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Abstract Background Proteoglycans are important tumor microenvironment extracellular matrix components. The regulation of key proteoglycans, such as decorin (DCN), by miRNAs has drawn attention since they have surfaced as novel therapeutic targets in cancer. Accordingly, this study aimed at identifying the impact of miR-181a in liver cancer and its regulatory role on the extracellular matrix proteoglycan, DCN, and hence on downstream oncogenes and tumor suppressor genes. Results DCN was under-expressed in 22 cirrhotic and HCC liver tissues compared to that in 11 healthy tissues of liver transplantation donors. Conversely, miR-181a was over-expressed in HCC liver tissues compared to that in healthy liver tissues. In silico analysis predicted that DCN 3’UTR harbors two high-score oncomiR-181a binding regions. This was validated by pmiRGLO luciferase reporter assay. Ectopic miR-181a expression into HuH-7 cells repressed the transcript and protein levels of DCN as assessed fluorometrically and by western blotting. DCN siRNAs showed similar results to miR-181a, where they both enhanced the cellular viability, proliferation, and clonogenicity. They also increased Myc and E2F and decreased p53 and Rb signaling as assessed using reporter vectors harboring p53, Rb, Myc, and E2F response elements. Our findings demonstrated that miR-181a directly downregulated the expression of its direct downstream target DCN, which in turn affected downstream targets related to cellular proliferation and apoptosis. Conclusion To our knowledge, this is the first study to unveil the direct targeting of DCN by oncomiR-181a. We also highlighted that miR-181a affects targets related to cellular proliferation in HCC which may be partly mediated through inhibition of DCN transcription. Thus, miR-181a could be a promising biomarker for the early detection and monitoring of liver cancer progression. This would pave the way for the future targeting of the oncomiR-181a as a therapeutic approach in liver cancer, where miR-181a-based therapy approach could be potentially combined with chemotherapy and immunotherapy for the management of liver cancer.

Background: Abortion is a spontaneous loss of pregnancy before 20 weeks. Approximately 42 million pregnancies end in abortion. The maternal infections that are transmissible from mother to fetus are caused by many pathogens, of which the TORCH complex contributes majorly to neonatal and infant deaths globally. The aim of this study is to detect the prevalence and types of infectious causes of abortion. One hundred aborted women admitted to King Faisal Medical Complex Maternity Hospital in Taif City between the period of 2018 and 2020 were enrolled in this study. The serological test reports (TORCH panel), as well as reports of hematological (CBC) and chemical parameters, were obtained from laboratory management system databases, reviewed, and then analyzed. The H&E-stained microscopic slides of their product of conception (POC) were examined under a microscope and compared with histopathological reports. The prevalence of TORCH infections was 8% in aborted women. Hepatitis B virus (HBV) and mixed TORCH infections constituted the highest percentage of TORCH pathogens in aborted women, constituting 6%. The most detected histopathological finding in seropositive cases (50%) was POC, with mixed inflammatory infiltrates and chronic endometritis, while in seronegative aborted women, POC was normal (64.1%). There is a statistically significant increase in the mean count of white blood cells in seropositive women. Therefore, it is important to provide health campaigns to bring awareness to the population about the risk factors of infectious agents to be avoided, especially during pregnancy.

Cognitive Radio (CR) offers a spectrum sharing solution to handle the massive amount of devices operating in the same spectrum. In this work a sub-Nyquist compressive sensing technique is proposed that allows secondary users to sense and utilize idle spectrum. Reconstruction of compressed sparse data is achieved through a dual stage sophisticated reconstruction algorithm. The reconstruction uses a classical fast Orthogonal Matching Persuit (OMP), followed by a new spiking deep Residual neural Network (ResNet) architecture. The proposed architecture is obtained through a novel distributed conversion technique that is proposed to convert deep architectures to a spiking neural networks. The reconstructed data is compared in terms of Peak Signal-to-Noise Ratio (PSNR), Mean Square Error (MSE) and Structural Similarity (SSIM) to the compressed data and the ground truth. Super Resolution Convolutional Neural Network (SRCNN) and a Deep ResNet are also used for reconstruction. The proposed algorithm outperforms SRCNN and the unconverted ResNet, specially at low Channel SNR (CSNR). In addition, the proposed algorithm results in a 68% reduction in both storage and energy requirements, which makes it suitable for implementation on User Equipment (UE).

Cardiovascular diseases remain a major public health burden worldwide. It was reported that vitamin D protects the cardiovascular system through several mechanisms mainly by hindering atherosclerosis development. Genetic variations in vitamin D metabolic pathway were found to affect vitamin D levels. This study aimed at investigating the association between single nucleotide polymorphisms in genes involved in vitamin D metabolism, CYP27B and CYP24A1; 25-hydroxyvitamin D (25(OH)D) levels; and susceptibility to acute coronary syndrome (ACS). One hundred and eighty-five patients and 138 healthy controls were recruited. CYP24A1 rs2762939 was genotyped using fast real-time PCR, while CYP24A1 rs4809960 and CYP27B1 rs703842 were genotyped using polymerase chain reaction followed by restriction fragment length polymorphism (PCR-RFLP). 25(OH)[D.sub.3] and 25(OH)[D.sub.2] levels were measured using ultra-performance liquid chromatography tandem mass spectrum. Vitamin D level was significantly lower in patients than controls (p Key words: myocardial infarction, 25(OH)D, single nucleotide polymorphism, CYP24A1, CYP27B1. Les maladies cardiovasculaires demeurent un fardeau de sante publique majeur a l'echelle mondiale. On a rapporte que la vitamine D permet de proteger le systeme cardiovasculaire par l'intermediaire de plusieurs modes d'action, principalement en retardant l'evolution de l'atherosclerose. On a observe que des variations genetiques des voies metaboliques de la vitamine D affectent les taux de vitamine D. Cette etude portait sur l'association entre des polymorphismes a nucleotide unique (ou SNP pour<>) dans des genes jouant un role dans le metabolisme de la vitamine D, CYP27B et CYP24A1, les taux de 25-hydroxyvitamine D (25(OH)D) et la susceptibilite au syndrome coronarien aigu. Nous avons inscrit 185 patients et 138 temoins en bonne sante. Nous avons genotype le rs2762939 du CYP24A1 a l'aide de la technique de PCR rapide en temps reel, tandis que le rs4809960 du CYP24A1 et le rs703842 du CYP27B1 ont ete genotypes a l'aide de la technique de PCR suivie du polymorphisme de longueur des fragments de restriction (ou RFLP pour<>). Nous avons mesure les taux de 25(OH)[D.sub.3] et de 25(OH)[D.sub.2] a l'aide de la chromatographie liquide d'ultra performance en tandem avec spectrometrie de masse. Nous avons observe que les taux de vitamine D etaient nettement moins eleves chez les patients que chez les temoins (p < 0,05). Le genotype GG du rs2762939 etait manifestement associe au risque d'apparition de syndrome coronarien aigu, mais sans proportionnalite avec les taux de vitamine D. Pour leur part, les variantes genetiques rs4809960 et rs703842 n'etaient pas associees avec le syndrome coronarien aigu ni avec les taux de 25(OH)D. La variante genetique rs2762939 du CYP24A1 est remarquablement associee avec le syndrome coronarien aigu. En contrepartie, les variantes rs4809960 et rs703842 ne sont pas associees avec la survenue d'un syndrome coronarien aigu. [Traduit par la Redaction] Mots-cles: infarctus du myocarde, 25(OH)D, polymorphisme a nucleotide unique, CYP24A1, CYP27B1., Introduction Cardiovascular disease (CVD) represents an immense burden worldwide. It is responsible for the death of 17.3 million per year, which accounts for 30% of the reported worldwide mortality, and [...]

Background: Abortion is a spontaneous loss of pregnancy before 20 weeks. Approximately 42 million pregnancies end in abortion. The maternal infections that are transmissible from mother to fetus are caused by many pathogens, of which the TORCH complex contributes majorly to neonatal and infant deaths globally. The aim of this study is to detect the prevalence and types of infectious causes of abortion. One hundred aborted women admitted to King Faisal Medical Complex Maternity Hospital in Taif City between the period of 2018 and 2020 were enrolled in this study. The serological test reports (TORCH panel), as well as reports of hematological (CBC) and chemical parameters, were obtained from laboratory management system databases, reviewed, and then analyzed. The H&E-stained microscopic slides of their product of conception (POC) were examined under a microscope and compared with histopathological reports. The prevalence of TORCH infections was 8% in aborted women. Hepatitis B virus (HBV) and mixed TORCH infections constituted the highest percentage of TORCH pathogens in aborted women, constituting 6%. The most detected histopathological finding in seropositive cases (50%) was POC, with mixed inflammatory infiltrates and chronic endometritis, while in seronegative aborted women, POC was normal (64.1%). There is a statistically significant increase in the mean count of white blood cells in seropositive women. Therefore, it is important to provide health campaigns to bring awareness to the population about the risk factors of infectious agents to be avoided, especially during pregnancy. [ABSTRACT FROM AUTHOR]

BACKGROUND: Nitric oxide (NO) may have a dual role in cancer. At low concentrations, endogenous NO promotes tumor growth and proliferation. However, at very high concentrations, it mediates cancer cell apoptosis and inhibits cancer growth. High levels of NO have been observed in blood of breast cancer (BC) patients, which increases tumor blood flow and promotes angiogenesis. To date, the regulation of NO-synthesizing enzyme, eNOS, by miRNAs has not been adequately investigated in BC. Therefore, the main aim of this study is to unravel the possible regulation of eNOS by miRNAs in BC and to examine their influence on NO production and BC progression. METHODS: Expression profile of eNOS in Egyptian BC patients and MDA-MB-231 cell lines was investigated using qRT-PCR. In-silico analysis was performed to predict a putative upstream regulator of eNOS. miR-744-5p was selected and its expression was quantified in BC tissues using qRT-PCR. MDA-MB-231 cells were cultured and transfected with miR-744-5p using lipofection method. NO levels were determined using Griess Reagent. Cellular viability and colony-forming ability were assessed using MTT and colony-forming assays; respectively. RESULTS: eNOS and miR-744-5p were significantly up-regulated in BC tissues compared to paired normal tissues. In-silico analysis revealed that miR-744-5p putatively binds to eNOS transcript with high binding scores. Transfection of MDA-MB-231 cells with miR-744-5p mimics resulted in a significant up-regulation of eNOS and consequently NO levels. In addition, miR-744-5p transfection led to an increase in cellular viability and colony-forming ability of the MDA-MB-231. CONCLUSION: miR-744-5p acts as an upstream positive regulator of the NO synthesizing enzyme, eNOS which in turn elevates NO levels. Furthermore, miR-744-5p is a novel oncogenic miRNA in BC. Thus, targeting miR-744/eNOS/NO axis may act as a therapeutic tool in TNBC. [ABSTRACT FROM AUTHOR]

Background and Aims: The role of miR-34a in hepatocellular carcinoma (HCC) is controversial and several unresolved issues remain, including its expression pattern and relevance to tumor etiology, tumor stage and prognosis, and finally, its impact on apoptosis. Methods: miR-34a expression was assessed in hepatitis C virus (HCV)-induced non-metastatic HCC tissues by RT-Q-PCR. Huh-7 cells were transfected with miR-34a mimics and the impact of miR-34a was examined on 84 pro-apoptotic/anti-apoptotic genes using PCR array; its net effect was tested on cell viability via MTT assay. Results: miR-34a expression was up-regulated in HCC tissues. Moreover, miR-34a induced a large set of pro-apoptotic/anti-apoptotic genes, with a net result of triggering apoptosis and repressing cell viability. Conclusions: HCC-related differential expression of miR-34a could be etiology-based or stage-specific, and low expression of miR-34a may predict poor prognosis. This study's findings also emphasize the role of miR-34a in apoptosis., Competing Interests: None