بررسی اثر مینوکسیدیل روی تکثیر و بقاء سلولهای بنیادی فولیکول موی موش سوری

سلولهای بنیادی فولیکول مو (HFSCs)، نقش اساسی در مورفوژنز فولیکول مو دارد، این سلولها قابلیت خود تکثیری داشته و پتانسیل تبدیل به اپیدرم، غدد سباسه و فولیکول مو را دارند. HFSCs در ناحیه Bulge که قسمتی از غلاف ریشه ای خارجی فولیکول مو است قرار دارند (1, 2). سلولهای بنیادی ناحیه Bulge خاصیت نگهدارنده لیبل (lRC)، را داشته و این سلولها سیکل رشد کندی در In vivo دارند . مطالعه روی سلولهای بنیادی فولیکول مو اهمیت زیادی در پزشکی ترمیمی مو دارد(3,4).\ud مینوکسیدیل مشتق پیریمیدینی است که در ابتدا بعنوان ماده کاهنده فشار خون مطرح بود، مینوکسیدیل باعث اتساع عروق محیطی می شود و بعنوان ماده تقویت کننده رشد فولیکول مو عمل می کند و رایجترین داروی مورد استفاده در آلوپسی آندروژنیک مطرح است، اثر موضعی مینوکسیدیل، بخاطر عمل مستقیم دارو است که باعث تحریک رویش مو می شود و اثرات غیر مستقیم آن شامل، گشاد کردن عروق و افزایش جریان خون پاپیلای درمی است(5). \ud مینوکسیدیل با روش های زیر باعث طولانی شدن فاز آناژن فولیکول مو می شود: الف) باعث القاء فاکتورهای رشدی مثل IGF-1, HGF, VEGF می شود، ب) با باز کردن کانالهای پتاسیمی باعث جلوگیری از آپوپتوز می شود و ج) شریان های فولیکول مو را گشاد کرده و جریان خون پاپیلای درمی را با اثر روی عضلات صاف جدار عروق افزایش می دهد(6,7).\ud محققان نشان داده اند که مینوکسیدیل، فولیکول موی در تلوژن را تحریک می کند و آن را بطرف آناژن سوق می دهد. و محققان دیگری نشان دادند که مینوکسیدیل کانال پتاسیمی را باز می کند و باعث رشد مستقیم مو می شود(8,9). با این حال اطلاعات کمی در مورد اثرات فارماکولوژیک این دارو و اثر آن روی سلولهای بنیادی فولیکول مو وجود دارد. در این مطالعه ما قصد داریم اثر دوزهای مختلف مینوکسیدیل را روی سلولهای بنیادی جدا شده از ناحیه Bulge موش سوری بررسی کنی

Trifluoperazine an Antipsychotic Drug and Inhibitor of Mitochondrial Permeability Transition Protects Cytarabine and Ifosfamide-Induced Neurotoxicity

The link between Ca2+ dysregulation, mitochondria damages, oxidative stress and cellular derangement is particularly evident in neurotoxicity induced by chemotherapeutic agents. In the current study, we investigated effects of trifluoperazine (TFP) as an inhibitor of calmodulin against the cytotoxicity induced by cytarabine (Ara-C) and Ifosfamide (IFOS) on isolated rat neurons and also the mechanisms involved in this toxicity. Isolated rat neurons were pretreated with TFP (100 µM) for 5 min at 37°C, then Ara-C (226 µM) and IFOS (290 µM) were added in separate experiments. After 3 h, the cytotoxicity, reactive oxygen species (ROS), lysosomal membrane destabilization, mitochondrial membrane potential (MMP), lipid peroxidation (LP), glutathione (GSH) and glutathione disulfide (GSSG) levels were measured. Ara-C and IFOS treatments caused a significant decrease in cellular viability, which was accompanied by ROS generation, GSSG/GSH ratio, lipid peroxidation and lysosomal and mitochondrial damages. On the other hand, TFP (100 µM) pre-treatment attenuated Ara-C and IFOS -induced decrease in cell viability. In addition, TFP (100 µM) pre-treatment significantly protected against Ara-C and IFOS -induced increase in ROS generation, lysosomal and mitochondrial damages, lipid peroxidation levels and decrease in GSH/GSSG ratio. Our data provided insights into the mechanism of protection by TFP against Ara-C and IFOS neurotoxicity, which is related, to neuronal ROS formation and mitochondrial damages

Needs assessment in research, Needs research

Background: There are many indications that there is a significant gap between the findings and information from the research and the actual needs of the gap. The need to identify basic issues and to carry out effective research around these issues is a research need research because this can be fruitful by the fact that human capital invests in solving real life problems. Research needs assessment is a complex and challenging process that begins by identifying potential research needs, with the prioritization of these needs, and will eventually be completed by providing a basis for allocating available resources to research topics. On the other hand, the design and implementation of need-level projects at each level requires the follow-up of a specific research design and pattern. An appropriate pattern should specify the purpose and scope of the implementation methods and other dimensions necessary for conducting a research need-assessment project. Method: The present study was conducted in a review using electronic and non-electronic sources of the past 10 years. RESULTS: The objectives of the research need-assessment, the establishment of the necessary framework for the application of research results and results through non-strategic implementation in the field of research; the basis for connecting and connecting as many decisions and researches through the basic research required by the organization or ministry; Research is based on the participation of all groups and factors involved in the organization. Today, there are different patterns of research projects in need assessment that are used by planners, but despite the diversity of the aforementioned patterns, none is superior to each other and their suitability depends on the educational and health project. Conclusion: The inappropriate allocation of resources and research credits will result in various and frequent damages and costs in the field of health. Therefore, the need assessment as a systematic method for identifying the needs of different areas and proposing measures that can address such needs It is considered that, since different subjects and objectives require different approaches and methods of need assessment, it requires a combination of qualitative and quantitative research methods for data collection and the use of existing information

Pathogenic Mechanisms and Therapeutic Implication in Nickel-induced Cell Damage

BACKGROUND:Nickel (Ni) is mostly applied in plenty industrial sections like printing inks, welding, alloy, electronics and electrical professions. Occupational or environmental exposure to nickel may lead to cancer, allergy reaction, nephrotoxicity, hepatotoxicity, neurotoxicity as well as cell damage, apoptosis and oxidative stress. METHOD:In here we focused on published studies about cell death, carcinogenicity, allergy reactions and neurotoxicity, and promising agents for prevention and treatment the toxicity by Ni. RESULTS:Our review showed that in last years, more researches have focused on reactive oxygen species formation, oxidative stress, DNA damages, apoptosis, interaction with involving receptors in allergy and mitochondrial damages in neuron induced by Ni. CONCLUSION:The gathering data in this paper provides useful information about the main toxicities induced by Ni also, their fundamental mechanisms, and how to discover new ameliorative agents for prevention and treatment, by reviewing agents with protective and therapeutic consequences on Ni induced toxicity