Radioprotective effect of Cerebrolysin in the Rat's Brain Tissues.

AIM: The aim of this study is to evaluate radioprotective effects of Cerebrolysin (CBL) in rats' brain tissues after local irradiation. BACKGROUND: CBL has demonstrated antioxidant, anti-inflammatory, and tissue repair properties. In this study, the radioprotective effects of CBL in the brain tissues of rats after Irradiation (IR) (50 mg/ kg) were evaluated. OBJECTIVE: The levels of different oxidative stress markers, including malondialdehyde (MDA), nitric oxide (NO), glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) were examined after treatment with radiation and CBL. METHODS: First, 20 male adult Wistar rats weighing 180-200 g were used. The animals were exposed to a single fraction of 15Gy using a linear accelerator unit at a dose rate of 200 cGy/mine. In this study, to check the amount of oxidative stress following the IR, the level of four markers MDA, NO, GPx, CAT, and SOD were examined and measured using the spectrophotometric method and purchased kits. RESULTS: The results showed that compared to the IR group, the administration of CBL increases the levels of GPX and SOD significantly (p < 0.05). CONCLUSION: Our finding suggests that CBL has radioprotective effects on the brain by enhancing antioxidant defense mechanisms.

Efficiency of Hesperidin against Liver Fibrosis Induced by Bile Duct Ligation in Rats.

Introduction: Bile duct ligation (BDL) and subsequent cholestasis are associated with oxidative stress and liver injury and fibrosis. Hesperidin (3,5,7-trihydroxyflavanone 7-rhamnoglucoside) is a flavanone glycoside abundant in citrus fruits. It has positive effects on diabetic retinopathy, reduced platelet aggregation, and blood flow alterations and has the potential to reduce liver injury in oxidative stress. The aim of this study was to evaluate the hepatoprotective effects of hesperidin on BDL-induced liver injury in rats. Methods: A total of 48 adult male Wistar rats were equally allocated to six eight-rat groups, namely, a healthy group, a sham group, a BDL+Vehicle group (BDL plus treatment with distilled water), a BDL+VitC group (BDL plus treatment with vitamin C 4.25 µg/kg), a BDL+Hesp100 group (BDL plus treatment with hesperidin 100 mg/kg/day), and a BDL+Hesp200 group (BDL plus treatment with hesperidin 200 mg/kg/day). Treatments were orally provided for 21 consecutive days. Finally, rats were sacrificed through heart blood sampling. Blood samples were centrifuged, and liver function, oxidative stress, and antioxidant parameters were assessed. Liver tissue was also assessed for oxidative stress, antioxidant, and histological parameters. The expression of inflammatory genes, namely, TGFß1, iNOS, Caspase-3, and α-SMA, was measured through polymerase chain reaction. Findings. Hesperidin supplementation was associated with significant decrease in the levels of liver enzymes, bilirubin, nitric oxide, malondialdehyde, protein carbonyl, and inflammatory gene expression; significant increase in the levels of total antioxidant capacity, glutathione, and superoxide dismutase and catalase enzyme activity; and significant improvement in the histological morphology and structure of the liver parenchyma. Conclusion: Hesperidin has significant positive effects on liver morphology and structure, inflammation, fibrosis, and oxidative stress in rats with BDL-induced cholestatic liver injury.

The effect of vitamin D on morphine preference in rats: Possible biochemical and DRD2-GDNF signaling.

INTRODUCTION: Despite half a century of research on vitamin D (Vit. D), its link to substance abuse and dependence has only been discussed in recent decades. Evidence also shows the involvement of Vit. D in the evolution of dopaminergic neurons in the nucleus accumbens, an increase in the expression of tyrosine hydroxylase, and the regulation of dopaminergic processes. The novel idea for this work is taken from a hypothesis given about the effectiveness of Vit. D on dopamine signaling pathway. It is therefore presumed that Vit. D can be considered an effective therapeutic approach for narcotic addiction and substance abuse. METHODS: The animals were assigned into six groups (control, vehicle, Morphine [Mor.], and Vit. D [250, 500, and 1000 IU/kg, i.p.]). Following each conditioning session in a conditioned place preference (CPP) model, the animals received Vit. D. Afterward, the locomotor activity of the animals was assessed using open-field apparatus. Malondialdehyde (MDA), nitric oxide (NO), catalase (CAT), superoxide dismutase (SOD), thiol, and total antioxidant capacity (TAC) were measured in the brain. The relative DRD2 and GDNF expressions (%) were also measured in the hippocampus. RESULTS: Vit. D administration after Mor. caused a significant increase in the place preference index in the acquisition phase (p < .05). Vit. D altered the oxidation/antioxidation profiles (CAT, SOD, MDA, NO, TAC, and Thiol). Vit. D was more effective than Mor. in the expression of GDNF (p < .0001); however, in the expression of DRD2, this was only the case for 1000 IU Vit. D (p < .0001). CONCLUSIONS: Considering the increased place preference index induced by Mor., it can be concluded that Vit. D interacts via the oxidative pathway and DRD2-GDNF signaling to potentiate the Mor. effect.

The Effect of Heat-Killed Lactobacillus plantarum on Oxidative Stress and Liver Damage in Rats with Bile Duct Ligation-Induced Hepatic Fibrosis.

This study is aimed at evaluating the effects of heat-killed Lactobacillus plantarum (L. plantarum) on cholestatic liver injury induced by bile duct ligation (BDL) in rats. Rats in the first group were healthy (normal control) and in the second group underwent abdominal incision (sham control). Rats in the third and fourth groups underwent common bile duct ligation and were treated with either oral distilled water (BDL control group) or heat-killed L. plantarum (BDL + L. plantarum) for 28 days. Finally, rats were sacrificed, blood samples were analyzed through biochemical methods, liver and ileum tissue tissues were histologically assessed, and the expression of the αSMA, TNF-α, IL-6, and IL-10 genes in the liver and ZO-1 gene in ileum tissues were assessed through real-time PCR. The levels of bilirubin, liver function enzymes, NO, MDA, and carbonyl protein in the BDL + L. plantarum group were significantly lower than in the BDL control group (P ≤ 0.05). SOD and CAT activity in BDL + L. plantarum group was significantly greater than the BDL control group 1.4 and 3.0 times, respectively (P ≤ 0.001). Moreover, in the BDL + L. plantarum group, the expression of the α-SMA, TNF-α, and IL-6 genes was significantly lower (3.1, 2.9, and 2.5 times), and IL-10 and ZO-1 genes were significantly greater than the BDL control group by 2.1 and 3.6 times, respectively (P ≤ 0.05). The histological assessment also confirmed the greater effectiveness of heat-killed L. plantarum in improving the morphology and parenchymal structure of the liver. Taken together, our results suggest that heat-killed L. plantarum strains are potential therapeutic agents for hepatic fibrosis.

Protection against Morphine-Induced Inhibitory Avoidance Memory Impairment in Rat by Curcumin: Possible Role of Nitric Oxide/ cAMP-Response Element Binding Protein Pathway.

Background: Although a substantial body of research suggests curcumin (CUR) has the preventive potential in memory impairment, the mechanism by which CUR prevents memory loss is still being investigated. This study employs an inhibitory avoidance (IA) model to investigate whether CUR can prevent morphine (Mor)-induced memory impairment as well as the possible role of cAMP-response element binding (CREB) protein, and nitric oxide (NO) signaling in this mechanism. Methods: This experimental study was conducted at the Animal Lab of the Physiology Research Center, Kashan University of Medical Sciences (Kashan, Iran) in 2018. Forty rats were randomly divided into four groups: control, CUR (pretreatment gavage of CUR [10 mg/Kg] for 35 days), Mor (7.5 mg/Kg, i.p.), and CUR+Mor (n=10 per group). Following the evaluation of the IA memory and locomotor activity of the animals, the CREB protein expression in the hippocampus and NO metabolites (NOx) level in the brain tissue were also investigated. The data were analyzed using Sigmaplot software (version 14.0) by using the ANOVA, Kruskal-Wallis, Holm-Sidak, and Dunn's post hoc tests. P<0.05 was considered to be statistically significant. Results: In the Mor group, the IA memory of the rats was significantly impaired (P=0.001). CUR prevented the Mor-induced IA memory impairment (P=0.075). While the Mor treatment decreased the phosphorylated CREB (p-CREB) expression, the CUR+Mor cotreatment increased p-CREB expression (P=0.010). Nevertheless, the Mor treatment increased the total CREB expression (P=0.010). The NOx concentration in the brain tissue was decreased following the Mor treatment (P=0.500) but increased after the CUR+Mor cotreatment (P=0.001). Conclusion: The present findings suggest that CUR prevents the memory impairment of rats, possibly through NO and its downstream CREB signaling.

L-Lysine Ameliorates Diabetic Nephropathy in Rats with Streptozotocin-Induced Diabetes Mellitus.

Introduction: Diabetic nephropathy is one of the leading causes of end-stage renal disease worldwide. Uncontrolled hyperglycemia and subsequent production of glycation end-products activate the paths which lead to diabetic nephropathy. The aim of this study was to assess the effects of L-lysine on antioxidant capacity, biochemical factors, kidney function, HSP70 level, and the expression of the TGFß, VEGF, and RAGE genes in rats with streptozocin-induced diabetes mellitus. Methods: Thirty-two male Wistar rats were randomly allocated to four eight-rat groups, namely, a healthy group, a diabetic group treated with vehicle (DM + vehicle), a diabetic group treated with L-lysine (DM + Lys), and a healthy group treated with L-lysine (healthy + Lys). Rats in the DM + Lys and the healthy + Lys groups were treated with L-lysine 0.15%. The levels of fasting blood glucose, insulin, HbA1C, advanced glycation end-products (AGEs), lipid profile, serum creatinine, blood urea nitrogen, glomerular filtration rate, urine microalbumin, oxidative stress parameters, kidney histology and morphology, and TGFß, VEGF, and RAGE gene expressions were assessed. Findings. An eight-week treatment with L-lysine significantly reduced the levels of fasting blood glucose, AGEs, kidney function parameters, oxidative stress parameters, lipid profile, and the TGFß, VEGF, and RAGE gene expression and significantly increased the levels of serum insulin and tissue HSP70. Conclusion: Treatment with L-lysine seems to slow down the progression of diabetic nephropathy.

The Protective Effects of Securigera securidaca Seed Extract on Liver Injury Induced by Bile Duct Ligation in Rats.

This study is aimed at evaluating the effects of Securigera securidaca (SS) seed extract on cholestatic liver injury induced by bile duct ligation (BDL) in rats. Total polyphenols and flavonoids in SS seed extract were determined using a colorimetric assay, and their components were quantified using HPLC. Rats in four groups underwent BDL at the common bile duct and were treated for 21 days with either oral distilled water as vehicle, vitamin C, 100 mg/kg SS seed extract, or 200 mg/kg SS seed extract. Rats in the fifth group underwent abdominal incision without BDL and were treated with distilled water, and rats in the sixth group were healthy and received nothing. Finally, rats were sacrificed, blood samples were analyzed through biochemical methods, liver tissues were histologically assessed, and the expression of the TGFß-1, iNOS, caspase-3, and α-SMA genes in the liver was assessed through real-time PCR. BDL significantly increased, and SS seed extract significantly decreased the serum levels of bilirubin and liver function enzymes. Moreover, SS seed extract suppressed the expression of the TGFß-1, iNOS, caspase-3, and α-SMA genes, reduced the levels of nitric oxide, malondialdehyde, and protein carbonyl, and increased the levels of glutathione, total antioxidant capacity, and SOD and catalase enzyme activity in the serum and liver. Extract at a dose of 100 mg/kg had significant positive effects on liver morphology and parenchyma structure in a dose-dependent manner.

MiR-33-5p Regulates CREB to Induce Morphine State-dependent Memory in Rats: Interaction with the µ Opioid Receptor.

The aim of the present study was to examine the hypothesis that miR-33-5p attenuates morphine state-dependent (StD) memory via the µ opioid receptor by regulating cyclic AMP response element-binding protein (CREB). The effects of post-training morphine and morphine StD memory and their interaction with pre-test naloxone were evaluated using a single-trial inhibitory avoidance paradigm. Then, the hippocampal miR-33-5p gene and pCREB/CREB protein expression profiles were evaluated using quantitative real-time PCR and western blotting, respectively. We found that while post-training morphine and morphine StD memory respectively up- and down-regulate the miR-33-5p expression profile in the hippocampus, the reverse results are true for the expression of pCREB/CREB. Pre-test naloxone antagonized the response. Overall, our findings suggest that the expression levels of miR-33-5p in the hippocampus set the basis for morphine StD memory with low miR-33-5p enabling state dependency. The mechanism is mediated via miR33-5p and CREB signaling with the interaction of the µ opioid receptor. This finding may be used as a potential strategy for ameliorating morphine-induced memory-related disorders.

Pentylenetetrazol and Morphine Interaction in a State-dependent Memory Model: Role of CREB Signaling.

INTRODUCTION: State-dependent (STD) memory is a process, in which the learned information can be optimally retrieved only when the subject is in the state similar to the encoding phase. This phenomenon has been widely studied with morphine. Several studies have reported that Pentylenetetrazole (PTZ) impairs memory in experimental animal models. Due to certain mechanistic interactions between morphine and PTZ, it is hypothesized that PTZ may interfere with the morphine-STD. The cyclic adenosine monophosphate Response Element-Binding (CREB) is considered as the main downstream marker for long-term memory. This study was designed to determine the possible interaction between PTZ and morphine STD and the presumable changes in CREB mRNA. METHODS: In an Inhibitory Avoidance (IA) model, posttraining morphine (2.5, 5, and 7.5 mg/ kg-i.p.) was used. The pre-test morphine was evaluated for morphine-induced STD memory. Moreover, the effect of a pre-test PTZ (60 mg/kg-i.p.) was studied along with morphine STD. Locomotion testing was carried out using open-field. Eventually, using real-time-PCR, the CREB mRNA changes in the hippocampus were evaluated. RESULTS: Posttraining MOR (7.5 mg/kg-i.p.) impaired IA memory (P<0.001). The pre-test injection of similar doses of morphine recovered the morphine-induced memory impairment (P<0.001). The pre-test PTZ impaired the IA memory recall (P<0.001); however, the pre-test PTZ along with morphine STD potentiated the morphine-induced STD (P<0.001). Alterations in CREB mRNA were observed in all groups. No difference was seen in the locomotor activity. CONCLUSION: Presumably, the certain interactive effect of PTZ on morphine-induced STD is mediated through gamma-aminobutyric acid and opioid systems via CREB signaling.

Cardioprotective effects of cerebrolysin on the lesion severity and inflammatory factors in a rat model of isoproterenol-induced myocardial injury.

BACKGROUND: Myocardial injury (MI) is an important heart condition and a major cause of morbidity and mortality worldwide. The current study was designed to investigate the cardioprotective effects of cerebrolysin (CLY) on the lesion severity and inflammatory factors in male rats using isoproterenol (ISO)-induced MI model. METHODS: MI in rats was induced by injecting ISO (100 mg/kg) subcutaneously (sc) on the first 2 days. Then, CLY (5 ml/kg) was injected intraperitoneally (ip) post-treatment for 7 days. On the 3rd day, creatine phosphokinase (CK-MB) and cardiac troponin I (cTnI) levels in serum and, on the 10th day, the TNF-α and IL6 levels in serum and heart tissue were measured by enzyme-linked immunosorbent assay (ELISA). Finally, the heart of each rat was dissected out and stained for histopathological examination. RESULTS: On the 3rd day, the serum CK-MB and cTnI levels in the ISO and CLY + ISO groups were significantly increased compared with that in the control and CLY + Sal groups. One week after the induction of MI, ISO administration showed a significant increase in the serum level of TNF-α in the ISO group compared with that in the control and CLY + Sal groups. Also, our findings showed only a moderate reduction in inflammatory cell infiltration and extent of edema following CLY treatment in the CLY + ISO group. Also, CLY induced vascular proliferation in the heart tissue. CONCLUSIONS: We conclude that the severity of pathological changes induced by ISO in MI (e.g. inflammation and edema) can be limited by CLY treatment.

Low-dose ethanol ameliorates amnesia induced by a brief seizure model: the role of NMDA signaling.

Objective: The present study aimed to evaluate the ameliorative effect of low-dose ethanol (Eth) on amnesia induced by a brief seizure model and the role of N-methyl D-aspartate (NMDA) signaling in this event. Materials and Methods: Four groups of rats (total number = 36; n = 9, each group) were used: control, Eth (0.5 g/kg/i.p.), pentylenetetrazole (PTZ) (60 mg/kg/i.p.), and Eth+PTZ. Eth was administered for 6 days before the single injection of PTZ, at minute dose that cannot induce memory impairment. The consequences of Eth pretreatment, coadministered with PTZ, were studied in an inhibitory avoidance (IA) memory model. The PTZ was injected 30 min prior to the IA memory test. Thereafter, locomotion, liver enzymes, and the Real-time PCR for NR1 subunit of NMDA receptor were studied. The statistical analyses were performed using the parametric/nonparametric ANOVA and the post-hoc tests. Results: Our findings revealed that Eth pretreatment significantly improved the IA memory impairment induced by PTZ (P < 0.001), and indicated no change in locomotion and serum ALT, but significantly differed for AST between the PTZ and PTZ groups (P = < 0.05). The Real-time PCR results indicate the decreased NR1 mRNA expression in Eth and PTZ groups and the increased NR1 mRNA expression in Eth+PTZ group, compared to the control group (P < 0.001); however, the NR1 mRNA expression was increased in the Eth+PTZ group, compared to PTZ group (P < 0.001). Conclusion: The present study provides evidence that the low-dose Eth can improve the amnesia induced by a brief seizure model presumably via NMDA signaling in a rat.

Ameliorative effects of cerebrolysin against isoproterenol-induced myocardial injury in male rats.

AIMS: Myocardial injury (MI) is the principal cause of death from cardiovascular disease (CVD). The present study was conducted to investigate the ameliorative and antioxidant effects of cerebrolysin (CBL) on isoproterenol-induced MI in rats. METHODS: MI was induced in the rats by subcutaneously injecting 100 mg/kg of isoproterenol (ISO) in the first two days. The serum levels of creatine phosphokinase (CK-MB) and cardiac troponin I (cTnI) were measured on the third day to confirm MI. The post-treatment involved intraperitoneally injecting 5 ml/kg of CBL for 7 days. Nitric oxide (NO), malondialdehyde (MDA) in the heart tissue and catalase (CAT) and serum levels of superoxide dismutase (SOD) and glutathione peroxidase (GPX) were measured on the 10th day using the enzyme-linked immunosorbent assay (ELISA). Histopathological examinations of the heart tissue were also performed. FINDINGS: The present results suggested significant increases in CK-MB, cTnI, MDA and NO. A significant decrease was also observed in the ISO-treated rats in certain antioxidant enzymes, including CAT and GPX. CBL administration showed a significant ameliorative increase against the oxidative ISO-induced damage. Moreover, the histopathological findings showed lower levels of the infiltration of inflammatory cells and edema and vascular proliferation in the CBL-treated rats. SIGNIFICANCE: The present histopathological and biochemical findings attributed antioxidant properties to CBL in the rat myocardium and suggested protective effects on ISO-induced MI.

Exposure to GSM 900-MHz mobile radiation impaired inhibitory avoidance memory consolidation in rat: Involvements of opioidergic and nitrergic systems.

The use of mobile phones is increasing, and the main health concern is the possible deleterious effects of radiation on brain functioning. The present study aimed to examine the effects of exposure to a global system for mobile communication (GSM) with mobile phones on inhibitory avoidance (IA) memory performance as well as the involvement of endogenous opioids and nitric oxide (NO) in this task. Male Wistar rats, 10-12 weeks old, were used. The results showed that four weeks of mobile phone exposure impaired IA memory performance in rats. The results also revealed that post-training, but not pre-training, as well as pre-test intracerebroventricular (i.c.v.) injections of naloxone (0.4, 4 and 40 ng/rat), dose-dependently recovered the impairment of IA memory performance induced by GSM radiation. Additionally, the impairment of IA memory performance was completely recovered in the exposed animals with post-training treatment of naloxone (40 ng/rat) plus pre-test i.c.v. injections of L-arginine (100 and 200 nmol/rat). However, pre-test i.c.v. injections of L-NAME (10 and 20 nmol/rat), impaired IA memory performance in the animals receiving post-training naloxone (40 ng/rat). In the animals receiving post-training naloxone treatment, the impairment of IA memory performance due to pre-test i.c.v. injections of L-NAME was recovered by the pre-test co-administration of L-arginine. It was concluded that the recovery from impairment of IA memory in GSM-exposed animals with post-training naloxone treatment was the result of blockade of the opioidergic system in early memory consolidation as well as activation of the nitrergic system in the retrieval phase of memory.

Immunization with a recombinant fusion protein protects mice against Helicobacter pylori infection.

More than 50% of the world's population is infected with the bacterium Helicobacter pylori. If left untreated, infection with H. pylori can cause chronic gastritis and peptic ulcer disease, which may progress into gastric cancer. Owing to the limited efficacy of anti-H. pylori antibiotic therapy in clinical practice, the development of a protective vaccine to combat this pathogen has been a tempting goal for several years. In this study, a chimeric gene coding for the antigenic parts of H. pylori FliD, UreB, VacA, and CagL was generated and expressed in bacteria and the potential of the resulting fusion protein (rFUVL) to induce humoral and cellular immune responses and to provide protection against H. pylori infection was evaluated in mice. Three different immunization adjuvants were tested along with rFUVL: CpG oligodeoxynucleotides (CpG ODN), Addavax, and Cholera toxin subunit B. Compared to the control group that had received PBS, vaccinated mice showed significantly higher cellular recall responses and antigen-specific IgG2a, IgG1, and gastric IgA antibody titers. Importantly, rFUVL immunized mice exhibited a reduction of about three orders of magnitude in their stomach bacterial loads. Thus, adjuvanted rFUVL might be considered as a promising vaccine candidate for the control of H. pylori infection.

Immunization with recombinant FliD confers protection against Helicobacter pylori infection in mice.

Nearly half of the world's population is infected with Helicobacter pylori. Clinical manifestations of this infection range from gastritis and peptic ulcers to gastric adenocarcinoma and lymphoma. Due to the emerging of antibiotic resistant strains and poor patient compliance of the antibiotic therapy, there is increasing interest in the development of a protective vaccine against H. pylori infection. The bacterial protein FliD forms a capping structure on the end of each flagellum which is critical to prevent depolymerization and structural degradation. In this study, the potential of FliD as a prospective H. pylori subunit vaccine was assessed. For this purpose, immunogenicity and protective efficacy of recombinant FliD (rFliD) from H. pylori was evaluated in C57BL/6 mice. Purified rFliD was formulated with different adjuvants and administered via subcutaneous or oral route. Subcutaneous immunization with rFliD elicited predominantly mixed Th1 and Th17 immune responses, with high titers of specific IgG1 and IgG2a. Splenocytes of immunized mice exhibited strong antigen-specific memory responses, resulting in the secretion of high amounts of IFN-γ and IL-17, and low levels of IL-4. Immunization with rFliD caused a significant reduction in H. pylori bacterial load relative to naïve control mice (p < 0.001), demonstrating a robust protective effect. Taken together, these results suggest that subcutaneous vaccination with rFliD formulated with CpG or Addavax could be considered as a potential candidate for the development of a subunit vaccine against H. pylori infection.

Effects Following Intracerebroventricular Injection of Immunosuppressant Cyclosporine A On Inhibitory Avoidance Learning and Memory in Mice.

BACKGROUND: Protein phosphatase-2B or calcineurin (CN) is the main phosphatase and a critical regulator of cellular pathways for learning, memory, and plasticity. Cyclosporine A(CyA), a phosphatase and peptidyl-prolyl cis/trans isomerase inhibitor, is a common immune suppressant extensively used in tissue transplantation. To further clarify the role of CN in different stages of learning and memory, the aim of the present study was to evaluate the role of CyA in an inhibitory avoidance (IA) model in mice. MATERIALS AND METHODS: Using intracerebroventricular (ICV) injection of different doses of CyA (0.5, 5, and 50 nM) at different periods (pre-/post-training and pre-test), the effect of the drug was evaluated in a step-down IA paradigm. The latency of step-down (sec) was considered a criterion for memory performance. RESULTS: The pre-training injections of CyA (0.5, 5 nM), however not of 50 nM, impaired IA learning acquisition. The post-training injection of high-dose CyA (50 nM) impaired memory consolidation. The pre-test ICV CyA injection did not impair memory retrieval; the ICV injection of CyA caused no change in locomotion. CONCLUSION: These findings suggest that CyA selectively interferes with acquisition, retention, but not retrieval, of information processing in mice. Given the crucial role of CN in common signaling pathway of memory performance and cognition, it could be a probable therapeutic target in the treatment of a wide variety of neurological conditions involving memory.

In Silico Design of a Chimeric Protein Containing Antigenic Fragments of Helicobacter pylori; A Bioinformatic Approach.

Helicobacter pylori is a global health problem which has encouraged scientists to find new ways to diagnose, immunize and eradicate the H. pylori infection. In silico studies are a promising approach to design new chimeric antigen having the immunogenic potential of several antigens. In order to obtain such benefit in H. pylori vaccine study, a chimeric gene containing four fragments of FliD sequence (1-600 bp), UreB (327-334 bp),VacA (744-805 bp) and CagL(51-100 bp) which have a high density of B- and T-cell epitopes was designed. The secondary and tertiary structures of the chimeric protein and other properties such as stability, solubility and antigenicity were analyzed. The in silico results showed that after optimizing for the purpose of expression in Escherichia coli BL21, the solubility and antigenicity of the construct fragments were highly retained. Most regions of the chimeric protein were found to have a high antigenic propensity and surface accessibility. These results would be useful in animal model application and accounted for the development of an epitope-based vaccine against the H. pylori.

Comparing the effect of whole body massage by a specialist nurse and patients' relatives on blood cortisol level in coronary patients.

BACKGROUND: Cardiovascular diseases such as acute coronary syndrome and myocardial infarction are often accompanied by severe anxiety over the likelihood of death. Cortisol has been known as a stress hormone. However, there are controversies about the effect of massage therapy on blood cortisol level. Furthermore, no study is available on the difference between massage applied by a nurse specialist or by patients' relatives on blood cortisol level. This study was aimed to compare the effect of massage applied by a nurse specialist and patients' relatives on blood cortisol level among the patients admitted in coronary care unit (CCU). METHODS: In a randomized controlled trial, ninety patients hospitalized at CCU were randomly placed in three groups: massage by a nurse; massage by patients' relatives and control group. The two massage groups received a session of whole body massage. The control group received the routine care. Data were analyzed using analysis of variance, chi-square and Fischer exact tests, Kruskal-Wallis and Wilcoxon Signed Ranks tests. RESULTS: The mean age of participants was 58.43 ± 14.23 years. None of the participants had the history of massage therapy. In the group massaged by a nurse, the median blood cortisol level was 281.90 nanomoles, which were decreased to 197.00 after the intervention (P < 0.007). The median blood cortisol level in the group massaged by the patients' relatives and the control group did not affect significantly. CONCLUSION: Massage therapy decreased the blood cortisol level in the group that received massage by a specialist nurse. It can be recommended that massage therapy be used in patients admitted in CCU.

Intra-CA1 administration of FK-506 (tacrolimus) in rat impairs learning and memory in an inhibitory avoidance paradigm.

OBJECTIVES: Calcineurin (CN) is a main phosphatase and a critical regulator of cellular pathways for learning, memory, and plasticity. The FK-506 (tacrolimus), a phosphatase inhibitor, is a fungal-derived agent and a common immune suppressant extensively used for tissue transplantation. To further clarify the role of CN in different stages of learning and memory the main aim of this study was to evaluate the role of FK-506 in an inhibitory avoidance model. MATERIALS AND METHODS: Using different doses of FK-506 (0.5, 5, and 50 nM) in the CA1 of hippocampus at different times (before, after the training and also before the test), the effect of drug was evaluated in a step-through inhibitory avoidance paradigm. The latency of entering to the dark compartment was considered as a criterion for memory. RESULTS: The pre-training intra-CA1 injections of FK-506 impaired inhibitory avoidance (IA) learning acquisition. In addition, the post-training intra-CA1 injections of FK-506 at 1, 2, and 3 hr relative to training impaired memory consolidation. Moreover, the pre-test intra-CA1 injections of FK-506 impaired memory retrieval. CONCLUSION: These findings suggest that the FK-506 selectively interferes with acquisition, retention, and retrieval of information processing in CA1 of hippocampus. Given the crucial role of CN in common signaling pathway of higher functions such as memory performance and cognition, in future it would be a probable therapeutic target in the treatment of a wide verity of neurological conditions involving memory.

Review of sport-induced groin injuries.

CONTEXT: Groin injuries are among the most common injuries co-existing with sports. The aim of this review was to outline the epidemiology and identify risk factors, as well as examine preventative and interventional measures for reducing the occurrence of this form of injury among athletes. EVIDENCE ACQUISITION: An electronic, systematic search for relevant keywords, either separately or in combination was sought in the academic scientific databases. RESULTS: Groin injuries, acute or chronic, consist of a high percentage of injuries that manifest with pain. Despite the specific tendency for injury among some sports, such injuries make up 2-5% of sport-induced injuries. There are few available reports on lower limb injuries, especially groin injuries, in Iran. Numerous factors predispose to groin injuries. A lengthy list of preventive/ treatment measures, from preliminary to sophisticated, have been proposed. CONCLUSIONS: Although using a programmed strategy designed to decrease the risk of groin injuries by taking a strategic approach to exercise may alleviate complications, in some cases the chronic nature of the injury may threaten the professional life of the athlete. More research is required to plan suitable programs for reducing the risk of this type of injury in athletes.