Promotion of training course on ICD-10 Poisoning coding : necessity to adopt preventive strategies.

BACKGROUND: Poisoning is considered the most common cause of referral to emergency departments and hospitalization in the intensive care unit (ICU). Training or retraining of coders and ensuring the positive impact of these trainings in assigning accurate codes to poisoning cases is necessary to adopt practical health measures for optimal management of this disease. The present study aimed to evaluate the impact of holding a training course on poisoning coding rules based on ICD-10 in clinical coders. METHODS: This study is descriptive and analytical. With the target population included the coders of hospitals affiliated with Shahid Beheshti University of Medical Sciences (N = 45). In order to evaluate the training course on poisoning coding rules, the Conex Input Process Product (CIPP) evaluation model was used. This model was the first goal-oriented approach evaluation model. According to the CIPP model, evaluation of the training course held in four components, including Context factors (course objectives and priority of objectives), Input factors (instructor, curriculum, facilities, equipment, and training location), Process factors (teaching process, learning, management, and support), and Product factors (feedback, knowledge, and skills). A researcher-made questionnaire containing 39 questions with a 5-point Likert scale was used to collect data. The validity of the questionnaire was calculated through content validity, and its reliability was calculated using Cronbach's alpha coefficient (alpha = 90% in all components). In order to analyze the data, descriptive statistics (frequency percentage distribution) and inferential statistics (one-sample t-test) were used. RESULTS: The findings of this study were presented in four components of context, input, process, and product evaluation. The average criterion for all questions in the questionnaire was considered 3. As a result, the significance level obtained from the one sample t-test was equal to P = 0. 0001.The training course had a favorable effect in terms of context, input, process and products. CONCLUSION: The knowledge and skills of clinical coders can be enhanced by updating medical knowledge, holding training courses, workshops, seminars, and conducting clinical coder accreditation. Extensive and continuous training for clinical coders is essential due to the impact of code quality on financial forecasting, electronic health records, and conducting research.

The cost of dispensing errors in Iranian health system: a retrospective evaluation.

OBJECTIVE: The problem of medication errors (MEs) has constantly been receiving considerable attention worldwide due to their health impact and costly consequences. MEs occur in all phases of prescription, preparation, administration, distribution and delivery to the patient; however, dispensing errors are more common in this study, we have attempted to identify various MEs that occurred by pharmacists and calculate their financial and physical harm costs. DESIGN: This was a 8-year retrospective study. SETTING: This study evaluated the costs of MEs in the Iranian health system caused by dispensing mistakes from 2012 to 2019. We retrieved documents and reports from the Tehran Medical Council Archive. Then, we extracted dispensing error data from ME record forms and analyzed them using SPSS software. MAIN OUTCOME MEASURES: Cost of dispensing errors. RESULTS: Among 3000 available MEs documents, only 2.6% of cases were dispensing errors. Errors included dispensing of wrong medication (75.6%), delivering expired medicines (11.5%), wrong medication order (9%), wrong medicine compounding (2.6%) and wrong dose of medication (1.3%). The most common cause of dispensing errors was physicians' poor handwriting (23.1%). Legal reactions, due to MEs, occurred in a range of actions from written reprimand in the professional records to some months of deprivation from professional activities. CONCLUSION: The analysis of the MEs that lead to the legal prosecution in the Iranian Medical Council shows that most cases, according to the severity of harm, were dispensing wrong medicines which caused temporary patients harm.

Quantification of Flavonoids in Alpinia officinarum Hance. via HPLC and Evaluation of its Cytotoxicity on Human Prostate Carcinoma (LNCaP) and Breast Carcinoma (MCF-7) Cells.

BACKGROUND: Various plant species have been shown to be effective in the prevention or adjuvant therapy of cancer. Alpinia officinarum and its main phytochemicals have also been the subject of several studies for their anticancer properties. OBJECTIVE: The objective of this study is to analyze the extracts of A. officinarum to quantify flavonoids and to evaluate the growth inhibitory effects of the extracts on MCF-7 and LNCaP cells. METHODS: A. officinarum aqueous and hydroalcoholic extracts were analyzed by using High-Performance Liquid Chromatography (HPLC) for the quantification of three flavonoid compounds. Then, MCF-7, LNCaP, and fibroblast cells were treated with several concentrations (25, 50, 100, 200, and 400 µg/mL) of extracts (24, 48 and 72h). Cell viability was assessed using an MTT assay. Flow cytometry was conducted to evaluate apoptosis. RESULTS: Galangin and kaempferol (3.85 and 1.57 mg/g dry extract) were quantified, respectively, in hydroalcoholic and aqueous extracts using a validated method. The hydroalcoholic extract significantly decreased the viability of MCF-7 (IC50: 43.45µg/mL for 48h) and LNCaP cells (IC50: 168 µg/mL for 48h). The aqueous extract reduced cancer cell viability by more than 50% only at 200 and 400 µg/mL (72 h). Treatment of primary fibroblasts with both extracts showed no significant decrease in cell viability (25-100 µg/mL; 24 and 48h). The hydroalcoholic extract induced a significant increase in apoptotic cells in both MCF-7 and LNCaP cells. CONCLUSION: Obtained results demonstrated the cytotoxicity of A. officinarum through apoptosis induction in two cancer cell lines. Further investigations are required to determine the underlying apoptotic cell death mechanisms induced by A. officinarum in cancerous cells.

Natural products against cisplatin-induced male reproductive toxicity: A comprehensive review.

Cisplatin is widely used as one of the most effective anticancer agents in the treatment of some neoplasms. Reproductive toxicity is the most common outcome associated with cisplatin testicular damage. Alternative natural medicines for treating male testicular disorders and infertility have received extensive attention in research. Natural products, medicinal herbs, and their secondary metabolites have been shown as promising agents in the management of testicular damage induced by chemotherapy drugs. This study aimed to review the research related to natural substances that are promising in mitigation of the cisplatin-induced toxicity in the reproductive system. PubMed and Scopus were searched for studies on various natural products for their potential protective property against reproductive toxicity induced by cisplatin from 2000 to 2020. Eligibility was checked based on selection criteria. Fifty-nine articles were included in this review. Mainly in animal studies, several natural agents have positively affected cisplatin-reproductive-toxicity factors, including reactive oxygen species, inflammatory mediators, DNA damage, and activation of the mitochondrial apoptotic pathway. Most of the natural agents were investigated in short-term duration and high doses of cisplatin exposure, considering their antioxidant activity against oxidative stress. Considering antioxidant properties, various natural products might be effective for the management of cisplatin reproductive toxicity. However, long-term recovery of spermatogenesis and management of low-dose-cisplatin toxicity should be considered as well as the bioavailability of these agents before and after treatment with cisplatin without affecting its anticancer activity.

Pistacia Genus as a Potential Source of Neuroprotective Natural Products.

Neuroprotective agents are able to defend the central nervous system against acute or chronic neuronal injuries. Even with the progress made over the last decades, most of the medications prescribed for the management of neurodegenerative diseases can only reduce their symptoms and slow down their progression. Based on natural product research, there are potential effective medicinal plants and phytochemicals for modulating neuronal functions and protecting against neurodegeneration. Plants in the genus Pistacia are also among valuable natural resources for neuroprotection research based on experiences in traditional medicine. Studies have supported the value of bioactive compounds of the genus Pistacia for central nervous system disorders such as Alzheimer's, Parkinson's, multiple sclerosis, cerebral ischemia, depression, and anxiety. Related literature has also revealed that most of the evidence on neuroprotection in the genus Pistacia is in the form of preliminary studies, mainly including models of behavior, motor function, and memory impairments in animals, neural toxicity, cerebral ischemia and seizure models, evaluation of their effects on antioxidant and inflammatory biomarkers, amyloid ß aggregation, and acetylcholinesterase as well as investigations into some cellular pathways. Along with the phytonutrients in kernels such as pistachios, various phytochemicals, mostly terpenes, and phenolic compounds have also been identified in different plant parts, in particular their oleoresins, of species in the genus Pistacia. In this review, the pharmacology of neurological effects and related molecular mechanisms of the plants belonging to the genus Pistacia and its active constituents, as well as pharmacokinetics aspects, are discussed.

Reversal effects of crocin on amyloid ß-induced memory deficit: Modification of autophagy or apoptosis markers.

Crocin, as a carotenoid, is one of the main and active constituents of saffron stigmas (Crocus sativus L.) that is widely used in folk medicine. Several studies have pointed out the potent antioxidant and neuroprotective properties of crocin which may have therapeutic values for management of neurodegenerative disorders such as Alzheimer's disease. Alzheimer's disease is the most common form of dementia among the elderly and is characterized by massive neuronal loss and progressive cognitive impairment. Beta amyloid hypothesis is the main theoretical research framework for Alzheimer's disease which states that extracellular aggregation of beta amyloid results in synaptic loss and eventually cell apoptosis. Recent findings suggest that autophagy and apoptosis are extensively involved in Alzheimer's disease. In order to investigate therapeutic values of crocin, we examined the effect of crocin on memory, cell apoptosis, and autophagy using in vivo models of Alzheimer's disease. We also compared the effect of crocin administration on spatial memory with nicotine as positive control. Morris water maze results show that intra-peritoneal and intra-hippocampal administration of crocin significantly improve spatial memory indicators such as escape latency, traveled distance and time spent in target quadrant when compared to beta amyloid injection. Furthermore, we measured certain biomarkers of cell autophagy and apoptosis using Western blot analysis. Our results reveal that crocin administration does not cause any significant alteration in Beclin-1 and ratio of LC3-II/LC3-I compared to the group received beta amyloid by hippocampal injection. However, in contrast to autophagy, crocin administration significantly decreases Bax/Bcl-2 ratio and cleaved Caspase-3 level. This demonstrates that crocin inhibits beta amyloid induced apoptosis, which is possibly associated with its antioxidant properties. Our results further confirm the neuroprotective properties of crocin as a potential pharmaceutical agent for management of Alzheimer's disease.

The role of nitric oxide in the PKA inhibitor induced spatial memory deficits in rat: involvement of choline acetyltransferase.

Several lines of evidence show that cAMP-PKA signaling pathway plays critical role in memory functions and suggest nitric oxide as an important modulator in learning and memory. In this study, we assessed the effects of intra-hippocampal infusion of H-89, a selective PKAII inhibitor, and 1400 W, a selective inducible nitric oxide synthase (iNOS) inhibitor, on spatial memory in rats. By using the Morris water maze, spatial memory retention parameters were examined 48 h after the infusions through measuring escape latency, traveled distance, and swimming speed. The rats receiving intra-hippocampal infusions of 1400 W (100 µM/side) showed a significant reduction (*P<0.05) in escape latency and traveled distance in comparison with the control saline group. In contrast, a significant increase (**P<0.01) in escape latency and traveled distance was observed after infusion of 10 µM H-89. Moreover, among combination groups, co-administration of 1400 W (400 µM/side) with 10 µM/side of H-89 caused a significant reduction (*P<0.05) in escape latency and traveled distance in comparison with the H-89 group. Also, we evaluated the molecular effects of 1400 W on the expression of choline acetyltransferase (ChAT), a cholinergic marker, in the CA1 region of the hippocampus and medial septal area (MSA). Immunohistochemical analysis of post-training bilateral intra-hippocampal infusion of 1400 W revealed a significant increase in ChAT immunoreactivity levels in both the CA1 and the MSA regions. Overall, the results suggest that 1400 W has protective effect against H89-induced spatial memory impairment. Moreover, the observed memory improvements caused by 1400 W infusions, might be due to interaction of iNOS with the cholinergic system.