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.

Novel Point and Combo-Mutations in the Genome of Hepatitis B Virus-Genotype D: Characterization and Impact on Liver Disease Progression to Hepatocellular Carcinoma

<div><p>Background</p><p>The contribution of chronic hepatitis B virus (HBV) infection in the pathogenesis of hepatocellular carcinoma (HCC) through progressive stages of liver fibrosis is exacerbated by the acquisition of naturally occurring mutations in its genome. This study has investigated the prevalence of single and combo mutations in the genome of HBV-genotype D from treatment naïve Indian patients of progressive liver disease stages and assessed their impact on the disease progression to HCC.</p><p>Methods</p><p>The mutation profile was determined from the sequence analysis of the full-length HBV genome and compared with the reference HBV sequences. SPSS 16.0 and R software were used to delineate their statistical significance in predicting HCC occurrence.</p><p>Results</p><p>Age was identified as associated risk factor for HCC development in chronic hepatitis B (CHB) patients (p≤0.01). Beyond the classical mutations in basal core promoter (BCP) (A1762T/G1764A) and precore (G1862T), persistence of progressively accumulated mutations in enhancer-I, surface, HBx and core were showed significant association to liver disease progression. BCP_T1753C, core_T147C, surface_L213I had contributed significantly in the disease progression to HCC (p<0.05) in HBeAg positive patients whereas precore_T1858C, core_I116L, core_P130Q and preS1_S98T in HBeAg negative patients. Furthermore, the effect of individual mutation was magnified by the combination with A1762T/G1764A in HCC pathogenesis. Multivariate risk analysis had confirmed that core_P130Q [OR 20.71, 95% CI (1.64–261.77), p = 0.019] in B cell epitope and core_T147C [OR 14.58, 95% CI (1.17–181.76), p = 0.037] in CTL epitope were two independent predictors of HCC in HBeAg positive and negative patients respectively.</p><p>Conclusions</p><p>Thus distinct pattern of mutations distributed across the entire HBV genome may be useful in predicting HCC in high-risk CHB patients and pattern of mutational combinations may exert greater impact on HCC risk prediction more accurately than point mutations and hence these predictors may support the existing surveillance strategies in proper management of the patients.</p></div

Frequencies of naturally occurring single and combination of mutations accumulated in the HBV genome were found significantly higher in hepatocellular carcinoma (HCC) than non-HCC patients.

<p>p<0.05 was considered as significant. ** indicates p>0.05.</p

Frequencies of mutations showing escalating trend with the progression of the liver diseases from no liver fibrosis (nLF) or liver fibrosis (LF) to liver cirrhosis (LC) and hepatocellular carcinoma (HCC).

<p>Significant mutations were indicated in bold (p≤0.05) and marginal significant values were represented in italics.</p><p>Frequencies of mutations showing escalating trend with the progression of the liver diseases from no liver fibrosis (nLF) or liver fibrosis (LF) to liver cirrhosis (LC) and hepatocellular carcinoma (HCC).</p

Multivariate analysis to identify independent risk factors for HCC development in HBeAg positive and negative patients.

<p>p value <0.05 was considered as significant.</p><p>Multivariate analysis to identify independent risk factors for HCC development in HBeAg positive and negative patients.</p

Clinical, biochemical and demographic profile of sixty-eight patients included in the study.

<p>SD =  Standard deviation; NS =  Not significant; ALT =  Alanine aminotransferase; AST = Aspartate aminotransferase; INR =  International normalized ratio; ALP = Alkaline phosphatase; IU =  International unit; Δ Parameters presented as Mean±SD; β parameters presented as Median [Range]; δ Mutations with statistically significant difference between the groups are presented.</p><p>Clinical, biochemical and demographic profile of sixty-eight patients included in the study.</p

Distribution pattern of HBV/genotype C and HBV/genotype D in hepatocellular carcinoma (HCC) (A) and in liver cirrhotic (LC) (B) patients.

<p>HBV genotypes were detected from sequence analysis of five clones of amplified HBx or HBs region from chromosomal DNA and serum viral DNA using virus specific primer pairs. This will amplify replicating virus in liver tissue and circulating virus in serum. Genotypes of Integrated viruses were determined from sequence analysis of five clones of Alu-PCR product. T = tumor, NT = adjacent non-tumor and LC = liver cirrhosis.</p

List of primers used to generate PCR products and promoter construct.

<p>List of primers used to generate PCR products and promoter construct.</p

Baseline characteristics and biochemical parameters of LC and HCC patients.

<p>Baseline characteristics and biochemical parameters of LC and HCC patients.</p

Quantification of ROS generated after HBV/genotype D and HBV/genotype C infection.

<p>Huh7 cells were transfected with control pTriEX vector and pTriEX-HBV/D and pTriEX-HBV/C plasmids, which contain 1.2× HBV genome independently. After 48 hours, cells were treated with DCFDA and DCF positive cells were quantified on (A) FACSCaliber and (B) Confocal microscope. Scale bar corresponds to 20 µm. <i>p</i><0.05 was considered as significant.</p