The TRIPOD (Transparent Reporting of a multivariable prediction model for Individual Prognosis Or Diagnosis) Statement includes a 22-item checklist, which aims to improve the reporting of studies developing, validating, or updating a prediction model, whether for diagnostic or prognostic purposes. The TRIPOD Statement aims to improve the transparency of the reporting of a prediction model study regardless of the study methods used. This explanation and elaboration document describes the rationale; clarifies the meaning of each item; and discusses why transparent reporting is important, with a view to assessing risk of bias and clinical usefulness of the prediction model. Each checklist item of the TRIPOD Statement is explained in detail and accompanied by published examples of good reporting. The document also provides a valuable reference of issues to consider when designing, conducting, and analyzing prediction model studies. To aid the editorial process and help peer reviewers and, ultimately, readers and systematic reviewers of prediction model studies, it is recommended that authors include a completed checklist in their submission. The TRIPOD checklist can also be downloaded from www.tripod-statement.org.

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Transparent Reporting of a multivariable prediction model for Individual Prognosis or Diagnosis (TRIPOD): explanation and elaboration.

Introduction: Ventilator-induced Lung Injury: Not Only Air Leaks Ventilation-induced Pulmonary Edema and Related Findings: A Historical Perspective Ventilation-induced Pulmonary Edema: Hydrostatic or Permeability Edema? Experimental Evidence for Increased Vascular Transmural Pressure Evidence for Alterations in Alveolar–Capillary Permeability Contributions of the Static and Dynamic Lung Volume Components to Ventilator-induced Edema High-volume Lung Edema Low Lung Volume Injury Effects of High-volume Ventilation on Abnormal Lungs Effects of High-volume Ventilation on Injured Lungs Interaction between Severe Alveolar Flooding and Mechanical Ventilation Effects of Resting the Lung on Ventilator-induced Lung Injury Possible Mechanisms of Ventilation-induced Lung Injury Mechanisms of Increased Vascular Transmural Pressure Mechanisms of Altered Permeability Clinical Relevance

Ventilator-induced lung injury: lessons from experimental studies.

Prediction models are developed to aid health-care providers in estimating the probability or risk that a specific disease or condition is present (diagnostic models) or that a specific event will occur in the future (prognostic models), to inform their decision making. However, the overwhelming evidence shows that the quality of reporting of prediction model studies is poor. Only with full and clear reporting of information on all aspects of a prediction model can risk of bias and potential usefulness of prediction models be adequately assessed. The Transparent Reporting of a multivariable prediction model for Individual Prognosis Or Diagnosis (TRIPOD) Initiative developed a set of recommendations for the reporting of studies developing, validating, or updating a prediction model, whether for diagnostic or prognostic purposes. This article describes how the TRIPOD Statement was developed. An extensive list of items based on a review of the literature was created, which was reduced after a Web-based survey and revised during a 3-day meeting in June 2011 with methodologists, health-care professionals, and journal editors. The list was refined during several meetings of the steering group and in e-mail discussions with the wider group of TRIPOD contributors. The resulting TRIPOD Statement is a checklist of 22 items, deemed essential for transparent reporting of a prediction model study. The TRIPOD Statement aims to improve the transparency of the reporting of a prediction model study regardless of the study methods used. The TRIPOD Statement is best used in conjunction with the TRIPOD explanation and elaboration document. To aid the editorial process and readers of prediction model studies, it is recommended that authors include a completed checklist in their submission (also available at www.tripod-statement.org).

https://www.bmj.com/content/bmj/350/bmj.g7594.full.pdf

Transparent reporting of a multivariable prediction model for individual prognosis or diagnosis (TRIPOD): The TRIPOD statement

Prediction models are developed to aid health care providers in estimating the probability or risk that a specific disease or condition is present (diagnostic models) or that a specific event will occur in the future (prognostic models), to inform their decision making. However, the overwhelming evidence shows that the quality of reporting of prediction model studies is poor. Only with full and clear reporting of information on all aspects of a prediction model can risk of bias and potential usefulness of prediction models be adequately assessed. The Transparent Reporting of a multivariable prediction model for Individual Prognosis Or Diagnosis (TRIPOD) Initiative developed a set of recommendations for the reporting of studies developing, validating, or updating a prediction model, whether for diagnostic or prognostic purposes. This article describes how the TRIPOD Statement was developed. An extensive list of items based on a review of the literature was created, which was reduced after a Web-based survey and revised during a 3-day meeting in June 2011 with methodologists, health care professionals, and journal editors. The list was refined during several meetings of the steering group and in e-mail discussions with the wider group of TRIPOD contributors. The resulting TRIPOD Statement is a checklist of 22 items, deemed essential for transparent reporting of a prediction model study. The TRIPOD Statement aims to improve the transparency of the reporting of a prediction model study regardless of the study methods used. The TRIPOD Statement is best used in conjunction with the TRIPOD explanation and elaboration document. To aid the editorial process and readers of prediction model studies, it is recommended that authors include a completed checklist in their submission (also available at www.tripod-statement.org).

Transparent Reporting of a multivariable prediction model for Individual Prognosis Or Diagnosis (TRIPOD): The TRIPOD Statement

Acute lung injury in humans is characterized histopathologically by neutrophilic alveolitis, injury of the alveolar epithelium and endothelium, hyaline membrane formation, and microvascular thrombi. Different animal models of experimental lung injury have been used to investigate mechanisms of lung injury. Most are based on reproducing in animals known risk factors for ARDS, such as sepsis, lipid embolism secondary to bone fracture, acid aspiration, ischemia-reperfusion of pulmonary or distal vascular beds, and other clinical risks. However, none of these models fully reproduces the features of human lung injury. The goal of this review is to summarize the strengths and weaknesses of existing models of lung injury. We review the specific features of human ARDS that should be modeled in experimental lung injury and then discuss specific characteristics of animal species that may affect the pulmonary host response to noxious stimuli. We emphasize those models of lung injury that are based on reproducing risk factors for human ARDS in animals and discuss the advantages and disadvantages of each model and the extent to which each model reproduces human ARDS. The present review will help guide investigators in the design and interpretation of animal studies of acute lung injury.

Animal models of acute lung injury.

Reassembly of lipid-protein complexes of pulmonary surfactant. Proposed mechanism of interaction.

We have isolated and partially characterized the protein found in surface-active material from adult human lungs, and have determined the time of appearance of this protein in amniotic fluid. Fluids were drawn at gestational ages from 12 to 44 wk, and were assayed for their concentration of apoprotein by an agglutination immunoassay. Surfactant apoprotein ((defined as that protein which is reproducibly found in purified preparations of surface active material) was usually first detected from 30 to 32 wk gestation, and its concentration increased almost fivefold to a maximum at 37 wk. The change in apoprotein concentration was approximately paralleled by the change in phospholipid concentration. At all gestational ages there was wide variability in both phospholipid and apoprotein concentrations, and the time of appearance of the apoprotein in amniotic fluid differed among fetuses. The results suggest that the presence of surfactant apoprotein in amniotic fluid is coincident with the biochemical and morphological maturation of the fetal lung, and are additional evidence that this apoprotein is cosecreted with the lipids of surface-active material.

Appearance of paoproteins of pulmonary surfactant in human amniotic fluid.

In the last 10 years there has been an increased appreciation of the changes in lung cell populations that occur in association with the acute respiratory failure often induced by traumatic injury. Early events result in an accumulation in the lung of platelets, neutrophils, monocytes, and macrophages, a release of substances having potent cardiopulmonary and metabolic effects, and an ensuing edema and transudation of materials from the interstitium and capillaries into the alveoli. Further progression of the injury results in significant decreases in the number of endothelial and type I epithelial cells and a subsequent hyperplasia of fibroblasts and type II-like epithelial cells. Major sequelae of the latter stage of the disease are interstitial and interalveolar fibrosis, probably resulting from the increased number of fibroblasts present. The activity and composition of pulmonary surfactant are often perturbed. This review will discuss mechanisms that may be involved in these processes, with major emphasis on cell-cell interactions mediated through polypeptide growth factors. We describe the properties of certain growth factors commonly associated with inflammatory and wound healing reactions, discuss their cellular origins, and speculate on their possible roles in mediating the structural and physiological responses seen in the lung during acute respiratory failure. The majority of work done with lung cells has concentrated on interactions between macrophages and fibroblasts, and it is evident that macrophages are capable of producing mitogens affecting the proliferation of fibroblasts. However, from the results of studies that are less developed, it is possible that epithelial cells and immunologically stimulated cells could also be involved in these actions. We conclude that the homeostasis of lung cell populations may be influenced by both growth-stimulating and growth-inhibiting substances and potentially could involve interactions through growth factors of fibroblasts, macrophages, lymphocytes, alveolar epithelial cells, endothelial cells, and platelets. At this time the information on these purported interactions is quite limited and there are far more questions than answers.

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Regulation of lung cell proliferation by polypeptide growth factors.

Surfactant proteins A and D (SP-A and SP-D) are believed to participate in the pulmonary host defense and the response to lung injury. In order to understand the effects of prematurity and lung injury on these proteins, we measured the amounts of SP-A and SP-D and their mRNAs in three groups of animals: (1) nonventilated premature baboon fetuses; (2) neonatal baboons delivered prematurely at 140 d gestation age (ga) and ventilated with PRN O2; (3) animals of the same age ventilated with 100% O2 to induce chronic lung injury. In nonventilated fetuses, tissue and lavage SP-A were barely detectable in baboons of 125 and 140 d ga, but they equaled or exceeded adult SP-A concentrations (g/g lung dry wt) at 175 d (term gestation, 185 d). In contrast, SP-D was readily detectable in tissue and lavage at 125 and 140 d ga. When the baboons of 140 d ga were ventilated for 10 d with 100% oxygen to produce chronic lung injury, the tissue concentration of SP-A was five times greater than that of normal adults; SP-D 16-...

https://www.atsjournals.org/doi/pdf/10.1164/ajrccm.160.3.9806061

Richard J. King

Papers

Reassembly of lipid-protein complexes of pulmonary surfactant. Proposed mechanism of interaction.

Appearance of paoproteins of pulmonary surfactant in human amniotic fluid.

Regulation of lung cell proliferation by polypeptide growth factors.

Surfactant proteins A and D in premature baboons with chronic lung injury (Bronchopulmonary dysplasia). Evidence for an inhibition of secretion.

Project MERIT standards.