Temporal-Fault Diagnosis for Critical-Decision Making in Discrete-Event Systems.

Since its appearance in AI, model-based diagnosis is intrinsically set-oriented. Given a sequence of observations, the diagnosis task generates a set of diagnoses, or candidates, each candidate complying with the observations. What all the approaches in the literature have in common is that a candidate is invariably a set of faulty elements (components, events, or otherwise). In this paper, we consider a posteriori diagnosis of discrete-event systems (DESs), which are described by networks of components that are modeled as communicating automata. The diagnosis problem consists in generating the candidates involved in the trajectories of the DES that conform with a given temporal observation. Oddly, in the literature on diagnosis of DESs, a candidate is still a set of faulty events, despite the temporal dimension of trajectories. In our view, when dealing with critical domains, such as power networks or nuclear plants, set-oriented diagnosis may be less than optimal in explaining the supposedly abnormal behavior of the DES, owing to the lack of any temporal information relevant to faults, along with the inability to discriminate between single and multiple occurrences of the same fault. Embedding temporal information in candidates may be essential for critical-decision making. This is why a temporal-oriented approach is proposed for diagnosis of DESs, where candidates are sequences of faults. This novel perspective comes with the burden of unbounded candidates and infinite collections of candidates, though. To cope with, a notation based on regular expressions on faults is adopted. The diagnosis task is supported by a temporal diagnoser, a flexible data structure that can grow over time based on new observations and domain-dependent scenarios.

Influence of surface properties on the electrical conductivity of silicon nanomembranes.

Because of the large surface-to-volume ratio, the conductivity of semiconductor nanostructures is very sensitive to surface chemical and structural conditions. Two surface modifications, vacuum hydrogenation (VH) and hydrofluoric acid (HF) cleaning, of silicon nanomembranes (SiNMs) that nominally have the same effect, the hydrogen termination of the surface, are compared. The sheet resistance of the SiNMs, measured by the van der Pauw method, shows that HF etching produces at least an order of magnitude larger drop in sheet resistance than that caused by VH treatment, relative to the very high sheet resistance of samples terminated with native oxide. Re-oxidation rates after these treatments also differ. X-ray photoelectron spectroscopy measurements are consistent with the electrical-conductivity results. We pinpoint the likely cause of the differences.PACS: 73.63.-b, 62.23.Kn, 73.40.Ty.

[Effect of transforming growth factor-beta1 on proliferation and apoptosis of mononuclear cells of cord blood].

To explore the mechanism of transforming growth factor-beta1 (TGF-beta1) effect on umbilical cord blood mononuclear cells proliferation and apoptosis, 5-bromo-2'-deoxyurine (BrdU) incorporation assay was adopted to detect effect of TGF-beta1 on synthesis of DNA in cells. Western blot method was used to examine effect of TGF-beta1 on expression of cyclin A, Cyclin D1, CDK2 and CDK4 in G1 phase of cell cycle. Giemsa staining and flow cytometry (FCM) were performed to detected effect of TGF-beta1 on cell apoptosis. The results showed that (1) after culture of cells with IMDM containing 10% FBS, 10% FBS + 1 ng/ml TGF-beta1, 10% FBS + 2 ng/ml TGF-beta1 or 10% FBS + 5 ng/ml TGF-beta1 for 12 hours the OD values of TGF-beta1 group were significantly lower than control group (P <0.01); after culture for 24 hours the OD values of 1 ng/ml TGF-beta1 group had no significant difference compared with control group (P >0.05), but the OD values of 2 ng/ml and 5 ng/ml TGF-beta1 groups were significantly lower than control group (P <0.05). (2) 2 ng/ml TGF-beta1 could significantly inhibit the production of cyclin A, cyclin D1, CDK2 and CDK4, the protein levels were significantly lower than control group. (3) when the cells were co-cultured with 2 ng/ml TGF-beta1 for 12 and 24 hours, Giemsa staining and FCM detection could display typical apoptosis, the apoptosis rates were 14.42% and 31.98%, while apoptosis rate in control were 4.71% and 5.76%. It is concluded that TGF-beta1 can inhibit production of G1 cyclins and CDKs of umbilical cord blood mononuclear cells, arrest cells in the G1 phase of cell cycle and induce cell apoptosis. Thus, TGF-beta1 may be an important negative modulator in hematopoiesis.