No abstract

An H5N1 avian influenza A virus was transmitted to humans in Hong Kong in 1997. Although the virus causes systemic infection and is highly lethal in chickens because of the susceptibility of the hemagglutinin to furin and PC6 proteases, it is not known whether it also causes systemic infection in humans. The clinical outcomes of infection in Hong Kong residents ranged widely, from mild respiratory disease to multiple organ failure leading to death. Therefore, to understand the pathogenesis of influenza due to these H5N1 isolates, we investigated their virulence in mice. The results identified two distinct groups of viruses: group 1, for which the dose lethal for 50% of mice (MLD50) was between 0.3 and 11 PFU, and group 2, for which the MLD50 was more than 103 PFU. One day after intranasal inoculation of mice with 100 PFU of group 1 viruses, the virus titer in lungs was 107 PFU/g or 3 log units higher than that for group 2 viruses. Both types of viruses had replicated to high titers (>106 PFU/g) in the lungs by day 3 and maintained these titers through day 6. More importantly, only the group 1 viruses caused systemic infection, replicating in nonrespiratory organs, including the brain. Immunohistochemical analysis demonstrated the replication of a group 1 virus in brain neurons and glial cells and in cardiac myofibers. Phylogenetic analysis of all viral genes showed that both groups of Hong Kong H5N1 viruses had formed a lineage distinct from those of other viruses and that genetic reassortment between H5N1 and H1 or H3 human viruses had not occurred. Since mice and humans harbor both the furin and the PC6 proteases, we suggest that the virulence mechanism responsible for the lethality of influenza viruses in birds also operates in mammalian hosts. The failure of some H5N1 viruses to produce systemic infection in our model indicates that multiple, still-to-be-identified, factors contribute to the severity of H5N1 infection in mammals. In addition, the ability of these viruses to produce systemic infection in mice and the clear differences in pathogenicity among the isolates studied here indicate that this system provides a useful model for studying the pathogenesis of avian influenza virus infection in mammals.

The purpose of this study was to evaluate the effect of temperature on shrinkage and the histologic properties of glenohumeral joint capsular tissue. Six fresh-frozen cadaveric shoulders were used for this study. Seven joint capsule specimens were taken from different regions from each glenohumeral joint and assigned to one of seven treatment groups (37 degrees, 55 degrees, 60 degrees, 65 degrees, 70 degrees, 75 degrees, 80 degrees C) using a randomized block design. Specimens were placed in a tissue bath heated to one of the designated temperatures for 10 minutes. Specimens treated with temperatures at or above 65 degrees C experienced significant shrinkage compared with those treated with a 37 degrees C bath. The posttreatment lengths in the 70 degrees, 75 degrees, and 80 degrees C groups were significantly less than the pretreatment lengths. Histologic analysis revealed significant thermal alteration characterized by hyalinization of collagen in the 65 degrees, 70 degrees, 75 degrees, and 80 degrees C groups. This study demonstrated that temperatures at or above 65 degrees C caused significant shrinkage of glenohumeral joint capsular tissue. These results are consistent with histologic findings, which revealed significant thermal changes of collagen in the 65 degrees, 70 degrees, 75 degrees, and 80 degrees C groups. To verify the validity of laser application for shrinkage of joint capsule, studies designed to compare these findings with the effects of laser energy must be performed.

Abstract. From a series of experimental studies with pigs (12-16 kg), either pulmonary edema or liver failure emerged as a distinct pathogenetic expression of fumonisin B 1 (FB 1 ) toxicosis. The primary determinant as to which pathogenetic consequence developed was the quantity (dose) of the mycotoxin fed or intubated per kilogram of body weight per day. Pigs intubated with a minimum of 16 mg FB 1 /kg/day developed severe interlobular edema with or without hydrothorax and variably severe pulmonary edema. Pigs intubated with < 16 mg FB 1 /kg/day or pigs fed diets containing 200 mg FB 1 /kg of feed developed marked icterus and hepatocellular necrosis. The spectrum of degrees of severity of pulmonary edema observed in the experimental pigs allowed rational speculation regarding evolution of the pathologic changes.In 1988, the chemical structures of the fumonisins, a group of related mycotoxins elaborated by certain strains of Fusarium moniliforme, were published.

The purpose of this in vivo study was to analyze the short-term tissue response of joint capsule to monopolar radiofrequency energy and to compare the effects of five power settings at 65 degrees C on heat distribution in joint capsule. In 12 mature Hampshire sheep, the medial and lateral aspects of both stifles were treated with monopolar radiofrequency energy under arthroscopic control in a single uniform pass to the synovial surface. The radiofrequency generator power settings were 0, 10, 15, 20, 25, and 30 watts (N = 8/group). The electrode tip temperature was 65 degrees C. Histologic analysis at 7 days after surgery revealed thermal damage of capsule at all radiofrequency power settings. The lesion's cross-sectional area, depth, vascularity, and inflammation were commensurate with radiofrequency power. Tissue damage was indicated by variable inflammatory cell infiltration, fusion of collagen, pyknosis of fibroblasts, myonecrosis, and vascular thrombosis, whereas synovial hyperplasia, fibroblast proliferation, and rowing of sarcolemmal nuclei demonstrated regenerative processes. This study revealed that radiofrequency power settings and heat loss through lavage solution play a significant role in heat distribution and morphologic alterations in joint capsule after arthroscopic application of monopolar radiofrequency energy.