Quantifying the potential of automated dynamic solar shading in office buildings through integrated simulations of energy and daylight

The façade design is and should be considered a central issue in the design of energy-efficient buildings. That is why dynamic façade components are increasingly used to adapt to both internal and external impacts, and to cope with a reduction in energy consumption and an increase in occupant comfort. To gain a complete picture of any façade’s performance and subsequently carry out a reasonable benchmarking of various façade alternatives, the total energy consumption and indoor environment need to be considered simultaneously. We quantified the potential of dynamic solar shading façade components by using integrated simulations that took energy demand, the indoor air quality, the amount of daylight available, and visual comfort into consideration. Three types of façades were investigated (without solar shading, with fixed solar shading, and with dynamic solar shading), and we simulated them with various window heights and orientations. Their performance was evaluated on the basis of the building’s total energy demand, its energy demand for heating, cooling and lighting, and also its daylight factors. Simulation results comparing the three façade alternatives show potential for significant energy reduction, but greater differences and conflicting tendencies were revealed when the energy needed for heating, cooling and artificial lighting were considered separately. Moreover, the use of dynamic solar shading dramatically improved the amount of daylight available compared to fixed solar shading, which emphasises the need for dynamic and integrated simulations early in the design process to facilitate informed design decisions about the façade.     

Chest radiographic data acquisition and quality assurance in multicenter studies

Dorsal fusion with the internal fixator has become the standard treatment of instabilities and deformities of the thoracolumbar spine. With our new device, the modular spine fixator (MSF), which has been specially designed for short-distance instrumentations, we have increasingly been treating unstable injuries of the thoracolumbar spine by one-level stabilization. Prerequisite is an accurate evaluation of the indication, including CT and MRI to assess the involvement of the intervertebral disc and the ligamental structures. The operative technique differs in some details from the procedure in more-multi-level instrumentations, especially concerning the application of the pedicle screws. The instrumentation is always combined with posterior allogenic bone grafting. Since the beginning of 1993 we also perform anterior autogenic transpedicular bone grafting. Between January 1991 and July 1995, 57 one-level stabilizations with the MSF were performed. Of the 57 patients operated on 39, 27 men and 12 women, with an average age of 41 years, have had a clinical and radiographic follow-up examination so far, on average, 27 months after the accident. Seventeen patients were completely free of pain and 17 patients (were only) sensitive to weather changes or had minor pain during great physical stress. Five patients had pain even during slight physical stress or at rest. The preoperatively measured Cobb angle was 15.1 degrees on average, after the operation 5.2 degrees, and at the time of the follow-up examination amounted to 8.1 degrees. The patients' range of motion was normal. Only five minor complications have been seen. No implant fatigue failure has been noted in this series. We derive from these results that, for correct indications, one-level stabilization can be performed successfully and should be firmly established in the operative treatment of unstable fractures of the thoracolumbar spine.     

Cortical input to the basal forebrain

The arborization pattern and postsynaptic targets of corticofugal axons in basal forebrain areas have been studied by the combination of anatomical tract-tracing and pre- and postembedding immunocytochemistry. The anterograde neuronal tracer Phaseolus vulgaris leucoagglutinin was iontophoretically delivered into different neocortical (frontal, parietal, occipital), allocortical (piriform) and mesocortical (insular, prefrontal) areas in rats. To identify the transmitter phenotype in pre- or postsynaptic elements, the tracer staining was combined with immunolabeling for either glutamate or GABA, or with immunolabeling for choline acetyltransferase or parvalbumin. Tracer injections into medial and ventral prefrontal areas gave rise to dense terminal arborizations in extended basal forebrain areas, particularly in the horizontal limb of the diagonal band and the region ventral to it. Terminals were also found to a lesser extent in the ventral part of the substantia innominata and in ventral pallidal areas adjoining ventral striatal territories. Similarly, labeled fibers from the piriform and insular cortices were found to reach lateral and ventral parts of the substantia innominata, where terminal varicosities were evident. In contrast, descending fibers from neocortical areas were smooth, devoid of terminal varicosities, and restricted to the myelinated fascicles of the internal capsule en route to more caudal targets. Ultrastructural studies obtained indicated that corticofugal axon terminals in the basal forebrain areas form synaptic contact primarily with dendritic spines or small dendritic branches (89%); the remaining axon terminals established synapses with dendritic shafts. All tracer labeled axon terminals were immunonegative for GABA, and in the cases investigated, were found to contain glutamate immunoreactivity. In material stained for the anterograde tracer and choline acetyltransferase, a total of 63 Phaseolus vulgaris leucoagglutinin varicosities closely associated with cholinergic profiles were selected for electron microscopic analysis. From this material, 37 varicosities were identified as establishing asymmetric synaptic contacts with neurons that were immunonegative for choline acetyltransferase, including spines and small dendrites (87%) or dendritic shafts (13%). Unequivocal evidence for synaptic interactions between tracer labeled terminals and cholinergic profiles could not be obtained in the remaining cases. From material stained for the anterograde tracer and parvalbumin, 40% of the labeled terminals investigated were found to establish synapses with parvalbumin-positive elements; these contacts were on dendritic shafts and were of the asymmetrical type. The present data suggest that corticofugal axons innervate forebrain neurons that are primarily inhibitory and non-cholinergic; local forebrain axonal arborizations of these cells may represent a mechanism by which prefrontal cortical areas control basal forebrain cholinergic neurons outside the traditional boundaries of pallidal areas.     

Assessment of genomic damage in colorectal cancer by DNA fingerprinting: prognostic applications

PURPOSE: Here we evaluate the prognostic significance of the relative value of genomic damage assessed by DNA fingerprinting in colorectal cancer. MATERIALS AND METHODS: Sixty-three tumor and paired normal mucosa samples were included in the study. Genomic damage was assessed by comparative analysis of paired normal and tumor tissue DNA fingerprints by the arbitrarily primed polymerase chain reaction (AP-PCR). Decreases and increases of intensity in bands were computed and referred to the total number of visualized bands per case. An index reflecting the genomic damage fraction (GDF), with separated values for losses and gains, was obtained for each tumor. This index was used to determine molecular and clinicopathologic correlates after exclusion of eight cases displaying microsatellite instability. RESULTS: Fifty-five cases were considered for the statistical analysis. The average fraction of altered bands per tumor was 0.287+/-0.121. When losses and gains were computed separately, the average fraction of changes was 0.126+/-0.113 and 0.161+/-0.120, respectively. Tumors lacking a ras mutation showed an increased GDF, primarily because of a higher fraction of gains. Tumors that were at advanced Dukes' stages and that were poorly differentiated also displayed a higher GDF. Finally, disease-free survival was significantly diminished in tumors with a GDF greater than 0.314 (P < .001). The prognostic significance of the GDF was independent of Dukes' stage (Cox multivariate analysis, P = .005). CONCLUSION: The degree of genomic damage assessed by unbiased DNA fingerprinting correlates with genotypic, phenotypic, and clinical variables in colorectal carcinoma and may be useful in assessing prognosis in colorectal cancer.     

Improved exercise tolerance following enhanced external counterpulsation: cardiac or peripheral effect?

Tissue damage, inflammation and necrosis are hallmarks of myocardial infarction. In the present study significant elevations of serum alpha-1-antitrypsin were noted in coronary artery disease and angina cases. Interestingly chronic rheumatic heart disease which is also characterized by tissue injury. Inflammation revealed normal levels of serum alpha-1-antitrypsin. The level in chronic rheumatic heart disease was 3.37 +/- 0.57 mumol/mt/ml (control level was 3.37 +/- 0.54 mumol/mt/ml). The corollary of these observations is that in heart diseases acute phase response in terms of enhanced levels of alpha-1-antitrypsin differ depending on the causative factors. Except chronic rheumatic heart disease, in all other stressful states studied there is (to a certain degree) an altered systemic homeostasis and haemostasis. On the other hand chronic rheumatic heart disease encompass certain amount of acute phase status in terms of tissue damage and inflammation does exist unaccompanied by altered systemic homeostasis and haemostasis. However, bacteriological etiologies predominate the triggered immune responses. It is hypothesised that serum alpha-1-antitrypsin enhancement will not occur even though acute phase state exists if specific immune responses are also a part of the disease manifestation.     

MHC class I-restricted lysis of human oligodendrocytes by myelin basic protein peptide-specific CD8 T lymphocytes

Multiple sclerosis (MS) is considered to be an autoimmune disease that is directed either at myelin or at its cell of origin, the oligodendrocytes (OL). The inflammatory lesions in the central nervous system contain multiple myelin Ag-restricted and nonrestricted cell populations with the potential to mediate tissue injury. Previous studies indicate that it is possible to generate MHC class I-restricted myelin peptide-specific cytotoxic CD8 T cells, and that human adult OLs express MHC class I molecules in vitro. The purpose of this study was to demonstrate that myelin basic protein peptide-specific CD8 T cells could induce OL injury. We generated CD8 T cell lines from six healthy donors and five MS patients, and all cell lines were HLA-A2 positive. The obtained CD8 cell lines induced lysis of HLA-A2- but not HLA-A3-transfected HMy2.C1R cells in the presence of myelin basic protein peptide 110-118. In the absence of exogenous peptide, the CD8 T cell lines were cytotoxic to HLA-A2 but not to non-HLA-A2 OLs. Cytotoxicity was blocked with anti-MHC class I-blocking Ab. These results support the postulate that autoreactive CD8 cytotoxic T cells can contribute to the tissue injury in MS.