Statistical and computational analysis for corruption and poverty model using Caputo-type fractional differential equations

Since there is a clear correlation between poverty and corruption, mathematicians have been actively researching the concept of poverty and corruption in order to develop the optimal strategy of corruption control. This work aims to develop a mathematical model for the dynamics of poverty and corruption. First, we study and analyze the indicators of corruption and poverty rates by applying the linear model along with the Eviews program during the study period. Then, we present a prediction of poverty rates for 2023 and 2024 using the results of the standard problem-free model. Next, we formulate the model in the frame of Caputo fractional derivatives. Fundamental properties, including equilibrium points, basic reproduction number, and positive solutions of the considered model are obtained using nonlinear analysis. Sufficient conditions for the existence and uniqueness of solutions are studied via using fixed point theory. Numerical analysis is performed by using modified Euler method. Moreover, results about Ulam-Hyers stability are also presented. The aforementioned results are presented graphically. In addition, a comparison with real data and simulated results is also given. Finally, we conclude the work by providing a brief conclusion

Pro106Leu MPL mutation is associated with thrombocytosis and a low risk of thrombosis, splenomegaly and marrow fibrosis

The P106L mutation in the human myeloproliferative leukemia virus oncogene (MPL) was shown to be associated with hereditary thrombocythemia in Arabs. The clinical and bone marrow (BM) features of P106L mutation are unknown. Genetic databases at two tertiary hospitals in Saudi Arabia were searched to identify patients with the MPL P106L mutation. Clinical data were collected retrospectively and the BM aspirates and biopsies were independently reviewed by two hematopathologists. In total, 115 patients were included. Median age was 33 years of which 31 patients were pediatric and 65 were female. The mutation was homozygous in 87 patients. Thrombocytosis was documented in 107 patients, with a median platelet count of 667 × 109/L. The homozygous genotype was associated with a higher platelet count. Thirty-three patients had an evaluable BM and clustering of megakaryocytes was observed in 30/33 patients. At the time of last follow-up, 114 patients were alive. The median follow-up was 7.8 years from the time of thrombocytosis. No patients developed disease progression to myelofibrosis. The P106L mutation was associated with marked thrombocytosis at a younger age and with a low risk of thrombosis, splenomegaly, and marrow fibrosis. The BM demonstrated normal or hypocellular marrow with megakaryocyte clusters

Axial Spondylometaphyseal Dysplasia Is Caused by C21orf2 Mutations

Axial spondylometaphyseal dysplasia (axial SMD) is an autosomal recessive disease characterized by dysplasia of axial skeleton and retinal dystrophy. We conducted whole exome sequencing and identified C21orf2 (chromosome 21 open reading frame 2) as a disease gene for axial SMD. C21orf2 mutations have been recently found to cause isolated retinal degeneration and Jeune syndrome. We found a total of five biallelic C21orf2 mutations in six families out of nine: three missense and two splicing mutations in patients with various ethnic backgrounds. The pathogenic effects of the splicing (splice-site and branch-point) mutations were confirmed on RNA level, which showed complex patterns of abnormal splicing. C21orf2 mutations presented with a wide range of skeletal phenotypes, including cupped and flared anterior ends of ribs, lacy ilia and metaphyseal dysplasia of proximal femora. Analysis of patients without C21orf2 mutation indicated genetic heterogeneity of axial SMD. Functional data in chondrocyte suggest C21orf2 is implicated in cartilage differentiation. C21orf2 protein was localized to the connecting cilium of the cone and rod photoreceptors, confirming its significance in retinal function. Our study indicates that axial SMD is a member of a unique group of ciliopathy affecting skeleton and retina

A haplotype analysis of C<i>21orf2</i> in family F3.

<p>The sib patients inherited different C<i>21orf2</i> haplotypes from the parents, respectively, which ruled out <i>C21orf2</i> as a disease gene in this family.</p

Clinical, radiographic and genetic findings of the axial SMD subjects.

<p>Clinical, radiographic and genetic findings of the axial SMD subjects.</p

<i>C21orf2</i> mutations in axial SMD.

<p><i>C21orf2</i> mutations in axial SMD.</p

<i>C21orf2</i> expression during chondrocyte induction.

<p>Relative mRNA expression of mouse <i>C21orf2</i> (<i>1810043G02Rik)</i> in induced (red lines) and un-induced (blue lines) ATDC5 cells. (A-B) The expression of <i>1810043G02Rik</i> measured by real-time PCR using two primer sets; (C-E) Expression of chondrocyte marker genes (<i>Col2a1</i>, <i>Agc1</i> and <i>Col10a1</i>), indicating the differentiation of induced ATDC5 cell to chondrocyte. All the expression values were presented relatively to the ones of day 0, which was set as 1. *: P< 0.05, **: P< 0.01, ***: P< 0.001; induced versus un-induced by t-test. n = 3.</p