Chronic heat stress induces lung injury in broiler chickens by disrupting the pulmonary blood-air barrier and activating TLRs/NF-κB signaling pathway.

As an important respiratory organ, the lung is susceptible to damage during heat stress due to the accelerated breathing frequency caused by an increase in environmental temperature. This can affect the growth performance of animals and endanger their health. This study aimed to explore the mechanism of lung tissue damage caused by heat stress. Broilers were randomly divided into a control group (Control) and a heat stress group (HS). The HS group was exposed to 35°C heat stress for 12 h per d from 21-days old, and samples were taken from selected broilers at 28, 35, and 42-days old. The results showed a significant increase in lactate dehydrogenase (LDH) activity in the serum and myeloperoxidase (MPO) activity in the lungs of broiler chickens across all 3 age groups after heat stress (P < 0.01), while the total antioxidant capacity (T-AOC) was significantly enhanced at 35-days old (P < 0.01). Heat stress also led to significant increases in various proinflammatory factors in serum and expression levels of HSP60 and HSP70 in lung tissue. Histopathological results showed congestion and bleeding in lung blood vessels, shedding of pulmonary epithelial cells, and a large amount of inflammatory infiltration in the lungs after heat stress. The mRNA expression of TLRs/NF-κB-related genes showed an upward trend (P < 0.05) after heat stress, while the mRNA expression of MLCK, a gene related to pulmonary blood-air barrier, significantly increased after heat stress, and the expression levels of MLC, ZO-1, and occludin decreased in contrast. This change was also confirmed by Western blotting, indicating that the pulmonary blood-air barrier is damaged after heat stress. Heat stress can cause damage to the lung tissue of broiler chickens by disrupting the integrity of the blood-air barrier and increasing permeability. This effect is further augmented by the activation of TLRs/NF-κB signaling pathways leading to an intensified inflammatory response. As heat stress duration progresses, broiler chickens develop thermotolerance, which gradually mitigates the damaging effects induced by heat stress.

Artificial intelligence computed tomography helps evaluate the severity of COVID-19 patients: A retrospective study.

BACKGROUND: Computed tomography (CT) is a noninvasive imaging approach to assist the early diagnosis of pneumonia. However, coronavirus disease 2019 (COVID-19) shares similar imaging features with other types of pneumonia, which makes differential diagnosis problematic. Artificial intelligence (AI) has been proven successful in the medical imaging field, which has helped disease identification. However, whether AI can be used to identify the severity of COVID-19 is still underdetermined. METHODS: Data were extracted from 140 patients with confirmed COVID-19. The severity of COVID-19 patients (severe vs. non-severe) was defined at admission, according to American Thoracic Society (ATS) guidelines for community-acquired pneumonia (CAP). The AI-CT rating system constructed by Hangzhou YITU Healthcare Technology Co., Ltd. was used as the analysis tool to analyze chest CT images. RESULTS: A total of 117 diagnosed cases were enrolled, with 40 severe cases and 77 non-severe cases. Severe patients had more dyspnea symptoms on admission (12 vs. 3), higher acute physiology and chronic health evaluation (APACHE) II (9 vs. 4) and sequential organ failure assessment (SOFA) (3 vs. 1) scores, as well as higher CT semiquantitative rating scores (4 vs. 1) and AI-CT rating scores than non-severe patients (P<0.001). The AI-CT score was more predictive of the severity of COVID-19 (AUC=0.929), and ground-glass opacity (GGO) was more predictive of further intubation and mechanical ventilation (AUC=0.836). Furthermore, the CT semiquantitative score was linearly associated with the AI-CT rating system (Adj R 2=75.5%, P<0.001). CONCLUSIONS: AI technology could be used to evaluate disease severity in COVID-19 patients. Although it could not be considered an independent factor, there was no doubt that GGOs displayed more predictive value for further mechanical ventilation.

The etiology of achalasia: An immune-dominant disease.

There is accumulating evidence suggesting that an autoimmune component is involved in esophageal achalasia. An increase in immune cells, cytokines, chemokines, and autoimmune antibodies in serum and infiltration of immune cells in tissues support the view that immune-mediated inflammation is a crucial pathogenesis of inhibitory neuron degeneration in the lower esophageal sphincter. Infection of viruses such as the herpes virus family has been suspected of provoking the autoimmune reaction. Meanwhile, previous reports on immunogenetics have proposed that specific risk alleles on the human leukocyte antigen complex define the susceptible population to achalasia. In this study we reviewed current knowledge regarding the immune-related factors of achalasia, including immunology, viral infection and immunogenetic variations.

Multiplex immunoassays reveal increased serum cytokines and chemokines associated with the subtypes of achalasia.

BACKGROUND: Achalasia is an esophageal motility disorder with unknown etiology. Previous findings indicate that immune-mediated inflammatory process causes inhibitory neuronal degeneration. This study was designed to evaluate levels of serological cytokines and chemokines in patients with achalasia. METHODS: We collected information from forty-seven patients with achalasia who underwent peroral endoscopic myotomy. Control samples were collected from forty-seven age- and sex-matched healthy people. The concentrations of serological cytokines and chemokines were analyzed by Luminex xMAP immunoassay. Serological and clinical data were compared between groups. KEY RESULTS: Compared with healthy controls, achalasia patients had significantly increased concentrations of eleven cytokines and chemokines, namely, TGF-ß1 (P < .001), TGF-ß2 (P < .001), TGF-ß3 (P < .001), IL-1ra (P < .001), IL-17 (P = .005), IL-18 (P < .001), IFN-γ (P < .001), MIG (P < .001), PDGF-BB (P < .001), IP-10 (P = .003), and SCGF-B (P < .001). Gene ontology (GO) and network functional enrichment analysis revealed regulation of signaling receptor activity and receptor-ligand activity were the most related pathways of these cytokines and chemokines. Levels of twelve cytokines and chemokines were significantly increased in type III compared with I/II achalasia, namely, TGF-ß2, IL-1ra, IL-2Ra, IL-18, MIG, IFN-γ, SDF-1a, Eotaxin, PDGF-BB, IP-10, MCP-1, and TRAIL. CONCLUSIONS AND INFERENCES: Patients with achalasia exhibited increased levels of serological cytokines and chemokines. Levels of cytokines and chemokines were significantly increased in type III than in type I/II achalasia. Cytokines and chemokines might contribute to the inflammatory development of achalasia.