Miracle-dz/UniFAR-FTUs huggingface dataset:
Self-Assembled Metal Colloid Monolayers: An Approach to SERS Substrates

The self-assembly of monodisperse gold and silver colloid particles into monolayers on polymer-coated substrates yields macroscopic surfaces that are highly active for surface-enhanced Raman scattering (SERS). Particles are bound to the substrate through multiple bonds between the colloidal metal and functional groups on the polymer such as cyanide (CN), amine (NH2), and thiol (SH). Surface evolution, which can be followed in real time by ultraviolet-visible spectroscopy and SERS, can be controlled to yield high reproducibility on both the nanometer and the centimeter scales. On conducting substrates, colloid monolayers are electrochemically addressable and behave like a collection of closely spaced microelectrodes. These favorable properties and the ease of monolayer construction suggest a widespread use for metal colloid-based substrates.
Hyperkalemia: A Review

Potassium is the principal intracellular cation, and maintenance of the distribution of potassium between the intracellular and the extracellular compartments relies on several homeostatic mechanisms. When these mechanisms are perturbed, hypokalemia or hyperkalemia may occur. This review covers hyperkalemia, that is, a serum potassium concentration exceeding 5 mmol/L. The review includes a discussion of potassium homeostasis and the etiologies of hyperkalemia and focuses on the prompt recognition and treatment of hyperkalemia. This disorder should be of major concern to clinicians because of its propensity to cause fatal arrhythmias. Hyperkalemia is easily diagnosed, and rapid and effective treatments are readily available. Unfortunately, treatment of this life-threatening condition is often delayed or insufficiently attentive or aggressive.
The effect of lutein and zeaxanthin supplementation on metabolites of these carotenoids in the serum of persons aged 60 or older.

PURPOSE To investigate the effect of lutein supplementation at doses of 2.5, 5.0, and 10 mg/d for 6 months on distribution of these carotenoids and their metabolites in the serum of elderly human subjects, with and without age-related macular degeneration. To determine whether supplementation with lutein can interact with the serum levels of other dietary carotenoids, retinol, and alpha-tocopherol. METHODS Forty-five subjects received daily supplements of lutein (containing 5% zeaxanthin) for 6 months and were followed up for another 6 months after supplementation. Blood was collected at various intervals and lutein, zeaxanthin, and their metabolites in the sera were quantified by normal-phase high-performance liquid chromatography (HPLC)-UV/visible detection. Other dietary carotenoids, retinol, and alpha-tocopherol were identified and quantified on a C18 reversed phase HPLC column. RESULTS After 6 months of supplementation with 10 mg of lutein, the increases in the mean serum levels from baseline were: 210 to 1000 nM/L (P < 0.0001) for lutein and 56 to 95 nM/L (P < 0.0001) for zeaxanthin. Similarly, the mean concentrations (nM/L) of carotenoid metabolites increased from 49 to 98 (P < 0.0001) for 3-hydroxy-beta,epsilon-caroten-3'-one (3'-oxolutein); 31 to 80 (P < 0.0001) for 3'-hydroxy-epsilon,epsilon-caroten-3-one; and 19 to 25 (P < 0.0001) for epsilon,epsilon-carotene-3,3'-dione. The serum levels of these carotenoids gradually decline within 6 months after supplementation. CONCLUSIONS The increase in the serum levels of lutein/zeaxanthin correlates with increases in the serum levels of their metabolites that have previously been identified in the ocular tissues. Elderly human subjects with and without AMD can safely take supplements of lutein up to 10 mg/d for 6 months with no apparent toxicity or side effects.
A comparative study on phasor and frequency measurement techniques in power systems

The objective of this paper is to make a comparative study on different phasor and frequency measurement algorithms available for power systems. The dynamic nature of the power system signals has made the estimation of frequency and phasors difficult. Over the years, many digital algorithms have been developed to overcome these difficulties and to provide accurate real-time frequency and phasor measurements. In this paper, four different algorithms for frequency estimation and three different algorithms for phasor estimation are studied and compared. A case study is performed by considering a three-phase voltage signal with time-varying amplitude and frequency to verify the effectiveness of these estimation algorithms.
Kisspeptin/KISS1R signaling potentiates extravillous trophoblast adhesion to type‐I collagen in a PKC‐ and ERK1/2‐dependent manner

During the first trimester of human pregnancy, cytotrophoblasts proliferate within the tips of the chorionic villi to form cell columns that anchor the placenta to the uterus. This migration coincides with a widespread change in the adhesion molecule repertoire of these trophoblasts. Kisspeptin and its receptor, KISS1R, are best known as potent triggers of gonadotropin‐releasing hormone secretion. The kisspeptin/KISS1R signaling system is also highly expressed in the human placenta, where it was demonstrated to inhibit extra‐villous trophoblast (EVT) migration and invasion in vitro. Here we show that kisspeptin, in a dose‐ and time‐dependent manner, induces increased adhesion of human EVTs to type‐I collagen, a major component of the human placenta. This increased adhesion was both rapid and transient, suggesting that it likely occurred through the activation of KISS1R secondary effectors such as PKC and ERK, which underwent rapid and transient kisspeptin‐dependent activation in EVTs. We then showed that inhibition of both PKC and ERK1/2 attenuated the kisspeptin‐dependent increase in EVT adhesion, suggesting that these molecules are key positive regulators of trophoblast adhesion. We therefore propose that kisspeptin/KISS1R signaling potentiates EVT adhesion to type‐I collagen via “inside‐out signaling. ” Furthermore, kisspeptin treatment increased mouse blastocyst adhesion to collagen I, suggesting that kisspeptin signaling is a key regulator of trophoblast function during implantation as well as early placentation. Mol. Reprod. Dev. 81: 42–54, 2014. © 2013 Wiley Periodicals, Inc.
A new storage structure design of Surakarta chess based on location

Surakarta chess is one of Computer Olympiad chesses. Its Chessboard is irregular. The logical structure of Surakarta chess is studied. A new storage structure of realizing the computer game program of Surakarta chess is presented. Representation of chessboard and chessman are presented by using the new storage structure. It is quite easy to judge the position relation of chess pieces with the storage structure. And it is very convenient to implement the move judging algorithm and capture judging algorithm, and the chess rules. This storage structure has referential value to accomplish the computer game programs of other sorts of chesses.
Examination of ‘lipotoxicity’ in skeletal muscle of high‐fat fed and ob/ob mice

Excess lipid accumulation resulting from an elevated supply of plasma fatty acids is linked to the pathogenesis of the metabolic syndrome and heart disease. The term ‘lipotoxicity’ was coined to describe how lipid accumulation leads to cellular dysfunction and death in non‐adipose tissues including the heart, pancreas and liver. While lipotoxicity has been shown in cultured skeletal muscle cells, the degree of lipotoxicity in vivo and the functional consequences are unresolved. We studied three models of fatty acid overload in male mice: 5 h Intralipid® and heparin infusion, prolonged high fat feeding (HFF) and genetic obesity induced by leptin deficiency (ob/ob mice). Markers of apoptosis, proteolysis and autophagy were assessed as readouts of lipotoxicity. The Intralipid® infusion increased caspase 3 activity in skeletal muscle, demonstrating that enhancing fatty acid flux activates pro‐apoptotic pathways. HFF and genetic obesity increased tissue lipid content but did not influence apoptosis. Gene array analysis revealed that HFF reduced the expression of 31 pro‐apoptotic genes. Markers of autophagy (LC3β and beclin‐1 expression) were unaffected by HFF and were associated with enhanced Bcl2 protein expression. Proteolytic activity was similarly unaffected by HFF or in ob/ob mice. Thus, contrary to our previous findings in muscle culture in vitro and in other non‐adipose tissues in vivo, lipid overload did not induce apoptosis, autophagy or proteolysis in skeletal muscle. A broad transcriptional suppression of pro‐apoptotic proteins may explain this resistance to lipid‐induced cell death in skeletal muscle.
Antidepressants for smoking cessation.

BACKGROUND There are two reasons to believe antidepressants might help in smoking cessation. First, depression may be a symptom of nicotine withdrawal, and smoking cessation sometimes precipitates depression. Second, nicotine may have antidepressant effects that maintain smoking for some smokers. Antidepressants may substitute for this effect. OBJECTIVES The aim of this review is to assess the effectiveness of antidepressant medications in aiding long term smoking cessation. The drugs include bupropion; doxepin; fluoxetine; imipramine; moclobemide; nortriptyline; paroxetine; selegiline; sertraline, tryptophan and venlafaxine. SEARCH STRATEGY We searched the Cochrane Tobacco Addiction Group trials register which includes trials indexed in MEDLINE, EMBASE, SciSearch and PsycLIT, and other reviews and meeting abstracts, in September 2001. SELECTION CRITERIA We considered randomized trials comparing antidepressant drugs to placebo or an alternative therapeutic control for smoking cessation. We excluded trials with less than 6 months follow-up. DATA COLLECTION AND ANALYSIS We extracted data in duplicate on the type of study population, the nature of the drug therapy, the outcome measures, method of randomisation, and completeness of follow-up. The main outcome measure was abstinence from smoking after at least six months follow-up in patients smoking at baseline. We used the most rigorous definition of abstinence for each trial, and biochemically validated rates if available. Where appropriate, we performed meta-analysis using a fixed effects model. MAIN RESULTS There was one trial each of moclobemide, sertraline and venlafaxine, two of fluoxetine and nortriptyline, and five trials of bupropion, one of which tested long term use to prevent relapse. Nortriptyline and bupropion both increased cessation. In one trial the combination of bupropion and nicotine patch produced slightly higher quit rates than patch alone. REVIEWER'S CONCLUSIONS Some antidepressants (bupropion and nortriptyline) can aid smoking cessation. It is not clear whether these effects are specific for individual drugs, or would occur with any antidepressant.
Image-Based Automated Defect Recognition via Statistical Learning of Minkowski Functionals

The adoption of image-based automated defect recognition (ADR) systems as standard tools for industrial inspection requires that such systems have extremely high levels of performance. To accomplish this goal it is often necessary to exploit every available constraint or information available about the specific inspection problem to be tackled. We propose an inspection method for the detection of flaws in aluminum castings that explores two broadly applicable assumptions: (i) defect-free industrial parts are abundant and standardized; (ii) statistically, the characteristics that distinguish defective from non-defective regions show no preferential a priori direction or orientation. The first observation leads to the use of a reference-based approach to ADR, in which a set of registered images of defect-free parts is used to build a statistical model for normalcy. The second observation suggests the use of Minkowski functionals, due to their invariance properties, to build signatures for the identification of defects. The proposed method was tested on 800 2D radiographic images of 100 aluminum cylinder heads. Our approach yielded a 100% detection rate with a 4% false alarm rate. These promising results demonstrate the potential of the approach.
Cross-Resistance within the Protease Inhibitor Class

Protease inhibitors (PIs) inhibit HIV-1 replication by binding to the active site of the viral protease and preventing it from binding and cleaving its natural polyprotein substrate. HIV-1 resists PI drug action by selecting for variants that have developed mutations that counteract drug binding to the viral protease. Although the protease gene consists of only 99 codons, the frequency of polymorphisms is relatively high [1,2]. Of these, at least 42 mutations across 27 codons have been correlated with loss of responsiveness to PI therapy [3,4]. However, the actual number of resistance-associated sites may be much higher [1,4]. The drug-associated mutations that occur in the HIV-1 genome have been divided into two groups: primary and accessory (sometimes referred to as secondary or compensatory) mutations [5–7]. Primary mutations are considered to directly confer drug resistance, whilst also often reducing the replicative capacity or ‘fitness’ of the virus, thus reducing their pathogenic potential [8,9]. Accessory mutations occur after primary mutations have developed, and are thought to compensate for the loss of viral fitness resulting from the primary mutations [10,11]. Therefore, a virus containing both primary and accessory mutations can potentially replicate in the presence of drug and attain a level of viral fitness equivalent to the wild-type virus in the absence of drug. The identification of drug-related mutations in the protease gene is continually being updated and revised as to their clinical relevance [4,12]. Figure 1 shows the current mutations associated with PI selection [12]. Since the role of the protease in the life cycle of HIV-1 is to cleave the gag and pol polyproteins, accessory mutations can also occur in the cleavage sites (for example, gag p7/p1 and p1/p6), compensating for the effects of resistance mutations in the protease, and restoring viral fitness [13]. Cross-resistance occurs when mutations, selected by one drug, confer resistance to another drug. A number of primary mutations selected by individual PIs do confer some cross-resistance to others (for example, 82A, 90M, Figure 1) [12]. The exceptions to this are a mutation at codon 48 that confers high-level resistance to saquinavir and mutations at codons 30 and 88, which are associated specifically with nelfinavir resistance. The majority of accessory mutations play a role in resistance to all molecules within the PI class [12], and the accumulation of multiple mutations gives rise to the highest levels of PI resistance [14]. Therefore, if one PI selects for a certain number of mutations, the virus may only need to accumulate one or two extra mutations relevant to the second PI in order for high-level cross-resistance to occur. This review will discuss the role of accessory mutations in viral replicative fitness, the level of cross-resistance detected after PI failure and the options that remain following prior PI failure.
Autism‐like behavioral phenotypes in BTBR T+tf/J mice

Autism is a behaviorally defined neurodevelopmental disorder of unknown etiology. Mouse models with face validity to the core symptoms offer an experimental approach to test hypotheses about the causes of autism and translational tools to evaluate potential treatments. We discovered that the inbred mouse strain BTBR T+tf/J (BTBR) incorporates multiple behavioral phenotypes relevant to all three diagnostic symptoms of autism. BTBR displayed selectively reduced social approach, low reciprocal social interactions and impaired juvenile play, as compared with C57BL/6J (B6) controls. Impaired social transmission of food preference in BTBR suggests communication deficits. Repetitive behaviors appeared as high levels of self‐grooming by juvenile and adult BTBR mice. Comprehensive analyses of procedural abilities confirmed that social recognition and olfactory abilities were normal in BTBR, with no evidence for high anxiety‐like traits or motor impairments, supporting an interpretation of highly specific social deficits. Database comparisons between BTBR and B6 on 124 putative autism candidate genes showed several interesting single nucleotide polymorphisms (SNPs) in the BTBR genetic background, including a nonsynonymous coding region polymorphism in Kmo. The Kmo gene encodes kynurenine 3‐hydroxylase, an enzyme‐regulating metabolism of kynurenic acid, a glutamate antagonist with neuroprotective actions. Sequencing confirmed this coding SNP in Kmo, supporting further investigation into the contribution of this polymorphism to autism‐like behavioral phenotypes. Robust and selective social deficits, repetitive self‐grooming, genetic stability and commercial availability of the BTBR inbred strain encourage its use as a research tool to search for background genes relevant to the etiology of autism, and to explore therapeutics to treat the core symptoms.
Towards an immunity-based anomaly detection system for network traffic

This paper proposes an immunity-based anomaly detection system for network traffic. The system is inspired by the specificity and diversity of the immune system; the system has a user-specific agent for every user, and diverse agents make a decision whether network traffic is normal or abnormal. The system makes use of multiple user profiles, which account for normal user traffic, while conventional anomaly detections have used only the single user profile. The use of multiple profiles leads to an improvement in detection accuracy. In addition, this paper proposes an evaluation framework for the immunity-based anomaly detection system. The evaluation framework is capable of evaluating the differences in detection accuracy between internal and external anomalies. In experiments, the immunity-based method outperformed the conventional method. For internal masquerader detection, the average false acceptance rate was 11.21% with no false alarms. For virus detection, four random-scanning worms and the simulated metaserver worm were detected with no false acceptances and no false alarms, while a simulated passive worm was successfully detected on some of accounts.
Beneficial Effects of Magnesium Treatment on Heart Rate Variability and Cardiac Ventricular Function in Diabetic Rats

Background: Diabetes mellitus induces life-threatening cardiovascular complications such as cardiac autonomic neuropathy and ventricular dysfunction and is associated with hypomagnesemia. In this study, we investigated the short-term effects of magnesium (Mg2+) treatment on streptozotocin (STZ)-induced diabetic cardiac complications. Methods: Adult Wistar rats were treated once with STZ (50 mg/kg, intraperitoneally [ip]) or vehicle (citrate) and then daily for 7 days with MgSO4 (270 mg/kg, ip) or saline. On the eighth day, in vivo tail-pulse plethysmography was recorded for heart rate variability (HRV) analysis, and ex vivo Langendorff-based left ventricular (LV) pressure–volume parameters were measured using an intraventricular balloon. Measurements of plasma lipid and Mg2+ levels as well as blood glucose and cardiac tissue Mg2+ levels were also performed. Results: Treatment with Mg2+ prevented diabetes-induced alterations in the standard deviation of the averages of normal-to-normal (NN) intervals (SDANN), root mean square differences of successive NN intervals (RMSSD), heart rate, and low-frequency (LF) power–high-frequency (HF) power ratio. In addition, Mg2+ restored orthostatic stress-induced changes in SDANN, RMSSD, and LF–HF ratio in diabetic rats. In isolated hearts, Mg2+ reversed the diabetes-induced decrease in LV end-diastolic elastance and the right shift of end-diastolic equilibrium volume intercept, without altering LV-developed pressure or end-systolic elastance. However, Mg2+ did not prevent the elevation in blood glucose, total cholesterol, and triglycerides or the decrease in high-density lipoprotein cholesterol in diabetes. Plasma- or cardiac tissue Mg2+ was not different among the treatment groups. Conclusion: These results suggest that Mg2+ treatment may attenuate diabetes-induced reduction in HRV and improve LV diastolic distensibility, without preventing hyperglycemia and dyslipidemia. Thus, Mg2+ may have a modulatory role in the early stages of diabetic cardiovascular complications.
WATER AND METHANOL MASER SURVEY OF PROTOSTARS IN THE ORION MOLECULAR CLOUD COMPLEX

The results of a maser survey toward 99 protostars in the Orion molecular cloud complex are presented. The target sources are low-mass protostars identified from infrared observations. Single-dish observations were carried out in the water maser line at 22 GHz and the methanol class I maser lines at 44, 95, and 133 GHz. Most of the detected sources were mapped to determine the source positions. Five water maser sources were detected, and they are excited by HH 1–2 VLA 3, HH 1–2 VLA 1, L1641N MM1/3, NGC 2071 IRS 1/3, and an object in the OMC 3 region. The water masers showed significant variability in intensity and velocity with time scales of 1 month or shorter. Four methanol emission sources were detected, and those in the OMC 2 FIR 3/4 and L1641N MM1/3 regions are probably masers. The methanol emission from the other two sources in the NGC 2071 IRS 1–3 and V380 Ori NE regions are probably thermal. For the water masers, the number of detections per protostar in the survey region is about 2%, which suggests that the water masers of low-mass protostars are rarely detectable. The methanol class I maser of low-mass protostars is an even rarer phenomenon, with a detection rate much smaller than 1%.
Mechanical Stressing of Integrin Receptors Induces Enhanced Tyrosine Phosphorylation of Cytoskeletally Anchored Proteins*

Physical forces play a fundamental role in the regulation of cell function in many tissues, but little is known about how cells are able to sense mechanical loads and realize signal transduction. Adhesion receptors like integrins are candidates for mechanotransducers. We used a magnetic drag force device to apply forces on integrin receptors in an osteoblastic cell line and studied the effect on tyrosine phosphorylation as a biochemical event in signal transduction. Mechanical stressing of both the β1 and the α2 integrin subunit induced an enhanced tyrosine phosphorylation of proteins compared with integrin clustering. Application of cyclic forces with a frequency of 1 Hz was more effective than a continuous stress. Using Triton X-100 for cell extraction, we found that tyrosine-phosphorylated proteins became physically anchored to the cytoskeleton due to mechanical integrin loading. This cytoskeletal linkage was dependent on intracellular calcium. To see if mechanical integrin stressing induced further downstream signaling, we analyzed the activation of mitogen-activated protein (MAP) kinases and found an increased phosphorylation of MAP kinases due to mechanical stress. We conclude that integrins sense physical forces that control gene expression by activation of the MAP kinase pathway. The cytoskeleton may play a key role in the physical anchorage of activated signaling molecules, which enables the switch of physical forces to biochemical signaling events.
Power flow management in active networks

This paper proposes a new method to manage the active power in the distribution systems, a function under the framework of the active network (AN) concept. An application of the graph theory is introduced to cope with the optimal power generation (DGs/Cells dispatch) and interarea power flows. The algorithm is implemented in a distributed way supported by the multi-agent system (MAS) technology. Simulations show how the method works in cases of optimal operation, congestion management, and power generation cost change.