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Range image segmentation into planar and quadric surfaces using an improved robust estimator and genetic algorithm.

This paper presents a novel range image segmentation method employing an improved robust estimator to iteratively detect and extract distinct planar and quadric surfaces. Our robust estimator extends M-estimator Sample Consensus/Random Sample Consensus (MSAC/RANSAC) to use local surface orientation information, enhancing the accuracy of inlier/outlier classification when processing noisy range data describing multiple structures. An efficient approximation to the true geometric distance between a point and a quadric surface also contributes to effectively reject weak surface hypotheses and avoid the extraction of false surface components. Additionally, a genetic algorithm was specifically designed to accelerate the optimization process of surface extraction, while avoiding premature convergence. We present thorough experimental results with quantitative evaluation against ground truth. The segmentation algorithm was applied to three real range image databases and competes favorably against eleven other segmenters using the most popular evaluation framework in the literature. Our approach lends itself naturally to parallel implementation and application in real-time tasks. The method fits well, into several of today's applications in man-made environments, such as target detection and autonomous navigation, for which obstacle detection, but not description or reconstruction, is required. It can also be extended to process point clouds resulting from range image registration.

Algorithms↗

[Diagnosis of cholestatic disorders].

BACKGROUND: Cholestasis is known as an etiologically diverse clinical entity which requires a broad differential diagnostic workup. In the majority of patients, history, clinical examination, clinical chemical analysis, and abdominal ultrasound enable the differentiation between extrahepatic and intrahepatic cholestasis. This review summarizes our current knowledge in the diagnosis of cholestatic disorders. METHODS: In regard to clinical practice, diagnostic tools and new developments in imaging and molecular genetics are discussed including an algorithm for the diagnostic workup of cholestatic patients. CONCLUSION: Ultrasound and computed tomography have represented the most important primary imaging techniques in hepatobiliary disorders over the last 2 decades. The direct visualization either by endoscopic retrograde cholangiopancreatography (ERCP) or percutaneous transhepatic cholangiography (PTC) still remains the gold standard in the evaluation of the extrahepatic bile duct. In the past decade, magnetic resonance cholangiopancreatography (MRCP) has increasingly been established as a noninvasive alternative, thereby reducing the necessity of ERCP as an invasive exploration of the biliary system. Liver biopsy is indicated for the histologic grading and staging of intrahepatic cholestatic disorders. Recently, molecular genetic studies have elucidated several mutations in genes of hepatobiliary transporters which are responsible for hereditary forms of cholestasis in man. Thus, molecular genetics may be of interest in single cases of unclassified cholestasis or familial syndromes and will contribute to the routine diagnosis of hereditary cholestatic syndromes in the future. In summary, application of these diagnostic tools will finally lead to an unequivocal diagnosis in the majority of cholestatic patients with consecutive rational therapy.

Biopsy↗

Historical aspects of idiopathic generalized epilepsies.

Early in these proceedings, the origin of the three terms in the title, "idiopathic generalized epilepsy," is discussed with respect to their significance over time, and typical misunderstandings. In the mid-20th century, a rather chaotic use of a multitude of often loosely defined terms had developed, which increasingly became an obstacle to a meaningful international discussion. The International League against Epilepsy (ILAE) took the initiative to develop an internationally accepted terminology with a classification system consisting of a classification of seizures (1981) and a classification of syndromes (1989). The Idiopathic Generalized Epilepsies are one of its four major groups emerging from a double dichotomy of generalized versus localization-related and idiopathic versus symptomatic. The inclusion of biologic aspects such as syndrome-specific ages of onset ("age-related syndromes") or syndrome-specific relations of seizure occurrence to the sleep-wake cycle ("Epilepsy with Grand Mal on Awaking") meant that the syndrome classification merged the more biological views of the German school with the more neurophysiological ones of the French. Apart from establishing a common international language concerning epilepsy, the International Classification of Epilepsies and Epileptic Syndromes became an important stimulator of research, especially concerning the idiopathic epilepsies. In particular, genetic and functional imaging investigations aim at a better understanding of these conditions. It is now understood that most idiopathic syndromes have a--sometimes complex--genetic background, but we are also becoming aware of the inappropriateness of the time-honored term "generalized" and part of our dichotomies. Both localization-related and "generalized" idiopathic epilepsies seem to share a principle of ictogenesis based on functional anatomic pathogenic networks, and we seem to move toward understanding them as functional system disorders of the brain.

Electroencephalography↗

Olfactory maps and odor images.

The understanding of neuronal processing of olfactory stimuli has been furthered by genetic studies and specialized imaging of particular neuronal populations. Selective optical imaging of odor-induced presynaptic and postsynaptic glomerular activity in the olfactory bulb/antennal lobe has visualized odorant-responsive receptor repertoires and shown a more confined odor image at the level of projection neurons compared to their olfactory receptor neuron input. Genetic tracing of projection neurons connected to particular glomeruli has revealed a somewhat dispersed spatial map of termination areas for these neurons both in insects and in vertebrates. Modifications of the glomerular odor map have resulted in altered percepts of the corresponding odors.

Animals↗

[Towards a molecular psychiatry].

Recent research data from psychopharmacology, brain imaging and molecular genetics support the notion of a new psychiatric frontier: that of molecular psychiatry. Identification of different subtypes of neurotransmitter receptors and their changes in density and sensitivity in response to endogenous ligands and/or psychotropic drugs may account for the clinical expression of various behavioral phenomena, including some psychiatric disorders. Brain imaging, in particular positron-emission tomographic evaluations, are likely to change psychiatric nosology. New diagnostic elements derived from these scanners will allow to associate psychotic states to neuroreceptor changes. Molecular genetics has shown that bipolar affective disorder can be caused by a single gene. A strong linkage seems to exist between a gene locus on chromosome 11 and bipolar illness. An amyloid gene located on chromosome 21 has also been shown to be strongly related to familial Alzheimer's disease. While genetic heterogeneity limits the screening value of these findings, the powerful techniques of molecular biology have entered the field of psychiatry. Ethical issues regarding DNA immortality, gene cloning and gene therapy will strengthen this relationship.

Bipolar Disorder↗

[Functional imaging of neurocognitive dysfunction in attention deficit hyperactivity disorder].

Attention Deficit Hyperactivity Disorder (ADHD) is a neurobiological disorder of early childhood onset. Defining symptoms are chronic impairments of attention, impulse control and motor hyperactivity that frequently persist until adulthood. Miscellaneous causes of the disorder have been discussed. Accumulating evidence from imaging- and molecular genetic studies strengthened the theory of ADHS being a predominantly inherited disorder of neurobiological origin. In the last 15 years, non-invasive brain imaging methods were successfully implemented in pediatric research. Functional magnetic resonance imaging studies gave major insight into the neurobiological correlates of executive malfunction, inhibitory deficits and psychomotoric soft signs. These findings are in good accordance with brain morphometric data indicating a significant volumetric decrease of major components of striato-thalamo-cortical feedback loops, primarily influencing prefrontal executive functioning (e.g. basal ganglia). Empirical evidence points to a broad array of associated behavioral disturbances like deficient visuomotor abilities and oculomotor dysfunctions. This paper reviews the current empirical evidence derived from prior imaging studies. Special emphasis is given to the relevance of oculomotor dysfunctions in clinical and research settings, as well as their assessment in the MR environment.

Attention Deficit and Disruptive Behavior Disorder↗

Etiology and neurobiology of social anxiety disorder.

Social anxiety disorder (SAD) is influenced by multiple genetic and environmental factors. Imaging genomics combines genotyping with neuroradiological techniques, such as functional MRI (fMRI) and positron emission tomography (PET), to investigate samples relevant to psychiatric pathophysiology. Neuroanatomical areas implicated in SAD include the amygdala, prefrontal cortex, hippocampus, and striatum. Recent investigations have suggested that allelic polymorphisms may play a role in the disorder; 2 candidate genes, the serotonin transporter (SLC6A4) and catechol-O-methyl transferase (COMT), are described. The biology of extinction learning is relevant to therapeutic approaches that aim to augment existing psychotherapies. In the future, novel uses of imaging genomics integrated with rational, biologically informed treatments will offer a more refined understanding of this complex and disabling disorder.

Brain↗

Women's acceptance of MRI in breast cancer surveillance because of a familial or genetic predisposition.

Magnetic resonance imaging (MRI) of the breasts is a promising screening modality for early detection in women at increased breast cancer risk. We investigated the subjective experiences with MRI and the preferences for MRI, mammography or clinical breast examination in 178 high-risk women adhering to a breast cancer surveillance programme. MRI was reported to cause limited discomfort. About 44% preferred MRI as a screening test (mammography: 14%). MRI provided the most reassurance of breast cancer being absent in case of a favourable test result. MRI seems to be acceptable as a screening test for women at increased breast cancer risk and is preferred by them over mammography.

Adult↗

Imaging physiologic dysfunction of individual hippocampal subregions in humans and genetically modified mice.

We have developed a variant of functional magnetic resonance imaging (fMRI) designed to be sensitive to static neuronal function. This method is based on resting instead of dynamic changes in oxygen-dependent signal and therefore allows for a spatial resolution that can detect signal from different hippocampal subregions in human subjects as well as in mice. We found that hippocampal signal was significantly diminished in elderly subjects with memory decline compared to age-matched controls, and different subjects showed dysfunction in different subregions. Among healthy elders, signal intensity from the subiculum was correlated selectively with memory performance. This method does not require an activation task; it can be used in anesthetized normal and in genetically modified and cognitively impaired mice. In mice the signal was found to be sufficiently sensitive to detect functional changes in the absence of underlying anatomical changes.

Aged↗

Unsealed radioactive materials in medical practice in New Zealand.

Information has been collected on numbers and types of radionuclide procedures in medical practice in New Zealand over a three-month period in the latter half of 1973. For in vivo procedures data on the age and sex of patients and the activities of radioactive materials administered were also collected. The changes in numbers of such procedures carried out over a seven-year period are discussed. A genetic radiation dose to the population of 0.24 mrad per person is derived for the year 1973, about 0.20 mrad of this dose arising from diagnostic procedures and 64 percent being attributable to brain imaging. Whereas formerly genetic doses have been estimated from data on activities of 131I and 32P used, this is no longer possible.

Adult↗

Autosomal dominant partial epilepsy with auditory features: description of a new family.

PURPOSE: To report the clinical and genetic study of a new family with autosomal dominant partial epilepsy with auditory features (ADPEAF). METHODS: All the living affected members underwent a full clinical, neurophysiological, and magnetic resonance imaging (MRI) study. Genetic analysis was performed by typing their DNA with seven microsatellite markers previously found to cosegregate with ADPEAF on chromosome 10q24. RESULTS: The three living affected members had a childhood onset of rare and drug-responsive tonic-clonic seizures constantly preceded by a humming sensation. Routine and sleep electroencephalograms revealed rare and inconstant focal abnormalities over both temporal regions. MRI detected atrophy with increased T2 signal in the subcortical lateral portion of the right temporal lobe in one case. Analysis of 10q24 polymorphic alleles showed the same haplotype in all three affected members but different alleles in unaffected individuals. CONCLUSIONS: ADPEAF is a distinct condition with homogeneous clinical features. Genetic findings are consistent with linkage of ADPEAF to chromosome 10q24.

Adolescent↗

IgVH determined genetic restriction of a non-internal image monoclonal anti-idiotypic vaccine against Semliki Forest virus.

Two monoclonal anti-idiotypic antibodies (ab2 mAb), designated 1.13A112 (IgG2a) and 1.13A321 (IgG1) and induced against Semliki Forest virus (SFV)-neutralizing mAb UM 1.13, were investigated with regard to their vaccine potential. 1.13A321 was coupled with glutaraldehyde to keyhole limpet haemocyanin (KLH) and mixed with the adjuvant Quil A. Then when injected subcutaneously into BALB/c mice, it evoked high levels of SFV-neutralizing anti-anti-idiotypic antibodies in serum. In contrast, 1.13A112 had to be indirectly cross-linked to KLH with anti-mouse immunoglobulin to induce a low neutralizing antibody response. Competition binding assay revealed that 1.13A112 and 1.13A321 were completely competitive. Furthermore, SFV neutralization by UM 1.13 and anti-anti-idiotypic (ab3) serum was blocked equally well by either ab2 mAb. These results indicate that ab1 (UM 1.13) and ab3 share at least one antigen-combining site-related idiotope. Induction of SFV-neutralizing antibodies is genetically restricted. Rabbit anti-anti-idiotypic sera against 1.13A321 and 1.13A112 contained no SFV-neutralizing activity. Moreover, in DBA/2, C57BL/6J, CAL-20, and CB-20 mice 1.13A321 did not develop SFV-neutralizing ab3 antibodies in contrast to BALB.K, 129, SWISS, and BAB-14 mice. CAL-20, CB-20, and BAB-14 mice are congenic strains with an inbred background of BALB/c. CB-20 mice derived both IgCH and IgVH from donor strain C57BL/Ka, while BAB-14 mice derived IgCH from C57BL/Ka mice but retained IgVH from BALB/c mice. Clearly, induction of SFV-neutralizing antibodies by 1.13A321 in BAB-14 mice is dependent on IgVH of BALB/c origin. The results suggest that 1.13A321 binds to a paratope-associated recurring idiotope and almost certainly does not bear the internal image of the discontinuous neutralization epitope recognized by mAb UM 1.13. The latter suggestion is sustained by the observation that 1.13A112 and 1.13A321 do not bind to cell receptors.

Animals↗

Molecular cytogenetics: unraveling of the genetic composition of individual cells by fluorescence in situ hybridization and digital imaging microscopy.

Molecular biology techniques allow the unraveling of the genetic alterations that cause or accompany malignant disease. Since tumors are often heterogeneous, biochemical analysis of tissue homogenates is of limited diagnostic value. This paper gives examples of methods that are presently operational to analyze the genetic composition of individual cells. They are based on fluorescence in situ hybridization (FISH) and digital imaging microscopy. First, the current status of indirect and direct FISH staining methods with respect to probe labeling, detection sensitivity, multiplicity, and DNA resolution is summarized. Microscope hardware as well as charge-coupled device (CCD) cameras required for FISH analysis are then described. Applications potentially important for the analysis of urological malignancies, such as the automated enumeration of chromosomal abnormalities (counting of dots in interphase cells) and high-resolution DNA mapping on highly extended chromatin, are described in detail. Finally, the limitations of the present methodology and its future prospects are discussed.

Chromosome Mapping↗

[Hypertrophic cardiomyopathy].

Hypertrophic cardiomyopathy (HCM) counts as one of primary diseases emanating from the myocardium. In approximately 60% of the cases a familial autosomal dominant trait of disease inheritance was determined. In the majority of the cases a mutation in one of the known 14 disease-causing genes could be proven. With a prevalence of 0.2% HCM is one of the most common genetic heart diseases. The genetic causes, the clinical manifestations as well as the clinical progression are heterogeneous. At present, echocardiography is the most important diagnostic tool. It remains to be seen how the results from magnetic resonance imaging and molecular genetic diagnosis will have impact on the disease management in the future. The prognosis varies according to the localization, the degree of hypertrophy and, in some cases, on the underlying genetic mutation. Sudden death (SD) is a significant risk of the disease in young people. A systematic stratification of patients at a higher risk of SD is desperately needed. The implantation of an AICD is the most effective preventive measure against SD. The basis medication therapy of symptomatic patients uses calcium antagonists or beta-blockers. In high-degree heart failure the typical therapy is applied mainly in combination with beta-blockers and, if indicated, also with antiarrhythmics. When a high degree of outflow obstruction is present, transcoronary ablation of septum hypertrophy (TASH; synonym: percutaneous transluminal septal myocardial ablation [PTSMA]) or myectomy Ercan be performed. Heart transplantion is performed only in very few patients with terminal heart failure. Even though HCM is one of the best-documented genetically based heart diseases, only a few prospective studies and registries have been established, which have produced guidelines and recommendations for diagnostics and therapy. The ACC/ESC Expert Consensus Document is very helpful in this respect. Therefore, there is still a great need for systematic prospective analyses in large patient populations.

Adrenergic beta-Antagonists↗

In vivo neuroreceptor imaging in attention-deficit/hyperactivity disorder: a focus on the dopamine transporter.

There is converging evidence of the role of catecholamine dysregulation in the underlying pathophysiology of attention-deficit/hyperactivity disorder (ADHD). The dopamine transporter (DAT) is known to be a key regulator of dopamine, and recent genetic, treatment, and imaging studies have highlighted the role of DAT in ADHD. There is an emerging literature on in vivo neuroreceptor imaging of DAT in ADHD and control subjects reported by a number of groups internationally. A comprehensive review of existing imaging studies of DAT binding in ADHD shows that six of eight independent studies by six different groups have reported increased DAT binding in (mostly) treatment-naïve children and adults with ADHD. Although there is fair agreement regarding the presence and direction of abnormal DAT binding, there remains disagreement as to the magnitude of the finding and the importance of many potentially confounding variables, including clinical characteristics and imaging methodology. Three studies by three different groups have reported decreased DAT binding after methylphenidate treatment. Interpretation of the latter finding awaits clarification of the issue of timing of drug administration and imaging to disentangle receptor occupancy from downregulation.

Age Factors↗

A synthesis of current findings regarding neurobiological correlates and treatment of suicidal behavior.

Considerable progress has been made in the study of neurobiological correlates of suicidal behavior. These studies have confirmed the link between reduced serotonergic function and serious suicidal acts. They have localized the changes to the ventral prefrontal cortex and suggested how genetics, childhood rearing, alcoholism, substance abuse, gender, age, and cholesterol intake can modulate suicide rates through effects on the serotonergic system. Future studies need to apply this knowledge in the development of in vivo brain imaging and molecular genetic probes for study of high-risk patients. Identification of high-risk groups is essential for the conduct of controlled treatment trials, which are presently almost entirely lacking in suicidal populations. Previous clinical trials of medications and psychotherapies have targeted axis I or axis II disorders but not the predisposition to suicidal acts. Controlled treatment in high-risk patients must be undertaken to identify interventions that can reduce the propensity for suicidal acts. Such interventions will supplement current treatment strategies that target the associated psychiatric illness and reduce the opportunities to attempt suicide in high-risk patients by hospitalization.

Animals↗

[The German competence network stroke: researching -- promoting -- networking].

BACKGROUND: Stroke is the most frequent neurologic disease, one of the most frequent reasons for disability and the third most frequent cause of death in Germany. Only the coordination of prevention, therapy in the acute setting and rehabilitation will improve the socioeconomic burden of stroke. IMPLEMENTATION AND RESULTS: The Competence Net Stroke (www.schlaganfallnetz.de) substantially contributes to these efforts by linking leading research groups together, improving communication, exchanging knowledge between clinicians, researchers and patients, as well as advancing public health science and quality assurance. Since the initiation of the Competence Net Stroke by the German Ministry of Education and Research in 1999, researchers and clinicians have implemented and expanded corporate databanks that jointly answer pressing questions in stroke imaging, epidemiology, and genetics. The progress that has been made is largely due to the formation of joint standard protocols at several independent institutions. The multicenter approach enabled the competence net to build up specialized criteria in magnetic resonance imaging (MRI). These criteria guide the clinician to those patients, who profit from thrombolysis beyond the 3-h time window. In addition, the Competence Net Stroke succeeded in reliably detecting cerebral hemorrhage with MRI. PROGRESSION AND PERSPECTIVES: Since 2005, and the beginning of the third funding period, the Competence Net Stroke consists of nine sub-nets. The integrative, rather than dominating, structure eases flexible reactions to new developments and findings in research. The Competence Net Stroke can more straightforwardly adopt new, promising research areas and end funding of those which are unsuccessful. The future and continuity of the Competence Net Stroke are secured by the acquisition of alternative funding such as "Sonderforschungsbereiche", the sixth European framework program, industrial partners, and health insurance.

Clinical Competence↗