Proteome analysis of rat hippocampus following morphine-induced amnesia and state-dependent learning

Morphine's effects on learning and memory processes are well known to depend on synaptic plasticity in the hippocampus. Whereas the role of the hippocampus in morphine-induced amnesia and state-dependent learning is established, the biochemical and molecular mechanisms underlying these processes are poorly understood. The present study intended to investigate whether administration of morphine can change the expression level of rat hippocampal proteins during learning of a passive avoidance task. A step-through type passive avoidance task was used for the assessment of memory retention. To identify the complex pattern of protein expression induced by morphine, we compared rat hippocampal proteome either in morphine-induced amnesia or in state-dependent learning by two-dimensional gel electerophoresis and combined mass spectrometry [MS and MS/MS]. Post-training administration of morphine decreased step-through latency. Pre-test administration of morphine induced state-dependent retrieval of the memory acquired under post-training morphine influence. In the hippocampus, a total of 18 proteins were identified whose MASCOT [Modular Approach to Software Construction Operation and Test] scores were inside 95% confidence level. Of these, five hippocampal proteins altered in morphine-induced amnesia and ten proteins were found to change in the hippocampus of animals that had received post-training and pre-test morphine. These proteins show known functions in cytoskeletal architecture, cell metabolism, neurotransmitter secretion and neuroprotection. The findings indicate that the effect of morphine on memory formation in passive avoidance learning has a morphological correlate on the hippocampal proteome level. In addition, our proteomic screen suggests that morphine induces memory impairment and state-dependent learning through modulating neuronal plasticity

Foxp3 gene expression in multiple sclerosis patients pre- and post mesenchymal stem cell therapy

Multiple Sclerosis [MS] is an inflammatory demyelinating and neurodegenerative disorder of the central nervous system [CNS], which mainly affects young adults. Activated T lymphocytes promote the neuro-inflammatory cascade of MS by secreting pro-inflammatory cytokines and play a significant role in its pathogenesis. T lymphocytes may trigger the inflammation, which in turn leads to axonal loss and neurodegeneration observed in the course of MS. Currently, there is no cure for MS, however, one of the most promising neuroprotective research tools consists of the use of bone marrow derived mesenchymal stem cells [MSC]. This method promotes immune system regulation and possibly induces neurological repair and re-myelination of the damaged axons. Recent studies have shown that MSC exert an immune regulatory function and induce T regulatory-cell proliferation, therefore, it may serve as a potentially useful treatment for immune-mediated diseases such as MS. In this pilot study a group of MS patients underwent MSC therapy and we assayed the expression of an X-linked transcription factor, FoxP3, as a specific marker of T Regulatory cells in peripheral blood, prior to and after the treatment. Using q RT-PCR for measurement of expression of FoxP3 by peripheral blood mononuclear cells, we found that in all subjects, except for one, the expression of FoxP3 at 6 months after intrathecal injection of MSC was significantly higher than the levels prior to treatment. Such significant enhanced expression of FoxP3 associated with clinical stability. Findings from this pilot study further support the potential of bone marrow derived MSC for treatment of MS patients

[HELLP syndrome: after delivery and favorable response to corticosteroid therapy: a case report in Bank Meli Iran hospital]

HELLP syndrome is a multisystem disease and a pregnancy complication consisting of Hemolysis, Elevated Liver enzyme level and low Platelet count. [1] We report on a patient with postpartum presentation. The patient was a 28 years old female at 30th wee, of her third pregnancy referred to bank melli hospital complaining of fever, chills, dysuria and frequency and admitted with diagnosis of urinary tract infection. After few days disease was progressed and abnormal laboratory tests ensued. Due to worsening general condition the pregnancy was terminated. After delivery platelet count decreased and she met all criteria of HELLP syndrome and received corticosteroid and the disease improved. Pathogenesis of HELLP syndrome is vague and there are different hypotheses all common in endothelial damage, vasospasm and coagulation system activation. This syndrome can present in the third trimester of pregnancy [%69] or after delivery [%31]. In most patient with post partum presentation, the disease is manifested during the first 48 hours after delivery. Corticosteroid therapy in all patient with complete HELLP syndrome [hemolysis, elevated liver enzyme level and low platelet count] is recommended. We reported on patient with complete HELLP syndrome presented post partum and good response to corticosteroid therapy

[Epigenetic of autoimmune diseases: a focus on systemic lupus erithematosis]

The genetic bases of most of the autoimmune diseases are identified with specified gene luci. Most of these diseases are multifactorial with considerable effect of environmental factors. But it is not yet obviously clear that how these factors can affect on genetic factors. These environmental mechanisms which affect on gene expression are called "epigenetics". In this article we will discuss about "epigenetics of autoimmune diseases

[Triplet repeats in human genome and neuromuscular diseases]

In recent years, a new mechanism of genetic disease has been discovered: the expansion of the triplet DNA sequences [tri-nucleotides] that either interrupt or compromise a gene. The presence of these expansions, sometimes containing thousands of tri-nucleotide repeats lead to processing of DNA and RNA that result in specific diseases. It remains mysterious that how this expansion in a single allele may exert a dominant effect and how the extent of the expansion increases the severity of the disease remain mysteries. This article describes a novel type of genome instability, expansion of tri-nucleotide repeats, originally discovered in 1991 upon cloning the gene responsible for fragile X syndrome. It has proved to be a general phenomenon responsible for a growing number of human neurological disorders. Besides apparent medical importance, the discovery of tri-nucleotide repeat expansion unraveled a fundamental problem in classical view of human genetics: a non-Mendelian type of inheritance called anticipation. Understanding the mechanisms of repeat expansion and the molecular pathways originally from these expansions expression to human diseases became a formidable task for modern biology. Here we discuss the major breakthroughs made in this field during the last decade, with an emphasis on molecular models of repeat expansion