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Y Ni

Publications and source records attributed to Y Ni.

112 records · Page 7Linked to original sources

Role of contrast agent perfusion and of diffusion in the NMR signal enhancement of liver lesions.

Both perfusion and diffusion contribute to NMR signal enhancement after intravenous injection of a nonspecific contrast agent. In the present study the roles of perfusion and diffusion in the contrast enhancement of induced liver lesions in the rat and the rabbit were evaluated. This was done by comparing Gd-DOTA absolute enhancement signal-to-noise versus time plots of various lesions with the findings from microangiography and histology. Four types of enhancement could be recognized. Diffusion was the major factor in the delayed enhancement seen in lesions that had large extravascular diffusion space.

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Mn-DPDP enhanced MRI in experimental bile duct obstruction.

To assess both the effect of Mn-DPDP as a hepatobiliary-specific contrast agent in bile duct obstruction and the relative role of liver and kidney in the elimination of this agent from the body, an animal experiment was set up. Twelve rats were used and divided into three groups. In group 1 the common bile duct was ligated, in group 2 bile duct ligation was limited to one lobe, and group 3 served as control. Magnetic resonance T1-weighted SE images were obtained before and after the injection of 25 mumol/kg of Mn-DPDP during the first 2 h and at day 1, 2, 3, 4, and, in some animals, up to 21 days. In normal rats the absolute enhancement signal-to-noise ratio (S/N) versus time plots obtained from the liver after Mn-DPDP injection returned to precontrast values within 24 h. In the group with common bile duct ligation, important liver enhancement persisted up to 21 days. In the group with selective obstruction, liver intensity normalized after 3 days. The S/N plots from spleen, renal cortex, and obstructed liver lobe showed similarities in time course. The present data indicate that Mn elimination is strongly impaired in the presence of bile duct obstruction. Renal glomerular filtration is ineffective in eliminating Mn from the body. The persisting splenic and renal cortical enhancement suggests that free Mn or some Mn-DPDP metabolite either is strongly bound to plasma proteins and acts as a blood pooling agent and/or is uptaken by the splenic or renal parenchyma.

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Characterization of avian reovirus strain-specific polymorphisms.

Avian reoviruses have been associated with several pathologic conditions, but correlative relationships between genotypes and specific diseases have not been demonstrated. Six avian reoviruses (883, 176, 81-5, S1133, FC, and TX) were selected for this study, and a comparative study of the pathogenic properties of the viruses in chickens, following peroral and footpad inoculation, was carried out, along with a comparison of the electrophoretic mobility of viral genomic segments and viral proteins encoded by the gene segments. The pathogenic properties of the viruses were shown to be diverse, with three distinct pathotypes being defined: Pathotype I (883) caused only a syndrome that we have termed "transient digestive system disorder" (TDSD); Pathotype II (FC, TX, and S1133) caused only "viral arthritis syndrome" (VAS), whereas Pathotype III (176 and 81-5) caused both TDSD and VAS. Likewise, the genomes of the viruses were shown to be extremely polymorphic, with a maximum of five segments co-migrating between any two strains. Considerable variation in the electrophoretic mobility of the encoded proteins also was demonstrated with pronounced variation in the molecular size of the sigma 4 protein, the purported viral attachment protein, being evident. These results show that the genomes of avian reoviruses were extremely polymorphic, preventing correlation between genotypes and pathotypes. But these studies have provided us with the genetic elements needed to characterize the gene functions involved in viral pathogenesis.

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A comparative study of avian reovirus pathogenicity: virus spread and replication and induction of lesions.

This study examined the relationship of avian reovirus spread and replication to induction of lesions and the relevant role of the S1 segment encoding a virus-neutralizing antigen. One-day-old broiler chickens were infected via footpad or orally with two virus strains (883 and 176) that differ greatly in virulence and a reassortant (R44) that has the S1 segment from 176 and the remaining genome segments from 883. Virus replication and histological lesions in various tissues (heart, liver, spleen, kidney, bursa, hock joint, and bone marrow) were measured at 2-day intervals until day 8 postinoculation. The virulent strain 176 spread to and replicated efficiently in all tissues examined and caused extensive and severe lesions, whereas the mild strain 883 was detected only in tissues near inoculation sites and caused only minimal lesions. The appearance of lesions correlated with the presence of viral replication in each tissue tested. Together, these results indicate that induction of lesions, or pathogenicity, is directly related to virus spread and replication. Reassortant R44 behaved like strain 176 in chicken embryo fibroblasts (CEFs), i.e., both replicated much faster and produced larger plaques than strain 883. In broiler chickens, however, R44 behaved like strain 883, replicating and inducing lesions to an extent that was fat lower than that of strain 176. These results suggest that the S1 segment alone is capable of determining viral replication and plaque formation in cultured CEFs but is not sufficient to determine the virus spread and replication and the pathological change in broiler chickens.

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