Control of early viral and bacterial distribution and disease by natural antibodies

Natural antibodies are often dismissed from immunological analysis as "background," but they may play an important role in conferring immunity against infections. In antibody-free mice infected with various viruses or with Listeria monocytogenes, viral or bacterial titers in peripheral organs, including the kidney and brain, were 10 to 100 times greater than in antibody-competent mice (and enhanced their susceptibility to some infections), and titers in secondary lymphoid organs were 10 to 100 times lower than in antibody-competent mice. Thus, natural antibodies play a crucial role by preventing pathogen dissemination to vital organs and by improving immunogenicity through enhanced antigen-trapping in secondary lymphoid organs.     

Dimensionality control of electronic phase transitions in nickel-oxide superlattices

The competition between collective quantum phases in materials with strongly correlated electrons depends sensitively on the dimensionality of the electron system, which is difficult to control by standard solid-state chemistry. We have fabricated superlattices of the paramagnetic metal lanthanum nickelate (LaNiO(3)) and the wide-gap insulator lanthanum aluminate (LaAlO(3)) with atomically precise layer sequences. We used optical ellipsometry and low-energy muon spin rotation to show that superlattices with LaNiO(3) as thin as two unit cells undergo a sequence of collective metal-insulator and antiferromagnetic transitions as a function of decreasing temperature, whereas samples with thicker LaNiO(3) layers remain metallic and paramagnetic at all temperatures. Metal-oxide superlattices thus allow control of the dimensionality and collective phase behavior of correlated-electron systems.     

ECTRODACTYLY (SPLIT-HAND DEFORMITY) IN THE DOG

Radiographs of 14 dogs with ectrodactyly of the forelimb were evaluated and the defect classified according to the site of division of the longitudinal axis of the paw. The majority of separations occurred between metacarpal bones one and two, although separations were also noted between metacarpal bones two and three, two and four, and three and four. Other lesions noted in affected limbs included digit contracture, digit aplasia, metacarpal hypoplasia and metacarpal fusions. Bilateral involvement was noted in only one of 14 cases. No breed or sex predisposition was found and there was equal involvement of the left and right limbs.     

Oropharyngeal dysphagias in the dog: A cinefluorographic analysis of experimentally induced and spontaneously occurring swallowing disorders

Cinefluorography and videofluorography were used to record and analyze functional swallowing deficits of 12 dogs with spontaneously occurring oropharyngeal dysphagias and six experimental dogs with selected neurectomies. Ten of the 12 dogs had dysphagias affecting the cricopharyngeal stage of the oropharyngeal phase of swallowing. Two dogs had mixed oropharyngeal dysphagias. Clinical signs of cricopharyngeal dysphagia could not be differentiated from those of dysphagias due to pharyngeal or mixed oropharyngeal deficits. Signs of cricopharyngeal dysphagia consisted of: 1) repeated attempts to swallow; 2) excessive head movement; 3) dropping food from the mouth after unsuccessful swallowing attempts; 4) reingestion of dropped food. Nine of these dogs had cinefluorographic evidence of asynchrony between the normal pharyngeal contraction and relaxation, and subsequent cricopharyngeal relaxation and contraction. Only one dog demonstrated a consistent cricopharyngeal non-opening (achalasia). Seven of the dogs responded dramatically to cricopharyngeal myotomy. Two dogs with mixed oropharyngeal dysphagias had poor contractility of the pharyngeal muscles in addition to cricopharyngeal dysphagia. Clinical and cinefluorographic evaluation following cricopharyngeal myotomy of one dog verified exacerbation of functional deficits due to the iatrogenic cricopharyngeal chalasia. Esophagopharyngeal reflux accentuated the contrast medium retention in the pharynx and laryngotracheal aspiration. The need was stressed for careful differentiation between cricopharyngeal dysphagia and dysphagias involving the pharyngeal stage. Four experimental dogs with selective bilateral neurectomies of branches of the glossopharyngeal (IX) and vagus (X) nerves were evaluated clinically and cinefluorographically in an attempt to identify the pathogenesis of cricopharyngeal dysphagia. The variable results in the four dogs and the observed recovery in two dogs suggested that peripheral motor nerve deficits are not a major cause of cricopharyngeal dysphagia. Glossopharyngeal neurectomy in two dogs induced a profound functional disorder involving the pharyngeal and cricopharyngeal stages and the esophageal phase of swallowing. This would support a new hypothesis that the glossopharyngeal nerve is sensory to the esophagus as well as the pharynx, and may play a major role in disorders of the pharynx, upper esophageal sphincter, and esophagus, including congenital or acquired megaesophagus.     

Congenital portosystemic shunt in dogs and cats

An overview of the circulation of the liver and of the pathogenesis of hepatic encephalopathy as a result of portal vascular anomalies is given. Clinical signs associated with portal systemic shunts are described on the basis of 16 cases, 14 dogs and 2 cats. These animals ranged in age at the time of presentation from 4 months to 7 years. The predominant abnormality observed were central nervous signs, which differed in severity. The different techniques of contrast angiography allowing demonstration of a portal systemic shunt are presented along with a discussion of the pros and cons of each. Additionally the significance of making portal venous pressure measurements prior to each angiography is also explained. In most cases mesenteric portography was chosen. Based on their location the anomalies could be categorized as intrahepatic (4 dogs) or extrahepatic (10 dogs, 2 cats). In both groups breeds of various size are represented. The extrahepatic shunts could be further described as portal-caval (n = 5), portal-phrenic (n = 4) and portal-azygos (n = 3). In five of the older animals angiography showed in addition some hepatic perfusion by the portal vein. Laboratory evaluation revealed increased resting blood ammonia concentrations (greater than 200-912 micrograms/100 ml) in all animals. Seven dogs had definitely subnormal BUN concentrations (less than 10 mg%) and ten dogs low total plasma protein levels (less than 5.4 g%). Free amino acids (24) were determined in four dogs and a lowered hepatic encephalopathy index (less than 1.64) found. Medical palliative therapy to control the clinical signs is discussed. The only effective long term therapy is, however, surgery. The shunt vessel is narrowed so that a greater volume of portal blood reaches the liver. Experience gained from the surgical therapy of 14 animals is presented. Ten of these survived well without requiring further therapy at a later time. Finally the etiology, prognosis, and differential diagnosis are summarized.     

Further purification and characterisation of horse IgE

Horse IgE was isolated from a serum pool collected from foals naturally infected with endoparasites. The serum was precipitated with ammonium sulfate, delipidated with dextran sulfate and further purified by gel filtration, anionic exchange, immunosorption or preparative polyacrylamide gelelectrophoresis. By these methods IgE could be isolated at a purity of 81%. The sera from rabbits immunized with the purified horse serum fractions were tested using reversed passive cutaneous anaphylaxis and an enzyme linked immunosorbent assay (ELISA). By the ELISA method cross reaction of rabbit anti horse IgE sera to human, mouse and rat myeloma IgE was demonstrated. Rat myeloma IgE also served to monitor the production of antibodies to horse IgE in rabbits.     

Blood catalsase polymorphism: some immunological aspects

The immunological properties of the erythrocyte catalase of mice-normal (wild type) strain, one lacking catalase (acatalasemic), and four with only slight catalase activity (hypocatalasemic strains)-have been investigated. Agardiffusion tests and antigen titration of red-cell lysates against rabbit antiserum to catalase from normal mouse blood showed that immunologically identical catalase protein was present in large amounts in the acatalasemic as well as in the hypocatalasemic mutant strains. Despite lack of catalatic activity, the erythrocytes lacking catalase as well as those with only a little catalase contain catalase protein that has been modified at the site of enzyme activity, although the antigenic determinants are identical with those of normal catalase protein. This mutation is purely structural, being characterized by modification of the enzyme active site but not of the antigenic site.