This report describes the development of an experimental head injury model capable of producing diffuse brain injury in the rodent. A total of 161 anesthetized adult rats were injured utilizing a simple weight-drop device consisting of a segmented brass weight free-falling through a Plexiglas guide tube. Skull fracture was prevented by cementing a small stainless-steel disc on the calvaria. Two groups of rats were tested: Group 1, consisting of 54 rats, to establish fracture threshold; and Group 2, consisting of 107 animals, to determine the primary cause of death at severe injury levels. Data from Group 1 animals showed that a 450-gm weight falling from a 2-m height (0.9 kg-m) resulted in a mortality rate of 44% with a low incidence (12.5%) of skull fracture. Impact was followed by apnea, convulsions, and moderate hypertension. The surviving rats developed decortication flexion deformity of the forelimbs, with behavioral depression and loss of muscle tone. Data from Group 2 animals suggested that the cause of death was due to central respiratory depression; the mortality rate decreased markedly in animals mechanically ventilated during the impact. Analysis of mathematical models showed that this mass-height combination resulted in a brain acceleration of 900 G and a brain compression gradient of 0.28 mm. It is concluded that this simple model is capable of producing a graded brain injury in the rodent without a massive hypertensive surge or excessive brain-stem damage.

Healthy adults who had not been exposed to antimicrobial agents for the preceding 4 weeks were examined for intestinal carriage of Clostridium dif®cile. The 1234 individuals examined were composed of seven groups: three classes of university students, hospital workers at two hospitals, employees of a company and self-defence force personnel at a local station. Overall, 94 (7.6%) individuals were positive for C. dif®cile by faecal culture but carriage rates among the study groups ranged from 4.2% to 15.3%. Typing by PCR ribotyping and pulsed-®eld gel electrophoresis demonstrated clusters of carriers colonised by a single type in each of three groups, indicating that cross-transmission of C. dif®cile can occur in community settings. Follow-up culture was performed on 38 C. dif®cile-positive individuals and C. dif®cile was isolated again from 12 (32%) of them 5± 7 months after the initial culture; six (50%) of these 12 individuals had a new strain on repeat culture. Two or more family members were C. dif®cile-positive in ®ve of 22 families examined. C. dif®cile with an identical type was isolated from persons within a family in only one family. These results suggest that intestinal carriage by healthy adults may play a role as a reservoir for community-acquired C. dif®cile-associated diarrhoea, but that cross-transmission of C. dif®cile does not occur frequently among family members at home.

The aim of the present study was to investigate the colonization status of Clostridium difficile in healthy individuals. In total, 139 healthy adults from two study groups were examined at intervals of 3 months. Among the 18 positive subjects, the number of subjects from whom C. difficile was isolated once, twice, three times or four times was 10 (55 . 6 %), three (16 . 7 %), two (11 . 1 %) and three (16 . 7 %), respectively. In the student group, different subjects were colonized by different PCR ribotype/PFGE types. However, the same PCR ribotype/PFGE types of C. difficile were isolated from different subjects in the employee group, indicating that cross-transmission may have occurred in this group. Continuous colonization by the same PCR ribotype/PFGE type was only observed in three subjects. C. difficile-positive subjects were significantly more densely colonized by enterococci (P , 0 . 05) than C. difficile-negative subjects: subjects that were found to be C. difficile-positive three or four times appeared to have higher concentrations of enterococci. The present results demonstrate that, although colonization by a C. difficile strain is transient in many cases, there are healthy individuals that are colonized persistently by C. difficile. They also suggest that dense colonization of the intestine by enterococci may be associated with C. difficile colonization.

These results suggest that mitoK ATP channels are downstream of PKC in the mechanism of infarct-size limitation by A1-receptor activation and that the anti-infarct tolerance afforded by opening of mitoK ATP channels is associated with preservation of mitochondrial function during ischemia/reperfusion.