An Accelerated Homotopy Perturbation Method for Solving Nonlinear Two-Dimensional Volterra-Fredholm Integrodifferential Equations

We propose and apply coupling of the variational iteration method (VIM) and homotopy perturbation method (HPM) to solve nonlinear mixed Volterra-Fredholm integrodifferential equations (VFIDE). In this approach, we use a new formula called variational homotopy perturbation method (VHPM) and variational accelerated homotopy perturbation method (VAHPM). This approach is based on the form of He’s polynomials and on a new form of He’s polynomials. We discuss the convergence of the technique. Some numerical examples are introduced to verify the efficiency of this technique

The origin of fracture in the I-ECAP of AZ31B magnesium alloy

Magnesium alloys are very promising materials for weight-saving structural applications due to their low density, comparing to other metals and alloys currently used. However, they usually suffer from a limited formability at room temperature and low strength. In order to overcome those issues, processes of severe plastic deformation (SPD) can be utilized to improve mechanical properties, but processing parameters need to be selected with care to avoid fracture, very often observed for those alloys during forming. In the current work, the AZ31B magnesium alloy was subjected to SPD by incremental equal-channel angular pressing (I-ECAP) at temperatures varying from 398 K to 525 K (125 °C to 250 °C) to determine the window of allowable processing parameters. The effects of initial grain size and billet rotation scheme on the occurrence of fracture during I-ECAP were investigated. The initial grain size ranged from 1.5 to 40 µm and the I-ECAP routes tested were A, BC, and C. Microstructures of the processed billets were characterized before and after I-ECAP. It was found that a fine-grained and homogenous microstructure was required to avoid fracture at low temperatures. Strain localization arising from a stress relaxation within recrystallized regions, namely twins and fine-grained zones, was shown to be responsible for the generation of microcracks. Based on the I-ECAP experiments and available literature data for ECAP, a power law between the initial grain size and processing conditions, described by a Zener–Hollomon parameter, has been proposed. Finally, processing by various routes at 473 K (200 °C) revealed that route A was less prone to fracture than routes BC and C

68Ga-PSMA PET/CT in Initial Diagnosis and Bone Metastasis Evaluation in Saudi Patients with High-Grade Prostate Cancer

We present the first study performed in Saudi Arabia to evaluate 68Ga-PSMA PET/CT in prostate cancer (PCa) initial diagnosis and its added value in bone metastases (BM) diagnosis in such patients. Twenty-six male patients underwent prostate histopathological examination and all imaging studies (68Ga-PSMA PET/CT and CT); all of them were confirmed with high-grade PCa. Patients' mean PSA levels and Gleason score were 5.12±1.12 and 7.0±0.9, respectively. 68Ga-PSMA PET/CT (20/26; sensitivity of 76.9%) was superior to traditional CT (18/26; sensitivity of 69.2%) in PCa detection. There was a non-significant association (P=0.206) between patients' age and BM. Based on bone scintigraphy (BS), in patients without BM (n=16), 68Ga-PSMA PET/CT detected metastasis-suspicious lesions in six patients (37.5%) and negative results in ten patients (62.5%). 68Ga-PSMA PET/CT showed no false-negative cases among patients with confirmed BM using BS. In conclusion, 68Ga-PSMA PET/CT performed well in PCa initial diagnosis in Saudi male patients with high-grade tumors. 68Ga-PSMA PET/CT also accurately detected BM in all PCa patients with confirmed BM by BS. Larger prospective studies are urgently required to compare 68Ga-PSMA PET/CT diagnostic performance with other standard modalities in PCa and BM diagnosis

Deletion of retinoic acid-related orphan receptor gamma reduces body weight and hepatic lipids in mice by modulating the expression of lipid metabolism genes

Aim: Retinoic acid-related orphan receptor γ (RORγ) functions as a ligand-dependent transcription factor and its loss has been shown to affect the circadian expression of lipid metabolism genes. However, its effect on body weight gain and hepatic lipids is not well understood. In this study, we investigated the impact of Rorγ gene deletion on changes in body weight and hepatic lipids.Methods: Body weight and lipids were analyzed in the plasma and liver. Expression of lipid metabolism genes in the liver was evaluated in wild type and Rorγ knockout mice.Results: We show that deletion of RORγ results in reduced body weight and fewer lipids in the liver. Analysis of gene expression showed that deletion of Rorγ resulted in an overall lower expression of genes and transcription factors involved in lipid biosynthesis. We observed a decrease in the gene expression of cholesterol biosynthesis, efflux, and esterification but an increase in bile acid synthesis. There was a decrease in fatty acid and triglycerides biosynthesis genes and an increase in the fatty acid uptake genes. The decrease in the expression of lipid biosynthesis genes was accompanied by the decrease in the sterol response element binding protein (Srebp) genes. We observed an increase in the expression of peroxisome proliferator-activated receptor alpha (Ppara) and a decrease in the expression of acetyl-CoA carboxylase 2 (Acc2) genes.Conclusion: Our data suggest that RORγ regulates body weight and lipid metabolism genes and its modulation may be beneficial for the management of obesity and related lipid metabolic disorders

Molecular Analysis of Congenital Hypothyroidism in Saudi Arabia:SLC26A7 Mutation Is a Novel Defect in Thyroid Dyshormonogenesis

Abstract Context Congenital hypothyroidism (CH) is the most common neonatal endocrine disorder, affecting one in 3000 to 4000 newborns. Since the introduction of a newborn screening program in 1988, more than 300 cases have been identified. The underlying genetic defects have not been systematically studied. Objective To identify the mutation spectrum of CH-causing genes. Methods Fifty-five patients from 47 families were studied by next-generation exome sequencing. Results Mutations were identified in 52.7% of patients (29 of 55) in the following 11 genes: TG, TPO, DUOX2, SLC26A4, SLC26A7, TSHB, TSHR, NKX2-1, PAX8, CDCA8, and HOXB3. Among 30 patients with thyroid dyshormonogenesis, biallelic TG mutations were found in 12 patients (40%), followed by biallelic mutations in TPO (6.7%), SLC26A7 (6.7%), and DUOX2 (3.3%). Monoallelic SLC26A4 mutations were found in two patients, one of them coexisting with two tandem biallelic deletions in SLC26A7. In 25 patients with thyroid dysgenesis, biallelic mutations in TSHR were found in six patients (24%). Biallelic mutations in TSHB, PAX 8, NKX2-1, or HOXB3 were found once in four different patients. A monoallelic CDCA8 mutation was found in one patient. Most mutations were novel, including three TG, two TSHR, and one each in DUOX2, TPO, SLC26A7, TSHB, NKX2-1, PAX8, CDCA8, and HOXB3. SLC26A7 and HOXB3 were novel genes associated with thyroid dyshormonogenesis and dysgenesis, respectively. Conclusions TG and TSHR mutations are the most common genetic defects in Saudi patients with CH. The prevalence of other disease-causing mutations is low, reflecting the consanguineous nature of the population. SLC26A7 mutations appear to be associated with thyroid dyshormonogenesis. </jats:sec