Policies to decrease low-acuity emergency department (ED) use have traditionally assumed that EDs are a substitute for unavailable primary care (PC). However, such policies can exacerbate ED overcrowding, rather than ameliorate it, if patients use EDs to complement, rather than substitute, their PC use. We tested whether Medicaid managed care enrolees visit the ED for nonemergent and PC treatable conditions to substitute for or to complement PC. Based on consumer choice theory, we modelled county-level monthly ED visit rate as a function of PC supply and used 2012–2015 New York Statewide Planning and Research Cooperative System (SPARCS) outpatient data and non-linear least squares method to test substitution vs complementarity. In the post-Medicaid expansion period (2014–2015), ED and PC are substitutes state-wide, but are complements in highly urban and poorer counties during nights and weekends. There is no evidence of complementarity before the expansion (2012–2013). Analyses by PC provider demonstrate that the relationship between ED and PC differs depending on whether PC is provided by physicians or advanced practice providers. Policies to reduce low-acuity ED use via improved PC access in Medicaid are likely to be most effective if they focus on increasing actual appointment availability, ideally by physicians, in areas with low PC provider supply. Different aspects of PC access may be differently related to low-acuity ED use.

The emergence of 2019 novel coronavirus disease (COVID-19) is currently a global concern. In this study, our goal was to explore the changing expression levels of acute-phase reaction proteins (APRPs) in the serum of COVID-19 patients and to elucidate the immunological characteristics of COVID-19. In the study design, we recruited 72 COVID-19 patients, including 22 cases of mild degree, 38 cases of moderate degree and 12 cases of severe degree. We also recruited 20 patients with community-acquired pneumonia (CAP) and 20 normal control subjects as a comparison. Fasting venous blood was taken to detect the content of complement 3 (C3), complement 4 (C4), C-reactive protein (CRP), serum amyloid A (SAA) and prealbumin (PA). When compared the COVID-19 group with the CAP and normal control groups, respectively, the mean value of CRP and SAA in the COVID-19 group (including mild, moderate and severe patients) had increased significantly (P < 0.01), whereas the mean values of C3, C4 and PA decreased (P < 0.01). For the asymptomatic or mild symptomatic patients with COVID-19, the actual aggravation of disease may be more advanced than the clinical appearances. Meanwhile, the statistical analyses indicated that the development of COVID-19 brought about a significant increase in the content of CRP and SAA (P < 0.01), and a decline in the content of C3, C4 and PA (P < 0.01). These findings suggested that the changes in the level of APRPs could be used as indicators to identify the degree and progression of COVID-19, and the significant changes might demonstrate the aggravation of disease. This study provided a new approach to improve the clinical management plan and prognosis of COVID-19.

The present study investigated the effects of condensed tannins (CT) on intestinal immune function in on-growing grass carp (Ctenopharyngodon idella). A total of 540 healthy grass carp were fed six diets containing different levels of CT (0, 10·00, 20·00, 30·00, 40·00 and 50·00 g/kg diet) for 70 d and then challenged with Aeromonas hydrophila for 14 d. The results showed that, compared with the control group, dietary CT (1) induced intestinal histopathological lesions and aggravated enteritis; (2) decreased lysozyme and acid phosphatase activities, complement 3 (C3), C4 and IgM contents and down-regulated the Hepcidin, liver-expressed antimicrobial peptide (LEAP)-2A, LEAP-2B, Mucin2 and β-defensin-1 mRNA levels in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) (P < 0·05); (3) down-regulated the mRNA levels of anti-inflammatory cytokines transforming growth factor (TGF)-β1, TGF-β2 (not in MI and DI), IL-4/13A (not IL-4/13B), IL-10 and IL-11 partly correlated with target of rapamycin (TOR) signalling; and (4) up-regulated the mRNA levels of pro-inflammatory cytokines interferon-γ2, IL-1β, IL-6, IL-8 (not in PI), IL-12p35, IL-12p40, IL-15 and IL-17D partly related to NF-κB signalling in the intestine of on-growing grass carp. Overall, the results indicated that CT could impair the intestinal immune function, and its potential regulation mechanisms were partly associated with the TOR and NF-κB signalling pathways. Finally, based on the percentage weight gain and enteritis morbidity, the maximum allowable levels of CT for on-growing grass carp (232·22–890·11 g) were estimated to be 18·6 and 17·4 g/kg diet, respectively.

This study aimed to investigate the impacts of dietary threonine on intestinal immunity and inflammation in juvenile grass carp. Six iso-nitrogenous semi-purified diets containing graded levels of threonine (3·99–21·66 g threonine/kg) were formulated and fed to fishes for 8 weeks, and then challenged with Aeromonas hydrophila for 14 d. Results showed that, compared with optimum threonine supplementation, threonine deficiency (1) decreased the ability of fish against enteritis, intestinal lysozyme activities (except in the distal intestine), acid phosphatase activities, complement 3 (C3) and C4 contents and IgM contents (except in the proximal intestine (PI)), and it down-regulated the transcript abundances of liver-expressed antimicrobial peptide (LEAP)-2A, LEAP-2B, hepcidin, IgZ, IgM and β-defensin1 (except in the PI) (P<0·05); (2) could up-regulate intestinal pro-inflammatory cytokines TNF-α, IL-1β, IL-6, IL-8 and IL-17D mRNA levels partly related to NF-κB signalling; (3) could down-regulate intestinal anti-inflammatory cytokine transforming growth factor (TGF)-β1, TGF-β2, IL-4/13A (not IL-4/13B) and IL-10 mRNA levels partly by target of rapamycin signalling. Finally, on the basis of the specific growth rate, against the enteritis morbidity and IgM contents, the optimum threonine requirements were estimated to be 14·53 g threonine/kg diet (4·48 g threonine/100 g protein), 15.05 g threonine/kg diet (4·64 g threonine/100 g protein) and 15·17 g threonine/kg diet (4·68 g threonine/100 g protein), respectively.

Recently published work as described by the authors highlighted the extent of Complement activity in bovine milk. Localised mastitis infection occurring in the mammary glands of dairy cows is readily detectable by the levels of somatic cells in milk. Thus, it is opportune to monitor Complement activity in milks in association with the animal's innate immune response to mammary infection. Preliminary screening of milk samples taken randomly showed that milk with a high somatic cell count (SCC) reduced growth of the Complement-sensitive strain E. coli O111 to a greater extent (P < 0·05) than when the marker microorganism was grown in milk heated for the purpose of inactivating Complement. A follow-up study set out to determine the effect on Complement activity when a sub-clinical mastitis infection was induced in the mammary gland of four lactating dairy cows. The effect of Str. dysgalactiae spp. dysgalactiae inoculation into selected individual udder quarters of the mammary glands of each animal was followed by monitoring of SCC levels in the milks from the segregated udder samples during subsequent milking. At 72 and 96 h post inoculation (PI), the SCCs for the challenged quarter were increased compared to normal values. At the same time, the bactericidal sequestration assay identified increased E. coli O111 inhibition that can be directly linked to greater Complement activity in those quarter milks affected by induced inflammation. Thus, it can be identified that the high SCC milks were more effective in limiting E. coli O111 growth. Milks from the unchallenged quarters in all four cows were significantly less effective at reducing growth of the assay strain (P < 0·05).

An ELISA assay targeting specific activation components of the Complement pathways confirmed that greater bacterial inhibition observed during the bactericidal sequestration assay was attributable to higher Complement activity in the milk samples from the affected quarters, i.e., with higher SCC. The induced infection was confirmed as self-limiting in three of the affected animals and their SCC returned to normal levels within 14 d PI, while the fourth cow required brief antibiotic intervention.

We give sufficient conditions for a graph to be traceable and Hamiltonian in terms of the Wiener index and the complement of the graph, which correct and extend the result of Yang [‘Wiener index and traceable graphs’, Bull. Aust. Math. Soc.88 (2013), 380–383]. We also present sufficient conditions for a bipartite graph to be traceable and Hamiltonian in terms of its Wiener index and quasicomplement. Finally, we give sufficient conditions for a graph or a bipartite graph to be traceable and Hamiltonian in terms of its distance spectral radius.

While the Complement protein system in human milk is well characterised, there is little information on its presence and activity in bovine milk. Complement forms part of the innate immune system, hence the importance of its contribution during milk ingestion to the overall defences of the neonate. A bactericidal sequestration assay, featuring a Complement sensitive strain, Escherichia coli 0111, originally used to characterise Complement activity in human milk was successfully applied to freshly drawn bovine milk samples, thus, providing an opportunity to compare Complement activities in both human and bovine milks. Although not identical in response, the levels of Complement activity in bovine milk were found to be closely comparable with that of human milk. Differential counts of Esch. coli 0111 after 2 h incubation were 6·20 and 6·06 log CFU/ml, for raw bovine and human milks, respectively – the lower value representing a stronger Complement response. Exposing bovine milk to a range of thermal treatments e.g. 42, 45, 65, 72, 85 or 95 °C for 10 min, progressively inhibited Complement activity by increasing temperature, thus confirming the heat labile nature of this immune protein system. Low level Complement activity was found, however, in 65 and 72 °C heat treated samples and in retailed pasteurised milk which highlights the outer limit to which high temperature, short time (HTST) industrial thermal processes should be applied if retention of activity is a priority. Concentration of Complement in the fat phase was evident following cream separation, and this was also reflected in the further loss of activity recorded in low fat variants of retailed pasteurised milk. Laboratory-based churning of the cream during simulated buttermaking generated an aqueous (buttermilk) phase with higher levels of Complement activity than the fat phase, thus pointing to a likely association with the milk fat globule membrane (MFGM) layer.

Let $G$ be a graph of order $n\geq 6$ with minimum degree ${\it\delta}(G)\geq 4$. Arkin and Hassin [‘Graph partitions with minimum degree constraints’, Discrete Math. 190 (1998), 55–65] conjectured that there exists a bipartition $S,T$ of $V(G)$ such that $\lfloor n/2\rfloor -2\leq |S|,|T|\leq \lceil n/2\rceil +2$ and the minimum degrees in the subgraphs induced by $S$ and $T$ are at least two. In this paper, we first show that $G$ has a bipartition such that the minimum degree in each part is at least two, and then prove that the conjecture is true if the complement of $G$ contains no complete bipartite graph $K_{3,r}$, where $r=\lfloor n/2\rfloor -3$.

The brain undergoes many changes in chemistry and structure during normal aging. For example, it dries and shrinks. Neurons are lost from some regions and there is also neuronal atrophy and loss of synaptic branching. The extent of such losses remains controversial for all but a few subcortical regions of the brain. Decreases in glucose metabolism and in some pre-and post-synaptic neurotransmitter indices have also been reported. Many systems, however, remain entirely unexplored. The evidence to date also indicates that there is great regional specificity in the effects, and that humans show considerable variability between individuals. Of interest is the fact that some of the changes most clearly demonstrated in normal aging - such as loss of dopaminergic neurons of the substantia nigra and cholinergic neurons of the medial basal forebrain - also occur in a much accentuated form in neurodegenerative diseases such as Parkinson's disease and Alzheimer disease. The small loss of these systems in normal aging may account for the shuffling gait, stooped posture and memory loss in the elderly. A phenomenon seen in neurodegenerative diseases, but not in normal aging, is the appearance of chronic inflammation in the brain. The suggestion that the progress of such diseases might be slowed by treatment with anti-inflammatory agents has, in the case of Alzheimer disease, gained some support from 19 epidemiological studies and one very small clinical trial. Clearly more detailed clinical trials are required, and caution must be used because of the undesirable side effects of currently available anti-inflammatory agents.