EXCLI Journal https://www.excli.de/index.php/excli <center><img class="img-responsive" src="/public/site/images/lindemann/Lucida_logo_neu_geschrieben.PNG" alt="EXCLI Journal Logo"></center> <p>EXCLI Journal publishes original research reports, authoritative reviews and case reports of experimental and clinical sciences.</p> <div class="toggleBox"><input id="toggleContent" name="toggleContent" type="checkbox"> <label class="open" for="toggleContent">More...</label> <label class="close" for="toggleContent">Less...</label> <div> <p><strong>EXCLI Journal </strong>(eISSN 1611-2156)&nbsp;is particularly keen to keep a broad view of science and technology, and therefore welcomes papers which bridge disciplines and may not suit the narrow specialism of other journals. Although the general emphasis is on biological sciences, studies from the following fields are explicitly encouraged:</p> <p>Immunology, toxicology, ergonomics, neurosciences, psychology, occupational medicine, clinical and preclinical studies, drug development, pharmacology, environmental health, chemistry including analytical chemistry, biochemistry, cell biology, genetics, forensic medicine, oncology and cancer research, proteomics, systems biology, hepatology and gastroenterology, aging research, psychiatric research, behavioral sciences.</p> </div> </div> IfADo - Leibniz Research Centre for Working Environment and Human Factors, Dortmund en-US EXCLI Journal 1611-2156 <p>Authors who publish in this journal agree to the following terms:</p> <ul> <li>The authors keep the copyright and grant the journal the right of first publication under the terms of the Creative Commons Attribution license, <a href="https://creativecommons.org/licenses/by/4.0/" target="_blank" rel="noopener">CC BY 4.0</a>. This licencse permits unrestricted use, distribution and reproduction in any medium, provided that the original work is properly cited.</li> <li>The use of general descriptive names, trade names, trademarks, and so forth in this publication, even if not specifically identified, does not imply that these names are not protected by the relevant laws and regulations.</li> <li>Because the advice and information in this journal are believed to be true and accurate at the time of publication, neither the authors, the editors, nor the publisher accept any legal responsibility for any errors or omissions presented in the publication. The publisher makes no guarantee, express or implied, with respect to the material contained herein.</li> <li>The authors can enter into additional contracts for the non-exclusive distribution of the journal's published version by citing the initial publication in this journal (e.g. publishing in an institutional repository or in a book).</li> </ul> Effect of ADCY3 and ADCY8 Gene Polymorphisms to Hepatocellular Carcinoma Risk https://www.excli.de/index.php/excli/article/view/3437 <p><strong>ABSTRACT</strong></p> <p><strong>Background</strong>: Hepatocellular carcinoma (HCC) is the result of a combination of multiple genetic and environmental factors, but its etiology and pathogenesis remain unclear. <strong>Aim of the study</strong>: Our aim was to determine whether variations in <em>ADCY3</em> and <em>ADCY8</em> correlate with HCC risk indices in Chinese Han people. <strong>Methods:</strong> A total of 434 patients with HCC and 442 healthy controls were recruited for this case-control study. Six single nucleotide polymorphisms (SNPs) of <em>ADCY3</em> and <em>ADCY8</em> were genotyped with Agena MassARRAY platform, and association analysis was performed in multiple genetic models. Odds ratios (OR) and 95% confidence intervals (CI) were calculated by unconditional logistic regression for risk assessment. <strong>Results:</strong> We found that <em>ADCY8-</em>rs7813092 significantly increased the risk of HCC in genotype model (<em>p</em> = 0.021) and dominant model (<em>p</em> = 0.036). In stratified analyses by age, rs6545800 (<em>p</em> = 0.029), rs6545814 (<em>p</em> = 0.027), and rs713586 (<em>p</em> = 0.032) of<em> ADCY3 </em>as well as rs7813092 (<em>p</em> = 0.027) of<em> ACDY8</em> were significantly associated with an increased risk of HCC among participates older than 55 years. While <em>ACDY8</em>-rs7829589 increased HCC risk among the people who are less than or equal to 55 years old. <strong>Conclusion:</strong> This study provided evidence for the impact of <em>ADCY3</em> and <em>ADCY8</em> polymorphisms on HCC susceptibility in Chinese patients. These findings may contribute to the development of the early diagnosis of HCC.</p> xu chao Copyright (c) 20 THE EFFECT OF LUWAK COFFEE ON MEMORY PERFORMANCE AND INTESTINAL MICROBIOME IN MICE (MUS MUSCULUS) https://www.excli.de/index.php/excli/article/view/3432 <p>Coffee is one of the most consumed drinks by humans. The benefits of coffee as an antioxidant can stimulate brain performance by improving memory, focus strengthening, and increasing alertness. One type of coffee used is civet coffee, which uses the civet's digestive system (<em>Paradoxurus hermaphrodites</em>). This study aims to determine the effect of giving coffee on mice's memory performance in the hippocampus and its relationship with the microbiome. This study used 24 male mice (Mus musculus) divided into three treatment groups P1 (100 mg/kg BW), P2 (200 mg/kg BW), and P3 (control), which were given orally for 30 days. The spatial memory performance was observed by observing mice's ability to explore Y-maze and NOR (Novel Object Recognition). Microbial observations were carried out by isolating mice feces using the (Total Plate Count) method. The results of this study indicate that the administration of 200 mg/kg BW of civet coffee was able to show a pattern of increasing memory ability of mice in the NOR test as shown by an increase in NPC (Neural Progenitor Cells) cells and a decrease in apoptotic cells in the hippocampus. However, gut microbes concentration, including total bacteria, Escherichia coli, and lactic acid bacteria, was not altered following coffee treatments.</p> Mardilah HK Berry Juliandi Rika Indri Astuti Copyright (c) 20 THE UPWARD TREND OF METASTASIS LINKING TO CLINICOPATHODEMOGRAPHY AND COLORECTAL TISSUES' KEY CELL CYCLE-AND MUCIN STABILIZING MOLECULES IN CRC PATIENTS https://www.excli.de/index.php/excli/article/view/3431 <p>We aimed to evaluate the various clinicopathodemographical, epidemiological, and molecular players of cumulatively worldwide metastatic colorectal cancer (CRC) in CRC patients from a highly-populated area in northeastern Iran to pinpoint metastasis risk. A retrospective clinical material-based cohort including a total of 6260 registered CRC patients, of whom 3829 underwent surgery, from rigional university hospitals, during 2006-2016, were analyzed for the clinicopathodemographic aspects of age, sex, stage of CRC, history of smoking, type-2 diabetes (T2D), hypertension, body-mass-index (BMI), familial/occupational status, post-surgery survival period and mRNA/protein expression of mucin stabilizer (B3GALNT2), mucin I<strong> (</strong>MUC1), key cell cycle molecules (i.e., P53 and Ki67), and MMR-related genes. Factors were set to estimate the risk of metastatic CRC and mortality. Predominant adenocarcinomatous CRCs were found in colon. Post-surgery survival period of metastatic CRC patients was remarkably longer in patients aged&gt;50 compared to those aged&lt;50 years, and worse in females than males. B3GALNT2<sup>high</sup>, MUC<sup>high</sup>, P53<sup>low</sup> and Ki67<sup>high</sup> mRNA/protein expression in the metastatic stage III CRC along with T2D and hypertension were associated with increased metastasis/mortality, with more worsening in males, older, BMI &gt;25, urban residing-and-employed individuals, indicative of non-genetic attributable factors. Overall, B3GALNT2, MUC1, and “Ki67” can be used as promising biomarkers for prognosis and early diagnosis of increasingly/predominantly non-genetic/environmental originated metastatic CRCs.</p> Jalil Mehrzad Ali Ghorbani Ranjbary Abbas Abdollahi Saman Hosseinkhani Abbas Tabatabaee Hesam Dehghani Copyright (c) 20