Do local banks credits to private sector and domestic direct investments affect FDI inflow? (Malaysia evidence)

This study analysis the factors affecting foreign direct investment inflow in manufacturing sector in Malaysia in between 1974 to 2009, mainly focused on two determinants; domestic credit to private sector by local commercial banks and domestic direct investment. Growth Domestic product and the Trade Openness are also included in the model respectively; the results indicate that Gross Domestic Product of manufacturing, Trade openness, domestic credit to private sector and domestic direct investment significantly influenced the level of foreign direct investment inflow into Malaysia. This study manipulate the cointegration test method and Vector Auto Regression Granger causality between logarithm of foreign direct investment, domestic credit to private sector and domestic direct investment respectively which illustrates both variables are cointegrated and also Granger caused of foreign direct investment

The determinants of FDI inflow in manufacturing sector of Malaysia

The role of foreign direct investment (FDI) to create competition,technology transfer, reducing unemployment and generating productive economic growth is undeniable. Therefore, policy makers and economists seek to identify the factors that affect FDI in different sectors. Accordingly, this study investigated the determinants of FDI in manufacturing sector of Malaysia over the period from 2000 to 2009. Using quarterly data, this research found a positive and significant effect of domestic credit to private sector provided by banking system and development expenditure of government on FDI.Meanwhile, the effect of the global financial recession of 2007–2008 on FDI inflow to Malaysia was positive and significant, though due to this recession reduction of the world aggregate FDI reduced the growth of FDI inflow to the manufacturing sector of Malaysia. The effect of corruption on FDI’s growth was also negative and significan

Study on MRI Changes in Phenylketonuria in Patients Referred to Mofid Hospital/Iran

How to Cite This Article: Karimzadeh P, Ahmadabadi F, Jafari N, Shariatmadari F, Nemati H, Ahadi A, Karimi Dardashti S, Mirzarahimi M, Dastborhan Z, Zare Noghabi J. Study on MRI Changes in Phenylketonuria in Patients Referred to Mofid Hospital. Iran J Child Neurol. 2014 Spring 8(2):53-56.ObjectivePhenylketonuria is one of the most common metabolic disorders and the first known cause of mental retardation in pediatrics. As Screening for phenylketonuria (PKU) is not a routine neurometabolic screening test for neonates in Iran, many PKU cases may be diagnosed after developing the clinical symptoms. One of the findings of PKU is myelination disorders, which is seen as hypersignal regions in T2-weighted (T2W) and FLAIR sequences of brain MRI. The aim of our study was to assess MRI changes in PKU patients referred to Mofid Children’s Hospital, 2010-2011.Materials & MethodsWe studied all PKU cases referred to our clinic as a referral neurometabolic center in Iran for brain MRI and assessed the phenylalanine level at the time of Imaging. The mean phenylalanine level (in one year), clinical manifestations,and MRI pattern based on Thompson scoring, were evaluated.ResultsThe mean age of our study group was 155±99 months and the mean diagnosis age was 37±27.85 months. There were 15 patients with positive and 15 with negative family history. The mean phenylalanine level at the time of imaging was 9.75±6.28 and the mean 1 year phenylalanine level was 10.28±4.82. Seventy percent of our patients had MRI involvement, in whom 20% showed atrophic changes, in addition to white matter involvement. Based on modified Thompson scoring, the score for our study group was 4.84.The maximum involvement in MRI was in occipital region, followed by parietal, frontal, and temporal zones. There was not any correlation between MRI score and patients’ age. But we found significant relationship between MRI score andthe age of regimen cessation. No correlation was seen between phenylalanine level (at the time of Imaging) and MRI score. But there was a relationship between mean 1 year phenylalanine level and MRI score.ConclusionAccording to the results of this study, brain MRI and white matter involvement can be used for evaluation of long-term control of phenylalanine level in PKU cases. References1. Blau Nenad. Phenylketonuria and BH4 Deficiencies. London: UNI-MED; 2010.2. Buck PS. The child who never grew. Woodbine House; 1992.3. Rezvani I, Melvin JJ. Defects in metabolism of amino acids. In: Kliegman RM, Stanton BF, St. Geme J, Behrman RE, editors. Nelson Textbook of Pediatrics. 19th ed. USA: Elsevier; 2011. p. 418-22.4. Menkes J, Wilcox WR. Inherited Metabolic Diseases of nervous system. In: Menkes JH, editor Child neurology. 7th ed. Philadelphia: Lippincott Williams&Wilkins; 2006. p. 34-36.5. Aicardi J. Diseases of the nervous system in childhood. London: Mac Keith press; 2009.6. Enns GM, Cowan TM, Klein O, Packman S. Aminoacidemias and organic acidemias. In: Swaiman KF. Swaimans Pediatric Neurology principle and practice. 5th ed. China: Saunders; 2012. p. 330-7.7. Barkovich J. Toxic and Metabolic Brain disorders. In: Barkovich J, editor Pediatric Neuroimaging. 4th ed. USA: Lippincott William&Wilkins;2005. p. 88-92.8. Van der knaap MS. Phenylketonuria. In: Van der knaap MS, Valk J, editor. Magnetic resonance of Myelination and Myelin Disorders. 3rd ed. Germany: Springer; 2005. p. 285-90.9. Manara R, Burlina AP, Citton V, Ermani M, Vespignani F, Carollo C, et al. Brain MRI diffusion-Weighted imaging in patients with classical phenylketonuria: Neuroradiology (2009)51:803-12.10. Möller HE, Weglage J, Bick U, Wiedermann D, Feldmann R, Ullrich K. Brain imaging and proton Magnetic Resonance Spectroscopy in Patients with Phenylketonuria Pediatrics 2003;112(6 Pt 2):1580-3.11. Phillips MD, McGraw P, Lowe MJ, Mathews VP, Hainline BE. Diffusion-Weighted Imaging of White Matter Abnormalities in Patients with Phenylketonuria. AJNR Am J Neuroradiol 2001 Sep;22(8):1583-6.12. Cleary MA, Walter JH, Wraith JE, Jenkins JP, Alani SM, Tyler K, et al. Magnetic resonance Imaging of the Brain in Phenyl ketonuria. Lancet 1994;344(8915):87-90

Methylmalonic Acidemia: Diagnosis and Neuroimaging Findings of This Neurometabolic Disorder (An Iranian Pediatric Case Series)

How To Cite This Article: Karimzadeh P, Jafari N, Jabbehdari S, Taghdiri MM, Nemati H, Saket S, Alaee MR, Ghofrani M, Tonakebni SH. Methylmalonic Acidemia: Diagnosis and Neuroimaging Findings of This Neurometabolic Disorder (An Iranian Pediatric Case Series). Iran J Child Neurol. 2013 Summer; 7(3): 63-66. ObjectiveMethylmalonic acidemia is one of the inborn errors of metabolism resulting in the accumulation of acylcarnitine in blood and increased urinary methylmalonic acid excretion. This disorder can have symptoms, such as neurological and gastrointestinal manifestations, lethargy, and anorexia.Materials & MethodsThe patients who were diagnosed as methylmalonic acidemia in the Neurology Department of Mofid Children’s Hospital in Tehran, Iran, between 2002 and 2012 were included in our study. The disorder was confirmed by clinical findings, neuroimaging findings, and neurometabolic and geneticassessment in reference laboratory in Germany. We assessed the age, gender, past medical history, developmental status, clinical manifestations, and neuroimaging findings of 20 patients with methylmalonic acidemia.ResultsEighty percent of the patients were offspring of consanguineous marriages. Half of the patients had Failure to thrive (FTT) due to anorexia; 85% had history of developmental delay or regression, and 20% had refractory seizure, which all of them were controlled. The patients with methylmalonic acidemia were followed for approximately 5 years and the follow-up showedthat the patients with early diagnosis had a more favorable clinical response in growth index, refractory seizure, anorexia, and neurodevelopmental delay. Neuroimaging findings included brain atrophy, basal ganglia involvement (often in putamen), and periventricular leukomalacia.ConclusionAccording to the results of this study, we suggest that early assessment and diagnosis have an important role in the prevention of disease progression and clinical signs.References:1. Trinh BC, Melhem ER, Barker PB. Multi-slice proton MR spectroscopy and diffusion-weighted imaging in methylmalonic acidemia: report of two cases and review of the literature. AJNR Am J Neuroradiol 2001;22(5):831-3.2. Mahoney MJ, Bick D. Recent advances in the inherited methylmalonic acidemias. Acta Paediatr Scand1987;76(5):689-96.3. Radmanesh A, Zaman T, Ghanaati H, Molaei S, Robertson RL, ZamaniAA. Methylmalonic acidemia: brain imaging findings in 52 children and a review of the literature.Pediatr Radiol 2008 Oct;38(10):1054-61.4. Cantani A. [Methylmalonic acidemia: classification, diagnosis and therapy]. KlinPadiatr 1983;195(6):388-93.5. Avery ME, First LR, Pediatric Medicine, 2nd ed. Williams & Wilkins, Waverly Company; 1994. p.1075.6. Matsui SM, Mahoney MJ, Resenberg LE. The natural history of the inherited methylmalonic acidemias. N Engl J Med 1983;308(15):857-61.7. Holliday MA, Barrat M, Arner ED. Pediatric Nephrology, 3rd ed. William and Wilkins 1994; p. 890.8. Soda H, Yoshida I, Aramaki S, Kuriya N, Aoki K, Inokuchi T, et al. Renal handling of methylmalonic acid in a uraemic patient with vitamin B12 unresponsive methylmalonica cidaemia. J Inherit Metab Dis 1996;19(1):90-1.9. Imen M, Hanene B, Ichraf K, Aida R, Ilhem T, Naziha K, et al. Methylmalonic acidemia and hyperglycemia: an unusual association. Brain Dev 2012;34(2):113-4.10. Ma X, Zhang Y, Yang Y, Liu X, Yang Z, Bao X, et al. Epilepsy in children with methylmalonic acidemia: electroclinical features and prognosis. Brain Dev 2011;33(9):790-5.11. Brismar J, Ozand PT. CT and MR of the brain in disorders of the propionate and methylmalonatemetabolism. AJNR Am J Neuroradiol 1994;15(8):1459-73.12. Nicolaides P, Leonard J, Surtees R. Neurological outcome of methylmalonic acidaemia. Arch Dis Child 1998;78:508-12.

Evaluation of One Hundred Pediatric Muscle Biopsies During A 2-Year Period in Mofid Children And Toos Hospitals

 How to Cite This Article:Nilipor Y, Shariatmadari F, Abdollah gorji F, Rouzrokh M, Ghofrani M, Karimzadeh P, Taghdiri MM,  Delavarkasmaei H, Ahmadabadi F, Bakhshandeh bali MK, Nemati H, Saket S, Jafari N, Yaghini O, Tonekaboni SH.  Evaluation of One Hundred Pediatric Muscle Biopsies During A 2-Year Period in Mofid Children And Toos Hospitals. Iran J Child Neurol. 2013 Spring;7(2):17-21. ObjectiveMuscle biopsy is a very important diagnostic test in the investigation of a child with suspected neuromuscular disorder. The goal of this study was to review and evaluate pediatric muscle biopsies during a 2-year period with focus on histopathology diagnosis and correlations with other paraclinicstudies.Materials & MethodsWe investigated 100 muscle biopsies belonging to patients with clinical impression of neuromuscular disorder. These patients have been visited consecutively by pediatric neurologists during 2010 to 2012. Samples were investigated by standard enzyme histochemical and immunohistochemical techniques.ResultSixty-nine (69%) males and 39 (39%) females with a mean age of 5.7 years were evaluated. Major pathologic diagnoses were Muscular dystrophy (48 cases), Neurogenic atrophy (18 cases), nonspecific myopathic atrophy (12cases), congenital myopathy (6 cases), storage myopathies (4 cases) and in 6 cases there was no specific histochemical pathologic finding. EMG was abnormal in 79 cases. Degree of correlation between EMG and biopsy result was significant in children ≥ 2 years of age.ConclusionThis study confirms the high diagnostic yields of muscle biopsyespecially only if standard and new techniques such as enzyme study and immunohistochemistry are implemented. Also, we report 11 cases of Merosin negative congenital muscular dystrophy. This is the largest documented case series of Merosin deficient congenital muscular dystrophy reported from Iran. References1. Harvey B. Sarnat. Evaluation and Investigation. In:Kliegman. Stanton.Schor. Behrman.Nelson Text Book of Pediatrics.19th edition.Philadelphia: Elsevier,2011. P.2109-2112. 2. Harvey B. Sarnat and John H Menkes. Disease of TheMotore Unit. In: John H Menkes, Harvey B Sarnat, Bernard L Maria. Child Neurology. 7th edition.california: lippincott,2006.p.969-972.3. Marius Kuras Skram, Sasha Gulati, Erik Larrson. Muscle Biopsies In Children-An Evaluation Of Histopathology And Clinical Valueduring A 5-Year Period. Upsala J Med Sci 2009 March:114 (1);41-45.4. Owji M, Modaressi F. Diagnosis of Myopathies Using Histology. Histochemistry, Immunohistochemistry and Electron Microscopy 2010,12 (4):434 -440.5. Dua T, Das M, Kabra M. Spectrum of Floppy Children in Indian Scenario. Indian Pediatric J 2001, 38:1236-1243.6. Rabie M, Jossiphov J, Nevo Y. Electromyography accuracy compared to muscle biopsy in childhood. J Child Neurol 2007 jul; 22(7):803.8.