فهرست مطالب

  • Volume:6 Issue:2, 2013
  • تاریخ انتشار: 1391/11/01
  • تعداد عناوین: 6
  • Navid Goodarzi, Mohammad Hossein Ghahremani, Rassoul Dinarvand Page 65
  • Hamid Abdollahia, Maryam Teymouria, Sara Khademib Page 66
    The biological effects of space radiations on astronauts are the main concern in deep space missions. Many investigations have been made to find the best way to overcome those problems in extended space travels. There are some studies showing that radiofrequency radiation can induce adaptive responses in human cells and animals during which they become more resistant against challenging doses of mutagenic agents such as high levels of radiation. We suggest that radiofrequency radiation as an agent that induces adaptive response may help astronauts in space flights. Exposure to radiofrequency radiation before or during space missions while choosing the optimised dosimetric parameters such as determined power density and frequency and duration of exposure can help astronauts in their travels.
    Keywords: Radiofrequency radiation, Space mission, Astronauts, Adaptive response, Hypothesis
  • Rovshan M. Ismailovcorresponding Page 70
    Global variation in heart failure (HF) prevalence and mortality rates is evident and multiple factors have been hypothesised to explain such non-random distribution. The author hypothesised that this non-random HF distribution could be attributed, in part, to individual variation in the level of erythropoietin (EPO), a hormone and a possible cardioprotectant. Such individual EPO variation can be explained by hypoxia resulting from regional differences in geographic elevation. This hypothesis was justified using results from various animal-based and clinical studies. In addition, data from the population-based Healthcare Cost and Utilization Project was used. The global distribution of HF can be explained, in part, by the geographic landscape. Prospective studies based on the author’s hypothesis may provide new treatment opportunities for such an important health issue as HF. In addition, this hypothesis may demonstrate new insights into the mechanism of HF.
    Keywords: Erythropoietin, Heart failure, Altitude
  • Zahra Piria, Abdolreza Esmaeilzadehb, Mehri Hajikhanmirzaeic Page 75
    Pancreatic cancer is an aggressive type of malignancy. Generally, its promotion and progression are due to the disturbance in some cellular and molecular mechanisms, particularly deregulation of programmed cell death or apoptosis. Certainly, loss of counterbalance between generation and cell death will lead to the tumoural mass development in various tissues, such as pancreas.From earlier decades, a variety of treatments as chemotherapy, radiation and surgery have been employed in order to pancreatic cancer remedial purposes, which are associated with infirm medical outcome. Therefore, with regard to the anti-cancerous and pro-apoptotic properties of the cytokine interleukin-25 (IL-25), the authors intend to anticipate a new therapeutic strategy. IL-25 – known as IL-17E – is one of the major factors responsible for death receptor-mediated pathway. Broadly, its receptor is located on multifarious cells such as pancreatic cancerous cells. We proposed to select four groups of C57BL/6 mice, for IL-25 gene inoculation, via mesenchymal stem cells as a vector, in order to increase exposure of cancerous cells to IL-25. IL-25 could activate apoptotic mediators including tumour necrosis factor receptor associated factor (TRAF6), Fas-Associated protein with Death Domain (FADD) and caspases consequently. Probably this method will be efficient in pancreatic malignancy treatment, via inducing apoptosis in pancreatic tumoural cells.
    Keywords: Pancreatic cancer, IL, 25, Mesenchymal stem cells, Apoptosis, Syngeneic mice model, Immunotherapy
  • Muzammal Hussaina, Aqeel Javeeda, Muhammad Ashrafa, Amjad Riazb, Ijaz Alic, Aamir Ghafoord Page 80
    The pathobiology of allergic bronchial asthma is mediated by over-expressed T helper type 2 (Th2)-biased immune responses to harmless environmental antigens, leading to airway inflammation and hyper-responsiveness. These Th2 responses are normally suppressed by functional T regulatory cells (Tregs), which maintain the airway tolerance. However, the Tregs activity is conceived to be compromised in allergic asthmatics. The curative therapy to counteract this immune dysregulation is not available so far, and to devise such a remedy is the current research impetus in allergic asthma therapeutics. One of the novel insights is to consider a Tregs-directed immunoregulatory therapy that could harness endogenous Tregs to redress the Th2/Tregs imbalance, thus enhancing the airway tolerance. Aspirin or acetylsalicylic acid (ASA) is a prototype non-steroidal anti-inflammatory drug that possesses intriguing immunopharmacological attributes. For example, it can enhance the number or the frequency of functional Tregs, especially natural CD4+ CD25+ FoxP3+ Tregs, either directly or by inducing tolerogenic activity in dendritic cells (DCs). It is also considered to be beneficial for the induction of immunological tolerance in autoimmunity and graft rejection. This raises the question whether ASA, if exploited optimally, may be used to induce and harness endogenous Tregs activity for redressing Th2/Tregs imbalance in allergic asthma. In this paper, we hypothesise that ASA may help to counteract the underlying immune dysregulation in allergic asthma by promoting airway tolerance. Nevertheless, the future research in this regard will selectively need to be targeted to allergic asthma models, which are ASA insensitive, as ASA has some adverse background and is contraindicated in asthmatics who are sensitive to it.
    Keywords: Aspirin, Allergic asthma, Airway tolerance, Regulatory T cells
  • Tehseen Fatima Alia, Tabinda Hasanb Page 85
    Osteogenesis imperfecta as the name suggests, is a bone disorder characterised by imperfect bone mineralisation and development. The key defect lies in the osteoblast–osteoid cycle, leading to insufficient calcification and consequently weak bones. Osteogenesis imperfecta patients are prone to fractures. Till date, numerous growth hormone/synthetic analogues have been used therapeutically in osteogenesis imperfecta patients and they do provide temporary relief, but not without numerous unwanted side effects. The intervention offered by such treatments is mainly at the symptomatic level, with temporary pain relief and some degree of mineralisation of available osteoids; but the root cause of the disease remains unattended. Such treatment modalities fail to promote mesenchymal stem cell osteogenic differentiation and tackle the fundamental deficiency of osteoids. This paper suggests a unique and hitherto unimplemented approach for treatment of osteogenesis imperfecta at the cellular level through application of a natural source, ‘Brown algae isolated phlorotannins’, which promote mesenchymal stem cell differentiation by increasing alkaline phosphatase activity, calcific mineralisation and total protein and collagen synthesis. This natural extract, when integrated directly with mesenchymal stem cells, will boost cellular differentiation into healthy bone-forming cells. The modality will strengthen the bone intrinsically and without the adverse reactions of routine pharmacotherapeutic agents.
    Keywords: Osteogenesis imperfecta, Mesenchymal stem cell, Osteoblast, Phlorotannin, Brown Algae