TOWARDS REAL-TIME CUSTOMIZED MANAGEMENT OF SUPPLY AND DEMAND CHAINS

Our focus herein is on developing an effective taxonomy for the simultaneous and real-timemanagement of supply and demand chains.More specifically,the taxonomy is developed in terms ofits underpinning components and its research foci.From a components perspective,we first considerthe value chain of supplier,manufacturer,assembler,retailer,and customer,and then develop aconsistent set of definitions for supply and demand chains based on the location of the customer orderpenetration point.From a research perspective,we classify the methods that are employed in themanagement of these chains,based on whether supply and/or demand are flexible or fixed.Interestingly,our taxonomy highlights a very critical research area at which both supply and demandare flexible,thus manageable.Simultaneous management of supply and demand chains sets the stagefor mass customization which is concerned with meeting the needs of an individualized customermarket.Simultaneous and real-time management of supply and demand chains set     

连载一洋兰

在中国兰花的栽培有悠久的历史，中国在《易经》中已有“同心之言，其臭如兰”的说法。孔子在过隐谷时，见幽兰独茂，叹曰：“夫兰当为王者香，今乃与众草为伍；譬贤者不逢时？鄙夫为伦也。”以兰花的幽香来比喻人之高雅。     

连载一洋兰

在中国，兰花的栽培有悠久的历史，中国在《易经》中已有“同心之言，其臭如兰”的说法。孔子在过隐谷时，见幽兰独茂，叹曰：“夫兰当为王者香，今乃与众草为伍；譬贤者不逢时？鄙夫为伦也。”以兰花的幽香来比喻人之高雅。     

Effects of different friction stir welding conditions on the microstructure and mechanical properties of copper plates

Friction stir welding is a new and innovative welding method used to fuse materials. In this welding method, the heat generated by friction and plastic flow causes significant changes in the microstructure of the material, which leads to local changes in the mechanical properties of the weld. In this study, the effects of various welding parameters such as the rotational and traverse speeds of the tool on the microstructural and mechanical properties of copper plates were investigated; additionally, Charpy tests were performed on copper plates for the first time. Also, the effect of the number of welding passes on the aforementioned properties has not been investigated in previous studies. The results indicated that better welds with superior properties are produced when less heat is transferred to the workpiece during the welding process. It was also found that although the properties of the stir zone improved with an increasing number of weld passes, the properties of its weakest zone, the heat-affected zone, deteriorated.     

Arsenite transport in plants

Arsenic is a metalloid which is toxic to living organisms. Natural occurrence of arsenic and human activities have led to widespread contamination in many areas of the world, exposing a large section of the human population to potential arsenic poisoning. Arsenic intake can occur through consumption of contaminated crops and it is therefore important to understand the mechanisms of transport, metabolism and tolerance that plants display in response to arsenic. Plants are mainly exposed to the inorganic forms of arsenic, arsenate and arsenite. Recently, significant progress has been made in the identification and characterisation of proteins responsible for movement of arsenite into and within plants. Aquaporins of the NIP (nodulin26-like intrinsic protein) subfamily were shown to transport arsenite in planta and in heterologous systems. In this review, we will evaluate the implications of these new findings and assess how this may help in developing safer and more tolerant crops.     

Mutations in genes encoding ribonuclease H2 subunits cause Aicardi-Goutières syndrome and mimic congenital viral brain infection

Aicardi-Goutières syndrome (AGS) is an autosomal recessive neurological disorder, the clinical and immunological features of which parallel those of congenital viral infection. Here we define the composition of the human ribonuclease H2 enzyme complex and show that AGS can result from mutations in the genes encoding any one of its three subunits. Our findings demonstrate a role for ribonuclease H in human neurological disease and suggest an unanticipated relationship between ribonuclease H2 and the antiviral immune response that warrants further investigation.     

An analogue of the ℤ<Subscript>4</Subscript>-Goethals code in non-primitive length

This paper constructs a cyclic ?₄-code with a parity-check matrix similar to that of Goethals code but in length 2^m + 1, for all m ≥ 4. This code is a subcode of the lifted Zetterberg code for m even. Its minimum Lee weight is shown to be at least 10, in general, and exactly 12 in lengths 33, 65. The authors give an algebraic decoding algorithm which corrects five errors in these lengths for m = 5, 6 and four errors for m > 6.     

A central role for calcineurin in protein misfolding neurodegenerative diseases

Accumulation of misfolded/unfolded aggregated proteins in the brain is a hallmark of many neurodegenerative diseases affecting humans and animals. Dysregulation of calcium (Ca²⁺) and disruption of fast axonal transport (FAT) are early pathological events that lead to loss of synaptic integrity and axonal degeneration in early stages of neurodegenerative diseases. Dysregulated Ca²⁺ in the brain is triggered by accumulation of misfolded/unfolded aggregated proteins in the endoplasmic reticulum (ER), a major Ca²⁺ storing organelle, ultimately leading to neuronal dysfunction and apoptosis. Calcineurin (CaN), a Ca²⁺/calmodulin-dependent serine/threonine phosphatase, has been implicated in T cells activation through the induction of nuclear factor of activated T cells (NFAT). In addition to the involvement of several other signaling cascades, CaN has been shown to play a role in early synaptic dysfunction and neuronal death. Therefore, inhibiting hyperactivated CaN in early stages of disease might be a promising therapeutic strategy for treating patients with protein misfolding diseases. In this review, we briefly summarize the structure of CaN, inhibition mechanisms by which immunosuppressants inhibit CaN, role of CaN in maintaining neuronal and synaptic integrity and homeostasis and the role played by CaN in protein unfolding/misfolding neurodegenerative diseases.     

ATM protein kinase: the linchpin of cellular defenses to stress

ATM is the most significant molecule involved in monitoring the genomic integrity of the cell. Any damage done to DNA relentlessly challenges the cellular machinery involved in recognition, processing and repair of these insults. ATM kinase is activated early to detect and signal lesions in DNA, arrest the cell cycle, establish DNA repair signaling and faithfully restore the damaged chromatin. ATM activation plays an important role as a barrier to tumorigenesis, metabolic syndrome and neurodegeneration. Therefore, studies of ATM-dependent DNA damage signaling pathways hold promise for treatment of a variety of debilitating diseases through the development of new therapeutics capable of modulating cellular responses to stress. In this review, we have tried to untangle the complex web of ATM signaling pathways with the purpose of pinpointing multiple roles of ATM underlying the complex phenotypes observed in AT patients.     

Recessive LAMC3 mutations cause malformations of occipital cortical development

The biological basis for regional and inter-species differences in cerebral cortical morphology is poorly understood. We focused on consanguineous Turkish families with a single affected member with complex bilateral occipital cortical gyration abnormalities. By using whole-exome sequencing, we initially identified a homozygous 2-bp deletion in LAMC3, the laminin γ3 gene, leading to an immediate premature termination codon. In two other affected individuals with nearly identical phenotypes, we identified a homozygous nonsense mutation and a compound heterozygous mutation. In human but not mouse fetal brain, LAMC3 is enriched in postmitotic cortical plate neurons, localizing primarily to the somatodendritic compartment. LAMC3 expression peaks between late gestation and late infancy, paralleling the expression of molecules that are important in dendritogenesis and synapse formation. The discovery of the molecular basis of this unusual occipital malformation furthers our understanding of the complex biology underlying the formation of cortical gyrations.