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Abstract Aim: The aim of this randomised, split-mouth, single-blind study was to determine the efficacy of controlled-release delivery of chlorhexidine gluconate 2.5 mg (PerioChipTM) in patients with residual bleeding pockets (>5 mm) at least 3 months following oral hygiene and root debridement phase therapy. Material and Methods: 26 patients (non-smokers) were screened and potential study sites identified. Clinical parameters recorded at baseline and all subsequent visits were plaque index (PI), pocket probing depth (PPD), bleeding index (BI) and clinical attachment level (CAL). All study sites were debrided using ultrasonic instrumentation. PerioChips (PC) were placed in the selected sites of two quadrants (left or right) whilst identified sites in the remaining quadrants were left without adjunctive antimicrobial treatment. Clinical measurements were made at follow-up visits after 1, 3 and 6 months. Mean changes from baseline in PPD, BI and CAL were calculated with the patient as the experimental unit and comparability between the treatments was determined using t-tests. Results: At baseline there were no significant differences between PC and control sites for mean PI, PD, BI or CAL. The mean (SE) reductions in PPD for PC and control treatments were: 0.47 (0.1), 0.46 (0.1); 0.76 (0.1), 0.55 (0.1); 0.78 (0.1), 0.45 (0.1) for months 1, 3 and 6 respectively. Only at month 6 did the difference between treatments approach statistical significance (p=0.06). Mean (SE) reductions in CAL over the same periods were: 0.17 (0.1), 0.04 (0.08); 0.38 (0.1), 0.21 (0.1); 0.43 (0.1), 0.15 (0.09) p=0.048. Mean (SE) reduction in BI between PC and control treatments only reached statistical significance at 6 months: 1.08 (0.1), 0.59 (0.1) p=0.05. Conclusion: These data suggest that PerioChipTM is beneficial for patients on maintenance therapy although the benefit is not apparent until 6 months after placement. [ABSTRACT FROM AUTHOR]

Objective: We examined the hypothesis that exogenous stimulation with thyrotropin-releasing hormone immediately before umbilical cord clamping can improve thermoregulation in near-term lambs delivered by cesarean. Study Design: Twin lambs were injected with either saline solution alone (control, n = 12) or thyrotropin-releasing hormone in saline solution (n = 16) and were immediately placed in a warm (30 degrees C; n = 14) or cool (15 degrees C; n = 14) ambient temperature. In vivo measurements of temperature control (colonic temperature, oxygen consumption, and incidence of shivering) were then performed during the first 6 hours after birth, in conjunction with plasma thyroid hormone measurements. Brown adipose tissue was then sampled for measurement of uncoupling protein 1 abundance. Results: Plasma triiodothyronine concentrations were significantly higher in lambs treated with thyrotropin-releasing hormone than in control lambs between 3 and 6 hours after birth, as were plasma thyroxine concentrations 1 and 5 hours after birth. Delivery temperature had no effect on plasma thyroid hormone concentrations. At 6 hours after birth the abundance of uncoupling protein 1 was higher in lambs treated with thyrotropin-releasing hormone than in control lambs. Lambs treated with thyrotropin-releasing hormone exhibited a lower incidence of shivering than did control lambs between 5 and 6 hours after birth, and an effect of ambient temperature on the incidence of shivering was observed only in the control group. From 3 to 6 hours after birth colonic temperature was significantly higher in cool-delivered lambs treated with thyrotropin-releasing hormone than in the control group. Oxygen consumption was higher in cool-delivered lambs than warm-delivered lambs, but this was not influenced by thyrotropin-releasing hormone. Irrespective of delivery temperature, lambs treated with thyrotropin-releasing hormone possessed more pericardial adipose tissue and hepatic glycogen than did control lambs. Conclusion: Thyrotropin-releasing hormone treatment stimulated thyroid hormone secretion in the neonatal lamb and improved thermoregulation during the first 6 hours after birth in near-term lambs delivered by cesarean under cool conditions. [ABSTRACT FROM AUTHOR]

Abstract Background Although the epidemiology of scrapie has been broadly understood for many years, attempts to introduce voluntary or compulsory controls to eradicate the disease have frequently failed. Lack of precision in defining the risk factors on farm has been one of the challenges to designing control strategies. This study attempted to define which parts of the annual flock management cycle represented the greatest risk of infection to naive lambs exposed to the farm environment at different times. Results In VRQ/VRQ lambs exposed to infected sheep at pasture or during lambing, and exposed to the buildings in which lambing took place, the attack rate was high and survival times were short. Where exposure was to pasture alone the number of sheep affected in each experimental group was reduced, and survival times were longer and related to length of exposure. Conclusion At the flock level, eradication and control strategies for scrapie must take into account the need to decontaminate buildings used for lambing, and to reduce (or prevent) the exposure of lambs to infected sheep, especially in the later stages of incubation, and at lambing. The potential for environmental contamination from pasture should also be considered. Genotype selection may still prove to be the only viable tool to prevent infection from contaminated pasture, reduce environmental contamination and limit direct transmission from sheep to sheep.

Abstract Background In order to study the sites of uptake and mechanisms of dissemination of scrapie prions in the natural host under controlled conditions, lambs aged 14 days and homozygous for the VRQ allele of the PrP gene were infected by the oral route. Infection occurred in all lambs with a remarkably short and highly consistent incubation period of approximately 6 months. Challenge of lambs at approximately eight months of age resulted in disease in all animals, but with more variable incubation periods averaging significantly longer than those challenged at 14 days. This model provides an excellent system in which to study the disease in the natural host by virtue of the relatively short incubation period and close resemblance to natural infection. Results Multiple sites of prion uptake were identified, of which the most important was the Peyer's patch of the distal ileum. Neuroinvasion was detected initially in the enteric nervous system prior to infection of the central nervous system. At end stage disease prion accumulation was widespread throughout the entire neuraxis, but vacuolar pathology was absent in most animals that developed disease at 6–7 months of age. Conclusion Initial spread of detectable PrP was consistent with drainage in afferent lymph to dependent lymph nodes. Subsequent accumulation of prions in lymphoid tissue not associated with the gut is consistent with haematogenous spread. In addition to macrophages and follicular dendritic cells, prion containing cells consistent with afferent lymph dendritic cells were identified and are suggested as a likely vehicle for carriage of prions from initial site of uptake to the lymphoreticular system, and as potential carriers of prion protein in blood. It is apparent that spongiform change, the characteristic lesion of scrapie and other prion diseases, is not responsible for the clinical signs in sheep, but may develop in an age dependent manner.