Нормативно-правові аспекти дослідження витрат торговельних підприємств

У статті досліджено міжнародні та національні нормативно-правові акти, що розкривають суть та методологічні аспекти формування витрат підприємств у бухгалтерському і податковому обліку. (In the article are investigated standard-legal sources that open methodological aspects of formation of costs of the enterprises in the accounting and tax account.

Identification of Novel <i>GRM1</i> Mutations and Single Nucleotide Polymorphisms in Prostate Cancer Cell Lines and Tissues

<div><p>Metabotropic glutamate receptor 1 (GRM1) signaling has been implicated in benign and malignant disorders including prostate cancer (PCa). To further explore the role of genetic alterations of <i>GRM1</i> in PCa, we screened the entire human <i>GRM1</i> gene including coding sequence, exon-intron junctions, and flanking untranslated regions (UTRs) for the presence of mutations and single nucleotide polymorphisms (SNPs) in several PCa cell lines and matched tumor-normal tissues from Caucasian Americans (CAs) and African Americans (AAs). We used bidirectional sequencing, allele-specific PCR, and bioinformatics to identify the genetic changes in <i>GRM1</i> and to predict their functional role. A novel missense mutation identified at C1744T (582 Pro > Ser) position of <i>GRM1</i> gene in a primary AA-PCa cell line (E006AA) was predicted to affect the protein stability and functions. Another novel mutation identified at exon-intron junction of exon-8 in C4-2B cell line resulted in alteration of the <i>GRM1</i> splicing donor site. In addition, we found missense SNP at T2977C (993 Ser > Pro) position and multiple non-coding mutations and SNPs in 3′-UTR of <i>GRM1</i> gene in PCa cell lines and tissues. These novel mutations may contribute to the disease by alterations in <i>GRM1</i> gene splicing, receptor activation, and post-receptor downstream signaling.</p></div

Genotype status of mutations and SNPs identified in <i>GRM1</i> gene in matched prostate tumor-normal tissues.

a<p>DSSC: Downstream to stop codon.</p

Bioinformatics prediction of splicing site motif (donor/acceptor).

<p>Twenty one base pair sequence flanking of mutation site with wild type (<b>A</b>) and mutant allele (<b>B</b>) was tested for prediction of splicing site motif (donor or acceptor).</p

Genotype status of non-synonymous and synonymous mutations and polymorphisms identified in <i>GRM1</i> gene in prostate cancer cell lines.

a<p>Novel mutations identified in our study.</p>b<p>Mis: Missense mutation.</p

Genotype status of downstream non-coding polymorphisms identified in <i>GRM1</i> gene in prostate cancer cell lines.

a<p>DSSC: Downstream to stop codon.</p

Location of the novel identified mutations and polymorphisms in different domains of GRM1 receptor.

<p>Location of the novel identified mutations and polymorphisms in different domains of GRM1 receptor.</p

Schematic presentation of the identified mutations and polymorphisms of full-length <i>GRM1</i> gene in prostate cancer cell lines and tissues.

<p>Schematic presentation of the identified mutations and polymorphisms of full-length <i>GRM1</i> gene in prostate cancer cell lines and tissues.</p

Allele-specific PCR genotyping of novel missense mutation identified in exon-8 of <i>GRM1</i> gene in prostate tumors.

<p>Presence of C-allele showed amplification of a 439 bp fragment and presence of T-allele showed amplification of a 267 bp fragment. A nonspecific fragment of 706 bp was amplified in all samples.</p

Mapping of PARK2 and PACRG Overlapping Regulatory Region Reveals LD Structure and Functional Variants in Association with Leprosy in Unrelated Indian Population Groups

<div><p>Leprosy is a chronic infectious disease caused by <i>Mycobacterium Leprae</i>, where the host genetic background plays an important role toward the disease pathogenesis. Various studies have identified a number of human genes in association with leprosy or its clinical forms. However, non-replication of results has hinted at the heterogeneity among associations between different population groups, which could be due to differently evolved LD structures and differential frequencies of SNPs within the studied regions of the genome. A need for systematic and saturated mapping of the associated regions with the disease is warranted to unravel the observed heterogeneity in different populations. Mapping of the PARK2 and PACRG gene regulatory region with 96 SNPs, with a resolution of 1 SNP per 1 Kb for PARK2 gene regulatory region in a North Indian population, showed an involvement of 11 SNPs in determining the susceptibility towards leprosy. The association was replicated in a geographically distinct and unrelated population from Orissa in eastern India. <i>In vitro</i> reporter assays revealed that the two significantly associated SNPs, located 63.8 kb upstream of PARK2 gene and represented in a single BIN of 8 SNPs, influenced the gene expression. A comparison of BINs between Indian and Vietnamese populations revealed differences in the BIN structures, explaining the heterogeneity and also the reason for non-replication of the associated genomic region in different populations.</p></div