The Impact of State Fiscal Policy on States\u27 Resilience Entering the Great Recession

The U.S. economy entered the Great Recession in December 2007 and exited in June 2009. This national statistic obscures a wealth of state-level data shedding light on the policies and conditions that helped some states withstand that recessionary shock for a time. In this study, we used that state-level data in a parametric regression model, known as survival analysis, to estimate the effects that a state’s fiscal policy had on the timing of its entry into the Great Recession. Consistent with earlier, more general, studies focusing on economic growth, we found that taxes have the potential to hasten the start of a state’s recession, while expenditures could defer that event. However, not all types of taxes and expenditures were equivalent in terms of their effect on recessionary timing. Most notably, our results showed that corporate income taxes had a different timing effect than sales, property, and individual income taxes. In addition, although total expenditures tended to delay the Great Recession’s onset, relatively few individual expenditure types had a statistically-significant impact on recessionary timing. Overall, our results suggest that, while taxes likely increase a state’s recessionary risk and expenditures likely decrease it, that narrative is an oversimplification of the complex role played by fiscal policy in determining a state\u27s ability to resist a negative economic shock like the Great Recession

Frequency and Phase Synchronization in Stochastic Systems

The phenomenon of frequency and phase synchronization in stochastic systems requires a revision of concepts originally phrased in the context of purely deterministic systems. Various definitions of an instantaneous phase are presented and compared with each other with special attention payed to their robustness with respect to noise. We review the results of an analytic approach describing noise-induced phase synchronization in a thermal two-state system. In this context exact expressions for the mean frequency and the phase diffusivity are obtained that together determine the average length of locking episodes. A recently proposed method to quantify frequency synchronization in noisy potential systems is presented and exemplified by applying it to the periodically driven noisy harmonic oscillator. Since this method is based on a threshold crossing rate pioneered by S.O. Rice the related phase velocity is termed Rice frequency. Finally, we discuss the relation between the phenomenon of stochastic resonance and noise-enhanced phase coherence by applying the developed concepts to the periodically driven bistable Kramers oscillator.Comment: to appear in the Chaos focus issue on "Control, communication, and synchronization in chaotic dynamical systems

Resistant gonorrhoea: east meets west

In 2016 and 2018, two treatment failures of ceftriaxone and azithromycin, used in combination, were reported in the UK in men who contracted gonococcal infections in Asia,1, 2 once again suggesting that antimicrobial resistance of Neisseria gonorrhoeae is spreading. These treatment failures indicate the potentially waning efficacy and usefulness of this combination, which is currently recommended as the first-line therapy. Surveillance of antimicrobial resistance is paramount if resistance patterns of these and other antimicrobials are to be recognised in a timely manner that enables meaningful intervention and prevention of the spread of resistant organisms. Antimicrobial susceptibility testing (phenotyping) for antimicrobial resistance is considered the gold-standard test. There are some key limitations to the more commonly used methods of genotyping, such as N gonorrhoeae multi-antigen sequence typing (NG-MAST) and multilocus sequence typing (MLST), which indicate associated antimicrobial resistance determinants but do not directly identify antimicrobial resistance. The genotypes of N gonorrhoeae strains that are identified by use of these methods, which include antimicrobial resistance determinants, often do not correlate directly with the mean inhibitory concentrations of antimicrobials against these strains

Antimicrobial Resistance in Neisseria gonorrhoeae: Proceedings of the STAR Sexually Transmitted Infection-Clinical Trial Group Programmatic Meeting

The goal of the Sexually Transmitted Infection Clinical Trial Group\u27s Antimicrobial Resistance (AMR) in Neisseria gonorrhoeae (NG) meeting was to assemble experts from academia, government, nonprofit and industry to discuss the current state of research, gaps and challenges in research and technology and priorities and new directions to address the continued emergence of multidrug-resistant NG infections. Topics discussed at the meeting, which will be the focus of this article, include AMR NG global surveillance initiatives, the use of whole genome sequencing and bioinformatics to understand mutations associated with AMR, mechanisms of AMR, and novel antibiotics, vaccines and other methods to treat AMR NG. Key points highlighted during the meeting include: (i) US and International surveillance programs to understand AMR in NG; (ii) the US National Strategy for combating antimicrobial-resistant bacteria; (iii) surveillance needs, challenges, and novel technologies; (iv) plasmid-mediated and chromosomally mediated mechanisms of AMR in NG; (v) novel therapeutic (eg, sialic acid analogs, factor H [FH]/Fc fusion molecule, monoclonal antibodies, topoisomerase inhibitors, fluoroketolides, LpxC inhibitors) and preventative (eg, peptide mimic) strategies to combat infection. The way forward will require renewed political will, new funding initiatives, and collaborations across academic and commercial research and public health programs

Role of Gonococcal Neisserial Surface Protein A (NspA) in Serum Resistance and Comparison of Its Factor H Binding Properties with Those of Its Meningococcal Counterpart

Neisseria gonorrhoeae, the causative agent of gonorrhea, has evolved several mechanisms to subvert complement, including binding of the complement inhibitor factor H (FH). We previously reported FH binding to N. gonorrhoeae independently of lipooligosaccharide (LOS) sialylation. Here we report that factor H-like protein 1 (FHL-1), which contains FH domains 1 through 7 and possesses complement-inhibitory activity, also binds to N. gonorrhoeae The ligand for both FH and FHL-1 was identified as neisserial surface protein A (NspA), which has previously been identified as a ligand for these molecules on Neisseria meningitidis As with N. meningitidis NspA (Nm-NspA), N. gonorrhoeae NspA (Ng-NspA) bound FH/FHL-1 through FH domains 6 and 7. Binding of FH/FHL-1 to NspA was human specific; the histidine (H) at position 337 of domain 6 contributed to human-specific FH binding to both Ng- and Nm-NspA. FH/FHL-1 bound Nm-NspA better than Ng-NspA; introducing Q at position 73 (loop 2, present in Ng-NspA) or replacing V and D at positions 112 and 113 in Nm-NspA loop 3 with A and H (Ng-NspA), respectively, reduced FH/FHL-1 binding. The converse Ng-NspA to Nm-NspA mutations increased FH/FHL-1 binding. Binding of FH/FHL-1 through domains 6 and 7 to N. gonorrhoeae increased with truncation of the heptose I (HepI) chain of LOS and decreased with LOS sialylation. Loss of NspA significantly decreased serum resistance of N. gonorrhoeae with either wild-type or truncated LOS. This report highlights the role for NspA in enabling N. gonorrhoeae to subvert complement despite LOS phase variation. Knowledge of FH-NspA interactions will inform the design of vaccines and immunotherapies against the global threat of multidrug-resistant gonorrhea

Timing is everything: Drivers of interannual variability in blue whale migration.

Blue whales need to time their migration from their breeding grounds to their feeding grounds to avoid missing peak prey abundances, but the cues they use for this are unknown. We examine migration timing (inferred from the local onset and cessation of blue whale calls recorded on seafloor-mounted hydrophones), environmental conditions (e.g., sea surface temperature anomalies and chlorophyll a), and prey (spring krill biomass from annual net tow surveys) during a 10 year period (2008-2017) in waters of the Southern California Region where blue whales feed in the summer. Colder sea surface temperature anomalies the previous season were correlated with greater krill biomass the following year, and earlier arrival by blue whales. Our results demonstrate a plastic response of blue whales to interannual variability and the importance of krill as a driving force behind migration timing. A decadal-scale increase in temperature due to climate change has led to blue whales extending their overall time in Southern California. By the end of our 10-year study, whales were arriving at the feeding grounds more than one month earlier, while their departure date did not change. Conservation strategies will need to account for increased anthropogenic threats resulting from longer times at the feeding grounds

Mechanisms of quadriceps muscle weakness in knee joint osteoarthritis: the effects of prolonged vibration on torque and muscle activation in osteoarthritic and healthy control subjects

Introduction: A consequence of knee joint osteoarthritis (OA) is an inability to fully activate the quadriceps muscles, a problem termed arthrogenic muscle inhibition (AMI). AMI leads to marked quadriceps weakness that impairs physical function and may hasten disease progression. The purpose of the present study was to determine whether g-loop dysfunction contributes to AMI in people with knee joint OA. Methods: Fifteen subjects with knee joint OA and 15 controls with no history of knee joint pathology participated in this study. Quadriceps and hamstrings peak isometric torque (Nm) and electromyography (EMG) amplitude were collected before and after 20 minutes of 50 Hz vibration applied to the infrapatellar tendon. Between-group differences in pre-vibration torque were analysed using a one-way analysis of covariance, with age, gender and body mass (kg) as the covariates. If the g-loop is intact, vibration should decrease torque and EMG levels in the target muscle; if dysfunctional, then torque and EMG levels should not change following vibration. One-sample t tests were thus undertaken to analyse whether percentage changes in torque and EMG differed from zero after vibration in each group. In addition, analyses of covariance were utilised to analyse between-group differences in the percentage changes in torque and EMG following vibration. Results: Pre-vibration quadriceps torque was significantly lower in the OA group compared with the control group (P = 0.005). Following tendon vibration, quadriceps torque (P < 0.001) and EMG amplitude (P ≤0.001) decreased significantly in the control group but did not change in the OA group (all P > 0.299). Hamstrings torque and EMG amplitude were unchanged in both groups (all P > 0.204). The vibration-induced changes in quadriceps torque and EMG were significantly different between the OA and control groups (all P < 0.011). No between-group differences were observed for the change in hamstrings torque or EMG (all P > 0.554). Conclusions: g-loop dysfunction may contribute to AMI in individuals with knee joint OA, partially explaining the marked quadriceps weakness and atrophy that is often observed in this population

Diverse CD81 proteins support hepatitis C virus infection.

Hepatitis C virus (HCV) entry is dependent on CD81. To investigate whether the CD81 sequence is a determinant of HCV host range, we expressed a panel of diverse CD81 proteins and tested their ability to interact with HCV. CD81 large extracellular loop (LEL) sequences were expressed as recombinant proteins; the human and, to a low level, the African green monkey sequences bound soluble HCV E2 (sE2) and inhibited infection by retrovirus pseudotype particles bearing HCV glycoproteins (HCVpp). In contrast, mouse or rat CD81 proteins failed to bind sE2 or to inhibit HCVpp infection. However, CD81 proteins from all species, when expressed in HepG2 cells, conferred susceptibility to infection by HCVpp and cell culture-grown HCV to various levels, with the rat sequence being the least efficient. Recombinant human CD81 LEL inhibited HCVpp infectivity only if present during the virus-cell incubation, consistent with a role for CD81 after virus attachment. Amino acid changes that abrogate sE2 binding (I182F, N184Y, and F186S, alone or in combination) were introduced into human CD81. All three amino acid changes in human CD81 resulted in a molecule that still supported HCVpp infection, albeit with reduced efficiency. In summary, there is a remarkable plasticity in the range of CD81 sequences that can support HCV entry, suggesting that CD81 polymorphism may contribute to, but alone does not define, the HCV susceptibility of a species. In addition, the capacity to support viral entry is only partially reflected by assays measuring sE2 interaction with recombinant or full-length CD81 proteins