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This research belongs focuses on the effects of financial instability on the rest of the economy. The article observes the dynamic changes of the shock spillovers between systemic stress and the rest of the German economy. In that way, the net emitters and receivers of shocks are observed throughout time, as previous research found that systemic stress is not always the predictor of other economic activity. The analysis utilizes Diebold and Yilmaz (2009, 2012) spillover index approach within the vector autoregression model. One step further is taken as well, as the changes of dynamics are observed throughout the entire period. As the macroprudential and monetary policymakers have to track the interrelationships between these variables over time, the approach in the study is straightforward and easy to interpret. The timing and intensity of the specific measures are important in practice, and such an approach enables the policymakers to meet these criteria.

Strong correlations have been shown between systemic oxidative stress (SOS) and the occurrence, metastasis, and prognosis of many types of cancers. It is yet unknown how SOS levels relate to the prognosis of esophageal squamous cell carcinoma (ESCC). The current research aims to explore the prognostic role of systemic oxidative stress index (SOSI) on ESCC receiving neoadjuvant immunochemotherapy (nICT). Retrospective recruitment was used to identify 224 nICT-treated ESCC patients. In order to determine the integrative score of SOSI, logistic regression analyses were utilized to screen independent risk variables, with disease-free survival (DFS) serving as the dependent variable. Given the non-linear relationship between SOSI and DFS, the best threshold was determined using a restricted cubic spline (RCS) model. Independent variable determination was executed using a cox regression analysis. For prognostic prediction, a risk categorization method based on recursive partitioning analysis (RPA) was also created. Four SOS-related indicators, including albumin, creatinine, blood urea nitrogen, and direct bilirubin, were used to establish the SOSI. The ideal threshold of SOSI, shown by the non-linear relationship between DFS and SOSI (P<0.001), was used to compare between two groups. As a potential prognostic factor for those nICT-treated ESCC patients, SOSI showed a strong correlation with both DFS and overall survival (OS). Patients with low SOSI had better DFS (55.1% vs. 85.5%, P<0.001) and OS (72.6% vs. 79.1%, P=0.013). Then, a new staging that included TNM and SOSI based on RPA algorithms was produced. In terms of prognostication, the RPA model performed significantly better than TNM classification. SOSI is a simple and useful score based on available SOS-related indices. In ESCC receiving nICT, low SOSI is found to be an important factor of better prognosis.

The main objective of this paper is to construct high-frequency composite indicators of financial stress for Croatia that will enable the monitoring of the total level of financial stress and its components on the domestic financial market. Emphasis is put on the choice of variables appropriate for small, open, highly euroized economies characterised by bank-centric financial systems dominantly owned by foreign banks, shallow financial markets and dependence on foreign capital.

The DJ-1 protein, known as an oxidative stress sensor, plays an important role in immunological processes. Using DJ-1 gene knock-out mice, we identified DJ-1 as a positive regulator in systemic lupus erythematosus (SLE). DJ-1 deficiency significantly alleviated skin lesion, splenomegaly, lymphadenopathy, while reducing multiple autoantibodies and immunoglobulin levels. Moreover, DJ-1 deficiency provided protection against renal hypertrophy and decreased glomerular deposition of immunoglobulin, ultimately leading to reduced albuminuria and SLE activity. These findings demonstrate that DJ-1 expression critically influences the progression of lupus-like disease.

Introduction A recent metabolomic screen of sera from patients with Systemic Lupus Erythematosus (SLE) found reduction of antioxidants and substrates for energy generation. These metabolic alterations may underlie one of the most common features of SLE - fatigue. The metabolomic studies also noted reduced omega-3 fatty acids, which are powerful anti- oxidants. This deficiency may be causally related to oxidative stress, inflammation, disease activity, and fatigue in SLE. Supplementation of omega-3 fatty acids using fish oil in SLE has been shown to reduce oxidative stress in other studies. The objective of this study is to evaluate the effect of fish oil supplementation on clinical measures of fatigue, quality of life, and disease activity as part of a randomized clinical trial. Methods Fifty SLE patients recruited in outpatient clinics were randomized 1:1 to fish oil supplementation or olive oil placebo, and blinded to their treatment group. At baseline and after 6 months of treatment, RAND Short Form-36 (RAND SF-36), Fatigue Severity Scale (FSS), SLE Disease Activity Index (SLEDAI), and Physician Global Assessment (PGA) were completed; serum was also collected for soluble mediator analysis. Results Thirty-two patients completed the study. PGA improved significantly in the fish oil group compared with the placebo group ( p  = 0.015). The RAND SF-36 Energy/fatigue and Emotional well-being scores demonstrated improvement trends ( p  = 0.092 and 0.070). No clear difference was seen in FSS and SLEDAI ( p  = 0.350 and p  = 0.417). Erythrocyte sedimentation rate and serum IL-12 were reduced ( p  = 0.008 and p  = 0.058); while serum IL-13 was increased by fish oil supplementation ( p  = 0.033). Conclusions In this randomized, placebo-controlled 6-month trial, SLE patients randomized to fish oil supplementation demonstrated improvement in their PGA, RAND SF-36, and some circulating inflammatory markers. Trial registration ClinicalTrials.gov Identifier: NCT02021513 (registered 13 December 2013).

Bullying is a common childhood experience that involves repeated mistreatment to improve or maintain one’s status. Victims display long-term social, psychological, and health consequences, whereas bullies display minimal ill effects. The aim of this study is to test how this adverse social experience is biologically embedded to affect short- or long-term levels of C-reactive protein (CRP), a marker of low-grade systemic inflammation. The prospective population-based Great Smoky Mountains Study (n = 1,420), with up to nine waves of data per subject, was used, covering childhood/adolescence (ages 9–16) and young adulthood (ages 19 and 21). Structured interviews were used to assess bullying involvement and relevant covariates at all childhood/adolescent observations. Blood spots were collected at each observation and assayed for CRP levels. During childhood and adolescence, the number of waves at which the child was bullied predicted increasing levels of CRP. Although CRP levels rose for all participants from childhood into adulthood, being bullied predicted greater increases in CRP levels, whereas bullying others predicted lower increases in CRP compared with those uninvolved in bullying. This pattern was robust, controlling for body mass index, substance use, physical and mental health status, and exposures to other childhood psychosocial adversities. A child’s role in bullying may serve as either a risk or a protective factor for adult low-grade inflammation, independent of other factors. Inflammation is a physiological response that mediates the effects of both social adversity and dominance on decreases in health.

Systemic lupus erythematosus (SLE) is a heterogeneous disease with unpredictable patterns of activity. Patients with similar activity levels may have different prognosis and molecular abnormalities. In this study, we aimed to measure the main differences in drug-induced gene expression signatures across SLE patients and to evaluate the potential for clinical data to build a machine learning classifier able to predict the SLE subset for individual patients. SLE transcriptomic data from two cohorts were compared with drug-induced gene signatures from the CLUE database to compute a connectivity score that reflects the capability of a drug to revert the patient signatures. Patient stratification based on drug connectivity scores revealed robust clusters of SLE patients identical to the clusters previously obtained through longitudinal gene expression data, implying that differential treatment depends on the cluster to which patients belongs. The best drug candidates found, mTOR inhibitors or those reducing oxidative stress, showed stronger cluster specificity. We report that drug patterns for reverting disease gene expression follow the cell-specificity of the disease clusters. We used 2 cohorts to train and test a logistic regression model that we employed to classify patients from 3 independent cohorts into the SLE subsets and provide a clinically useful model to predict subset assignment and drug efficacy.

To assess the prevalence of atherosclerotic cardiovascular disease (ASCVD) and its individual phenotypes of coronary artery disease (CAD), peripheral artery disease (PAD), and cerebrovascular disease by age and sex in a large US cohort of hospitalized patients with systemic lupus erythematosus (SLE). A nested case-control study of adults with and without SLE was conducted from the January 1, 2008, through December 31, 2014, National Inpatient Sample. Hospitalized patients with SLE were matched (1:3) by age, sex, race, and calendar year to hospitalized patients without SLE. The prevalences of CAD, PAD, and cerebrovascular disease were evaluated, and associations with SLE were determined after adjustment for common cardiovascular risk factors. Among the 252,676 patients with SLE and 758,034 matched patients without SLE, the mean age was 51 years, 89% were women, and 49% were white. Patients with SLE had a higher prevalence of ASCVD vs those without SLE (25.6% vs 19.2%; OR, 1.45; 95% CI, 1.44-1.47; P<.001). After multivariable adjustment, SLE was associated with a greater odds of ASCVD (adjusted odds ratio [aOR], 1.46; 95% CI, 1.41-1.51). The association between SLE and ASCVD was observed in women and men and was attenuated with increasing age. Also, SLE was associated with increased odds of CAD (aOR, 1.42; 95% CI, 1.40-1.44), PAD (aOR, 1.25; 95% CI, 1.22-1.28), and cerebrovascular disease (aOR, 1.68; 95% CI, 1.65-1.71). In hospitalized US patients, SLE was associated with increased ASCVD prevalence, which was observed in both sexes and was greatest in younger patients.

Subtle and asymptomatic nature of high blood pressure results in increase in mortality and morbidity. Dentists may play a vital role in identifying patients with suspected hypertension who are not yet diagnosed to refer them timely to physicians for diagnosis and management of the condition. The aim of this study was to compare the oral health status using decayed, missing, filled teeth (DMFT) index and perceived stress score using perceived stress scale (PSS-10) between systemically healthy dental patients, and patients with undiagnosed and known hypertension attending dental out-patient department of Combined Military Hospital (CMH) Lahore Medical College & Institute of Dentistry, Lahore, Pakistan. It is a cross-sectional descriptive study in which 108 patients participated selected through purposive sampling method, 36 in each group. According to Kruskal Wallis H test, there were significant associations seen among the three groups with age (p < 0.001), DMFT (p < 0.001), and PSS-10 scores (p = 0.003). According to Spearman’s matrix correlations, moderate positive correlations were observed between mean arterial pressure (MAP) and DMFT (r = 0.46, p < 0.001), and MAP and age (r = 0.38, p = 0.001), DMFT and PSS-10 (r = 0.47, p < 0.001), and DMFT and age (r = 0.33, p = 0.004) in healthy and patients with undiagnosed hypertension. It may be concluded that patients with raised blood pressure have higher perceived stress and deteriorated oral health.

Background Low-grade systemic inflammation has been reported in many psychiatric diseases and is described as a non-severe state of the inflammatory response. Post-traumatic stress disorder (PTSD) is a chronic psychiatric disorder characterized by symptoms of avoidance, re-experiencing and hyperarousal that develop secondary to a serious traumatic event. The trauma itself creates psychological and biological changes in the individual, apart from PTSD. This complex situation has still not been clarified and researchers have tended to research on inflammatory processes. Systemic immune inflammation index (SII), as a new index related to inflammation, is a comprehensive value based on peripheral lymphocyte, neutrophil and platelet counts. SII has been used as a marker of subclinical inflammation and prognosis in various studies. Although the presence of inflammation in PTSD was tried to be demonstrated through cytokines, inflammatory variables such as neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR) and SII, which are low-cost and easily shown in routine examinations, have not been studied before. Method We compared PTSD patients with healthy controls. 160 subjects (80 PTSD and 80 controls) were enrolled for study. All patients were evaluated with Structured clinical study form for DSM-V Axis 1 disorders. Exclusion criteria were as follows: presence of PTSD symptoms shorter than one month, presence of psychiatric comorbidity, being diagnosed with psychotic disorder, bipolar disorder, autism spectrum disorder, presence of mental retardation, being under psychotropic drug treatment, presence of a neurological disease that may cause serious disability (epilepsy, cerebrovascular disease), migraine, presence of organic brain damage, smoking, alcohol and substance use disorder, presence of a chronic disease such as diabetes mellitus, hypertension, hyperlipidemia, chronic lung diseases, being in pregnancy and breastfeeding, presence of heart disease were determined as exclusion criteria. Additionally, patients with diseases that could affect the leukocyte count (hematopoietic disease, malignancy, acute infection, acute or chronic renal failure, liver failure) and medication use (chemotherapy, history of glucocorticoid use in the last three months) were not included in the study. Patients who smoked more than fifteen cigarettes per day and had a body mass index > 30 were also excluded. SII is calculated as follows; SII = platelet count x neutrophil count / lymphocyte count. Results Sociodemographic data were comparable among groups. Neutrophil and platelet levels of PTSD patients were significantly higher than controls although both groups’ values were in normal range. Moreover, NLR, PLR and SII were significantly higher in PTSD group. Conclusion We found that NLR, PLR and SII values, which are easily calculable and cost-effective markers of systemic inflammation, were significantly higher in PTSD patients than in the control group. These values may be considered to identify patients who may benefit from adjuvant anti-inflammatory pharmacological treatment on top of psychotherapeutic treatment.