A computer program is written for the calculation of differential neutron flux spectra in the high energy region. This program utilizes as input data the saturated specific activity of threshold foil detectors, the cross section as a function of energy for the foil's primary reaction, and a first guess of the incident neurtron flux spectrum. The program is an iterative type not depending upon the assumption of any particular spectrum shape. Output data consists of the differential neurtron flux energy spectrum and error statement. Experience has shown that this program converges after a few iterations to within 10 percent of the spectrum given by the last previous iteration. (Author)
No abstract is provided for this article.
The plastic collapse response of structural steel elliptical hollow section (EHS) profiles in compression is examined in this paper. As an initial step, a parametric study to identify the factors that determine which plastic mechanisms would arise has been carried out using finite element (FE) results from the current work and experimental data from the literature. Following this, an analytical model to describe the split flip disc plastic collapse mechanism in compressed EHS is derived. The parameters controlling the shape and size of the plastic hinges have been investigated and found to be of key importance; hence, special care has been taken in their definition. Finally, the analytically derived load- displacement curves have been compared with FE results. The comparisons have revealed good agreement, confirming the ability of the developed analytical models to predict the plastic collapse response of elliptical tubes.
The Second Edition of Asthma and COPD: Basic Mechanisms and Clinical Management continues to provide a unique and authoritative comparison of asthma and COPD. Written and edited by the world's leading experts, it continues to be a comprehensive review of the most recent understanding of the basic mechanisms of both conditions, specifically comparing their etiology, pathogenesis, and treatments. Each chapter considers Asthma and COPD in side-by-side contrast and comparison not in isolation - in the context of mechanism, triggers, assessments, therapies, and clinical management. This title presents the latest and most comprehensive understandings of the mechanisms of inflammation in both Asthma and COPD. It provides most extensive reference to primary literature on both Asthma and COPD in one source. It offers easy-to-read summaries of the latest advances alongside clear illustrations.
No abstract is provided for this article.
Tolerance to the direct bronchodilator effects of β2-agonists does not appear to occur in asthma. However, it is not known whether this is true for the nonbronchodilator effects of these agents, which protect the airways against bronchoconstrictive stimuli.
Summary Human granulocyte–macrophage colony‐stimulating factor (GM‐CSF) reporter constructs containing up to 3·3 kb of upstream promoter sequence were transiently transfected into both Jurkat and HUT78 human T‐cell lines. In Jurkat cells, stimulation with phorbol 12‐myristate 13‐acetate (PMA) plus phytohemaglutinin (PHA) produced robust increases in reporter activity, whereas HUT78 cells showed low levels of reporter induction attributable to constitutive nuclear factor (NF)‐κB activity. Following mutation of either the proximal NF‐κB site (−85/−76) or the activator protein1 (AP‐1) motif within the conserved lymphokine element 0 (CLE0) site (−54/−31), reporter activity was markedly reduced in both cell lines. Despite this dependence on NF‐κB and CLE0/AP‐1, GM‐CSF reporter activity was unaffected by dexamethasone in either cell line. Similarly, an NF‐κB‐dependent reporter was also not repressed by dexamethasone, yet GM‐CSF release from HUT78 T cells was inhibited. These data therefore confirm a critical role for both NF‐κB and CLE0 sites in GM‐CSF promoter activation and indicate that NF‐κB may not mediate glucocorticoid‐dependent repression of GM‐CSF in these cells.
To assess the inter- and intra- observer reproducibility for strut count, strut apposition and strut tissue coverage measurements with optical coherence tomography (OCT).Ten drug-eluting stents (244 frames, 1712 struts) imaged with OCT nine months after implantation were analysed by two independent analysts. One of the analysts repeated the analysis of five stents (120 frames, 795 struts) one week later. Offline analysis was performed with the proprietary LightLab Imaging software. The number of struts was counted and lumen and stent area contours were traced. Tissue coverage thickness was measured at 360 degrees of vessel circumference and in front of every individual strut. The number of malapposed struts was determined. There was good agreement for strut number count (Kendall's Tau-b 0.90 for inter- and 0.94 for intra- observer variability). The relative difference for lumen area, stent area and tissue coverage measurements was around 1%. There was complete inter- and intra- observer agreement for malapposed struts classification (4 out of 1708 struts, Kappa=1).In a Corelab setting, the inter- and intra- observer reproducibility for strut count, strut apposition and strut tissue coverage measurements with OCT is excellent. This emphasises the value of OCT as a tool for the clinical long-term assessment of stents.
Abstract Selected, extended paper from the SDSS 2019 special session ECCS/TC8 – Structural Stability This paper presents the development and assessment of an innovative cross‐section design method for structural steel circular and elliptical hollow sections (CHS and EHS) – the generalised slenderness‐based resistance method (GSRM). A numerical simulation programme was first conducted to expand the data pool for CHS and EHS. Finite element (FE) models were established, validated against existing test data and then utilised for parametric studies, where a total of over 3 700 cross‐section resistance data were numerically generated. The development of the GSRM for CHS and EHS is then presented. Key design parameters, including the reference resistances and the generalised local slenderness, are initially defined. The general design procedure is subsequently introduced. Two design alternatives for CHS and EHS – a strength‐based approach, and a deformation‐based approach based on the continuous strength method (CSM), are developed and presented. Finally, the proposed GSRM is assessed using the previously collected test results and freshly generated FE data, where excellent accuracy and consistency in the resistance predictions are clearly revealed for all loading scenarios. Subsequent reliability analyses demonstrate that the current partial safety factor used in EN 1993‐1‐1 can be applied to the GSRM, achieving an appropriate level of reliability.
INTRODUCTION Spontaneous perforation of the bile duct (SPBD) or idiopathic bile duct perforation is a rare but potentially fatal disorder that requires urgent diagnosis and management. Most of the cases present insidiously in infancy, although as in our case, SPBD can occur in an older child. The more common case presentation is a healthy infant developing progressive symptoms. Less commonly, the presentation is that of an acute surgical abdomen. The typical age of patients with SPBD is between 2 and 20 weeks, although the age range varies from birth to 7 years (2,3,5–7,9–18). Although the etiology is often unknown, distal biliary obstruction from either a stone or stricture is a postulated mechanism. In cases of suspected distal biliary obstruction, biliary intestinal anastomosis is recommended (2,6,8,10–15). We present a case of a 34-month-old male who presented with an acute abdomen. Radiographic studies suggested a bile leak, and the patient was taken emergently to endoscopic retrograde cholangiopancreatography (ERCP) which provided the diagnosis of a bile duct leak at the junction of the common and cystic duct and allowed decompression and endoscopic treatment. CASE REPORT A 3-year-old, former 26-week preterm male infant presented to the emergency department after a 2-day history of abdominal pain, nausea and vomiting. The patient had been well until the acute onset 2 days before admission of postprandial pain, nausea and multiple episodes of nonbloody, nonbilious emesis. On the day before admission, he was diagnosed with acute gastroenteritis with instructions for home oral hydration. Continued pain and vomiting resulted in dehydration and hospital admission. There was no history of fever, respiratory symptoms, diarrhea, rash, ill contacts, possible ingestions or abdominal trauma. The patient had been receiving levothyroxine for hypothyroidism of prematurity since the neonatal period. The patient was twin B of a 26-week gestation and received approximately 12 weeks of intravenous nutrition in the neonatal intensive care unit. Twin A died during the neonatal period awaiting liver and small-bowel transplantation for cirrhosis and short-bowel syndrome after necrotizing enterocolitis. During physical examination, the patient was febrile, tachycardic, tachypneic and irritable. The patient weighed 15 kg. The abdomen was distended with voluntary guarding and severe discomfort with palpation and percussion. There was no hepatosplenomegaly, mass or palpable ascites. The rest of the examination findings was normal. Laboratory evaluation showed leukocytosis (18 000/μL), a normal platelet count and hemoglobin. Serum bicarbonate was 12 mmol/L; potassium, 3.0 mmol/L; glucose, 130 mg/dL; blood urea nitrogen, 18 mg/dL; aspartate aminotransferase, 132 IU/L; alanine aminotransferase, 178 IU/L; alkaline phosphatase, 366 IU/L; total bilirubin, 2.2 mg/dL and conjugated bilirubin, 0.5 mg/dL. The remainder of the serum chemistries, albumin, amylase and lipase were normal. Prothrombin time was elevated at 16.4 seconds. A computed tomographic scan of the abdomen with intravenous contrast (Fig. 1) showed a distended gallbladder with a significant amount of fluid surrounding the portahepatis, mesenteric edema and a dilated common bile duct of approximately 5 mm with a stone at the duodenal papilla. Intravenous fluid resuscitation and broad-spectrum antibiotics were started.FIG. 1: Computed tomographic scan image at initial presentation. Black arrow demonstrates common bile duct stone at duodenal papilla and adjacent fluid in peritoneal space.Because of a suspected perforation of the bile duct, the patient underwent emergent ERCP performed under general anesthesia. An Olympus TJF-160 duodenoscope was used to cannulate the major papilla with a sphincterome, and contrast injection demonstrated 2 small stones in the distal common bile duct. A sphincterotomy was performed over a guide wire, and the stones were extracted with a balloon extraction catheter. A balloon occlusion cholangiogram demonstrated a bile leak at the region of junction of the common hepatic duct and cystic duct (Fig. 2). A 5-cm 7F internal biliary stent was deployed across the leak.FIG. 2: Endoscopic retrograde cholangiopancreatography image after cholangiographic injection. White arrow demonstrates bile leak as white blush. Black arrow demonstrates 2 stones at distal common bile duct.The patient tolerated the procedure well and was treated with intravenous antibiotics, fluids and internal biliary drainage. The ileus and abdominal pain resolved by postoperative day 4, and the patient was discharged on day 7. Of note, the patient had no previous imaging studies, laboratory evidence or symptoms suggestive of choledocholithiasis despite such risks as prematurity and total parenteral nutrition. One month after discharge, the stent was removed at endoscopy, and a repeat cholangiogram was concerning for a possible stricture at the level of the common hepatic duct. The patient remained asymptomatic without further therapy. Six weeks later, the result of abdominal ultrasound was normal without evidence of ductal dilatation. The patient's clinical course and liver function test results, including γ-glutamyl transpeptidase, have remained normal for 11 months. DISCUSSION Although uncommon, SPBD is frequently cited as the second most common indication for jaundice requiring surgical intervention in infancy (2,3,5–15). Since the initial description by Dijkstra (1) in 1932, there have been approximately 150 cases described in the literature. Most of the patients have a normal newborn and perinatal course and present with insidious symptoms including abdominal distension, ascites, fluctuating acholic stools and jaundice, poor weight gain, emesis, intermittent fever, irritability and abdominal or inguinal hernias that can become progressively bile stained (2,3,6–9,11,13–18). Laboratory studies are variable but may be helpful. Serum aminotransferase levels and bilirubin can be normal or elevated, although alkaline phosphatase and γ-glutamyl transpeptidase are often elevated. There may be leukocytosis, anemia, thrombocytosis and elevations of inflammatory markers (2–9,11–17). Ultrasonography or abdominal computed tomography can identify ascites and biliary ductal dilatation, stones or sludge (2,4,6,8,15–17). If the patient is clinically stable, a radionucleotide hepatobiliary scan (ie, cholescintigraphy) is highly sensitive and specific for a bile duct leak (2–4,6–10,14–17). Spontaneous perforation of the bile duct is somewhat of a misnomer as the “spontaneity” of the perforation may be secondary to one or multiple etiologies as in our patient. These include trauma, ischemia, infection, distal bile duct stenosis or obstruction secondary to stones or sludge, reflux of pancreatic secretions secondary to pancreaticobiliary malformations and congenital malformation or weakness of the bile duct wall (2–15,17,18). First proposed by Johnston (18) in 1961 and further expanded by Lilly et al. (5) in 1974, the most commonly accepted unifying theory is that there exists a localized embryogenic defect at the junction of the common bile duct and cystic duct that is susceptible to a variety of insults and therefore prone to rupture. Most of perforations are on the anterior wall of the common bile duct at the junction of the cystic duct (2,4,5,8,9,11–15,17,18). Previously, there was almost universal consensus in the literature supporting surgical intervention for SPBD (2–18). During the initial exploration, an operative cholangiogram is performed to ascertain the location of the perforation and to assess for distal obstruction (2,3,5–8,10,11,13–15,17). For nonobstructive perforation of the common or hepatic duct, drainage of the biliary leak is recommended by placing an external drain at or near the site of the perforation without intervention to the bile duct itself (2,4–17). A cholecystostomy tube may be placed for postoperative management until the perforation has sealed (2,5–8,12,15,17). With simple conservative drainage, most of the perforations seal with decompression and drainage (2,4–15,17). In cases of SPBD with distal biliary obstruction unrelieved by the cholangiogram, most authors recommend a biliary-intestinal anastomosis (2,6–8,10–15,17). Surgical repair of the bile duct is controversial because of possible biliary stricture formation postoperatively, and T-tube drainage is no longer recommended (2,5,13,16). Endoscopic retrograde cholangiopancreatography has been a useful diagnostic and therapeutic procedure in children since the 1980s (19). Endoscopic retrograde cholangiopancreatography has long been used to both diagnose and treat choledocholithiasis (20–24). To date, we are unaware of any reports in the literature describing the role of ERCP in the diagnosis and primary treatment of SPBD in children. In our case, ERCP was used as the initial cholangiographic technique and the primary therapy, sparing the need for exploratory surgery. Although there are relatively few centers with the resources and personnel available for pediatric ERCP, this experience suggests that when the proper equipment and endoscopic expertise are available, ERCP may be an alternative therapy of SPBD in infants and children.
