[The use of assessment instruments in the rehabilitation of accident victims]. / Der Einsatz von Assessmentverfahren in der Rehabilitation von Unfallverletzten.

Within the course of rehabilitation management the Verwaltungs-Berufsgenossenschaft (VBG) has started to measure the outcomes to assure the quality of rehabilitation processes using assessment instruments. The measures included some aspects of activity and participation in accordance with the International Classification of Functioning, Disability and Health (ICF). The present paper describes the generic and condition-specific instruments used in the this study to assess the health-related quality-of-life, discusses their selection and illustrates their incorporation into management practice. The assessment process constitutes a consistent system to prove the effects of rehabilitation and their persistence. The first experience shows that the assessment-based quality management system can be recommended for permanent modelling of structures, processes and outcomes to improve the efficacy and cost-effectiveness of rehabilitation.

Intelligent systems in the context of surrounding environment.

We investigate the behavioral patterns of a population of agents, each controlled by a simple biologically motivated neural network model, when they are set in competition against each other in the minority model of Challet and Zhang. We explore the effects of changing agent characteristics, demonstrating that crowding behavior takes place among agents of similar memory, and show how this allows unique "rogue" agents with higher memory values to take advantage of a majority population. We also show that agents' analytic capability is largely determined by the size of the intermediary layer of neurons. In the context of these results, we discuss the general nature of natural and artificial intelligence systems, and suggest intelligence only exists in the context of the surrounding environment (embodiment).

Effect of scalp infiltration with lidocaine on the circulatory response to craniotomy.

BACKGROUND: The purpose of the present study was to evaluate the influence of infiltration anesthesia of the projected line of incision in the skin of head on the hemodynamic response of the circulatory system, and the essential dose of opioids in 100 patients who underwent craniotomy. MATERIAL AND METHODS: The patients were divided into 4 groups: IA - brain tumors, no infiltration anesthesia; IB - cerebral aneurysms, no infiltration anesthesia; IIA - brain tumors + infiltration anesthesia; IIB - cerebral aneurysms + infiltration anesthesia. In the patients from groups IIA and IIB, the projected line of skin incision was injected with a 1% lidocaine solution (9.94+/-1.95 ml) five minutes before commencing surgery. RESULTS: No statistically significant differences were found between the various groups in regards to their weight, the time between infusion of the first dose of fentanyl and skin incision, the mean heart rates at time points T1 (prior to induction of anesthesia), T2 (prior to skin incision) or T3 (after skin incision), or mean arterial pressure values (MAP) at time points T1 or T2. A significant increase in MAP values (P<0.05) caused by skin incision was recorded in groups IA (from 95.2+/-9.85 to 119+/-10.6 mm Hg) and IB (from 88.4+/-11.5 to 100.3+/-11.4 mm Hg). In group IIA, MAP increased insignificantly, while in group IIB the MAP values did not change. CONCLUSIONS: Infiltration anesthesia of the projected line of skin incision in the head enabled maintenance of stability in the circulatory system and lower doses of opioids administered before commencing surgery.

Scale dependent dimension of luminous matter in the universe.

We suggest a geometrical model for the distribution of luminous matter in the Universe, where the apparent dimension, D(l), increases linearly with the logarithm of the scale l. Beyond the correlation length, xi, the Universe is homogeneous, and D = 3. Comparison with data from the SARS redshift catalog, and the LEDA database provides a good fit with a correlation length xi approximately 300 Mpc. This type of scaling structure was recently discovered in a simple reaction-diffusion "forest-fire" model, indicating a broad class of scaling phenomena.

Adaptive learning by extremal dynamics and negative feedback.

We describe a mechanism for biological learning and adaptation based on two simple principles: (i) Neuronal activity propagates only through the network's strongest synaptic connections (extremal dynamics), and (ii) the strengths of active synapses are reduced if mistakes are made, otherwise no changes occur (negative feedback). The balancing of those two tendencies typically shapes a synaptic landscape with configurations which are barely stable, and therefore highly flexible. This allows for swift adaptation to new situations. Recollection of past successes is achieved by punishing synapses which have once participated in activity associated with successful outputs much less than neurons that have never been successful. Despite its simplicity, the model can readily learn to solve complicated nonlinear tasks, even in the presence of noise. In particular, the learning time for the benchmark parity problem scales algebraically with the problem size N, with an exponent k approximately 1.4.

Solitons in the one-dimensional forest fire model.

Fires in the one-dimensional Bak-Chen-Tang forest fire model propagate as solitons, resembling shocks in Burgers turbulence. The branching of solitons, creating new fires, is balanced by the pairwise annihilation of oppositely moving solitons. Two distinct, diverging length scales appear in the limit where the growth rate of trees, p, vanishes. The width of the solitons, w, diverges as a power law, 1/p, while the average distance between solitons diverges much faster as d approximately exp(pi2/12p).

Scale-dependent dimension in the forest fire model

The forest fire model is a reaction-diffusion model where energy, in the form of trees, is injected uniformly, and burned (dissipated) locally. We show that the spatial distribution of fires forms a geometric structure where the fractal dimension varies continuously with the length scale. In the three-dimensional model, the dimensions vary from zero to three, proportional with ln(l), as the length scale increases from l approximately 1 to a correlation length l=xi. Beyond the correlation length, which diverges with the growth rate p as xi approximately p(-2/3), the distribution becomes homogeneous. We suggest that this picture applies to the "intermediate range" of turbulence where it provides a natural interpretation of the extended scaling that has been observed at small length scales. Unexpectedly, it might also be applicable to the spatial distribution of luminous matter in the universe. In the two-dimensional version, the dimension increases to D=1 at a length scale l approximately 1/p, where there is a crossover to homogeneity, i.e., a jump from D=1 to D=2.

Automatic vigilance: the attention-grabbing power of approach- and avoidance-related social information.

The automatic processing of information was investigated, varying valence (positive vs. negative) and relevance (other-relevant traits [ORT] vs. possessor-relevant traits [PRT]; G. Peeters, 1983) of stimuli. ORTs denote unconditionally positive or negative consequences for persons in the social environment of the holder of the trait (e.g., honest, brutal) whereas PRTs denote unconditionally positive or negative consequences for the trait holder (e.g., happy, depressive). In 2 experiments using the Stroop paradigm, larger interference effects were found for ORTs than PRTs. This is due to the behavior-relatedness of ORTs. In a go/no-go lexical decision task (Experiment 3), participants either had to withdraw their finger from a pressed key (i.e., "avoid") or had to press a key (i.e., "approach") if a word was presented. Responses to negative ORTs were relatively faster in the withdraw condition, whereas positive ORTs were relatively faster in the press condition.

Onset of type 1 diabetes: a dynamical instability.

Type 1 diabetes is a disease characterized by progressive loss of beta-cell function due to an autoimmune reaction affecting the islets of Langerhans. It is now generally accepted that cytokines are implicated in the pathogenesis of autoimmune diseases. Animal studies have shown that interleukin-1beta, tumor necrosis factor-alpha, and interferon-gamma affect type 1 diabetes development profoundly. It has been suggested that beta-cells are destroyed by cytokine-induced free radical formation before cytotoxic T-helper (Th)-lymphocytes and/or autoantibody-mediated cytolysis. This hypothesis is known as the "Copenhagen model." We introduce a mathematical model encompassing the various processes within this framework. The model is expressed in rate equations describing the changes in numbers of beta-cells, macrophages, and Th-lymphocytes. Being concerned with the earliest events, we explore the conditions necessary to maintain self-sustained beta-cell elimination based on the feedback between immune cells and insulin-producing cells. The motivation for this type of analysis becomes clear when we consider the multifactorial and complicated nature of the disease. Indeed, recent research has provided detailed information about the different factors that contribute to the development of the disease, stressing the importance of incorporating these findings into a more general picture. A mathematical formalism allows for a more comprehensive description of the biological problem and can reveal nonintuitive properties of the dynamics. Despite the rather complicated structure of the equations, our main conclusion is simple: onset of type 1 diabetes is due to a collective, dynamical instability, rather than being caused by a single etiological factor.

Learning from mistakes.

We re-examine the commonly held view that learning and memory necessarily require potentiation of synapses. A simple neuronal model of self-organized learning with no positive reinforcement is presented. The strongest synapses are selected for propagation of activity. Active synaptic connections are temporarily "tagged" and subsequently depressed if the resulting output turns out to be unsuccessful. Thus, all learning occurs by mistakes. The model operates at a highly adaptive state with low activity. Previously stored patterns may be swiftly retrieved when the environment and the demands of the brain change. The combined process of: (i) activity selection by extremal "winner-take-all" dynamics; and (ii) the subsequent weeding out of synapses may be viewed as synaptic Darwinism. We argue that all the features of the model are biologically plausible and discuss our results in light of recent experiments by Fitzsimonds et al. on back-propagation of long-term depression, by Xu et al. on facilitation of long-term depression in the hippocampus by behavioural stress, and by Frey and Morris on synaptic tagging.

Criticality and scaling in evolutionary ecology.

Fluctuations in ecological systems are known to involve a wide range of spatial and temporal scales, often displaying self-similar (fractal) properties. Recent theoretical approaches are trying to shed light on the nature of these complex dynamics. The results suggest that complexity in ecology and evolution comes from the network-like structure of multispecies communities that are close to instability. If true, these ideas might change our understanding of how complexity emerges in the biosphere and how macroevolutionary events could be decoupled from microevolutionary ones.

Prostate development requires Sonic hedgehog expressed by the urogenital sinus epithelium.

The prostate gland develops from the urogenital sinus by a testosterone-dependent process of ductal morphogenesis. Sonic hedgehog (Shh) is expressed in the urogenital sinus epithelium and the time course of expression coincides with the formation of the main prostatic ducts. Expression is most abundant in the lumen of the urogenital sinus and in the contiguous proximal duct segments. The initial upregulation of Shh expression in the male urogenital sinus depends on the presence of testosterone. The function of Shh was examined in the male urogenital sinus which was transplanted under the renal capsule of an adult male host mouse. Blockade of Shh function by a neutralizing antibody interferes with Shh signaling and abrogates growth and ductal morphogenesis in the transplanted tissue. These observations show that testosterone-dependent Shh expression in the urogenital sinus is necessary for the initiation of prostate development.

Dynamics of money.

We present a dynamical many-body theory of money in which the value of money is a time dependent "strategic variable" that is chosen by the individual agents. The value of money in equilibrium is not fixed by the equations, and thus represents a continuous symmetry. The dynamics breaks this continuous symmetry by fixating the value of money at a level which depends on initial conditions. The fluctuations around the equilibrium, for instance in the presence of noise, are governed by the "Goldstone modes" associated with the broken symmetry. The idea is illustrated by a simple network model of monopolistic vendors and buyers.

Interferon-responsive protein kinase (p68) and proliferating cell nuclear antigen are inversely distributed in head and neck squamous cell carcinoma.

PKR (protein kinase, interferon-responsive) is a ribosomal-associated protein kinase found in all human cells. When activated by dsRNA or polyanionic substances, PKR efficiently inhibits cellular protein synthesis. PKR expression has been correlated with cellular differentiation in a number of tumor types, including squamous cell carcinoma of the head and neck region. Although transfection of PKR into mouse fibroblasts and yeast cells inhibits proliferation, it is not known if modulation of native PKR levels occurs during cellular proliferation and differentiation in human normal and neoplastic tissues. To determine whether PKR expression was inversely related to proliferative activity in vivo, we used double-label immunohistochemistry to colocalize PKR and the proliferation marker, proliferating cell nuclear antigen (PCNA), in a series of head and neck squamous cell carcinomas. Overall, neoplasms demonstrating high levels of PKR showed low levels of PCNA immunoreactivity; carcinomas with low levels of PKR expressed high levels of PCNA. Within individual tumors, PKR and PCNA showed an inverse regional distribution: PKR was located predominantly in the center of tumor nests, while PCNA was restricted to the periphery. Patients whose tumors expressed high levels of both PKR and PCNA had the longest mean disease-free survival. These findings support the hypothesis that PKR levels are modulated in cell proliferation and differentiation in head and neck squamous cell carcinoma. Further studies are needed to clarify the mechanisms underlying the antiproliferative activity of PKR.

Protease antigen recovery decreases the specificity of bromodeoxyuridine detection in formalin-fixed tissue.

Incorporation of halogenated nucleotide analogues is often used to assess DNA synthesis and to quantitate cellular proliferation. Multiple antibodies have been developed to bromodeoxyuridine (BrdUrd) and it is the most frequently utilized substrate. Because the immunodetection of incorporated BrdUrd requires DNA denaturation or nuclease digestion, most of these antibodies are not reactive in tissues or cells fixed with crosslinking agents. Antigen retrieval techniques utilizing protease digestion restore BrdUrd antigenicity and permit the detection of BrdUrd in formalin-fixed tissue. However, during the development of a double label immunohistochemical protocol to quantitate proliferating alveolar Type II cells, we noted nucleus-specific staining in lung sections from animals that had not received BrdUrd. Therefore, we systematically analyzed the specificity of the immunohistochemical detection of incorporated BrdUrd in formalin-fixed tissue after protease digestion. Enzymatic antigen recovery diminished the specificity of the BrdUrd reaction product and caused false-positive staining with the BU-1, B44, and BR3 monoclonal antibodies. Staining was less prominent with Bu20a but was more specific. Protease antigen recovery may decrease the specificity of BrdUrd immunodetection. Appropriate controls are required when enzymatic digestion is used to detect incorporated BrdUrd in formalin-fixed tissue. The type and duration of fixation, antibody to BrdUrd, protease, and tissue may affect the specificity of the staining pattern.

Human mastication modulated by experimental trigeminal and extra-trigeminal painful stimuli.

This paper describes the modulation of human deliberately unilateral mastication by trigeminal and extra-trigeminal standardized painful stimuli. Series with 15 s of gum-chewing before induction of pain, during pain and after pain were quantitatively assessed by jaw-closing muscle electromyography (EMG) and kinematics of the lower jaw. Four different painful stimuli were used: cold stimulation of the frontal region, cold stimulation of the dominant hand, capsaicin stimulation of the hard palate, and pressure pain stimulation of the temporomandibular joint (TMJ). Intensity and quality of perceived pain were rated on visual analogue scales (VAS) and McGill's Pain Questionnaires (MPQ). Analysis of the data showed that frontal cold stimulation was the least painful test and was associated with the fewest changes in masticatory function. Cold stimulation of the hand and palatal capsaicin stimulation caused significant increases in peak amplitudes of EMG bursts from all jaw-closing muscles and faster jaw movements whereas TMJ pressure pain produced significantly lower peak EMG amplitudes. The present results suggest that nociceptive input from different tissues and even extra-trigeminal regions may modulate trigeminal motor function in selective ways. Thus, clinical observations of changes in masticatory function may not always be due to pain in the orofacial region and therefore do not necessitate orofacial treatment.

Intratracheal administration of hepatocyte growth factor/scatter factor stimulates rat alveolar type II cell proliferation in vivo.

Alveolar epithelial injury occurs universally in common respiratory illnesses associated with diffuse lung damage. After alveolar injury, type II cells proliferate and reestablish epithelial integrity, thereby restoring normal lung structure and function. However, the regulation of type II cell proliferation and alveolar epithelial repair is poorly understood. Hepatocyte growth factor/scatter factor (HGF/SF) is a heparin-binding growth factor that has been shown to be mitogenic for cultured alveolar type II cells. In this study, we determined the effect of intratracheal instillation of rhHGF/SF on type II cell proliferation in vivo. To quantify the alveolar type II cell proliferative response, we developed a double-label immunohistochemical technique to detect replicating alveolar type II cells in formalin-fixed lung sections that utilized the identification of proliferating cells by bromodeoxyuridine (BrdUrd) incorporation into DNA and alveolar type II cells by 3F9 immunoreactivity. BrdUrd detection was optimized by enzymatic antigen recovery and silver intensification of the horseradish peroxidase reaction product. Intratracheal instillation of rhHGF/SF induced a time- and dose-dependent increase in type II cell proliferation. The type II cell labeling index increased to 12.3 +/- 6.0% 48 h after 1.0 mg/kg rhHGF/SF administration, compared with 2.6 +/- 0.9% after PBS instillation. To compare the normal type II cell reparative response with the level of proliferation after exogenous rhHGF/SF administration, we measured the specific alveolar type II cell labeling index in rat lung sections obtained from animals exposed to hyperoxia for 50 h and then allowed to recover in room air. After 1 day of recovery, the alveolar type II cell labeling index was 0.45 +/- 0.2%. The specific labeling index increased to 5.4 +/- 1.3% at 2 days and then declined to 0.31 +/- 0.16% 5 days after hyperoxia exposure. In animals not exposed to hyperoxia, the alveolar type II cell labeling index was 0.6 +/- 0.14%. These studies demonstrated that intratracheal instillation of rhHGF/SF promoted alveolar type II cell proliferation in vivo. The maximal level of type II cell proliferation after rhHGF/SF administration was more than twice that reached during recovery from hyperoxia exposure. Thus, intratracheal instillation of HGF/SF may provide a potential strategy to promote type II cell proliferation and augment alveolar epithelial repair after lung injury.

Psychophysical and electrophysiological responses to experimental pain may be influenced by sedation: comparison of the effects of a hypnotic (propofol) and an analgesic (alfentanil).

Sedation may influence the responses of some experimental pain models used to test analgesic efficacy. In this study we compared the effects of a sedative (propofol) and analgesic (alfentanil) on: nociceptive reflex to single and repeated electrical stimulations; mechanical pressure pain; and evoked potentials elicited by nociceptive (electrical and laser) and non-nociceptive (acoustical) stimulation. We studied 12 healthy volunteers with two subanaesthetic concentrations of propofol and two analgesic concentrations of alfentanil. Both propofol and alfentanil increased the threshold for nociceptive reflex to single electrical stimulations, but only alfentanil increased the threshold for nociceptive reflex to repeated electrical stimulations. The pressure pain tolerance thresholds were increased significantly by alfentanil, whereas propofol significantly decreased the thresholds (hyperalgesia). Propofol and alfentanil induced similar reductions in the amplitudes of the evoked potentials elicited by nociceptive (electrical and laser) and non-nociceptive (acoustical) stimulation, whereas only alfentanil reduced the perceived pain to nociceptive stimulations. We have shown that sedation can influence both the psychophysical and electrophysiological responses of some experimental pain tests used to measure analgesic efficacy, and that propofol in subhypnotic doses, has no analgesic effect on painful electrical and heat stimulations, but has a hyperalgesic effect on mechanical pressure pain.

Pain perception and brain evoked potentials in patients with angina despite normal coronary angiograms.

OBJECTIVE: To evaluate the role of nociception in patients with angina despite normal coronary angiograms and to investigate whether any abnormality is confined to visceral or somatosensory perception. METHODS: Perception, pain threshold, and brain evoked potentials to nociceptive electrical stimuli of the oesophageal mucosa and the sternal skin were investigated in 10 patients who had angina but normal coronary angiograms, no other signs of cardiac disease, and normal upper endoscopy. Controls were 10 healthy volunteers. The peaks of the evoked potential signal were designated N for negative deflections and P for positive. Numbers were given to the peaks in order of appearance after the stimulus. The peak to peak amplitudes (P1/N1, N1/P2) were measured in microV. RESULTS: (1) Angina pectoris was provoked in seven patients following continuous oesophageal stimulation. (2) Distant projection of pain occurred after continuous electrical stimulation of the oesophagus in four patients and in no controls. (3) Patients had higher oesophageal pain thresholds (median 16.3 mA v 7.3 mA, P = 0.02) to repeated stimuli than controls, whereas the values did not differ with respect to the skin. There were no intergroup differences in thresholds to single stimuli. (4) Patients had substantially reduced brain evoked potential amplitudes after both single oesophageal (P1/N1, median values: 7.2 microV, controls: 29.0 microV; N1/P2: 16.5 microV, controls: 66.0 microV; P < 0.001 for both) and skin (N1/P2: 13.5 microV; controls: 76.0 microV; P < 0.001) stimuli despite the similar pain thresholds. CONCLUSION: Central nervous system responses to visceral and somatosensory nociceptive input are altered in patients who have angina despite normal coronary angiograms.