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Suspecting a werewolf is responsible for the murders and mysterious disappearances of other park residents who wander into the woods, Ambrose mounts a defense. He buys an immaculate tombstone for his dog and begins to slowly dig a grave for him. Meeting with the local congregation, Ambrose, who could hear a rasping in the werewolf's breathing, monitors the people around him for similar issues. He encounters Gloria's husband, who is encased in an iron lung, but Gloria suspects Ambrose of trying to kill her husband when he accidentally disconnects the machine; she throws him out. His suspicions fall on the church's pastor, Father Roger Smith, who has developed a wheeze after years of chain smoking. He suggests Ambrose visit the church, prompting him to take a local shuttle from his house, where he meets another suspect, James Griffin, who is a friend of Smith's and has a similar wheeze from asthma. Uncomfortable with Ambrose's habits and lifestyle, the three women convince James to privately transport Ambrose. Ambrose goes to a gun shop and convinces the owner to create silver bullets. Ambrose learns that James had also previously purchased silver ammunition. The tombstone arrives, and Ambrose puts it in his back yard, still digging the grave. Complaints of this and the smell of his dog's decomposition gets Ambrose observed by the police, who become concerned for his well being. Despite this, Ambrose convinces them not to interfere.

Bovine tuberculosis, caused by Mycobacterium tuberculosis var. bovis (M. bovis), is an important enzootic disease affecting mainly cattle, worldwide. Despite the implementation of national campaigns to eliminate the disease, bovine tuberculosis remains recalcitrant to eradication in several countries. Characterizing the host response to M. bovis infection is crucial for understanding the immunopathogenesis of the disease and for developing better control strategies. To profile the host responses to M. bovis infection, we analyzed the transcriptome of whole blood cells collected from experimentally infected calves with a virulent strain of M. bovis using RNA transcriptome sequencing (RNAseq). Comparative analysis of calf transcriptomes at early (8 weeks) versus late (20 weeks) aerosol infection with M. bovis revealed a divergent and unique profile for each stage of infection. Notably, at the early time point, transcriptional upregulation was observed among several of the top-ranking canonical pathways involved in T-cell chemotaxis. At the late time point, enrichment in the cell mediated cytotoxicity (e.g., Granzyme B) was the predominant host response. These results showed significant change in bovine transcriptional profiles and identified networks of chemokine receptors and monocyte chemoattractant protein (CCL) coregulated genes that underline the host-mycobacterial interactions during progression of bovine tuberculosis in cattle. Further analysis of the transcriptomic profiles identified potential biomarker targets for early and late phases of tuberculosis in cattle. Overall, the identified profiles better characterized identified novel immunomodulatory mechanisms and provided a list of targets for further development of potential diagnostics for tuberculosis in cattle.

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In 2008 the U.S. Department of Homeland Security (DHS) published Protective Action Guides (PAGs) for radiological dispersal devices (RDDs) and improvised nuclear devices (INDs). Guidance was offered to protect members of the public in the early, intermediate and late phases of response to terrorist attacks with radiological devices. The optimization (of radiation protection) process was recommended for late-phase recovery in circumstances of widespread contamination with radioactive material. The purpose of this Report is to provide guidance on optimizing decision making for late-phase recovery from a major RDD or IND incident. In light of the March 2011 Fukushima Dai-ichi Nuclear Power Plant (NPP) accident, the scope was expanded to include nuclear accidents.

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Yusuke Nakashima, Yuka Sasaki, Takeo Watanabe; Masking that disrupts late phases of visual processing eliminates location specificity of visual perceptual learning. Journal of Vision 2023;23(9):5151.

Patients with acute respiratory distress syndrome (ARDS) often develop severe diaphragmatic and limb skeletal muscle dysfunction. Impaired muscle function in ARDS is associated with increased mortality, increased duration of mechanical ventilation, and functional disability in survivors. In this review, we propose that muscle dysfunction in ARDS can be categorized into an early and a late phase. These early and late phases are based on the timing in relationship to lung injury and the underlying mechanisms. The early phase occurs temporally with the onset of lung injury, is driven by inflammation and disuse, and is marked predominantly by muscle atrophy from increased protein degradation. The ubiquitin-proteasome, autophagy, and calpain-caspase pathways have all been implicated in early-phase muscle dysfunction. Late-phase muscle weakness persists in many patients despite resolution of lung injury and cessation of ongoing acute inflammation-driven muscle atrophy. The clinical characteristics and mechanisms underlying late-phase muscle dysfunction do not involve the massive protein degradation and atrophy of the early phase and may reflect a failure of the musculoskeletal system to regain homeostatic balance. Owing to these underlying mechanistic differences, therapeutic interventions for treating muscle dysfunction in ARDS may differ during the early and late phases. Here, we review clinical and translational investigations of muscle dysfunction in ARDS, placing them in the conceptual framework of the early and late phases. We hypothesize that this conceptual model will aid in the design of future mechanistic and clinical investigations of the skeletal muscle system in ARDS and other critical illnesses.

We propose, on the basis of observations of animal models and clinical studies, that muscle wasting in patients with ARDS can be divided into early and late phases. These phases differ in pathophysiology and potential underlying mechanisms and can be identified by their relationship to the time course of lung injury, recovery, and resolution. In this review, we will summarize major recent findings regarding clinical and mechanistic investigations into muscle wasting in ARDS and frame them in the context of the early and late phases. We propose that this conceptual framework will enhance the design of future clinical and mechanistic investigations and aid in tailoring therapies designed to treat muscle wasting in ARDS.

The early and late phases of muscle wasting in acute respiratory distress syndrome. The early phase of muscle wasting begins with the onset of lung injury and is caused by lung and systemic inflammation and to a lesser degree disuse, both leading to muscle atrophy. The late phase of muscle wasting begins as lung function recovers and acute systemic inflammation resolves. Disuse continues in many patients during the late phase. Muscle function deteriorates in the early phase, and dysfunction persists in many patients during the late phase, which may last for years despite resolution of lung injury and cessation of ongoing muscle atrophy. Factors mediating recovery trajectories in the late phase are poorly understood

The late phase of muscle dysfunction begins following resolution of the early acute lung and systemic inflammation characteristic of the early phase, usually following the first few days of illness and during the recovery phase of lung injury. Muscle atrophy may continue into the late phase, driven by disuse, but this factor usually resolves once patients are no longer bedridden. Similar to early-phase wasting, late-phase muscle weakness may occur from persistent or unresolved nerve or NMJ injury [30, 31].

The characteristic feature of late-phase muscle wasting is that muscle dysfunction persists despite recovery and resolution of lung injury in many patients [8, 20]. Factors such as age, baseline (pre-ARDS) muscle function, medications administered during or after the ICU stay, comorbidities, route of muscle injury (nerve versus NMJ versus myofiber), and nutrition may contribute to both the degree of injury and the rate of muscle functional recovery. However, the clinical characteristics associated with complete, partial, or failed recovery of muscle function in ARDS survivors (Fig. 1) are generally poorly understood. e24fc04721