Social inequality, social networks, and health: a scoping review of research on health inequalities from a social network perspective.

BACKGROUND: This review summarises the present state of research on health inequalities using a social network perspective, and it explores the available studies examining the interrelations of social inequality, social networks, and health. METHODS: Using the strategy of a scoping review, as outlined by Arksey and O'Malley (Int J Sci Res Methodol 8:19-32, 2005), our team performed two searches across eight scientific, bibliographic databases including papers published until October 2021. Studies meeting pre-defined eligibility criteria were selected. The data were charted in a table, and then collated, summarised, and reported in this paper. RESULTS: Our search provided a total of 15,237 initial hits. After deduplication (n = 6,168 studies) and the removal of hits that did not meet our baseline criteria (n = 8,767 studies), the remaining 302 full text articles were examined. This resulted in 25 articles being included in the present review, many of which focused on moderating or mediating network effects. Such effects were found in the majority of these studies, but not in all. Social networks were found to buffer the harsher effects of poverty on health, while specific network characteristics were shown to intensify or attenuate the health effects of social inequalities. CONCLUSIONS: Our review showed that the variables used for measuring health and social networks differed considerably across the selected studies. Thus, our attempt to establish a consensus of opinion across the included studies was not successful. Nevertheless, the usefulness of social network analysis in researching health inequalities and the employment of health-promoting interventions focusing on social relations was generally acknowledged in the studies. We close by suggesting ways to advance the research methodology, and argue for a greater orientation on theoretical models. We also call for the increased use of structural measures; the inclusion of measures on negative ties and interactions; and the use of more complex study designs, such as mixed-methods and longitudinal studies.

Role of Catalyst in Optimizing Fluid Catalytic Cracking Performance During Cracking of H-Oil-Derived Gas Oils.

Three H-Oil gas oils, heavy atmospheric gas oil (HAGO), light vacuum gas oil (LVGO), heavy vacuum gas oil (HVGO), and two their blends with hydrotreated straight run vacuum gas oils (HTSRVGOs) were cracked on two high unit cell size (UCS) lower porosity commercial catalysts and two low UCS higher porosity commercial catalysts. The cracking experiments were performed in an advanced cracking evaluation fluid catalytic cracking (FCC) laboratory unit at 527 °C, 30 s catalyst time on stream, and catalyst-to-oil (CTO) variation between 3.5 and 7.5 wt/wt The two high UCS lower porosity catalysts were more active and more coke selective. However, the difference between conversion of the more active high UCS lower porosity and low UCS higher porosity catalysts at 7.5 wt/wt CTO decreased in the order 10% (HAGO) > 9% (LVGO) > 6% (HVGO) > 4% (80% HTSRVGO/20% H-Oil VGO). Therefore, the catalyst performance is feedstock-dependent. The four studied catalysts along with a blend of one of them with 2% ZSM-5 were examined in a commercially revamped UOP FCC VSS unit. The lower UCS higher porosity catalysts exhibited operation at a higher CTO ratio achieving a similar conversion level with more active higher UCS lower porosity catalysts. However, the higher UCS lower porosity catalysts made 0.67% Δ coke that was higher than the maximum acceptable limit of 0.64% for this particular commercial FCC unit (FCCU), which required excluding the HVGO from the FCC feed blend. The catalyst system containing ZSM-5 increased the LPG yield but did not have an impact on gasoline octane. It was found that the predominant factor that controls refinery profitability related to the FCCU performance is the FCC slurry oil (bottoms) yield.

Tolerance and threshold in the extrinsic coagulation system.

This paper focus on the quest for mechanisms that are able to create tolerance and an activation threshold in the extrinsic coagulation cascade. We propose that the interplay of coagulation inhibitor and blood flow creates threshold behavior. First we test this hypothesis in a minimal, four dimensional model. This model can be analysed by means of time scale analysis. We find indeed that only the interplay of blood flow and inhibition together are able to produce threshold behavior. The mechanism relays on a combination of raw substance supply and wash-out effect by the blood flow and a stabilization of the resting state by the inhibition. We use the insight into this minimal model to interpret the simulation results of a large model. Here, we find that the initiating steps (TF that produces together with fVII(a) factor Xa) does not exhibit threshold behavior, but the overall system does. Hence, the threshold behavior appears via the feedback loop (in that fIIa produces indirectly fXa that in turn produces fIIa again) inhibited by ATIII and blood flow.

Spatial reorganization of cortical motor output maps of stump muscles in human upper-limb amputees.

Spatial changes of the motor cortical representation of the biceps brachii muscle (stump muscle) were studied in ten patients with long-standing amputations at the level of the forearm. Motor output maps were established by focal transcranial magnetic stimulation on a skull surface grid overlying the motor cortex. Characteristics of the motor output map were its spatial extension (number of effective stimulation sites), the maximal response amplitude and the center of gravity (COG) of the spatial distribution of response amplitudes. The extension of the stump muscle motor maps was increased (ratio: 1.5+/-0.3 versus 1.0+/-0.3 in control group; P<0.05) and the stump muscle motor responses were much larger (ratio: 2.6+/-0.6 versus 1.0+/-0.5 in the control group; P<0.05). The COG of the stump muscle map was significantly shifted laterally by, on average, 6.0+/-7.7 mm (range, -3.4-21 mm; P<0.05), either reflecting gross changes of local cortical excitability or structural anatomic reorganization.