Purpose-As multinational firms seek to acquire competitive cost advantages through global sourcing, it is also important for them to develop effective strategies to reduce possible damage of a negative country-of-origin (COO) effect. This study aims to examine whether brand image and evaluation mode could alleviate a negative COO effect. Design/methodology/approach-A 2(COO) £ 2(brand) £ 2(evaluation mode) experimental design was employed in order to examine whether brand and COO effects on product evaluation vary under different evaluation modes. The data were analyzed by a repeated measure MANOVA. Findings-The results showed that products made in favourable countries were rated higher in joint evaluation mode than in separate evaluation mode. Conversely, products made in unfavourable countries were better evaluated in separate evaluation mode than in joint evaluation mode. The results of the study are not in favour of the notion that a strong brand image could overcome the negative effect of COO. Research limitations/implications-Conclusions of the study suggest that the COO effect plays an equally important role in consumer product evaluation for both strong and weak brands. Thus, even for a product with strong brand image, the negative consequences of COO stemming from consumerš unfavourable attitudes towards the manufacturing country are not likely to be completely eliminated. Moreover, to alleviate the negative impact of unfavourable COO, marketers may want to avoid direct comparison between products made in unfavourable countries with those made in favourable countries, regardless of their brand strength. Practical implications-When marketing a product made in an unfavourable country, marketers should manage to create a selling environment facilitating a separate evaluation mode. In contrast, marketers should proactively manage to display products from favourable countries along with those from unfavourable countries in order to further enhance quality perceptions. Originality/value-The results of the study could help marketers employ advantageous merchandizing or advertising strategies to lessen the negative effect of COO.

The aims of this study were to compare the quality of life (QOL) between subjects with and without heroin use and to examine the association of QOL with sociodemographic characteristics, characteristics of heroin use, family support, and depression among heroin users at entry to a methadone maintenance treatment program. A group of 123 heroin users who visited an outpatient addiction treatment clinic in southern Taiwan for methadone maintenance treatment were recruited into this study. We also recruited 106 subjects who had never used heroin as the control group. Their QOL status was assessed by the short form of the Taiwan Version of the World Health Organization Questionnaire on Quality of Life (the WHOQOL-BREF Taiwan version). The level of QOL between subjects with and without heroin use was compared, and the correlates of QOL among heroin users were examined. Heroin users had poorer QOL than nonusers in the physical, psychological, and social relationship domains but not the environment domain of the WHOQOL-BREF after controlling for the influences of other factors. In addition, heroin users with obvious depression had poorer QOL in all four domains than those without obvious depression. Also, heroin users who perceived higher family support had better QOL in the social relationship and environment domains. Heroin users had poorer QOL than nonusers in multiple domains. Relief of depressive symptoms and enhancement of family support should be important strategies to improve QOL in heroin users.

Objectives We aimed to examine whether the C-reactive protein (CRP) level could be used to differentiate between major depressive disorder (MDD) and bipolar II disorder (BD II). Methods Ninety-six healthy controls, 88 BD II and 72 MDD drug-naïve patients in their major depressive episodes were enrolled. The fasting plasma level of high-sensitivity CRP was assessed at baseline and after treatment. Results The BD II patients presented significantly higher 17-item Hamilton Depression Rating Scale (HDRS) scores and CRP levels at baseline when adjustment for age, gender, and body mass index (P < 0.001 and P < 0.001, respectively). After treatment the CRP levels remained significantly different (P < 0.001), although the HDRS score was not significantly different between the BD II and MDD patients. A receiver-operating characteristic analysis showed that a baseline CRP level of 621.6 ng/mL could discriminate between BD II and MDD, with an area under the curve of 0.816 and a sensitivity and specificity of 0.699 and 0.882, respectively. Furthermore, the baseline CRP level greater than 621.6 ng/ml had 28.2 higher odds of a diagnosis of BD II (P < 0.001, 95% confidence interval: 10.96-72.35). Conclusions The level of CRP plays a role of biomarker to differentiate between MDD and BD II depression in both their depressed and euthymic state.

The diagnosis of Bipolar II disorder (BD-II) is currently based on the patients' description of symptoms and clinical behavioral observations. This study explored the possibility of miRNA in peripheral blood (serum) as a specific biomarker for BD-II. We identified 6 candidate miRNAs to differentiate BD-II patients from controls using next-generation sequencing. We then examined these candidate miRNAs using real-time PCR in the first cohort (as training group) of 79 BD-II and 95 controls. A diagnostic model was built based on these candidate miRNAs and then tested on an individual testing group (BD-II: n = 20, controls: n = 20). We found that serum expression levels of miR-7-5p, miR-23b-3p, miR-142-3p, miR-221-5p, and miR-370-3p significantly increased in BD-II compared with controls in the first cohort, whereas that of miR-145-5p showed no significant difference. The diagnostic power of the identified miRNAs was further analyzed using receiver-operating characteristic (ROC). Support vector machine (SVM) measurements revealed that a combination of the significant miRNAs reached good diagnostic accuracy (AUC: 0.907). We further examined an independent testing group and the diagnostic power reached fair for BD-II (specificity = 90%, sensitivity = 85%). We constructed miRNA panels using SVM model, which may aid in the diagnosis for BD-II.Bipolar disorder (BD) has several subtypes. Bipolar I disorder (BD-I) and bipolar II disorder (BD-II) are two of the most commonly seen subtypes of BD. BD-I and BD-II differ in clinical presentation: BD-I involves one or more manic or mixed episodes in addition to one or more major depressive episodes. BD-II is characterised by at least one hypomanic episode with one or more major depressive episodes 1,2 . BD-II has become the focus of increasing attention and has been recognised as a unique disorder. Its prevalence rate ranges from 3% to 11% 3 . Nevertheless, because of the complex spectrum of symptoms, the diagnosis of BD remains subjective. Diagnosing BD is challenging because patients typically regard hypomanic episodes as a positive mood status or experience, and they only seek medical help during depressive episodes 4 . BD is initially misdiagnosed at a rate of approximately 40% and typically requires approximately 5-12 years to be correctly diagnosed and treated appropriately 5,6 . Delayed diagnosis and inefficacious treatment of BD-II may lead to a prolonged course, more affective episodes, and an increased suicide rate, adding further to its socioeconomic burden 5,7 .Accumulating evidence reveals that microribonucleic acids (miRNAs) are involved in many biological processes such as neurogenesis, neuroproliferation, and synaptic plasticity in the central nervous system 8,9 . Different expressions of peripheral miRNA have been reported in several mental disorders including schizophrenia, major depressive disorder, and Alzheimer disease [10][11][12] . Changes in peripheral miRNA may be correlated with changes in neuroendocrine or neuroimmune responses 13 . Because brain tissue ...

We conclude that plasma BDNF profiles in different mental disorders are not affected by BDNF Val66Met gene variants, but by the process and progression of the illness itself.