Expressibility-Enhancing Strategies for Quantum Neural Networks

Quantum neural networks (QNNs), represented by parameterized quantum circuits, can be trained in the paradigm of supervised learning to map input data to predictions. Much work has focused on theoretically analyzing the expressive power of QNNs. However, in almost all literature, QNNs' expressive power is numerically validated using only simple univariate functions. We surprisingly discover that state-of-the-art QNNs with strong expressive power can have poor performance in approximating even just a simple sinusoidal function. To fill the gap, we propose four expressibility-enhancing strategies for QNNs: Sinusoidal-friendly embedding, redundant measurement, post-measurement function, and random training data. We analyze the effectiveness of these strategies via mathematical analysis and/or numerical studies including learning complex sinusoidal-based functions. Our results from comparative experiments validate that the four strategies can significantly increase the QNNs' performance in approximating complex multivariable functions and reduce the quantum circuit depth and qubits required.Comment: 16 pages, 11 figure

Global MicroRNA Characterization Reveals That miR-103 Is Involved in IGF-1 Stimulated Mouse Intestinal Cell Proliferation

MicroRNAs play extensive roles in cellular development. Analysis of the microRNA expression pattern during intestinal cell proliferation in early life is likely to unravel molecular mechanisms behind intestinal development and have implications for therapeutic intervention. In this study, we isolated mouse intestinal crypt cells, examined the differences in microRNA expression upon IGF-1 stimulated proliferation and identified miR-103 as a one of the key regulators. Mouse intestinal crypt cells were cultured and treated with IGF-1 for 24 h. MicroRNA microarray showed that multiple microRNAs are regulated by IGF-1, and miR-103 was the most sharply down-regulated. Expression of miR-103 in mouse intestinal crypt cells was confirmed by real-time Q-PCR. Sequence analyses showed that, among the 1040 predicted miR-103 target genes, CCNE1, CDK2, and CREB1 contain complementary sequences to the miR-103 seed region that are conserved between human and mouse. We further demonstrated that miR-103 controls the expression level of these three genes in mouse crypt cells by luciferase assay and immunoblotting assay. Taken together, our data suggest that in mouse intestinal crypt cells, miR-103 is part of the G1/S transition regulatory network, which targets CCNE1, CDK2, and CREB1 during IGF-1 stimulated proliferation

Improved on an improved remote user authentication scheme with key agreement

Recently, Kumari et al. pointed out that Chang et al.’s scheme “Untraceable dynamic-identity-based remote user authentication scheme with verifiable password update” not only has several drawbacks, but also does not provide any session key agreement. Hence, they proposed an improved remote user authentication Scheme with key agreement on Chang et al.’s Scheme. After cryptanalysis, they confirm the security properties of the improved scheme. However, we determine that the scheme suffers from both anonymity breach and he smart card loss password guessing attack, which are in the ten basic requirements in a secure identity authentication using smart card, assisted by Liao et al. Therefore, we modify the method to include the desired security functionality, which is significantly important in a user authentication system using smart card

MiR-584 mediates post-transcriptional expression of lactoferrin receptor in Caco-2 cells and in mouse small intestine during the perinatal period

MicroRNAs function as gene expression modulators that are critical for mammalian development. Lactoferrin receptor on the apical membrane of enterocytes has been suggested to play key roles in the absorption of lactoferrin-bound iron from breast milk. The objective of this study was to identify mechanisms of microRNA mediated post-transcriptional regulation of the lactoferrin receptor. Sequence analyses revealed that the miR-584 sequence is identical in human, mouse and rat, and there is a conserved region complementary to the seed region (5' nucleotides 2-8) of miR-584 within the lactoferrin receptor mRNA-3'-untranslated region. miR-584 was further found to co-localize with lactoferrin receptor mRNA in mouse small intestine. The 3'-untranslated region of human lactoferrin receptor mRNA was cloned into pGL3-control luciferase reporter vector. By luciferase reporter assays in HEK293 cells, miR-584 mimic specifically repressed the reporter activity in a dose-dependent manner. miR-584 mimic reduced endogenous lactoferrin receptor protein expression in Caco-2 cells, without significantly affecting the mRNA level. We also determined that miR-584 expression is inversely correlated with lactoferrin receptor mRNA and protein expression. Taken together, we propose that miR-584 contributes to the post-transcriptional expression of lactoferrin receptor during the perinatal period. These findings demonstrate a novel example of how microRNAs may be involved in regulation of nutrient metabolism in the newborn

Growth factor TGF- β induces intestinal epithelial cell (IEC-6) differentiation: MiR-146b as a regulatory component in the negative feedback loop

TGF-β is a potent pleiotropic factor that promotes small intestinal cell differentiation. The role of microRNAs in the TGF-β induction of intestinal epithelial phenotype is largely unknown. We hypothesized that microRNAs are functionally involved in TG

Biochemical and molecular impacts of lactoferrin on small intestinal growth and development during early life

Postnatal modeling of the intestinal epithelium has long-term impacts on the healthy development of infants and relies largely on nutrient composition of the diet. Lactoferrin (Lf) is among the various human milk trophic factors that facilitate the infant intestinal adaptation. Hydrolysis of Lf is minimal at the prevailing postprandial pH of infants, and Lf may therefore have greater biological potential in infants than in adults. Lf bidirectionally stimulates concentration-dependent proliferation and differentiation of small intestinal epithelial cells, and therefore affects small intestinal mass, length, and epithelial digestive enzyme expression. A 105 kDa Lf receptor (LfR) specifically mediates the uptake of Lf into enterocytes and crypt cells. Mechanistically, the complex of Lf and LfR is internalized through clathrin-mediated endocytosis; both iron-free apo-Lf and iron-saturated holo-Lf activate the PI3K/Akt pathway, whereas only apo-Lf triggers ERK1/2 signaling. Lf enters the nucleus, where it can stimulate thymidine incorporation into crypt cells, regulating transcription of genes such as TGFb1. In the fetus, the plasma membrane LfR is at the highest abundance in the small intestine, and the receptor gene is tightly controlled at multiple levels. Aspecific microRNA, miR-584, is involved in the posttranscriptional regulation of LfR, and in the human LfR DNA promoter, 2 Sp1 binding sites have been characterized functionally. Finally, cell proliferation and global gene expression reveal that native bovine Lf can perform biological activities similar to those exerted by human Lf in postnatal small intestinal development

miR-214 regulates lactoferrin expression and pro-apoptotic function in mammary epithelial cells

Lactoferrin (Lf) is an abundantly expressed protein in human milk. Lactoferrin exhibits several important biological functions, and its expression is regulated by multiple environmental factors. Cellular endogenous factors, however, have not been extensively studied with regard to lactoferrin gene expression. In this study, we showed that lactoferrin gene expression and function are directly targeted by miR-214 in HC11 and MCF7 cells. In the lactoferrin mRNA 39 untranslated region (UTR) of human, mouse, rat, pig, bovine, camel, and goat species, there is a conserved region that perfectly matches the seed region of miR-214. Transfection of miR-214 mimic in HEK293 cells dose-dependently inhibited the activity of pGL3-control vector containing lactoferrin mRNA 3′UTR downstream of the luciferase gene. In HC11 cells, miR-214 overexpression inhibited the induction of lactoferrin expression by β-estradiol (E2) and dexamethasone-prolactin-insulin (DPI). Furthermore, in MCF7 cells, overexpression of miR-214 markedly decreased lactoferrin expression (P < 0.05), and inhibition of endogenous miR-214 expression increased lactoferrin expression and cellular apoptotic activities (P < 0.05). In summary, our data showed that miR-214 is directly involved in lactoferrin expression and lactoferrin mediated cancer susceptibility (proapoptotic activities) in mammary epithelial cells

Forty-four miRNAs were significantly correlated with mouse crypt cell proliferation upon IGF-1 treatment.

<p>Hierarchical clustering analysis was performed using Euclidian distance. Each row represents relative levels of expression for a significantly regulated single microRNA and each column represents the relative expression level of a single replicate relative to control (<i>P</i><0.01). Colors on the figure represent the scaled fold-change between samples within a gene. Control group was set to 0.</p