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Abstract Background The stigma of tuberculosis (TB) poses a significant challenge to TB control because it leads to delayed diagnosis and non-adherence. However, few studies on TB-related stigma have been completed in China. The aim of the current study was to explore the status of TB-related stigma and its associated predictive factors among TB patients in Dalian, Northeast China. Methods An institution-based, cross-sectional survey was conducted among outpatients at Dalian Tuberculosis Hospital in Liaoning Province, Northeast China. Data were collected by using a questionnaire that measured TB-related stigma, treatment status, anxiety, social support, doctor-patient communication and so on. A multiple linear regression model was used to determine the predictors of TB-related stigma. Results A total of 601 eligible participants were recruited. The mean score for TB-related stigma was 9.07, and the median score was 10. The average scores for anxiety, social support and doctor-patient communication were 4.03, 25.41 and 17.17, respectively. Multiple linear regression analysis revealed that patients who were female (β = 1.19, 95% CI: 0.38–2.01, P

Abstract Doctor–patient trust is not strong in China, but studies examining this factor remain insufficient. The present study aimed to explore the effect of doctor–patient communication, medical service quality, and service satisfaction on patient trust in doctors. Five hundred sixty-four patients with tuberculosis participated in this cross-sectional study in Dalian, China. They completed questionnaires assessing socio-demographic characteristics, doctor–patient communication, medical service quality, service satisfaction and patient trust in medical staff. A structural equation model was applied to examine the hypotheses, and all the study hypotheses were supported: (1) doctor–patient communication, medical service quality and service satisfaction were positively associated with building doctor–patient trust; (2) service quality positively mediated the relationship between doctor–patient communication and trust; (3) medical service satisfaction positively mediated the relationship between doctor–patient communication and trust; (4) medical service satisfaction positively mediated the relationship between medical service quality and doctor–patient trust; and (5) medical service quality and service satisfaction were the positively sequential mediators between communication and doctor–patient trust. Based on these findings, improvements in doctor–patient communication, medical service quality, and service satisfaction are the important issues contributing to the rebuilding of doctor–patient trust in medical service delivery.

Abstract Background Non-adherence to tuberculosis (TB) treatment is the most important cause of poor TB outcomes, and improving support for TB patients is a primary priority for governments, but there has been little research on the effects of family, social and national policy support factors on TB treatment adherence. The current study evaluated treatment adherence among newly diagnosed TB patients in Dalian, north-eastern China, and determined the effects of family, society, and national policy support factors on treatment adherence. Methods A cross-sectional survey was conducted among newly diagnosed TB patients treated at the outpatient department of Dalian Tuberculosis Hospital from September 2019 to January 2020. Data were collected using a questionnaire that measured medication adherence, family support, social support, and national policy support and so on. Differences between groups were assessed using Chi-square tests and Fisher’s exact tests. Ordinal logistic regression analysis was used to determine the predictors of adherence. Results A total of 481 newly diagnosed TB patients were recruited, of whom 45.7% had good adherence, and 27.4 and 26.8% had moderate and low adherence, respectively. Patients who had family members who frequently supervised medication (OR:0.34, 95% CI:0.16–0.70), family members who often provided spiritual encouragement (OR:0.13, 95% CI:0.02–0.72), a good doctor-patient relationship (OR:0.61, 95% CI:0.40–0.93), more TB-related knowledge (OR:0.49, 95% CI:0.33–0.72) and a high need for TB treatment policy support (OR:0.38, 95% CI:0.22–0.66) had satisfactory medication adherence. However, patients who had a college degree or higher (OR:1.69, 95% CI:1.04–2.74) and who suffered adverse drug reactions (OR:1.45, 95% CI:1.00–2.11) were more likely to have lower adherence. Conclusions Our findings suggested that non-adherence was high in newly diagnosed TB patients. Patients who had family members who frequently supervised medication and provided spiritual encouragement and a good doctor-patient relationship and TB-related knowledge and a high need for policy support contributed to high adherence. It is recommended to strengthen medical staff training and patient and family health education and to increase financial support for improving adherence.

Background/Aims: Vasopressin is a powerful stimulator of vascular calcification, augmenting osteogenic signaling in vascular smooth muscle cells (VSMCs) including up-regulation of the transcription factors core-binding factor α-1 (CBFA1), msh homeobox 2 (MSX2), and SRY-Box 9 (SOX9), as well as of tissue-nonspecific alkaline phosphatase (ALPL). Vasopressin-induced osteogenic signaling and calcification require the serum- & glucocorticoid-inducible kinase 1 (SGK1). Known effects of SGK1 include up-regulation of Na+/H+ exchanger 1 (NHE1). NHE1 further participates in the regulation of reactive oxygen species (ROS). NHE1 has been shown to participate in the orchestration of bone mineralization. The present study, thus, explored whether vasopressin modifies NHE1 expression and ROS generation, as well as whether pharmacological inhibition of NHE1 disrupts vasopressin-induced osteogenic signaling and calcification in VSMCs. Methods: Human aortic smooth muscle cells (HAoSMCs) were treated with vasopressin in the absence or presence of SGK1 siRNA, SGK1 inhibitor GSK-650394, and NHE1 blocker cariporide. Transcript levels were determined by using qRT-PCR, protein abundance by western blotting, ROS generation with 2’,7’-dichlorofluorescein diacetate (DCFDA) fluorescence, as well as ALP activity and calcium content by using colorimetric assays. Results: Vasopressin significantly enhanced the NHE1 transcript and protein levels in HAoSMCs, effects significantly blunted by SGK1 inhibition with GSK-650394 or SGK1 siRNA. Vasopressin increased ROS accumulation, an effect significantly blocked by NHE1 inhibitor cariporide. Vasopressin further significantly increased osteogenic markers CBFA1, MSX2, SOX9, and ALPL transcript levels, as well as ALP activity and calcium content in HAoSMCs, all effects significantly blunted by SGK1 silencing or in the presence of GSK-650394 and cariporide. Conclusion: Vasopressin stimulates NHE1 expression and ROS generation, an effect dependent on SGK1 and required for vasopressin-induced stimulation of osteogenic signaling and calcification of VSMCs.

Objectives The aim of this study was to analyse the status regarding inequities in adult obesity and central obesity in China. Thus, income-related inequality for both diseases and the underlying factors were examined.Methods and design The China Health and Nutrition Survey (CHNS)—conducted from 1997 to 2011—included 128 307 participants; in this study, 79 566 individuals classified as obese and 65 250 regarded as suffering from central obesity according to the CHNS were analysed. A body mass index greater than 27 was considered indicative of obesity; men and women with a waist circumference of more than 102 cm and 80 cm, respectively, were considered as suffering from central obesity. The concentration index was employed to analyse inequality in adult obesity and central obesity. The decomposition of this index based on a probit model was used to calculate the horizontal inequality index.Results The prevalence of adult obesity increased from 8.34% in 1997 to 17.74% in 2011, and that of central obesity increased from 6.52% in 1997 to 16.79% in 2011. The horizontal inequality index for adult obesity decreased from 0.1377 in 1997 to 0.0164 in 2011; for central obesity, it decreased from 0.0806 in 1997 to −0.0193 in 2011. The main causes of inequality for both diseases are, among others, economic status, marital status and educational attainment.Conclusions From 1997 to 2011, the prevalence of adult obesity and central obesity increased annually. The pro-rich inequalities in both adult and central obesity decreased from 1997 to 2011. The inequality in central obesity was more prominent in the low-income group in 2011. Future policies may need to address obesity reduction among the poor.

Background /Aims: Accumulating evidence indicates that endothelial inflammation is one of the critical determinants in pathogenesis of atherosclerotic cardiovascular disease. Our previous studies had demonstrated that Vaccariae prevented high glucose or oxidative stress-triggered endothelial dysfunction in vitro. Very little is known about the potential effects of hypaphorine from Vaccariae seed on inflammatory response in endothelial cells. Methods: In the present study, we evaluated the anti-inflammatory effects of Vaccariae hypaphorine (VH) on lipopolysaccharide (LPS)-challenged endothelial EA.hy926 cells. The inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), monocyte chemoattractant protein 1 (MCP-1) and vascular cellular adhesion molecule-1 (VCAM-1) were measured by real-time PCR (RT-PCR). The expressions of adenosine monophosphate-activated protein kinase (AMPK), acetyl-CoA carboxylase (ACC), toll-like receptor 4 (TLR4), peroxisome proliferator-activated receptor γ (PPARγ) were detected by Western blotting or immunofluorescence. Results: We showed that LPS stimulated the expressions of TNF-α, IL-1β, MCP-1, VCAM-1 and TLR4, but attenuated the phosphorylation of AMPK and ACC as well as PPARγ protein levels, which were reversed by VH pretreatment. Moreover, we observed that LPS-upregulated TLR4 protein expressions were inhibited by PPARγ agonist pioglitazone, and the downregulated PPARγ expressions in response to LPS were partially restored by knockdown of TLR4. The negative regulation loop between TLR4 and PPARγ response to LPS was modulated by AMPK agonist AICAR (5-Aminoimidazole-4-carboxamide riboside or acadesine) or A769662. Conclusions: Taken together, our results suggested that VH ameliorated LPS-induced inflammatory cytokines production in endothelial cells via inhibition of TLR4 and activation of PPARγ, dependent on AMPK signalling pathway.

Oxidized low-density lipoprotein (ox-LDL) accumulation is one of the critical determinants in endothelial dysfunction in many cardiovascular diseases such as atherosclerosis. C1q/TNF-related protein 9 (CTRP9) is identified to be an adipocytokine with cardioprotective properties. However, the potential roles of CTRP9 in endothelial function remain largely elusive. In the present study, the effects of CTRP9 on the proliferation, apoptosis, migration, angiogenesis, nitric oxide (NO) production and oxidative stress in human umbilical vein endothelial cells (HUVECs) exposed to ox-LDL were investigated. We observed that treatment with ox-LDL inhibited the proliferation, migration, angiogenesis and the generation of NO, while stimulated the apoptosis and reactive oxygen species (ROS) production in HUVECs. Incubation of HUVECs with CTRP9 rescued ox-LDL-induced endothelial injury. CTRP9 treatment reversed ox-LDL-evoked decreases in antioxidant enzymes including heme oxygenase-1 (HO-1), nicotinamide adenine dinucleotide phosphate (NAD(P)H) dehydrogenase quinone 1, and glutamate-cysteine ligase (GCL), as well as endothelial nitric oxide synthase (eNOS). Furthermore, CTRP9 induced activation of peroxisome proliferator-activated receptor γ co-activator 1α (PGC1-α) and phosphorylation of adenosine monophosphate-activated protein kinase (AMPK). Of interest, AMPK inhibition or PGC1-α silencing abolished CTRP9-mediated antioxidant enzymes levels, eNOS expressions, and endothelial protective effects. Collectively, we provided the first evidence that CTRP9 attenuated ox-LDL-induced endothelial injury by antioxidant enzyme inductions dependent on PGC-1α/AMPK activation. [ABSTRACT FROM AUTHOR]

Abstract Endothelial lesion response to injurious stimuli is a necessary step for initiating inflammatory cascades in blood vessels. Hypaphorine (Hy) from different marine sources is shown to exhibit anti-inflammatory properties. However, the potential roles and possible molecular mechanisms of Hy in endothelial inflammation have yet to be fully clarified. We showed that Hy significantly inhibited the positive effects of lipopolysaccharide (LPS) on pro-inflammatory cytokines expressions, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), monocyte chemoattractant protein 1 (MCP-1) and vascular cellular adhesion molecule-1 (VCAM-1), as well as induction of the phosphorylation of Akt and mTOR in HMEC-1 cells. The downregulated peroxisome proliferator-activated receptor γ (PPAR-γ) and upregulated toll-like receptor 4 (TLR4) expressions in LPS-challenged endothelial cells were prevented by Hy. Inhibition of both PI3K and mTOR reversed LPS-stimulated increases in TLR4 expressions and decreases in PPAR-γ levels. Genetic silencing of TLR4 or PPAR-γ agonist pioglitazone obviously abrogated the levels of pro-inflammatory cytokines in LPS-treated HMEC-1 cells. These results suggest that Hy may exert anti-inflammatory actions through the regulation of TLR4 and PPAR-γ dependent on PI3K/Akt/mTOR signal pathways. Hy may be considered as a therapeutic agent that can potentially relieve or ameliorate endothelial inflammation-associated diseases. [ABSTRACT FROM AUTHOR]

Background: Activation of macrophage is involved in many inflammation diseases. Lipopolysaccharide (LPS) is a powerful inflammatory signal contributing to monocytes/macrophages activation associated with increased proinflammatory cytokines expressions. We recently identified that vaccarin was expected to protect endothelial cells from injury. Hypaphorine was abundantly found in vaccaria semen. However, the potential roles and underlying mechanisms of vaccaria hypaphorine on macrophage inflammation have been poorly defined. Methods: This study was designed to determine the effects of vaccaria hypaphorine on LPS-mediated inflammation in RAW 264.7 cells. Results: In this study, we demonstrated that vaccaria hypaphorine dramatically ameliorated LPS-induced nitric oxide (NO) release and productions of proinflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, IL-10, monocyte chemoattractant protein 1 (MCP-1) and prostaglandin E2 (PGE2) in RAW 264.7 cells. LPS-stimulated expressions of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were down-regulated by vaccaria hypaphorine. Furthermore, vaccaria hypaphorine retarded LPS-induced phosphorylation of ERK, nuclear factor kappa beta (NFκB), NFκB inhibitor IκBα, and IKKβ. Immunofluorescence staining revealed that vaccaria hypaphorine eliminated the nuclear translocation of NFκB in LPS-treated RAW 264.7 cells. Conclusion: It was seen that vaccaria hypaphorine counteracted inflammation via inhibition of ERK or/and NF?B signaling pathways. Collectively, we concluded that vaccaria hypaphorine can be served as an anti-inflammatory candidate. [ABSTRACT FROM AUTHOR]