Miracle-dz/UniFAR-FTUs huggingface dataset:
How Justified is Abandoning Money in the Conduct of Monetary Policy in Australia on the Grounds of Instability in the Money‐Demand Function?

The role of money in the design and conduct of monetary policy has reemerged as an important issue in both advanced and developing economies, especially since the 2007 global financial crisis. A growing body of recent literature suggests that the causal relationship between money supply growth and inflation remains intact across countries and over time and that this relation is not conditional on the stability of the money&#8208;demand function or whether money is endogenous or exogenous. Moreover, critical for a rule&#8208;based monetary policy is the presence of a long&#8208;run stable money&#8208;demand function, rather than a short&#8208;run money&#8208;demand model that may exhibit instability for many reasons, including problems with estimating a money&#8208;demand model with high&#8208;frequency data. Provided that a stable money&#8208;demand function exists, it could be useful to establish long&#8208;run equilibrium relations among money, output, prices, and exchange rates, as the classical monetary theory suggests. Within this analytical framework, this paper addresses the question of whether money has any role in the conduct of monetary policy in Australia. The conventional wisdom is that the money&#8208;demand function in Australia has been unstable since the mid&#8208;1980s due to financial deregulation and reforms; this led to a change in the strategy of monetary policy for price stability in the form of inflation targeting that ignores money insofar as inflation and its control are concerned. This paper reports empirical findings for Australia, obtained from a longer quarterly data series over the period 1960Q1&#8211;2015Q1, which suggest that instability in the narrow&#8208;money&#8208;demand function in Australia was primarily due to the exclusion of variables which have become important in the deregulated environment since the 1980s. These findings are confirmed by an expanded form of the narrow&#8208;money&#8208;demand function that was found stable over the past two decades, although it experienced multiple structural breaks over the study period. The paper draws the conclusion that abandoning the monetary aggregate as an instrument of monetary policy in Australia, under a rule&#8208;based monetary policy such as inflation targeting, cannot be justified by instability in the money&#8208;demand function or even by lack of a causal link between money supply growth and inflation.
The Ca2+-dependent protein kinase CPK3 is required for MAPK-independent salt-stress acclimation in Arabidopsis

Plants use different signalling pathways to respond to external stimuli. Intracellular signalling via calcium-dependent protein kinases (CDPKs) or mitogen-activated protein kinases (MAPKs) present two major pathways that are widely used to react to a changing environment. Both CDPK and MAPK pathways are known to be involved in the signalling of abiotic and biotic stresses in animal, yeast and plant cells. Here, we show the essential function of the CDPK CPK3 (At4g23650) for salt stress acclimation in Arabidopsis thaliana, and test crosstalk between CPK3 and the major salt-stress activated MAPKs MPK4 and MPK6 in the salt stress response. CPK3 kinase activity was induced by salt and other stresses after transient overexpression in Arabidopsis protoplasts, but endogenous CPK3 appeared to be constitutively active in roots and leaves in a strictly Ca(2+) -dependent manner. cpk3 mutants show a salt-sensitive phenotype comparable with mutants in MAPK pathways. In contrast to animal cells, where crosstalk between Ca(2+) and MAPK signalling is well established, CPK3 seems to act independently of those pathways. Salt-induced transcriptional induction of known salt stress-regulated and MAPK-dependent marker genes was not altered, whereas post-translational protein phosphorylation patterns from roots of wild type and cpk3 plants revealed clear differences. A significant portion of CPK3 was found to be associated with the plasma membrane and the vacuole, both depending on its N-terminal myristoylation. An initial proteomic study led to the identification of 28 potential CPK3 targets, predominantly membrane-associated proteins.
Drug-induced hyperploidy stimulates an antitumor NK cell response mediated by NKG2D and DNAM-1 receptors

ABSTRACT Formation of polyploid or aneuploid cells is a pathological hallmark of malignant tumors. Cell cycle checkpoint mechanisms play a crucial role in ensuring genomic integrity during mitosis, avoiding the generation of aneuploid cells. Additionally, cancer cell DNA ploidy is subjected to extrinsic controls operated by activation of adaptive immune responses mediated by T cells. NK cells exert a central role in the innate anticancer immunity; however, the mechanisms involved in the recognition of tumor cells by NK cells have not been fully elucidated. Herein, we report that drug-induced polyploidy in cancer cells activates antitumor responses mediated by NK cells. Thus, hyperploidy-inducing chemotherapeutic agents strongly upregulate the tumor expression of ligands for the NK cell activating receptors NKG2D and DNAM-1. Drug-induced hyperploidy modulated the repertoire of activating receptors and the cytokine profile of NK cells, rendering tumor cells more susceptible to NK cell-mediated lysis through the activation of NKG2D and DNAM-1 receptors. In addition, hyperploidization stimulated the production of IL-2 by CD4 T cells, which induced NK cell proliferation and activity. The stimulation of MICA, a key NKG2D ligand, in hyperploid cells was mainly mediated by ATM protein kinase. Likewise, pharmacological inhibition of key regulators of endoplasmic reticulum stress in certain cell models supports a role for this pathway in NKG2D ligand upregulation. Overall, our findings indicate that, besides the cytotoxic effect on tumor cells, the therapeutic activity of anti-mitotic drugs may be mediated by the induction of a coordinated antitumor immune response involving NK and T cells.
Activation of the alternative complement pathway in vitreous is controlled by genetics in age-related macular degeneration.

PURPOSE To determine if the progression of age-related macular degeneration (AMD) is associated with complement activation in the eye. METHODS Immunohistochemistry and ELISAs were used to determine the distribution, concentration, and activation of the alternative pathway complement proteases factor B (FB) and factor D (FD) and the central complement protein C3 in genotyped human postmortem donor eyes graded as having no or minimal drusen (category 1; controls), large drusen (category 3), and large drusen with advanced AMD (category 4). RESULTS C3, FB, and FD were present in vitreous and Bruch's membrane choroid (BM/C) interface of the macula of eyes in all tested AMD severity categories (n = 100). C3, FB, and FD were predominantly located to the choroidal vasculature and Bruch's membrane and, together with the serum proteins transferrin and albumin, elevated in BM/C extracts of category 4 eyes (n = 23) compared with category 1 eyes (n = 24). A significant increase in FB activation was found only in vitreous of category 4 eyes (n = 23) compared with category 1 eyes (n = 25). Genetic variants of complement factor H (CFH), C3, C2, and FB associated with increased risk of AMD were correlated with alternative pathway complement activation in vitreous, but not with complement proteins in BM/C protein extracts. CONCLUSIONS Increased activation of the alternative complement pathway in vitreous was controlled by disease stage and genetic variation in the complement pathway, supporting a role for complement activation in AMD disease pathogenesis.
Neither host-specific nor random: vascular epiphytes on three tree species in a Panamanian lowland forest.

BACKGROUND AND AIMS A possible role of host tree identity in the structuring of vascular epiphyte communities has attracted scientific attention for decades. Specifically, it has been suggested that each host tree species has a specific subset of the local species pool according to its own set of properties, e.g. physicochemical characteristics of the bark, tree architecture, or leaf phenology patterns. METHODS A novel, quantitative approach to this question is presented, taking advantage of a complete census of the vascular epiphyte community in 0.4 ha of undisturbed lowland forest in Panama. For three locally common host-tree species (Socratea exorrhiza, Marila laxiflora, Perebea xanthochyma) null models were created of the expected epiphyte assemblages assuming that epiphyte colonization reflected random distribution of epiphytes in the forest. KEY RESULTS In all three tree species, abundances of the majority of epiphyte species (69-81 %) were indistinguishable from random, while the remaining species were about equally over- or under-represented compared with their occurrence in the entire forest plot. Permutations based on the number of colonized trees (reflecting observed spatial patchiness) yielded similar results. Finally, a third analysis (canonical correspondence analysis) also confirmed host-specific differences in epiphyte assemblages. In spite of pronounced preferences of some epiphytes for particular host trees, no epiphyte species was restricted to a single host. CONCLUSIONS The epiphytes on a given tree species are not simply a random sample of the local species pool, but there are no indications of host specificity either.
Microstructural changes in the thalamus after mild traumatic brain injury: A longitudinal diffusion and mean kurtosis tensor MRI study

Abstract Primary objective: The primary aim of this study was to assess microstructural changes in the thalamus, hippocampus and corpus callosum with a fast mean kurtosis tensor (MKT) technique, in the acute and sub-acute phase after mTBI. It was hypothesized that MKT would differ between baseline and follow-up in patients. The secondary aim was to relate diffusion measures to symptoms of mTBI. Research design: A longitudinal case-control study. Methods and procedures: Twenty-seven patients with mTBI and 27 age- and gender-matched healthy controls were enrolled in the study. Patients were scanned within 2 weeks and 3 months after mTBI, while the controls were scanned once. Main outcomes and results: MKT decreased significantly (p = 0.02) from baseline to follow-up in the thalamus in patients. Compared to healthy subjects, thalamic MKT values were significantly larger in patients at baseline (p = 0.048). Secondary analysis revealed a significant decrease (p = 0.01) in fractional anisotropy in the splenium of corpus callosum from baseline to follow-up. Conclusions: The current study indicates microstructural changes in the thalamus and corpus callosum from within 14 days to 3 months after mTBI and suggests MKT as a potential biomarker after mTBI.
Influence of female sex on long-term mortality after acute coronary syndromes treated by percutaneous coronary intervention: a cohort study of 7304 patients

AimFemale sex has been associated with worse outcome after percutaneous coronary intervention (PCI) for acute coronary syndromes (ACS). We assessed the influence of female sex on the long-term outcome of patients undergoing PCI for ACS. This included an unadjusted analysis and a fully-adjusted multivariate analysis including a propensity score. MethodsThis was an observational cohort study involving 7304 patients who had PCI for ACS [ST-elevation myocardial infarction (STEMI), non-ST elevation (NSTE) ACS] between October 2003 and September 2010. We analysed the effect of female sex on outcome. ResultsThe primary end point was all-cause mortality, which was obtained from the UK Office of National Statistics at a median follow-up of 3.2 years (IQR: 1.5–4.6). Women were significantly older and had higher rates of diabetes mellitus compared with men. Over long-term follow-up, mortality was significantly higher in women with ACS compared with men; as a whole [all ACS: odds ratio (OR) 1.351, P<0.001] or when analysed by ACS type (NSTE ACS: OR 1.260, P=0.009; STEMI: OR 1.625, P<0.001). However, after adjustment using multivariate analysis, female sex was not an independent predictor of mortality in any ACS group (all ACS: OR 0.978, P=0.772; NSTE ACS: OR 0.954, P=0.603; STEMI: OR 1.081, P=0.567). This observation remained after the incorporation of a propensity score into the multivariate analysis [OR 0.95, 95% confidence interval 0.82–1.10]. ConclusionWomen presenting with ACS were older and had more baseline comorbidities. Female sex, however, does not appear to be an independent risk factor for mortality in our cohort.
Genetic classification and mutational spectrum of more than 600 patients with a Zellweger syndrome spectrum disorder

The autosomal recessive Zellweger syndrome spectrum (ZSS) disorders comprise a main subgroup of the peroxisome biogenesis disorders and can be caused by mutations in any of 12 different currently identified PEX genes resulting in severe multisystemic disorders. To get insight into the spectrum of PEX gene defects among ZSS disorders and to investigate if additional human PEX genes are required for functional peroxisome biogenesis, we assigned over 600 ZSS fibroblast cell lines to different genetic complementation groups. These fibroblast cell lines were subjected to a complementation assay involving fusion by means of polyethylene glycol or a PEX cDNA transfection assay specifically developed for this purpose. In a majority of the cell lines we subsequently determined the underlying mutations by sequence analysis of the implicated PEX genes. The PEX cDNA transfection assay allows for the rapid identification of PEX genes defective in ZSS patients. The assignment of over 600 fibroblast cell lines to different genetic complementation groups provides the most comprehensive and representative overview of the frequency distribution of the different PEX gene defects. We did not identify any novel genetic complementation group, suggesting that all PEX gene defects resulting in peroxisome deficiency are currently known. Hum Mutat 31:1–11, 2010. © 2010 Wiley‐Liss, Inc.
Phenotypic change from transformed to normal induced by benzoquinonoid ansamycins accompanies inactivation of p60src in rat kidney cells infected with Rous sarcoma virus

Three benzenoid ansamycin antibiotics (herbimycin, macbecin, and geldanamycin) were found to reduce the intracellular phosphorylation of p60src at a permissive temperature (33 degrees C) in a rat kidney cell line infected with a temperature-sensitive mutant of Rous sarcoma virus. This effect was accompanied by morphological changes from the transformed to the normal phenotype. The filamentous staining pattern of actin fibers was observed in the cells treated with these antibiotics at 33 degrees C. Removal of the antibiotics allowed the cells to revert to the transformed morphology. Ansamitocin, another benzenoid ansamycin, and naphthalenoid ansamycins such as streptovaricin and rifamycins did not show this effect. Pulse-labeling of the antibiotic-treated cultures with 32Pi showed a marked reduction of 32P radioactivity incorporated into p60src. A parallel experiment with [35S]methionine showed that synthesis of p60src was slightly inhibited. The immune complex prepared by mixing the herbimycin-treated cell extracts with antibody against p60src was inactive in vitro in phosphorylating the complex itself. On the contrary, the immune complex derived from untreated cells was active in vitro even in the presence of the antibiotics. These results suggest that benzoquinonoid ansamycins have no direct effect on src kinase but destroy its intracellular environment, resulting in an irreversible alteration of p60src and loss of catalytic activity.
An evaluation of the effectiveness of alcohol treatment, driver license actions and jail terms in reducing drunk driving recidivism in California.

AIM There has been long-standing interest in determining which sanctions work best to reduce drunk driving. This study examines the effectiveness of alcohol treatment, driver license actions and jail terms in reducing drunk-driving recidivism. DESIGN This quasi-experimental study examines the relationships between the sanctions that drivers convicted of driving-under-the-influence (DUI) receive and their subsequent reconviction of DUI, while statistically controlling for pre-existing differences among groups receiving different sanctions. Separate analyses were conducted for subjects having 0, 1 or 2 or more prior DUI convictions on their driving record. SETTING The study analyzes drunk driving reacidivism throughout the state of California. Participants. All drivers holding a California driver license who were convicted of DUI by a California court during 1990 and 1991 were selected for inclusion in the study. MEASUREMENTS A number of demographic, prior personal driving history and surrogate traffic environment measures were collected and used as covariates in the analyses. Data were also gathered on subsequent DUI reconvictions, and the number of days to first subsequent DUI reconviction, and used as outcome variables in the study. FINDINGS Results of the analyses showed that for all levels of prior DUI convictions, combining alcohol treatment with either driver license restriction or suspension is associated with the lowest DUI recidivism rates. CONCLUSIONS Based on this research, and the results of prior studies, it can be persuasively argued that combining license actions with alcohol treatment represents the most effective sanction combination for combating DUI recidivism.
Regulation of ROMK and channel-inducing factor (CHIF) in acute renal failure due to ischemic reperfusion injury.

BACKGROUND Acute renal failure caused by ischemia followed by reperfusion is often associated with severe hyperkalemia. The present study was undertaken to characterize the effects of renal ischemia and reperfusion on plasma potassium (K) and on the gene expression of channel-inducing factor (CHIF), a putative K channel regulator, and of ROMK, the distal nephron secretory K channel. METHODS The following groups of rats were studied: (1) sham operated (sham); (2) after one hour of ischemia by bilateral renal artery clamping (I), and after one hour of ischemia; (3) one hour of reperfusion (I-R 1 h); (4) 24 hours of reperfusion (I-R 24 h); (5) 48 hours of reperfusion (I-R 48 h); and (6) 72 hours reperfusion (I-R 72 h). The expression of CHIF and ROMK was examined by Northern blot hybridization in renal cortex, medulla, and papilla and in the colon. The abundance of ROMK protein was determined in the renal cortex and medulla by immunoblotting. RESULTS Maximal plasma creatinine and potassium levels after ischemia and reperfusion were 470 +/- 16 micromol/L, P < 0.0001 versus sham, and 9.65 +/- 0.33 mmol/L, P < 0.0001 versus sham, respectively. The expression of CHIF was significantly down-regulated in the medulla and papilla, with a maximal decrease of 80% at 48 to 72 hours. In contrast, a most significant increase in CHIF mRNA expression (250% of baseline) was noted in the colon after 24 to 48 hours of reperfusion. ROMK expression was reduced in the cortex and was completely abolished in the medulla at 48 to 72 hours of reperfusion. Ischemia and reperfusion injury significantly decreased ROMK protein abundance to 10% of control in the medullary fractions. CONCLUSIONS These results suggest that down-regulation of renal CHIF and ROMK may contribute at least partly to the hyperkalemia of acute renal failure after ischemia and reperfusion, while CHIF up-regulation in the colon may act as a compensatory mechanism of maintaining K balance via increased K secretion.
Increased allergen concentration enhances IFN‐γ production by allergic donor T cells expressing a peripheral tissue trafficking phenotype

Background: Clinically effective allergen‐specific immunotherapy correlates with decreased circulating allergen‐specific IL‐4+ T cells but increased IFN‐γ+ cells at sites of allergen challenge. Whether immunotherapy promotes trafficking of IFN‐γ+ T cells to peripheral tissues is unknown. As aeroallergen is administered at higher concentrations during immunotherapy than those encountered naturally, the effect of allergen concentration on adhesion molecule (CD62L and CD49d) and chemokine receptor (CCR3 and CCR5) expression by peripheral‐blood T cells was analysed in parallel with cytokine production.
Effect of a Lower Extremity Preventive Training Program on Physical Performance Scores in Military Recruits

Abstract Peck, KY, DiStefano, LJ, Marshall, SW, Padua, DA, Beutler, AI, de la Motte, SJ, Frank, BS, Martinez, JC, and Cameron, KL. Effect of a lower extremity preventive training program on physical performance scores in military recruits. J Strength Cond Res 31(11): 3146–3157, 2017—Exercise-based preventive training programs are designed to improve movement patterns associated with lower extremity injury risk; however, the impact of these programs on general physical fitness has not been evaluated. The purpose of this study was to compare fitness scores between participants in a preventive training program and a control group. One thousand sixty-eight freshmen from a U.S. Service Academy were cluster-randomized into either the intervention or control group during 6 weeks of summer training. The intervention group performed a preventive training program, specifically the Dynamic Integrated Movement Enhancement (DIME), which is designed to improve lower extremity movement patterns. The control group performed the Army Preparation Drill (PD), a warm-up designed to prepare soldiers for training. Main outcome measures were the Army Physical Fitness Test (APFT) raw and scaled (for age and sex) scores. Independent t tests were used to assess between-group differences. Multivariable logistic regression models were used to control for the influence of confounding variables. Dynamic Integrated Movement Enhancement group participants completed the APFT 2-mile run 20 seconds faster compared with the PD group (p < 0.001), which corresponded with significantly higher scaled scores (p < 0.001). Army Physical Fitness Test push-up scores were significantly higher in the DIME group (p = 0.041), but there were no significant differences in APFT sit-up scores. The DIME group had significantly higher total APFT scores compared with the PD group (p < 0.001). Similar results were observed in multivariable models after controlling for sex and body mass index (BMI). Committing time to the implementation of a preventive training program does not appear to negatively affect fitness test scores.