ABSTRACT
The origin of ADHD is multifactorial and both the aetiology and pathophysiology of ADHD are as yet incompletely understood. The monoamine deficit hypothesis of ADHD postulates a dysbalance in the interaction of the neurotransmitters dopamine, noradrenaline and serotonin. Pathophysiological mechanisms involved in ADHD include alterations in fronto-striatal circuits. The currently proposed animal models of ADHD are heterogeneous with regard to their pathophysiological alterations and their ability to mimic behavioural symptoms and to predict response to medication. Some evidence points to a genetic basis for ADHD which is likely to involve many genes of small individual effects. In summary, specific neurobiological substrates of ADHD are unknown and multiple genetic and environmental factors appear to act together to create a spectrum of neurobiological liability.
Subject(s)
Attention Deficit Disorder with Hyperactivity/physiopathology , Attention Deficit Disorder with Hyperactivity/psychology , Animals , Attention Deficit Disorder with Hyperactivity/genetics , Attention Deficit Disorder with Hyperactivity/therapy , Biofeedback, Psychology , Biogenic Monoamines/physiology , Brain Chemistry/physiology , Disease Models, Animal , Dopamine/physiology , Electroencephalography , Gene-Environment Interaction , Humans , Neurobiology , Neurotransmitter Agents/physiologyABSTRACT
BACKGROUND/AIMS: The purpose of the study was to investigate the intracellular survival of Porphyromonas gingivalis as a possible mechanism for maintaining periodontitis. METHODS: P. gingivalis strains, the strain ATCC 33277 and seven clinical isolates, were co-cultured with KB cells. The number of intracellular bacteria was determined up to 3 days after infection. In addition, the numbers of KB cells per well, the concentrations of the cytokines interleukin-1beta (IL-1beta), IL-6, IL-8 and tumour necrosis factor-alpha (TNF-alpha) and the arginine-specific amidolytic activity were measured. The 16S rRNA of P. gingivalis and the mRNA expression of IL-1beta, IL-6, IL-8, TNF-alpha and rgpA were also determined. RESULTS: All the P. gingivalis strains studied were able to survive within KB cells. In contrast to the reduced values of colony-forming units at day 3, equal and higher levels of 16S rRNA were seen in comparison to day 0. Arginine-specific amidolytic activity declined in all samples during infection. Expression of mRNA for rgpA was not found after infection of KB cells by P. gingivalis strains. IL-8 was detectable in all samples 2 days after infection with P. gingivalis strains. Principal components analysis underlined a correlation between the arginine-specific amidolytic activity 1 h after infection and both the released IL-8 and the mRNA expression of IL-8. Associations were found between the cultivable numbers of intracellular P. gingivalis and the mRNAs of IL-1, IL-6 and TNF-alpha at the day of infection. CONCLUSION: The results indicate survival of P. gingivalis within epithelial cells, possibly in a non-cultivable stage. Invasion into cells modulates the virulence properties of P. gingivalis as well as the inflammatory response of the cells.
Subject(s)
KB Cells/microbiology , Porphyromonas gingivalis/physiology , Adhesins, Bacterial/analysis , Cell Count , Coculture Techniques , Colony Count, Microbial , Cysteine Endopeptidases/analysis , Gingipain Cysteine Endopeptidases , Humans , Interleukin-1/analysis , Interleukin-1/genetics , Interleukin-6/analysis , Interleukin-6/genetics , Interleukin-8/analysis , Interleukin-8/genetics , Intracellular Space/microbiology , KB Cells/immunology , Porphyromonas gingivalis/enzymology , Porphyromonas gingivalis/immunology , RNA, Messenger/analysis , RNA, Ribosomal, 16S/analysis , Time Factors , Tumor Necrosis Factor-alpha/analysis , Tumor Necrosis Factor-alpha/genetics , VirulenceABSTRACT
PURPOSE: The aims of this study on hepatic arterial Doppler sonography were to ascertain interobserver and interequipment variability, to investigate any potential artificial influence of the ultrasonic contrast agent on the Doppler measurements and to compare the results in healthy and cirrhotic subjects. METHODS: Doppler sonography of the left hepatic artery was performed in nine healthy and nine cirrhotic subjects by three independent observers using three different devices. Continuous infusion of the ultrasonic contrast agent SHU 508A and placebo were administered in a double blind fashion. Systolic, mean and end diastolic peak velocities as well as resistive and pulsatility indices were measured. RESULTS: Equipment associated variances (5.8 - 12.7 %) of the five Doppler parameters were greater than interobserver variances (0.3 - 3.6 %). No significant differences were observed between the velocities using ultrasonic contrast agent and placebo. Systolic (65.9 +/- 3.6 vs. 47.7 +/- 4.2 cm/s mean +/- SE, p = 0.02) and mean peak velocity (35.4 +/- 1.6 vs. 24.5 +/- 1.8 cm/s, p = 0.007) were significantly higher in cirrhotic than in healthy subjects whereas the resistive and pulsatility indices were not different. CONCLUSIONS: Doppler sonography of the left hepatic artery performed by various observers is reproducible as long as the same device is used. Under clinical conditions, velocities are correctly measured with the use of ultrasonic contrast agent and are elevated in patients with cirrhosis.
Subject(s)
Contrast Media/administration & dosage , Hepatic Artery/diagnostic imaging , Liver Cirrhosis/diagnostic imaging , Polysaccharides , Ultrasonography, Doppler/instrumentation , Adult , Aged , Analysis of Variance , Blood Flow Velocity/physiology , Calibration , Double-Blind Method , Equipment Design , Female , Humans , Male , Middle Aged , Observer Variation , Prospective Studies , Pulsatile Flow/physiology , Reference Values , Ultrasonography, Doppler/statistics & numerical data , Vascular Resistance/physiologySubject(s)
Colitis, Ulcerative/diagnosis , Colitis, Ulcerative/therapy , Evidence-Based Medicine , Adolescent , Adult , Child , Colitis, Ulcerative/drug therapy , Colitis, Ulcerative/economics , Colitis, Ulcerative/surgery , Costs and Cost Analysis , Female , Humans , Male , Pregnancy , Recurrence , Remission Induction , Risk FactorsSubject(s)
Colitis, Ulcerative , Acute Disease , Administration, Oral , Adrenal Cortex Hormones/administration & dosage , Adrenal Cortex Hormones/therapeutic use , Aminosalicylic Acids/administration & dosage , Aminosalicylic Acids/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Aspirin/administration & dosage , Aspirin/therapeutic use , Azathioprine/administration & dosage , Azathioprine/therapeutic use , Colitis, Ulcerative/diagnosis , Colitis, Ulcerative/drug therapy , Colitis, Ulcerative/therapy , Cyclosporine/administration & dosage , Cyclosporine/therapeutic use , Drug Therapy, Combination , Follow-Up Studies , Humans , Immunosuppressive Agents/administration & dosage , Immunosuppressive Agents/therapeutic use , Mesalamine/administration & dosage , Mesalamine/therapeutic use , Prognosis , Prospective Studies , Randomized Controlled Trials as Topic , Recurrence , Remission Induction , Time FactorsABSTRACT
Since viral infections are believed to be one of the causes of sudden hearing loss we have used serological assays for herpes simplex virus (HSV), varicella zoster virus (VZV), and enterovirus as well as polymerase chain reaction for enterovirus to test 55 sudden hearing loss patients for viral infections. Serological screening of these patients for HSV and VZV failed to reveal significant differences between the patient group and the controls. In contrast, enterovirus sequences were detected by RT-PCR in 40% of the patient group, but in none of the controls, suggesting that enterovirus infections may be associated with sudden hearing loss.
