Manipulating the mandibular distraction site at different stages of consolidation.

PURPOSE: The purpose of this study was to define optimal timing and conditions for correcting an open bite side effect by manipulating the distraction site with orthodontic springs after mandibular distraction. MATERIALS AND METHODS: At 0, 1, 2, 3, and 8 weeks postdistraction, interarch springs were attached for 2 weeks to close distraction-produced open bites in 45 rabbits. Distractors were removed in half of the animals receiving spring treatment. Segment position was recorded by weekly direct measurements and radiographs. Tissue samples were collected at the end of spring application for microcomputerized tomography analysis and measurements of lateral symmetry. RESULTS: Orthodontic springs closed the open bite with or without distractors in place immediately after distraction and partially corrected the bite at later stages of bone consolidation. Distractor removal produced more rapid bite closure but also introduced lateral buckling of the distraction site during early consolidation. The lateral buckling was not observed if springs were applied after 2 weeks of consolidation. The amount of bite correction with orthodontic springs correlated with mineralization of the distraction site. CONCLUSION: During the consolidation period, a distraction site can be callus manipulated with orthodontic springs to correct an open bite. The amount of correction depended on when springs were placed and whether distractors were removed at the time of spring application.     

Glial cells participate in histamine inactivation in vivo

The ability of glial cells to take up histamine in vitro suggests that these cells may be involved in histamine inactivation. This prompted us to study the possible interactions between neuronal and glial processes which determine the histamine concentration in the synaptic cleft. In vitro experiments showed that the glial metabolic toxin, fluoroacetate (20 and 40mmol/l) depressed histamine uptake into cultured astroglial cells and dissociated hypothalamic cells of rats. For in vivo experiments, the push-pull superfusion technique was used. In anaesthetized rat, the anterior hypothalamic area was superfused through the push-pull cannula with artificial cerebrospinal fluid (aCSF) or with aCSF which contained fluoroacetate and the release of endogenous histamine was determined in the superfusate. Hypothalamic superfusion with fluoroacetate (20mmol/l) led to a pronounced increase in extracellular histamine. The effect of fluoroacetate was inhibited by 5μmol/l tetrodotoxin. Superfusion with Ca⁺⁺-free, Mg⁺⁺-rich (12mmol/l) aCSF inhibited the basal release rate of histamine. Under these conditions, 20mmol/l fluoroacetate did not modify the level of the amine in the superfusate. These data demonstrate that depression of glial function enhances the concentration of histamine in the extracellular space by slowing down the uptake of the amine into the glial cells. Thus, under in vivo conditions, glial cells are directly involved in the continuous removal of neuronal histamine from the synaptic cleft.     

Distribution of cerebello‐olivary degeneration in idiopathic late cortical cerebellar atrophy: Clinicopathological study of four autopsy cases

Late cortical cerebellar atrophy (LCCA) is a neurodegenerative disease which presents with slowly progressive cerebellar ataxia as a prominent symptom and is characterized neuropathologically by a limited main lesion to the cerebellar cortex and inferior olivary nucleus. To elucidate the features of lesions in the cerebellar cortex and inferior olivary nucleus, four autopsy cases suffering from idiopathic LCCA without other cortical cerebellar atrophies, such as alcoholic cerebellar degeneration, phenytoin intoxication, or hereditary cerebellar atrophy including spinocerebellar ataxia type 6, were examined. All affected patients had identical distinct features of cerebellar cortical lesions. In all four cases, the most obvious pathological finding throughout the cerebellum was loss of Purkinje cells, but the rarefaction of granular cell layers was observed only where loss of Purkinje cells was very severe, and thinning of the molecular layer was seen only where the rarefaction of granular cell layers was moderate to severe. Two patients presented with vermis dominant cerebellar cortical lesions, but the other two patients showed hemispheric dominant pathological changes. Neuronal loss of the inferior olivary nucleus was observed in the three autopsy cases. Two of the three cases had a prominent lesion in the dorsal part of the inferior olive and the cerebellar cortical lesion disclosed the vermis dominance, but the other patient, showing prominent neuronal loss in the ventral olivary nucleus, had a cerebellar hemisphere dominant lesion. The patient without neuronal loss in the inferior olivary nucleus had suffered from a shorter period of disease than the others and the rarefaction of granular cell layers and narrowing of the molecular layer of the cerebellar cortex were mild. Therefore, it is obvious that there are two types of cerebellar cortex lesions in idiopathic LCCA; one is vermis dominant and the other is cerebellar hemispheric dominant. The lesion of the inferior olivary nucleus occurs as a secondary degeneration after rarefaction of the granular cell layer and thinning of the molecular layer of the cerebellar cortex progresses. Furthermore, the distribution of the degeneration in the inferior olivary nucleus depends on the distribution of the cerebellar cortex lesions.     

The field topography of ERG components in man--I. The photopic luminance response.

A technique of multi-input systems analysis is used to explore the field topography of ERG responses to local luminance modulation. Variations in amplitude and wave form are studied within the central 23 degrees. Outside the fovea, the amplitude appears to follow a simple power law rx as a function of eccentricity r where x is approximately -2/3. The largest inter-subject variability is found in the fovea. Some nasal-temporal asymmetry is observed in all subjects with higher response densities in the temporal field outside the blind spot. The topography of the luminance response shares all these properties with the density of retinal cones.     

Hepatitis C-positive Donors in Heart Transplantation

Hepatitis C virus (HCV) can be transmitted to heart transplant recipients by donor organs. Mid-term results were reported using HCV-positive donors in patients at risk of imminent death (group I, n = 10), or in patients who otherwise would not have been offered heart transplantation (group II, n = 10) because of age (9/10) or associated medical risk (1/10). Medical records pertaining to patients receiving HCV-positive allografts between July 1994 and December 1999 were reviewed. The recipients consisted of 19 males and one female, with a median age of 54 years for group I and 66 for group II. The HCV RNA level, seroconversion of anti-HCV antibody, biochemical liver dysfunction, and causes of death were examined. Older recipients received reduced immunosuppression. Two patients in group II were HCV positive and were also retransplants. The hospital mortality rate was 10% in group I and 20% in group II; both hepatitis C-positive recipients died postoperatively prior to discharge. All predischarge deaths were related to multi-system organ failure (MSOF). All 17 survivors were HCV negative prior to transplant. Of these, 4/17 seroconverted. HCV RNA was detected in two of them. At a median follow-up of 26.4 months, 2/11 current survivors continue to test anti-HCV positive and are RNA negative. Three-year actual survival was 40% for group I and 70% in group II. Transplant coronary artery disease (TCAD) accounted for one postoperative death in group I. Current data show that four out of 11 survivors had developed TCAD at 3-year follow-up, yielding an actual freedom from TCAD rate of 12/17 (70%) at 3-year follow-up. Hepatitis C transmission using a donor heart as the reservoir is moderate (25%). Limited use of such donors is justified in selected patients. The risk for hepatic disease may be reduced by tailoring immunosuppression specifically for such recipients, particularly if they are at low risk of rejection. Further studies are necessary to define a possible association between HCV and TCAD.     

Effects of lysine-vasopressin and oxytocin on central cardiovascular control.

1 The cardiovascular effects of intravenous and intracisternal administration of neurohypophysial peptides were compared in dogs anaesthetized with chloralose. 2 Intravenous lysine-vasopressin (0.1 to 100 mu/kg) induced a dose-dependent increase in blood pressure and a decrease in heart rate. In contrast, intracisternal lysine-vasopressin (0.01 to 10 mu/kg induced a dose-related decrease in blood pressure and did not change heart rate. 3 Intracisternal oxytocin (1 and 10 mu/kg) increased blood pressure and did not change heart rate, whereas the same doses injected intravenously were inactive. 4 Pretreatment with guanethidine (15 mg/kg i.v. 24 h beforehand) abolished the hypotensive responses to intracisternal vasopressin but not the pressor action of intravenous vasopressin. 5 The pressor responses to central injections of oxytocin were not modified by guanethidine. 6 Hypotension elicited by intracisternal vasopressin was probably due to a decrease in sympathetic tone whereas the hypertension induced by intracisternal oxytocin was independent of variations in sympathetic tone.