A Study of Iran’s Comparative Advantage in Saffron, the Red Gold

Crop Production/Industries, Environmental Economics and Policy,

Impact of sanctions on bilateral trade of agricultural products between Iran and MENA region and the EU countries

This paper uses Generalized Method of Moments (GMM) estimation, gravity model, and dynamic panel data to evaluate the effect of the imposed sanctions against Iran on the value of the bilateral trade of agricultural products between Iran and its trading partners among the MENA and the EU countries during 2000 to 2014. The results show that the sanctions have had no effects on the trade flows between Iran and the MENA countries. However, they have meaningful impact on the Iran’s agricultural export to the EU countries, albeit they have caused a decrease in Iran’s agricultural import from this area. The annual precipitation in Iran, as a control variable, using in this paper has positive effects on the Iran’s agricultural export to the EU countries, nonetheless has negative effects on the Iran’s import from the mentioned countries. The overall country size of two trading partners’ variable has meaningful and direct effects on the mutual trade between Iran and the EU countries. According to the above outcomes, the imposed sanctions should be considered as an opportunity to the Iranian agricultural development and diversification of exports from the agriculture sector to the EU region as a wide range of non-oil products to compensate some of the costs on the Iranian economy caused by sanctions

Long-run Trend and Determinants of Terms of Trade of Iran

This paper examines the trend and determinants of terms of trade of Iran. Using a Vector-Error Correction model (VECM), two models has been estimated for Iran's economy. Terms of trade in model I is the net barter terms of trade; and in model II is the ratio of export to import unit values. Annual data of 1966-2012 and seasonal data of 1991-2011 have been used for respectively, model I and II. Four variables have been identified as main explanatory elements of variation in terms of trade over time; these variables are output, exchange rate, trade openness and oil prices. VEC model is used to capture the long-run interaction among variables. In first part of the article, the trend in terms of trade is evaluated to investigate whether there is a negative trend exists among TOT data as the Prebisch- Singer Hypothesis suggests there would be such a tendency in a commodity exporting country like Iran. Results show that there is not a significant decreasing trend in TOT data. VECM results show short-run causality from all variables to the terms of trade in. Also variables converged to their equilibrium levels. The correlation of the terms of trade is negative with exchange rate and positive with output, oil prices and trade openness in long-run. Keywords: Terms of Trade, Unit Root Test, VECM model JEL Classifications: F11; C8; C3

Fuel Switching Impacts of the Industry Sector under the Clean Development Mechanism: A General Equilibrium Analysis of Iran

The importance of international cooperation in reducing the Green House Gas (GHG) has been widely recognized. The primary tool for involving developing countries in carbon reduction without hindering their development is the clean development mechanism. In order to simulate numerically the impact of the Iran clean energy development of the industrial sector under the CDM, a computable general equilibrium (CGE) model is used. The numerical simulations reveal the growth potential and sustainable development benefits that represent the CDM for Iran, though the environmental impact in terms of carbon emission of sectors appears broadly mixed. Based on results some sectors benefit from these clean investment flows -including industry- other sectors show carbon emission increases, but the overall emission of the economy decrease and results in lower environmental costs in green GDP. Keywords: Clean Development Mechanism, Computable General Equilibrium, Industry Sector, Iran. JEL Classifications: D58, O13, Q56

Biallelic variants in OGDH encoding oxoglutarate dehydrogenase lead to a neurodevelopmental disorder characterized by global developmental delay, movement disorder, and metabolic abnormalities

PURPOSE: This study aimed to establish the genetic cause of a novel autosomal recessive neurodevelopmental disorder characterized by global developmental delay, movement disorder, and metabolic abnormalities. METHODS: We performed a detailed clinical characterization of 4 unrelated individuals from consanguineous families with a neurodevelopmental disorder. We used exome sequencing or targeted-exome sequencing, cosegregation, in silico protein modeling, and functional analyses of variants in HEK293 cells and Drosophila melanogaster, as well as in proband-derived fibroblast cells. RESULTS: In the 4 individuals, we identified 3 novel homozygous variants in oxoglutarate dehydrogenase (OGDH) (NM_002541.3), which encodes a subunit of the tricarboxylic acid cycle enzyme α-ketoglutarate dehydrogenase. In silico homology modeling predicts that c.566C>T:p.(Pro189Leu) and c.890C>A:p.(Ser297Tyr) variants interfere with the structure and function of OGDH. Fibroblasts from individual 1 showed that the p.(Ser297Tyr) variant led to a higher degradation rate of the OGDH protein. OGDH protein with p.(Pro189Leu) or p.(Ser297Tyr) variants in HEK293 cells showed significantly lower levels than the wild-type protein. Furthermore, we showed that expression of Drosophila Ogdh (dOgdh) carrying variants homologous to p.(Pro189Leu) or p.(Ser297Tyr), failed to rescue developmental lethality caused by loss of dOgdh. SpliceAI, a variant splice predictor, predicted that the c.935G>A:p.(Arg312Lys)/p.(Phe264_Arg312del) variant impacts splicing, which was confirmed through a mini-gene assay in HEK293 cells. CONCLUSION: We established that biallelic variants in OGDH cause a neurodevelopmental disorder with metabolic and movement abnormalities

Biallelic variants in OGDH encoding oxoglutarate dehydrogenase lead to a neurodevelopmental disorder characterized by global developmental delay, movement disorder, and metabolic abnormalities

Purpose: This study aimed to establish the genetic cause of a novel autosomal recessive neurodevelopmental disorder characterized by global developmental delay, movement disorder, and metabolic abnormalities.Methods: We performed a detailed clinical characterization of 4 unrelated individuals from consanguineous families with a neurodevelopmental disorder. We used exome sequencing or targeted-exome sequencing, cosegregation, in silico protein modeling, and functional analyses of variants in HEK293 cells and Drosophila melanogaster, as well as in proband-derived fibroblast cells.Results: In the 4 individuals, we identified 3 novel homozygous variants in oxoglutarate dehydrogenase (OGDH) (NM_002541.3), which encodes a subunit of the tricarboxylic acid cycle enzyme alpha-ketoglutarate dehydrogenase. In silico homology modeling predicts that c.566C > T:p.(Pro189Leu) and c.890C > A:p.(Ser297Tyr) variants interfere with the structure and function of OGDH. Fibroblasts from individual 1 showed that the p.(Ser297Tyr) variant led to a higher degradation rate of the OGDH protein. OGDH protein with p.(Pro189Leu) or p.(Ser297Tyr) variants in HEK293 cells showed significantly lower levels than the wild-type protein. Furthermore, we showed that expression of Drosophila Ogdh (dOgdh) carrying variants homologous to p.(Pro189Leu) or p.(Ser297Tyr), failed to rescue developmental lethality caused by loss of dOgdh. SpliceAI, a variant splice predictor, predicted that the c.935G > A:p.(Arg312Lys)/p.(Phe264_Arg312del) variant impacts splicing, which was confirmed through a mini-gene assay in HEK293 cells.Conclusion: We established that biallelic variants in OGDH cause a neurodevelopmental disorder with metabolic and movement abnormalities.(c) 2022 The Authors. Published by Elsevier Inc. on behalf of American College of Medical Genetics and Genomics. This is an open access article under the CC BY licensePeer reviewe

The clinical and genetic spectrum of autosomal-recessive TOR1A-related disorders.

In the field of rare diseases, progress in molecular diagnostics led to the recognition that variants linked to autosomal-dominant neurodegenerative diseases of later onset can, in the context of biallelic inheritance, cause devastating neurodevelopmental disorders and infantile or childhood-onset neurodegeneration. TOR1A-associated arthrogryposis multiplex congenita 5 (AMC5) is a rare neurodevelopmental disorder arising from biallelic variants in TOR1A, a gene that in the heterozygous state is associated to torsion dystonia-1 (DYT1 or DYT-TOR1A), an early-onset dystonia with reduced penetrance. While 15 individuals with TOR1A-AMC5 have been reported (less than 10 in detail), a systematic investigation of the full disease-associated spectrum has not been conducted. Here, we assess the clinical, radiological and molecular characteristics of 57 individuals from 40 families with biallelic variants in TOR1A. Median age at last follow-up was 3 years (0-24 years). Most individuals presented with severe congenital flexion contractures (95%) and variable developmental delay (79%). Motor symptoms were reported in 79% and included lower limb spasticity and pyramidal signs, as well as gait disturbances. Facial dysmorphism was an integral part of the phenotype, with key features being a broad/full nasal tip, narrowing of the forehead and full cheeks. Analysis of disease-associated manifestations delineated a phenotypic spectrum ranging from normal cognition and mild gait disturbance to congenital arthrogryposis, global developmental delay, intellectual disability, absent speech and inability to walk. In a subset, the presentation was consistent with fetal akinesia deformation sequence with severe intrauterine abnormalities. Survival was 71% with higher mortality in males. Death occurred at a median age of 1.2 months (1 week - 9 years) due to respiratory failure, cardiac arrest, or sepsis. Analysis of brain MRI studies identified non-specific neuroimaging features, including a hypoplastic corpus callosum (72%), foci of signal abnormality in the subcortical and periventricular white matter (55%), diffuse white matter volume loss (45%), mega cisterna magna (36%) and arachnoid cysts (27%). The molecular spectrum included 22 distinct variants, defining a mutational hotspot in the C-terminal domain of the Torsin-1A protein. Genotype-phenotype analysis revealed an association of missense variants in the 3-helix bundle domain to an attenuated phenotype, while missense variants near the Walker A/B motif as well as biallelic truncating variants were linked to early death. In summary, this systematic cross-sectional analysis of a large cohort of individuals with biallelic TOR1A variants across a wide age-range delineates the clinical and genetic spectrum of TOR1A-related autosomal-recessive disease and highlights potential predictors for disease severity and survival