Organic Food & Farming in Iran

An article on Irans Geography, agriculture and socio-economic condition, the historical development of the organic sector in Iran, its production structure and type of output as well as markets and future prospects

In silico prediction discontinuous B cell epitope peptide vaccine against leishmaniasis

Introduction: The kinetoplastid protozoan parasites of the genus Leishmania cause diseases for which treatment is difficult and there is still no vaccine for use in humans. Leishmanolysin is the major enzymatic protein component of the promastigote surface. Because of its role as a ligand involved in the interaction of the parasite with defensive systems of the host, including components of the complement system and the macrophage surface is an attractive candidate for designing peptide vaccines.  Methods and Results: In the current study, PEPOP was used to predict peptides from Leishmanolysin in the form of discontinuous B-cell epitopes. PEPOP identified segments comprised of accessible and sequence continuous amino acids. These segments were clustered according to their spatial distances using method of extensions: Optimized Nearest Neighbor (ONN), Optimized Flanking Nearest Neighbor (OFN), Optimized Patched segments Path (OPP), Traveling Salesman Problem (TSP), and Shortest Path (SHP). Each peptide sequence has been generally comprised of several segments. From 3D structure of Leishmanolysin, PEPOP identified 100 segments gathered in three clusters according to their spatial distances. In this study, we wanted to predict peptides from a specific region of the protein, the residue 264-345 on the active site of Leishmanolysin. It corresponds to the segments S34 to S48. The predicted peptides, which did not relate to this region (264-345) were removed and at last 29 peptides were selected. Conclusions: These results using bioinformatics analyses could be conducted in vaccine design against Leishmania infections

Positive correlation between ELF and RFelectromagnetic fieldon cancer risk

Extremely low frequency (ELF) and Radio frequency (RF) electromagnetic field may affect biological systems by raising generation free radicals by decline activities of glutathione peroxidase dismutase or increase in the lifetime of free radicals with inhibited pretreatment of cells antioxidant like that alpha tocopherol. ELF and  RF electromagnetic  field maycan damaged DNA  with raising level  hydroxyl radicals in cells and  it is  can interact DNA and form mainly 8-hydroxy-2′–deoxyguanosine( 8-OHdG) adducts. Many study showed   Electromagnetic field radiation(EMF) can change gene expression and conformation of protein. It may declineexpression of some genes such as superoxide dismutase orraise expressionof certain genes such as Hsps (heat shock proteins). ELF and RFelectromagnetic field   can effects on homeostasis Ca2+ and alteration in important cellular and molecular processes such as differentiation, proliferation, gene expression, cytoskeletal reorganization and metabolism. Use of radio frequency electromagneticfield onsatellite jamming in Iran and some country may can harmful to human health and it could be a risk factor for cancer

Association between ELF and RF electromagnetic field and Leukemia

     Extremely low frequency (ELF) electromagnetic field (ELF-EMFs) are widely employed in electrical appliances and different equipment such as television sets, ELF-EMFs can  affect biological systems by increasing production  ROS. The altered balance between ROS generation and elimination plays a critical role in a variety of pathologic conditions. ROS levels have been observed in several hematopoietic malignancies including acute and chronic myeloid leukemia. ELF-EMFs exposure significantly decreased Nitric oxide synthase (iNOS) protein expression Lower levels of NO have been demonstrated to exert a protective function in leukemic and melanoma cells and to inhibit effector caspases by S-nitrosylation. Also ELF-EMFs can decrease melatonin production by effects on N-acetyltransferase. Melatonin is an antioxidant, effective in protecting nuclear DNA. Transmitters emitting radio frequency electromagnetic fields (RF-EMFs) are usually not located in populated areas but some epidemiology studies showed association distance transmitters from residential area and leukemia.

Identification of B and T cell epitope peptide vaccines from IGF-1 Receptor in breast cancer

Introduction: The insulin-like growth factor-1 receptor (IGF-1R) plays a key role in proliferation, growth, differentiation, and development of several human malignancies including breast and pancreatic adenocarcinoma. IGF-1R targeted immunotherapeutic approaches are particularly attractive, as they may potentially elicit even stronger antitumor responses than traditional targeted approaches. Cancer peptide vaccines can produce immunologic responses against cancer cells by triggering helper T cell (Th) or cytotoxic T cells (CTL) in association with Major Histocompatibility Complex (MHC) class I or II molecules on the cell surface of antigen presenting cells.  Methods and Results: In our previous study, we set a technique based on molecular docking in order to find the best MHC class I and II binder peptides using GOLD. In the present work, molecular docking analyses on a library consisting of 30 peptides mimicking discontinuous epitopes from IGF-1R extracellular domain identified peptides 249 and 86, as the best MHC binder peptides to both MHC class I and II molecules. The receptors most often targeted by peptide 249 are HLA-DR4, HLA-DR3 and HLA-DR2 and those most often targeted by peptide 86 are HLA-DR4, HLA-DP2 , and HLA-DR3. Conclusions: These findings, based on bioinformatics analyses, can be conducted in further experimental analyses in cancer therapy and vaccine design

The neuroprotective effects of targeting key factors of neuronal cell death in neurodegenerative diseases: The role of ER stress, oxidative stress, and neuroinflammation

Neuronal loss is one of the striking causes of various central nervous system (CNS) disorders, including major neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and Amyotrophic lateral sclerosis (ALS). Although these diseases have different features and clinical manifestations, they share some common mechanisms of disease pathology. Progressive regional loss of neurons in patients is responsible for motor, memory, and cognitive dysfunctions, leading to disabilities and death. Neuronal cell death in neurodegenerative diseases is linked to various pathways and conditions. Protein misfolding and aggregation, mitochondrial dysfunction, generation of reactive oxygen species (ROS), and activation of the innate immune response are the most critical hallmarks of most common neurodegenerative diseases. Thus, endoplasmic reticulum (ER) stress, oxidative stress, and neuroinflammation are the major pathological factors of neuronal cell death. Even though the exact mechanisms are not fully discovered, the notable role of mentioned factors in neuronal loss is well known. On this basis, researchers have been prompted to investigate the neuroprotective effects of targeting underlying pathways to determine a promising therapeutic approach to disease treatment. This review provides an overview of the role of ER stress, oxidative stress, and neuroinflammation in neuronal cell death, mainly discussing the neuroprotective effects of targeting pathways or molecules involved in these pathological factors

Neuroprotective effect of cannabidiol on NTF-3 and IGF-1 genes expression

739-743Cannabidiol is a herbal compound that has been found to be effective in improvement of inflammatory demyelinating diseases and could be useful to increase supportive factors in remyelination. It is derived from Cannabis sativa known as Marijuana. The aim of this research was to investigate the changes in the expression of neuroprotective NTF-3 and IGF-1 genes with focus on multiple sclerosis (MS) disease after treating U373-MG glial cells with cannabidiol. In this regard U373-MG astrocyte cells were treated at timescales of 24 h, 48 h, and 72 h with doses of cannabidiol, the total cellular RNA was extracted and converted into cDNA. Eventually, changes in NTF-3 and IGF-1 gene expressions were evaluated by quantitative real time polymerase chain reaction (qRT-PCR). The results supported the theory that very low doses of the drug are neuroprotective for glial cells and CNS. Probably cannabidiol fulfills it by stimulating the growth and differentiation of oligodendrocyte precursor cells to become mature oligodendrocytes. However, further research work and application of complementary techniques are necessary to ensure trust worthy in vivo and in vitro results

Neuroprotective effect of cannabidiol on NTF-3 and IGF-1 genes expression

Cannabidiol is a herbal compound that has been found to be effective in improvement of inflammatory demyelinating diseases and could be useful to increase supportive factors in remyelination. It is derived from Cannabis sativa known as Marijuana. The aim of this research was to investigate the changes in the expression of neuroprotective NTF-3 and IGF-1 genes with focus on multiple sclerosis (MS) disease after treating U373-MG glial cells with cannabidiol. In this regard U373-MG astrocyte cells were treated at timescales of 24 h, 48 h, and 72 h with doses of cannabidiol, the total cellular RNA was extracted and converted into cDNA. Eventually, changes in NTF-3 and IGF-1 gene expressions were evaluated by quantitative real time polymerase chain reaction (qRT-PCR). The results supported the theory that very low doses of the drug are neuroprotective for glial cells and CNS. Probably cannabidiol fulfills it by stimulating the growth and differentiation of oligodendrocyte precursor cells to become mature oligodendrocytes. However, further research work and application of complementary techniques are necessary to ensure trust worthy in vivo and in vitro results