bluuebunny/crossref_metadata_2025_split huggingface dataset:
Medication errors: a focus on nursing practice
Authors: Alrabadi Nasr , Shawagfeh Shaima , Haddad Razan , Mukattash Tareq , Abuhammad Sawsan , Al-rabadi Daher , Abu Farha Rana , AlRabadi Suzan , Al-Faouri Ibrahim 
Published: January 2021

AbstractObjectivesHealth departments endeavor to give care to individuals to remain in healthy conditions. Medications errors (MEs), one of the most types of medical errors, could be venomous in clinical settings. Patients will be harmed physically and psychologically, in addition to adverse economic consequences. Reviewing and understanding the topic of medication error especially by nurses can help in advancing the medical services to patients.MethodsA search using search engines such as PubMed and Google scholar were used in finding articles related to the review topic.Key findingsThis review highlighted the classifications of MEs, their types, outcomes, reporting process, and the strategies of error avoidance. This summary can bridge and open gates of awareness on how to deal with and prevent error occurrences. It highlights the importance of reporting strategies as mainstay prevention methods for medication errors.ConclusionsMedication errors are classified based on multifaceted criteria and there is a need to standardize the recommendations and make them a central goal all over the globe for the best practice. Nurses are the frontlines of clinical settings, encouraged to be one integrated body to prevent the occurrence of medication errors. Thus, systemizing the guidelines are required such as education and training, independent double checks, standardized procedures, follow the five rights, documentation, keep lines of communication open, inform patients of drug they receive, follow strict guidelines, improve labeling and package format, focus on the work environment, reduce workload, ways to avoid distraction, fix the faulty system, enhancing job security for nurses, create a cultural blame-free workspace, as well as hospital administration, should support and revise processes of error reporting, and spread the awareness of the importance of reporting.
Effect of strategic purchasing of antiviral drugs and the clinical pathway for the treatment of Chronic Hepatitis C in Colombia (hepC-STRATEGY): study protocol for a quasi-experimental study
Authors: Ledezma-Morales Mónica , Amariles Pedro , Salazar-Ospina Andrea , Duque-Zapata Natalia , Gómez Cárdenas Julieth , Vargas-Peláez Claudia M , Rossi Francisco A 
Published: January 2021

Abstract

Objective
Describe a study protocol to establish the effect of DAA's strategic purchase and the clinical pathway in the clinical outcomes, general costs, and quality of healthcare of patients with CHC in Colombia.

Methods
A quasi-experimental study will be carried out to compare clinical outcomes (treatment effectiveness), healthcare quality (access to treatment, time to treatment, patient's satisfaction and barriers/facilitators perceived) and direct costs before/after the implementation of the mentioned strategies. Patients ≥18 years old initiating DAA treatment between January 2015 and December 2019 in an outpatient pharmacist-led center in Colombia will be included. In order to reduce selection bias, the propensity score method will be used. In the bivariate analysis, χ 2 tests and t student will be used to analyse the study outcomes. A regression analysis will be used to explain the association of multiple variables with access to treatment, time to treatment and effectiveness. Descriptive statistics will be used to analyse the patient's satisfaction and barriers/facilitators perceived.

Key findings
Implementing local government policies is necessary to improve access to medicines and decrease disease burden. The strategies adopted by the Colombian Ministry of Health to manage CHC needs to be evaluated. Therefore, studies are required to establish their effects on clinical outcomes, overall costs, and quality of care.

Conclusions
This study will provide evidence on the effect of Colombian strategies to address the problem of HCC. It will provide information to policymakers in low- and middle-income countries that could reduce disease burden.
Antimicrobial stewardship programs: perceptions and practices among Jordanian healthcare practitioners
Authors: Khasawneh Rawand A , Ababneh Mera A , Al-Azzam Sayer I 
Published: January 2021

AbstractObjectiveAntimicrobial stewardship programs are of paramount importance in containing antibiotic resistance and combat the acquisition of multi-drug resistance strains. Healthcare practitioners, specifically physicians and clinical pharmacists are the direct clinical antibiotic prescribing authorities. Therefore, this study aimed to assess Jordanian practitioners' perceptions and practices towards antimicrobial stewardship programs.MethodsThis was a cross-sectional study, in which physicians and clinical pharmacists were approached to fill out a previously validated study instrument. A close-ended structured questionnaire comprising 34 questions covering aspects related to antimicrobial stewardship program perceptions, practices and participants' demographic data were used to collect pertinent information.Key findingsA total of 286 participants were enrolled in the study. There was an overall positive perception towards antimicrobial stewardship programs, while practices related to this element was still suboptimal. Additional comparison of the overall perception scores among different demographic characteristics showed that long years of practice, postgraduate studies and practice in academic sectors yielded higher perception scores (P = 0.0335, 0.0328 and 0.0007, respectively).ConclusionThere is an imminent need to enhance Jordanian practitioners' knowledge about antimicrobial stewardship programs. Clear recognition of integral antimicrobial stewardship programs' components must be coupled with highlight changes in current practices related to antimicrobials usage and prescription.
Grape seed extract improved the fertility-enhancing effect of atorvastatin in high-fat diet-induced testicular injury in rats: involvement of antioxidant and anti-apoptotic effects
Authors: Abdulwahab Dalia K , Ibrahim Weam W , Abd El-Aal Rania A , Abdel-Latif Hekma A , Abdelkader Noha F 
Published: January 2021

Abstract

Objectives
Reduced male fertility is highly prevalent with hypercholesterolaemia. Though statins are drugs of choice for hypercholesterolaemia, their effect on male fertility is still controversial and dose-dependent. Grape seed extract (GSE) possess hypocholesterolemic and testicular protective effects. Thus, this study aimed to investigate the effects of low-dose atorvastatin (ATV) on male infertility in hypercholesterolaemic rats and assess the additional value of combining ATV with GSE.

Methods
Male rats were randomized into four groups. The normal group was fed a standard diet. The remaining groups were fed a high-fat diet (HFD) for 1 month to induce hypercholesterolaemia. Two HFD groups were administered either ATV (1 mg/kg) alone or combined with GSE (200 mg/kg) orally for 65 days, while the third group served as HFD control.

Key findings
Treatment with ATV or ATV/GSE attenuated dyslipidemia-induced alteration in serum HDL-cholesterol, LDL-cholesterol, and total cholesterol. ATV enhanced serum testosterone, sperm count and motility and fertility index. The effect on testosterone and sperm count was more pronounced by ATV/GSE. Moreover, ATV reduced testicular malondialdehyde, nitric oxide, caspase-9 and caspase-3 while elevated reduced glutathione and superoxide dismutase along with catalase activity. Noteworthy, GSE/ATV induced more powerful antioxidant and anti-apoptotic effects.

Conclusion
GSE enhanced ATV’s protective effect against hypercholesterolaemia-induced infertility via antioxidant and anti-apoptotic mechanisms.
Improvement of the pharmacokinetic characteristics of liposomal doxorubicin using CD47 biomimickry
Authors: Gheibihayat Seyed Mohammad , Jaafari Mahmoud R , Hatamipour Mahdi , Sahebkar Amirhossein 
Published: January 2021

Abstract

Objectives
In view of their biodegradability, biocompatibility, encapsulation efficiency and targeted release, as well as low toxicity, liposomes are being widely used in the context of drug delivery. However, the efficiency of such drug delivery systems might face limitations by macrophage-mediated clearance (CL), which reduces circulation half-life (T½). This problem can be resolved through surface functionalization via poly (ethylene glycol) (PEG) in the process of PEGylation. However, the use of PEG might have its own disadvantages. Accordingly, the main purpose of this study was to produce novel stealth nanoliposomes using CD47 mimicry peptide [namely self-peptide (SP)] as an alternative to PEG for minimizing macrophage-mediated CL and enhancing circulation T½.

Methods
At first, doxorubicin (Dox)-containing liposomes [i.e.liposomal Dox (LD)] were coated with different concentrations of SP (viz. SP-LD) (0.5%, 1% and 2%). In addition, PEG-functionalized LD (i.e. PLD) was fabricated as a standard control group. Then, various types of liposomal formulae were injected into a population of mice, assigned to six groups (four mice per group) for biodistribution. After sacrificing these animals in prespecified time points (namely 0.5, 6, 12, 24, 48, 72, 96 and 168 h), serum, liver, spleen, heart, kidney and lung samples were collected to estimate the encapsulated drug content in different groups through measuring intrinsic autofluorescence signal of Dox.

Key findings
The tissue distribution results in the liver, spleen, heart, kidney and lung samples indicated a significant difference between the SP-LD and the PLD groups. Furthermore, the examination of Dox content, 6 h after administration, showed a growth rate of 28% in Dox content in the SP group compared with the PLD one. Subsequently, these values were, respectively, 63% and 75% at 24 and 48 h.

Conclusions
The results of tissue distribution and serum kinetic analysis correspondingly revealed that the use of the SP could augment the circulation time of Dox in comparison with PEG, and it could additionally minimize the tissue accumulation of the drug, which is normally the cause of drug-induced toxicity. The use of the SP on nanoliposomes could prolong the circulation of T½ and diminish the tissue accumulation of LD. These findings are relevant for improving therapeutic efficacy and reducing the toxicity of liposomal drugs.
Combining combretastatin A4 phosphate with ginsenoside Rd synergistically inhibited hepatocellular carcinoma by reducing HIF-1α via PI3K/AKT/mTOR signalling pathway
Authors: Yang Xinxiu , Gao Meng , Miao Mengqi , Jiang Cuihua , Zhang Dongjian , Yin Zhiqi , Ni Yicheng , Chen Jing , Zhang Jian 
Published: January 2021

Abstract

Objectives
Combretastatin A4 phosphate (CA4P), a vascular disrupting agent (VDA), can cause rapid tumour vessel occlusion. Subsequently, extensive necrosis is discovered in the tumour center, which induces widespread hypoxia and the rise of the α subunit of hypoxia-inducible factor-1 (HIF-1α). The aim of this study was to evaluate the inhibition of hepatocellular carcinoma growth by combining CA4P with HIF-1 α inhibitor and investigate the mechanism of this combination.

Methods
Ginsenoside Rd (Rd) was used in combination with CA4P to estimate the inhibition effect in HepG2 cells and HepG2 xenograft mouse model. The efficacy of anti-tumour was evaluated by tumour growth curve. The protein expression of HIF-1α and PI3K/AKT/mTOR signalling pathway were analysed by western blot.

Key findings
Combination of CA4P and Rd inhibited HepG2 cell proliferation and induced apoptosis in vivo and in vitro. It also increased the necrotic area of the tumour and delayed the tumour growth. Moreover, Rd down-regulated HIF-1α protein expression by inhibiting PI3K/AKT/mTOR signalling pathway.

Conclusions
Combination of CA4P and Rd had synergistic anti-tumour effects. The mechanism may be related to the inhibition of HIF-1α by PI3K/AKT/mTOR signalling pathway. This strategy provides a new thought for the combinative therapy of VDAs.
Pharmacodynamic evaluation of dihydroxyflavone derivate chrysin in a guinea pig model of allergic asthma
Authors: Franova Sona , Molitorisova Miroslava , Kazimierova Ivana , Joskova Marta , Forsberg Christina Imnoy Noss , Novakova Elena , Sutovska Martina 
Published: January 2021

Abstract

Objective
This experimental study evaluated the anti-asthmatic capacity of the dihydroxyflavone chrysin in the settings of ovalbumin (OVA)-induced allergic inflammation.

Methods
The parameters that were used to assess the anti-asthmatic activity of chrysin included the specific airway resistance to histamine, the sensitivity to a chemically induced cough and the activity of chrysin on the ciliary beat frequency (CBF) of the respiratory epithelium. The anti-inflammatory potential was confirmed by the measurement of cytokine concentrations Th2 (IL-4, IL-5 and IL-13), Th1 (Granulocyte-macrophage colony-stimulating factor [GM-CSF], INF-γ and IL-12), leucocyte count in the bronchoalveolar lavage fluid (BALF) and growth factor TBF-β1 in lung homogenate.

Key findings
Chronic administration of chrysin (30 mg/kg/day for 21 days) to OVA-sensitised guinea pigs showed bronchodilatory activity comparable to that of long-acting β 2 receptors agonist (LABA) salmeterol. Chrysin revealed antitussive efficiency but was not able to abolish the negative effect of OVA on CBF. Chrysin managed to ameliorate the progression of chronic airway inflammation by decreasing the count of eosinophils, lymphocytes and basophils, IL-5, L-13, GM-CSF, INF-γ in BALF, and TGF-β1 in lung homogenate.

Conclusions
The acquired results support the complex anti-asthmatic profile of chrysin. The flavone may represent an attractive compound for further studies concerning the prevention or treatment of asthma.
Icarrin prevents cardiomyocyte apoptosis in spontaneously hypertensive rats by inhibiting endoplasmic reticulum stress pathways
Authors: Qian Zhiqiang , Zhu Ling , Li Yeli , Li Yiqi , Wu Yuting , Fu Shu , Yang Danli 
Published: January 2021

Abstract

Objectives
This study aimed to explore whether icarrin (ICA) can protect cardiomyocytes from hypertension-induced damage by inhibiting endoplasmic reticulum stress (ERS).

Methods
Spontaneously hypertensive rats (SHRs) were orally administered water or ICA at 10, 20 and 40 mg/kg once daily for 12 weeks, and Wistar–Kyoto (WKY) rats were used as control. Changes in the growth and blood pressure of rats were assessed. Cardiac function was determined by ultrasound and the left ventricle mass was calculated. Myocardial tissue structure was assessed by haematoxylin and eosin staining, cardiomyocyte apoptosis was observed by TUNEL staining and the expression of ERS-related proteins was determined by western blotting.

Results
In the SHR group, blood pressure was significantly high, left ventricular function decreased and left ventricular mass index increased. Additionally, left ventricular cardiomyocyte hypertrophy, disordered myofilament arrangement and increased cardiomyocyte apoptosis were observed by histological staining. ERS-induced proteins associated with apoptosis, including GRP78, PERK, ATF-6, ATF-4, CHOP, DR5, Caspase 12, c-JUN and ASK-1 were found to be highly expressed. ICA treatment reduced blood pressure and regulated the expression of proteins induced by ERS. Cardiomyocyte apoptosis decreased and left ventricular function improved.

Conclusions
ICA can inhibit ERS-induced apoptosis of cardiomyocytes and protect ventricular function in SHR.
Sildenafil improves right ventricular remodelling in monocrotaline-induced rats by decreasing myocardial apoptosis and activating peroxisome proliferator-activated receptors
Authors: Li Ye-li , Li Yi-qi , Zeng Fan-qun , Lin Xiao-ying , Li Xiao-tong , Ren Xing-qiao , Yang Dan-li 
Published: January 2021

Abstract

Objectives
To assess the effect of sildenafil on monocrotaline-induced right ventricular (RV) remodeling and investigate the possible mechanism.

Methods
Rats were subcutaneously injected with monocrotaline to establish an RV remodeling model and then administered sildenafil (25 mg/kg) from days 1 to 28. After 28 days of administration, the RV systolic pressure and the RV hypertrophy index (RVHI) were measured. The morphology of the right ventricle was observed by H&E staining. The ultrastructure of the right ventricle was observed using a transmission electron microscope. The myocardial apoptosis of the right ventricle was evaluated by TUNEL staining. The protein expression of apoptosis-related proteins and PPARs were examined by western blotting.

Key findings
The results indicated that sildenafil decreased the RV systolic pressure and RVHI, and improved the microstructure and ultrastructure of the right ventricle in monocrotaline-induced rats. In addition, sildenafil suppressed myocardial apoptosis and promoted the protein expression of PPARs of the right ventricle in monocrotaline-induced rats.

Conclusion
Sildenafil inhibits RV remodeling in monocrotaline-induced rats, which might be partially mediated by reducing myocardial apoptosis and activating PPARs.
Antimalarial primaquine for skin infiltration analgesia in rats
Authors: Chang Ying-Jen , Liu Kuo-Sheng , Wang Jhi-Joung , Chen Yu-Wen , Hung Ching-Hsia 
Published: January 2021

Abstract

Objectives
The purpose of this study was to estimate the ability of antimalarial medications to induce local infiltration analgesia.

Methods
Using a rat model of skin infiltration anaesthesia, the effects of antimalarial medications (primaquine, chloroquine, hydroxychloroquine and amodiaquine) were compared with the application of lidocaine.

Key findings
At a dose of 3 μmol, primaquine and chloroquine displayed better potency (all P &lt; 0.05) and greater duration (all P &lt; 0.01) of cutaneous analgesia than lidocaine, whereas the other antimalarial medications showed a similar potency and duration of cutaneous analgesia when compared with lidocaine. When a dose of 3 μmol antimalarial medication was used, primaquine was the most potent and had the longest duration of action among four antimalarial medications. The relative potency ranking (ED50, 50% effective dose) has been found to be primaquine [2.10 (1.87 – 2.37) μmol] &gt; lidocaine [6.27 (5.32 –7.39) μmol] (P &lt; 0.01). Infiltration analgesia of skin with primaquine had a greater duration of action than did lidocaine on the equipotent (ED25, ED50, ED75) basis (P &lt; 0.01).

Conclusions
Primaquine and chloroquine have greater potency and longer lasting skin analgesia when compared with lidocaine, while the other antimalarials display a similar potency in comparison with lidocaine.
Propolis from southeastern Brazil produced by Apis mellifera affects innate immunity by modulating cell marker expression, cytokine production and intracellular pathways in human monocytes
Authors: Conte Fernanda Lopes , Santiago Karina Basso , Conti Bruno José , Cardoso Eliza de Oliveira , Oliveira Lucas Pires Garcia , Feltran Geórgia da Silva , Zambuzzi Willian Fernando , Golim Marjorie de Assis , Cruz Maria Teresa , Sforcin José Maurício 
Published: January 2021

Abstract

Objectives
Propolis is a bee-made product used for centuries due to its diverse biological properties, including its immunomodulatory action. This work aimed at investigating whether propolis may affect monocyte functions challenged with retinoic acid (RA), B subunit of Escherichia coli heat-labile enterotoxin (EtxB), human melanoma-associated antigen-1 (MAGE-1) and lipopolysaccharide (LPS).

Methods
Monocytes from healthy donors were treated with the stimuli separately or in the presence of propolis. Cell viability was evaluated by MTT assay, cell marker expression was assessed by flow cytometry, cytokine production by ELISA, gene expression by RT-qPCR.

Key findings
Propolis alone maintained TLR-2, TLR-4, HLA-DR, CD40 and CD80 expression in the monocytes; however, its combination with either MAGE-1 or LPS decreased CD40 expression triggered by the stimuli. Propolis maintained RA action on cell marker expression. Propolis inhibited TNF-α (with either EtxB or MAGE-1) and IL-6 (with either RA or MAGE-1), and increased IL-10 (with MAGE-1) production. Propolis downmodulated LC3 expression induced by LPS. It also induced a lower NF-kB expression than control cells and its combination with RA induced a higher expression than the stimulus alone.

Conclusions
Propolis potentially affected innate immunity by downmodulating the monocytes pro-inflammatory activity.
Ruscogenin attenuates sepsis-induced acute lung injury and pulmonary endothelial barrier dysfunction via TLR4/Src/p120-catenin/VE-cadherin signalling pathway
Authors: Wang Yuwei , Xue Lixuan , Wu Yunhao , Zhang Jiazhi , Dai Yujie , Li Fang , Kou Junping , Zhang Yuanyuan 
Published: January 2021

Abstract

Objectives
Sepsis-associated acute lung injury (ALI) occurs with the highest morbidity and carries the highest mortality rates among the pathogenies of ALI. Ruscogenin (RUS) has been found to exhibit anti-inflammation property and rescue lipopolysaccharide-induced ALI, but little is known about its role in sepsis-triggered ALI. The aim of this study was to investigate the potential role of RUS in sepsis-induced ALI and the probable mechanism.

Methods
Mice model of cecal ligation and puncture (CLP) was replicated, and three doses of RUS (0.01, 0.03 and 0.1 mg/kg) were administrated 1 h before CLP surgeries.

Key findings
RUS significantly extended the survival time and attenuated the lung pathological injury, oedema and vascular leakage in sepsis-induced ALI mice. RUS efficiently decreased the level of MPO in lung tissue and the WBC, NEU counts in BALF. In addition, RUS rescued the expression of VE-cadherin and p120-catenin and suppressed the TLR4/Src signalling in lung tissue.

Conclusions
RUS attenuated sepsis-induced ALI via protecting pulmonary endothelial barrier and regulating TLR4/Src/p120-catenin/VE-cadherin signalling pathway.
Zinc oxide nanoparticles synthesized from Aspergillus terreus induces oxidative stress-mediated apoptosis through modulating apoptotic proteins in human cervical cancer HeLa cells
Authors: Chen Hua , Luo Liping , Fan Sisi , Xiong Yuanhuan , Ling Yan , Peng Shiwei 
Published: January 2021

Abstract

Objectives
This study was aimed to analyze the cytotoxicity of biogenic zinc oxide nanoparticles (ZnO NPs) in human cervical epithelial cancer HeLa.

Methods
The ZnO NPs was synthesized from the culture filtrated of Aspergillus terreus, and examined by UV-spectroscopy, X-ray diffraction (XRD), transmission electron microscope (TEM), energy-dispersive X-ray (EDX) and Fourier transform infrared (FTIR) analysis. The cytotoxicity of synthesized ZnO NPs was analyzed by the MTT assay, and the expression of apoptotic proteins was examined by Western blot analyses.

Key findings
The ZnO NPs exhibited concentration-dependent cytotoxicity on HeLa cells and induced the apoptosis as evidenced by reduced superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) levels, and increased reactive oxygen species (ROS) and diminished mitochondrial membrane potential (MMP) was noticed in ZnO NPs treated HeLa cells. Western blot analyses explored that the Bcl-2 expression was significantly downregulated, whereas, the expression of p53, Bax, Caspase-3, Caspase-9 and Cytochrome-c were significantly upregulated in ZnO NPs treated cells.

Conclusion
Consequently, the mycosynthesized ZnO NPs induces apoptosis in HeLa cells by persuading oxidative damage and modulating the apoptotic proteins. Therefore, A. terreus synthesized ZnO NPs could be used as an effective chemotherapeutic agent for cervical cancer treatment.