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Lung Injury

Lung Injury: A broad term encompassing damage or trauma to the lungs, often resulting in impaired respiratory function.
This can arise from a variety of causes, including infections, environmental exposures, or underlying medical conditions.
Accurate assessment and optimization of research protocols are crucial for enhancing reproducibility and advancing our understanding of lung injury pathogenesis and potential therapies.
PubCompare.ai provides data-driven decision making to support lung injury researchers in identifying the most effective methods and prodcuts for their studies.

Most cited protocols related to «Lung Injury»

Similar to the 2011 workshop, a Delphi method was used to solicit measurements of experimental ALI (Figure 2). In Round 1 (Table E2), the 50 participants were asked to complete an electronic survey, wherein they stated all the measurements that they thought would be helpful to assess 1) histological evidence of tissue injury, 2) alteration of the alveolar–capillary barrier, 3) presence of an inflammatory response, and 4) evidence of physiologic dysfunction. Here, we refer to “features” as a measurement or group of measurements that address a specific component of a domain. Additionally, we asked the participants whether a time criterion should be included in the definition of experimental ALI and, if yes, to suggest a time. This question was asked based on feedback from workshop participants that the time criterion of 24 hours was too short for some models of lung injury (e.g., viral pneumonia) (17 (link)).
All the responses obtained as a part of the first round were collated by the domain leads and organized into a questionnaire for Round 2 (Table E3). Specifically, in Round 2, participants were provided with a list of all the measurements obtained from Round 1 under each of the four original domains in the 2011 workshop report. Participants were asked to rate each measurement according to importance using a scale of 0–5 (0 = minimal importance, 5 = maximal importance). As a part of the “histological evidence of tissue injury” domain, measurements were grouped by anatomical location: 1) alveolar spaces, 2) alveolar epithelium, 3) vasculature, 4) alveolar septae, and 5) interstitium. As a part of the “alteration of the alveolar–capillary barrier” domain, measurements were grouped under 1) endothelial injury or dysfunction, 2) epithelial injury or dysfunction, 3) lung edema, and 4) transfer of plasma or lung constituents across the barrier. As a part of the “presence of an inflammatory response” domain, measurements were grouped under 1) soluble mediator profiles, 2) inflammatory cellular composition and characteristics, and 3) consequences of inflammation. Finally, as a part of the “evidence of physiologic dysfunction” domain, measurements were grouped under 1) gas exchange, 2) lung mechanics, 3) vital signs, and 4) other aspects of the physiological domain.
In Round 3, answers to the questions from Round 2 were collated and presented to the participants (Table E4). Participants were asked to choose the top 4–5 features that they considered “most relevant” to measure each domain. Those features selected as “most relevant” by 30% or more of the respondents were considered “relevant” for that domain for the purpose of this workshop. We noted that a 30% cutoff resulted in at least five measurements ranked as “most relevant” in each of the four domains by the panelists. This approach would maximize the numbers of relevant measurements available to the community and maintain consistency in the number of relevant measurements across the domains, thereby increasing flexibility in application to many experimental ALI models.
Publication 2022
Capillaries Cells Endothelium Epithelium Inflammation Injuries Lung Lung Injury Mechanics physiology Plasma Pneumonia, Viral Pulmonary Edema Signs, Vital Tissues
Patients were seen every three months during years 1 and 2 post treatment and then every 6 months until 4 years post treatment. Imaging was required at each visit for response and toxicity assessment using CT scans. Follow-up PET scans were required if progressive soft tissue abnormalities where noted on CT. Pulmonary function tests (FEV-1, DLCO, and arterial blood gases) were to be performed every 3 months for year 1 posttreatment and every 6 months for year 2 post treatment. Tumor measurements at each follow-up were carried out using the Response Evaluation Criteria in Solid Tumors (RECIST)12 (link) where a complete response (CR) is total tumor disappearance and partial response (PR) is decrease in the longest tumor diameter by 30% or more.
The primary endpoint of the study was two-year actuarial primary tumor control. Primary tumor control was defined as the absence of primary tumor failure. Primary tumor failure was defined based on meeting both of two criteria: 1. Local enlargement defined as at least a 20% increase in the longest diameter of the gross tumor volume per CT, and 2. Evidence of tumor viability. Tumor viability could be affirmed by either demonstrating PET imaging with uptake of a similar intensity as the pretreatment staging PET, or by repeat biopsy confirming carcinoma. Primary tumor failure included marginal failures occurring within 1 cm of the planning target volume (1.5-2.0 cm from the gross tumor volume). Failure beyond the primary tumor but within the involved lobe was collected separately from disseminated failure within uninvolved lobes. Local failure is the combination of primary tumor and involved lobe failure with local control being the absence of local failure.
Secondary endpoints included assessments of treatment-related toxicity, disease free survival and overall survival. Disease-free survival included separate assessments of local-regional failure (within the primary site, involved lobe, hilum, and mediastinum) and disseminated recurrence (failure beyond the local and regional sites).
The National Cancer Institute’s Common Toxicity Criteria (CTC) Version 3.0 was used for grading of adverse events13 (link). Certain adverse events attributable to study therapy were specified prospectively within the protocol for use in evaluating the secondary endpoint of treatment related toxicity including grade 3 measures of lung injury, esophageal injury, heart injury, and nerve damage as well as any grade 4-5 toxicity felt related to treatment. However, all adverse events reported by participating centers were collected and assessed.
Publication 2010
Arteries Biopsy Blood Gas Analysis Carcinoma Congenital Abnormality Feelings Heart Injuries Hypertrophy Injuries Lung Injury Mediastinum Neoplasms Nervousness Patients Recurrence Tests, Pulmonary Function Tissues Vision X-Ray Computed Tomography
The lung tissue was fixed in 10% formalin and then embedded in paraffin. Later, the tissue blocks were cut into 5-μm sections, placed onto glass slides and stained with hematoxylin and eosin (H&E), dehydrated, and mounted. Morphologic examinations in these tissues were evaluated by light microscopy in a blinded fashion. To examine the extent of lung injury, we considered its five pathological features, such as (i) presence of exudates, (ii) hyperemia/congestion, (iii) intra-alveolar hemorrhage/debris, (iv) cellular infiltration, and (v) cellular hyperplasia. The severity of each of these pathological features was evaluated by a score indicating 0 as absent/none, 1 as mild, 2 as to show moderate, and finally 3 for severe injury. Compilations of these values obtained from individual pathological features represent the lung injury score [7 (link),32 (link)].
Gr-1 is a 21- to 25-kDa myeloid differentiation protein and also known as Ly-6G/Ly-6C. This myeloid differentiation antigen is a glycosylphosphatidylinositol (GPI)-linked protein expressed on granulocytes and macrophages. In the bone marrow, expression levels of Gr-1 directly correlate with granulocyte differentiation and maturation [33 (link)]. To examine neutrophil infiltration in lungs we performed immunohistochemistry using anti-Gr-1 Ab (BioLegend, San Diego, CA, USA; Catalog No.: 108413) as described previously [7 (link)]. In brief, 10% formalin-fixed, paraffin-embedded lung tissues were dewaxed in xylene and rehydrated in a graded series of ethanol. The slides were heated in 0.92% citric acid buffer (Vector Laboratories, Burlingame, CA) at 95°C for 30 min. After cooling to room temperature, the slides were incubated with 2% H2O2 in 60% methanol and blocked in 2% normal rabbit serum/Tris-buffered saline. Anti-Gr-1 antibody (BioLegend) was then applied and incubated overnight. Vectastain ABC reagent and DAB kit (Vector Laboratories) were used to detect the immunohistochemical reaction. Slides were counterstained with 4′, 6-diamidino-2-phenylindole and examined under a phase contrast light microscope (Eclipse Ti-S; Nikon, Melville, NY, USA). Gr-1-positive staining cells were counted in 10 visual fields/section at × 200 magnification, and averaged number was calculated.
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Publication 2015
Antibodies, Anti-Idiotypic Bone Marrow Buffers Cells Citric Acid Cloning Vectors Differentiation Antigens Eosin Ethanol Exudate Formalin Glycosylphosphatidylinositols Granulocyte Hemorrhage Hyperemia Hyperplasia Immunohistochemistry Injuries Light Microscopy link protein Lung Lung Injury Macrophage Methanol Microscopy, Phase-Contrast Neutrophil Infiltration Normal Saline Paraffin Paraffin Embedding Peroxide, Hydrogen Physical Examination Proteins Rabbits Serum Tissues Xylene
The SARS-CoV (Beijing strain, PUMC01 isolate) used in this study was provided by Z. Wang and Y. Liu (Chinese Academy of Medical Sciences, Chinese National Human Genome Center). All mouse studies were approved by the Ministry of Health Science and Technology division of the People's Republic of China. We intranasally inoculated mice with 100 μl virus (105.23 TCID50). At day 2, mice were killed, and the lungs were removed for further analyses. We assessed lung injury scores as described previously30 (link).
Publication 2005
Chinese Genome, Human Lung Lung Injury Mus Severe acute respiratory syndrome-related coronavirus Strains Virus
The following data were collected from the hospital chart and analyzed: age, sex, body weight, body mass index, etiologies of ARDS, underlying diseases, Acute Physiology and Chronic Health Evaluation (APACHE) II score, Sequential Organ Failure Assessment (SOFA) score and lung injury score on the day of ICU admission.
Arterial blood gas, ARDS duration before ECMO, ventilator settings included tidal volume, respiratory rate, PEEP, peak inspiratory pressure, dynamic driving pressure (the difference between peak inspiratory pressure and PEEP) and FiO2 were recorded before ECMO initiation. After ECMO support, daily arterial blood gas, ventilator settings, ECMO settings (gas flow, blood flow and FiO2) and ECMO complications (oxygenator failure, blood clots in oxygenator or circuit, bleeding, infection or others) were recorded until ICU discharge.
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Publication 2017
Arteries Blood Circulation Body Weight Extracorporeal Membrane Oxygenation Index, Body Mass Infection Inhalation Lung Injury Oxygenators Patient Discharge physiology Positive End-Expiratory Pressure Pressure Respiratory Distress Syndrome, Adult Respiratory Rate Thrombus Tidal Volume

Most recents protocols related to «Lung Injury»

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Publication 2023
Albumins Anesthesia Animals Cytokine Diet Eosin Eucalyptus Food Histones Inhalation Injections, Intraperitoneal Injuries Institutional Animal Care and Use Committees Isoflurane Ketamine Lung Lung Injury Males Mice, Inbred C57BL Mus Obstetric Delivery Oropharynxs physiology Rivers Rodent Saline Solution Smoke Tissue Harvesting Xylazine
For histological analyses, the right lung of each mouse was perfused with PBS, inflated with 10% buffered formalin (ThermoFisher Scientific, Waltham, MA, USA), and stored at 4 °C until processing. Slices from each lobe of the right lung were trimmed and sent to the UAB Comparative Pathology Laboratory to be processed, paraffin embedded, sectioned onto slides and stained with hematoxylin and eosin (H and E). Semiquantitative grading of histopathological changes of all lung sections was performed by a board-certified surgical pathologist (L.N.). Severity of lung tissue injury included alveolar, peribronchial inflammation, perivascular neutrophil infiltration, pleuritis and tissue necrosis. Severity of tissue damage from all lung lobes was graded. Grade 0 showed no neutrophil infiltrate in lung tissue; grade 1 showed rare neutrophils in the alveolar, peribronchial or perivascular tissue; grade 2 showed dense neutrophil infiltrate within the alveolar spaces with no injury to alveolar tissue; grade 3 showed dense neutrophil infiltrate within the alveolar space and necrosis of involved alveolar tissue. H-score is a cumulative score, determined by the percentage of tissue area assigned each grade (0–3). Maximum grade was assigned to the most severely damaged lobe, representing the maximum infection per animal. Images of lung sections were taken on a Lionheart FX Automated Imaging microscope (BioTek, Winooski, VT, USA) using 10× objective. Scale bar represents 200 µm.
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Publication 2023
Animals Eosin Formalin Infection Inflammation Injuries Lung Lung Injury Microscopy Mus Necrosis Neutrophil Neutrophil Infiltration Operative Surgical Procedures Paraffin Pathologists Pleurisy Tissues

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Publication 2023
Eosin Ethanol Fibrosis Formaldehyde Lung Lung Injury Mus Pulmonary Fibrosis Xylene
The mice were sacrificed after anaesthetization, and fresh lungs were collected, fixed in 4% PFA buffer, embedded, and sliced into 5-μm thick sections. Then, the slices were stained with haematoxylin and eosin for lung injury assessment. HE-stained images were captured by microscopy (ZEISS) and viewed by two pathologists to evaluate the degree of lung injury as previously reported.9 (link)
Publication 2023
Buffers Eosin Lung Lung Injury Microscopy Mus Pathologists
The middle part of tissue samples was fixed in 4% paraformaldehyde, embedded in paraffin, and cut into sections with 1‐μm thickness. Then, the sections were stained with H&E (Yuanye Biotechnology, Shanghai, China) to examine histological changes and imaged using a light microscope (Olympus, Tokyo, Japan). Two blinded pathologists participated in the assessment of the degree of lung injury. A 4‐point scale was used: none (0), mild (1), moderate (2), or severe (3). The lung injury score was obtained by summing the resulting two scores.29
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Publication 2023
Light Microscopy Lung Injury Paraffin Embedding paraform Pathologists Tissues

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More about "Lung Injury"

Lung injury, also known as pulmonary injury or respiratory distress, is a broad term encompassing various forms of damage or trauma to the lungs.
This can arise from a multitude of causes, including infections (e.g., pneumonia, COVID-19), environmental exposures (e.g., air pollution, smoke inhalation), or underlying medical conditions (e.g., acute respiratory distress syndrome, pulmonary edema).
Accurate assessment and optimization of research protocols are crucial for enhancing reproducibility and advancing our understanding of lung injury pathogenesis and potential therapies.
The study of lung injury often involves the use of animal models, such as C57BL/6 mice, to investigate the underlying mechanisms and evaluate potential interventions.
Techniques like lipopolysaccharide (LPS) administration, a common method for inducing lung inflammation, and optical microscopy using instruments like the BX51 microscope, can provide valuable insights into the cellular and structural changes associated with lung injury.
The analysis of lung injury data can be facilitated by statistical software like SAS 9.4, while protein quantification assays, such as the BCA protein assay kit, can help researchers measure the levels of key biomarkers.
Additionally, image analysis tools like Image-Pro Plus can be utilized to quantify and visualize the morphological changes in lung tissue.
To enhance the reproducibility and accuracy of lung injury research, researchers can leverage data-driven decision-making platforms like PubCompare.ai.
This AI-powered tool allows researchers to identify the most effective methods and products from the scientific literature, pre-prints, and patents, enabling them to make informed decisions and optimize their experimental protocols.
By incorporating these insights and tools, lung injury researchers can advance their understanding of the pathogenesis of this complex condition and develop more effective therapies, ultimately improving patient outcomes.
Remember, one should always consult with medical professionals and follow approved protocols when conducting lung injury research.