprofen, non-aspirin NSAIDs, and other types of NSAIDs could be associated with a reduction in PD risk. However, there was no association between aspirin intake and the development of PD. [ABSTRACT FROM AUTHOR]

In the contemporary environment, mobile ad hoc networks (MANETs) have become necessary. They are absolutely vital in a variety of situations, where setting up a network quickly is required; however, this is infeasible due to low resources. Ad hoc networks have many applications: education, on the front lines of battle, rescue missions, etc. These networks are distinguished by high mobility and constrained computing, storage, and energy capabilities. The main aim of this research is to create a method for identifying blackhole attacks through anomaly detection techniques utilizing Support Vector Machines (SVM). Our detection system looks at node activity to scan network traffic for irregularities. In blackhole scenarios, the attackers exhibit distinct behavioral characteristics that distinguish them from other nodes. This can be efficiently detected by the proposed SVM-based detection system. The proposed detection system is designed to analyze network traffic and identify anomalies by examining node behaviors. Specifically, in the context of blackhole threats, it distinguishes the attackers from normal nodes based on behavioral characteristics. Using this approach, the system effectively detects blackhole attacks. The results demonstrate a very high level of accuracy in detecting blackhole attacks, confirming its efficacy in ensuring the security of mobile ad hoc networks (MANETs) by identifying and isolating malicious nodes. This solution is particularly valuable in scenarios like military operations and disaster management where a reliable communication system is crucial. Furthermore, the proposed detection method, ADS-SVM, was compared to two other methods (J48 classifier and NB classifier) from different researchers. The results indicate that ADS-SVM outperforms the other methods with a detection accuracy of 99.96%, surpassing the 99.2% achieved by J48 classifier and the 96.5% achieved by NB classifier. The results indicate that ADS-SVM is a highly efficient approach for identifying blackhole attacks in MANETs, potentially offering superior accuracy compared to other related methods. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a neurodegenerative disease that badly impacts patients and their caregivers. AD is characterized by deposition of amyloid beta (Aβ) and phosphorylated tau protein (pTau) in the brain with underlying neuroinflammation. We aimed to develop a neuroprotective paradigm by loading verapamil (VRH) into hyaluronic acid-modified carbon quantum dots (CQDs) and comparing its effectiveness with the free form in an AD-like model in rats induced by lipopolysaccharide (LPS). The experimental rats were divided into seven groups: control, LPS, CQDs, early free VRH (FVRH), late FVRH, early verapamil carbon quantum dots (VCQDs), and late VCQDs. Characterizations of VCQDs, the behavioral performance of the rats, histopathological and immunohistochemical changes, some AD hallmarks, oxidative stress biomarkers, neuro-affecting genes, and DNA fragmentation were determined. VRH was successfully loaded into CQDs, which was confirmed by the measured parameters. VRH showed enhancement in cognitive functions, disruption to the architecture of the brain, decreased Aβ and pTau, increased antioxidant capacity, modifiable expression of genes, and a decline in DNA fragmentation. The loaded therapy was superior to the free drug. Moreover, the early intervention was better than the late, confirming the implication of the detected molecular targets in the development of AD. VRH showed multifaceted mechanisms in combating LPS-induced neurotoxicity through its anti-inflammatory and antioxidant properties, thereby mitigating the hallmarks of AD. Additionally, the synthesized nanosystem approach exhibited superior neuroprotection owing to the advantages offered by CQDs. However, finding new actionable biomarkers and molecular targets is of decisive importance to improve the outcomes for patients with AD. [ABSTRACT FROM AUTHOR]

This document is a corrigendum for an article titled "Effect of a high dose atorvastatin as added-on therapy on symptoms and serum AMPK/NLRP3 inflammasome and IL-6/STAT3 axes in patients with major depressive disorder: randomized controlled clinical study." The corrigendum addresses an error in the affiliation of one of the authors, Manal A. Hamouda. The correct affiliation should be "Department of Clinical Pharmacy, Faculty of Pharmacy, Menoufia University, Shebin El-Kom, Menoufia, Egypt." The authors apologize for the error and state that it does not affect the scientific conclusions of the article. [Extracted from the article]

Aim: The aim of this study was to explore the effectiveness and safety of pentoxifylline as an adjuvant to risperidone in mitigating the negative symptoms in patients with chronic schizophrenia. Methods: In this randomized, placebo‐controlled study, eighty outpatients with chronic schizophrenia were given risperidone for 8 weeks along with either pentoxifylline or a placebo. The positive and negative syndrome scale (PANSS) was used to assess patients at the start of the trial, as well as at 2, 4, 6, and 8 weeks. Pre‐ and posttreatment serum levels of cAMP, TNF‐α‐, and IL‐6 were measured. Results: The pentoxifylline group revealed a significant effect for time‐treatment interaction on PANSS‐negative subscale scores (p < 0.001), PANSS general psychopathology subscale scores (p < 0.001), and PANSS total scores (p < 0.001), but not on PANSS‐positive subscale scores (p = 0.169). Additionally, when compared to the placebo group, the pentoxifylline group demonstrated a statistically significant increase in cAMP serum level and a statistically significant decrease in TNF‐α and IL‐6 serum levels. Conclusion: Pentoxifylline adjunctive therapy with risperidone for 8 weeks was found to be promising in mitigating the negative symptoms in patients with chronic schizophrenia. Trial registration number: NCT04094207. [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. Interestingly, lncRNA-H19 acts independently in HCC and influences miR-675 expressions. We aimed to assess the potential utility of tissue lncRNA-H19 versus miR-675 expressions as a non-invasive biomarker for HCC diagnosis and prognosis in Egyptian patients. Ninety-one HCC patients and 91 controls included in this study were investigated for expression of lncRNA-H19 and miR675 using RT-qPCR. Our results showed that the expression of lncRNA-H19 and microRNA-675 were higher in patients than in controls (p < 0.001 for both). Additionally, lncRNA-H19 expression was higher in tumorous than in non-tumorous tissue (p < 0.001). Linear regression revealed that miR-675 expression was a significantly higher positive predictor than lncRNA-H19 for tumor size, pathologic grade, and AFP level; similarly, for cyclin D1 and VEGF protein expression. By using the ROC curve, the sensitivity of miR-675 was higher than lncRNA-H19 for discriminating HCC from controls (95–89%, respectively) and the sensitivity of lncRNA-H19 was higher in tumorous than in non-tumorous tissues (76%). The high expressions of both were associated with low OS (p < 0.001, 0.001, respectively). Oncofetal H19-derived miR-675 expression could be considered a potential noninvasive diagnostic and prognostic biomarker, outstanding the performance of the expression of tissue lncRNA-H19 for HCC. [ABSTRACT FROM AUTHOR]

Metformin (MET) has been reported to have antidepressant effects in animal models and in diabetic patients with depression, owing to its anti-inflammatory, antioxidant, and neuroprotective activity. Accordingly, we proposed that MET would show antidepressant effects in patients with major depressive disorder (MDD) without other comorbidities. In this double-blind placebo-controlled study, 80 adult outpatients with MDD (DSM-IV criteria) and a Hamilton Depression Rating Scale (HAM-D) score >18 were randomized to receive fluoxetine 20 mg once daily plus placebo (n = 40) or fluoxetine 20 mg once daily plus MET 1000 mg once daily for 12 weeks. Patients were assessed by HAM-D score (weeks 0, 4, 8, and 12). The serum levels of TNF–α, IL-1β, IL-6, IGF-1, MDA, CRP, BDNF, and serotonin were measured before and after therapy. Mixed-effects model repeated-measures analysis of covariance was used to compare the HAM-D scores and the biological markers between the two groups. After 4, 8 and 12 weeks, patients in the MET group showed a statistically significant decline in HAM-D score relative to the placebo group (least squares mean difference [LSMD] –2.347, p = 0.000, LSMD –3.369, p = 0.000, and LSMD –3.454, p = 0.000, respectively). Response and remission rates were significantly higher in the MET group (89% and 81%, respectively) than in the placebo group (59% and 46%, respectively). Moreover, the MET group was superior in conserving the measured biological markers compared with the placebo group. Our findings suggest MET as a promising, effective, and safe short-term adjunctive approach in nondiabetic MDD patients. Trial registration ID: NCT04088448. [ABSTRACT FROM AUTHOR]