Tracking the COVID-19 crisis with high-resolution transaction data.

Payments systems generate vast amounts of naturally occurring transaction data rarely used for constructing official statistics. We consider billions of transactions from card data from a large bank, Banco Bilbao Vizcaya Argentaria, as an alternative source of information for measuring consumption. We show, via validation against official consumption measures, that transaction data complements national accounts and consumption surveys. We then analyse the impact of COVID-19 in Spain, and document: (i) strong consumption responses to business closures, but smaller effects for capacity restrictions; (ii) a steeper decline in spending in rich neighbourhoods; (iii) higher mobility for residents of lower-income neighbourhoods, correlating with increased disease incidence.

Fusion Learning on Multiple-Tag RFID Measurements for Respiratory Rate Monitoring.

Future advances in the medical Internet of Things (IoT) will require sensors that are unobtrusive and passively powered. With the use of wireless, wearable, and passive knitted smart garment sensors, we monitor infant respiratory activity. We improve the utility of multi-tag Radio Frequency Identification (RFID) measurements via fusion learning across various features from multiple tags to determine the magnitude and temporal information of the artifacts. In this paper, we develop an algorithm that classifies and separates respiratory activity via a Regime Hidden Markov Model compounded with higher-order features of Minkowski and Mahalanobis distances. Our algorithm improves respiratory rate detection by increasing the Signal to Noise Ratio (SNR) on average from 17.12 dB to 34.74 dB. The effectiveness of our algorithm in increasing SNR shows that higher-order features can improve signal strength detection in RFID systems. Our algorithm can be extended to include more feature sources and can be used in a variety of machine learning algorithms for respiratory data classification, and other applications. Further work on the algorithm will include accurate parameterization of the algorithm's window size.

Forehead or ear temperature measurement cannot replace rectal measurements, except for screening purposes.

BACKGROUND: Measuring rectal temperature in children is the gold standard, but ear or forehead measures are less traumatic and faster. The quality of non-invasive devices has improved but concerns remain whether they are reliable enough to substitute rectal thermometers. The aim was to evaluate in a real-life children population whether the forehead or ear temperature measurements could be used in screening to detect fever and if the agreement with the rectal temperature for different age groups is acceptable for clinical use. METHODS: Cross-sectional clinical study comparing temporal and tympanic temperatures to rectal temperature in 0-18-year-old children. The ear thermometer was a Pro 4000 Thermoscan, the temporal Exergen TAT. Rectal temperature ≥ 38.0 °C was defined as fever. RESULTS: Among 995 children, 39% had a fever. The ear thermometer had a significantly greater ability to detect fever than the temporal thermometer (AUC 0.972; 95% CI: 0.963-0.981 versus AUC 0.931; 95% CI: 0.915-0.947, p < 0.0001). Both devices had the lowest sensitivity in the youngest and oldest children, and only the ear thermometer reached a sensitivity above 90% in the 0.5-5-year age group. The Bland-Altman analysis showed that the 95% limits of agreement for the temporal thermometer was between - 1.2 to + 1.5 °C and for the ear thermometer between - 0.97 to + 1.07 °C. CONCLUSIONS: Based on a large sample of children, the temporal measurement of temperature is not currently recommendable, but with the technology used in this study the ear measurement proved useful for screening purposes, especially among children aged 6 months to 5 years. For the exact measurement of temperature, the rectal method is still recommended.

Detection of eastern equine encephalitis virus antibodies in moose (Alces americana), Maine, 2010.

Moose sera were collected from harvested animals during the 2010 hunting season in Maine. Of the 145 serum samples screened by plaque reduction neutralization test (PRNT), 16 (11%) had antibodies to eastern equine encephalitis virus (EEEV). Positive samples were collected from Aroostook County (n=13), Somerset County (n=2), and Piscataquis County (n=1) in northern and central Maine. Preliminary mosquito surveillance revealed the presence of enzootic and bridge vectors mosquitoes, including Culiseta (Climacura) melanura (Coquillett), Aedes (Aedimorphus) vexans (Meigen), and Coquillettidia (Coquillettidia) perturbans (Walker). Select mosquito species were tested by RT-PCR for the presence of EEEV. None were positive. This is the first report of EEEV in moose from Maine.

Changes in Purkinje cell firing and gene expression precede behavioral pathology in a mouse model of SCA2.

Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominantly inherited disorder, which is caused by a pathological expansion of a polyglutamine (polyQ) tract in the coding region of the ATXN2 gene. Like other ataxias, SCA2 most overtly affects Purkinje cells (PCs) in the cerebellum. Using a transgenic mouse model expressing a full-length ATXN2(Q127)-complementary DNA under control of the Pcp2 promoter (a PC-specific promoter), we examined the time course of behavioral, morphologic, biochemical and physiological changes with particular attention to PC firing in the cerebellar slice. Although motor performance began to deteriorate at 8 weeks of age, reductions in PC number were not seen until after 12 weeks. Decreases in the PC firing frequency first showed at 6 weeks and paralleled deterioration of motor performance with progression of disease. Transcription changes in several PC-specific genes such as Calb1 and Pcp2 mirrored the time course of changes in PC physiology with calbindin-28 K changes showing the first small, but significant decreases at 4 weeks. These results emphasize that in this model of SCA2, physiological and behavioral phenotypes precede morphological changes by several weeks and provide a rationale for future studies examining the effects of restoration of firing frequency on motor function and prevention of future loss of PCs.

Response to ethanol induced ataxia between C57BL/6J and 129X1/SvJ mouse strains using a treadmill based assay.

More sensitive assays of mouse motor ataxia may provide a better understanding of the pathological profile. Treadmill gait analysis using ventral imaging allows for unhindered access to the ambulating mouse. In contrast to genetic mutations or exogenous brain injury, ethanol (EtOH) allows for the detection of dose dependent changes in motor behavior, which can be used to assess an assay's detection sensitivity. EtOH induced ataxia was assessed in C57BL/6J (B6) and 129X1/SvJ (129) mice using the DigiGait imaging system. Gait was analyzed across EtOH dosage (1.75, 2.25 and 2.75 g/kg) in each strain using a linear mixed effects model. Overall, 129 mice displayed greater susceptibility to EtOH ataxia than their B6 counterparts. In both strains, hind paws exhibited greater sensitivity to EtOH dosage than fore paws. Across most variables analyzed, only a modest EtOH-induced change in motor behavior was observed in each strain with the 1.75 g/kg EtOH doses failing to elicit significant change. These data indicate the ability to detect motor differences between strains, yet only moderate ability to detect change across EtOH dosage using the automated treadmill. Rotarod assays, however, were able to detect motor impairment at lower doses of EtOH. The significant, but opposite changes in paw placement with increasing EtOH doses highlight strain-specific differences in biophysical adaptations in response to acute EtOH intoxication.

ETS1 regulates the expression of ATXN2.

Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant disorder caused by the expansion of a CAG tract in the ATXN2 gene. The SCA2 phenotype is characterized by cerebellar ataxia, neuropathy and slow saccades. SCA2 foreshortens life span and is currently without symptomatic or disease-modifying treatments. Identifying function-specific therapeutics for SCA2 is problematic due to the limited knowledge of ATXN2 function. As SCA2 is likely caused by a gain-of-toxic or gain-of-normal function like other polyglutamine disorders, targeting ATXN2 expression may represent a valid therapeutic approach. This study characterized aspects of ATXN2 expression control using an ATXN2 promoter-luciferase (luc) reporter construct. We verified the fidelity of construct expression by generating transgenic mice expressing the reporter construct. High reporter expression was seen in the cerebellum and olfactory bulb in vivo but there was relatively low expression in other tissues, similar to the expression of endogenous ataxin-2. We verified the second of two possible start codons as the functional start codon in ATXN2. By evaluating deletions in the ATXN2 promoter, we identified an E-twenty six (ETS)-binding site required for ATXN2 expression. We verified that endogenous ETS1 interacted with the ATXN2 promoter by an electromobility supershift assay and chromatin immunoprecipitation polymerase chain reaction. ETS1 overexpression increased ATXN2-luc (ATXN2-luciferase) as well as endogenous ATXN2 expression. Deletion of the putative ETS1-binding site abrogated the effects on the expression of ATXN2-luc. A dominant negative ETS1 and an ETS1 short-hairpin RNA both reduced ATXN2-luc expression. Our study broadens the understanding on the transcriptional control of ATXN2 and reveals specific regulatory features of the ATXN2 promoter that can be exploited therapeutically.

Cholinergic modulation of mesolimbic dopamine function and reward.

The substantial health risk posed by obesity and compulsive drug use has compelled a serious research effort to identify the neurobiological substrates that underlie the development these pathological conditions. Despite substantial progress, an understanding of the neurochemical systems that mediate the motivational aspects of drug-seeking and craving remains incomplete. Important work from the laboratory of Bart Hoebel has provided key information on neurochemical systems that interact with dopamine (DA) as potentially important components in both the development of addiction and the expression of compulsive behaviors such as binge eating. One such modulatory system appears to be cholinergic pathways that interact with DA systems at all levels of the reward circuit. Cholinergic cells in the pons project to DA-rich cell body regions in the ventral tegmental area (VTA) and substantial nigra (SN) where they modulate the activity of dopaminergic neurons and reward processing. The DA terminal region of the nucleus accumbens (NAc) contains a small but particularly important group of cholinergic interneurons, which have extensive dendritic arbors that make synapses with a vast majority of NAc neurons and afferents. Together with acetylcholine (ACh) input onto DA cell bodies, cholinergic systems could serve a vital role in gating information flow concerning the motivational value of stimuli through the mesolimbic system. In this report we highlight evidence that CNS cholinergic systems play a pivotal role in behaviors that are motivated by both natural and drug rewards. We argue that the search for underlying neurochemical substrates of compulsive behaviors, as well as attempts to identify potential pharmacotherapeutic targets to combat them, must include a consideration of central cholinergic systems.

Comparison of intracanal EndoSequence Root Repair Material and ProRoot MTA to induce pH changes in simulated root resorption defects over 4 weeks in matched pairs of human teeth.

INTRODUCTION: Intracanal mineral trioxide aggregate (MTA) may provide an alternative to calcium hydroxide in the treatment of external inflammatory root resorption. This in vitro study using human matched pairs of teeth compared white ProRoot MTA (WMTA; (Dentsply Tulsa Dental Specialties, Tulsa, OK) and an alternative material with purportedly improved handling properties, EndoSequence Root Repair Material (ES; Brasseler USA, Savannah, GA), by measuring pH in simulated root surface resorptive defects after intracanal placement. The null hypothesis tested was that there is no difference between WMTA and ES. METHODS: Bilaterally matched pairs (n = 24) of extracted, human, single-rooted teeth were instrumented to apical size 50/.06, and root surface cavities were prepared at 5 mm and 2 mm from the apex. Root canals of experimental matched pairs (n = 20) were filled with WMTA or ES; control pairs (n = 4) were filled with calcium hydroxide (positive control [POS]) or saline (negative control [NEG]). Teeth were sealed coronally and apically and immersed in saline. The pH in root surface cavities was measured at 20 minutes, 3 hours, 24 hours, 1 week, 2 weeks, 3 weeks, and 4 weeks. RESULTS: The pH at 5 mm when compared with the 2-mm level was significantly higher for the WMTA, ES, and POS groups (P < .05, paired t tests); therefore, each level was analyzed separately. At both the 2-mm and 5-mm levels, significant pH changes occurred over time in the WMTA, ES (both P < .0001, repeated-measures analysis of variance), and POS (P < .0001, Friedman test) groups and not in the NEG group (mean pH = 7.32 ± 0.04, P > .05). There were no differences between WMTA and ES at 20 minutes and 3 hours at both levels or at 24 hours at 5mm. The pH of WMTA was higher than ES by 24 hours at the 2-mm level (8.79 vs 8.56, P < .05, paired t test) and after 1 week at the 5-mm level (8.91 vs 8.05, P < .0001) and was thereafter always significantly higher in WMTA compared with ES (P < .0001). The null hypothesis was rejected. CONCLUSIONS: In matched pairs of teeth, intracanal placement of WMTA compared with ES resulted in a higher pH in simulated root resorption defects that was time and root level dependent.

Injection of CART (cocaine- and amphetamine-regulated transcript) peptide into the nucleus accumbens reduces cocaine self-administration in rats.

Cocaine- and amphetamine-regulated transcript (CART) peptides appear to modulate various effects of psychostimulant drugs. Injections of CART peptide into the nucleus accumbens (NAcc) inhibit locomotion produced by systemic injections of the psychostimulants cocaine and amphetamine. Intra-NAcc injections of CART peptide also inhibit locomotion produced by microinfusions of dopamine into the NAcc, suggesting that the effects of CART peptides may be due to an interaction with the dopaminergic system in the NAcc. We sought to determine if this inhibitory effect of CART peptide generalizes to other measures of dopaminergic function such as reward/reinforcement by testing the effect of bilateral intra-NAcc CART infusions (0, 0.25, 1.0 and 2.5 microg per side) on cocaine and food self-administration. One group of rats self-administered cocaine (0.75 mg/kg per 140 microl IV infusion) on a progressive ratio schedule. A separate group received 45 mg food pellets on the same progressive ratio schedule. Bilateral intra-NAcc injections of CART peptide dose-dependently decreased the number of cocaine infusions, the breakpoint of cocaine self-administration, and the total number of bar presses on the cocaine-associated lever. There were no effects of CART injections on the breakpoint for food reward. Thus, we conclude that injections of CART into the NAcc appear to functionally antagonize a major site of action for cocaine self-administration in rats.

The nicotinic acetylcholine receptor antagonist mecamylamine prevents escalation of cocaine self-administration in rats with extended daily access.

RATIONALE: Escalation from moderate to excessive drug intake is a hallmark of human addiction that can be modeled in rats by giving them longer daily access time to self-administer cocaine. Nicotine and cocaine are commonly coabused drugs in humans and recent work in animals suggests that activation of nicotinic acetylcholine receptors (nAChR) can increase cocaine self-administration. OBJECTIVES: Determine the role of nAChR in the escalation of cocaine self-administration. METHODS: Control rats self-administered cocaine (0.75 mg/kg/infusion) for either 1 or 6 h per day. Experimental groups had the nAChR antagonist mecamylamine (MEC) added to the cocaine solution for 5 days after the transition from short (1 h per day) to long access (6 h per day) for cocaine self-administration. After 5 days, MEC was removed from the cocaine solution. RESULTS: Control rats and rats that received a low dose of MEC (7 microg/infusion) with cocaine increased their average hourly intake over 5 days of 6 h per day cocaine access. Rats that received a higher dose of MEC (70 microg/infusion) did not increase their intake of cocaine during 6 h access but continued to self-administer cocaine. When MEC was removed, this group showed an escalation in cocaine self-administration. MEC did not alter cocaine intake in a group that had continuous 1 h access. CONCLUSIONS: Antagonism of nAChRs during the initial exposure to extended cocaine self-administration access time prevented escalation of, but did not eliminate, drug intake. These findings indicate that MEC-sensitive nAChRs are critical for determining cocaine intake as a function of longer access time.

Resorptive response of rhBMP2 simulating infection in an anterior lumbar interbody fusion with a femoral ring.

RhBMP-2 has been available for general use since July of 2002. No literature regarding its use with femoral ring allografts exists. This case demonstrates how a resorptive effect of rhBMP-2 with a femoral ring allograft on host bone at the interbody fusion site can easily be confused with infection. Spine surgeons should be aware of this effect to avoid unnecessary antibiotic use or additional surgery.

Protease-activated receptor signaling increases epithelial antimicrobial peptide expression.

Epithelial tissues provide both a physical barrier and an antimicrobial barrier. Antimicrobial peptides of the human beta-defensin (hBD) family are part of the innate immune responses that play a role in mucosal defense. hBDs are made in epithelia including oral epithelium where the bacterial load is particularly great. hBD-2 and hBD-3 are up-regulated in response to bacterial stimuli. Previous studies show that hBD-2 expression in human gingival epithelial cells (GEC) is stimulated by both nonpathogenic and pathogenic bacteria, including Porphyromonas gingivalis, a Gram-negative pathogen associated with periodontitis. Present evidence suggests that hBD-2 expression in GEC uses several signaling pathways, including an NF-kappaB-mediated pathway but without apparent LPS-TLR4 signaling. Protease-activated receptors (PAR) are G-protein-coupled receptors that mediate cellular responses to extracellular proteinases. P. gingivalis secretes multiple proteases that contribute to its virulence mechanisms. To determine whether PAR signaling is used in hBD-2 induction, GEC were stimulated with wild-type P. gingivalis or mutants lacking one or more proteases. hBD-2 mRNA expression was reduced in GEC stimulated with single protease mutants (11-67% compared with wild type), strongly reduced in double mutants (0.1-16%), and restored to wild-type levels (93%) in mutant with restored protease activity. Stimulation by wild type was partially blocked by inhibitors of phospholipase C, a main signaling pathway for PARs. Expression of hBD-3 was unaffected. Peptide agonist of PAR-2, but not PAR-1 activator, also induced hBD-2 in GEC. Thus, P. gingivalis proteases are directly involved in regulation of hBD-2 in cultured GEC, and this induction partially uses the PAR-2 receptor and signaling pathway.

Operant self-administration of ethanol in C57BL/6 mice lacking beta-endorphin and enkephalin.

To test whether endogenous opioid peptides are necessary for the rewarding effects of ethanol, we examined operant oral self-administration of ethanol in mice congenic to the C57BL/6J strain but lacking expression of beta-endorphin, enkephalin or both peptides. The influences of prandial state, schedule interval and type, and ethanol concentration were all examined. Food-restricted subjects were tested in postprandial and preprandial states and subsequently at normal body weight when feeding ad libitum (ad lib). Operant studies were conducted using fixed ratio (FR) intervals of 2 and 8 as well as a progressive ratio (PR) interval of 2. The main significant effect relevant to our hypothesis was increased responding by female mice lacking beta-endorphin under ad lib feeding conditions and only for lower ethanol concentrations (3% and 6%). Importantly, all subjects including those lacking both beta-endorphin and enkephalins learned to self-administer ethanol similarly to wild-type mice and maintained responding for ethanol under a variety of procedural variables. Consequently, the two opioid peptides believed to be the endogenous ligands for the micro-opioid receptor (MOR) were not necessary to shape or perpetuate ethanol-reinforced operant responding. These results suggest that the rewarding effects of ethanol do not require beta-endorphin or enkephalin signaling.

Resource utilization and coexistence of three species of Pogonomyrmex ants in an Upper Sonoran Grassland Community.

In an Upper Sonoran Grassland Community, three species of Pogonomyrmex ants coexist. Due to the similarity in their diets and the apparent limitation of food, coexistence is aided by the differential utilization of the available food, according to size and type. Interspecific differences in morphology, physiology and microhabitat nesting sites facilitate this division. Differences in morphology enable the foragers to handle and collect seeds of different size and, consequently, type. Differences in desiccation resistance enable the foragers to be active at different times and, consequently, incorporate different amounts of insect material into their diets. Differences in microhabitat nest sites offers the foragers different proportions of the desired food resource.