Chiral QCD, General QCD Parameterization and Constituent Quark Models

Several recent papers -using effective QCD chiral Lagrangians- reproduced results obtained with the general QCD parameterization (GP). These include the baryon 8+10 mass formula, the octet magnetic moments and the coincidental nature of the "perfect" -3/2 ratio between the magnetic moments of p and n. Although we anticipated that the GP covers the case of chiral treatments, the above results explicitly exemplify this fact. Also we show by the GP that -in any model or theory (chiral or non chiral) reproducing the results of exact QCD- the Franklin (Coleman Glashow) sum rule for the octet magnetic moments must be violated.Comment: 10 pages, Latex; abridged version (same results), removed some reference

On Paragrassmann Differential Calculus

Explicit general constructions of paragrassmann calculus with one and many variables are given. Relations of the paragrassmann calculus to quantum groups are outlined and possible physics applications are briefly discussed. This paper is the same as the original 9210075 except added Appendix and minor changes in Acknowledgements and References. IMPORTANT NOTE: This paper bears the same title as the Dubna preprint E5-92-392 but is NOT identical to it, containing new results, extended discussions, and references.Comment: 19p

Octet magnetic moments and the Coleman-Glashow sum rule violation in the chiral quark model

Baryon octet magnetic moments when calculated within the chiral quark model, incorporating the orbital angular momentum as well as the quark sea contribution through the Cheng-Li mechanism, not only show improvement over the non relativistic quark model results but also gives a non zero value for the right hand side of Coleman-Glashow sum rule. When effects due to spin-spin forces between constituent quarks as well as `mass adjustments' due to confinement are added, it leads to an excellent fit for the case of p, \Sigma^+, \Xi^o and violation of Coleman-Glashow sum rule, whereas in almost all the other cases the results are within 5% of the data.Comment: 5 RevTeX pages, accepted for publication in PRD(Rapid Communication

Determination of the chiral coupling constants c3 and c4 in new pp and np partial-wave analyses

As a first result of two new partial-wave analyses, one of the pp and another one of the np scattering data below 500 MeV, we report a study of the long-range chiral two-pion exchange interaction which contains the chiral coupling constants c1, c3, and c4. By using as input a theoretical value for c1 we are able to determine in pp as well as in np scattering accurate values for c3 and c4. The values determined from the pp data and independently from the np data are in very good agreement, indicating the correctness of the chiral two-pion exchange interaction. The weighted averages are c3 = -4.78(10) / GeV and c4 = 3.96(22) / GeV, where the errors are statistical. The value of c3 is best determined from the pp data and that of c4 from the np data.Comment: 9 pages, 1 figure. Accepted for publication in Phys. Rev.

Distinct clinical symptom patterns in patients hospitalised with COVID-19 in an analysis of 59,011 patients in the ISARIC-4C study

COVID-19 is clinically characterised by fever, cough, and dyspnoea. Symptoms affecting other organ systems have been reported. However, it is the clinical associations of different patterns of symptoms which influence diagnostic and therapeutic decision-making. In this study, we applied clustering techniques to a large prospective cohort of hospitalised patients with COVID-19 to identify clinically meaningful sub-phenotypes. We obtained structured clinical data on 59,011 patients in the UK (the ISARIC Coronavirus Clinical Characterisation Consortium, 4C) and used a principled, unsupervised clustering approach to partition the first 25,477 cases according to symptoms reported at recruitment. We validated our findings in a second group of 33,534 cases recruited to ISARIC-4C, and in 4,445 cases recruited to a separate study of community cases. Unsupervised clustering identified distinct sub-phenotypes. First, a core symptom set of fever, cough, and dyspnoea, which co-occurred with additional symptoms in three further patterns: fatigue and confusion, diarrhoea and vomiting, or productive cough. Presentations with a single reported symptom of dyspnoea or confusion were also identified, alongside a sub-phenotype of patients reporting few or no symptoms. Patients presenting with gastrointestinal symptoms were more commonly female, had a longer duration of symptoms before presentation, and had lower 30-day mortality. Patients presenting with confusion, with or without core symptoms, were older and had a higher unadjusted mortality. Symptom sub-phenotypes were highly consistent in replication analysis within the ISARIC-4C study. Similar patterns were externally verified in patients from a study of self-reported symptoms of mild disease. The large scale of the ISARIC-4C study enabled robust, granular discovery and replication. Clinical interpretation is necessary to determine which of these observations have practical utility. We propose that four sub-phenotypes are usefully distinct from the core symptom group: gastro-intestinal disease, productive cough, confusion, and pauci-symptomatic presentations. Importantly, each is associated with an in-hospital mortality which differs from that of patients with core symptoms

Delayed mucosal antiviral responses despite robust peripheral inflammation in fatal COVID-19

Background While inflammatory and immune responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in peripheral blood are extensively described, responses at the upper respiratory mucosal site of initial infection are relatively poorly defined. We sought to identify mucosal cytokine/chemokine signatures that distinguished coronavirus disease 2019 (COVID-19) severity categories, and relate these to disease progression and peripheral inflammation. Methods We measured 35 cytokines and chemokines in nasal samples from 274 patients hospitalized with COVID-19. Analysis considered the timing of sampling during disease, as either the early (0–5 days after symptom onset) or late (6–20 days after symptom onset) phase. Results Patients that survived severe COVID-19 showed interferon (IFN)-dominated mucosal immune responses (IFN-γ, CXCL10, and CXCL13) early in infection. These early mucosal responses were absent in patients who would progress to fatal disease despite equivalent SARS-CoV-2 viral load. Mucosal inflammation in later disease was dominated by interleukin 2 (IL-2), IL-10, IFN-γ, and IL-12p70, which scaled with severity but did not differentiate patients who would survive or succumb to disease. Cytokines and chemokines in the mucosa showed distinctions from responses evident in the peripheral blood, particularly during fatal disease. Conclusions Defective early mucosal antiviral responses anticipate fatal COVID-19 but are not associated with viral load. Early mucosal immune responses may define the trajectory of severe COVID-19

Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses

To understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1–11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely