Miracle-dz/UniFAR-FTUs huggingface dataset:
Automated telephone screening for problem drinking.

OBJECTIVE This study assessed test-retest reliability and criterion validity for an automated version of the Alcohol Use Disorders Identification Test (AUDIT), a screening tool for alcohol-related problems. Participants' willingness to use such a system to learn about and change their drinking behavior was also assessed. METHOD Participants were 202 callers recruited through newspaper ads and flyers asking for volunteers concerned about their drinking and willing to help test a new method of screening and referral for alcohol problems. Participants were divided into two groups. The first group of subjects recruited received the Telephone-Linked Communications (TLC)-AUDIT twice, administered a week apart. The second group received the TLC-AUDIT once and a human-administered AUDIT once, also a week apart. RESULTS Test-retest reliability was assessed in 102 participants; the intraclass correlation of AUDIT scores between both administrations was . 87; kappa for nonproblem versus problem drinking (AUDIT score of 8 or above) was . 89. The validity study compared the TLC-AUDIT scores of the next 100 participants to AUDIT questions administered by a human interviewer. The intraclass correlation was . 94; kappa was . 75. Seventy-five percent of all participants who screened positive for problem drinking agreed they would "talk to a computer again to learn more about your drinking pattern and how to deal with it". CONCLUSIONS Automated telephone technology can be used to administer the AUDIT instrument with high levels of reliability and validity. This technology could be used to deliver behavioral change interventions.
Is easier always better?

A common theme in modern advertisements is that the product or service that is being offered is better because it is easier or faster. Every year, advancements in technology make the daily chores of life easier. These innovations have accelerated in the last two decades. We have GPS devices to give step-by-step directions, phones to remember a phone directory of numbers, and digital calendars to remind us up to the minute on our appointments. We also have new software, which has made staying in touch with friends, paying bills and filing our taxes a child’s play. This has indeed helped most people to focus their energy and time on their jobs productively. Technology has freed us from the heaviest of manual labors and the tedium of mundanemental tasks, but has there been a cost? Apart from the reduction of exercise endurance and increase in the incidence of obesity, there may be just as significant effects on the mental health of individuals in the long term. There are multiple studies to suggest that people who have higher pre-morbid cognitive functioning (are cognitively very active) have slower onset of dementia and better prognosis (Daffner, 2010). The current young and middle age population is the future geriatric cohort at risk for cognitive disorders. This could imply that the incidence of dementia and other cognitive disorders is likely to drastically rise in the years to come. ACTIVE (Advanced Cognitive Training for Independent and Vital Elderly) study was a multicenter, randomized controlled trial to examine the long-term outcomes of cognitive interventions on the daily functioning of older individuals living independently. This study showed that cognitive training could delay the rate of the neurocognitive decline (Willis et al., 2006, Ball et al., 2002). Cognitive stimulation therapy has shown to benefit cognition in people with mild to moderate dementia over and above any medication effects (Woods et al., 2012). Some neurologists, in fact, encourage patients with mild cognitive impairment to work on crosswords or other activities to slow the progress of the disease. This could imply that neurologists or even primary care physicians may advise their patients in the future to limit the use of electronic devices used for navigation, calendars and other activities. Is this trend of easing the human effort—physical or mental—beneficial for the mankind? Is this system, where a fraction of the human work force works hard tomake the life of the rest easier and better, advantageous to the evolution of the human race? Are we at risk of losing our intellect and memory as a species in this course ofmodernization? Long-term longitudinal studies may throw some light on this issue.
A Secreted Protein with Plant-Specific Cysteine-Rich Motif Functions as a Mannose-Binding Lectin That Exhibits Antifungal Activity1[W]

Ginkbilobin2 is shown to exert antifungal activity through its interaction with a1,2-linked mannose chains of fungal cell wall mannan, which provides clues to the molecular function of the DUF26 protein family. Plants have a variety of mechanisms for defending against plant pathogens and tolerating environmental stresses such as drought and high salinity. Ginkbilobin2 (Gnk2) is a seed storage protein in gymnosperm that possesses antifungal activity and a plant-specific cysteine-rich motif (domain of unknown function26 [DUF26]). The Gnk2-homologous sequence is also observed in an extracellular region of cysteine-rich repeat receptor-like kinases that function in response to biotic and abiotic stresses. Here, we report the lectin-like molecular function of Gnk2 and the structural basis of its monosaccharide recognition. Nuclear magnetic resonance experiments showed that mannan was the only yeast (Saccharomyces cerevisiae) cell wall polysaccharide that interacted with Gnk2. Gnk2 also interacted with mannose, a building block of mannan, with a specificity that was similar to those of mannose-binding legume lectins, by strictly recognizing the configuration of the hydroxy group at the C4 position of the monosaccharide. The crystal structure of Gnk2 in complex with mannose revealed that three residues (asparagine-11, arginine-93, and glutamate-104) recognized mannose by hydrogen bonds, which defined the carbohydrate-binding specificity. These interactions were directly related to the ability of Gnk2 to inhibit the growth of fungi, including the plant pathogenic Fusarium spp. , which were disrupted by mutation of arginine-93 or the presence of yeast mannan in the assay system. In addition, Gnk2 did not inhibit the growth of a yeast mutant strain lacking the α1,2-linked mannose moiety. These results provide insights into the molecular basis of the DUF26 protein family.
Substrate and acute temperature effects on turtle heart and liver mitochondria.

The oxidative properties of heart and liver mitochondria from the Western painted turtle (Chrysemys picta bellii) were characterized on the basis of substrate preferences and temperature sensitivity. Turtle heart and liver mitochondria oxidize most substrates at 2- and 10-fold less, respectively, than rates obtained from the corresponding rat mitochondria. Krebs cycle intermediates, ketone bodies, and glutamate were oxidized at similarly high rates by turtle heart mitochondria (70.0-121.2 nmol O.min-1.mg protein-1). Fatty acylcarnitines were oxidized at approximately one-half of the above rates, and rates of amino acid oxidation were either not detectable or very low. Heart mitochondria oxidize ketone bodies at rates as high as pyruvate plus malate. Liver mitochondria oxidized Krebs cycle intermediates, amino acids, and fatty acids at similarly low rates (3.0-8.0 nmol O.min-1.mg protein-1). Typically, succinate was oxidized at the highest rates, 20.6 +/- 4.0 and 121.2 +/- 1.2 nmol O.min-1.mg protein-1, for liver and heart, respectively. Values for the rate of change of oxidation with a 10 degrees C increase (Q10) from heart and liver mitochondria oxidizing glutamate were calculated over the range 25-5 degrees C in 5 degrees C intervals; over the range 10-5 degrees C, Q10 values were 3.2 and 19.8, respectively. Q10 values calculated over the higher temperature intervals were lower. It is suggested that the large difference in temperature sensitivity between mitochondria from these two tissues and the ability of the heart mitochondria to oxidize ketone bodies at high rates are adaptations to recover from the long anoxic overwintering bouts experienced by this species.
Isoform-specific Regulation of Insulin-dependent Glucose Uptake by Akt/Protein Kinase B*

Recent data have implicated the serine/threonine protein kinase Akt/protein kinase B (PKB) in a diverse array of physiological pathways, raising the question of how biological specificity is maintained. Partial clarification derived from the observation that mice deficient in either of the two isoforms, Akt1/PKBα or Akt2/PKBβ, demonstrate distinct abnormalities, i.e. reduced organismal size or insulin resistance, respectively. However, the question still persists as to whether these divergent phenotypes are due exclusively to tissue-specific differences in isoform expression or distinct capacities for signaling intrinsic to the two proteins. Here we show that Akt2/PKBβ-/- adipocytes derived from immortalized mouse embryo fibroblasts display significantly reduced insulin-stimulated hexose uptake, clearly establishing that the partial defect in glucose disposal in these mice derives from lack of a cell autonomous function of Akt2/PKBβ. Moreover, in adipocytes differentiated from primary fibroblasts or immortalized mouse embryo fibroblasts, and brown preadipocytes the absence of Akt2/PKBβ resulted in reduction of insulin-induced hexose uptake and glucose transporter 4 (GLUT4) translocation, whereas Akt1/PKBα was dispensable for this effect. Most importantly, hexose uptake and GLUT4 translocation were completely restored after re-expression of Akt2/PKBβ in Akt2/PKBβ-/- adipocytes, but overexpression of Akt1/PKBα at comparable levels was ineffective at rescuing insulin action to normal. These results show that the Akt1/PKBα and Akt2/PKBβ isoforms are uniquely adapted to preferentially transmit distinct biological signals, and this property is likely to contribute significantly to the ability of Akt/PKB to play a role in diverse processes.
Association between apolipoprotein E epsilon4 and the rate of cognitive decline in community-dwelling elderly individuals with and without dementia.

OBJECTIVE To determine whether the apolipoprotein E epsilon4 allele (apoE epsilon4) is associated with cognitive decline in individuals with and without dementia, we conducted a 4-year longitudinal study of subjects with a range of cognitive function. SETTING At baseline, respondents (n=511) were randomly selected according to age and Mini-Mental State Examination score from a community-based study of dementia among noninstitutionalized persons aged 65 to 84 years. Respondents were examined at baseline and followed up in 3 annual visits. At baseline, subjects were classified as having normal cognitive function, minimal dementia, or dementia, according to criteria from the Cambridge Examination for Mental Disorders of the Elderly (CAMDEX) and the Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition. Of the 511 respondents at baseline, 405 who were examined at least 2 times are included in this analysis. MAIN OUTCOME MEASURES Cognitive decline was determined by a slope estimating yearly change in score on the neuropsychological test, the CAMCOG (the cognitive section of the CAMDEX), and its sub-scales of memory and nonmemory functions. RESULTS Among the subjects who had normal cognitive function at baseline, apoE epsilon4 carriers showed a significantly greater decline (P<.001) in score on the CAMCOG compared with noncarriers. Differences in decline on the memory and nonmemory subtests were also significant (P<.001). Rates of cognitive decline were not related to apoE epsilon4 status in the groups with minimal dementia and dementia. CONCLUSIONS In our community-based sample, apoE epsilon4 was associated with the rate of cognitive decline prior to the clinically symptomatic phase of dementia. Knowing the apoE epsilon4 status of those already symptomatic for dementia may not improve knowledge about a patient's prognosis.
Associations of IL-23 with polypoidal choroidal vasculopathy.

PURPOSE To determine the relationship between the levels of intraocular inflammatory cytokines and polypoidal choroidal vasculopathy (PCV). METHODS Prospective cohort study. Sixty-two patients with PCV and 36 control subjects were studied. The levels of cytokines, chemokines, and growth factors in the aqueous humor samples from PCV patients and control subjects were assessed for significant associations with PCV. Logistic regression analysis was used to compute the odds ratios (ORs) and 95% confidence intervals (CIs) after the study populations were divided into quartiles. RESULTS In PCV patients, IL-4, IL-10, and IL-23 were significantly higher than in the controls. Logistic analyses showed a significantly high risk for IL-23 (OR for the highest quartile compared with the lowest quartile: 16.3; 95% CI: 3.5-75.2), VEGF (5.7; 1.2-26.1), and IL-4 (4.0; 1.3-12.7). IL-10 and IL-4, but not IL-23, were significantly correlated with the VEGF levels in PCV patients (IL-10: ρ = 0.477, IL-4: ρ = 0.281). The elevated levels of IL-5, IL-10, IL-4, IL-23, and IL-1α were found to be significantly associated with exudative lesion(s) in the fluorescein angiograms. CONCLUSIONS The significant associations between elevated levels of IL-23 with PCV and its activity strongly suggest an involvement of inflammatory processes in the etiology of PCV, presumably independent of VEGF. (www.umin.ac.jp/ctr number, UMIN000003854.).
The Labour Market in the Visegrad Group Countries : Selected Aspects

The aim of this paper is to compare selected aspects related to the labour market in the Visegrad Group countries. Inparticular, attention is paid to the analysis of labour force inactivity, the period of being unemployed and selected institutional arrangements related to the unemployment benefit systems. The research method is based on the analysis of statistical data and a review of institutional arrangements existing in each of the four countries. The analysis shows that there are differences related to the duration and the generosity of unemployment benefit systems. In terms of unemployment, the worst situation is to be found in Slovakia (especially, due to problems with an unemployment rate above the EU average, a high youth unemployment rate, and a significant proportion of long-term unemployed). In 2016 the shortest statutory duration of unemployment benefits was in Hungary, while the relatively least favourable benefit system seemed to exist in Poland.
(99m)Tc-3P-RGD2 micro-single-photon emission computed tomography/computed tomography provides a rational basis for integrin αvβ3-targeted therapy.

PURPOSE This study was to demonstrate the utility of (99m)Tc-3P-RGD2 micro-single-photon emission computed tomography/computed tomography (SPECT/CT) for the integrin αvβ3 expression quantification in NCI-H446 and A549 lung cancer xenografts. MATERIALS AND METHODS (99m)Tc-3P-RGD2 was prepared with high radiochemical purity (97%±2%) and showing high in vitro stability. The in vitro affinities of (99m)Tc-3P-RGD2 to NCI-H446 and A549 tumor cells were analyzed with γ-counter, while the in vivo uptakes in NCI-H446 and A549 xenografts were evaluated with micro-SPECT/CT. The region of interest was drawn over the tumor site and contralateral muscle on the SPECT/CT image, and the tumor to nontumor (T/NT) ratio was calculated to estimate αvβ3 expression and tumor uptake. The expressions of integrin αvβ3 in vitro and in vivo were analyzed using a flow cytometer and immunofluorescence. RESULTS Micro-SPECT/CT demonstrated focal uptake in the tumors. T/NT ratio in NCI-H446 xenografts was significantly higher compared with the A549 tumor model, as 5.92±0.82 and 3.62±0.91, respectively, with p<0.05. In addition, integrin αvβ3 expression in NCI-H446 cells was significantly higher compared with the A549 cells, which was consistent with the imaging data. A linear relationship was observed between (99m)Tc-3P-RGD2 uptake and αvβ3 expression (R(2)=0.7667, p<0.001). CONCLUSION (99m)Tc-3P-RGD2 SPECT/CT could be used to quantify integrin αvβ3 expression within tumors, providing a rational basis for integrin αvβ3-targeted cancer therapy.
Bone resorption by isolated chick osteoclasts in culture is stimulated by murine spleen cell supernatant fluids (Osteoclast‐Activating Factor) and inhibited by calcitonin and prostaglandin E2

The question of whether any of the agents known to activate bone resorption in vivo or in organ cultures acts directly on the osteoclast or via intermediate target cells that secondarily secrete locally paracrine factors is important for our understanding of bone remodeling. In an attempt to clarify this issue for some of the agents, we have taken advantage of the recent progress in obtaining and culturing relatively pure populations of osteoclasts. We performed an in vitro bone‐resorbing assay in which isolated and partially purified chick osteoclasts were cultured on devitalized, paired and standardized bone disks prepared from rat calvaria prelabeled with both 45Ca and 3H‐proline. Some of the isolated osteoclasts attached to the devitalized bone matrix, formed a ruffled border, and acidified the bone‐resorbing compartment that they established with the matrix, thereby indicating that they resorbed bone in a physiologic manner. Salmon calcitonin added to these cultures (0.3 U/ml = 60 ng/ml) and prostaglandin E2 (PGE2) (10−6M) inhibited both basal and stimulated 45Ca and 3H‐proline release. Neither parathyroid hormone (PTH) 1–34 (1 U/ml), 1,25‐(OH)2‐D3 (10−8 and 10−9M), nor interleukin 1 (IL‐1) (purified from P388D1 macrophage culture supernatant fluids or recombinant murine IL‐1‐alpha) (100 ng/ml) stimulated bone resorption in these cultures. In contrast, supernatant fluids from concanavalin A (Con‐A)‐activated murine spleen cell cultures (murine osteoclast‐activating factor; OAF) consistently and significantly induced a 3‐ to 5‐fold stimulation of bone resorption in this system.
Identification of Inactivation Determinants in the Domain IIS6 Region of High Voltage-activated Calcium Channels*

We have recently reported that transfer of the domain IIS6 region from rapidly inactivating R-type (α1E) calcium channels to slowly inactivating L-type (α1C) calcium channel confers rapid inactivation (Stotz, S. C., Hamid, J., Spaetgens, R. L., Jarvis, S. E., and Zamponi, G. W. (2000) J. Biol. Chem. 275, 24575–24582). Here we have identified individual amino acid residues in the IIS6 regions that are responsible for these effects. In this region, α1C and α1Echannels differ in seven residues, and exchanging five of those residues individually or in combination did not significantly affect inactivation kinetics. By contrast, replacement of residues Phe-823 or Ile-829 of α1C with the corresponding α1E residues significantly accelerated inactivation rates and, when substituted concomitantly, approached the rapid inactivation kinetics of R-type channels. A systematic substitution of these residues with a series of other amino acids revealed that decreasing side chain size at position 823 accelerates inactivation, whereas a dependence of the inactivation kinetics on the degree of hydrophobicity could be observed at position 829. Although these point mutations facilitated rapid entry into the inactivated state of the channel, they had little to no effect on the rate of recovery from inactivation. This suggests that the development of and recovery from inactivation are governed by separate structural determinants. Finally, the effects of mutations that accelerated α1C inactivation could still be antagonized following coexpression of the rat β2a subunit or by domain I–II linker substitutions that produce ultra slow inactivation of wild type channels, indicating that the inactivation kinetics seen with the mutants remain subject to regulation by the domain I–II linker. Overall, our results provide novel insights into a complex process underlying calcium channel inactivation.
Hydroxychloroquine’s Efficacy as an Antiplatelet Agent Study in Healthy Volunteers

Background: With the inflammatory model of atherosclerosis taking center stage, anti-inflammatory drugs hold a promising place in the therapy of cardiovascular disease (CVD). Recent studies showed that hydroxychloroquine (HCQ) was protective against thrombovascular events in lupus erythematosus and traditional cardiovascular risk factors in patients with rheumatoid arthritis. Some preliminary experimental data have shown that it may prevent platelet activation too. Objective: To evaluate the antiplatelet activity of HCQ when given alone and in combination with aspirin (ASA) and compare it with ASA alone and ASA plus clopidogrel (CLOP) in healthy human volunteers. Methods: In part 1 of the study, 8 volunteers were given HCQ for 7 days. In part 2, 12 volunteers were randomly assigned in a 1:1:1 ratio to the 3 groups in which 2 of the 3 treatments, ASA, ASA plus CLOP, and ASA plus HCQ, were given in the 2 treatment periods separated by a 14-day washout period using the incomplete block design. Inhibition of platelet aggregation (IPA) was measured by light transmission aggregometry. Results: When arachidonic acid (AA) was used as agonist, HCQ given alone showed a significant reduction in platelet aggregation (11.0% ± 4.2%, P = .03). The IPA was significantly increased when ASA plus HCQ was compared with ASA alone (31.2% ± 8.1%, P = .002). This synergistic effect was not seen with adenosine diphosphate and collagen as agonists. Levels of serum 11-dehydrothromboxane B2, a stable marker of thromboxane A2 production, were not significantly different between the groups. There was also a significant decrease in fibrinogen and erythrocyte sedimentation rate values when HCQ was used alone or in combination with ASA. Conclusion: This study suggests that HCQ has antiplatelet properties possibly through the AA pathway (downstream to thromboxane A2 production). With possible additional beneficial effects over the traditional CVD risk factors, larger studies in the future might explore HCQ’s potential as an antiplatelet agent.
Interfirm learning in environmental safety: evidence from the bakken

ABSTRACT This paper examines whether firm learning economies lead to reduced environmental incidents in Bakken unconventional oil drilling. We model the relationship between environmental safety and learning in preventing environmental incidents. We do not find evidence that firm or interfirm learning leads to increased environmental safety. We do find evidence that idiosyncratic quality of matches between firms and subcontractors is associated with improved environmental safety.
Anti-Eavesdropping Scheme Based on Quadrature Spatial Modulation

To resist the passive eavesdropping while reserving the same hardware cost and receiver structure of the legitimate receiver, a secure quadrature spatial modulation (QSM) scheme is proposed in this letter. Instead of the information symbol, a mixture of the information symbol and artificial noise is transmitted through the activated transmit antennas. The mixed signals are designed, so that the artificial noise is cancelled at the legitimate receiver but cause random interference to the eavesdropper. The secrecy rate is analyzed and the optimal power allocation between the artificial noise and the information signal is investigated. The influence of the number of the eavesdropper’s antennas is discussed. Simulation results show that, for multiple-input-single-output systems, the proposed secure QSM scheme achieves the best secrecy performance among the existing similar schemes by using less radio frequency chains. For multiple-input-multiple-output systems, the secure QSM scheme performs better than the existing secure SM scheme does under the same power constraint and transmission rate.