Robust Adaptive Depth Control of Hybrid Underwater Glider in Vertical Plane

Hybrid underwater glider (HUG) is an advanced autonomous underwater vehicle with propellers capable of sustainable operations for many months. Under the underwater disturbances and parameter uncertainties, it is difficult that the HUG coordinates with the desired depth in a robust manner. In this study, a robust adaptive control algorithm for the HUG is proposed. In the descend and ascend periods, the pitch control is designed using backstepping technique and direct adaptive control. When the vehicle approaches the target depth, the surge speed control using adaptive control combined with the pitch control is used to keep the vehicle at the desired depth with a constant cruising speed in the presence of the disturbances. The stability of the proposed controller is verified by using the Lyapunov theorem. Finally, the computer simulation using the numerical method is conducted to show the effectiveness of the proposed controller for a hybrid underwater glider system

Inhibitory effect of a tyrosine-fructose Maillard reaction product, 2,4-bis(p-hydroxyphenyl)-2-butenal on amyloid-β generation and inflammatory reactions via inhibition of NF-κB and STAT3 activation in cultured astrocytes and microglial BV-2 cells

<p>Abstract</p> <p>Background</p> <p>Amyloidogenesis is linked to neuroinflammation. The tyrosine-fructose Maillard reaction product, 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal, possesses anti-inflammatory properties in cultured macrophages, and in an arthritis animal model. Because astrocytes and microglia are responsible for amyloidogenesis and inflammatory reactions in the brain, we investigated the anti-inflammatory and anti-amyloidogenic effects of 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal in lipopolysaccharide (LPS)-stimulated astrocytes and microglial BV-2 cells.</p> <p>Methods</p> <p>Cultured astrocytes and microglial BV-2 cells were treated with LPS (1 μg/ml) for 24 h, in the presence (1, 2, 5 μM) or absence of 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal, and harvested. We performed molecular biological analyses to determine the levels of inflammatory and amyloid-related proteins and molecules, cytokines, Aβ, and secretases activity. Nuclear factor-kappa B (NF-κB) DNA binding activity was determined using gel mobility shift assays.</p> <p>Results</p> <p>We found that 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal (1, 2, 5 μM) suppresses the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) as well as the production of nitric oxide (NO), reactive oxygen species (ROS), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) in LPS (1 μg/ml)-stimulated astrocytes and microglial BV-2 cells. Further, 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal inhibited the transcriptional and DNA binding activity of NF-κB--a transcription factor that regulates genes involved in neuroinflammation and amyloidogenesis via inhibition of IκB degradation as well as nuclear translocation of p50 and p65. Consistent with the inhibitory effect on inflammatory reactions, 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal inhibited LPS-elevated Aβ₄₂levels through attenuation of β- and γ-secretase activities. Moreover, studies using signal transducer and activator of transcription 3 (STAT3) siRNA and a pharmacological inhibitor showed that 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal inhibits LPS-induced activation of STAT3.</p> <p>Conclusions</p> <p>These results indicate that 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal inhibits neuroinflammatory reactions and amyloidogenesis through inhibition of NF-κB and STAT3 activation, and suggest that 2,4-bis(<it>p</it>-hydroxyphenyl)-2-butenal may be useful for the treatment of neuroinflammatory diseases like Alzheimer's disease.</p

Combinatorial growth of Si nanoribbons

Silicon nanoribbons (Si NRs) with a thickness of about 30 nm and a width up to a few micrometers were synthesized. Systematic observations indicate that Si NRs evolve via the following sequences: the growth of basal nanowires assisted with a Pt catalyst by a vapor-liquid-solid (VLS) mechanism, followed by the formation of saw-like edges on the basal nanowires and the planar filling of those edges by a vapor-solid (VS) mechanism. Si NRs have twins along the longitudinal < 110 > growth of the basal nanowires that also extend in < 112 > direction to edge of NRs. These twins appear to drive the lateral growth by a reentrant twin mechanism. These twins also create a mirror-like crystallographic configuration in the anisotropic surface energy state and appear to further drive lateral saw-like edge growth in the < 112 > direction. These outcomes indicate that the Si NRs are grown by a combination of the two mechanisms of a Pt-catalyst-assisted VLS mechanism for longitudinal growth and a twin-assisted VS mechanism for lateral growth

Maxillary incisor inclination of skeletal Class III patients treated with extraction of the upper first premolars and two-jaw surgery: Conventional orthognathic surgery vs surgery-first approach.

Objective: To investigate the differences in the amount and pattern of the maxillary incisor (MXI) inclination change in skeletal Class III patients treated with extraction of the maxillary first premolars (MXP1) and two-jaw surgery (TJS) between conventional orthognathic surgery (COS) and surgery-first approach (SFA). Materials and Methods: The study included 60 skeletal Class III patients who had normal maxillary position, prognathic mandible, and mild crowding in the maxillary arch (#4 mm). The patients were divided into group 1 (COS, n 5 36) and group 2 (SFA, n 5 24). Lateral cephalograms were taken before treatment (T0), 1 month before surgery (T1), within 1 month after surgery (T2), and after debonding (T3) for COS patients and at T0, T2, and T3 for SFA patients. After measurement of the skeletodental variables, statistical analyses were performed. Results: During T0–T2, the amount of MXI inclination change (DU1-SN) in group 1 was significantly larger than that in group 2 (212.8u vs 24.4u; P , .001). During T2–T3, DU1-SN in groups 1 and 2 occurred in opposite directions (3.8u vs 25.9u; P , .001). However, the total amount of DU1-SN during T0–T3 was not different between groups 1 and 2 (29.0u vs 210.3u). At T3 the U1-SN values for groups 1 and 2, respectively, moved closer to normal according to the values of the normal range rate (all 83%), relative percentage ratio (102.4% and 100.1%), and achievement ratio (77.7% and 97.8%). Conclusions: The results of this study might provide basic data for predicting the amount and pattern of MXI inclination change in SFA for skeletal Class III TJS patients.OAIID:oai:osos.snu.ac.kr:snu2014-01/102/0000004298/4SEQ:4PERF_CD:SNU2014-01EVAL_ITEM_CD:102USER_ID:0000004298ADJUST_YN:NEMP_ID:A072100DEPT_CD:852CITE_RATE:1.184FILENAME:parkhm-sfa-mxi-ao-2014.pdfDEPT_NM:치의과학과SCOPUS_YN:YCONFIRM:

Differential effect of NF-κB activity on β-catenin/Tcf pathway in various cancer cells

Abstractβ-Catenin/Tcf and NF-κB pathways play an important role in biological functions. We determined the underlying mechanisms of differential interaction between two pathways in various human cancer cell lines. NF-κB positively regulated β-catenin/Tcf pathways in human glioblastoma, whereas it has an opposite effect on β-catenin/Tcf pathways in colon, liver, and breast cancer cells. Expression of lucine zipper tumor suppressor 2 (lzts2) was positively regulated by NF-κB activity in colon, liver, and breast cancer cells, whereas negatively regulated in glioma cells. Downregulation of lzts2 increased the β-catenin/Tcf promoter activity and inhibited NF-κB-induced modulation of the nuclear translocation of β-catenin. These data indicate that the differential crosstalk between β-catenin/Tcf and NF-κB pathway in various cancer cells is resulted from the differences in the regulation of NF-κB-induced lzts2 expression

A Case of Acrodermatitis Enteropathica Localized on the Hands and Feet with a Normal Serum Zinc Level

Acrodermatitis enteropathica is classified as a congenital autosomal recessive type and an acquired transient type. This disease manifests as acral and periorificial dermatitis, alopecia, intractable diarrhea, and failure to thrive. Whereas the autosomal hereditary type is caused by malabsorption of zinc in the intestine, the acquired type is caused by low nutritional support or decreased peripheral release of zinc from blood. We experienced a case of a 5-month old, breast feeding, full-term female presenting with only acral bullous dermatitis without diarrhea, periorificial dermatitis and an abnormal serum zinc level

PDGFR-β-Positive Perivascular Adventitial Cells Expressing Nestin Contribute to Fibrotic Scar Formation in the Striatum of 3-NP Intoxicated Rats

Perivascular cells expressing platelet-derived growth factor receptor beta (PDGFR-β) have recently been implicated in fibrotic scar formation after acute brain injury, but their precise identity and detailed morphological characteristics remain elusive. This study sought to characterize and define the cellular phenotype of vascular-associated cells expressing PDGFR-β in the striatum of rats treated with the mitochondrial toxin 3-nitropropionic acid (3-NP). In the control striatum, PDGFR-β-positive cells were invariably localized on the abluminal side of smooth muscle cells of larger caliber vessels, and demonstrated morphological features typical of perivascular fibroblasts. PDGFR-β expression increased and expanded to almost all vessels, including microvessels in the lesion core, at 7 days after 3-NP injection. The cells expressing PDGFR-β had ultrastructural features of fibroblasts undergoing active collagen synthesis: large euchromatic nuclei with a prominent nucleolus, well-developed rough endoplasmic reticulum (rER) with dilated cisterns and extracellular collagen fibrils. By 14 days, PDGFR-β-positive cells had somata located at a distance from the vasculature, and their highly ramified, slender processes overlapped with those from other cells, thus forming a plexus of processes in the extravascular space of the lesion core. In addition, their ultrastructural morphology and spatial correlation with activated microglia/macrophages were elaborated by three-dimensional reconstruction. Using a correlative light- and electron-microscopy technique, we found that the intermediate filament proteins nestin and vimentin were induced in PDGFRβ-positive fibroblasts in the lesion core. Collectively, our data suggest that perivascular PDGFR-β-positive fibroblasts are distinct from other vascular cell types, including pericytes and contribute to fibrotic scar formation in the lesion core after acute brain injury. Nestin and vimentin play critical roles in the structural dynamics of these reactive fibroblasts