Upward Three-Dimensional Grid Drawings of Graphs

A \emph{three-dimensional grid drawing} of a graph is a placement of the vertices at distinct points with integer coordinates, such that the straight line segments representing the edges do not cross. Our aim is to produce three-dimensional grid drawings with small bounding box volume. We prove that every $n$-vertex graph with bounded degeneracy has a three-dimensional grid drawing with $O(n^{3/2})$ volume. This is the broadest class of graphs admiting such drawings. A three-dimensional grid drawing of a directed graph is \emph{upward} if every arc points up in the z-direction. We prove that every directed acyclic graph has an upward three-dimensional grid drawing with $(n^3)$ volume, which is tight for the complete dag. The previous best upper bound was $O(n^4)$. Our main result is that every $c$-colourable directed acyclic graph ($c$ constant) has an upward three-dimensional grid drawing with $O(n^2)$ volume. This result matches the bound in the undirected case, and improves the best known bound from $O(n^3)$ for many classes of directed acyclic graphs, including planar, series parallel, and outerplanar

Acute Pulmonary Edema

clinical practice T h e ne w e ngl a nd jou r na l o f m e dic i ne A 62-year-old man presents with a three-day history of progressive dyspnea, nonproductive cough, and low-grade fever. He had been hospitalized two years earlier for congestive heart failure. His blood pressure is 95/55 mm Hg, his heart rate 110 beats per minute, his temperature 37.9°C, and his oxygen saturation while breathing ambient air 86 percent. Chest auscultation reveals rales and rhonchi bilaterally. A chest radiograph shows bilateral pulmonary infiltrates consistent with pulmonary edema and borderline enlargement of the cardiac silhouette. How should this patient be evaluated to establish the cause of the acute pulmonary edema and to determine appropriate therapy? the clinical problem The following two fundamentally different types of pulmonary edema occur in humans: cardiogenic pulmonary edema (also termed hydrostatic or hemodynamic edema) and noncardiogenic pulmonary edema (also known as increased-permeability pulmonary edema, acute lung injury, or acute respiratory distress syndrome). Although they have distinct causes, cardiogenic and noncardiogenic pulmonary edema may be difficult to distinguish because of their similar clinical manifestations. Knowledge of the cause of acute pulmonary edema has important implications for treatment. Patients with cardiogenic pulmonary edema typically are treated with diuretics and afterload reduction, although the underlying cause may require other treatment, including coronary revascularization. 1 Patients with noncardiogenic pulmonary edema who require mechanical ventilation should be ventilated with a low tidal volume (6 ml per kilogram of predicted body weight) and a plateau airway pressure less than 30 cm of water. This lung-protective strategy of ventilation reduces mortality in patients with acute lung injury. 2,3 In addition, for patients with severe sepsis, recombinant activated protein C 4 and low-dose hydrocortisone 5 should be considered. Prompt diagnosis of the cause of acute pulmonary edema with the use of noninvasive methods, supplemented by catheterization of the pulmonary artery when there is diagnostic uncertainty, facilitates timely and appropriate treatment. Accurate diagnosis of acute pulmonary edema requires an understanding of microvascular fluid exchange in the lun

Acute Pulmonary Edema

clinical practice T h e n e w e ng l a n d j o u r na l o f m e dic i n e A 62-year-old man presents with a three-day history of progressive dyspnea, nonproductive cough, and low-grade fever. He had been hospitalized two years earlier for congestive heart failure. His blood pressure is 95/55 mm Hg, his heart rate 110 beats per minute, his temperature 37.9°C, and his oxygen saturation while breathing ambient air 86 percent. Chest auscultation reveals rales and rhonchi bilaterally. A chest radiograph shows bilateral pulmonary infiltrates consistent with pulmonary edema and borderline enlargement of the cardiac silhouette. How should this patient be evaluated to establish the cause of the acute pulmonary edema and to determine appropriate therapy? the clinical problem The following two fundamentally different types of pulmonary edema occur in humans: cardiogenic pulmonary edema (also termed hydrostatic or hemodynamic edema) and noncardiogenic pulmonary edema (also known as increased-permeability pulmonary edema, acute lung injury, or acute respiratory distress syndrome). Although they have distinct causes, cardiogenic and noncardiogenic pulmonary edema may be difficult to distinguish because of their similar clinical manifestations. Knowledge of the cause of acute pulmonary edema has important implications for treatment. Patients with cardiogenic pulmonary edema typically are treated with diuretics and afterload reduction, although the underlying cause may require other treatment, including coronary revascularization. 1 Patients with noncardiogenic pulmonary edema who require mechanical ventilation should be ventilated with a low tidal volume (6 ml per kilogram of predicted body weight) and a plateau airway pressure less than 30 cm of water. This lung-protective strategy of ventilation reduces mortality in patients with acute lung injury. 2,3 In addition, for patients with severe sepsis, recombinant activated protein C 4 and low-dose hydrocortisone 5 should be considered. Prompt diagnosis of the cause of acute pulmonary edema with the use of noninvasive methods, supplemented by catheterization of the pulmonary artery when there is diagnostic uncertainty, facilitates timely and appropriate treatment. Accurate diagnosis of acute pulmonary edema requires an understanding of microvascular fluid exchange in the lun

Anatomic Repair of Posteromedial Meniscocapsular Separation Using an All-Inside Technique

Separation of the posteromedial meniscocapsular junction (PMC) is a unique injury seen in patients with disruption of the anterior cruciate ligament. PMC tears may go unrecognized despite preoperative magnetic resonance imaging and diagnostic arthroscopy of the medial compartment. Unrepaired lesions may lead to persistent laxity of the knee after anterior cruciate ligament reconstruction. Inside-out repair techniques risk iatrogenic injury to the articular cartilage during needle passage and require dissection of the posteromedial knee for suture retrieval. Previous all-inside techniques have required specialized implants and repaired PMC lesions with direct visualization of the tear. The presented all-inside technique is an easily reproducible, cost-effective means to anatomically repair separation of the PMC. The technique provides the surgeon direct visualization and full arthroscopic access to the lesion, making repair technically easy and efficient

The mouse as an investigational model for preterm labor

Preterm labor continues to be a leading cause of perinatal morbidity and mortality. In many cases the etiology of preterm labor is unknown. However, much interest has been generated surrounding the infectious causes of preterm labor. Because data suggest that preterm labor is preceded by a cascade of complex events, in vivo observations in humans and in vitro experiments using human tissue may not be sufficient to answer questions regarding its etiology. The murine model holds significant promise in delineating the chronology and specifics regarding the events precipitating preterm labor