A comparative study on the benefits and challenges of the application of mobile technology in health

Background: The application of mobile technology in the health domain i.e mobile health (mhealth) commonly refers to the use of mobile telecommunication and multi-media technologies for providing health services and public health systems. Some scholars consider mobile health as a subsystem of health technology which, due to the existing conditions, has become more significant compared to other interventions in this field. The present study intends to investigate the global approach on mobile health technology on the one hand, and its benefits and challenges on the other. Materials and Methods: As a comparative-descriptive study conducted in 2011, the present study has tried to explore mhealth technology strategies in public health domain, different types of mhealth interventions and benefits of using mhealth as well as its challenges and obstacles. The data were collected through informational sources such as articles, books, magazines and valid websites. Then, the status of the countries were compared and analyzed as far as the development of this technology is concened. Results:Based on the findings of the study, one of the criteria affecting the development of mhealth is the high penetration of mobile phone. By October, 2011, the estimated number of mobile users has been over 5 billion showing a penetration coefficient of 76. The review of the research on the obstacles and challenges experienced in moving towards the development of this technology by World Health Organization revealed that prioritization and increasing knowledge level are the most significant obstacles in the way to develop this technology. Discussions: Mhealth technology has been provided in most countries with the aim of promoting public health and accelerating the supply of health services. Having a penetration coefficient of over 90 in Iran, it can be predicted that this country can take effective steps towards development of this technology

Designing an organizational memory model for reporting the medical errors

Background: The increasing growth in the volume of the data in the organizations and the resultant challenges due to medical errors during the last two decades have made the necessity of reporting and managing medical errors more apparent. Organizational memory (OM) has been known as one of the tools appropriate for implementing knowledge management. The goal of the present study is to design an organizational memory model for medical departments of the teaching and medical centers of Charmahal va Bakhtiyari province in Iran. Materials and Methods: This study is descriptive - applied in nature and its population consisted of the personnel of teachingmedical centers in Charmahal va Bakhtiyari province. Identifying the processes was performed through observation and the required data for identifying and reporting the medical errors was collected through conducting one structured interview with 65 personnel from the medical departments of 5 centers under research. OMs were derived through library research and online search. Based on the results of need-analysis and reviewing of the models, the proposed model was prepared and then was judged and evaluated by the medical professionals through Delphi test technique. Results: The personnel who took part in the study believed if they have access to the data and information required for reporting the medical errors, they will have a better performance (85). they regarded the use of organizational memory as a necessity (98) and enumerated the occurrence of errors, slowness of the work, irregularity, discontent and wonderlessness of the customers as some challenges resulting from human error and system fault (86). Discussions: Organizational memory system which relates organizational knowledge to job functions related to reporting the errors not to recognize the wrongdoer but to prevent error repetition, is one of the requirements of the medical centers which can promote the efficiency and organizational learning

Applying Proteomics to Study Crosstalk at the Cartilage-Subchondral Bone Interface in Osteoarthritis: current Status and Future Directions

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Glucose transporter Glut-1 is detectable in pen-necrotic regions in many human tumor types but not normal tissues: Study using tissue microarrays

The hypoxic tumor microenvironment is associated with malignant progression and poor treatment response. The glucose transporter Glut-1 is a prognostic factor and putative hypoxia marker. So far, studies of Glut-1 in cancer have utilised conventional immunohistochemical analysis in a series of individual biopsy or surgical specimens. Tissue microarrays, however, provide a rapid, inexpensive means of profiling biomarker expression. To evaluate hypoxia markers, tissue cores must show architectural features of hypoxia, i.e. viable tissue surrounding necrotic regions. Glut-1 may be a useful biomarker to validate tissue microarrays for use in studies of hypoxia-regulated genes in cancer. In this study, we carried out immunohistochemical detection of Glut-1 protein in many tumor and normal tissue types in a range of tissue microarrays. Glut-1 was frequently found in peri-necrotic regions, occurring in 9/34 lymphomas, 6/12 melanomas, and 5/16 glioblastomas; and in 43/54 lung, 22/84 colon, and 23/60 ovarian tumors. Expression was rare in breast (6/40) and prostate (1/57) tumors, and in normal tissue, was restricted to spleen, tongue and CNS endothelium. In conclusion, tissue microarrays enable the observation of Glut-1 expression in peri-necrotic regions, which may be linked to hypoxia, and reflect previous studies showing differential Glut-1 expression across tumor types and non malignant tissue

Gastrointestinal malformations in Gorgan, North of Iran: Epidemiology and associated malformations

The aim of this prospective study was to evaluate the prevalence and pattern of gastrointestinal malformations (GIM) among Iranian newborns in Gorgan, North of Iran. From 1998 through 2003, 37,951 live births in Dezyani hospital in Gorgan, North of Iran, were screened for gastrointestinal malformations. Clinical and demographic factors of diagnosed cases were recorded in a pre-designed questionnaire for analysis; sex, ethnicity, type of GIM and associated anomalies. The overall prevalence rate of gastrointestinal malformations was 10 per 10,000 births. The imperforate anus (5 per 10,000) was the commonest birth defect in gastrointestinal tract. The prevalence rate of GIM was 8.2 per 10,000 in males and 10.7 per 10,000 in females. According to the parental ethnicity, the prevalence rates of GIM were 6.7, 15.8 and 17.6 per 10,000 in Fars, Turkman, and Sistani, respectively. There were eight cases (21%) with associated anomalies. The prevalence rate of GIM in North of Iran is not similar to the previous studies in Iran and Middle East and ethnic background may be a causative factor in the rate of GIM in this area. © 2006 Springer-Verlag

Carprofen inhibits the release of matrix metalloproteinases 1, 3, and 13 in the secretome of an explant model of articular cartilage stimulated with interleukin 1β

Introduction: Arthritic diseases are characterized by the degradation of collagenous and noncollagenous extracellular matrix (ECM) components in articular cartilage. The increased expression and activity of matrix metalloproteinases (MMPs) is partly responsible for cartilage degradation. This study used proteomics to identify inflammatory proteins and catabolic enzymes released in a serum-free explant model of articular cartilage stimulated with the pro-inflammatory cytokine interleukin 1β (IL-1β). Western blotting was used to quantify the release of selected proteins in the presence or absence of the cyclooxygenase-2 specific nonsteroidal pro-inflammatory drug carprofen. Methods: Cartilage explant cultures were established by using metacarpophalangeal joints from horses euthanized for purposes other than research. Samples were treated as follows: no treatment (control), IL-1β (10 ng/ml), carprofen (100 μg/ml), and carprofen (100 μg/ml) + IL-1β (10 ng/ml). Explants were incubated (37°C, 5% CO2) over twelve day time courses. High-throughput nano liquid chromatography/mass spectrometry/mass spectrometry uncovered candidate proteins for quantitative western blot analysis. Proteoglycan loss was assessed by using the dimethylmethylene blue (DMMB) assay, which measures the release of sulfated glycosaminoglycans (GAGs). Results: Mass spectrometry identified MMP-1, -3, -13, and the ECM constituents thrombospondin-1 (TSP-1) and fibronectin-1 (FN1). IL-1β stimulation increased the release of all three MMPs. IL-1β also stimulated the fragmentation of FN1 and increased chondrocyte cell death (as assessed by β-actin release). Addition of carprofen significantly decreased MMP release and the appearance of a 60 kDa fragment of FN1 without causing any detectable cytotoxicity to chondrocytes. DMMB assays suggested that carprofen initially inhibited IL-1β-induced GAG release, but this effect was transient. Overall, during the two time courses, GAG release was 58.67% ± 10.91% (SD) for IL-1β versus 52.91% ± 9.35% (SD) with carprofen + IL-1β. Conclusions: Carprofen exhibits beneficial anti-inflammatory and anti-catabolic effects in vitro without causing any detectable cytotoxicity. Combining proteomics with this explant model provides a sensitive screening system for anti-inflammatory compounds

Ameliorative effects of PACAP against cartilage degeneration. Morphological, immunohistochemical and biochemical evidence from in vivo and in vitro models of rat osteoarthritis

© 2015 by the authors; licensee MDPI, Basel, Switzerland. Osteoarthritis (OA); the most common form of degenerative joint disease, is associated with variations in pro-inflammatory growth factor levels, inflammation and hypocellularity resulting from chondrocyte apoptosis. Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide endowed with a range of trophic effects in several cell types; including chondrocytes. However; its role in OA has not been studied. To address this issue, we investigated whether PACAP expression is affected in OA cartilage obtained from experimentally-induced OA rat models, and then studied the effects of PACAP in isolated chondrocytes exposed to IL-1β in vitro to mimic the inflammatory milieu of OA cartilage. OA induction was established by histomorphometric and histochemical analyses. Changes in PACAP distribution in cartilage, or its concentration in synovial fluid (SF), were assessed by immunohistochemistry and ELISA. Results showed that PACAP abundance in cartilage tissue and SF was high in healthy controls. OA induction decreased PACAP levels both in affected cartilage and SF. In vitro, PACAP prevented IL-1β-induced chondrocyte apoptosis, as determined by MTT assay; Hoechst staining and western blots of apoptotic-related proteins. These changes were also accompanied by decreased i-NOS and COX-2 levels, suggesting an anti-inflammatory effect. Altogether, these findings support a potential role for PACAP as a chondroprotective agent for the treatment of OA

Spatial distribution of multiple sclerosis disease

زمینه و هدف: مالتیپل اسکلروزیس (MS) یک بیماری نورولوژیکی مزمن سیستم اعصاب مرکزی می باشد که بوسیله التهاب، تخریب میلین و آسیب اکسونی مشخص می شود. هدف از این تحقیق تعیین کلی شیوع مکانی-فضایی این بیماری در استان چهار محال و بختیاری می باشد. روش بررسی: در این مطالعه توصیفی و تحلیلی 479 مورد بیمار که بین سال های 1371 تا پایان سال 1390 بر اساس فاکتورهای تشخیصی MC Donald WI به طور قطعی در گروه تشخیصی بیماری قرار گرفته بودند وارد مطالعه و اطلاعات سن، جنس، سال تشخیص بیماری و آدرس آن ها از پرونده بیماران استخراج گردید. پس از جمع آوری اطلاعات بیماری و داده های مکانی، شروع به ساختن نقشه توزیع جغرافیایی بیماری نموده و با محاسبه شیوع و استاندارد کردن بیماری بر حسب جمعیت، نقشه شیوع بیماری در شهرستان ها و بخش های استان تهیه شد. نقشه سازی در محیط نرم افزار Arc GIS صورت گرفت. برای نقشه سازی شیوع بیماری از روشquantitie (مقادیر موجود) استفاده گردید. یافته ها: شهرستان شهرکرد با 7/59 بیشترین و شهرستان کوهرنگ با 1 کمترین تعداد بیماری را داشتند. در بخش های بازفت، میانکوه و منج هیچگونه مورد بیماری وجود نداشت. توزیع بیماری بیشتر در سمت شرق و شمال شرق استان بود. میزان شیوع در شهرستان شهرکرد 95/87 و در لردگان 84/11 در هر صدهزار نفر بود که بیشترین و کمترین میزان شیوع را به خود اختصاص داده اند. نتیجه گیری: توزیع و شیوع بیشتر بیماری در نیمه شرقی استان می تواند به دلیل شهرهای بزرگی همچون شهرکرد، بروجن و فرخشهر باشد، لذا به نظر می رسد MS یک بیماری است که بیشتر در مناطق شهری شیوع پیدا می کند، همچنین در این مطالعه با توجه به شیوع پایین تر بیماری در مناطق سردسیر، لازم است در مطالعات بعدی علاوه بر وجود جمعیت، عوامل محیطی مکانی نیز بررسی گردن

Clusterin secretion is attenuated by the proinflammatory cytokines interleukin‐1β and tumor necrosis factor‐α in models of cartilage degradation

The protein clusterin has been implicated in the molecular alterations that occur in articular cartilage during osteoarthritis (OA). Clusterin exists in two isoforms with opposing functions, and their roles in cartilage have not been explored. The secreted form of clusterin (sCLU) is a cytoprotective extracellular chaperone that prevents protein aggregation, enhances cell proliferation and promotes viability, whereas nuclear clusterin acts as a pro-death signal. Therefore, these two clusterin isoforms may be putative molecular markers of repair and catabolic responses in cartilage and the ratio between them may be important. In this study, we focused on sCLU and used established, pathophysiologically relevant, in vitro models to understand its role in cytokine-stimulated cartilage degradation. The secretome of equine cartilage explants, osteochondral biopsies and isolated unpassaged chondrocytes was analyzed by western blotting for released sCLU, cartilage oligomeric protein (COMP) and matrix metalloproteinases (MMP) 3 and 13, following treatment with the proinflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α. Release of sulfated glycosaminoglycans (sGAG) was determined using the dimethylmethylene blue assay. Clusterin messenger RNA (mRNA) expression was quantified by quantitative real-time polymerase chain reaction. MMP-3, MMP-13, COMP, and sGAG release from explants and osteochondral biopsies was elevated with cytokine treatment, confirming cartilage degradation in these models. sCLU release was attenuated with cytokine treatment in all models, potentially limiting its cytoprotective function. Clusterin mRNA expression was down-regulated 7-days post cytokine stimulation. These observations implicate sCLU in catabolic responses of chondrocytes, but further studies are required to evaluate its role in OA and its potential as an investigative biomarker

Benzamil sensitive ion channels contribute to volume regulation in canine chondrocytes

Background and Purpose: Chondrocytes exist within cartilage and serve to maintain the extracellular matrix. It has been postulated that osteoarthritic (OA) chondrocytes lose the ability to regulate their volume, affecting extracellular matrix production. In previous studies, we identified expression of epithelial sodium channels (ENaC) in human chondrocytes, but their function remained unknown. Although ENaC typically has Na+ transport roles, it is also involved in the cell volume regulation of rat hepatocytes. ENaC is a member of the degenerin (Deg) family, and ENaC/Deg-like channels have a low conductance and high sensitivity to benzamil. In this study, we investigated whether canine chondrocytes express functional ENaC/Deg-like ion channels and, if so, what their function may be. Experimental Approach: Canine chondrocytes were harvested from dogs killed for unassociated welfare reasons. We used immunohistochemistry and patch-clamp electrophysiology to investigate ENaC expression and video microscopy to analyse the effects of pharmacological inhibition of ENaC/Deg on cell volume regulation. Key Results: Immunofluorescence showed that canine chondrocytes expressed ENaC protein. Single-channel recordings demonstrated expression of a benzamil-sensitive Na+ conductance (9 pS), and whole-cell experiments show this to be approximately 1.5 nS per cell with high selectivity for Na+. Benzamil hyperpolarized chondrocytes by approximately 8 mV with a pD2 8.4. Chondrocyte regulatory volume decrease (RVI) was inhibited by benzamil (pD2 7.5) but persisted when extracellular Na+ ions were replaced by Li+. Conclusion and Implications: Our data suggest that benzamil inhibits RVI by reducing the influx of Na+ ions through ENaC/Deg-like ion channels and present ENaC/Deg as a possible target for pharmacological modulation of chondrocyte volume