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Festuca grass, a multipurpose and vital resource, is experiencing crises of sustainability and degradation due to increased demand and mismanagement. Through a survey research approach, this study aimed to develop sustainable management and utilization strategies for Festuca grass. We employed purposive and random sampling techniques for data collection, focusing on the Festuca grass potential in Borena-Sayint Worehimenu National Park. Interviews, key informant surveys, focus group discussions, and field observations were also conducted. We employed quantitative and qualitative data analysis techniques to ensure a comprehensive approach to deriving insights from the collected data. The findings indicate that Festuca grass has a lifespan of two to four years and fully matures within two years. Products derived from Festuca grass vary according to the maturity level. The results also highlight the demand for Festuca grass and the potential availability of market demand. Harvesting frequency, inappropriate management practices, biased resource sharing, and unauthorized exploitation are basic challenges related to grass resource sustainability. The establishment of certified user groups, domestication of private stocks, revision of resource-sharing protocols, and periodic monitoring are among the possible potential strategic utilization options identified by user groups. A modified strategic framework for the sustainable management and utilization of Festuca grass was developed. This framework outlines four dominant management clusters that are interconnected with each other. Sustainable management of Festuca grass contributes to both environmental conservation and community wellbeing. It advocates for inclusive, community-based approaches that balance ecological preservation with socioeconomic needs. The sustainability of Festuca grass resources is precarious and could face a significant decline or total loss if the current management practices remain unchanged in the coming decades. To ensure the effective utilization and management of Festuca grass, it is imperative to implement periodic resource monitoring, conduct stakeholder meetings, and apply a sustainable management framework. The responsibility for sustaining Festuca grass resources lies with governmental organizations, academic and research institutions, nongovernmental organizations, professional associations, and user communities.

Objectives: Visceral leishmaniasis remains a deadly parasitic disease with diagnostic complexities. Currently, point-of-care chest imaging is gaining momentum in the diagnosis of infectious diseases. Respiratory symptoms are common in visceral leishmaniasis. Here we aimed to systematically synthesize the evidence on the utility of chest imaging on the diagnosis and management of patients with visceral leishmaniasis., Methods: We searched PubMed, Scopus, Web of Science, ScienceDirect, and Google Scholar databases for studies reporting chest imaging findings in patients with visceral leishmaniasis, published in English from database inception to November 2022. We used the Joanna Briggs Institute checklists to evaluate the risk of bias. The protocol of this systematic review was registered with the Open Science Framework: https://doi.org/10.17605/OSF.IO/XP24W., Results: Of 1792 studies initially retrieved, 17 studies with 59 participants were included. Of the 59 patients, 51% (30) had respiratory symptoms and 20% (12) were human immunodeficiency virus co-infected. Chest X-ray, high-resolution computed tomography, and chest ultrasound findings were available for 95% (56), 93% (55), and 2% (1) of the patients, respectively. The most common findings were pleural effusion (20%; 12), reticular opacities (14%; 8), ground-glass opacities (12%; 7), and mediastinal lymphadenopathies (10%; 6). High-resolution computed tomography was more sensitive than chest X-ray and detected lesions that were lost on chest X-ray, 62% (37) versus 29% (17). In almost all cases, regression of the lesions was observed with treatment. Microscopy of pleural or lung biopsy detected amastigotes. Polymerase chain reaction yield was better in pleural and bronchoalveolar lavage fluids. A parasitological diagnosis from pleural and pericardial fluid was possible in AIDS patients. Overall, the risk of bias was low., Conclusions: Visceral leishmaniasis patients frequently had abnormal findings on high-resolution computed tomography. Chest ultrasound is a useful alternative in resource-limited settings to aid in diagnosis and subsequent treatment follow-up, especially when routine tests yield negative results despite clinical suspicion., Competing Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (© The Author(s) 2023.)

Background: Exposure to wood smoke (WS) increases the risk for chronic bronchitis more than exposure to cigarette smoke (CS), but the underlying mechanisms are unclear., Objective: The effect of WS and CS on mucous cell hyperplasia in mice and in human primary airway epithelial cells (AECs) was compared with replicate the findings in human cohorts. Responsible WS constituents were identified to better delineate the pathway involved, and the role of a tumor protein p53 ( Tp53 ) gene polymorphism was investigated., Methods: Mice and primary human AECs were exposed to WS or CS and the signaling receptor and pathway were identified using short hairpin structures, small molecule inhibitors, and Western analyses. Mass spectrometric analysis was used to identify active WS constituents. The role of a gene variant in Tp53 that modifies proline to arginine was examined using nasal brushings from study participants in the Lovelace Smokers Cohort, primary human AECs, and mice with a modified Tp53 gene., Results: WS at 25-fold lower concentration than CS increased mucin expression more efficiently in mice and in human AECs in a p53 pathway-dependent manner. Study participants who were homozygous for p53 arginine compared with the proline variant showed higher mucin 5AC (MUC5AC) mRNA levels in nasal brushings if they reported WS exposure. The WS constituent, oxalate, increased MUC5AC levels similar to the whole WS extract, especially in primary human AECs homozygous for p53 arginine, and in mice with a modified Tp53 gene. Further, the anion exchange protein, SLC26A9, when reduced, enhanced WS- and oxalate-induced mucin expression., Discussion: The potency of WS compared with CS in inducing mucin expression may explain the increased risk for chronic bronchitis in participants exposed to WS. Identification of the responsible compounds could help estimate the risk of pollutants in causing chronic bronchitis in susceptible individuals and provide strategies to improve management of lung diseases. https://doi.org/10.1289/EHP9446.

Our previous studies showed that cigarette smokers who are exposed to wood smoke (WS) are at an increased risk for chronic bronchitis and reduced lung function. The present study was undertaken to determine the mechanisms for WS-induced adverse effects. We studied the effect of WS exposure using four cohorts of mice. C57Bl/6 mice were exposed for 4 or 12 weeks to filtered air, to 10 mg/m(3) WS for 2 h/d, to 250 mg/m(3) cigarette smoke (CS) for 6 h/d, or to CS followed by WS (CW). Inflammation was absent in the filtered air and WS groups, but enhanced by twofold in the bronchoalveolar lavage of the CW compared with CS group as measured by neutrophil numbers and levels of the neutrophil chemoattractant, keratinocyte-derived chemokine. The levels of the anti-inflammatory lipoxin, lipoxin A4, were reduced by threefold along with cyclo-oxygenase (COX)-2 and microsomal prostaglandin E synthase (mPGES)-1 in airway epithelial cells and PGE2 levels in the bronchoalveolar lavage of CW compared with CS mice. We replicated, in primary human airway epithelial cells, the changes observed in mice. Immunoprecipitations showed that WS blocked the interaction of aryl hydrocarbon receptor (AHR) with AHR nuclear transporter to reduce expression of COX-2 and mPGES-1 by increasing expression of AHR repressor (AHRR). Collectively, these studies show that exposure to low concentrations of WS enhanced CS-induced inflammation by inducing AHRR expression to suppress AHR, COX-2, and mPGES-1 expression, and levels of PGE2 and lipoxin A4. Therefore, AHRR is a potential therapeutic target for WS-associated exacerbations of CS-induced inflammation.

Despite implications for carcinogenesis and other chronic diseases, basic mechanisms of p53 and its variants in suppressing Bcl-2 levels are poorly understood. Bcl-2 sustains mucous cell metaplasia, whereas p53(-/-) mice display chronically increased mucous cells. Here we show that p53 decreases bcl-2 mRNA half-life by interacting with the 5' untranslated region (UTR). The p53-bcl-2 mRNA interaction is modified by the substitution of proline by arginine within the p53 proline-rich domain (PRD). Accordingly, more mucous cells are present in primary human airway cultures with p53(Arg) compared with p53(Pro). Also, the p53(Arg) compared with p53(Pro) displays higher affinity to and activates the promoter region of SAM-pointed domain-containing Ets-like factor (SPDEF), a driver of mucous differentiation. On two genetic backgrounds, mice with targeted replacement of prolines in p53 PRD show enhanced expression of SPDEF and Bcl-2 and mucous cell metaplasia. Together, these studies define the PRD of p53 as a determinant for chronic mucous hypersecretion.

Cigarette smoke contains numerous chemical compounds, including abundant reactive oxygen/nitrogen species and aldehydes, and many other carcinogens. Long-term cigarette smoking significantly increases the risk of various lung diseases, including chronic obstructive pulmonary disease and lung cancer, and contributes to premature death. Many in vitro and in vivo studies have elucidated mechanisms involved in cigarette smoke-induced inflammation, DNA damage, and autophagy, and the subsequent cell fates, including cell death, cellular senescence, and transformation. In this Translational Review, we summarize the known pathways underlying these processes in airway epithelial cells to help reveal future challenges and describe possible directions of research that could lead to better management and treatment of these diseases.

Interferon γ (IFN-γ)-induced cell death is mediated by the BH3-only domain protein, Bik, in a p53-independent manner. However, the effect of IFN-γ on p53 and how this affects autophagy have not been reported. The present study demonstrates that IFN-γ down-regulated expression of the BH3 domain-only protein, Bmf, in human and mouse airway epithelial cells in a p53-dependent manner. p53 also suppressed Bmf expression in response to other cell death-stimulating agents, including ultraviolet radiation and histone deacetylase inhibitors. IFN-γ did not affect Bmf messenger RNA half-life but increased nuclear p53 levels and the interaction of p53 with the Bmf promoter. IFN-γ-induced interaction of HDAC1 and p53 resulted in the deacetylation of p53 and suppression of Bmf expression independent of p53's proline-rich domain. Suppression of Bmf facilitated IFN-γ-induced autophagy by reducing the interaction of Beclin-1 and Bcl-2. Furthermore, autophagy was prominent in cultured bmf(-/-) but not in bmf(+/+) cells. Collectively, these observations show that deacetylation of p53 suppresses Bmf expression and facilitates autophagy.

Extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) are members of the mitogen-activated protein kinase super family that can mediate cell proliferation and apoptosis. The Ras-Raf-MEK-ERK signaling cascade controlling cell proliferation has been well studied but the mechanisms involved in ERK1/2-mediated cell death are largely unknown. This review focuses on recent papers that define ERK1/2 translocation to the nucleus and the proteins involved in the cytosolic retention of activated ERK1/2. Cytosolic retention of ERK1/2 denies access to the transcription factor substrates that are responsible for the mitogenic response. In addition, cytosolic ERK1/2, besides inhibiting survival and proliferative signals in the nucleus, potentiates the catalytic activity of some proapoptotic proteins such as DAP kinase in the cytoplasm. Studies that further define the function of cytosolic ERK1/2 and its cytosolic substrates that enhance cell death will be essential to harness this pathway for developing effective treatments for cancer and chronic inflammatory diseases.