Information-seeking process and clinical scenario solving: introduction of a new tool in nursing education.

BACKGROUND: Nursing education has recently undergone changes to improve care. These changes require innovative and transformative strategies in nursing education. Search as learning is one of the educational methods this study was conducted to determine the effect of the information searching process on scenario-based learning in nursing students. METHODS: This study is a single group semi-experimental study that was conducted on 38 nursing students in 2021. Students first drew a concept map according to their existing knowledge about two scenarios (diabetes and trauma). The students then searched the medical databases and drew another concept map after the search. Data were analyzed using descriptive statistics, paired mean tests and Pearson correlation coefficients. RESULTS: The results showed that the mean scores of the participants in the diabetes scenario before and after the search were 18.32 ± 5.50 and 19.13 ± 7.54, respectively, and those in the trauma scenario were 18.58 ± 7.69 and 29.61 ± 7, respectively (P < 0.01). The mean scores of the details of the conceptual map before and after the search in terms of themes, number of levels and relationships were statistically significant. In both scenarios, there was a positive correlation (p < 0.01) between learning and the number of correct webpages (r = 0.74 for trauma and r = 0.64 for diabetes), as well as between search time and the amount of learning (r = 0.77 for trauma and 0.64 for diabetes). CONCLUSIONS: The results showed that search as learning in nursing education scenarios led to student learning. It is recommended that nurse educators use this method as a tool in nursing education to increase students' awareness and develop their thinking skills. Further research is recommended to determine the effectiveness of this method with other educational methods.

Ermin deficiency leads to compromised myelin, inflammatory milieu, and susceptibility to demyelinating insult.

Ermin is an actin-binding protein found almost exclusively in the central nervous system (CNS) as a component of myelin sheaths. Although Ermin has been predicted to play a role in the formation and stability of myelin sheaths, this has not been directly examined in vivo. Here, we show that Ermin is essential for myelin sheath integrity and normal saltatory conduction. Loss of Ermin in mice caused de-compacted and fragmented myelin sheaths and led to slower conduction along with progressive neurological deficits. RNA sequencing of the corpus callosum, the largest white matter structure in the CNS, pointed to inflammatory activation in aged Ermin-deficient mice, which was corroborated by increased levels of microgliosis and astrogliosis. The inflammatory milieu and myelin abnormalities were further associated with increased susceptibility to immune-mediated demyelination insult in Ermin knockout mice. Supporting a possible role of Ermin deficiency in inflammatory white matter disorders, a rare inactivating mutation in the ERMN gene was identified in multiple sclerosis patients. Our findings demonstrate a critical role for Ermin in maintaining myelin integrity. Given its near-exclusive expression in myelinating oligodendrocytes, Ermin deficiency represents a compelling "inside-out" model of inflammatory dysmyelination and may offer a new paradigm for the development of myelin stability-targeted therapies.

Safety of Intraparenchymal Injection of Allogenic Placenta Mesenchymal Stem Cells Derived Exosome in Patients Undergoing Decompressive Craniectomy Following Malignant Middle Cerebral Artery Infarct, A Pilot Randomized Clinical Trial.

Background: Malignant middle cerebral artery infarct (mMCAI) largely contributes to high mortality and physical disability among adults. Surviving individuals may not have proper outcomes and suffer from severe lasting disabilities. Utilization of stem cells and paracrine factor for regenerative purposes is considered as a potential strategy for patients with neurological deficits. While preclinical stroke studies have shown that mesenchymal stem cells (MSCs) reduce post-treatment neurological deficits and prevent disability and also promote recovery, few randomized clinical trials (RCT) have assessed exosome therapy in humans. Methods: In this RCT, we assessed the safety of intraparenchymal injection placenta MSC-derived Exosome in mMCAI patients with average age of 62 years between January, 2019, till September, 2020. The study was done in a single-center as an open-label RCT, with a 3-months follow-up. Primary outcomes assessed the safety and also disability indexes were followed. Results: Five mMCAI patients were included with mean NIHSS: 17.6 ± 5.02. The mean MRS was 3.25 ± 0.95 in three patients. No serious adverse events were observed. Hematoma or local reaction as excessive edema were not seen at the site of injection. Conclusions: Intraparenchymal implantation of MSC-EXO showed no post-interventional adverse effects in five ischemic stroke patients. It is proposed Local injection Exosome treatment following mMCAI can be safe and in future, it would be applied as a supportive, restorative and preventive treatment in patients who suffer from acute ischemic stroke and post ischemic disability.

The Serum Level of Midkine in Patients With Multiple Sclerosis and Neuromyelitis Optica.

INTRODUCTION: Midkine (MK), a heparin-binding growth factor, is involved in neurological diseases by mediating the inflammatory responses through enhancing the leukocyte migration. The present study assesses the serum concentration of this growth factor among newly developed Multiple Sclerosis (MS) and Neuromyelitis Optica (NMO) patients. METHODS: The present research, as a cross-sectional study, was performed at Isfahan University of Medical Sciences, Isfahan City, Iran. All samples were selected from patients who visited Kashani and Alzahra hospitals for two years (2014 to 2016). The MK level was assessed in 80 new MS cases, 80 NMO patients, and 80 healthy subjects. After collecting blood sera samples, MK serum level was measured using the ELISA. The obtained data were analyzed in SPSS. RESULTS: The Mean±SD MK level was 1038.58±44.73 pg/mL in the MS group, which was significantly higher than the Mean±SD MK level in the NMO (872.62±55.42 pg/mL) and control groups (605.02±9.42 pg/mL). CONCLUSION: Overall, these results demonstrated that MK plays a prominent role in inflammatory reactions and neuroautoimmune diseases, especially in MS. So, the MK level may be used for earlier diagnosis and also prevention of disease progression by using a special inhibitor.

A systematic review of extracellular vesicles as non-invasive biomarkers in glioma diagnosis, prognosis, and treatment response monitoring.

The present systematic review was done to investigate the possible application of Extracellular vesicles (EVs) in the diagnosis, prognosis, and treatment response monitoring of gliomas using available literature to wrap up the final applicable conclusion in this regard. we searched PubMed/MEDLINE, Scopus, and ISI Web of Science databases. Authors evaluated the quality of the included studies by the QUADAS-2 tool. In total, 2037 published datasets were retrieved through systematic search. Upon screening for eligibility, 35 datasets were determined as eligible. Exosome was the EV-subtype described in the majority of studies, and most datasets used serum as the primary EVs isolation source. EVs isolation was primarily conducted by ultracentrifugation. 31 datasets reported that EVs hold considerable potential for being used in diagnostics, with the majority reporting different types of miRNAs as biomarkers. Besides, 8 datasets reported that EVs could be a potential source of prognostic biomarkers. And finally, 3 datasets reported that EVs might be a reliable strategy for monitoring therapy response in glioma patients. According to the findings of the current systematic review, it seems that miR-301, miR-21, and HOTAIR had the highest diagnostic accuracy. However, heterogeneous and limited evidence regarding prognosis and treatment response monitoring precludes us from drawing a practical conclusion regarding EVs.

Stem Cell-Derived Exosomes as Treatment for Stroke: a Systematic Review.

BACKGROUND: The therapeutic potential of stem cells may largely be mediated by paracrine factors contained in exosomes released from intracellular endosomes. A systematic review was performed to identify the effects of stem cell-derived exosomes for their ability to induce restorative effects in animal models of stroke. METHODS: PubMed, Scopus, and ISI Web of Science databases were searched for all available articles testing stem cell-derived exosomes as therapeutic interventions in animal models of stroke until April 2020. The STAIR scale was used to assess the quality of the included studies. RESULTS: A total of 994 published articles were identified in the systematic search. After screening for eligibility, a total of 16 datasets were included. Type of cerebral ischemia was transient in majority studies and most studies used rat or mice adipose tissue-derived stem cells/bone marrow-derived stem cells. Eight studies indicated improved functional recovery while 8 were able to show reduced infarct volume as a result of exosome therapy. The beneficial effects were mainly attributed to reduced inflammation and oxidative stress, enhanced neurogenesis, angiogenesis, and neurite remodeling. Also, 4 studies demonstrated that exosomes hold great promise as an endogenous drug delivery nano-system. CONCLUSION: In preclinical studies, use of stem cell-derived exosomes is strongly associated with improved neurological recovery and reduced brain infarct volume following stroke. Improved preclinical study quality in terms of treatment allocation reporting, randomization and blinding will accelerate needed progress towards clinical trials that should assess feasibility and safety of this therapeutic approach in humans. Graphical abstract.

A plethora of carbapenem resistance in Acinetobacter baumannii: no end to a long insidious genetic journey.

Acinetobacter baumannii, notorious for causing nosocomial infections especially in patients admitted to intensive care unit (ICU) and burn units, is best at displaying resistance to all existing antibiotic classes. Consequences of high potential for antibiotic resistance has resulted in extensive drug or even pan drug resistant A. baumannii. Carbapenems, mainly imipenem and meropenem, the last resort for the treatment of A. baumannii infections have fallen short due to the emergence of carbapenem resistant A. baumannii (CRAB). Though enzymatic degradation by production of class D ß-lactamases (Oxacillinases) and class B ß-lactamases (Metallo ß-lactamases) is the core mechanism of carbapenem resistance in A. baumannii; however over-expression of efflux pumps such as resistance-nodulation cell division (RND) family and variant form of porin proteins such as CarO have been implicated for CRAB inception. Transduction and outer membrane vesicles-mediated transfer play a role in carbapenemase determinants spread. Colistin, considered as the most promising antibacterial agent, nevertheless faces adverse effects flaws. Cefiderocol, eravacycline, new ß-lactam antibiotics, non-ß-lactam-ß-lactamase inhibitors, polymyxin B-derived molecules and bacteriophages are some other new treatment options streamlined.

The effect of propolis supplementation on clinical symptoms in patients with coronavirus (COVID-19): A structured summary of a study protocol for a randomised controlled trial.

OBJECTIVES: This study aims to assess the effect of propolis supplementation on clinical symptoms in patients with coronavirus (COVID-19). TRIAL DESIGN: This is a Double-Blind, Placebo-Controlled, Parallel Arm, Randomized Phase ΙΙ Clinical Trial. PARTICIPANTS: Patients with the confirmed COVID-19 based on the PCR test are eligible to participate in the trial if they are 18 to 75 years of age and have no history of the current use of warfarin or propolis supplement and presence of sensitivity to bee products. Patients will be recruited from the Al-Zahra hospital in Isfahan city, Isfahan, Iran. INTERVENTION AND COMPARATOR: Participants (N=40) in the intervention group will receive an identical propolis tablet (containing 300 mg Iranian green propolis extract) three times a day for a period of 2 weeks. Participants (N=40) in the control group will receive an identical placebo tablet (containing 300 mg microcrystalline cellulose) three times a day for 2 weeks. All tablets are prepared by the Reyhan Naghsh Jahan Pharmaceutical Co., Isfahan, Iran. MAIN OUTCOMES: The main outcomes are changes in the coronavirus disease's clinical symptoms including duration and severity from baseline to the end of 2 weeks. RANDOMIZATION: Eligible patients will be randomly allocated in a 1:1 ratio to the intervention or control group. Randomization will be performed on the basis of permuted block sizes of 4 and will be stratified according to sex categories. Randomization sequences will be prepared by the trial's pharmacist with the use of random-number tables. BLINDING (MASKING): The trial-group assignment will be concealed from all participants, clinicians, and investigators throughout the trial. To ensure blinding, randomization sequences will be kept in identical, opaque, sealed, sequentially numbered envelopes. Only the trial's pharmacist has access to the randomization list. Also, the placebo tablet will be similar to the propolis tablet in terms of texture, taste, color, odor, and weight. Both tablets will be provided in containers that are completely identical in weight, shape, labelling, and packaging. NUMBERS TO BE RANDOMIZED (SAMPLE SIZE): The calculated total sample size is 80 patients, with 40 patients in each group. TRIAL STATUS: The protocol is Version 1.0, October 10, 2020. Recruitment began August 22, 2020, and is anticipated to be completed by March 21, 2021. TRIAL REGISTRATION: The name of the trial register: The effect of propolis supplementation on clinical symptoms in patients with coronavirus (COVID-19): A randomized, double-blind, placebo-controlled clinical trial. IRCT registration number: IRCT20200802048267N1 . Date of trial registration: 20 October 2020, retrospectively registered. FULL PROTOCOL: The full protocol is attached as an additional file, accessible from the Trials website (Additional file 1). In the interest of expediting the dissemination of this material, the familiar formatting has been eliminated; this Letter serves as a summary of the key elements of the full protocol.

Association Study between Functional Polymorphisms of MMP9 Gene Promoter and Multiple Sclerosis Susceptibility in an Iranian Population.

BACKGROUND: Matrix metalloproteinase-9 (MMP-9) polymorphisms, C-1562 T and -90 (CA) n repeats, which influence transcriptional activity of this gene, are proposed to play a role in MS susceptibility and its development. In the present study, the possible association of MMP-9 polymorphisms in Iranian MS patients is studied. METHODS: Association of MMP-9 mentioned gene polymorphisms with MS susceptibility was evaluated in unrelated Iranian subjects referred to Al-Zahra Hospital, Isfahan, Iran during 2014 to 2017. RESULTS: -1562 T allele of MMP-9 was associated with increased MS risk. However, we found no overall significant effect of -90 (CA)n repeat on MS susceptibility. CONCLUSION: For as much as MMP-9 molecule is a potential target for MS therapy, to determine whether any of MMP-9 polymorphisms influence MS susceptibility in Iranian MS patients or not, concerning the significant influence of T allele on MS susceptibility and the non-significant association regarding CA repeats, further research is needed before proposing any definite conclusion.

MicroRNA-29b variants and MxA expression change during interferon beta therapy in patients with relapsing-remitting multiple sclerosis.

BACKGROUND: Multiple sclerosis is a chronic inflammatory demyelinating disease of the central nervous system (CNS) characterized by immune-mediated demyelination and axonal injury. Myelin-reactive IFN-γ-producing Th1 cells has been shown to play an important role in the development of MS. MicroRNAs (miRNAs) are a new class of small non-coding RNA molecules about 22 nucleotides long which regulate gene expression post-transcriptionally by binding to 3' UTR of their mRNA targets, and resulting in degradation or transcriptional repression of the targeted mRNA. Accumulating evidence supports that miRNA dysregulation is linked to the pathogenesis of autoimmune diseases that include MS. miR-29b expression has been shown to be upregulated in memory CD4+T cells from relapsing-remitting MS (RR-MS) patients, which may reflect chronic Th1 inflammation. Interferon beta (IFN-ß) benefits patients with MS and reduces symptoms of the RR-MS. MxA is induced by type I interferon and predicts IFN-ß response in MS patients. The aim of this study was to evaluate miR-29b variants and MxA expression and serum IFN-γ level in responders and non-responders to IFN-ß treatment. METHODS: A total of 70 IFN-ß treated RR-MS patients including 35 responders and 35 non-responders were enrolled. We analyzed the expression level of miR-29b variants and MxA using the peripheral blood of MS patients treated with IFN-ß for more than one year. Real-time RT-PCR was performed to analyze miR-29b variants and MxA expression one year after initiation of IFN-ß therapy. Serum cytokine level was measured by ELISA. RESULTS: The results indicated that the expression level of miR-29b-3p changed related to IFN-ß response. Moreover, miR-29b-5p was downregulated under IFN-ß treatment in responders versus non-responders. MxA level was significantly decreased in the responders. There was no change in IFN-γ level following treatment with IFN-ß in the MS patients. CONCLUSIONS: Our results might provide fundamentals for the development of new markers of the biological effects of IFN-ß therapy.

Novel mutation in HTRA1 in a family with diffuse white matter lesions and inflammatory features.

OBJECTIVE: To investigate the possible involvement of germline mutations in a neurologic condition involving diffuse white matter lesions. METHODS: The patients were 3 siblings born to healthy parents. We performed homozygosity mapping, whole-exome sequencing, site-directed mutagenesis, and immunoblotting. RESULTS: All 3 patients showed clinical manifestations of ataxia, behavioral and mood changes, premature hair loss, memory loss, and lower back pain. In addition, they presented with inflammatory-like features and recurrent rhinitis. MRI showed abnormal diffuse demyelination lesions in the brain and myelitis in the spinal cord. We identified an insertion in high-temperature requirement A (HTRA1), which showed complete segregation in the pedigree. Functional analysis showed the mutation to affect stability and secretion of truncated protein. CONCLUSIONS: The patients' clinical manifestations are consistent with cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL; OMIM #600142), which is known to be caused by HTRA1 mutations. Because some aspects of the clinical presentation deviate from those reported for CARASIL, our study expands the spectrum of clinical consequences of loss-of-function mutations in HTRA1.

Elevated serum level of IL-4 in neuromyelitis optica and multiple sclerosis patients.

Mediators have important roles in the pathogenesis of autoimmune diseases. Interleukin 4 (IL-4) is one of the most important cytokines that has a regulatory effect on immune cells. In the current study, the serum level of IL-4 was assessed in the newly diagnosed neuromyelitis optica (NMO) and multiple sclerosis (MS) patients compared to healthy subjects. ELISA technique was used for assessment of the serum level of IL-4, and data analysis was performed by SPSS software. Serum level of IL-4 was elevated in both NMO and MS patients compared with healthy individuals (P < .001), but no statistically significant difference was identified between MS and NMO patients (P = .071). Furthermore, gender (female) and AQP4-Ab had significant impacts on the level of IL-4 in NMO patients (P < .001). These data show the crucial role of IL-4 in the pathogenesis of NMO and MS diseases. However, we suggest future studies to investigate the serum level of IL-4 in NMO and MS patients to clarify more roles of this cytokine in the pathogenesis of both diseases.

Comparison of acute ischemic stroke evaluation and the etiologic subtypes between university and nonuniversity hospitals in Isfahan, Iran.

BACKGROUND AND PURPOSE: Performing a proper causative workup for ischemic stroke patients is essential as it guides the direction of primary and secondary preventions. We aim to investigate the etiological evaluation of these patients in university and nonuniversity hospitals. METHOD: We enrolled subjects from the Persian Registry of Cardiovascular Disease-stroke. Stroke patients were categorized base on an etiological-based classification (Trial of Org 10172 in Acute Stroke Treatment or TOAST) into five groups. We also separated patients with ischemic stroke of undetermined etiology due to incomplete standard evaluation from ischemic stroke of undetermined etiology due to negative standard evaluation. The etiological subtypes and diagnostic evaluations were compared between the two hospital groups. RESULT: Ischemic stroke of undetermined etiology was the most common subtype overall (43%). The prevalence of ischemic stroke of undetermined etiology (incomplete standard evaluation) was significantly higher in patients evaluated in nonuniversity hospitals versus university hospital (46.2% vs. 22.3%). Patients with ischemic stroke of undetermined etiology (negative standard evaluation) and large-artery atherosclerosis were significantly more prevalent in university hospitals (10.3% vs. 4.6% and 13.9% vs. 4.4%, respectively). All diagnostic workups were performed more significantly for university hospital patients. Patients with Ischemic stroke of undetermined etiology (negative standard evaluation). Patients were significantly younger (64.91 ± 14.44 vs. 71.42 ± 12.93) and had lower prevalence of risk factors such as hypertension (48.5% vs. 65.4%) and diabetes (19.4% vs. 33.1%) than patients in ischemic stroke of undetermined etiology (incomplete standard evaluation) subgroup. University hospital patients had better clinical outcomes in terms of mortality and degree of disability during one-year follow-up. CONCLUSION: The high clinical burden of ischemic stroke of undetermined etiology especially in nonuniversity hospitals shows the rational for promoting ischemic stroke evaluation and providing specialized stroke centers for these hospitals in a developing country like Iran.

Evaluation of glucose-6-phosphate dehydrogenase serum level in patients with multiple sclerosis and neuromyelitis optica.

Background: Multiple sclerosis (MS) and neuromyelitis optica (NMO) are both demyelinating disorders and oxidative stress is suggested to have a role in their pathogenesis. Glucose-6-phosphate dehydrogenase (G6PD) produces nicotinamide adenine dinucleotide phosphate (NADPH) via the pentose phosphate pathway. NADPH is not only involved in the synthesis of fatty acids necessary for myelination, but also it is involved in the defense against oxidative stress. Prescribing supplementary vitamin D as a part of the MS treatment plan can increase G6PD gene expression. The aim of this study was to determine the serum level of G6PD in patients with MS and NMO and its relationship with vitamin D, since it is yet to be explored thoroughly. Methods: In this case-control study, subjects were divided into three experimental and control groups. The experimental groups comprised 50 patients with relapsing-remitting MS (RRMS) who had a history of vitamin D consumption, 50 newly-diagnosed MS patients, and 50 patients with NMO. Control group included 65 healthy individuals. Serum level of G6PD was measured and compared among these groups. Results: No significant difference was seen between the G6PD level in patients with MS and NMO, but it should be noted that this level was significantly lower than the healthy group. G6PD serum level was significantly higher in patients with MS who had previously consumed supplementary vitamin D compared to those who had not. Conclusion: G6PD deficiency is observed in patients with MS and NMO. Also, supplementary vitamin D may induce favorable results on the G6PD level.

Preoperative Mechanical Bowel Evacuation Reduces Intraoperative Bleeding and Operation Time in Spinal Surgery.

STUDY DESIGN: Randomized clinical trial. PURPOSE: In this study, we evaluated the effect of mechanical evacuation of the bowels prior to operation on intraoperative bleeding. OVERVIEW OF LITERATURE: Bleeding is the most significant complication in patients undergoing spinal surgery. METHODS: We randomly divided 108 individuals planned to undergo spinal surgery into two age-, sex-, and co-morbidity (especially preoperative hemoglobin [Hb])-matched groups of 54. The treatment group was administered polyethylene glycol (PEG) before the operation, whereas the control group was not. The exact amount (mL) of bleeding during operation, operative time, and approximate amount of blood transfused were recorded. The volume of bleeding and Hb level were also recorded 24 and 48 hours postoperatively. RESULTS: T-tests revealed that intraoperative bleeding, the volume of transfusion, and operative time were significantly lower in the treatment group than in the control group. Statistically significant correlations of intraoperative bleeding with age, body mass index (BMI), preoperative Hb levels, operative time, the volume of transfusion, hospitalization time, and 24- and 48-hour postoperative bleeding were observed (p =0.001, all). Repeated measures analysis of covariance after adjusting the covariate variables revealed that the volume of bleeding showed a near-significant trend in the treatment group compared with that in the control group (p =0.056). Diabetic females had the highest bleeding amount between the groups (p =0.03). Bleeding was higher in patients with higher BMI (p =0.02) and was related to operative time (p =0.001) in both the groups. CONCLUSIONS: Preoperative gastrointestinal tract evacuation by PEG administration can decrease intraoperative bleeding in spinal surgeries; however, more research is imperative regarding PEG administration in surgical procedures for this purpose.

TRPC6 Mutational Analysis in Iranian Children With Focal Segmental Glomerulosclerosis.

INTRODUCTION: Focal segmental glomerulosclerosis (FSGS) ranks among nephrotic syndromes. Research shows that FSGS is brought about by several genes including transient receptor potential cation channel subfamily c member 6 (TRPC6). This study aimed to investigate TRPC6 gene in Iranian FSGS children. MATERIALS AND METHODS: Twenty-six FSGS patients were included. They were all under 16 years old. Polymerase chain reaction amplification and sequencing were performed to examine exons 2 and 13 of TRPC6 gene. RESULTS: Sampling was performed when the patients had a mean age of 9.26 ± 3.19 years. Sixteen children were boys (61.5%); male-female ratio was 1.35:1. Four patients (15.4%) were diagnosed with TRPC6 variants. Three missense nonsynonymous mutations (C121S, D130V, and G162R) and 1 synonymous mutation (I111I) were detected. All variants were novel; in silico analysis predicted D130V and G162R as pathogenic. Patients with and without mutations were not different significantly regarding age at disease onset, sex, consanguinity, hypertension, hematuria, serum creatinine and albumin, rate of progression to kidney failure, response to steroids, and resistance to cyclosporine A and cyclophosphamide. CONCLUSIONS: This study examined exons 2 and 13 of TRPC6 gene in Iranian FSGS children. Four novel TRPC6 variants were detected; in silico analysis showed that 2 variants (D130V and G162R) could be pathogenic. It could be concluded that TRPC6 may be useful for genetic screening in Iranian FSGS children.

Opium Addiction and Ischemic Stroke in Isfahan, Iran: A Case-Control Study.

BACKGROUND: The effect of opium addiction (OA) on cerebrovascular disease is controversial. The aim of this study was to clarify this relationship in Iranian patients with ischemic stroke. METHODS: In a case-control study, 672 patients with ischemic stroke and 293 controls without a previous history of cerebrovascular or cardiovascular diseases were compared. OA as well as other risk factors such as diabetes mellitus (DM), hypertension (HTN), hyperlipidemia, tobacco smoking (TS) were compared between the 2 groups. RESULTS: OA percentage, TS, TS amount (pack/year), HTN and DM history were significantly higher in the case group compared to controls (p < 0.05). After regression analysis between risk factors, a significant difference remained between 2 groups with regards to HTN (OR 4.21, 95% CI 3.05-5.81, p < 0.001), TS (OR 2.33, 95% CI 1.51-3.59, p < 0.001), and OA (OR 2.36, 95% CI 1.16-4.85, p = 0.018). CONCLUSION: Our study showed OA is a risk factor for stroke. However, a follow-up study with a larger cohort is required to confirm the results.

Polymorphisms at activated protein C cleavage sites of factor V: Are they important in the absence of factor V Leiden?

Background: Activated protein C (APC) inactivates factor V (FV) by cleavage of its heavy chain at Arg306, Arg506, Arg679, and Lys994. Mutational changes, which abolish APC cleavage sites, may predispose thrombosis by altering the inactivation process of FV. FV Leiden (FVL) (Arg506Glu) has been demonstrated as a strong risk factor for thrombosis. In the current study, we have studied whether mutations in the cleavage sites of FV for APC, not due to FVL, would have a role in presenting APC resistance (APCR) and initiation of a cerebral thrombotic event. Methods: A group of 22 patients with a history of cerebral venous thrombosis (CVT), who were not carriers of FVL enrolled in the study. The patients who had conditions associated with acquired APCR were excluded from the study. APCR test was performed on the remaining 16 patients, which showed APCR in 4 plasma samples. DNA sequencing was performed on four exons of FV of APCR patients, encoding Arg306, Arg506, Arg679, and Lys994. Results: Mutations were not found within nucleotides encoding the cleavage sites; neither was found within their close upstream and downstream sequences. Conclusion: Our results show that polymorphisms affecting cleavage sites of FV other than Arg506Glu it would be less likely to be the basis for APCR and its increased thrombosis susceptibility. In addition, it emphasizes on the importance of screening for APCR in the patients diagnosed with CVT.