The effects of glial cells inhibition on spatial reference, reversal and working memory deficits in a rat model of traumatic brain injury (TBI).

AIMS: Evidence suggests that glial cells are influenced by Traumatic brain injury (TBI). Both protective and damaging roles have been attributed to reactive glial cells, but their role after TBI has not been well understood. In this study, the role of glial cells in TBI-induced cognitive impairment was investigated. MATERIALS AND METHODS: Male rats were randomly assigned to the following groups: Sham + PBS, sham + FC, TBI + PBS, and TBI + FC. FC (1 nmol/1 µl), a glial cell inhibitor, was injected into the lateral ventricle 10 min after TBI induction and it was repeated every 24 h until the seventh day. On days 8-13 post-injury, reference and reverse memory and on days 8-16 post-injury, working memory was assessed using the Morris water maze test. RESULTS: Brain-injured rats exhibited significant impairments in acquisition and retrieval phases of reference and reverse memory compared to sham rats and FC administration could not attenuate the deteriorative effect of TBI in different learning tasks. TBI rats showed impairment in acquisition (but not retrieval) of working memory. Sham animals which received FC showed a deficit in reversal memory acquisition and retrieval of reference memory compared to sham + PBS rats. CONCLUSION: The present study demonstrates that memory deficit induced by TBI cannot be improved by FC, and glial cells inhibition in uninjured animals causes impairments in reversal memory acquisition and retrieval of reference memory. Our results suggest that in addition to essential role of glial cells for memory formation in normal situation, their responses after TBI may have preventive effect against memory impairments.

HIWI2 rs508485 Polymorphism Is Associated with Non-obstructive Azoospermia in Iranian Patients.

BACKGROUND: The PIWI-interacting RNA (piRNA) pathway has an essential role in transposon silencing, meiosis progression, spermatogenesis, and germline maintenance. HIWI genes are critical for piRNA biogenesis and function. Therefore, polymorphisms in HIWI genes contribute to spermatogenesis defects and can be considered as risk factors for male infertility. The aim of the present study was to investigate the association between the HIWI2 gene rs508485 polymorphism and non-obstructive azoospermia. METHODS: A total of 121 Iranian men with idiopathic azoospermia and 100 fertile controls were genotyped for HIWI2 rs508485 (T>C) polymorphism using Tetra-ARMS PCR. The presence of eight sequence-tagged site (STS) markers from the Y chromosome AZF region was also investigated by Multiplex PCR (M-PCR). RESULTS: Thirteen (10.74%) patients showed Y chromosome microdeletions and therefore were excluded from the study. rs508485 in the 3'UTR of HIWI2 was associated with increased risk of azoospermia in our studied population with a P-value of 0.035 and odds ratio of 2.00 (CI 95%: 1.04-3.86). CONCLUSIONS: We provide evidence for an association between genetic variation in the HIWI2 gene involved in the piRNA pathway and idiopathic non-obstructive azoospermia in Iranian patients. Therefore, piRNA pathway gene variants can be considered as risk factors for male infertility.

TRAIL gene expression analysis in multiple sclerosis patients.

BACKGROUND: Multiple sclerosis (MS) as an autoimmune disorder in which the insulating covers of neurons in the Central Nervous System are destructed. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is an immunomodulatory molecule to protect against T cells hyper activation. METHODS: In this Case-control study, we compare TRAIL gene expression in peripheral blood between 50 relapse remitting MS patients and 50 healthy controls by TaqMan Real time PCR. All the patients were negative for HLA-DRB1*15 susceptible allele, normal serum vitamin D, responder to Interferon beta. All the health individuals were matched to patients. Also, we tried to find correlation between TRAIL gene expression and clinical characteristics of patients. RESULTS: No statistically significant difference was found in TRAIL mRNA expression between MS patients and controls (p> 0.05). There was no correlation in the TRAIL expression and age of onset, disease duration and Expanded Disability Status Scale of Kurtzke (EDSS). As IFN-b may have stimulatory effects on immunoregulatory function of TRAIL and all of our patients were treated with interferon beta and were responder, it lead to no significant change in TRAIL expression. We suggest comparing between responders and non-responders should be investigated.