Miracle-dz/UniFAR-FTUs huggingface dataset:
Soy-Dairy Protein Blend or Whey Protein Isolate Ingestion Induces Similar Postexercise Muscle Mechanistic Target of Rapamycin Complex 1 Signaling and Protein Synthesis Responses in Older Men1234

Background: Previous work demonstrated that a soy-dairy protein blend (PB) prolongs hyperaminoacidemia and muscle protein synthesis in young adults after resistance exercise. Objective: We investigated the effect of PB in older adults. We hypothesized that PB would prolong hyperaminoacidemia, enhancing mechanistic target of rapamycin complex 1 (mTORC1) signaling and muscle protein anabolism compared with a whey protein isolate (WPI). Methods: This double-blind, randomized controlled trial studied men 55–75 y of age. Subjects consumed 30 g protein from WPI or PB (25% soy, 25% whey, and 50% casein) 1 h after leg extension exercise (8 sets of 10 repetitions at 70% one-repetition maximum). Blood and muscle amino acid concentrations and basal and postexercise muscle protein turnover were measured by using stable isotopic methods. Muscle mTORC1 signaling was assessed by immunoblotting. Results: Both groups increased amino acid concentrations (P < 0.05) and mTORC1 signaling after protein ingestion (P < 0.05). Postexercise fractional synthesis rate (FSR; P ≥ 0.05), fractional breakdown rate (FBR; P ≥ 0.05), and net balance (P = 0.08) did not differ between groups. WPI increased FSR by 67% (mean ± SEM: rest: 0.05% ± 0.01%; postexercise: 0.09% ± 0.01%; P < 0.05), decreased FBR by 46% (rest: 0.17% ± 0.01%; postexercise: 0.09% ± 0.03%; P < 0.05), and made net balance less negative (P < 0.05). PB ingestion did not increase FSR (rest: 0.07% ± 0.03%; postexercise: 0.09% ± 0.01%; P ≥ 0.05), tended to decrease FBR by 42% (rest: 0.25% ± 0.08%; postexercise: 0.15% ± 0.08%; P = 0.08), and made net balance less negative (P < 0.05). Within-group percentage of change differences were not different between groups for FSR, FBR, or net balance (P ≥ 0.05). Conclusions: WPI and PB ingestion after exercise in older men induced similar responses in hyperaminoacidemia, mTORC1 signaling, muscle protein synthesis, and breakdown. These data add new evidence for the use of whey or soy-dairy PBs as targeted nutritional interventions to counteract sarcopenia. This trial was registered at clinicaltrials.gov as NCT01847261.
MICROTUBULE ORGANIZATION 1 Regulates Structure and Function of Microtubule Arrays during Mitosis and Cytokinesis in the Arabidopsis Root1[W]

MICROTUBULE ORGANIZATION 1 (MOR1) is a plant member of the highly conserved MAP215/Dis1 family of microtubule-associated proteins. Prior studies with the temperature-sensitive mor1 mutants of Arabidopsis (Arabidopsis thaliana), which harbor single amino acid substitutions in an N-terminal HEAT repeat, proved that MOR1 regulates cortical microtubule organization and function. Here we demonstrate by use of live cell imaging and immunolabeling that the mor1-1 mutation generates specific defects in the microtubule arrays of dividing vegetative cells. Unlike the universal cortical microtubule disorganization in elongating mor1-1 cells, disruption of mitotic and cytokinetic microtubule arrays was not detected in all dividing cells. Nevertheless, quantitative analysis identified distinct defects in preprophase bands (PPBs), spindles, and phragmoplasts. In nearly one-half of dividing cells at the restrictive temperature of 30°C, PPBs were not detected prior to spindle formation, and those that did form were often disrupted. mor1-1 spindles and phragmoplasts were short and abnormally organized and persisted for longer times than in wild-type cells. The reduced length of these arrays predicts that the component microtubule lengths are also reduced, suggesting that microtubule length is a critical determinant of spindle and phragmoplast structure, orientation, and function. Microtubule organizational defects led to aberrant chromosomal arrangements, misaligned or incomplete cell plates, and multinucleate cells. Antiserum raised against an N-terminal MOR1 sequence labeled the full length of microtubules in interphase arrays, PPBs, spindles, and phragmoplasts. Continued immunolabeling of the disorganized and short microtubules of mor1-1 at the restrictive temperature demonstrated that the mutant mor1-1L174F protein loses function without dissociating from microtubules, providing important insight into the mechanism by which MOR1 may regulate microtubule length.
A low fidelity mathematical model of a biomimetic AUV for multi-vehicle cooperation

While the advantages of operating AUVs within a multi-vehicle scenario are apparent, the complications associated with the underwater environment have provided a barrier preventing the successful operation of a self-organising group of Autonomous Underwater Vehicles (AUVs). Although AUV technology has matured sufficiently to overcome these challenges, the development of suitable coordination algorithms that take into account the various nuisances of the underwater environment is still a relatively unexplored area of development. In order to design such algorithms a validated mathematical model representing the dynamics and kinematics of the vehicle is required to represent each group member. However, the fidelity of the model has to be taken into consideration in order to ensure a practical simulation time is achieved when multiple vehicles are being simulated. Consequently, this paper describes a validated high fidelity model of the biomimetic AUV RoboSalmon and the techniques utilised to reduce the model's fidelity to improve the simulation run time. Once validated, the low fidelity model is used to analyse the efficiency and effectiveness of coordination algorithms based on the behavioural mechanisms associated with fish in school structures. The results demonstrate that by using look-up tables to replace certain aspects of the high fidelity model allows for a tenfold decrease in the simulation run time while maintaining an accurate representation of the AUVs dynamics. The results from the simulations involving the coordination algorithms demonstrated a dependency on certain configuration parameters to ensure the formation of a stable group structure.
Activation of Peroxisome Proliferator-Activated Receptor α by Substituted Urea-Derived Soluble Epoxide Hydrolase Inhibitors

Soluble epoxide hydrolase (sEH) plays a major role in regulating vascular epoxyeicosatrienoic acid metabolism and function, and substituted urea derivatives that inhibit sEH activity reduce blood pressure in hypertensive rats. We found that substituted urea derivatives containing a dodecanoic acid group, besides effectively inhibiting sEH, increased peroxisome proliferator-activated receptor (PPAR) α activity. In PPARα transfected COS-7 cells, treatment with 10 μM N-cyclohexyl-N′-dodecanoic acid urea (CUDA) or N-adamantanyl-N′-dodecanoic acid urea (AUDA) produced 6- and 3-fold increases, respectively, in PPARα activation. Neither CUDA nor AUDA activated PPARδ or PPARγ directly, indicating selectivity for PPARα. CUDA did not alter PPARα protein expression, and it competitively inhibited the binding of Wy-14643 (pirinixic acid) to the ligand binding domain of PPARα, suggesting that it functions as a PPARα ligand. CUDA and AUDA were metabolized to chain-shortened β-oxidation products, a process that reduced their potency as sEH inhibitors and their ability to bind and activate PPARα. N,N′-Dicylclohexylurea and N-cyclohexyl-N′-dodecylurea, sEH inhibitors that do not contain a carboxylic acid group, did not activate PPARα. In HepG2 cells, CUDA increased the expression of the PPARα-responsive gene carnitine palmitoyltransferase 1A. We conclude that CUDA and AUDA, by virtue of their carboxylic acid substitution, activate PPARα in addition to potently inhibiting sEH. Further development of these compounds could lead to a class of agents with hypotensive and lipid-lowering properties that may be valuable for the prevention and treatment of cardiovascular disease.
Bibliometrical Analysis on Destructive Innovation Research in China

Disruptive innovation theory has become a hot issue in the field of enterprise innovation and strategic management. Based on 627 papers for disruptive innovation field collected by journals and in China Knowledge Internet (CNKI) since 2003, analysis are made by bibliometrics. Citespace Software is applied. Quantity of issuing, key words, issuing authors and issuing authorizations for disruptive innovation research field in China are systematically reviewed and summarized in the article. Some characteristics on disruptive innovation research field in China are gained to supply reference and information to relative scholars for subsequent researches. Keywords-disruptive innovation; bibliometrics; citespace
Electrothermal modeling and characterization of carbon interconnects with negative temperature coefficient of the resistance

Among many outstanding properties of carbon-based interconnects, it is of great interest for nanoelectronics applications the possibility to have an electrical resistance almost insensitive or even decreasing with temperature increase. This behavior has been theoretically predicted and experimentally proven for carbon nanotubes and graphene nanoribbons, but only in controlled conditions, and for limited ranges of geometrical dimensions and temperature. This paper demonstrates the possibility of observing such a desirable behavior in large dimension carbon nanotubes and graphene conductors, made by self-assembly of short tubes and graphene flakes, respectively. The electro-thermal characterization of a 150μm-long carbon conductor clearly shows the possibility of having a negative temperature coefficient of the resistance.
The A-Kinase Anchoring Protein (AKAP) Glycogen Synthase Kinase 3β Interaction Protein (GSKIP) Regulates β-Catenin through Its Interactions with Both Protein Kinase A (PKA) and GSK3β *

The A-kinase anchoring protein (AKAP) GSK3β interaction protein (GSKIP) is a cytosolic scaffolding protein binding protein kinase A (PKA) and glycogen synthase kinase 3β (GSK3β). Here we show that both the AKAP function of GSKIP, i.e. its direct interaction with PKA, and its direct interaction with GSK3β are required for the regulation of β-catenin and thus Wnt signaling. A cytoplasmic destruction complex targets β-catenin for degradation and thus prevents Wnt signaling. Wnt signals cause β-catenin accumulation and translocation into the nucleus, where it induces Wnt target gene expression. GSKIP facilitates control of the β-catenin stabilizing phosphorylation at Ser-675 by PKA. Its interaction with GSK3β facilitates control of the destabilizing phosphorylation of β-catenin at Ser-33/Ser-37/Thr-41. The influence of GSKIP on β-catenin is explained by its scavenger function; it recruits the kinases away from the destruction complex without forming a complex with β-catenin. The regulation of β-catenin by GSKIP is specific for this AKAP as AKAP220, which also binds PKA and GSK3β, did not affect Wnt signaling. We find that the binding domain of AKAP220 for GSK3β is a conserved GSK3β interaction domain (GID), which is also present in GSKIP. Our findings highlight an essential compartmentalization of both PKA and GSK3β by GSKIP, and ascribe a function to a cytosolic AKAP-PKA interaction as a regulatory factor in the control of canonical Wnt signaling. Wnt signaling controls different biological processes, including embryonic development, cell cycle progression, glycogen metabolism, and immune regulation; deregulation is associated with diseases such as cancer, type 2 diabetes, inflammatory, and Alzheimer's and Parkinson's diseases.
A novel EBG microstrip line with noise suppression

In this paper, a novel microstrip transmission line structure based on the electromagnetic bandgap (EBG) is proposed to suppress simultaneous switching noise (SSN) with good transmission performance. Different from the common microstrip lines, in which the conductor line is uniform and EBG is etched on the ground plane to suppress SSN, the proposed microstrip transmission line applies EBG structure to conductor line instead of ground plane. The simulation results show that the novel microstrip line can exhibit better noise suppression performance than common microstrip line with EBG structure etched on ground plane.
Characterization of inhibition of M2 ion channel activity by BL-1743, an inhibitor of influenza A virus

The influenza A virus M2 integral membrane protein has ion channel activity that can be inhibited by the antiviral drug amantadine. Recently, a spirene-containing compound, BL-1743 (2-[3-azaspiro (5,5)undecanol]-2-imidazoline), that inhibits influenza virus growth was identified (S. Kurtz, G. Lao, K. M. Hahnenberger, C. Brooks, O. Gecha, K. Ingalls, K.-I. Numata, and M. Krystal, Antimicrob. Agents Chemother. 39:2204-2209, 1995). We have examined the ability of BL-1743 to inhibit the M2 ion channel when expressed in oocytes of Xenopus laevis. BL-1743 inhibition is complete as far as can be measured by electrophysiological methods and is reversible, with a reverse reaction rate constant of 4.0 x 10(-3) s(-1). In contrast, amantadine inhibition is irreversible within the time frame of the experiment. However, BL-1743 inhibition and amantadine inhibition have similar properties. The majority of isolated influenza viruses resistant to BL-1743 are also amantadine resistant. In addition, all known amino acid changes which result in amantadine resistance also confer BL-1743 resistance. However, one BL-1743-resistant virus isolated, designated M2-I35T, contained the change Ile-35-->Thr. This virus is >70-fold more resistant to BL-1743 and only 10-fold more resistant to amantadine than the wild-type virus. When the ion channel activity of M2-I35T was examined in oocytes, it was found that M2-I35T is BL-1743 resistant but is reversibly inhibited by amantadine. These findings suggest that these two drugs interact differently with the M2 protein transmembrane pore region.
Characterization of monoclonal antibodies to Marburg virus nucleoprotein (NP) that can be used for NP‐capture enzyme‐linked immunosorbent assay

After the first documented outbreak of Marburg hemorrhagic fever identified in Europe in 1967, several sporadic cases and an outbreak of Marburg hemorrhagic fever have been reported in Africa. In order to establish a diagnostic system for Marburg hemorrhagic fever by the detection of Marburg virus nucleoprotein, monoclonal antibodies to the recombinant nucleoprotein were produced. Two clones of monoclonal antibodies, MAb2A7 and MAb2H6, were efficacious in the antigen‐capture enzyme‐linked immunosorbent assay (ELISA). At least 40 ng/ml of the recombinant nucleoprotein of Marburg virus was detected by the antigen‐capture ELISA format. The epitope of the monoclonal antibody (MAb2A7) was located in the carboxy‐terminus of nucleoprotein from amino acid position 634 to 647, while that of the MAb2H6 was located on the extreme region of the carboxy‐terminus of the Marburg virus nucleoprotein (amino acid position 643–695). These monoclonal antibodies strongly interacted with the conformational epitopes on the carboxy‐terminus of the nucleoprotein. Furthermore, these two monoclonal antibodies were reacted with the authentic Marburg virus antigens by indirect immunofluorescence assay. These data suggest that the Marburg virus nucleoprotein‐capture ELISA system using the monoclonal antibodies is a promising technique for rapid diagnosis of Marburg hemorrhagic fever. J. Med. Virol. 76:111–118, 2005. © 2005 Wiley‐Liss, Inc.
Rat models of cardiometabolic diseases: baseline clinical chemistries, and rationale for their use in examining air pollution health effects

Abstract Individuals with cardiovascular and metabolic diseases (CVD) are shown to be more susceptible to adverse health effects of pollutants. Rodent models of CVD are used for examining susceptibility variations. CVD models developed by selective inbreeding are shown to represent the etiology of human disease and metabolic dysfunction. The goal of this article was to review the origin and the pathobiological features of rat models of varying CVD with or without metabolic syndrome and healthy laboratory rat strains to allow better interpretation of the data regarding their susceptibility to air pollutant exposures. Age-matched healthy Sprague–Dawley (SD), Wistar (WIS) and Wistar Kyoto (WKY), and CVD-prone spontaneously hypertensive (SH), Fawn-Hooded hypertensive (FHH), SH stroke-prone (SHSP), SHHF/Mcc heart failure obese (SHHF) and insulin-resistant JCR:LA-cp obese (JCR) rat models were considered for this study. The genetics and the underlying pathologies differ between these models. Normalized heart weights correlated with underlying cardiac disease while wide differences exist in the number of white blood cells and platelets within healthy strains and those with CVD. High plasma fibrinogen and low angiotensin converting enzyme activity in FHH might relate to kidney disease and associated hypertension. However, other obese strains with known kidney lesions do not exhibit decreases in ACE activity. The increased activated partial thromboplastin time only in SHSP correlates with their hemorrhagic stroke susceptibility. Increases plasma lipid peroxidation in JCR might reflect their susceptibility to acquire atherosclerosis. These underlying pathologies involving CVD and metabolic dysfunction are critical in interpretation of findings related to susceptibility variations of air pollution health effects.
In vitro activity of CI-919 (AT-2266), an oral antipseudomonal compound

We tested CI-919 (AT-2266), a nalidixic acid analog, against 555 gram-positive and gram-negative bacteria, using microbroth or agar dilution methods. The activity of CI-919 was compared with those of cephalosporins, tobramycin, ticarcillin, dicloxacillin, rifampin, chloramphenicol, ampicillin, and trimethoprimsulfamethoxazole. The minimal inhibitory concentrations of CI-919 for 90% of isolates were (in micrograms per milliliter): Pseudomonas spp. (including Pseudomonas aeruginosa), 4.0; Enterobacteriaceae, 0.5; Staphylococcus spp. , 2.0; Haemophilus influenzae, 0.12; Campylobacter jejuni, 0.12; and enterococci, 16. The minimal inhibitory concentrations of CI-919 for 90% of 82 tobramycin-resistant, gram-negative strains was 4.0 micrograms/ml. CI-919 was bactericidal for most isolates, showing no cross-resistance with unrelated antimicrobial agents, and was stable for 11 weeks at temperatures ranging from 22 to -70 degrees C. Inoculum size and media pH had little effect on the antibacterial activity of CI-919 for nine strains tested. CI-919 may be useful as an oral antibiotic for the treatment of infections due to diverse bacteria, including P. aeruginosa.
Lifestyle Intervention in Overweight Individuals With a Family History of Diabetes

OBJECTIVE To assess the effect of lifestyle intervention over 2 years on changes in weight, coronary heart disease (CHD) risk factors, and incidence of diabetes in overweight individuals with a parental history of diabetes. RESEARCH DESIGN AND METHODS Participants (n = 154), who were 30–100% over ideal body weight, had one or both parents with diabetes, and were currently nondiabetic, were randomly assigned to 2-year treatments focused on diet (decreasing calories and fat intake), exercise (goal of 1,500 kcal/week of moderate activity), or the combination of diet plus exercise or to a no-treatment control group. Subjects were reassessed at 6 months, 1 year, and 2 years. RESULTS At 6 months, the groups differed significantly on measures of eating, exercise, and fitness; weight losses in the diet and diet-plus-exercise groups were significantly > in the exercise and control conditions. Weight losses were associated with positive changes in CHD risk factors. After 6 months, there was gradual deterioration of behavioral and physiological changes, so that at 2 years, almost no between-group differences were maintained. Differences between groups in risk of developing diabetes were of borderline significance (P = 0.08). Strongest predictors were impaired glucose tolerance at baseline, which was positively related to risk of developing diabetes, and weight loss from baseline to 2 years, which was negatively related; in all treatment groups, a modest weight loss of 4.5 kg reduced the risk of type 2 diabetes by ∼ 30% compared with no weight loss. CONCLUSIONS Although initially successful, the interventions studied here were not effective in producing long-term changes in behavior, weight, or physiological parameters. However, weight loss from 0 to 2 years reduced the risk of developing type 2 diabetes. Since modest weight loss significantly reduced risk of type 2 diabetes, further research is needed to determine how best to increase the percentage of subjects achieving at least a modest weight loss.
Factors Leading to Hip Subluxation and Dislocation in Femoral Lengthening of Unilateral Congenital Short Femur

Congenital short femur is a rare and complex deformity. For it to be treated in the most accurate way, we must know of every possible complication. The purpose of this study was to determine the factors leading to hip subluxation or dislocation in patients with an unilateral congenital short femur who underwent a femoral lengthening procedure. Forty-four patients with congenital unilateral short femora types I, II, and IIIA were seen between 1981 and 1993 at Alfred I. duPont Hospital for Children. Seventeen patients had type I, 9 patients had type II, and 18 patients had type IIIA. Twenty patients underwent simultaneous lengthening of the femur and tibia, and 24 patients had primary lengthening of the femur. Eleven patients had an epiphysiodesis of the contralateral femur for residual leg length discrepancies of <6 cm. We observed that in patients with type IIIA, the acetabular dysplasia is severe, as well as the coxa vara deformity, and is associated with progressive subluxation and dislocation of the hip with lengthening. We believe that the combined abnormality of coxa vara and bow of the femoral shaft contributes to hip subluxation and dislocation in congenital short femur in association with an acetabular dysplasia prior to the lengthening. We recommend correction of the varus bow of the femur and the neck-shaft angle to 120° and the acetabular index to <25° prior to lengthening of type IIIA femora.
Indigenous People’s Environmental Concerns: The Missing Piece in Ongoing Administrative and Political Decentralization in Africa

Decentralization is assumed to make national governments more accountable and enables local people to get involved in governance decisions. This study examines the relationships and whether decentralization activities, policies and regulations support indigenous concerns for the environment. Much of the pristine and local lands globally have already been degraded through overexploitation of natural resources leading to significant loss of environmental benefits to people, especially the marginalized and indigenous communities. Using citizen-over-state and state-over-citizen theory, the influence of national level policies on local policies and vice versa is examined. Two sets of data are analyzed: reports from conservation organizations and peer reviewed publications. The other data is obtained from the World Bank and the Food and Agricultural Organization data base. All African countries are analyzed. The findings show that many national policies and regulations do not support and have no relationship with indigenous peoples’ environmental values, thus undermining local sustainable lifestyles. The more focus on economic development as an outcome is turning out to be a dominant force in driving exploitation of resources and eroding indigenous peoples’ cultural and environment values. While a few policies and regulations have some correlation with indigenous values, they have no significant influence in terms of producing sustainable local level environmental outcomes.