Vol 55, No 12 (2017)

Published: 2017-12-16


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    Hepatotoxicity is one of the clinically adverse effects of ecstasy (3, 4-methylenedioxymethamphetamine; MDMA) consumption. The detoxification tissue, liver, plays a central role in maintaining circulating levels of glucose and lipid. Hypoglycemia and hypotriglyceridemia have been reported due to ecstasy abuse. Ghrelin is a 28-amino-acid peptide secreted predominantly from the stomach. It has been demonstrated that ghrelin has hepatoprotective effects and is able to increase blood glucose concentration. In the current study, we explored the effect of hepatotoxic dose of MDMA and therapeutic use of exogenous ghrelin on the serum levels of glucose and lipids in four groups of rats. MDMA caused a severe and transient reduction in circulating levels of glucose and triglyceride and increased serum LDL. However, cholesterol and HDL levels remained unchanged. Meanwhile, altered hepatic architecture was observed with intracellular vacuolation that may indicate intracellular accumulation of lipid droplets. In addition, following ghrelin administration, the blood sugar levels improved and LDL levels returned to the baseline value, and ghrelin treatment did not improve triglycerides levels. These results showed that MDMA causes hypoglycemia, hypotriglyceridemia, and hyper LDL-cholesterolemia. To our knowledge, this is the first report showing ghrelin administration could improve hypoglycemia and normalize LDL levels induced by MDMA and partially restore hepatic architecture.

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    Breast cancer imposes a considerable amount of cancer-related mortality and morbidity among women worldwide. Many efforts are in progress to reduce the disease burden and amongst the bacterial-based products received considerable attention as potential anti-cancer drugs. In the present study, the effect of recombinant pro-inflammatory outer membrane protein (HopH) of Helicobacter pylori on the angiogenic factor and tumor development in metastatic breast cancer model was evaluated. The HopH gene was cloned into Pet28a vector, induced by IPTG and expressed and purified by Ni-NTA affinity chromatography. The expressed protein was confirmed by SDS-page. The breast cancer tumor induction was performed using Breast cancer cell line (4T1). The mice were divided into different groups and underwent treatment by recombinant HopH and Herceptin, subsequently. The treatment effectiveness on tumor size was followed, and the expression level of vascular endothelial growth factor was evaluation by real time PCR. The SDS-PAGE analysis confirmed the expression of HopH protein with an approximate 34KD weight. Based on our results, the expression level of VEGF was significantly reduced in HopH-treated mice group comparing to the control and Herceptin group. Our results have shown that the recombinant HopH protein can effectively reduce VEGF expression in breast cancer tumor which was associated with reduction of tumor size. The HopH protein can be considered as a potential anti-cancer agent for future cancer therapeutic studies.

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    5-fluorouracil (5-FU) is one of the major components of many standard regimens for chemotherapy of colorectal cancer (CRC) and some other malignancies. Given the known relationship between thymidylate synthase (TS) and methylenetetrahydrofolate reductase (MTHFR) activity and 5-FU metabolism, this study investigated the impact of selected functional polymorphisms of the TS and MTHFR genes on chemotherapy resistance in 5 human CRC cell lines. HCT116, SW1116, HT29/219, LS180, and Caco-2 CRC cells were cultured as monolayer and their chemosensitivity to 5-FU, oxaliplatin, and irinotecan was determined by MTT assay. Genomic DNA was extracted from the cultured cells, and a 6-bp insertion or deletion (6-bp ins/del) polymorphism in 3´-UTR of the TS gene was determined by the PCR-RFLP method. Genotyping of MTHFR 677 C/T and 1298A/C single nucleotide polymorphism (SNP) was also performed by MS-PCR and PCR-RFLP, respectively. Caco-2 with the homozygous TS 6-bp ins/ins and MTHFR 677 T/T and 1298 C/C genotype, was the most 5-FU resistant cell line. HCT116 with the homozygous TS 6-bp del/del and MTHFR 1298 A/A and heterozygous MTHFR 677 C/T genotype was the least 5-FU resistant cell. LS180, the second most 5-FU resistant cell line, was heterozygous for all three polymorphic sits. HT29/219 and SW1116 cells with homozygous TS 6-bp ins/ins and heterozygous MTHFR 677 C/T and 1298 A/C genotypes had intermediate 5-FU sensitivity. The results indicate that TS 3´-UTR 6-bp insertion and MTHFR 677T and 1298C alleles increase 5-FU resistance in CRC cells. No relationship was observed between TS and MTHFR genotypes and oxaliplatin or irinotecan sensitivity in these cells.

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    Polycystic ovarian syndrome (PCOS) is an endocrine metabolic disorder with unclear etiopathogenesis among reproductive age women. Evidences show genetic susceptibility and environmental factors were associated with PCOS. The aim of this study was to find the association between urinary concentrations of Bisphenol-A as an endocrine disrupting chemical (EDC) and PCOS. A case-control study was conducted in 51 samples in each group. All cases were selected from women who diagnosed with PCOS at Gynecology and infertility center. The control group was selected from women who had clinical file in the center due to previous problem and came for routine check-up and pap smear. The participants were asked to collect a first-morning urine sample before any medical interventions. Total BPA in urine were measured with High Performance Liquid Chromatography (HPLC) method. Comparison of BPA level between two groups shows significantly higher level in PCOS group compared with control group (3.34 ± 2.63 vs 1.43 ± 1.57 ng/mL, P-value <0.001). Using logistic regression analysis, BPA as the main dependent variable, was significantly associated with PCOS with adjusted Odds Ratio (OR) equal to 1.53 (95% CI: 1.14-2.05, P-value =0.004). The results of this study indicated that BPA may play a major role in the PCOS pathogenesis. Further investigations with better design are necessary to confirm this association.

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    In recent decades, the relation of carotid artery intima-media thickness (IMT) as a marker of atherosclerosis with snoring and sleep disorders has been drawing attention. The aim of this study was to evaluate the relation of carotid arteries IMT with snoring in type 2 diabetic patients. This cross-sectional study was performed on type 2 diabetes patients referring to Mashhad University of Medical Sciences' clinics. The stop Bang, Epworth sleepiness scale, and Stanford questionnaires were used for evaluation of daily sleepiness and snoring. For assessment of carotid artery thickness, Madison X8 ultrasound with 10 MHz superficial probes was utilized. The data were entered into SPSS software, and then the ANOVA test with Turkey, chi-square comparison technique, and Kruskal Wallis with Mann-Whitney U technique was used. The level of significance was considered P≤0.05. In total 80 patients (37 snorers and 43 non-snorers) entered the study. The mean carotid artery IMT in the group of snoring patients (0.72±0.17) was significantly higher than non-snorers (0.56±0.17) (P<0.001). Frequency of daily based on Stanford and ESS questionnaires was 23.8% and 39.2%. The association of sleepiness and snoring was confirmed by Stanford and ESS questionnaires with P=0.026 and P=0.007. Patients with higher risk of apnea had higher thickness of the mean carotid artery IMT (P<0.001). The mean carotid artery IMT had a positive significant relation with age (P=0.002), serum creatinine level (P<0.002), blood cholesterol (P=0.02) and HbAIC level (P=0.04). Findings of this study provides evidence on the relation of carotid artery IMT in diabetic patients with snoring independent of other effective factors. Also, results showed that snoring is associated with increased daily sleepiness and patients with higher risk of apnea had higher thickness of the mean carotid artery IMT.

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    Preterm premature rupture of membranes (PPROM) is a condition leading to an increased risk of maternal and neonatal morbidity and mortality in pregnant women. To prevent this complication, some studies have proposed using prophylactic progesterone. However, due to lack of sufficient relevant data, there is still need for further studies in this regard. This study was performed to determine the effect of rectal progesterone on the latent phase and maternal and neonatal outcome variables in females with PPROM. During the present randomized clinical trial study (IRCT201512077676N4), a total of 120 patients with PPROM at pregnancy ages between 26 and 32 weeks were randomly assigned to 2 equal intervention and control groups. In the intervention group, progesterone suppositories (400 mg per night) were administered until delivery or completion of the 34th gestational week and was compared with placebo effect in control group. The latent phase and maternal and neonatal outcome variables were compared between the two groups. The mean age of patients was 29.56±5.66 (19-42) and 29.88±5.57 (17-40) years in the intervention and control group, respectively. The two groups were almost identical in the confounding factors. The median latent phase was 8.5 days in the intervention group vs. 5 days in the control group in the 28th-30th weeks of gestation, which was significantly higher in the intervention group (P=0.001). Among maternal and neonatal outcome variables, only the mean birth-weight was significantly higher in the intervention group than that in the controls (1609.92±417.28 gr vs. 1452.03±342.35 gr, P=0.03). Administration of progesterone suppository in patients with PPROM at gestational ages of 28 to 30 weeks is effective in elongating the latent phase and increasing birth-weight with no significant complications.

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    Ischemic stroke is an important cause of death and disability in the world. Brain ischemia causes damage to brain cell, and among brain neurons, pyramidal neurons of the hippocampal CA1 region are more susceptive to ischemic injury. Recent findings suggest that neurotrophic factors protect against ischemic cell death. A dietary component of Rosa damascene extract possibly is associated with expression of neurotrophic factors mRNA following ischemia, so it can have therapeutic effect on cerebral ischemia. The present study attempts to evaluate the neuroprotective effect of Rosa damascene extract on adult rat hippocampal neurons following ischemic brain injury. Forty-eight adult male Wistar rats (weighing 250±20 gr and ages 10-12 weeks) used in this study, animals randomly were divided into 6 groups including Control, ischemia/ reperfusion (IR), vehicle and three treated groups (IR+0.5, 1, 2 mg/ml extract). Global ischemia was induced by bilateral common carotid arteries occlusion for 20 minutes. The treatment was done by different doses of Rosa damascena extract for 30 days. After 30 days cell death and gene expression in neurons of the CA1 region of the hippocampus were evaluated by Nissl staining and real time PCR assay. We found a significant decrease in NGF, BDNF and NT3 mRNA expression in neurons of CA1 region of the hippocampus in ischemia group compared to control group (P<0.0001). Our results also revealed that the number of dark neurons significantly increases in ischemia group compared to control group (P<0.0001). Following treatment with Rosa damascene extract reduced the number of dark neurons that was associated with NGF, NT3, and BDNF mRNA expression. All doses level had positive effects, but the most effective dose of Rosa damascena extract was 1 mg/ml. Our results suggest that neuroprotective activity of Rosa damascena can enhance hippocampal CA1 neuronal survival after global ischemia.

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    Cerebral ischemic stroke is a common leading cause of disability. Flaxseed is a richest plant-based source of antioxidants. In this study, the effects of flaxseed oil (FSO) pretreatment on functional motor recovery and gene expression and protein content of neurotrophic factors in motor cortex area in rat model of brain ischemia/reperfusion (I/R) were assessed. Transient middle cerebral artery occlusion (tMCAo) in rats was used as model brain I/R. Rats (6 in each group) were randomly divided into four groups of Control (Co+normal saline [NS]), Sham (Sh+NS), tMCAo+NS and tMCAo+FSO. After three weeks of pretreatment with vehicle or FSO (0.2 ml~800 mg/kg body weight), the rats were operated in sham and ischemic groups. Ischemia was induced for 1 h and then reperfused. After 24 h of reperfusion, neurological examination was performed, and animals were sacrificed, and their brains were used for molecular and histopathological studies. FSO significantly improved the functional motor recovery compared with tMCAo+NS group (P<0.05). A significant reduction in brain-derived neurotrophic factor (BDNF) and glial cell-derived neurotrophic factor (GDNF) mRNAs and protein levels were observed in the tMCAo+NS group compared with Co+NS and Sh+NS group (P<0.05). A significant increase of BDNF and GDNF mRNAs and proteins was recorded in the tMCAo+FSO group compared with Co+NS, Sh+NS and tMCAO+NS groups (P<0.05). The results of the current study demonstrated that pretreatment with FSO had neuroprotective effects on motor cortex area following cerebral ischemic stroke by increasing the neurotrophic factors (BDNF, GDNF).

Case Report(s)

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    Metachondromatosis which was first described in 1971 by Maroteaux is a rare genetic disease consisting of osteochondromas and enchondromas, caused by loss of function of the PTPN11 gene. It is distinct from other cartilaginous tumors such as multiple osteochondromas and hereditary multiple exostosis by the distribution and orientation of lesions, and pattern of inheritance. In Metachondromatosis osteochondromas typically occur in hands, feet, femur, and tibia while enchondromas commonly affect the pelvic bones and femurs. Both tumors are generally reported to regress in adulthood. To the best of our knowledge only one case of Chondrosarcoma has been reported, and our case is the second reported case of Chondrosarcoma in metachondromatosis.

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    A 59-year-old man presented with proximal myopathy, myalgia, and weight loss, with the initial markedly elevated serum creatine kinase at 11,000 U/L. Due to his refusal for muscle biopsy, he was initially treated as inflammatory myositis and responded well with the corticosteroids. However, he subsequently had a relapse of the symptoms with more extensive systemic involvement, i.e., hypercalcemia, lymphadenopathy and subcutaneous nodules. Finally, a biopsy of the thigh and subcutaneous nodule revealed non-caseating granulomatous inflammation, consistent with sarcoidosis. He responded well to the corticosteroids, and finally, azathioprine was added as a steroid-sparing agent. Including our series, there are 103 cases of symptomatic muscle involvement in sarcoidosis patients published in the English literature to date. Further pool analysis of the cases will be reported in this review.

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    Paraplegia is an exceedingly rare neurologic complication after off-pump coronary artery bypass graft (OPCAB) surgery commonly caused by spinal cord ischemia (SCI). SCI is not a well unknown clinical phenomenon in the postoperative course. SCI has been reported after noncardiac surgery in otherwise healthy subjects in whom only one risks factor i.e. severe hypotension has been documented. SCI has also been reported as a rare complication among the other neurologic sequels of cardiac surgery. We report a case of paraplegia in a patient with metabolic syndrome and multiples risk factors after an OPCAB. This patient may be considered as an interesting case as no any ischemic event was found in the imaging modalities and culprit lesion may be attributed to 1-left internal thoracic artery use as an important blood perfusion to anterior spinal artery vasculature and 2-Disc herniation at intervertebral space of T as a culprit lesion 3-transient intraoperative hypotension. The patient was managed by lower extremities physiotherapy and skin care, however, after 3months of follow-up, no evidence of recovery was detected.