Capabilities of the Intelligent Manufacturing Enterprise

Manufacturing enterprises encounter pressure to digitalize and increase their intelligence as their environments demand improved productivity and agility. Based on existing research on intelligent enterprises, manufacturing enterprises, and data technologies, the authors developed an explanatory model for the derivation of a definition of the intelligent manufacturing enterprise. This paper expands the formerly developed model by presenting the characteristics of the intelligent manufacturing enterprise and the capabilities needed to become such an enterprise

Defining the Intelligent Manufacturing Enterprise

Manufacturing enterprises encounter pressure to digitalize and increase their intelligence as their environments demand increased productivity and agility. Based on existing research on intelligent enterprises, manufacturing enterprises, and data technologies, developing the definition of an intelligent manufacturing enterprise is required. Current research lacks historically derived definitions of these dynamic fields, as well as a model of their overlap. An explanatory model is proposed to define the intelligent manufacturing enterprise, its characteristics, and the capabilities needed to become such an enterprise. This model is derived through qualitative and quantitative methods utilizing content analysis. This paper describes the content analysis methodology as well as the derived definition of the intelligent manufacturing enterprise

Oxygen impairs oligodendroglial development via oxidative stress and reduced expression of HIF-1α

The premature increase of oxygen tension may contribute to oligodendroglial precursor cell (OPC) damage in preterm infants. Fetal OPCs are exposed to low oxygen tissue tensions not matched when cells are cultured in room air. Maturation (A2B5, O4, O1, MBP, CNP, arborization), oxidative stress (nitrotyrosine Western blot, NRF2 and SOD2 expression), apoptosis (TUNEL), proliferation (Ki67), and expression of transcription factors regulated by Hypoxia-Inducible-Factor-1-alpha (Hif-1α) expressed in OPCs (Olig1, Olig2, Sox9, Sox10) were assessed in rat OPCs and OLN93 cells cultured at 5% O2 and 21% O2. Influences of Hif-1α were investigated by Hif-1α luciferase reporter assays and Hif-1α-knockdown experiments. At 21% O2, cell proliferation was decreased and process arborization of OPCs was reduced. Expression of MBP, CNP, Olig1, Sox9 and Sox10 was lower at 21% O2, while Nrf2, SOD2, nitrotyrosine were increased. Apoptosis was unchanged. Luciferease reporter assay in OLN93 cells indicated increased Hif-1α activity at 5% O2. In OLN93 cells at 5% O2, Hif-1α knockdown decreased the expression of MBP and CNP, similar to that observed at 21% O2. These data indicate that culturing OPCs at 21% O2 negatively affects development and maturation. Both enhanced oxidative stress and reduced expression of Hif-1α-regulated genes contribute to these hyperoxia-induced changes

Some psychological benefits of urban nature: Mental vitality from time spent in nearby nature.

A one-time era of vast energy and natural resources allowed an industrial civilization to emerge and flourish. This gift of resources allowed for the building of modern society’s infrastructure and the flood of goods and services. Those resources, however, were never limitless. The coming decline in resource availability and quality will significantly alter individual and community life patterns, and initiate a drawn-out transition to a new normal. These changes in the biophysical basis of everyday life will tax our social, emotional and attentional capacities. Individuals will struggle to remain clearheaded and effective while coping with immutable biophysical limits. It is here that psychology will play a major role since what is being faced is not a technological or political challenge but an existential one. Psychological research posits that time spent in nature restores our mental effectiveness, emotional outlook and subjective well-being. Furthermore, the full psychological benefits of nature may not require exceptional natural environments such as scenic parks, exquisite gardens or immense green spaces. Everyday nature, even that judged to be mundane, may suffice. This is an important notion since nature in small-scale neighborhood settings is inexpensive to maintain and widely accessible to the vast majority of people. This chapter explores this idea, first by developing the theoretical basis for using ordinary nature to restore mental and social effectiveness and second by presenting a study of two designed residential neighborhoods that differ dramatically on the quality and amount of nearby nature. Results of the study are consistent with theory and prior research in indicating that residents who committed to spending time outdoors in their neighborhood showed greater mental clarity and effectiveness, regardless of the quality of the surrounding natural settings. Considered together, the theory and results support the suggestion that exposure to nearby nature significantly benefits mental functioning even in the absence of superlative design features. Time spent in everyday nature, which is available to most people, is as effective as experiencing the breathtaking beauty of extraordinary natural settings. The chapter presents these findings as having important implications for citizens who must maintain their mental clarity and emotional stability while responding to trying environmental circumstances. Even under a business-as-usual resource scenario, budget constraints and existing land use patterns make it difficult to create new natural areas. A scenario that includes a reduction of net energy surplus and a descent in natural resource availability makes these findings all the more useful.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/136087/1/De Young, R., K. Scheuer, T. Brown, T. Crow & J. Stewart (2017) Some psychological benefits of urban nature, in Columbus, A. M. (Ed.) Advances in Psychology Research 116 (Pp. 93-120).pdfDescription of De Young, R., K. Scheuer, T. Brown, T. Crow & J. Stewart (2017) Some psychological benefits of urban nature, in Columbus, A. M. (Ed.) Advances in Psychology Research 116 (Pp. 93-120).pdf : Main articl

Postnatal myelination of the immature rat cingulum is regulated by GABAB receptor activity

Myelination of axons in the neonatal brain is a highly complex process primarily achieved by oligodendroglial cells (OLs). OLs express receptors for gamma-aminobutyric acid (GABA) which is released from cortical interneurons on a basal level, while glial cells can be a source of GABA, too. We investigated GABA-induced oligodendroglial maturation, proliferation, apoptosis, and myelin production after pharmacological inhibition of GABA(A) and GABA(B) in the neonatal rat brain. Daily injections of the reverse GABA(A) receptor agonist (DMCM) and the GABA(B) receptor antagonist (CGP35348) were performed from postnatal day 6 (P6) to P11. MBP expression was examined by Western blots and immunohistochemistry. Furthermore, we determined the number of CC1(+)OLIG2(+) and CNP(+)OLIG2(+) cells to assess maturation, the number of PCNA(+)OLIG2(+) oligodendrocytes to assess proliferation, the number of oligodendrocyte precursor cells (PDGFR alpha(+)OLIG2(+)), and apoptosis of OLs (CASP3A(+)OLIG2(+)) as well as apoptotic cells in total (CASP3A(+)DAPI(+)) at P11 and P15. In addition, we analyzed the expression Pdgfr alpha and CNP. MBP expression was significantly reduced after CGP treatment at P15. In the same animal group, CNP expression and CNP(+)OLIG2(+) cells decreased temporarily at P11. At P15, the proliferation of PCNA(+)OLIG2(+) cells and the number of PDGFR alpha(+)OLIG2(+) cells increased after GABA(B) receptor antagonization whereas no significant differences were visible in the Pdgfr alpha gene expression. No changes in apoptotic cell death were observed. CGP treatment induced a transient maturational delay at P11 and deficits in myelin expression at P15 with increased oligodendroglial proliferation. Our in vivo study indicates GABA(B) receptor activity as a potential modulator of oligodendroglial development

Determining ‘Age at Death’ for Forensic Purposes using Human Bone by a Laboratory-based Analytical Method

Determination of age-at-death (AAD) is an important and frequent requirement in contemporary forensic science and in the reconstruction of past populations and societies from their remains. Its estimation is relatively straightforward and accurate (±3 years) for immature skeletons by using morphological features and reference tables within the context of forensic anthropology. However, after skeletal maturity (>35 yrs) estimates become inaccurate, particularly in the legal context. In line with the general migration of all the forensic sciences from reliance upon empirical criteria to those which are more evidence-based, AAD determination should rely more-and-more upon more quantitative methods. We explore here whether well-known changes in the biomechanical properties of bone and the properties of bone matrix, which have been seen to change with age even after skeletal maturity in a traceable manner, can be used to provide a reliable estimate of AAD. This method charts a combination of physical characteristics some of which are measured at a macroscopic level (wet & dry apparent density, porosity, organic/mineral/water fractions, collagen thermal degradation properties, ash content) and others at the microscopic level (Ca/P ratios, osteonal and matrix microhardness, image analysis of sections). This method produced successful age estimates on a cohort of 12 donors of age 53–85 yr (7 male, 5 female), where the age of the individual could be approximated within less than ±1 yr. This represents a vastly improved level of accuracy than currently extant age estimation techniques. It also presents: (1) a greater level of reliability and objectivity as the results are not dependent on the experience and expertise of the observer, as is so often the case in forensic skeletal age estimation methods; (2) it is purely laboratory-based analytical technique which can be carried out by someone with technical skills and not the specialised forensic anthropology experience; (3) it can be applied worldwide following stringent laboratory protocols. As such, this technique contributes significantly to improving age estimation and therefore identification methods for forensic and other purposes

Bromine measurements in ozone depleted air over the Arctic Ocean

In situ measurements of ozone, photochemically active bromine compounds, and other trace gases over the Arctic Ocean in April 2008 are used to examine the chemistry and geographical extent of ozone depletion in the arctic marine boundary layer (MBL). Data were obtained from the NOAA WP-3D aircraft during the Aerosol, Radiation, and Cloud Processes affecting Arctic Climate (ARCPAC) study and the NASA DC-8 aircraft during the Arctic Research of the Composition of the Troposphere from Aircraft and Satellites (ARCTAS) study. Fast (1 s) and sensitive (detection limits at the low pptv level) measurements of BrCl and BrO were obtained from three different chemical ionization mass spectrometer (CIMS) instruments, and soluble bromide was measured with a mist chamber. The CIMS instruments also detected Br2. Subsequent laboratory studies showed that HOBr rapidly converts to Br2 on the Teflon instrument inlets. This detected Br2 is identified as active bromine and represents a lower limit of the sum HOBr + Br2. The measured active bromine is shown to likely be HOBr during daytime flights in the arctic. In the MBL over the Arctic Ocean, soluble bromide and active bromine were consistently elevated and ozone was depleted. Ozone depletion and active bromine enhancement were confined to the MBL that was capped by a temperature inversion at 200–500 m altitude. In ozone-depleted air, BrO rarely exceeded 10 pptv and was always substantially lower than soluble bromide that was as high as 40 pptv. BrCl was rarely enhanced above the 2 pptv detection limit, either in the MBL, over Alaska, or in the arctic free troposphere

Effect of pancreatic and/or renal transplantation on diabetic autonomic neuropathy

Thirty-nine Type 1 (insulin-dependent) diabetic patients were studied prospectively after simultaneous pancreas and kidney (n=26) and kidney grafting alone (n=13) by measuring heart rate variation during various manoeuvers and answering a standardized questionnaire every 6 to 12 months post-transplant. While age, duration of diabetes, and serum creatinine (168.1±35.4 vs 132.7±17.7 mgrmol/l) were comparable, haemoglobin A1 levels were significantly lower (6.6±0.2 vs 8.5±0.3%; p<0.01) and the mean observation time longer (35±2 vs 25±3 months; p<0.05) in the pancreas recipients when compared with kidney transplanted patients. Heart rate variation during deep breathing, lying/standing and Valsalva manoeuver were very similar in both groups initially and did not improve during follow-up. However, there was a significant reduction in heart rate in the pancreas recipient group. Autonomic symptoms of the gastrointestinal and thermoregulatory system improved more in the pancreas grafted subjects, while hypoglycaemia unawareness deteriorated in the kidney recipients. This study suggests that long-term normoglycaemia by successful pancreatic grafting is able to halt the progression of autonomic dysfunction

In Vitro P38MAPK Inhibition in Aged Astrocytes Decreases Reactive Astrocytes, Inflammation and Increases Nutritive Capacity After Oxygen-Glucose Deprivation

Proper astroglial functioning is essential for the development and survival of neurons and oligodendroglia under physiologic and pathological circumstances. Indeed, malfunctioning of astrocytes represents an important factor contributing to brain injury. However, the molecular pathways of this astroglial dysfunction are poorly defined. In this work we show that aging itself can drastically perturb astrocyte viability with an increase of inflammation, cell death and astrogliosis. Moreover, we demonstrate that oxygen glucose deprivation (OGD) has a higher impact on nutritive loss in aged astrocytes compared to young ones, whereas aged astrocytes have a higher activity of the anti-oxidant systems. P38MAPK signaling has been identified to be upregulated in neurons, astrocytes and microglia after ischemic stroke. By using a pharmacological p38 alpha specific inhibitor (PH-797804), we show that p38MAPK pathway has an important role in aged astrocytes for inflammatory and oxidative stress responses with the subsequent cell death that occurs after OGD.Deutsche Forschungsgemeinschaft (SCHE 2078/2-1). Forderverein fur fruhgeborene Kinder an der Charite e.V. Basque Government Postdoc (2017_1_0095