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Background Firearm violence is an intensifying public health problem in the United States. News reports shape the way the public and policy makers understand and respond to health threats, including firearm violence. To better understand how firearm violence is communicated to the public, we aimed to determine the extent to which firearm violence is framed as a public health problem on television news and to measure harmful news content as identified by firearm-injured people. Methods This is a quantitative content analysis of Philadelphia local television news stories about firearm violence using a database of 7,497 clips. We compiled a stratified sample of clips aired on two randomly selected days/month from January-June 2021 from the database ( n  = 192 clips). We created a codebook to measure public health frame elements and to assign a harmful content score for each story and then coded the clips. Characteristics of stories containing episodic frames that focus on single shooting events were compared to clips with thematic frames that include broader social context for violence. Results Most clips employed episodic frames (79.2%), presented law enforcement officials as primary narrators (50.5%), and included police imagery (79.2%). A total of 433 firearm-injured people were mentioned, with a mean of 2.8 individuals shot included in each story. Most of the firearm-injured people featured in the clips (67.4%) had no personal information presented apart from age and/or gender. The majority of clips (84.4%) contained at least one harmful content element. The mean harmful content score/clip was 2.6. Public health frame elements, including epidemiologic context, root causes, public health narrators and visuals, and solutions were missing from most clips. Thematic stories contained significantly more public health frame elements and less harmful content compared to episodic stories. Conclusions Local television news produces limited public health coverage of firearm violence, and harmful content is common. This reporting likely compounds trauma experienced by firearm-injured people and could impede support for effective public health responses to firearm violence. Journalists should work to minimize harmful news content and adopt a public health approach to reporting on firearm violence.

Atr is a serine/threonine kinase, known to sense single-stranded DNA breaks and activate the DNA damage checkpoint by phosphorylating Chek1, which inhibits Cdc25, causing cell cycle arrest. This pathway has not been implicated in neuroregeneration. We show that in Drosophila sensory neurons removing Atr or Chek1, or overexpressing Cdc25 promotes regeneration, whereas Atr or Chek1 overexpression, or Cdc25 knockdown impedes regeneration. Inhibiting the Atr-associated checkpoint complex in neurons promotes regeneration and improves synapse/behavioral recovery after CNS injury. Independent of DNA damage, Atr responds to the mechanical stimulus elicited during regeneration, via the mechanosensitive ion channel Piezo and its downstream NO signaling. Sensory neuron-specific knockout of Atr in adult mice, or pharmacological inhibition of Atr-Chek1 in mammalian neurons in vitro and in flies in vivo enhances regeneration. Our findings reveal the Piezo-Atr-Chek1-Cdc25 axis as an evolutionarily conserved inhibitory mechanism for regeneration, and identify potential therapeutic targets for treating nervous system trauma. The Atr-Check1 pathway is involved in cell cycle and the DNA damage response. Here, the authors show that the Atr-Check1 pathway can inhibit axon regeneration in response to Piezo-mediated mechanosensation, affecting functional recovery.

A neuron’s regenerative capacity is governed by its intrinsic and extrinsic environment. Both peripheral and central neurons exhibit cell-type-dependent axon regeneration, but the underlying mechanism is unclear. Glia provide a milieu essential for regeneration. However, the routes of glia-neuron signaling remain underexplored. Here, we show that regeneration specificity is determined by the axotomy-induced Ca 2+ transients only in the fly regenerative neurons, which is mediated by L-type calcium channels, constituting the core intrinsic machinery. Peripheral glia regulate axon regeneration via a three-layered and balanced modulation. Glia-derived tumor necrosis factor acts through its neuronal receptor to maintain calcium channel expression after injury. Glia sustain calcium channel opening by enhancing membrane hyperpolarization via the inwardly-rectifying potassium channel (Irk1). Glia also release adenosine which signals through neuronal adenosine receptor (AdoR) to activate HCN channels (Ih) and dampen Ca 2+ transients. Together, we identify a multifaceted glia-neuron coupling which can be hijacked to promote neural repair. Limited neuron regeneration is the key barrier to recovery after central nervous system damage. Here, the authors show that axon regeneration is regulated by glia in a multi-layered manner controlling regeneration-dependent neuronal calcium channels.

Traumatic brain injury (TBI) induces immune dysfunction that can be captured clinically by an increase in the neutrophil-to-lymphocyte ratio (NLR). However, few studies have characterized the temporal dynamics of NLR post-TBI and its relationship with hospital-acquired infections (HAI), resource utilization, or outcome. We assessed NLR and HAI over the first 21 days post-injury in adults with moderate-to-severe TBI (n = 196) using group-based trajectory (TRAJ), changepoint, and mixed-effects multivariable regression analysis to characterize temporal dynamics. We identified two groups with unique NLR profiles: a high (n = 67) versus a low (n = 129) TRAJ group. High NLR TRAJ had higher rates (76.12% vs. 55.04%, p = 0.004) and earlier time to infection (p = 0.003). In changepoint-derived day 0–5 and 6–20 epochs, low lymphocyte TRAJ, early in recovery, resulted in more frequent HAIs (p = 0.042), subsequently increasing later NLR levels (p ≤ 0.0001). Both high NLR TRAJ and HAIs increased hospital length of stay (LOS) and days on ventilation (p ≤ 0.05 all), while only high NLR TRAJ significantly increased odds of unfavorable six-month outcome as measured by the Glasgow Outcome Scale (GOS) (p = 0.046) in multivariable regression. These findings provide insight into the temporal dynamics and interrelatedness of immune factors which collectively impact susceptibility to infection and greater hospital resource utilization, as well as influence recovery.

Atr is a serine/threonine kinase, known to sense single-stranded DNA breaks and activate the DNA damage checkpoint by phosphorylating Chek1, which inhibits Cdc25, causing cell cycle arrest. This pathway has not been implicated in neuroregeneration. We show that in Drosophila sensory neurons, removing Atr or Chek1, or overexpressing Cdc25 promotes regeneration, whereas Atr or Chek1 overexpression, or Cdc25 knockdown impedes regeneration. Inhibiting the Atr-associated checkpoint complex in neurons promotes regeneration and improves synapse/behavioral recovery after CNS injury. Independent of DNA damage, Atr responds to the mechanical stimulus elicited during regeneration, via the mechanosensitive ion channel Piezo and its downstream NO signaling. Sensory neuron-specific knockout of Atr in adult mice, or pharmacological inhibition of Atr-Chek1 in mammalian neurons in vitro and in flies in vivo enhance regeneration. Our findings reveal the Piezo-Atr-Chek1-Cdc25 axis as an evolutionarily conserved inhibitory mechanism for regeneration, and identify potential therapeutic targets for treating nervous system trauma. Competing Interest Statement The authors have declared no competing interest.

Lymph node fibroblastic reticular cells (FRCs) respond to signals from activated T cells by releasing nitric oxide, which inhibits T cell proliferation and restricts the size of the expanding T cell pool. Whether interactions with FRCs also support the function or differentiation of activated CD8 + T cells is not known. Here we report that encounters with FRCs enhanced cytokine production and remodeled chromatin accessibility in newly activated CD8 + T cells via interleukin-6. These epigenetic changes facilitated metabolic reprogramming and amplified the activity of pro-survival pathways through differential transcription factor activity. Accordingly, FRC conditioning significantly enhanced the persistence of virus-specific CD8 + T cells in vivo and augmented their differentiation into tissue-resident memory T cells. Our study demonstrates that FRCs play a role beyond restricting T cell expansion—they can also shape the fate and function of CD8 + T cells. Fibroblastic reticular cells (FRCs) are dynamic regulators of lymphoid tissue structure. Turley and colleagues show FRCs also support activated T cells by producing IL-6, which confers an advantage to CD8+ T cell memory responses.

The long battle over the Century Freeway apparently ended Tuesday with announcement of an agreement that will lead to construction of a 17.3-mile freeway between Norwalk and Los Angeles International Airport, providing for rapid transit and at least 3,700 housing...

The long battle over the Century Freeway apparently ended Tuesday with announcement of an agreement that will lead to construction of a 17.3-mile freeway between Norwalk and Los Angeles International Airport, providing for rapid transit and at least 3,700 housing...

The long battle over the Century Freeway apparently ended Tuesday with announcement of an agreement that will lead to construction of a 17.3-mile freeway between Norwalk and Los Angeles International Airport, providing for rapid transit and at least 3,700 housing...

The long battle over the Century Freeway apparently ended Tuesday with announcement of an agreement that will lead to construction of a 17.3-mile freeway between Norwalk and Los Angeles International Airport, providing for rapid transit and at least 3,700 housing...