What Constitutes a Good Model? An Analysis of Models for Mortgage Backed Securities

The U.S. agency mortgage backed securities (MBS) market is deep and highly liquid, yet modeling MBS is extremely challenging. This paper applies market participants' desired requirements for a good pricing model to MBS pricing models provided by six of the top MBS dealers. We find that five out of the six models fall short of the desired requirements. The five models are highly correlated, but less correlated with the best model, indicating potential herding among MBS analysts. The most undesirable property of the failed models is the high correlation with the underlying interest rate and options markets.Mortgage-backed securities, option-adjusted spreads, market efficiency

Are Interest Rate Derivatives Spanned by the Term Structure of Interest Rates?

We investigate whether the same finite dimensional dynamic system spans both interest rates (the yield curve) and interest rate options (the implied volatility surface). We find that the options market exhibits factors independent of the underlying yield curve. While three common factors are adequate to capture the systematic movement of the yield curve, we need three additional factors to capture the movement of the implied volatility surface.Factors; principal component; LIBOR; swaps; swaptions; yield curve; implied volatility surface.

Post trade allocation: how much are bunched orders costing your performance?

Individual trade orders are often bunched into a block order for processing efficiency, where in post execution, they are allocated into individual accounts. Since Regulators have not mandated any specific post trade allocation practice or methodology, entities try to rigorously follow internal policies and procedures to meet the minimum Regulatory ask of being procedurally fair and equitable. However, as many have found over the years, there is no simple solution for post trade allocation between accounts that results in a uniform distribution of returns. Furthermore, in many instances, the divergences between returns do not dissipate with more transactions, and tend to increase in some cases. This paper is the first systematic treatment of trade allocation risk. We shed light on the reasons for return divergence among accounts, and we present a solution that supports uniform allocation of return irrespective of number of accounts and trade sizes.Comment: 16 pages, 2 figures, 12 table

Investigating Chronotype Orientation on Daily and Weekly Rhythm Fluctuations in Preschoolers Working Memory Performance

Background: Chronopsychology researches claim that cognitive processes performance during learning in the educational environment in times of the day and days of the week fluctuate, and working memory is essential among these cognitive processes. The research aimed to study the rhythm of daily and weekly working memory performance of preschoolers based on their chronotype (morningness and eveningness) orientation.Methods: The research method is causal-comparative. The participants are 100 preschool children in Tehran that were selected based on purposive sampling. Their working memory was tested at different time intervals of (8, 11, 13, and 15) and weekly (Saturday, Sunday, Monday, Tuesday and Wednesday). Saturday also considered as the first day of the week. Data collection instrument were children morningness-eveningness preference (CMEP) in the form of questionnaire and working memory test. Data analysis based on a mixed analysis of variance.Results: The results showed that preschoolers working memory performance during different days of the week and time of day was different (P < 0.01). There was a significant difference between children in different groups regarding memory at different hours of the day, but on different days of the week, there was no significant difference in memory performance (P < 0.01).Conclusion: According to the findings, teachers and clinicians are suggested to consider the importance of circadian rhythm parameters in assessing cognitive function in patients and healthy people. Awareness of individual differences of the morningness-eveningness type can be very effective in designing training programs and preventive health associated matters with each type

Increased Prevalence 12308 A > G mutation in Mitochondrial tRNALeu (CUN) Gene Associated with earlier Age of Onset in Friedreich Ataxia

How to Cite this Article: Heidari MM, Khatami M, Houshmand M, Mahmoudi E, Nafissi Sh .Increased Prevalence 12308 A > G mutation in MitochondrialtRNALeu (CUN) Gene Associated with earlier Age of Onset in Friedreich Ataxia. Iranian Journal of Child Neurology 2011;5(4):25-31.Objective Friedreich ataxia (FRDA) is an inherited recessive disorder. Mitochondrial DNA is a candidate modifying factor for FRDA.The purpose of this study was to investigate the relationship between the tRNALeu (CUN) 12308 A> G mutation and age of onset in Friedreich ataxia.Materials & Methods The 12308 A> G substitution in mitochondrial tRNALeu (CUN) was examined in DNA samples from 30 Friedreich ataxia patients and 48 control subjects by temporal temperature gradient gel electrophoresis (TTGE) and sequencing. Logistic regression was used to determine of cutoff age of onset.ResultsTwenty-two patients had the 12308 A> G mutation, and we found that its overall prevalence was significantly higher in 20 patients aged 17 years or younger than in 2 patients aged over 17 years (90% versus 10%). The 12308 A> G mutation lies in a region that has been highly conserved between species.Conclusion Our results show that the 12308 A > G mutation is associated with earlier age of onset in Friedreich ataxia. Thus, this mutation might cause the younger age of onset in FRDA.References Grabczyk E, Usdin K. The GAA*TTC triplet repeat expanded in Friedreich ataxia impedes transcription elongation by T7 RNA polymerase in a length and supercoil dependent manner. Nucleic Acids Res 2000;28(14):2815-22.Sakamoto N, Chastain PD, Parniewski P, Ohshima K, Pandolfo M, Griffith JD, et al. Sticky DNA: self association properties of long GAA.TTC repeats in R.R.Y triplex structures from Friedreich ataxia. Mol Cell1999;3(4):465-75.Lodi R, Cooper JM, Bradley JL, Manners D, Styles P, Taylor DJ, et al. Deficit of in vivo mitochondrial ATP production in patients with Friedreich ataxia. Proc Natl Acad Sci U S A 1999;96(20):11492-5.Babcock M, de Silva D, Oaks R, Davis-Kaplan S, Jiralerspong S, Montermini L, et al. Regulation of mitochondrial iron accumulation by Yfh1p, a putative homolog of frataxin. Science 1997;276(5319):1709-12.Wilson RB, Roof DM. Respiratory deficiency due to loss of mitochondrial DNA in yeast lacking the frataxin homologue. Nat Genet 1997;16(4):352-7.Ramazzotti A, Vanmansart V, Foury F. Mitochondrial functional interactions between frataxin and Isu1p, the iron-sulfur cluster scaffold protein, in Saccharomycescerevisiae. FEBS Lett 2004;557(1-3):215-20.Foury F, Cazzalini O. Deletion of the yeast homologue of the human gene associated with Friedreich ataxiaelicits iron accumulation in mitochondria. FEBS Lett1997;411(2-3):373-7.Foury F, Talibi D. Mitochondrial control of iron homeostasis. A genome wide analysis of gene expression in a yeast frataxin-deficient strain. J Biol Chem 2001;276(11):7762-8.Koeppen AH. Friedreich ataxia: pathology, pathogenesis, and molecular genetics. J Neurol Sci 2011;303(1-2):1-12.Kish SJ, Bergeron C, Rajput A, Dozic S, Mastrogiacomo F, Chang LJ, et al. Brain cytochrome oxidase in Alzheimer’s disease. J Neurochem 1992;59(2):776-9.Schapira AH. Mitochondrial complex I deficiency in Parkinson’s disease. Adv Neurol 1993;60(1):288-91.Lu F, Selak M, O’Connor J, Croul S, Lorenzana C, Butunoi C, et al. Oxidative damage to mitochondrial DNA and activity of mitochondrial enzymes in chronicactive lesions of multiple sclerosis. J Neurol Sci2000;177(2):95-103.Bradley JL, Blake JC, Chamberlain S, Thomas PK, Cooper JM, Schapira AH. Clinical, biochemical and molecular genetic correlations in Friedreich ataxia. Hum Mol Genet 2000;9(2):275-82.Rotig A, de Lonlay P, Chretien D, Foury F, Koenig M, Sidi D, et al. Aconitase and mitochondrial iron-sulphur protein deficiency in Friedreich ataxia. Nat Genet1997;17(2):215-7.van den Ouweland JM, Bruining GJ, Lindhout D, Wit JM, Veldhuyzen BF, Maassen JA. Mutations in mitochondrial tRNA genes: non-link age with syndromes of Wolfram and chronic progressive external ophthalmoplegia. Nucleic Acids Res 1992;20(4):679-82.Harding AE. Friedreich ataxia: a clinical and genetic study of 90 families with an analysis of early diagnostic criteria and intrafamilial clustering of clinical features. Brain 1981;104(3):589-620.Geoffroy G, Barbeau A, Breton G, Lemieux B, Aube M, Leger C, et al. Clinical description and roentgenologic evaluation of patients with Friedreich ataxia. Can J Neurol Sci 1976;3(4):279-86.Campuzano V, Monter mini L, Molto MD, Pianese L, Cossee M, Cavalcanti F, et al. Friedreich ataxia: autosomal recessive disease caused by an intronic GAA triplet repeat expansion. Science 1996;271(5254):1423-7.Tan DJ, Bai RK, Wong LJ. Comprehensive scanning of somatic mitochondrial DNA mutations in breast cancer. Cancer Res 2002;62(4):972-6.Sanchez M, Anitua E, Azofra J, Andia I, Padilla S, Mujika I. Comparison of surgically repaired Achilles tendon tearsusing platelet-rich fibrin matrices. Am J Sports Med2007;35(2):245-51.Anderson S, Bankier AT, Barrell BG, de Bruijn MH, Coulson AR, Drouin J, et al. Sequence and organization of the human mitochondrial genome. Nature1981;290(5806):457-65.22. Marmolino D. Friedreich ataxia: past, present and future.Brain Res Rev 2011;67(1-2):311-30.Houshmand M, Mahmoudi T, Panahi MS, Seyedena Y,Saber S, Ataei M. Identification of a new human mt DNA polymorphism (A14290G) in the NADH dehydrogenase subunit 6 gene. Braz J Med Biol Res 2006;39(6):725-30.Rona RJ, Reynolds A, Allsop M, Morris RW, Morgan M, Mandalia S. Audit from preschool developmental surveillance of vision, hearing, and language referrals. Arch Dis Child 1991;66(8):921-6.Heidari MM, Houshmand M, Hosseinkhani S, Nafissi S, Scheiber-Mojdehkar B, Khatami M. A novel mitochondrial heteroplasmic C13806A point mutation associated with Iranian Friedreich ataxia. Cell Mol Neurobiol 2009;29(2):225-33.Covarrubias D, Bai RK, Wong LJ, Leal SM. Mitochondrial DNA variant interactions modify breast cancer risk. J Hum Genet 2008;53(10):924-8.Pulkes T, Sweeney MG, Hanna MG. Increased risk of stroke in patients with the A12308G polymorphism in mitochondria. Lancet 2000;356(9247):2068-9.Wei YH. Oxidative stress and mitochondrial DNA mutations in human aging. Proc Soc Exp Biol Med1998;217(1):53-63.Hess JF, Parisi MA, Bennett JL, Clayton DA. Impairment of mitochondrial transcription termination by a point mutation associated with the MELAS subgroup of mitochondrial encephalomyopathies. Nature 1991;351(6323):236-9.

Ability of Ultrasonography in Detection of Different Extremity Bone Fractures; a Case Series Study

Introduction: Despite radiography being the gold standard in evaluation of orthopedic injuries, using bedsideultrasonography has several potential supremacies such as avoiding exposure to ionizing radiation, availabilityin pre-hospital settings, being extensively accessible, and ability to be used on the bedside. The aim of thepresent study is to evaluate the diagnostic accuracy of ultrasonography in detection of extremity bone fractures.Methods: This study is a case series study, which was prospectively conducted on multiple blunt trauma patients,who were 18 years old or older, had stable hemodynamic, Glasgow coma scale 15, and signs or symptomsof a possible extremity bone fracture. After initial assessment, ultrasonography of suspected bones was performedby a trained emergency medicine resident and prevalence of true positive and false negative findingswere calculated compared to plain radiology. Results: 108 patients with the mean age of 44.6 § 20.4 years werestudied (67.6% male). Analysis was done on 158 sites of fracture, which were confirmed with plain radiography.91 (57.6%) cases were suspected to have upper extremity fracture(s) and 67 (42.4%) to have lower ones.The most frequent site of injuries were forearm (36.7%) in upper limbs and leg (27.8%) in lower limbs. Prevalenceof true positive and false negative cases for fractures detected by ultrasonography were 59 (64.8%) and 32(35.52%) for upper and 49 (73.1%) and 18 (26.9%) for lower extremities, respectively. In addition, prevalence oftrue positive and false negative detected cases for intra-articular fractures were 24 (48%) and 26 (52%), respectively.Conclusion: The present study shows the moderate sensitivity (68.3%) of ultrasonography in detectionof different extremity bone fractures. Ultrasonography showed the best sensitivity in detection of femur (100%)and humerus (76.2%) fractures, respectively. It had low sensitivity in detection of in intra-articular fractures

Effect of Morningness-Eveningness Chronotype on Daily and Weekly Fluctuations in Aggression in Preschool Children

Background: The present study aimed at studying the morningness-eveningness chronotype (MEC) of daily and weekly biorhythm fluctuations in the aggression of preschool children. Methods: This was a causal-comparative study. The statistical population was preschool children in Tehran. One hundred children were selected through purposive sampling. They were examined at different times of day (08:00, 10:00, 13:00 and 15:00) and different days of the week (Saturday, Sunday, Monday, Tuesday and Wednesday). The data collection tool used was the MEC questionnaire for children, a behavioral questionnaire for preschool children and a self-report questionnaire about aggression. The data was analyzed using mixed ANOVA. Results: The results showed that the aggressive behavior of pre-school children in the educational environment varies throughout the day and week. Also, the aggressive performance of preschool children in the morning differed from that of mid-session children or evening-type children in the educational environment during the week (P<0.01). Conclusion: The results of the behavioral questionnaire showed that the effect of the group on the level of aggression was not significant, but the effect of the day of the week and time of day was significant

Urine and milk iodine concentrations in healthy and congenitally hypothyroid neonates and their mothers

Wstęp: Częste występowanie wrodzonej niedoczynności tarczycy (CH, congenital hypothyroidism) w Iranie skłoniło autorów do oceny roli jodu w etiologii CH, opierając się na porównaniu jego stężenia w moczu zdrowych noworodków i noworodków z wrodzoną niedoczynnością tarczycy oraz w mleku i moczu ich matek. Materiał i metody: W tym przekrojowym badaniu zmierzono stężenie jodu w moczu (UIC, urinary iodine concentration) noworodków z CH oraz UIC i stężenie jodu w mleku (MIC, milk iodine concentration) ich matek, a następnie porównano je z wynikami otrzymanymi w grupie kontrolnej. Wartości UIC zmierzone u noworodków i karmiących matek podzielono na 3 kategorie: niskie UIC < 150 mg/l, średnie - 150-230 mg/l i wysokie > 230 mg/l. Analogiczne kategorie przyjęto dla MIC: niskie 180 mg/l. Wyniki: Mediana UIC u noworodków z CH (n = 68) i u zdrowych noworodków (n = 179) wynosiła odpowiednio 300,5 i 290,5 mg/dl, (P > 0,05). Mediana UIC w grupach badanej i kontrolnej wynosiła odpowiednio 150 i 130 mg/l (P > 0,05). Mediana MIC w grupie badanej była większa niż w grupie kontrolnej (210 mg/l v. 170 mg/l, P < 0,05). Stwierdzono dodatnią korelację między UIC u noworodków i MIC u ich matek. Nie wykazano wyraźnej zależności między UIC i stężeniem TSH w surowicy u noworodków oraz UIC I MIC u matek. Wnioski: Spożycie sodu w badanej populacji było prawidłowe. Nadmierna podaż sodu może być czynnikiem ryzyka CH, jednak w badaniu wykazano brak korelacji między MIC I UIC u matek i podobne wartości mediany UIC u noworodków w obu grupach, dlatego do sformułowania jednoznacznych wniosków potrzebne są dalsze badania. (Endokrynol Pol 2010; 61 (4): 371-376)Introduction: In view of the high prevalence of Congenital Hypothyroidism (CH) in Iran, in this study we evaluated the role of iodine in the aetiology of CH by comparing urine and milk iodine concentrations in healthy and congenitally hypothyroid neonates and their mothers. Material and methods: In a cross-sectional study, urinary iodine concentrations (UIC) in newborns with CH, as well as UIC and the milk iodine concentrations (MIC) of their mothers, were measured and compared with a control group. The lower, mid, and upper range of UIC for neonates and lactating mothers was considered to be 230 mg/L, and lower, mid, and upper range of MIC was considered to be 180 mg/L, respectively. Results: The median UICs in subjects with CH (n = 68) and healthy subjects (n = 179) were 300.5 and 290.5 mg/L, respectively (P > 0.05). The median UICs in the case and control groups were 150 and 130 mg/L, respectively (P > 0.05). The median MIC in the case group was higher than in the control group (210 mg/L v. 170 mg/L, P < 0.05).There was a positive correlation between newborn UIC and MIC. There was no significant correlation between newborn UIC and serum TSH, maternal UIC and maternal MIC, or newborn UIC and serum TSH. Conclusions: There is no inadequacy in iodine intake in the studied population. Iodine excess could be a possible risk factor for CH, but there were findings, such as lack of correlation between maternal MIC and UIC, and the median neonatal UIC, which was similar in the two groups, so, drawing conclusions should be done with some caution and requires further studies. (Pol J Endocrinol 2010; 61 (4): 371-376