Acute injury of the ligaments of the knee: magnetic resonance evaluation

Eleven acutely injured knees and 13 normal knees were examined by magnetic resonance imaging (MRI) to assess the value of this modality in detecting acute ligamentous injury of the knee. The presence of torn ligaments in the injured knees was determined by arthroscopy and/or arthrotomy in ten cases and clinical follow-up in one case. The anterior and posterior cruciate ligaments (ACL and PCL) were demonstrated by sagittal spin echo (SE) images through the intercondylar notch (TE = 30 ms; TR = 2,000 ms). The tibial and fibular collateral ligaments (TCL and FCL) were evaluated on coronal SE images (TE = 30 ms, TR = 200 or 530 ms; TE = 120 ms, TR = 2,000 or 2,120 ms). The ACL and PCL were considered torn on MR if they appeared disrupted or were not seen in their normal anatomical positions. The collateral ligaments were considered torn if abnormal high-intensity signal was noted in adjacent soft tissues on TE = 120 ms images or if disruption of a ligament was apparent. Eleven of 15 torn ligaments and 80 of 81 normal ligaments were correctly identified by these criteria. It is concluded that MR imaging may be useful in detecting acute injury of ligaments of the knee.     

Inhibition of Salmonella typhimurium Invasion by Host Cell Expression of Secreted Bacterial Invasion Proteins

Pathogenic Salmonella species initiate infection of a host by inducing their own uptake into intestinal epithelial cells. An invasive phenotype is conferred to this pathogen by a number of proteins that are components of a type III secretion system. During the invasion process, the bacteria utilize this secretion system to release proteins that enter the host cell and apparently interact with unknown host cell components that induce alterations in the actin cytoskeleton. To investigate the role of secreted proteins as direct modulators of invasion, we have evaluated the ability of Salmonella typhimurium to enter mammalian cells that express portions of the Salmonella invasion proteins SipB and SipC. Plasma membrane localization of SipB and SipC was achieved by fusing carboxyl- and amino-terminal portions of each invasion protein to the intracellular carboxyl-terminal tail of a membrane-bound eukaryotic receptor. Expression of receptor chimeras possessing the carboxyl terminus of SipB or the amino terminus of SipC blocked Salmonella invasion, whereas expression of their chimeric counterparts had no effect on invasion. The effect on invasion was specific for Salmonella since the perturbation of uptake was not extended to other invasive bacterial species. These results suggest that Salmonella invasion can be competitively inhibited by preventing the intracellular effects of SipB or SipC. In addition, these experiments provide a model for examining interactions between bacterial invasion proteins and their host cell targets.     

Regneration in free grafts of normal and denervated muscles in the rat: morphology and histochemistry.

Intact soleus and extensor digitorum longus muscles in the rat were freely grafted to the contralateral leg after either no preliminary treatment or 14 days prior denervation. Normal muscle grafts during the first week were characterized by a central zone of degenerating original muscle fibers (disappearing by 7-9 days) and a peripheral zone, containing regenerating muscle as well as small numbers of surviving original muscle fibers. A radial gradient of regeneration was establihed, with more mature muscle at the periphery and less mature muscle toward the center. Denervated grafts were characterized by rapid degeneration (within 2-3 days) of original muscle fibers in the central area, rapid appearance of regenerating muscle fibers (e.g. cross striations by 5 days) with uniform levels of differentiation throughout the graft and larger numbers of surviving original muscle fibers at the periphery. During the first week, stages of muscle differentiation in denervated grafts were attained 1-2 days earlier than comparable stages in normal grafts. Later stages of muscle differentiation were similar in both types of grafts. Histochemical studies revealed a loss of enzyme activity (phosphorylase, ATPase and SDH) in the center of early (2-4-day) normal and denervated grafts. Denervated grafts, however, possessed a thicker peripheral rim of enzymatically active surviving muscle fibers than normal grafts. In both types of grafts the old muscle fibers in the center were replaced by enzymatically active regenerating muscle fibers which stained uniformaly (ATPase) until 30 days. By 60 days a mixed fiber pattern had developed. Muscle spindles were found within the grafts.     

Levels of O6-methylguanine acceptor protein in tissues of rats and their relationship to carcinogenicity and aging

N-nitroso compounds react with cellular DNA to produce various damaging adducts, one of the more important being O6-alkylguanine. DNA restoration is accomplished by transfer of the alkyl group to a cysteine residue of an acceptor protein. The levels of acceptor activity were compared in several tissues from well-fed and dietary-restricted inbred SD rats 30-1,194 days of age. Striking and consistent differences were found in the levels of acceptor activity in different tissues from both groups; these levels corresponded to their sensitivity to tumorigenesis by alkylating agents. Acceptor activity levels were highest in the liver and somewhat less in the spleen; there were significantly lower levels in brain and kidney. The random loss with time in the integrity of DNA may cause alterations in cellular function or limit cellular proliferation, thus leading to senescence and death. DNA repair processes may alter the rate of accumulation of damage, thereby affecting potential longevity. There were no significant age-associated changes in the ability of cells from either dietary group to remove DNA adducts and there was no evidence of alterations in the acceptor protein with age that would compromise its functional activity.     

Stability two years after mandibular advancement with and without suprahyoid myotomy: an experimental study

Ten adult rhesus monkeys underwent mandibular advancement surgery of 4-6 mm with and without suprahyoid myotomy. Serial lateral cephalograms using radiopaque bone markers were obtained during maxillomandibular fixation and for 96 weeks after release of fixation to determine the effects of suprahyoid myotomy on short-term and long-term adaptations in the advanced mandible. The non-myotomy group exhibited a significant reduction in the length of the advanced mandible (relapse) during the fixation period but showed no significant change in mandibular length after release of fixation. The myotomy group exhibited no relapse during the fixation period and after release of fixation displayed a slight but statistically significant increase in mandibular length. This supports the hypothesis that stretching of the suprahyoid musculature as a result of mandibular advancement surgery is a major factor leading to skeletal relapse.     

Epinephrine-induced cardiac arrhythmias in rabbits exposed to trichloroethylene: Potentiation by ethanol

Studies were conducted to examine the role of trichloroethylene metabolites in epinephrine-induced cardiac arrhythmias in rabbits exposed to trichloroethylene. Rabbits were exposed for 1 hr to 2000, 4000, 6000, or 8000 ppm trichloroethylene under dynamic airflow conditions, and epinephrine was infused iv until arrhythmias occurred after 7.5, 15, 30, 45, and 60 min of exposure and also 15 and 30 min postexposure. Serial blood samples collected at these times were analyzed for trichloroethylene and the two major metabolites, trichloroethanol and trichloroacetic acid. Blood levels of trichloroethylene and the incidence of arrhythmias increased with increasing exposure levels of trichloroethylene, while no differences were seen in trichloroethanol and trichloroacetic acid blood levels among groups exposed to 4000, 6000, and 8000 ppm trichloroethylene. Rabbits receiving chloral hydrate (50 mg/kg, iv), a trichloroethylene intermediate metabolite, generated blood levels of trichloroethanol and trichloroacetic acid 40–100 times greater than rabbits that had been exposed to 8000 ppm trichloroethylene but developed essentially no arrhythmias in response to epinephrine. The data indicate that trichloroethylene, rather than its metabolites, sensitizes the rabbit myocardium to epinephrine-induced cardiac arrhythmias.