SUMMARY The aim of the present study was to investigate whether removal of all amalgam fillings was associated with long-term changes in health complaints in a group of patients who attributed subjective health complaints to amalgam fillings. Patients previously examined at the Norwegian Dental Biomaterials Adverse Reaction Unit were included in the study and assigned to a treatment group (n = 20) and a reference group (n = 20). Participants in the treatment group had all amalgam fillings replaced with other restorative materials. Follow-ups took place 3 months, 1 and 3 years after removal of all amalgam fillings. There was no intervention in the reference group. Subjective health complaints were measured by numeric rating scales in both groups. Analysis of covariance was used to compare changes in health complaints over time in the two groups. In the treatment group, there were significant reductions in intra-oral and general health complaints from inclusion into study to the 3-year follow-up. In the reference group, changes in the same period were not significant. Comparisons between the groups showed that reductions in intra-oral and general health complaints in the treatment group were significantly different from the changes in the reference group. The mechanisms behind this remain to be identified. Reduced exposure to dental amalgam, patientcentred treatment and follow-ups, and elimination of worry are factors that may have influenced the results.

Cognitive functioning was compared in 29 children diagnosed with fetal alcohol syndrome (FAS), 35 children with fetal alcohol effects (FAE), and 66 psychotropic drugs-exposed (PDE) children using Wechsler tests and the neuropsychological test battery NEPSY. In the FAS group, verbal IQ (VIQ=78), performance IQ (PIQ=77), and full scale IQ (FSIQ=75) were significantly lower as compared to the FAE and PDE groups. In the PDE group VIQ and FSIQ were significantly higher than in the FAE group. In the FAS group, processing speed (PS) was significantly lower than the other three factors. In the FAE group, perceptual organization (PO) was significantly higher, whereas PS was significantly lower than the other factors. In the PDE group, verbal comprehension (VC) was significantly higher than the other factors. Attention subscales on the NEPSY were significantly lower in all the three groups. Prenatal alcohol exposure affects IQ levels more than exposure to psychotropic drugs. Attentional problems were found in all children when tested with the NEPSY in all groups.

Changes in glucose levels are known to directly alter gene expression. A number of previous studies have found that these effects are in part mediated by modulating the levels and the activity of transcription factors. We have investigated an alternative mechanism by which glucose might regulate gene expression by modulating levels of a transcriptional repressor. We have focused on Id2, which is a protein that indirectly regulates gene expression by sequestering certain transcription factors and preventing them from forming functional dimers. Id2 targets include the class A basic helix-loop-helix transcription factors and the sterol regulatory element-binding protein (SREBP)-1. We demonstrate that increases in glucose levels cause a rapid increase in levels of Id2 in J774.2 macrophages, and a number of lines of evidence indicate that this is via the hexosamine pathway because 1) the effect of glucose requires glutamine; 2) the effect of glucose is mimicked by low levels of glucosamine; 3) the effect of glucose is inhibited by azaserine, an inhibitor of glutamine:fructose-6-phosphate amidotransferase (GFAT); and 4) adenoviral mediated overexpression of GFAT increases levels of Id2. We go on to show that increases in Id2 can have functional effects on metabolic genes, because Id2 blocked the SREBP-1-induced induction of hormone-sensitive lipase (HSL) promoter activity, whereas Id2 alone does not modulate activity of the HSL promoter. In summary, these studies define a new mechanism by which glucose uses the hexosamine pathway to regulate gene expression by increasing levels of a transcriptional repressor. E proteins; diabetes; atherosclerosis IT IS WELL RECOGNIZED that changes in glucose levels have direct effects of gene expression in a range of tissues (49). Gene expression events induced by normal physiological fluctuations in glucose levels play a critical role in the maintenance of proper glucose and lipid homeostasis. These effects have been thoroughly investigated mostly in liver, where changes in glucose levels play an important role in switching off gluconeogenesis and switching on glycolytic pathways (15, 17). Glucose also plays a key role in regulating the expression and release of insulin in the ␤-cells of the pancreas (45), and the insulin released subsequently plays an important role in the regulation of metabolic genes (17). However, persistent hyperglycemia associated with diabetes is known to contribute to a wide range of gene expression events associated with the development of diabetic complications (5). More recently, we and others (19,21,41,44) have shown that glucose has direct effects on genes controlling cholesterol ester metabolism in macrophages, and these findings have suggested a possible link between hyperglycemia and foam cell formation. The mechanisms by which glucose regulates gene expression in macrophages have not been characterized.A number of mechanisms have been implicated in glucosemediated regulation of gene expression (5). The hexosamine pathway has drawn particular attentio...

The findings indicate that the outcome of on-road assessment is most related to cognitive skills such as attention and processing speed in combination with cognitive flexibility.

The effect of electromyographic (EMG) biofeedback on frontalis and masseter muscle activity was compared with control conditions in two groups of patients with a diagnosis of myofascial pain dysfunction (MPD) syndrome. Patients were selected on the basis of clinical symptoms, radiographic evaluation, and a clinical examination. Depressed patients and patients with signs of a pathological condition in the temporomandibular joint were excluded. Both the experimental (EXP) and the control (CON) group went through two base-line screening sessions before treatment of the EXP group was started. Treatment consisted of eight biofeedback sessions, given twice a week for 4 weeks. Feedback was presented visually on a monitor. Treatment did not include any relaxation training. Control evaluations of both groups took place 1 week, 3 months, and 6 months after the end of treatment. The EXP group was able to reduce EMG levels in frontalis and masseter muscles significantly during training sessions. Follow-up data showed significantly reduced frontalis EMG levels in the EXP group after 3 and 6 months but not in the CON group. Both groups improved subjectively, as judged by reports on pain intensity and duration, but this improvement was significantly more pronounced in the EXP group. Objective clinical indices recorded throughout the study were uncorrelated with EMG changes or subjective reports. It is concluded that biofeedback training facilitated muscular relaxation and self-regulation in the EXP group and that visual EMG feedback, consisting of a patterning of frontalis and masseter muscle activity, can be recommended as an integrated part of MPD syndrome treatment.