Volume loss in the deep gray matter and thalamic subnuclei: a longitudinal study on disability progression in multiple sclerosis

Journal of Neurology - Volume loss in the deep gray matter (DGM) has been reported in patients with multiple sclerosis (MS) already at early stages of the disease and is thought to progress...     

Capturing the spatial variability of HIV epidemics in South Africa and Tanzania using routine healthcare facility data

Background

Large geographical variations in the intensity of the HIV epidemic in sub-Saharan Africa call for geographically targeted resource allocation where burdens are greatest. However, data available for mapping the geographic variability of HIV prevalence and detecting HIV ‘hotspots’ is scarce, and population-based surveillance data are not always available. Here, we evaluated the viability of using clinic-based HIV prevalence data to measure the spatial variability of HIV in South Africa and Tanzania.

Methods

Population-based and clinic-based HIV data from a small HIV hyper-endemic rural community in South Africa as well as for the country of Tanzania were used to map smoothed HIV prevalence using kernel interpolation techniques. Spatial variables were included in clinic-based models using co-kriging methods to assess whether cofactors improve clinic-based spatial HIV prevalence predictions. Clinic- and population-based smoothed prevalence maps were compared using partial rank correlation coefficients and residual local indicators of spatial autocorrelation.

Results

Routinely-collected clinic-based data captured most of the geographical heterogeneity described by population-based data but failed to detect some pockets of high prevalence. Analyses indicated that clinic-based data could accurately predict the spatial location of so-called HIV ‘hotspots’ in?>?50% of the high HIV burden areas.

Conclusion

Clinic-based data can be used to accurately map the broad spatial structure of HIV prevalence and to identify most of the areas where the burden of the infection is concentrated (HIV ‘hotspots’). Where population-based data are not available, HIV data collected from health facilities may provide a second-best option to generate valid spatial prevalence estimates for geographical targeting and resource allocation.

     

Reaction of sound and demineralised dentine to Carisolv in vivo and in vitro.

OBJECTIVES: The aim of the present study was to assess the structural reaction of intact dentine to Carisolv in vivo and in vitro. METHODS: For the in vivo study occlusal cavities were prepared in 48 caries-free molars in Wistar rats (age: three months) and Carisolv-solution was placed into the cavities of 24 M for 1, 10 and 20 min. Twenty four contralateral molars served as controls and were treated with an inert liquid containing purified water, carmellose and erythrosin for corresponding periods. For the in vitro study 24 rat molars were resected en bloc and fractured to expose an area of crown dentine area. Molars were demineralised with EDTA for eight weeks to expose the collagenous dentinal matrix. One half of the specimens was then coated with Carisolv-solution for 20 min. The other half served as a control and was coated with an inert solution for 20 min. RESULTS: In the in vivo specimens no signs of pulp cell damage were observed in the experimental group. The odontoblastic processes were destroyed in proximity to the floor of the cavity but were intact in the inner portion of dentinal tubules in experimental molars and a mechanical damage was noted in the control molars. In the in vitro specimens no structural discrepancy was detected between the experimental molars and the control molars in collagen fibrils of demineralised dentine. CONCLUSIONS: Carisolv causes destruction of cellular components of odontoblastic processes but does not attack healthy collagen fibrils.     

Efficiency of the polymer bur SmartPrep compared with conventional tungsten carbide bud bur in dentin caries excavation

SmartPrep is a rotating instrument for dentin caries excavation made from a special polymer. The manufacturer's product information stated that SmartPrep removes carious dentin selectively. This in vitro study compared the efficiency of SmartPrep with conventional tungsten carbide bud burs. Fifty extracted teeth were split in the center of a carious lesion. The 100 specimens were randomly divided into five groups. Five dentists were asked to excavate 10 teeth each: one half with SmartPrep and the corresponding half with conventional bud burs. The time needed for the caries excavation was measured. Subsequently, histological specimens were produced from all cavities and analyzed by light-microscope after Mallory-Azan-staining. The thickness of the remaining caries was measured (< 1 mm or > 1 mm). The time expended was analyzed using the paired t-test. The results were analyzed for the remaining caries and thickness of the carious layer for every tooth, using the non-parametric Wilcoxon test for combined random samples. A binary logistical regression was performed to determine the influence of the three variables (tooth, sections or bur) on the criteria "caries" or "carious layer thickness (> 1 mm)." The average time to excavate a cavity with SmartPrep was 208.1 seconds, and it was 228.32 seconds with conventional bud burs. The difference between the recorded times was not statistically significant (p > 0.05). In 37 of 50 teeth, the number of carious sections was higher in the SmartPrep group than in the bud bur group. In nine teeth, the quantity of carious sections was higher in the bud bur group than in the SmartPrep group. Four teeth showed no difference in the number of carious sections. The results were statistically significantly different (p < 0.001). In 30 teeth, the number of carious sections with a carious layer thicker than 1 mm was higher in the SmartPrep group compared with the bud bur group. In nine teeth, the number of carious sections was higher in the bud bur group than in the SmartPrep group. Eleven teeth showed no difference in thickness of the carious dentin layer. These results were statistically significantly different (p = 0.003). Binary logistical regression showed that only the variable "bur" (bud bur or SmartPrep) influenced the results concerning the criterion "caries" (p < 0.001).     

Systemic complement activation, lung injury, and products of lipid peroxidation.

Previously we have demonstrated that systemic activation of the complement system after intravenous injection of cobra venom factor (CVF) results in acute lung injury as reflected by increases in the vascular permeability of the lung as well as by morphologic evidence of damage to lung vascular endothelial cells. In using the vascular permeability of the lung as the reference, the current studies show a quantitative correlation between lung injury and the appearance in plasma of lipid peroxidation products (conjugated dienes) as well as increased concentrations of lactic dehydrogenase (LDH) and one of its isoenzymes (LDH-4). After injection of CVF, extracts of lungs also showed elevated levels of conjugated dienes, whereas no elevations were found in extracts of liver, kidney, and spleen. There was no evidence in CVF-injected rats of renal or hepatic injury as reflected by the lack of development of proteinuria and the failure to detect increased serum levels of liver-related enzymes. Other peroxidation products identified in plasma of CVF-injected rats involved hydroperoxides and fluorescent compounds with features of Schiff bases. Not surprisingly, malondialdehyde was not found to be a reliable plasma indicator of lipid peroxidation associated with oxygen radical-mediated lung vascular injury. In using a model of oxygen radical-independent lung injury induced by oleic acid, although large amounts of LDH and LDH-4 were found in the plasma, no increases in plasma levels of conjugated dienes were detected. In CVF-injected animals treated with interventions protective against lung injury (neutrophil depletion, catalase, hydroxyl radical scavengers, or iron chelators), there were striking reductions in the plasma levels of conjugated dienes, hydroperoxides, and fluorochromic products. Morphometric analysis of lung sections revealed that the protective interventions did not interfere with the accumulation of neutrophils in lung interstitial capillaries after systemic activation of complement. In vitro studies with phorbol-stimulated neutrophils failed to demonstrate appearance of conjugated dienes, suggesting that the dienes appearing in plasma of CVF-injected animals are not the result of autotoxic changes in neutrophils. The data presented in this paper suggest that acute lung injury mediated by oxygen radicals derived from phagocytic cells can be monitored by the appearance in plasma of products of lipid peroxidation.