The early, delayed, and systemic effects of acute traumatic brain injury (TBI) are the result of inflammatory mediators which initiate systemic inflammatory response syndrome (SIRS), subsequent complement deficits and coagulopathy. Once SIRS is triggered by acute inflammation, it can detrimentally self-propagate. Systemic inflammation causes tissue damage leading to further inflammation and damage, leaving the body in a vicious cycle of hyperinflammation. Therefore, important inflammatory mediators like interleukin (IL)-1 beta, IL-6 and tumour necrosis factor (TNF) alpha, are targeted in compensatory anti-inflammatory response syndrome (CARS) in an attempt to control the development of SIRS. The hypothalamus-pituitary (HPA)-axis and sympathetic nervous system (SNS) efferent limbs in CARS provide negative feedback for the production of inflammatory mediators. However, in the case of acute TBI, the activation of CARS often leads to the complication of immunosuppression which may result in multi-organ dysfunction syndrome (MODS) and mortality. In light of this, the activation of the SIRS following acute TBI does not bode well. If left uncontrolled, multiple systems will be implicated making it difficult to remedy.
Canetti, Goldreich, Goldwasser, and Micali (STOC 2000) introduced the notion of resettable zeroknowledge proofs, where the protocol must be zero-knowledge even if a cheating verifier can reset the prover and have several interactions in which the prover uses the same random tape. Soon afterwards, Barak, Goldreich, Goldwasser, and Lindell (FOCS 2001) studied the closely related notion of resettable soundness, where the soundness condition of the protocol must hold even if the cheating prover can reset the verifier to have multiple interactions with the same verifier's random tape. The main problem left open by this work was whether it is possible to have a single protocol that is simultaneously resettable zero knowledge and resettably sound. We resolve this question by constructing such a protocol.At the heart of our construction is a new non-black-box simulation strategy, which we believe to be of independent interest. This new strategy allows for simulators which "marry" recursive rewinding techniques (common in the context of concurrent simulation) with non-black-box simulation. Previous non-black-box strategies led to exponential blowups in computational complexity in such circumstances, which our new strategy is able to avoid.
Inflammation in the periventricular white matter (PWM) of hypoxic neonatal brain causes myelination disturbances. In this connection, macrophage colony-stimulating factor (M-CSF) has been reported to regulate release of proinflammatory cytokines that may be linked to PWM damage. We sought to determine if M-CSF derived from amoeboid microglial cells (AMC) would promote proinflammatory cytokine production by astrocytes in the PWM following hypoxic exposure, and, if so, whether it is associated with axon degeneration and myelination disturbances. In 1-day hypoxic rats, expression of M-CSF was upregulated in AMC. This was coupled with increased expression of CSF-1 receptor, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) in astrocytes, and TNF-receptor 1 and IL-receptor 1 on the axons. Neurofilament-200 immunopositive axons and myelin basic protein immunopositive processes appeared to undergo disruption in 14-days hypoxic rats. By electron microscopy, some axons showed degenerative changes affecting the microtubules and myelin sheath. Primary cultured microglial cells subjected to hypoxia showed enhanced release of M-CSF. Remarkably, primary cultured astrocytes treated with conditioned-medium derived from hypoxic microglia or M-CSF exhibited increased production of TNF-alpha and IL-1beta. Our results suggest that AMC-derived M-CSF promotes astrocytes to generate proinflammatory cytokines, which may be involved in axonal damage following a hypoxic insult.
Background Short-term recurrence of positive SARS-CoV-2 RNA PCR in discharged COVID-19 patients attracts the public’s concern. This study aimed to determine clinical and epidemiological results of such patients. Methods This retrospective study was conducted on 32 designated hospitals for COVID-19 patients discharged from January 14 th to March 10 th, 2020. After 28-day followed-up, re-positive patients confirmed by SARS-CoV-2 RNA RT-PCR were re-admitted to hospital for further treatments. All the close contacts of re-positive patients were asked 14-day self-segregating. Data of epidemiology, symptoms, laboratory tests and treatments were analyzed in re-positive patients and their close contacts were investigated. Results Of 1,282 discharged patients, 189 (14.74%) were tested re-positive of SARS-CoV-2 RNA during 28-day follow-up. The median time from discharge to re-positivity was 8 days (IQR 5-13). Patients in re-positive group were younger (34yr vs 45yr, p&0.001) with higher proportion of moderate symptoms (95.77% vs 84.35%, p&0.001) in the first hospitalization than negative group. During the second hospitalization, all re-positive patients showed normal in peripheral white blood cell and lymphocyte, and no new symptoms of COVID-19; 78.31% further improved on chest CT scan compared with the first discharge, yet 25.93% accepted antiviral therapy. The median time of re-positive to negative was 8 days (IQR 4-15). None of close contacts developed COVID-19. Conclusions Our data suggested that the short term recurrence of positive SARS-CoV-2 RNA in discharged patients is not a relapse of COVID-19, and the risk of onward transmission is very low. This provides important information for managing COVID-19 patients.
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