Socioeconomic Status and Health: Focusing on Co-Morbidity of Self Rated Health and Psychological Well-Being

Despite the well-documented associations between social and economic positions and diverse health conditions, the necessity and urgency of exploring the social and economic consequences of an array of health dimensions together have been proposed as a critical area of research to fully appreciate socioeconomic-health inequalities. The overall objective of the present study is to estimate the variance and covariation of two dimensions of health, i.e., self-rated health and psychological well-being, simultaneously, with specific attention to the social and economic influences, utilizing the multivariate response model. We use the 2005 National Health Interview Survey. Primary results indicate that variance in both self-rated health and psychological distress becomes attenuated with the adjustment of social and economic status, although variation in each outcome remains unexplained to some substantial degree. In addition, there is a strong and positive relationship between these two health outcomes in that individuals who are unhealthy tend also to have poor psychological resources (correlation = .34) and the substantial portion of co-morbidity between health conditions is attributable to the social and economic factors (about 37%)

Elastic p-12C scattering by using a cluster effective field theory

The elastic p-12C scattering at low energies is studied by using a cluster effective field theory (EFT), where the low-lying resonance states (s1/2, p3/2, d5/2) of 13N are treated as pertinent degrees of freedom. The low-energy constants of the Lagrangian are expressed in terms of the Coulomb-modified effective range parameters, which are determined to reproduce the experimental data for the differential cross-sections. The resulting theoretical predictions agree very well with the experimental data. The resulting theory is shown to give us almost identical phase shifts as obtained from the R-matrix approach. The role of the ground state of 13N below the threshold and the next-to-leading order in the EFT power counting are also discussed.Comment: 17 pages, 6 figure

Effects of a radiation dose reduction strategy for computed tomography in severely injured trauma patients in the emergency department: an observational study

<p>Abstract</p> <p>Background</p> <p>Severely injured trauma patients are exposed to clinically significant radiation doses from computed tomography (CT) imaging in the emergency department. Moreover, this radiation exposure is associated with an increased risk of cancer. The purpose of this study was to determine some effects of a radiation dose reduction strategy for CT in severely injured trauma patients in the emergency department.</p> <p>Methods</p> <p>We implemented the radiation dose reduction strategy in May 2009. A prospective observational study design was used to collect data from patients who met the inclusion criteria during this one year study (intervention group) from May 2009 to April 2010. The prospective data were compared with data collected retrospectively for one year prior to the implementation of the radiation dose reduction strategy (control group). By comparison of the cumulative effective dose and the number of CT examinations in the two groups, we evaluated effects of a radiation dose reduction strategy. All the patients met the institutional adult trauma team activation criteria. The radiation doses calculated by the CT scanner were converted to effective doses by multiplication by a conversion coefficient.</p> <p>Results</p> <p>A total of 118 patients were included in this study. Among them, 33 were admitted before May 2009 (control group), and 85 were admitted after May 2009 (intervention group). There were no significant differences between the two groups regarding baseline characteristics, such as injury severity and mortality. Additionally, there was no difference between the two groups in the mean number of total CT examinations per patient (4.8 vs. 4.5, respectively; p = 0.227). However, the mean effective dose of the total CT examinations per patient significantly decreased from 78.71 mSv to 29.50 mSv (p < 0.001).</p> <p>Conclusions</p> <p>The radiation dose reduction strategy for CT in severely injured trauma patients effectively decreased the cumulative effective dose of the total CT examinations in the emergency department. But not effectively decreased the number of CT examinations.</p

Protective Effect of Heme Oxygenase-1 on High Glucose-Induced Pancreatic β-Cell Injury

BackgroundGlucose toxicity that is caused by chronic exposure to a high glucose concentration leads to islet dysfunction and induces apoptosis in pancreatic β-cells. Heme oxygenase-1 (HO-1) has been identified as an anti-apoptotic and cytoprotective gene. The purpose of this study is to investigate whether HO-1 up-regulation when using metalloprotophyrin (cobalt protoporphyrin, CoPP) could protect pancreatic β-cells from high glucose-induced apoptosis.MethodsReverse transcription-polymerase chain reaction was performed to analyze the CoPP-induced mRNA expression of HO-1. Cell viability of INS-1 cells cultured in the presence of CoPP was examined by acridine orange/propidium iodide staining. The generation of intracellular reactive oxygen species (ROS) was measured using flow cytometry. Glucose stimulated insulin secretion (GSIS) was determined following incubation with CoPP in different glucose concentrations.ResultsCoPP increased HO-1 mRNA expression in both a dose- and time-dependent manner. Overexpression of HO-1 inhibited caspase-3, and the number of dead cells in the presence of CoPP was significantly decreased when exposed to high glucose conditions (HG). CoPP also decreased the generation of intracellular ROS by 50% during 72 hours of culture with HG. However, decreased GSIS was not recovered even in the presence of CoPP.ConclusionOur data suggest that CoPP-induced HO-1 up-regulation results in protection from high glucose-induced apoptosis in INS-1 cells; however, glucose stimulated insulin secretion is not restored

Signal Transduction Mechanisms Underlying Group I mGluR-mediated Increase in Frequency and Amplitude of Spontaneous EPSCs in the Spinal Trigeminal Subnucleus Oralis of the Rat

Group I mGluRs (mGluR1 and 5) pre- and/or postsynaptically regulate synaptic transmission at glutamatergic synapses. By recording spontaneous EPSCs (sEPSCs) in the spinal trigeminal subnucleus oralis (Vo), we here investigated the regulation of glutamatergic transmission through the activation of group I mGluRs. Bath-applied DHPG (10 μM/5 min), activating the group I mGluRs, increased sEPSCs both in frequency and amplitude; particularly, the increased amplitude was long-lasting. The DHPG-induced increases of sEPSC frequency and amplitude were not NMDA receptor-dependent. The DHPG-induced increase in the frequency of sEPSCs, the presynaptic effect being further confirmed by the DHPG effect on paired-pulse ratio of trigeminal tract-evoked EPSCs, an index of presynaptic modulation, was significantly but partially reduced by blockades of voltage-dependent sodium channel, mGluR1 or mGluR5. Interestingly, PKC inhibition markedly enhanced the DHPG-induced increase of sEPSC frequency, which was mainly accomplished through mGluR1, indicating an inhibitory role of PKC. In contrast, the DHPG-induced increase of sEPSC amplitude was not affected by mGluR1 or mGluR5 antagonists although the long-lasting property of the increase was disappeared; however, the increase was completely inhibited by blocking both mGluR1 and mGluR5. Further study of signal transduction mechanisms revealed that PLC and CaMKII mediated the increases of sEPSC in both frequency and amplitude by DHPG, while IP3 receptor, NO and ERK only that of amplitude during DHPG application. Altogether, these results indicate that the activation of group I mGluRs and their signal transduction pathways differentially regulate glutamate release and synaptic responses in Vo, thereby contributing to the processing of somatosensory signals from orofacial region

Out-of-Plane Strengthening of Unreinforced Masonry Walls by Glass Fiber-Reinforced Polyurea

Fiber-reinforced polymer reinforcement or polyurea reinforcement techniques are applied to strengthen unreinforced masonry walls (UMWs). The purpose of this experimental study is to verify the out-of-plane reinforcing effect of sprayed glass fiber-reinforced polyurea (GFRPU), which is a composite elastomer made of polyurea and milled glass fibers on UMW. The out-of-plane strengths and ductile behaviors based on various coating shapes are compared in this study. An empirical formula to describe the degree of reinforcement on the out-of-plane strength of the UMW is derived based on the experimental results. It is observed that the peak load-carrying capacity, ductility, and energy absorption capacity gradually improve with an increase in the strengthening degree or area. Compared with the existing masonry wall reinforcement method, the GFRPU technique is a construction method that can help improve the safety performance along with ease of construction and economic efficiency. Doi: 10.28991/CEJ-2022-08-01-011 Full Text: PD

In-Plane Strengthening of Unreinforced Masonry Walls by Glass Fiber-Reinforced Polyurea

Strengthening techniques have been employed in Korea to unreinforced masonry walls (UMWs) for several years to protect them from damage caused by the intermittent occurrence of earthquakes. Polyurea, which has a high tensile strength and elongation rate, can be utilized as a strengthening material to enhance the in-plane strength and ductility of UMWs. Glass fiber-reinforced polyurea (GFRPU) is a composite elastomer manufactured by progressively adding milled glass fiber to polyurea. The purpose of this study is to investigate the enhancement of the in-plane strength and ductility of UMWs using GFRPU, depending on the shape of the GFRPU coating on the wall. Four masonry wall specimens are tested with test variables of the number of strengthening sides and coating shapes. It is illustrated that the GFRPU reinforcement of masonry wall leads to enhanced load-carrying capacity, ductility, and energy absorption. An empirical formula to represent the degree of strengthening effected by GFRPU is proposed in this study. Doi: 10.28991/cej-2021-03091782 Full Text: PD

Cigarette smoke exacerbates mouse allergic asthma through Smad proteins expressed in mast cells

<p>Abstract</p> <p>Background</p> <p>Many studies have found that smoking reduces lung function, but the relationship between cigarette smoke and allergic asthma has not been clearly elucidated, particularly the role of mast cells. This study aimed to investigate the effects of smoke exposure on allergic asthma and its association with mast cells.</p> <p>Methods</p> <p>BALB/c mice were sensitized and challenged by OVA to induce asthma, and bone marrow-derived mast cells (BMMCs) were stimulated with antigen/antibody reaction. Mice or BMMCs were exposed to cigarette smoke or CSE solution for 1 mo or 6 h, respectively. The recruitment of inflammatory cells into BAL fluid or lung tissues was determined by Diff-Quik or H&E staining, collagen deposition by Sircol assay, penh values by a whole-body plethysmography, co-localization of tryptase and Smad3 by immunohistochemistry, IgE and TGF-β level by ELISA, expressions of Smads proteins, activities of signaling molecules, or TGF-β mRNA by immunoblotting and RT-PCR.</p> <p>Results</p> <p>Cigarette smoke enhanced OVA-specific IgE levels, penh values, recruitment of inflammatory cells including mast cells, expressions of smad family, TGF-β mRNA and proteins, and cytokines, phosphorylations of Smad2 and 3, and MAP kinases, co-localization of tryptase and Smad3, and collagen deposition more than those of BAL cells and lung tissues of OVA-induced allergic mice. CSE solution pretreatment enhanced expressions of TGF-β, Smad3, activities of MAP kinases, NF-κB/AP-1 or PAI-1 more than those of activated-BMMCs.</p> <p>Conclusions</p> <p>The data suggest that smoke exposure enhances antigen-induced mast cell activation via TGF-β/Smad signaling pathways in mouse allergic asthma, and that it exacerbates airway inflammation and remodeling.</p