A new secondary instability phenomenon of parametric sloshing

This paper reports on a new secondary instability phenomenon of parametric sloshing. Faraday first experimentally discovered the (1/2 sub-harmonic) parametric sloshing phenomenon in 1831. The parametric instability starts from a small disturbance on the free fluid surface, and then the sloshing amplitude of fluid increases exponentially and finally reaches a steady-state limit cycle oscillation. This parametric instability is called the first (linear) instability. The parametric sloshing experiment of this study discovers that in the case of the parametric excitation unchanged, the free fluid surface that is in a limit cycle oscillation might undergo a secondary instability. Under this circumstance, the sloshing amplitude of free surface increases sharply. The consequence is catastrophic – the fluid is splashed out of the tank. During the secondary instability, the sloshing mode (or energy) is transferred from the third mode to the first mode. The secondary instability, which is different from the first instability, is a nonlinear unstable process. The mechanism of the secondary instability is needed a further study

Exploration of Ideological and political education in Instrumental Analysis Teaching

Instrumental analysis is an elective course for biology majors. In undergraduate teaching design, there are many ideological and political elements that can be combined with professional knowledge. The core of this paper is to advocate the spirit of innovation and practice, scientifi c spirit, humanistic quality, patriotism, etc., and integrate ideological and political teaching into the course teaching, so as to jointly play the role of Ideological and political education

INSULIN RESISTANCE RELATED SIGNALING PATHWAYS IN THE LIVER

Over the past 20 years, the worldwide toll of diabetes has tripled to more than 400 million, which makes it one of the fastest-growing health challenges of the 21st century. There are three main categories of diabetes: type 1, type 2 and gestational diabetes mellitus. Among them, Type 2 diabetes(T2D) makes up to 90% of diabetes worldwide. Hyperglycemia can be effectively controlled by giving insulin injection for type 1 and gestational diabetes mellitus. However, because insulin resistance is one of the causes of T2D, those with T2D do not respond as well to insulin as those with T1D or gestational diabetes. Furthermore, our lack of knowledge about the underlying physiology of T2D makes it difficult to find reliable treatments. While high blood glucose concentration is one of the major symptoms of T2D, changes in lipid metabolism are characteristic of insulin resistance(IR). In the human body, the liver plays a major role in glucose homeostasis and lipid metabolism. Hence, this essay pro- vides an overview of signaling pathways in the liver and presents their interrelationship to better understand the underlying IR mechanism

FoxO gene family evolution in vertebrates

<p>Abstract</p> <p>Background</p> <p>Forkhead box, class O (FoxO) belongs to the large family of forkhead transcription factors that are characterized by a conserved forkhead box DNA-binding domain. To date, the FoxO group has four mammalian members: FoxO1, FoxO3a, FoxO4 and FoxO6, which are orthologs of DAF16, an insulin-responsive transcription factor involved in regulating longevity of worms and flies. The degree of homology between these four members is high, especially in the forkhead domain, which contains the DNA-binding interface. Yet, mouse FoxO knockouts have revealed that each FoxO gene has its unique role in the physiological process. Whether the functional divergences are primarily due to adaptive selection pressure or relaxed selective constraint remains an open question. As such, this study aims to address the evolutionary mode of FoxO, which may lead to the functional divergence.</p> <p>Results</p> <p>Sequence similarity searches have performed in genome and scaffold data to identify homologues of FoxO in vertebrates. Phylogenetic analysis was used to characterize the family evolutionary history by identifying two duplications early in vertebrate evolution. To determine the mode of evolution in vertebrates, we performed a rigorous statistical analysis with FoxO gene sequences, including relative rate ratio tests, branch-specific <it>d</it>_<it>N</it>/<it>d</it>_{<it>S </it>}ratio tests, site-specific <it>d</it>_<it>N</it>/<it>d</it>_{<it>S </it>}ratio tests, branch-site <it>d</it>_<it>N</it>/<it>d</it>_{<it>S </it>}ratio tests and clade level amino acid conservation/variation patterns analysis. Our results suggest that FoxO is constrained by strong purifying selection except four sites in FoxO6, which have undergone positive Darwinian selection. The functional divergence in this family is best explained by either relaxed purifying selection or positive selection.</p> <p>Conclusion</p> <p>We present a phylogeny describing the evolutionary history of the FoxO gene family and show that the genes have evolved through duplications followed by purifying selection except for four sites in FoxO6 fixed by positive selection lie mostly within the non-conserved optimal PKB motif in the C-terminal part. Relaxed selection may play important roles in the process of functional differentiation evolved through gene duplications as well.</p

A Comparative Study of Mouse Hepatic and Intestinal Gene Expression Profiles under PPARα Knockout by Gene Set Enrichment Analysis

Gene expression profiling of PPARα has been used in several studies, but fewer studies went further to identify the tissue-specific pathways or genes involved in PPARα activation in genome-wide. Here, we employed and applied gene set enrichment analysis to two microarray datasets both PPARα related respectively in mouse liver and intestine. We suggested that the regulatory mechanism of PPARα activation by WY14643 in mouse small intestine is more complicated than in liver due to more involved pathways. Several pathways were cancer-related such as pancreatic cancer and small cell lung cancer, which indicated that PPARα may have an important role in prevention of cancer development. 12 PPARα dependent pathways and 4 PPARα independent pathways were identified highly common in both liver and intestine of mice. Most of them were metabolism related, such as fatty acid metabolism, tryptophan metabolism, pyruvate metabolism with regard to PPARα regulation but gluconeogenesis and propanoate metabolism independent of PPARα regulation. Keratan sulfate biosynthesis, the pathway of regulation of actin cytoskeleton, the pathways associated with prostate cancer and small cell lung cancer were not identified as hepatic PPARα independent but as WY14643 dependent ones in intestinal study. We also provided some novel hepatic tissue-specific marker genes

Simultaneous slack budgeting and retiming for synchronous circuits optimization

Abstract- With the challenges of growing functionality and scaling chip size, the possible performance improvements should be considered in the earlier IC design stages, which gives more freedom to the later optimization. Potential slack as an effective metric of possible performance improvements is considered in this work which, as far as we known, is the first work that maximizes the potential slack by retiming for synchronous sequential circuit. A simultaneous slack budgeting and incremental retiming algorithm is proposed for maximizing potential slack. The overall slack budget is optimized by relocating the FFs iteratively with the MIS-based slack estimation. Compared with the potential slack of a well-known min-period retiming, our algorithm improves potential slack averagely 19.6 % without degrading the circuit performance in reasonable runtime. Furthermore, at the expense of a small amount of timing performance, 0.52 % and 2.08%, the potential slack is increased averagely by 19.89 % and 28.16 % separately, which give a hint of the tradeoff between the timing performance and the slack budget.

A comparative genome analysis of gene expression reveals different regulatory mechanisms between mouse and human embryo pre-implantation development

<p>Abstract</p> <p>Background</p> <p>Pre-implantation development is a crucial step in successful implantation and pregnancy in mammals. It has been studied in depth, but mostly in laboratory animal models. Less is known about the regulatory mechanism involved in the pre-implantation development in humans and about the comparative aspects.</p> <p>Methods</p> <p>Here, we employed the microarray datasets from the public database library of GEO and applied comparative analysis of genome wide temporal gene expression data based on statistical analysis and functional annotation for both mouse and human, demonstrating the discordance between the regulatory mechanisms of both mouse and human pre-implantation development.</p> <p>Results</p> <p>There were differences between mouse and human pre-implantation development both in the global gene expression pattern and in the expression changes of individual genes at each stage, including different major transient waves of transcription profiles and some stage-specific genes and significantly related pathways. There also appeared to be different functional changes from one stage to another between mouse and human.</p> <p>Conclusions</p> <p>The analysis presented here lead to interesting and complementary conclusions that the regulatory mechanism of human pre-implantation development is not completely the same as the mouse. Not as the fact that 1-cell to 2-cell stage is important for mouse pre-implantation development, the 4-cell stage and 8-cell stage are both essential for human. Unlike in mouse, of which most of pathways found were related to energy, RNA and protein metabolism, the identified pathways in human were mostly disease-related and associated with human pre-implantation embryonic development. All of these suggest that a further comparative analysis should be required for applying the result of mouse expression data to human research or therapy, particularly in pre-implantation developments. Our study provides several potential targets of genes and pathways for studying the regulatory mechanism of human pre-implantation development using mouse model.</p

Acetyl cholinesterase: a potential target for Alzheimer’s disease intervention

Alzheimer's disease is a neurological disorder in which the death of brain cells causes memory loss and cognitive decline. The role of treatment is not limited to pharmacology, but also involves many factors, such as the psychological, social, and economic aspects of the patient and family. It is important to consider the use of AChe inhibitors in patients with mild to moderate AD, despite cost issues and in the absence of any other immediate progression. Although there are allots of currently available inhibitor for acetyl cholinesterase but there is no selective potent inhibitor for AD. so, there is an urgent need discover of compounds that are active against Acetyl cholinesterase, along&nbsp; with there is need of molecular modeling for&nbsp; identifying functional groups that may be important for inhibiting Acetyl cholinesterase activity

Modulation of Actin Filament Dynamics by Inward Rectifying of Potassium Channel Kir2.1

Apart from its ion channel properties, the Kir2.1 channel has been found in tumors and cancer cells to facilitate cancer cell motility. It is assumed that Kir2.1 might be associated with cell actin filament dynamics. With the help of structured illumination microscopy (SIM), we show that Kir2.1 overexpression promotes actin filament dynamics, cell invasion, and adhesion. Mutated Kir2.1 channels, with impaired membrane expression, present much weaker actin regulatory effects, which indicates that precise Kir2.1 membrane localization is key to its actin filament remolding effect. It is found that Kir2.1 membrane expression and anchoring are associated with PIP2 affinity, and PIP2 depletion inhibits actin filament dynamics. We also report that membrane-expressed Kir2.1 regulates redistribution and phosphorylation of FLNA (filamin A), which may be the mechanism underlying Kir2.1 and actin filament dynamics. In conclusion, Kir2.1 membrane localization regulates cell actin filaments, and not the ion channel properties. These data indicate that Kir2.1 may have additional cellular functions distinct from the regulation of excitability, which provides new insight into the study of channel proteins