Prostaglandin-Independent Stimulation of Interleukin-6 Production by Fibrinogen Degradation Product D in Perfused Murine Liver

Bacterial endotoxin (LPS) and fibrinogen degradation product D (FDP-D) are both potent stimulators of interleukin-6 (IL-6) production in liver, however, there are differences in their metabolic effects. The aim of the present study was to compare the role of prostaglandins in the enhancement of IL-6 production by LPS or FDP-D in perfused mouse livers. Indomethacin inhibited the effect of LPS significantly but was ineffective in the case of FDP-D. Accordingly, production of prostaglandins D₂ and E₂ was not elevated following the addition of FDP-D, while their formation was increased several fold by LPS. At the same time interleukin-1 (IL-1) production in perfused liver rose markedly upon the addition of FDP-D. It is suggested that prostaglandins are not involved in the effects of FDP-D on the liver. The stimulatory effect of FDP-P on IL-6 production might be the consequence of elevated IL-1 levels.     

Conservative management of duodenal trauma: a multicenter perspective

The experience of eight trauma centers with duodenal injuries was analyzed to identify trends in operative management, sources of duodenal-related morbidity, and causes of mortality. During the 5-year period ending December 1988, 164 duodenal injuries were identified. Patient ages ranged from 5 to 78 years. There were 38 Class I, 70 Class II, 48 Class III, four Class IV, and four Class V injuries. Injury mechanism was penetrating in 102 (62%) patients and blunt in 62. Primary repair of the duodenal injury was performed in 117 (71%) patients, including 27 patients also managed with pyloric exclusion and 12 with tube duodenostomy. Duodenal resection with primary anastomosis was used in six (4%) patients and pancreatoduodenectomy was necessary in five (3%). There were 30 (18%) deaths. The cause of death was uncontrolled hemorrhage from severe hepatic or vascular injuries in 22 (73%) patients. In only two (1%) patients could death be attributed to the duodenal injury; each as the result of duodenal repair dehiscence and subsequent sepsis. Duodenal-related morbidity was documented in 29 (18%) patients, including 22 patients with intra-abdominal abscess, six with duodenal fistula, and five with frank duodenal dehiscence. In summary, this analysis demonstrated: 1) the great majority of duodenal injuries can be managed by simple repair; 2) tube duodenostomy is not a mandatory component of operative treatment; 3) pyloric exclusion is a useful adjunct for more complex injuries; 4) pancreatoduodenectomy is rarely necessary for civilian duodenal trauma; 5) morbidity following duodenal trauma is more dependent on associated intra-abdominal injuries than the extent of duodenal trauma; and 6) mortality following duodenal injuries is primarily related to associated vascular and hepatic trauma.     

Localization of a gene for otosclerosis to chromosome 15q25-q26

Among white adults otosclerosis is the single most common cause of hearing impairment. Although the genetics of this disease are controversial, the majority of studies indicate autosomal dominant inheritance with reduced penetrance. We studied a large multi- generational family in which otosclerosis has been inherited in an autosomal dominant pattern. Five of16 affected persons have surgically confirmed otosclerosis; the remaining nine have a conductive hearing loss but have not undergone corrective surgery. To locate the disease- causing gene we completed genetic linkage analysis using short tandem repeat polymorphisms (STRPs) distributed over the entire genome. Multipoint linkage analysis showed that only one genomic region, on chromosome 15q, generated a lod score >2.0. Additional STRPs were typed in this area, resulting in a lod score of 3.4. STRPs FES (centromeric) and D15S657 (telomeric) flank the 14. 5 cM region that contains an otosclerosis gene.