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Vibrational power flow contains two types of information, namely, vibration velocity and structural internal force, and is an important parameter for measuring vibration level and transmission. Structures are often under stress because of the working environment. This stress changes the vibration velocity and internal force of the structure. As a result, this stress affects the power flow. In practical engineering, structural stress often has a complex distribution. However, earlier studies mainly focused on the overall uniformly distributed stress, which cannot be applied to practical engineering vibration problems. The finite element method can handle this problem, but has several shortcomings, such as the lack of a clear explanation of the essential relationship between structural stress and vibration, the complicated process of applying specific stress, and the large number of calculations. This study considers the effect of general structural stress and determines the dynamic equation of a structure undergoing stress. By utilizing the orthogonality of specific order modes to decouple, we obtain the power flow analytical solution, which can be applied to structures with arbitrary distributed stress. Finally, we calculate and analyze the effect of structural stress on a welding plate. Results show that structural stress has a more significant effect on power flow than velocity and inner force and should be taken into account when considering vibration prediction and reduction in practical engineering. [ABSTRACT FROM AUTHOR]

To implement minimum power consumption of the link, cluster heads adopt the multi-hop manner for inter-cluster communication so as to forward the aggregation data to the relay nodes. This paper proposes a collaborative data aggregation in emerging sensor networks using a bio-level Voronoi diagram, which is an energy-efficient data aggregation protocol that integrates topology control, Multiple Access Control (MAC) and routing. The sensor nodes situated in the lower level of the diagram are responsible for listening and gathering data, and should be organized by optimal clustering node. In the inter-cluster communication stage, a particle swarm optimization algorithm is addressed to seek optimal transmission path which could simultaneously achieve the minimization of the maximum next hop distance between two nodes in the routing path and the minimization of the maximum hop count, so the minimization of whole network energy consumption is realized. The results of theoretical analysis and simulation results show that energy efficiency and synchronization accuracy of the proposed algorithm can be much better than with traditional routing protocols, and the energy consumption of nodes in the whole network can be more balanced. [ABSTRACT FROM AUTHOR]

The effect of welding residual stress on the vibration of underwater cylindrical shell is investigated. The welding residual stress of practical underwater structure, such as submarine, is widespread and complicate distributed. However, the earlier theoretical studies which mainly focused on the overall uniform distributed stress cannot be applied to deal with this practical vibration problem. In this paper, we offer a new theoretical analysis method aim at non-uniform distributed welding distributed stress. Based on the Flügge theory, considering the Fluid Structure Interaction (FSI), we derive the motion equations of the underwater cylindrical shell with welding residual stress. By means of a polynomial approximation and quadratic matrix linearization, we solve the nonlinear eigenvalue problem caused by the welding residual stress and FSI. Some numerical examples are used to validate our method and compare the welding residual stress-caused influence in the air and water. [ABSTRACT FROM AUTHOR]

The article presents a study which describes the posterior capsule rupture rates and visual outcomes after phacoemulsification, analyzes risk factors for poor vision, and compares results of faculty (F) and residents (R) from 2006-2010. It informs that visual success of all capsule ruptures was analyzed. The study concluded that the overall capsule rupture rate was 1.8 percent.

Inositol hexakisphosphate (lnsP6) levels rise and fall with neuronal excitation and silence, respectively, in the hippocampus, suggesting potential signaling functions of this inositol polyphosphate in hippocampal neurons. We now demonstrate that intracellular application of lnsP6 caused a concentration-dependent inhibition of autaptic excitatory postsynaptic currents (EPSCs) in cultured hippocampal neurons. The treatment did not alter the size and replenishment rate of the readily releasable pool in autaptic neurons. Intracellular exposure to lnsP6 did not affect spontaneous EPSCs or excitatory amino acid-activated currents in neurons lacking autapses. The lnsP6-induced inhibition of autaptic EPSCs was effectively abolished by coapplication of an antibody to synaptotagmin-1 C2B domain. Importantly, preabsorption of the antibody with a GST-WT synaptotagmin-1 C2B domain fragment but not with a GST-mutant synaptotagmin-1 C2B domain fragment that poorly reacted with the antibody impaired the activity of the antibody on the lnsP6-induced inhibition of autaptic EPSCs. Furthermore, K+ depolarization significantly elevated endogenous levels of lnsP6 and occluded the inhibition of autaptic EPSCs by exogenous lnsP6. These data reveal that lnsP6 suppresses excitatory neurotransmission via inhibition of the presynaptic synaptotagmin-1 C2B domain-mediated fusion via an interaction with the synaptotagmin Ca2+-binding sites rather than via interference with presynaptic Ca2+ levels, synaptic vesicle trafficking, or inactivation of postsynaptic ionotropic glutamate receptors. Therefore, elevated lnsP6 in activated neurons serves as a unique negative feedback signal to control hippocampal excitatory neurotransmission. [ABSTRACT FROM AUTHOR]

With the ubiquity of cellular phones, mobile applications with 2D barcodes have drawn a lot of attentions in recent years. When a user takes a barcode image with the camera in a mobile device, the captured image tends to be blurred due to camera shaking when the user presses the shutter. In addition, the captured image includes part of the complex background of the page with the barcode. In this paper, we point out that the above two issues, which have not been identified in previous works, deteriorate the accuracy of barcode recognition in the mobile computing. We then propose an efficient and effective algorithm to restore and extract 2D barcode from a complex background in a camera-shaken image. Compared with previous approaches, our algorithm outperforms in not only smaller running time but also higher accuracy of the barcode recognition in the mobile computing. [ABSTRACT FROM AUTHOR]

In this paper, we leverage network coding (NC) to reduce the bandwidth consumption for data broadcast (DB). We use the concept of mixing in a different way from the traditional NC. Traditional NC mixes all data items together. However, we mix each data item from only some data items according to the queried and stored data of receivers. Therefore, each receiver in our approach is required to receive fewer coded data to decode the required information, and the sender, thereby, is able to broadcast fewer data items. We formulate an optimization problem with integer-linear programming to minimize the bandwidth consumption in DB. We prove that the problem is NP-hard and design an approximation algorithm that can be implemented in the data server. In addition, we show that different mixings of data items lead to different decoding costs for receivers. We design an algorithm to optimally code the data items with the minimum decoding cost. [ABSTRACT FROM AUTHOR]

In this paper, we propose a bandwidth-efficient multicast routing mechanism using rectilinear Steiner trees for Internet Protocol (IP)-based low earth orbit (LEO) satellite networks. Different from existing work that minimizes the end-to-end delay, our mechanism minimizes the total bandwidth, i.e., the number of hops, for a multicast tree since the wireless bandwidth in satellite networks is a limited and scarce resource. We formulate the problem as an optimization problem and propose a distributed algorithm and a protocol to support the dynamic group membership for multicasting over LEO satellite networks. Our simulation results show that the trees created by our mechanism consume less bandwidth than the shortest path trees. The difference between the optimal solutions and the solutions obtained by our distributed algorithm is within 5%. Furthermore, our protocol has a limited overhead and can support a large number of group members. [ABSTRACT FROM AUTHOR]

Fairness in traffic management can improve the isolation between traffic streams, offer a more predictable performance, eliminate transient bottlenecks, mitigate the effect of certain kinds of denial-of-service attacks, and serve as a critical component of a quality-of-service strategy to achieve certain guaranteed services such as delay bounds and minimum bandwidths. In this paper, we choose a popular notion of fairness called max-min fairness and provide a rigorous definition in the context of input-queued switches. We show that being fair at the output ports alone or at the input ports alone or even at both input and output ports does not actually achieve an overall max-min fair allocation of bandwidth in a switch. Instead, we propose a new algorithm that can be readily implemented in a distributed fashion at the input and output ports to determine the exact max-min fair rate allocations for the flows through the switch. In addition to proving the correctness of the algorithm, we propose a practical scheduling strategy based on our algorithm. We present simulation results, using both real traffic traces and synthetic traffic, to evaluate the fairness of a variety of popular scheduling algorithms for input-queued switches. The results show that our scheduling strategy achieves better fairness than other known algorithms for input-queued switches and, in addition, achieves throughput performance very close to that of the best schedulers. [ABSTRACT FROM AUTHOR]

In this paper, we propose a new multicast delivery mechanism for bandwidth-demanding applications in IP networks. Our mechanism, referred to as Multiple-destination Overlay Multicast (MOM), combines the advantages of IP multicast and overlay multicast. We formulate the MOM routing problem as an optimization problem. We then design an algorithm based on Lagrangian relaxation on our formulation and propose a distributed protocol based on the algorithm. For network operators, MOM consumes less network bandwidth than both IP multicast and overlay multicast. For users, MOM uses less interface bandwidth than overlay multicast. [ABSTRACT FROM AUTHOR]

The article discusses the role of China's wildlife market in the spread of the coronavirus disease and mentions the wildlife protection law which should be revised by the Chinese legislature.

IP multicasting is an efficient group communication mechanism. It avoids transmitting packets from a sender to each of the receivers separately. Under the current IP multicast model, once having joined a group, the host will receive all data destined to the group from any source, irrespective of whether it wishes to receive them. This paper studies source filtering (SF) in IP multi-casting. Source filtering allows individual hosts to specify the reception of packets sent to a multicast group only from a list of source addresses or to explicitly identify a list of the sources whose data the hosts do not want to receive. We investigate the issue of source filtering in the context of multicast routing protocols, and provide support of source filtering for shared-tree based IP multicast routing. We also discuss how source filtering improves the performance of existing work on IP multicast. Finally, we provide analysis and conduct simulations to evaluate the performance of the proposed SF mechanism. The results show that our mechanism allows better bandwidth utilization and scalability than those without the capability of source filtering, thus achieving a truly efficient use of resources for IP multicasting. [ABSTRACT FROM AUTHOR]

The β-cell is equipped with at least six voltage-gated Ca2+ (Cav) channel α1-subunits designated Cav1.2, Cav1.3, Cav2.1, Cav2.2, Cav2.3, and Cav3.1. These principal subunits, together with certain auxiliary subunits, assemble into different types of Cav channels conducting L-, P/Q-, N-, R-, and T-type Ca2+ currents, respectively. The β cell shares customary mechanisms of Cav channel regulation with other excitable cells, such as protein phosphorylation, Ca2+-dependent inactivation, and G protein modulation How ever, the β-cell displays some characteristic features to bring these mechanisms into play. In islet β-cells. Cav channels can be highly phosphorylated under basal conditions and thus marginally respond to further phosphorylation. In β-cell lines, Cav channels can be surrounded by tonically activated protein phosphatases dominating over protein kinases; thus their activity is dramatically enhanced by inhibition of protein phosphatases. During the last 10 years, we have revealed some novel mechanisms of β-cell Cav channel regulation under physiological and pathophysiological conditions, including the involvement of exocytotic proteins, inositol hexakisphosphate, and type 1 diabetic serum. This minireview highlights characteristic features of customary mechanisms of Cav channel regulation in β-cells and also reviews our studies on newly identified mechanisms of β-cell Cav channel regulation. [ABSTRACT FROM AUTHOR]

In this issue of the JCI, Ciampi et at. report the identification of a novel oncogene in patients affected by radiation-associated thyroid papillary carcinomas (see the related article beginning on page 94). This oncogene derives from a paracentric inversion of the long arm of chromosome 7, which results in an in-frame fusion of the N-terminus of the A-kinase anchor protein 9 (AKAP9) gene with the C-terminal catalytic domain (exons 9-18) of the serine-threonine kinase BRAF. The resulting AKAP9-BRAF fusion protein shows constitutive kinase activity, and it is able to transmit mitogenic signals to the MAPK pathways and to promote malignant transformation of NIH3T3 cells. [ABSTRACT FROM AUTHOR]

Type 1 diabetes is an autoimmune disease of unknown etiology. Our previous work has shown that a factor present in serum from type 1 diabetic patients causes increased Ca2+ channel activity and apoptotic DNA fragmentation in pancreatic beta-cells. Here we examined the effects of type 1 diabetic serum on primary cerebellar granule cells (CGCs). In CGCs, exposure to type 1 diabetic serum did not cause increased apoptosis or changes in Ca2+ channel activity. However, patient serum did cause modulation of Ca2+ signals in a cell type with triangular soma that exhibited low voltage-gated Ca2+ currents. This cell was present primarily in cultures exposed to type 1 diabetic serum. The presence of low voltage-gated Ca2+ currents and long neuronal dendrites indicated that this unique cell was of neuronal origin and not of glial origin. [ABSTRACT FROM AUTHOR]

Focuses on a study which examined different components of leakage current in scaled n-metal oxide semiconductor field effect transistors with ultrathin gate oxides. Approaches; Results and discussion; Conclusion.

Heart rate variability (HRV) modulates both the sympathetic nervous system and the parasympathetic nervous system (PNS) of the autonomic nervous system. Mood disorder is one of the contributing factors to influence HRV. The warm-water footbath as a relaxing way is used to enhance the PNS. In this study, we intended to explore the association between HRV and a footbath in the mood disorder group. Methods: We recruited 14 young male study participants to receive a 30-minute warm-water footbath three times a week. Furthermore, we monitored the heart rates electrocardiographically before, during, and after the intervention. Results: This study showed that the footbath not only significantly enhanced standard deviation of NN (SDNN) intervals, high-frequency (HF) power, and low-frequency (LF) power during the first five minutes footbath (p < 0.01) but also increased all the parameters in five minutes after finishing the footbath. SDNN intervals, HF power, and LF power remained significantly upward in the next five minutes (p < 0.05). Conclusion: In line with previous studies, this study showed that a footbath elevated the PNS-related HRV parameters. We suggest that a warm-water footbath improves the PNS modulation possibly through baroreflex. In addition, those with cardiac conditions and depression should be particularly attentive to their condition during and following a footbath. [ABSTRACT FROM AUTHOR]

Background: Hexoses are important metabolic signals that respond to abiotic and biotic stresses. Cold stress adversely affects plant growth and development, limiting productivity. The mechanism by which sugars regulate plant cold tolerance remains elusive. Results: We examined the function of INVINH1, a cell wall invertase inhibitor, in tomato chilling tolerance. Cold stress suppressed the transcription of INVINH1 and increased that of cell wall invertase genes, Lin6 and Lin8 in tomato seedlings. Silencing INVINH1 expression in tomato increased cell wall invertase activity and enhanced chilling tolerance. Conversely, transgenic tomatoes over-expressing INVINH1 showed reduced cell wall invertase activity and were more sensitive to cold stress. Chilling stress increased glucose and fructose levels, and the hexoses content increased or decreased by silencing or overexpression INVINH1. Glucose applied in vitro masked the differences in chilling tolerance of tomato caused by the different expressions of INVINH1. The repression of INVINH1 or glucose applied in vitro regulated the expression of C-repeat binding factors (CBFs) genes. Transcript levels of NCED1, which encodes 9-cisepoxycarotenoid dioxygenase (NCED), a key enzyme in the biosynthesis of abscisic acid, were suppressed by INVINH1 after exposure to chilling stress. Meanwhile, application of ABA protected plant from chilling damage caused by the different expression of INVINH1. Conclusions: In tomato, INVINH1 plays an important role in chilling tolerance by adjusting the content of glucose and expression of CBFs. [ABSTRACT FROM AUTHOR]

Although the unique properties of wheat α-gliadin gene family are well characterized, little is known about the evolution and genomic divergence of α-gliadin gene family within the Triticeae. We isolated a total of 203 α-gliadin gene sequences from 11 representative diploid and polyploid Triticeae species, and found 108 sequences putatively functional. Our results indicate that α-gliadin genes may have possibly originated from wild Secale species, where the sequences contain the shortest repetitive domains and display minimum variation. A miniature inverted-repeat transposable element insertion is reported for the first time in α-gliadin gene sequence of Thinopyrum intermedium in this study, indicating that the transposable element might have contributed to the diversification of α-gliadin genes family among Triticeae genomes. The phylogenetic analyses revealed that the α-gliadin gene sequences of Dasypyrum, Australopyrum, Lophopyrum, Eremopyrum and Pseudoroengeria species have amplified several times. A search for four typical toxic epitopes for celiac disease within the Triticeae α-gliadin gene sequences showed that the α-gliadins of wild Secale, Australopyrum and Agropyron genomes lack all four epitopes, while other Triticeae species have accumulated these epitopes, suggesting that the evolution of these toxic epitopes sequences occurred during the course of speciation, domestication or polyploidization of Triticeae. [ABSTRACT FROM AUTHOR]

We propose a new code family, called extended shifted prime codes, and the universal encoding architecture for spectral amplitude coding optical code division multiple access systems using a two-code keying scheme. The proposed system can eliminate multiuser interference and suppress phase-induced intensity noise. In addition, we design the ESP codes to be an encoding/decoding architecture based on the array waveguide grating architecture and reduce the power loss and the complexity of the optical line terminal. The numerical results demonstrate that the proposed system with ESP codes outperforms the existing one-dimensional shifted prime codes system. [ABSTRACT FROM AUTHOR]

In this paper, we first study an important but unsolved dilemma in the literature of subspace clustering, which is referred to as "information overlapping-data coverage" challenge. Current solutions of subspace clustering usually invoke a grid-based Apriori-like procedure to identify dense regions and construct subspace clusters afterward. Due to the nature of monotonicity property in Apriori- like procedures, it is inherent that if a region is identified as dense, all its projected regions are also identified as dense, causing overlapping/redundant clustering information to be inevitably reported to users when generating clusters from such highly correlated regions. However, naive methods to filter redundant clusters will incur a challenging problem in the other side of the dilemma, called the "data coverage" issue. Note that two clusters may have highly correlated dense regions but their data members could be highly different to each other. Arbitrarily removing one of them may lose the coverage of data with clustering information, thus likely reporting an incomplete and biased clustering result. In this paper, therefore, we further propose an innovative algorithm, called "NOnRedundant Subspace Cluster mining" (NORSC), to efficiently discover a succinct collection of subspace clusters while also maintaining the required degree of data coverage. NORSC not only avoids generating the redundant clusters with most of the contained data covered by higher dimensional clusters to resolve the information overlapping problem but also limits the information loss to cope with the data coverage problem. As shown by our experimental results, NORSC is very effective in identifying a concise and small set of subspace clusters, while incurring time complexity in orders of magnitude better than that of previous works. [ABSTRACT FROM AUTHOR]

Transthyretin (TTR) is a transport protein for thyroxine and, in association with retinol-binding protein, for retinol, mainly existing as a tetramer in vivo. We now demonstrate that TTR tetramer has a positive role in pancreatic β-cell stimulus-secretion coupling. TTR promoted glucose-induced increases in cytoplasmic free Ca²+ concentration ([Ca²+]i) and insulin release. This resulted from a direct effect on glucose-induced electrical activity and voltage- gated Ca²+ channels. TTR also protected against β-cell apoptosis. The concentration of TTR tetramer was decreased, whereas that of a monomeric form was increased in sera from patients with type 1 diabetes. The monomer was without effect on glucose-induced insulin release and apoptosis. Thus, TTR tetramer constitutes a component in normal β-cell function. Conversion of TTR tetramer to monomer may be involved in the development of β-cell failure/ destruction in type 1 diabetes. [ABSTRACT FROM AUTHOR]

Multiple inositol polyphosphate phosphatase (MIPP) is an enzyme that, in vitro, has the interesting property of degrading higher inositol polyphosphates to the Ca[sup 2+] second messenger, inositol 1,4,5-trisphosphate (Ins(1,4,5)P[sub 3]), independently of inositol lipid breakdown. We hypothesized that a truncated cytosolic form of the largely endoplasmic reticulum-confined MIPP (cyt-MIPP) could represent an important new tool in the investigation of Ins(1,4,5) P[sub 3]dependent intracellular Ca[sup 2+] homeostasis. To optimize our ability to judge the impact of cyt-MIPP on intracellular Ca[sup 2+] concentration ([Ca[sup 2+]][sub i]) we chose a poorly responsive β-cell line (HIT M222.2) with an abnormally low [Ca[sup 2+]][sub i]. Our results show for the first time in an intact mammalian cell that cyt-MIPP expression leads to a significant enhancement of Ins(1,4,5)P[sub 3] concentration. This is achieved without a significant interference from other cyt-MIPP-derived inositol phosphates. Furthermore, the low basal [Ca[sup 2+]][sub i] of these cells was raised to normal levels (35 to 115 nM) when they expressed cyt-MIPP. Noteworthy is that the normal feeble glucose-induced Ca[sup 2+] response of HIT M2.2.2 cells was enhanced dramatically by mechanisms related to this increase in basal [Ca[sup 2+]][sub i]. These data support the use of cyt-MIPP as an important tool in investigating Ins(1,4,5)P[sub 3]dependent Ca[sup 2+] homeostasis and suggest a close link between Ins(1,4,5)P[sub 3] concentration and basal [Ca[sup 2+]][sub i], the latter being an important modulator of Ca[sup 2+] signaling in the pancreatic β-cell. [ABSTRACT FROM AUTHOR]

Voltage-gated calcium 3.1 (CaV3.1) channels are absent in healthy mouse β cells and mediate minor T-type Ca2+ currents in healthy rat and human β cells but become evident under diabetic conditions. Whether more active CaV3.1 channels affect insulin secretion and glucose homeostasis remains enigmatic. We addressed this question by enhancing de novo expression of β cell CaV3.1 channels and exploring the consequent impacts on dynamic insulin secretion and glucose homeostasis as well as underlying molecular mechanisms with a series of in vitro and in vivo approaches. We now demonstrate that a recombinant adenovirus encoding enhanced green fluorescent protein-CaV3.1 subunit (Ad-EGFPCaV3.1) efficiently transduced rat and human islets as well as dispersed islet cells. The resulting CaV3.1 channels conducted typical T-type Ca2+ currents, leading to an enhanced basal cytosolic-free Ca2+ concentration ([Ca2+]i). Ad-EGFP-CaV3.1-transduced islets released significantly less insulin under both the basal and first phases following glucose stimulation and could no longer normalize hyperglycemia in recipient rats rendered diabetic by streptozotocin treatment. Furthermore, Ad-EGFP-CaV3.1 transduction reduced phosphorylated FoxO1 in the cytoplasm of INS-1E cells, elevated FoxO1 nuclear retention, and decreased syntaxin 1A, SNAP-25, and synaptotagmin III. These effects were prevented by inhibiting CaV3.1 channels or the Ca2+-dependent phosphatase calcineurin. Enhanced expression of β cell CaV3.1 channels therefore impairs insulin release and glucose homeostasis by means of initial excessive Ca2+ influx, subsequent activation of calcineurin, consequent dephosphorylation and nuclear retention of FoxO1, and eventual FoxO1-mediated down-regulation of β cell exocytotic proteins. The present work thus suggests an elevated expression of CaV3.1 channels plays a significant role in diabetes pathogenesis. [ABSTRACT FROM AUTHOR]

Patients with amyotrophic lateral sclerosis (ALS) often show hallmarks of type 2 diabetes mellitus (T2DM). However, the causal link between ALS and T2DM has remained a mystery. We now demonstrate that 60% of ALS patients with T2DM (ALS-T2DM) have sera that exaggerated K+-induced increases in cytosolic free Ca2+ concentration ([Ca2+]i) in mouse islet cells. The effect was attributed to the presence of pathogenic immunoglobulin Gs (IgGs) in ALST2DM sera. The pathogenic IgGs immunocaptured the voltagedependent Ca2+ (CaV) channel subunit CaVα2δ1 in the plasmamembrane enhancing CaV1 channel-mediated Ca2+ influx and [Ca2+]i, resulting in impaired mitochondrial function. Consequently, impairments in [Ca2+]i dynamics, insulin secretion, and cell viability occurred. These data reveal that patients with ALS-T2DM carry cytotoxic ALS-T2DM-IgG autoantibodies that serve as a causal link between ALS and T2DM by immunoattacking CaαV2δ1 subunits. Our findings may lay the foundation for a pharmacological treatment strategy for patients suffering froma combination of these diseases. [ABSTRACT FROM AUTHOR]

Background: Urotensin-II (UII) rs228648 polymorphism has been reported to be associated with the risk of diabetes mellitus (DM) with inconsistent results. The present study sought to reassess the relationship between this polymorphism and susceptibility to DM by meta-analysis. Methods: Relevant eligible studies and whole genome association study (GWAS) data electronically searched were pooled to evaluate the strength of the association with odds ratios (ORs) and 95% confidence intervals (CIs). Results: Seven case–control studies involving 894 cases and 1186 controls were finally included in the meta-analysis. Overall analyses indicated that UII gene rs228648 variant was significantly associated with reduced risk of DM (allele, A vs. G: OR = 0.68, 95%CI = 0.56–0.82; dominant, AA+GA vs. GG: OR = 0.70, 95%CI = 0.53–0.91; homozygote, AA vs. GG: OR = 0.41, 95%CI = 0.28–0.61; recessive, AA vs. GA+GG: OR = 0.36, 95%CI = 0.19–0.71). In subgroup analyses based on ethnicity, the results showed a significant association of rs228648 polymorphism with decreased risk of DM in Chinese population under all five genetic models as well as in non-Chinese population under heterozygote and recessive models. Stratified analyses by specific type of DM also presented a significant association for common diabetes mellitus (CDM) under allele and homozygote as well as gestational diabetes mellitus (GDM) under all genetic models except for homozygote model. However, the synthetic analysis with GWAS data suggested an increased risk of DM with rs228648 effect allele in European population (OR = 1.01, 95%CI = 1.00–1.02). Conclusion: The present meta-analysis preliminarily suggested a potentially opposite role of rs228648 polymorphism associated with DM risk in the Chinese and European population. Further studies are in great request to verify the results. [ABSTRACT FROM AUTHOR]

The story of high mobility group protein B1 (HMGB1) in cancer is complicated and the function of HMGB1 in different cancers is uncertain. This review aims to retrieve literature regarding HMGB1 from English electronic resources, analyze and summarize the role of the HMGB1 signaling pathway in hepatocellular carcinoma (HCC), and provide useful information for carcinogenesis and progression of HCC. Results showed that HMGB1 could induce cell proliferation, differentiation, cell death, angiogenesis, metastasis, inflammation, and enhance immunofunction in in vitro and in vivo HCC models. HMGB1 and its downstream receptors RAGE, TLRs and TREM-1 may be potential anticancer targets. In conclusion, HMGB1 plays an important role in oncogenesis and represents a novel therapeutic target, which deserves further study. [ABSTRACT FROM AUTHOR]

Insulinomas cause neuroglycopenic symptoms, permanent neurological damage and even death. Current available therapies cannot satisfactorily treat malignant insulinomas and some benign insulinomas. The promising phototherapeutic results and harmless side effects of hypericin in some cancer treatments prompted us to explore possible anti-growth activity of photoactivated hypericin against RINm5F insulinoma cells and underlying mechanisms. We now show that detectable and maximal internalization of hypericin in RINm5F insulinoma cells occurred in 20 and 60 min respectively. Hypericin was considerably associated with the plasma membrane, appreciably localized in the sub-plasma membrane region and substantially accumulated in the cytoplasm. Photoactivated hypericin decreased the viability of RINm5F insulinoma cells due to its anti-proliferative and apoptotic actions. Photoactivation of hypericin inhibited cell proliferation reflected by decreased expression of the proliferation marker Ki-67 and cell-cycle arrest in the G0/G1-phase. The anti-proliferative effect resulted from down-regulation of phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular-signal-regulated kinase (ERK). Photoactivated hypericin triggered apoptosis through activation of caspase-3 and caspase-9 and elevation of the Bax-to B-cell lymphoma 2 (Bcl-2) ratio. The findings lay a solid foundation for implementation of hypericin-mediated photodynamic therapy in treatment of insulinomas. [ABSTRACT FROM AUTHOR]

The pancreatic β cell harbors α2-adrenergic and glucagon-like peptide-1 (GLP-1) receptors on its plasma membrane to sense the corresponding ligands adrenaline/noradrenaline and GLP-1 to govern glucose-stimulated insulin secretion. However, it is not known whether these two signaling systems interact to gain the adequate and timely control of insulin release in response to glucose. The present work shows that the α2-adrenergic agonist clonidine concentration-dependently depresses glucose-stimulated insulin secretion from INS-1 cells. On the contrary, GLP-1 concentration-dependently potentiates insulin secretory response to glucose. Importantly, the present work reveals that subthreshold α2-adrenergic activation with clonidine counteracts GLP-1 potentiation of glucose-induced insulin secretion. This counteractory process relies on pertussis toxin- (PTX-) sensitive Gi proteins since it no longer occurs following PTX-mediated inactivation of Gi proteins. The counteraction of GLP-1 potentiation of glucose-stimulated insulin secretion by subthreshold α2-adrenergic activation is likely to serve as a molecular mechanism for the delicate regulation of insulin release. [ABSTRACT FROM AUTHOR]

Instead of finding clusters in the full feature space, subspace clustering is an emergent task which aims at detecting clusters embedded in subspaces. Most of previous works in the literature are density-based approaches, where a cluster is regarded as a high-density region in a subspace. However, the identification of dense regions in previous works lacks of considering a critical problem, called "the density divergence problem" in this paper, which refers to the phenomenon that the region densities vary in different subspace cardinalities. Without considering this problem, previous works utilize a density threshold to discover the dense regions in all subspaces, which incurs the serious loss of clustering accuracy (either recall or precision of the resulting clusters) in different subspace cardinalities. To tackle the density divergence problem, in this paper, we devise a novel subspace clustering model to discover the clusters based on the relative region densities in the subspaces, where the clusters are regarded as regions whose densities are relatively high as compared to the region densities in a subspace. Based on this idea, different density thresholds are adaptively determined to discover the clusters in different subspace cardinalities. Due to the infeasibility of applying previous techniques in this novel clustering model, we also devise an innovative algorithm, referred to as DENCOS (DENsity COnscious Subspace clustering), to adopt a divide-and-conquer scheme to efficiently discover clusters satisfying different density thresholds in different subspace cardinalities. As validated by our extensive experiments on various data sets, DENCOS can discover the clusters in all subspaces with high quality, and the efficiency of DENCOS outperformes previous works. [ABSTRACT FROM AUTHOR]

Inositol pyrophosphates are recognized components of cellular processes that regulate vesicle trafficking, telomere length, and apoptosis. We observed that pancreatic β cells maintain high basal concentrations of the pyrophosphate diphosphoinositol pentakisphosphate (InsP7 or IP7). Inositol hexakisphosphate kinases (IP6Ks) that can generate IP7 were overexpressed. This overexpression stimulated exocytosis of insulin-containing granules from the readily releasable pool. Exogenously applied IP7 dose-dependently enhanced exocytosis at physiological concentrations. We determined that IP6K1 and IP6K2 were present in β cells. RNA silencing of IP6K1, but not IP6K2, inhibited exocytosis, which suggests that IP6K1 is the critical endogenous kinase. Maintenance of high concentrations of IP7 in the pancreatic β cell may enhance the immediate exocytotic capacity and consequently allow rapid adjustment of insulin secretion in response to increased demand. [ABSTRACT FROM AUTHOR]

Polycrystalline alkaline earth molybdate films, such as BaMoO4, SrMoO4 and CaMoO4, have been prepared by cell electrochemical method on molybdenum substrates in alkaline solutions at room temperature respectively. XRD patterns reveal that the films are well crystallized with single tetragonal scheelite structure. SEM observation shows that the grains of the films have regular pyramidal shape and the size of the grains is about 1-2 μm. Photoluminescence measurements at room temperature demonstrates that CaMoO4 film exhibits single green emission at 510 nm, and SrMoO4 film at 520 nm respectively at the excitation of 220 nm, and BaMoO4 film shows no emission. [ABSTRACT FROM AUTHOR]

In type 1 diabetes (T1D), there is a specific destruction of the insulin secreting pancreatic β cell. Although the exact molecular mechanisms underlying β cell destruction are not known, sera from T1D patients have been shown to promote Ca2+-induced apoptosis. We now demonstrate that apolipoprotein CIII (apoCIII) is increased in serum from T1D patients and that this serum factor both induces increased cytoplasmic free intracellular Ca2+ concentration ([Ca2+]i) and β cell death. The apoCIII-induced increase in [Ca2+]i reflects an activation of the voltage-gated L-type Ca2+ channel. Both the effects of T1D sera and apoCIII on the β cell are abolished in the presence of antibody against apoCIII. Increased serum levels of apoCIII can thus account for the increase in β cell [Ca2+]i and thereby β cell apoptosis associated with T1D. [ABSTRACT FROM AUTHOR]

Insulin secretion is controlled by the β cell's metabolic state, and the ability of the secretory granules to undergo exocytosis increases during glucose stimulation in a membrane potential-independent fashion. Here, we demonstrate that exocytosis of insulincontaining secretory granules depends on phosphatidylinositol 4-kinase (PI 4-kinase) activity and that inhibition of this enzyme suppresses glucose-stimulated insulin secretion. Intracellular application of phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate [PI(4,5)P[sub 2]] stimulated exocytosis by promoting the priming of secretory granules for release and increasing the number of granules residing in a readily releasable pool. Reducing the cytoplasmic ADP concentration in a way mimicking the effects of glucose stimulation activated PI 4-kinase and increased exocytosis whereas changes of the ATP concentration in the physiological range had little effect. The PI(4,5)P[sub 2]-binding protein Ca[sup 2+]-dependent activator protein for secretion (CAPS) is present in β cells, and neutralization of the protein abolished both Ca[sup 2+]- and PI(4,5)P[sub 2]-induced exocytosis. We conclude that ADPinduced changes in PI 4-kinase activity, via generation of PI(4,5)P[sub 2], represents a metabolic sensor in the β cell by virtue of its capacity to regulate the release competence of the secretory granules. [ABSTRACT FROM AUTHOR]

Presents a study on low-frequency charge pumping technique. Review of the theory governing the low-frequency charge pumping technique; Analysis of the tunneling effect on the low-frequency charge pumping technique; Discussion on the inaccuracies associated with the technique.

Cysteine string proteins (CSPs) are novel synaptic vesicle-associated protein components characterized by an N-terminal J-domain and a central palmitoylated string of cysteine residues. The cellular localization and functional role of CSP was studied in pancreatic endocrine cells. In situ hybridization and RT­PCR analysis demonstrated CSP mRNA expression in insulin-producing cells. CSP1 mRNA was present in pancreatic islets; both CSP1 and CSP2 mRNAs were seen in insulin-secreting cell lines. Punctate CSP-like immunoreactivity (CSP-LI) was demonstrated in most islets of Langerhans cells, acinar cells and nerve fibers of the rat pancreas. Ultrastructural analysis showed CSP-LI in close association with membranes of secretory granules of cells in the endo- and exocrine pancreas. Subcellular fractionation of insulinoma cells showed CSP1 (34⁄36 kDa) in granular fractions; the membrane and cytosol fractions contained predominantly CSP2 (27 kDa). The fractions also contained proteins of 72 and 70 kDa, presumably CSP dimers. CSP1 overexpression in INS-1 cells or intracellular administration of CSP antibodies into mouse ob/ob β-cells did not affect voltage-dependent Ca2+-channel activity. Amperometric measurements showed a significant decrease in insulin exocytosis in individual INS-1 cells after CSP1 overexpression. We conclude that CSP is associated with insulin secretory granules and that CSP participates in the molecular regulation of insulin exocytosis by mechanisms not involving changes in the activity of voltage-gated Ca2+-channels. [ABSTRACT FROM AUTHOR]