A three-year posthospital follow-up of adolescent and adult schizophrenics.
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Biomedical subjects
Publications and source records attributed to M Pollack.
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Exotoxin A is an extracellular enzyme that is produced by most clinical strains of Pseudomonas aeruginosa. It is a single-chain polypeptide (molecular weight, 71,000) with A and B fragments that mediate enzymatic and cell-binding functions, respectively. Exotoxin A catalyzes the transfer of the adenosine diphosphate-ribosyl moiety from nicotinamide-adenine dinucleotide to elongation factor 2, which results in the inactivation of the latter and the inhibition of protein biosynthesis. Exotoxin A is a potent cytotoxin and is lethal for a variety of animals, including subhuman primates. Produced in vivo during P. aeruginosa infections, exotoxin A apparently causes disease by inhibition of protein synthesis, direct cytopathic effects, and interference with cellular immune functions of the host. Antibodies to exotoxin A provide protection from some of the biochemical, pathologic, and lethal consequences of both experimental and clinical pseudomonas infections. Toxoid produced from exotoxin A is currently undergoing evaluation as a vaccine for possible use in the immunoprophylaxis against pseudomonas disease in humans.
Pseudomonas aeruginosa is an opportunistic pathogen whose adaptability, ubiquitousness, and pathogenicity are closely related. Both cell-associated and extracellular products of P. aeruginosa contribute to its virulence. Surface structures, including pili and the polysaccharide capsule or glycocalyx, appear to mediate the initial attachment of P. aeruginosa to its prospective host, thus permitting colonization. Extracellular enzymes such as alkaline protease, elastase, phospholipase C, and exotoxin A degrade infected tissues and promote bacterial invasion. When dissemination occurs, systemic disease results, often with fatal consequences. Although extracellular enzymes of P. aeruginosa figure prominently in local disease processes, exotoxin A and endotoxin are primarily responsible for systemic disease. The most protective antibodies presently known are directed toward the nontoxic portions of P. aeruginosa lipopolysaccharides that serve no known virulence function per se. However, there is preliminary evidence that the protective activity of these opsonic antibodies may be augmented by toxin-neutralizing antibodies directed toward the lipid A moiety of endotoxin and exotoxin A.
Control measures based on careful hospital surveillance are aimed primarily at minimizing environmental sources of Pseudomonas aeruginosa. Other important aspects of epidemiologic control include aggressive evaluation of outbreaks and limitation of antimicrobial use. Potent new antimicrobial chemotherapy has been developed, with most new agents of the beta-lactam and aminoglycoside classes. In spite of these developments, the likelihood of drug resistance seems great and the search for novel compounds continues. Of greatest appeal are approaches that augment host defences. Replacement or supplementation of circulating phagocytic cells is conceptually attractive, but this approach has encountered major technical problems and complications. More recently, there has been important progress in developing immunologic approaches aimed at augmenting circulating antibodies. Development of monoclonal antibodies and new methods for preparing hyperimmune globulins has produced forms of intervention that must be tested by clinical trials, but not all patients may benefit from augmentation of circulating antibodies to P. aeruginosa.
One case of choledochocele is reported, and the findings on CT, endoscopic retrograde cholangiopancreatography, and surgery are described. At surgery, in addition to choledochocele, a large choledochal cyst in the proximal common bile duct was discovered. Choledochocele can be diagnosed by CT and can be recognized by the finding of a cystic mass contiguous with the distal common bile duct that invaginates into the contrast-filled duodenum.
An infant born with multiplex congenita (Larsen's) syndrome developed respiratory distress 30 days following tracheostomy for relief of upper airway obstruction. The infant had structural and functional abnormalities of the thoracic cage. Tracheobronchoscopy revealed excessive compliance of the trachea with a tendency for collapse of the tracheal rings and obliteration of the tracheal lumen. Continuous positive airway pressure in the range of 20-25 cm H2O was used to maintain patency of the tracheal lumen and assure adequate ventilation. Hemodynamic and pulmonary barometric complications often observed when high levels of positive airway pressure are utilized in infants were not observed.