Local Labour Markets, Migration and Wage Determination: Theory and Evidence for the Wage Curve in New Zealand

Blanchflower and Oswald (1994) claim that there is a stable inverse relationship between the wages paid to workers and the local unemployment rate. Using micro data from a range of countries they find an unemployment elasticity of pay of around -0.1. We use a dynamic efficiency model based on Phelps (1994) to produce an upward-sloping locus of steady-state wage and employment rate outcomes. In our model, points along this locus are identified by local labour market shocks. In the long run, inter-regional equilibrium ensures that regions lie on a so-called Harris-Todaro condition, which is consistent with no net internal migration. Using a synthetic micro sample of 20,302 observations from the 1986, 1991 and 1996 New Zealand Censuses of Population and Dwellings, we then find support for this specification of the earnings equation. As predicted, the coefficient on the employment rate is positive, while the gross migration rate has a positive effect on wages. In contrast, Blanchflower and Oswald's specification is not robust to controlling for the possible presence of simultaneity bias, due to the endogeneity of unemployment. Separate gender regressions reveal that males, but not females, exhibit a positive employment elasticity of pay, possibly due to the greater labour supply elasticity of the latter group. Evidence that the wages of less geographically mobile groups of workers are also more responsive to changes in the local unemployment rate is found when occupations of different skill levels are analysed. Finally, we use a procedure developed by Lang and Gottschalk (1996) to show that our data set has permitted a 41 % gain in efficiency of the estimation of the employment elasticity of pay over previous New Zealand studies that used aggregate data

A multi-species simulation of mosquito disease vector development in temperate Australian tidal wetlands using publicly available data

Worldwide, mosquito monitoring and control programs consume large amounts of resources in the effort to minimise mosquito-borne disease incidence. On-site larval monitoring is highly effective but time consuming. A number of mechanistic models of mosquito development have been developed to reduce the reliance on larval monitoring, but none for Ross River virus, the most commonly occurring mosquito-borne disease in Australia. This research modifies existing mechanistic models for malaria vectors and applies it to a wetland field site in Southwest, Western Australia. Environmental monitoring data were applied to an enzyme kinetic model of larval mosquito development to simulate timing of adult emergence and relative population abundance of three mosquito vectors of the Ross River virus for the period of 2018–2020. The model results were compared with field measured adult mosquitoes trapped using carbon dioxide light traps. The model showed different patterns of emergence for the three mosquito species, capturing inter-seasonal and inter-year variation, and correlated well with field adult trapping data. The model provides a useful tool to investigate the effects of different weather and environmental variables on larval and adult mosquito development and can be used to investigate the possible effects of changes to short-term and long-term sea level and climate changes

Mutational Analysis of the Arf1•GTP/Arf GAP Interface Reveals an Arf1 Mutant that Selectively Affects the Arf GAP ASAP1

SummaryArf1 is a GTP binding protein that functions at a number of cellular sites to control membrane traffic and actin remodeling. Arf1 is regulated by site-specific GTPase-activating proteins (GAPs). The combined results of crystallographic and biochemical studies [1–3] have led to the proposal that Arf1 GAPs differ in the specific interface formed with Arf1. To test this hypothesis, we have used mutagenesis to examine the interaction of three Arf GAPs (ASAP1, AGAP1, and ArfGAP1) with switch 1, switch 2, and α helix3 of Arf1. The GAPs were similar in being affected by mutations in switch 1 and 2. However, effects of a mutation within α helix3 and specific mutations within switch 1 and 2 differed among the GAPs. The largest differences were observed with a change of isoleucine 46 to aspartate ([I46D]Arf1), which reduced ASAP1-induced catalysis by ∼10,000-fold but had a 3-fold effect on AGAP1. The reduction was due to an isolated effect on the catalytic rate, kcat. In vivo [I46D]Arf1 had no detectable effect on the Golgi apparatus but, instead, functioned as a constitutively active mutant in the cell periphery, affecting the localization of ASAP1 and paxillin. Based on our results, we conclude that the contribution of specific residues within switch 1 of Arf to binding and achieving a transition state toward GTP hydrolysis differs among Arf GAPs

Metatranscriptome of human faecal microbial communities in a cohort of adult men

The gut microbiome is intimately related to human health, but it is not yet known which functional activities are driven by specific microorganisms\u27 ecological configurations or transcription. We report a large-scale investigation of 372 human faecal metatranscriptomes and 929 metagenomes from a subset of 308 men in the Health Professionals Follow-Up Study. We identified a metatranscriptomic \u27core\u27 universally transcribed over time and across participants, often by different microorganisms. In contrast to the housekeeping functions enriched in this core, a \u27variable\u27 metatranscriptome included specialized pathways that were differentially expressed both across participants and among microorganisms. Finally, longitudinal metagenomic profiles allowed ecological interaction network reconstruction, which remained stable over the six-month timespan, as did strain tracking within and between participants. These results provide an initial characterization of human faecal microbial ecology into core, subject-specific, microorganism-specific and temporally variable transcription, and they differentiate metagenomically versus metatranscriptomically informative aspects of the human faecal microbiome

Variations of CYP3A activity induced by antiretroviral treatment in HIV-1 infected patients

Objective: To measure the in vivo variations of CYP3A activity induced by anti-HIV drugs in human immunodeficiency virus (HIV)1-positive patients. Methods: A low oral dose of midazolam (MID) (0.075mg) was given to the patients and the 30-min total 1-OH midazolam (1-OHMID)/MID ratio was determined. Patients were phenotyped either before the introduction of antiretroviral treatments (control group, 90 patients) or after a variable period of antiretroviral treatment (56 patients). Twenty-one subjects underwent multiple phenotyping tests (before and during the course of the treatment). Results: The median MID ratio was 3.51 in the control group (range 0.20-14.6). It was 5-fold higher in the group with efavirenz (28 patients; median, range: 16.0, 3.81-367; P<0.0001), 13-fold lower with nelfinavir (18 patients; 0.27, 0.06-36.3; P<0.0001), 17-fold lower with efavirenz+ritonavir (three patients; 0.21, 0.05-0.47; P=0.006), 50-fold lower with ritonavir (four patients; 0.07, 0.06-0.17; P=0.0007), and 7-fold lower with nevirapine+(ritonavir or nelfinavir or grapefruit juice) (three patients; 0.48, 0.03-1.83; P=0.03). CYP3A activity was lower in the efavirenz+ritonavir group (P=0.01) and in the ritonavir group (P=0.04) than in the nelfinavir group, although already strongly inhibited in the latter. Conclusion: The low-dose MID phenotyping test was successfully used to measure the in vivo variations of CYP3A activity induced by antiretroviral drugs. Efavirenz strongly induces CYP3A activity, while ritonavir almost completely inhibits it. Nelfinavir strongly decreases CYP3A activity, but to a lesser extent than ritonavir. The inhibition of CYP3A by ritonavir or nelfinavir offsets the inductive effects of efavirenz or nevirapine administered concomitantly. Finally, no induction of CYP3A activity was noticeable after long-term administration of ritonavir at low dosages (200mg/day b.i.d.) or of nelfinavir at standard dosages (2,500mg/day b.i.d.

Free 25-hydroxyvitamin D is low in obesity, but there are no adverse associations with bone health

Background: The mechanism and clinical significance of low circulating 25-hydroxyvitamin D [25(OH)D] in obese people are unknown. Low total 25(OH)D may be due to low vitamin D–binding proteins (DBPs) or faster metabolic clearance. However, obese people have a higher bone mineral density (BMD), which suggests that low 25(OH)D may not be associated with adverse consequences for bone. Objective: We sought to determine whether 1) vitamin D metabolism and 2) its association with bone health differ by body weight. Design: We conducted a cross-sectional observational study of 223 normal-weight, overweight, and obese men and women aged 25–75 y in South Yorkshire, United Kingdom, in the fall and spring. A subgroup of 106 subjects was also assessed in the winter. We used novel techniques, including an immunoassay for free 25(OH)D, a stable isotope for the 25(OH)D3 half-life, and high-resolution quantitative tomography, to make a detailed assessment of vitamin D physiology and bone health. Results: Serum total 25(OH)D was lower in obese and overweight subjects than in normal-weight subjects in the fall and spring (geometric means: 45.0 and 40.8 compared with 58.6 nmol/L, respectively; P < 0.001) but not in the winter. Serum 25(OH)D was inversely correlated with body mass index (BMI) in the fall and spring and in the winter. Free 25(OH)D and 1,25-dihydroxyvitamin D [1,25(OH)2D] were lower in obese subjects. DBP, the DBP genotype, and the 25(OH)D3 half-life did not differ between BMI groups. Bone turnover was lower, and bone density was higher, in obese people. Conclusions: Total and free 25(OH)D and 1,25(OH)2D are lower at higher BMI, which cannot be explained by lower DBP or the shorter half-life of 25(OH)D3. We speculate that low 25(OH)D in obesity is due to a greater pool of distribution. Lower 25(OH)D may not reflect at-risk skeletal health in obese people, and BMI should be considered when interpreting serum 25(OH)D as a marker of vitamin D status

Stability of the human faecal microbiome in a cohort of adult men

Characterizing the stability of the gut microbiome is important to exploit it as a therapeutic target and diagnostic biomarker. We metagenomically and metatranscriptomically sequenced the faecal microbiomes of 308 participants in the Health Professionals Follow-Up Study. Participants provided four stool samples—one pair collected 24–72 h apart and a second pair ~6 months later. Within-person taxonomic and functional variation was consistently lower than between-person variation over time. In contrast, metatranscriptomic profiles were comparably variable within and between subjects due to higher within-subject longitudinal variation. Metagenomic instability accounted for ~74% of corresponding metatranscriptomic instability. The rest was probably attributable to sources such as regulation. Among the pathways that were differentially regulated, most were consistently over- or under-transcribed at each time point. Together, these results suggest that a single measurement of the faecal microbiome can provide long-term information regarding organismal composition and functional potential, but repeated or short-term measures may be necessary for dynamic features identified by metatranscriptomics