31 research outputs found
Nonlinear Analysis of Auscultation Signals in TCM Using the Combination of Wavelet Packet Transform and Sample Entropy
Auscultation signals are nonstationary in nature. Wavelet packet transform (WPT) has currently become a very useful tool in analyzing nonstationary signals. Sample entropy (SampEn) has recently been proposed to act as a measurement for quantifying regularity and complexity of time series data. WPT and SampEn were combined in this paper to analyze auscultation signals in traditional Chinese medicine (TCM). SampEns for WPT coefficients were computed to quantify the signals from qi- and yin-deficient, as well as healthy, subjects. The complexity of the signal can be evaluated with this scheme in different time-frequency resolutions. First, the voice signals were decomposed into approximated and detailed WPT coefficients. Then, SampEn values for approximated and detailed coefficients were calculated. Finally, SampEn values with significant differences in the three kinds of samples were chosen as the feature parameters for the support vector machine to identify the three types of auscultation signals. The recognition accuracy rates were higher than 90%
Cocaine Preferentially Potentiates Fast Releasable Vesicle Pool in Mouse Dopaminergic Striatum In Vivo
BiophysicsSCI(E)CPCI-S(ISTP)0MEETING ABSTRACT2498A-499A10
Transient Receptor Potential V Channels Are Essential for Glucose Sensing by Aldolase and AMPK
Fructose-1,6-bisphosphate (FBP) aldolase links sensing of declining glucose availability to AMPK activation via the lysosomal pathway. However, how aldolase transmits lack of occupancy by FBP to AMPK activation remains unclear. Here, we show that FBP-unoccupied aldolase interacts with and inhibits endoplasmic reticulum (ER)-localized transient receptor potential channel subfamily V, inhibiting calcium release in low glucose. The decrease of calcium at contact sites between ER and lysosome renders the inhibited TRPV accessible to bind the lysosomal v-ATPase that then recruits AXIN:LKB1 to activate AMPK independently of AMP. Genetic depletion of TRPVs blocks glucose starvation-induced AMPK activation in cells and liver of mice, and in nematodes, indicative of physical requirement of TRPVs. Pharmacological inhibition of TRPVs activates AMPK and elevates NAD(+) levels in aged muscles, rejuvenating the animals' running capacity. Our study elucidates that TRPVs relay the FBP-free status of aldolase to the reconfiguration of v-ATPase, leading to AMPK activation in low glucose
SPINK1, PRSS1, CTRC, and CFTR genotypes influence disease onset and clinical outcomes in chronic pancreatitis
Objectives
Rare pathogenic variants in the SPINK1, PRSS1, CTRC, and CFTR genes have been strongly associated with a risk of developing chronic pancreatitis (CP). However, their potential impact on the age of disease onset and clinical outcomes, as well as their potential interactions with environmental risk factors, remain unclear. These issues are addressed here in a large Chinese CP cohort.
Methods
We performed targeted next-generation sequencing of the four CP-associated genes in 1061 Han Chinese CP patients and 1196 controls. To evaluate gene–environment interactions, the patients were divided into three subgroups, idiopathic CP (ICP; n = 715), alcoholic CP (ACP; n = 206), and smoking-associated CP (SCP; n = 140). The potential impact of rare pathogenic variants on the age of onset of CP and clinical outcomes was evaluated using the Kaplan–Meier model.
Results
We identified rare pathogenic genotypes involving the SPINK1, PRSS1, CTRC, and/or CFTR genes in 535 (50.42%) CP patients but in only 71 (5.94%) controls (odds ratio = 16.12; P < 0.001). Mutation-positive patients had significantly earlier median ages at disease onset and at diagnosis of pancreatic stones, diabetes mellitus and steatorrhea than mutation-negative ICP patients. Pathogenic genotypes were present in 57.1, 39.8, and 32.1% of the ICP, ACP, and SCP patients, respectively, and influenced age at disease onset and clinical outcomes in all subgroups.
Conclusions
We provide evidence that rare pathogenic variants in the SPINK1, PRSS1, CTRC, and CFTR genes significantly influence the age of onset and clinical outcomes of CP. Extensive gene–environment interactions were also identified
Insights into APC/C: from cellular function to diseases and therapeutics
Anaphase-promoting complex/cyclosome (APC/C) is a multifunctional ubiquitin-protein ligase that targets different substrates for ubiquitylation and therefore regulates a variety of cellular processes such as cell division, differentiation, genome stability, energy metabolism, cell death, autophagy as well as carcinogenesis. Activity of APC/C is principally governed by two WD-40 domain proteins, Cdc20 and Cdh1, in and beyond cell cycle. In the past decade, the results based on numerous biochemical, 3D structural, mouse genetic and small molecule inhibitor studies have largely attracted our attention into the emerging role of APC/C and its regulation in biological function, human diseases and potential therapeutics. This review will aim to summarize some recently reported insights into APC/C in regulating cellular function, connection of its dysfunction with human diseases and its implication of therapeutics
Метод расчета зависимости динамики доходов работников от уровня образования в Республике Беларусь
We report a study of the process e(+)e(-) -> (D*(D) over bar*)(0)pi(0) using e(+)e(-) collision data samples with integrated luminosities of 1092 pb(-1) at root s = 4.23 GeV and 826 pb(-1) at root s = 4.26 GeV collected with the BESIII detector at the BEPCII storage ring. We observe a new neutral structure near the (D*(D) over bar*)(0) mass threshold in the pi(0) recoil mass spectrum, which we denote as Z(c)(4025)(0). Assuming a Breit-Wigner line shape, its pole mass and pole width are determined to be (4025.5(-4.7)(+2.0) +/- 3.1) MeV/c(2) and (23.0 +/- 6.0 +/- 1.0) MeV, respectively. The Born cross sections of e(+)e(-) -> Z(c)(4025)(0)pi(0) -> (D*(D) over bar*)(0)pi(0) are measured to be (61.6 +/- 8.2 +/- 9.0) pb at root s = 4.23 GeV and (43.4 +/- 8.0 +/- 5.4) pb at root s = 4.26 GeV. The first uncertainties are statistical and the second are systematic.Funding: The BESIII Collaboration thanks the staff of BEPCII and the IHEP computing center for their strong support. This work is supported in part by the National Key Basic Research Program of China under Contract No. 2015CB856700; the National Natural Science Foundation of China (NSFC) under Contracts No. 11125525, No. 11235011, No. 11275266, No. 11322544, No. 11335008, and No. 11425524; the Chinese Academy of Sciences (CAS) Large-Scale Scientific Facility Program; the CAS Center for Excellence in Particle Physics (CCEPP); the Collaborative Innovation Center for Particles and Interactions (CICPI); the Joint Large-Scale Scientific Facility Funds of the NSFC and the CAS under Contracts No. 11179007, No. U1232201, and No. U1332201; the CAS under Contracts No. KJCX2-YW-N29 and No. KJCX2-YW-N45; the 100 Talents Program of the CAS; INPAC and the Shanghai Key Laboratory for Particle Physics and Cosmology; German Research Foundation DFG under Contract No. Collaborative Research Center CRC-1044; the Istituto Nazionale di Fisica Nucleare, Italy; the Ministry of Development of Turkey under Contract No. DPT2006K-120470; the Russian Foundation for Basic Research under Contract No. 14-07-91152; the U.S. Department of Energy under Contracts No. DE-FG02-04ER41291, No. E-FG02-05ER41374, No. DE-FG02-94ER40823, and No. DESC0010118; the U.S. National Science Foundation; the University of Groningen (RuG) and the Helmholtzzentrum fuer Schwerionenforschung GmbH (GSI), Darmstadt; and the WCU Program of National Research Foundation of Korea under Contract No. R32-2008-000-10155-0.</p