Compact Optimization Algorithms with Re-sampled Inheritance

The file attached to this record is the author's final peer reviewed version.Compact optimization algorithms are a class of Estimation of Distribution Algorithms (EDAs) characterized by extremely limited memory requirements (hence they are called \compact"). As all EDAs, compact algorithms build and update a probabilistic model of the distribution of solutions within the search space, as opposed to population-based algorithms that instead make use of an explicit population of solutions. In addition to that, to keep their memory consumption low, compact algorithms purposely employ simple probabilistic models that can be described with a small number of parameters. Despite their simplicity, compact algorithms have shown good performances on a broad range of benchmark functions and real-world problems. However, compact algorithms also come with some drawbacks, i.e. they tend to premature convergence and show poorer performance on non-separable problems. To overcome these limitations, here we investigate a possible algorithmic scheme obtained by combining compact algorithms with a non-disruptive restart mechanism taken from the literature, named Re-Sampled Inheritance (RI). The resulting compact algorithms with RI are tested on the CEC 2014 benchmark functions. The numerical results show on the one hand that the use of RI consistently enhances the performances of compact algorithms, still keeping a limited usage of memory. On the other hand, our experiments show that among the tested algorithms, the best performance is obtained by compact Differential Evolution with RI

Tissue distribution of the readthrough isoform of AQP4 reveals a dual role of AQP4ex limited to CNS

Translational readthrough (TRT) of aquaporin-4 (AQP4) has remarkably expanded the importance of this new post-transcriptional mechanism, as well as the regulation potential of AQP4. The TRT isoform of AQP4, named AQP4ex, is central for both AQP4 polarization and water channel activity in the central nervous system (CNS). Here we evaluate the relevance of the TRT mechanism by analyzing whether AQP4ex is also expressed in peripheral tissues and whether the expression of AQP4ex is necessary for its polarized expression as it occurs in perivascular astrocyte processes. To this purpose, AQP4ex null mice were used, and analysis was performed by immunolocalization and immunoblot. The results demonstrate that AQP4ex is expressed in kidney, stomach, trachea and skeletal muscle with the same localization pattern as the canonical AQP4 isoforms. AQP4ex protein levels vary from 6% to about 13% of the total AQP4 protein levels in peripheral tissues. Immunogold electron microscopy experiments demonstrated the localization of AQP4ex at the astrocytic endfeet, and experiments conducted on AQP4ex null mice CNS confirmed that the expression of AQP4ex is necessary for anchoring of the perivascular AQP4. Without the readthrough isoform, AQP4 assemblies are mis-localized, being uniformly distributed on the astrocyte processes facing the neuropile. No alteration of AQP4 polarization was found in AQP4ex null kidney, stomach, trachea or skeletal muscle, suggesting that AQP4ex does not have a role for proper membrane localization of AQP4 in peripheral tissues. We conclude that a dual role for AQP4ex is limited to the CNS

Molecular investigation of mtDNA A1555G, A3243G and A7445G mutations among the non syndromic hearing loss cases in Fars, Iran

Background: Hearing loss is a sensorineural disorder occuring in 1 out of 500 births. It happens due to some genetic/environmental causes or both. More than 60 of cases are noninherited and 80 non syndromic with autosomal recessive inheritance. In the present study we investigated the frequency of mtDNA A1555G, A3243 and A7445G mutations among the patients in Fars province.Materials and Methods: Seventy two non syndromic hearing loss subjects were studied. DNA was extracted using standard phenol-chloroform method. The screening of the mitochondrial gene mutations were performed using PCR-RFLP procedure. Finally, the possible mutations were confirmed by direct sequencing. Results: None of the A1555G, A3243G and A7445G mutations was detected in this study. However, destroying a MTTL1 restriction site for the investigation of A3243G mutation, revealed a G3316A with allelic variant of 1.4 in the deaf subjects. Conclusion: Our data indicated that the mitochondrial A1555G, A3243 and A7445G mutations have no role in auditory deficits in patients studied

Effect of 8 weeks resistance training on sphingosine-1-phosphate level and gene expression of SK1 enzyme, isoforms of MHCs in skeletal muscles of male Wistar Rats

Background and Objective: Sphingosine-1-phosphate (S1P) is involved in regulation of proliferation, differentiation, hypertrophy and anti-apoptosis and activation of satellite cells. This study was done to evaluated the effect of 8 weeks resistance training on sphingosine-1-phosphate level and gene expression of SK1 enzyme, isoforms of MHCs in skeletal muscles of male Wistar rats. Materials and Methods: This experimental study was done on Twenty four 8-week-old 190-250 gr male Wistar rats. The rats were allocated randomly into control (N=12) and training (N=12) groups. Resistance training was done using a 1 meter height ladder with 2 cm grid with an 85 degree incline, and weights attached to rat's tails. The content of S1P present in the chloroform layer was determined by means of high performance liquid chromatography (HPLC). Determination of relative mRNA expression was performed by Real-time PCR. Data were analyzed using SPSS-17, Kolmogorov-Smirnov and independent t-test. Results: Resistance exercise training increased the total content of S1P in FHL (fast-twitch) and soleus (slow-twitch) muscles in comparison with control group (P<0.05). Resistance exercise training changed the gene expression of FHL SK1, SOL SK1, FHL MHC I, Sol MHC I, FHL MHC IIa, Sol MHC IIa, FHL MHC IIb, Sol MHC IIb, FHL MHC IIx, Sol MHC IIx in comparison with control group (P<0.05). Conclusion: This study showed that S1P level and gene expression of SK1, MHCs increased at skeletal muscles after training

DFNB59 Gene Mutations and its Association with Deafness in Schoolchildren in Kohgilooyeh & Boyerahmad Province

Introduction & Objective: Hearing loss is a common disease affecting millions of people worldwide. Hearing loss can be caused due to genetic or environmental factors or even both. The genetic of hearing defect is highly heterogeneous and more than 100 genes are predicted to cause this disorder in humans. A newly identified gene (DFNB59) has been shown to cause deafness in some populations. Here we report mutation analysis for DFNB59 gene in 88 genetic non-syndromic hearing loss subjects. Materials & Methods: In this descriptive-lab based study which was conducted at the Cellular and Molecular Research Center of Shahrekord University of Medical Sciences, DNA was extracted from the peripheral blood samples using standard phenol chloroform procedure. Mutation analysis for DFNB59 gene was performed using PCR-SSCP/HA protocol. The suspected DFNB59 which was detected as shifted bands on PAGE were then confirmed by direct sequencing strategy. Results: Two DFNB59 polymorphisms including c.793C>G and c.793C>T were detected in 8 and 1 deaf subjects respectively. Conclusion: We conclude that there is no association between DFNB59 mutations and deafness in the studied patients in the region

Orthogonal arrays of particle assembly are essential for normal aquaporin-4 expression level in the brain

Astrocyte endfeet are endowed with aquaporin-4 (AQP4)-based assemblies called orthogonal arrays of particles (OAPs) whose function is still unclear. To investigate the function of OAPs and of AQP4 tetramers, we have generated a novel “OAP-null” mouse model selectively lacking the OAP forming M23-AQP4 isoform. We demonstrated that AQP4 transcript levels were not reduced by using qPCR. Blue native (BN)/SDS-PAGE and Western blot performed on OAP-null brain and primary astrocyte cultures showed the complete depletion of AQP4 assemblies, the selective expression of M1-AQP4-based tetramers, and a substantial reduction in AQP4 total expression level. Fluorescence quenching and super-resolution microscopy experiments showed that AQP4 tetramers were functionally expressed in astrocyte plasma membrane and their dimensions were reduced compared to wild-type assemblies. Finally, as shown by light and electron microscopy, OAP depletion resulted in a massive reduction in AQP4 expression and a loss of perivascular AQP4 staining at astrocyte endfeet, with only sparse labeling throughout the brain areas analyzed. Our study relies on the unique property of AQP4 to form OAPs, using a novel OAP-null mouse model for the first time, to show that (a) AQP4 assembly is essential for normal AQP4 expression level in the brain and (b) most of AQP4 is organized into OAPs under physiological conditions. Therefore, AQP4 tetramers cannot be used by astrocytes as an alternative to OAPs without affecting AQP4 expression levels, which is important in the physiological and pathological conditions in which OAP aggregation/disaggregation dynamics have been implicated