Performance evaluation of petrochemical firms accepted in Tehran stock exchange using DEA (window analysis)

In the past two decades, organizational performance management has become one of the most attractive topics of study. Each organization is needed to evaluate its system to determine the appropriateness and quality of your work in dynamic environments. Data envelopment analysis provides a theoretical framework for performance analysis and performance measurement. The data envelopment analysis (DEA) is a linear programming technique, whose main purpose is to compare and evaluate a number of similar decision making units which have different amounts of used inputs and produced outputs. Dynamic method of data envelopment analysis (window analysis), is a method that enables the calculation of performance over time and can result in improved outcomes.We use the model described in this paper, the performance of listed companies in the petrochemical industry review. The evaluation results are indicated with different companies. The results showed that the six companies are 80% more efficient

Performance evaluation of petrochemical firms accepted in Tehran stock exchange using DEA (window analysis)

In the past two decades, organizational performance management has become one of the most attractive topics of study. Each organization is needed to evaluate its system to determine the appropriateness and quality of your work in dynamic environments. Data envelopment analysis provides a theoretical framework for performance analysis and performance measurement. The data envelopment analysis (DEA) is a linear programming technique, whose main purpose is to compare and evaluate a number of similar decision making units which have different amounts of used inputs and produced outputs. Dynamic method of data envelopment analysis (window analysis), is a method that enables the calculation of performance over time and can result in improved outcomes.We use the model described in this paper, the performance of listed companies in the petrochemical industry review. The evaluation results are indicated with different companies. The results showed that the six companies are 80% more efficient

Performance evaluation of petrochemical firms accepted in Tehran stock exchange using DEA (window analysis)

In the past two decades, organizational performance management has become one of the most attractive topics of study. Each organization is needed to evaluate its system to determine the appropriateness and quality of your work in dynamic environments. Data envelopment analysis provides a theoretical framework for performance analysis and performance measurement. The data envelopment analysis (DEA) is a linear programming technique, whose main purpose is to compare and evaluate a number of similar decision making units which have different amounts of used inputs and produced outputs. Dynamic method of data envelopment analysis (window analysis), is a method that enables the calculation of performance over time and can result in improved outcomes.We use the model described in this paper, the performance of listed companies in the petrochemical industry review. The evaluation results are indicated with different companies. The results showed that the six companies are 80% more efficient

Simplified on-line monitoring system of MOSFET on-resistance based on a semi-empirical model

This work provides a solution allowing to monitor on-line the health of a power MOSFET adopted in a buck converter. In the considered application, the analysis is focused on the high-side switch, being a low-voltage power MOSFET. The monitoring system allows estimating the on-resistance of the device by measuring both output current and voltage drop across the switch. Moreover, a semi-empirical model is considered in order to account for the dependence of the on-resistance on operating temperature and gate driving voltage. The on-line implementation of such a model allows estimating on-resistance degradation in real-time with a high level of accuracy in a wide range of operating conditions. An on-line calibration procedure is also implemented in order to assess the on-resistance of fresh devices. Experimental results confirm the accuracy of the system (in conjunction with the proposed model) under different operating conditions: load current from 2A to 6A; device temperature up to 100\ub0C and gate to source voltage (VGS) from 6V to 10.5V. In the abovementioned conditions, an accuracy 642.6% is experimentally found. Hence, the system is able to properly estimate the degradation of on-resistance due to ageing conditions

Production of titanium tetrachloride (TiCl4) from titanium ores: A review

Titanium (Ti) is the ninth most abundant element on earth. The titanium mineral ores are widely distributed in different parts of the world. The two main ores of titanium include rutile (TiO2) and ilmenite (FeO.TiO2). It is aimed to provide the readers with an insight to the main processes currently employed to extract and recover titanium tetrachloride (TiCl4) from different titanium ores. Due to the crucial importance of TiCl4 catalyst in the synthesis and polymerization of polyolefins, the present work examines the literature and developments made in the processing of ilmenite and rutile ores for the extraction of TiCl4. The attention has been paid to the chlorination processes and the main parameters affecting the recovery of TiCl4. Different approaches developed to date are reviewed. Different processes, reaction mechanisms and conditions as well as the kinetic models developed for extraction and purification of TiCl4 in fluidized bed reactors are also reviewed. A literature survey on the combined fluidized bed reactor systems developed for achieving a high-grade synthetic rutile via selective chlorination of low-grade titanium ores having high metal oxides content such as magnesium oxide (MgO) and calcium oxide (CaO) is also reported. Different strategies adopted to avoid agglomeration process during the extraction process are discussed too

Polymerization of propylene in a minireactor: Effect of polymerization conditions on particle morphology

Gas phase polymerization of propylene was carried out in a semi-batch minireactor using a commercially supported Ziegler–Natta (ZN) catalyst. The influence of variables including monomer partial pressure, external electron donor, reaction temperature and time on the particle morphology and size distribution was investigated. Generally, more uniform fragmentation and particle densities were obtained at lower reaction rates. Monomer partial pressure showed a significant role of particle size and its distribution, the higher the monomer partial pressure, the broader particle size distribution was obtained. Polymerization pressure had a significant role on the morphology of particles. Wider cracks and more porosity were resulted from the polymerizations at higher pressures. Furthermore, a broader particle size distribution was obtained from the polymerization at higher pressures. The particle size analysis revealed the monomer partial pressure as the most effective parameter on the distribution of particles. The SEM images showed that three different steps could be distinguished in the development of particle morphology within the particle, showing the initiation and development of cracks and appearance of fragments inside the particle

A novel deletion mutation in ASPM gene in an Iranian family with autosomal recessive primary microcephaly

How to Cite This Article: Akbarizar E, Ebrahimpour M, Akbari S, Arzhanghi S, Abedini SS, Najmabadi H, Kahrizi K. A Novel Deletion Mutation in ASPM Gene in an Iranian Family with Autosomal Recessive Primary Microcephaly. Iran J Child Neurol.  2013 Spring;7(2):23-30. ObjectiveAutosomal recessive primary microcephaly (MCPH) is a neurodevelopmental and genetically heterogeneous disorder with decreased head circumference due to the abnormality in fetal brain growth. To date, nine loci and nine genes responsible for the situation have been identified. Mutations in the ASPM gene (MCPH5) is the most common cause of MCPH. The ASPM gene with 28 exons is essential for normal mitotic spindle function in embryonic neuroblasts.Materials & MethodsWe have ascertained twenty-two consanguineous families withintellectual disability and different ethnic backgrounds from Iran. Ten out of twenty-two families showed primary microcephaly in clinical examination. We investigated MCPH5 locus using homozygosity mapping by microsatellite marker. ResultSequence analysis of exon 8 revealed a deletion of nucleotide (T) in donor site of splicing site of ASPM in one family. The remaining nine families were not linked to any of the known loci. More investigation will be needed to detect the causative defect in these families.ConlusionWe detected a novel mutation in the donor splicing site of exon 8 of the ASPM gene. This deletion mutation can alter the ASPM transcript leading to functional impairment of the gene product. References1. Pattison L, Crow YJ, Deeble VJ, Jackson AP, Jafri H, Rashid Y, et al. A Fifth Locus for Primary Autosomal Recessive Microcephaly Maps to Chromosome 1q31. Am J Hum Genet 2000;67(6):1578-80.2. Darvish H, Esmaeeli-Nieh S, Monajemi G, Mohseni M, Ghasemi-Firouzabadi S, Abedini S, et al. A clinical and molecular genetic study of 112 Iranian families with primary microcephaly. Journal of Medical Genetics 2010;47(12):823-8.3. Tolmie JL, M M, JB S, D D, JM C. Microcephaly: genetic counselling and antenatal diagnosis after the birth of an affected child. Am JMed Genet 1987;27583-94.4. Cowie V. The genetics and sub-classification of microcephaly. J Ment Defic Res 1960;4:42-7. 5. Woods C. Human microcephaly. Curr Opin Neurobiol 2004;14(1):112-7.6. Kaindl AM PS, Kumar P, Kraemer N, Issa L, Zwirner A, Gerard B, Verloes A MS,et al.Many roads lead to primary autosomal recessive microcephaly. Prog Neurobiol 2010;90:363-83.7. Kumar A BS, Babu M, Markandaya M, Girimaji SC. Genetic analysis of primary microcephaly in Indian families: novel ASPM mutations. Clin Genet 2004;66:341-8.8. Jackson AP, Eastwood H, Bell SM, Adu J, Toomes C, Carr IM, et al. Identification of microcephalin, a protein implicated in determining the size of the human brain. The American Journal of Human Genetics 2002;71(1):136-42.9. Roberts E, Jackson AP, Carradice AC, Deeble VJ, Mannan J, Rashid Y, et al. The second locus for autosomal recessive primary microcephaly (MCPH2) maps to chromosome 19q13. 1-13.2. European journal of human genetics: EJHG  1999;7(7):815.10. Kousar R, Hassan MJ, Khan B, Basit S, Mahmood S, Mir A, et al. Mutations in WDR62 gene in Pakistani families with autosomal recessive primary microcephaly. BMC neurology 2011;11(1):119.11. Evans PD, Vallender EJ, Lahn BT. Molecular evolutionof the brain size regulator genes<i> CDK5RAP2</i>and<i> CENPJ</i>. Gene 2006;375:75-9.12. Nagase T, Nakayama M, Nakajima D, Kikuno R, Ohara O. Prediction of the coding sequences of unidentified human genes. XX. The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro. DNA research 2001;8(2):85-95. 13. Jamieson CR GC, Abramowicz MJ. Primary autosomal recessive microcephaly: homozygosity mapping of MCPH4 to chromosome 15. Am J Hum Genet 1999;65:1465-9.14. Genin A, Desir J, Lambert N, Biervliet M, Van Der Aa N, Pierquin G, et al. Kinetochore KMN network gene CASC5 mutated in Primary Microcephaly. Human molecular genetics 2012.15. Bond J, Roberts E, Mochida GH, Hampshire DJ, Scott S, Askham JM, et al. ASPM is a major determinant of cerebral cortical size. Nature genetics 2002;32(2):316-20.16. Fish JL, Kosodo Y, Enard W, Pääbo S, Huttner WB. Aspm specifically maintains symmetric proliferative divisions of neuroepithelial cells. Proceedings of the National Academy of Sciences 2006;103(27):10438-43.17. Leal G, Roberts E, Silva E, Costa S, Hampshire D, Woods C. A novel locus for autosomal recessive primary microcephaly (MCPH6) maps to 13q12.2. Journal of Medical Genetics 2003;40(7):540-2.18. Kumar A. Mutations in STIL, encoding a pericentriolar and centrosomal protein, cause primary microcephaly. The American Journal of Human Genetics 2009;84(2):286-90.19. Hussain MS, Baig SM, Neumann S, Nurnberg G, Farooq M, Ahmad I, et al. Atruncating mutation on CEP135 causes primary microcephaly and disturbed centrosomal function.AMJ,HumGenet 2012;90:871-8.20. Guernsey DL, Jiang H, Hussin J, Arnold M, Bouyakdan K, Perry S, et al. Mutations in centrosomal protein CEP152 in primary microcephaly families linked to MCPH4. The American Journal of Human Genetics 2010;87(1):40-51.21. Gul A, Hassan MJ, Mahmood S, Chen W, Rahmani S, Naseer MI, et al. Genetic studies of autosomal recessive primary microcephaly in 33 Pakistani families: novel sequence variants in ASPM gene. Neurogenetics 2006;7(2):105-10.22. Roberts E, Hampshire D, Springell K, Pattison L, Y C, Jafri H, et al. Autosomal recessive primary microcephaly: an analysis of locus heterogeneity and phenotypic variation. J Med Genet 2002;39:718–721.23. Woods CG BJ, Enard W. Autosomal recessive primary microcephaly (MCPH): a review of clinical, molecular, and evolutionary findings. Am J Hum Genet 2005 May;76(5):717-28.24. Kouprina N, Pavlicek A, Collins NK, Nakano M, Noskov VN, Ohzeki JI, et al. The microcephaly ASPM gene is expressed in proliferating tissues and encodes for a mitotic spindle protein. Human Molecular Genetics 2005;14(15):2155-65.25. Bond J, Scott S, Hampshire DJ, Springell K, Corry P, Abramowicz MJ, et al. Protein-Truncating Mutations in< i> ASPM</i> Cause Variable Reduction in Brain Size. The American Journal of Human Genetics 2003;73(5):1170-7.26. Pichon B, Vankerckhove S, Bourrouillou G, Duprez L, Abramowicz MJ. A translocation breakpoint disrupts the ASPM gene in a patient with primary microcephaly. European journal of Human Genetics 2004;12(5):419-21.27. Garshasbi.M, Motazacker M, Kahrizi K, Behjati F, Abedini S, Nieh S, et al. SNP array-based homozygosity mapping reveals MCPH1 deletion in family with autosomal recessive mental retardation and mild microcephaly. Hum Genet 2006 Feb;118(6):708-15.28. Jackson A, McHale D, Campbell D, Jafri H, Rashid Y, Mannan J, et al. Primary autosomal recessive microcephaly (MCPH1) maps to chromosome 8p22-pter. Am J Hum Genet 1998 Aug;63(2):541-6.29. Moynihan L, Jackson A, Roberts E, Karbani G, Lewis I, Corry P, et al. A third novel locus for primary autosomal recessive microcephaly maps to chromosome 9q34. Am J Hum Genet 2000 Feb;66(2):724-7.30. Bond J, Roberts E, Springell K, Lizarraga S, Scott S, Higgins J, et al. A centrosomalmechanism involving CDK5RAP2 and CENPJ controls brain size. Nat Genet.2005 Apr;37(4):353-5. Nat Genet 2005 Apr;37(4):353-5.31. Jamieson C, Govaerts C, Abramowicz M, J. Primary autosomal recessive microcephaly: homozygosity mapping of MCPH4 to chromosome 15. Am J Hum Genet. 1999;65:1465-9

In vitro intracellular trafficking of biodegradable nanoparticles dextran spermine in cancer cell lines.

The objective of the present study is to evaluate the effect of cationic dextran on the proliferation rate and biosynthetic activities of HT29, a human colonic adenocarcinoma, and MCF7, a human breast cancer cell line. Cationic dextran was prepared by means of reductive-amination between oxidised dextran and the natural oligoamine, spermine. Biological evaluations including cell proliferation assay, and cell cycle were studied. Flow cytometery was performed in order to determine the biological behaviour of cationic dextran after internalised into the cells. Our results clearly indicated that the cationic dextran was not toxic to the cells when the concentration was 5 μg/ml or lower. The results of the cell cycle flow cytometery indicated that the means of R2 in HT29, MCF7 and HeLa cells were less than 5 three days after treatment with 5 μg/ml of cationic dextran. We conclude that the toxicity of cationic dextran is dose dependent and it is not toxic at concentration lower than 5 μg/ml, and tolerable by the cells, and it can be used as a tool for gene delivery

Nintinol Self-Expandable Metallic Stenting in Management of Malignant Obstructive Jaundice: A Case Series

Background and Aims: Palliation therapy is the only available therapeutic method for most patients with tumor-induced obstructive jaundice. Metallic stents are now performed percutaneously as an alternative route to the endoscopic approach. It is widely accepted because of its safety, good patency rate, and minimal invasiveness. This study was designed to evaluate the long-term results of metallic self-expandable stent insertion in patients with malignant stenosis of the biliary tree. Methods: It is a longitudinal study of patients with percutaneously biliary stenting from September 2005 to March 2009. The patients had unresectable malignant biliary obstruction with unsuccessful endoscopic stenting and access. Percutaneous transhepatic cholangiogram performed after adequate local anesthesia, under sonographic or fluoroscopic guidance. Stenting or balloon dilation was performed through the hydrophilic guide wire. Among 50 patients, 45 stents were placed in biliary tree stenosis sites. Patients' follow-up was during the first, second, third, and then the sixth month after insertion of biliary stents. Stent patency was considered successful in our patients, when there were no lab results or sonographic appearance of biliary tree obstruction. Results: 10(20) patients' stent placement treatment failed because of unsuccessful technical procedure. The stenosis of biliary tract was complete and passage of guide wire was not possible through the tumor growth. 6 (15 ) patients with successful stent placements died within one month (mean, 22 days). Total serum bilirubin resolved to below 1.5 mg/dl within 30 days for 36 (90) patients with successful stent placements. Early complications not leading to death occurred in 28 of cases. The mean survival time for all patients who underwent stent placement was 140 days (16-420days). The mean patency rate for all stents was 147 days. Conclusions: Percutaneous biliary stenting is a safe procedure with few technical complications and a high success rate of palliation for patients with malignant biliary jaundice. Early complications are mostly managed conservatively and death is mainly due to systemic effects of the malignant disease