Cross-domain colorization of unpaired infrared images through contrastive learning guided by color feature selection attention.

In challenging lighting conditions, infrared detectors have become vital tools for enhancing visual perception, overcoming the limitations of visible cameras. However, inherent imaging principles and manufacturing constraints confine infrared imaging systems to grayscale, significantly impacting their utility. In comparison to visible imagery, infrared images lack detailed semantic information, color representation, and suffer from reduced contrast. While existing infrared image colorization techniques have made significant progress in improving color quality, challenges such as erroneous semantic color prediction and blurred depiction of fine details persist. Acquiring paired color images corresponding to real-world infrared scenarios poses substantial difficulties, exacerbating challenges in cross-domain colorization of infrared images. To address these critical issues, this paper introduces an innovative approach utilizing contrastive learning for unsupervised cross-domain mapping between unpaired infrared and visible color images. Additionally, we introduce a color feature selection attention module guiding rational infrared image coloring. The proposed method employs the Residual Fusion Attention Network (RFANet) as a generator, enhancing the encoder's ability to represent color and structural features. Furthermore, to ensure structural content consistency and enhance overall color style matching accuracy, we design a comprehensive joint global loss function integrating both detailed content and color style. Experimental evaluations on publicly available datasets demonstrate the superior performance of the proposed unsupervised cross-domain colorization method for infrared images compared to previous approaches.

Exposure to polystyrene nanoplastics induces hepatotoxicity involving NRF2-NLRP3 signaling pathway in mice.

Nanoplastic contamination has been of intense concern by virtue of the potential threat to human and ecosystem health. Animal experiments have indicated that exposure to nanoplastics (NPs) can deposit in the liver and contribute to hepatic injury. To explore the mechanisms of hepatotoxicity induced by polystyrene-NPs (PS-NPs), mice and AML-12 hepatocytes were exposed to different dosages of 20 nm PS-NPs in this study. The results illustrated that in vitro and in vivo exposure to PS-NPs triggered excessive production of reactive oxygen species and repressed nuclear factor erythroid-derived 2-like 2 (NRF2) antioxidant pathway and its downstream antioxidase expression, thus leading to hepatic oxidative stress. Moreover, PS-NPs elevated the levels of NLRP3, IL-1ß and caspase-1 expression, along with an activation of NF-κB, suggesting that PS-NPs induced hepatocellular inflammatory injury. Nevertheless, the activaton of NRF2 signaling by tert-butylhydroquinone mitigated PS-NPs-caused oxidative stress and inflammation, and inbihited NLRP3 and caspase-1 expression. Conversely, the rescuing effect of NRF2 signal activation was dramatically supressed by treatment with NRF2 inhibitor brusatol. In summary, our results demonstrated that NRF2-NLRP3 pathway is involved in PS-NPs-aroused hepatotoxicity, and the activation of NRF2 signaling can protect against PS-NPs-evoked liver injury. These results provide novel insights into the hepatotoxicity elicited by NPs exposure.

Effect of the Lipoxin Receptor Agonist BML-111 on Cigarette Smoke Extract-Induced Macrophage Polarization and Inflammation in RAW264.7 Cells.

Background: Macrophages are known to play a crucial role in the chronic inflammation associated with Chronic Obstructive Pulmonary Disease (COPD). BML-111, acting as a lipoxin A4 (LXA4) receptor agonist, has shown to be effective in protecting against COPD. However, the precise mechanism by which BML-111 exerts its protective effect remains unclear. Methods: In order to establish a cell model of inflammation, cigarette smoke extract (CSE) was used on the RAW264.7 cell line. Afterwards, an Enzyme-linked immunosorbent assay (ELISA) kit was employed to measure concentrations of tumor necrosis factor-α (TNF-α), interleukin-1beta (IL-1ß), interleukin-18 (IL-18), and interleukin-10 (IL-10) in the cell supernatants of the RAW264.7 cells.In this study, we examined the markers of macrophage polarization using two methods: quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis. Additionally, we detected the expression of Notch-1 and Hes-1 through Western blotting. Results: BML-111 effectively suppressed the expression of pro-inflammatory cytokines TNF-α, IL-1ß, and IL-18, as well as inflammasome factors NLRP3 and Caspase-1, while simultaneously up-regulating the expression of the anti-inflammatory cytokine IL-10 induced by CSE. Moreover, BML-111 reduced the expression of iNOS, which is associated with M1 macrophage polarization, and increased the expression of Arg-1, which is associated with M2 phenotype. Additionally, BML-111 downregulated the expression of Hes-1 and the ratio of activated Notch-1 to Notch-1 induced by CSE. The effect of BML-111 on inflammation and macrophage polarization was reversed upon administration of the Notch-1 signaling pathway agonist Jagged1. Conclusion: BML-111 has the potential to suppress inflammation and modulate M1/M2 macrophage polarization in RAW264.7 cells. The underlying mechanism may involve the Notch-1 signaling pathway.

Exposure to nanoplastics induces mitochondrial impairment and cytomembrane destruction in Leydig cells.

Plastic particle pollution poses an emerging threat to ecological and human health. Laboratory animal studies have illustrated that nano-sized plastics can accumulate in the testis and cause testosterone deficiency and spermatogenic impairment. In this study, TM3 mouse Leydig cells were in vitro exposed to polystyrene nanoparticles (PS-NPs, size 20 nm) at dosages of 50, 100 and 150 µg/mL to investigate their cytotoxicity. Our results demonstrated that PS-NPs can be internalized into TM3 Leydig cells and led to a concentration-dependent decline in cell viability. Furthermore, PS-NPs stimulation amplified ROS generation and initiated cellular oxidative stress and apoptosis. Moreover, PS-NPs treatment affected the mitochondrial DNA copy number and collapsed the mitochondrial membrane potential, accompanied by a disrupted energy metabolism. The cells exposed to PS-NPs also displayed a down-regulated expression of steroidogenesis-related genes StAR, P450scc and 17ß-HSD, along with a decrease in testosterone secretion. In addition, treatment with PS-NPs destructed plasma membrane integrity, as presented by increase in lactate dehydrogenase release and depolarization of cell membrane potential. In summary, these data indicated that exposure to PS-NPs in vitro produced cytotoxic effect on Leydig cells by inducing oxidative injury, mitochondrial impairment, apoptosis, and cytomembrane destruction. Our results provide new insights into male reproductive toxicity caused by NPs.

α-Pyrones with glucose uptake-stimulatory activity from the twigs of Cryptocarya wrayi.

Five new α-pyrones, cryptowratones A-E (1-5), and five known congeners (6-10), together with four other known compounds 11-14 were isolated from the twigs of Cryptocarya wrayi. The structures of the new compounds were elucidated on the basis of extensive spectroscopic data analysis and ECD calculations. All α-pyrones except 6 were evaluated for their stimulatory effects on glucose uptake in vitro with CHO-K1/GLUT4 cells. The positive control insulin displayed an approximate 42 ± 0.14% promotion on glucose uptake at 25 µM, compared with the CHO-K1/GLUT4 group. Compounds 1a/2a, 2, 3, and 10 showed a more significant stimulation of glucose uptake than insulin (25 µM) by 36 ± 0.08%, 27 ± 0.12%, 28 ± 0.12%, and 25 ± 0.12% at 1.5 µM, respectively. Immunofluorescence assays indicated the glucose uptake-stimulatory activity of α-pyrones might be correlated with increased GLUT4 translocation.

Lipoxin A4 promotes autophagy and inhibits overactivation of macrophage inflammasome activity induced by Pg LPS.

OBJECTIVE: To explore the role of lipoxin A4 (LXA4) on inflammasome and inflammatory activity in macrophages activated by Porphyromonas gingivalis lipopolysaccharide (PgLPS) one of the major causative agents of chronic periodontitis. METHODS: The mouse macrophage cell line RAW264.7 was used to produce an activated inflammation model. Markers of inflammasome and inflammatory activity and autophagy were assessed by ELISA, reverse transcription polymerase chain reaction (RT-PCR), and Western blot assay. RESULTS: Markers of inflammasome activity, inflammation and autophagy increased with Pg LPS concentration. They also increased with increasing exposure to Pg LPS up to 12h but decreased at 24h. However, markers of autophagy increased. Phosphorylated NF-κBp65 decreased with LXA4, which was similar to results obtained with the autophagy inducer, rapamycin. CONCLUSIONS: LXA4 promoted autophagy and inhibited activation of inflammasomes and inflammation markers in macrophage inflammation induced by PgLPS and this action was linked to the phosphorylation of NF-κB.

Automatic Lumbar Spine Tracking Based on Siamese Convolutional Network.

Deep learning has demonstrated great success in various computer vision tasks. However, tracking the lumbar spine by digitalized video fluoroscopic imaging (DVFI), which can quantitatively analyze the motion mode of the spine to diagnose lumbar instability, has not yet been well developed due to the lack of steady and robust tracking method. The aim of this work is to automatically track lumbar vertebras with rotated bounding boxes in DVFI sequences. Instead of distinguishing vertebras using annotated lumbar images or sequences, we train a full-convolutional siamese neural network offline to learn generic image features with transfer learning. The siamese network is trained to learn a similarity function that compares the labeled target from the initial frame with the candidate patches from the current frame. The similarity function returns a high score if the two images depict the same object. Once learned, the similarity function is used to track a previously unseen object without any adapting online. Our tracker is performed by evaluating the candidate rotated patches sampled around the previous target's position and presents rotated bounding boxes to locate the lumbar spine from L1 to L4. Results indicate that the proposed tracking method can track the lumbar vertebra steadily and robustly. The study demonstrates that the lumbar tracker based on siamese convolutional network can be trained successfully without annotated lumbar sequences.

Object Tracking Based on Vector Convolutional Network and Discriminant Correlation Filters.

Due to the fast speed and high efficiency, discriminant correlation filter (DCF) has drawn great attention in online object tracking recently. However, with the improvement of performance, the costs are the increase in parameters and the decline of speed. In this paper, we propose a novel visual tracking algorithm, namely VDCFNet, and combine DCF with a vector convolutional network (VCNN). We replace one traditional convolutional filter with two novel vector convolutional filters in the convolutional stage of our network. This enables our model with few memories (only 59 KB) trained offline to learn the generic image features. In the online tracking stage, we propose a coarse-to-fine search strategy to solve drift problems under fast motion. Besides, we update model selectively to speed up and increase robustness. The experiments on OTB benchmarks demonstrate that our proposed VDCFNet can achieve a competitive performance while running over real-time speed.

[Testicular injection of lipopolysaccharide: An effective method for establishing the mouse model of orchitis].

OBJECTIVE: To search for a method of establishing a reliable mouse model of orchitis and investigate the association of orchitis with the activation of the inflammasome. METHODS: We equally randomized 40 adult male KM mice into groups A (sham operation), B (intraperitoneal injection of lipopolysaccharide ï¼»LPSï¼½), C (unilateral testicular injection of glacial acetic acid ï¼»GAAï¼½), and D (unilateral testicular injection of LPS). At 3 weeks after modeling, we measured the sperm concentration and percentage of progressively motile sperm (PMS) in the epididymis by computer-assisted semen analysis, observed the pathological changes in the testis tissue by HE staining, and determined the expressions of the Caspase-1 and interleukin (IL)-1ß proteins by Western blot. RESULTS: The sperm concentration in the epididymis was significantly decreased in groups B (ï¼»25.74 ± 3.19ï¼½ ×106/ml), C (ï¼»17.16 ± 4.41ï¼½ ×106/ml) and D (ï¼»16.92 ± 7.13ï¼½ ×106/ml) as compared with that in group A (ï¼»28.20 ± 1.63ï¼½ ×106/ml) (all P < 0.05), even more significantly in B than in C and D (P < 0.01), and so was PMS in groups B (ï¼»29.57 ± 2.16ï¼½%), C (ï¼»18.10 ± 2.38ï¼½%) and D (ï¼»7.34 ± 1.63ï¼½%) in comparison with group A (ï¼»59.34 ± 1.10ï¼½%) (P < 0.01), even more significantly in B and C than in D (P < 0.01). Light microscopy revealed different degrees of pathological changes in the testis tissue, most significant in group D, followed by C and B. Both the expressions of Caspase-1 and IL-1ß were remarkably up-regulated in groups B, C and D compared with those in group A (P < 0.01), even more markedly in D than in B and C (P < 0.05). CONCLUSIONS: Unilateral testicular injection of LPS is a more efficient method than either unilateral testicular injection of GAA or intraperitoneal injection of LPS for establishing the mouse model of orchitis. Orchitis may be pathologically associated with the activation of the NLRP3 inflammasome.

BML-111, a lipoxin receptor agonist, protects against acute injury via regulating the renin angiotensin-aldosterone system.

BACKGROUND: The renin angiotensin-aldosterone system (RAAS) and lipoxins (LXs) have similar roles in many processes. We previously reported that BML-111, a Lipoxin receptor agonist, inhibited chronic injury hepatic fibrosis by regulating RAAS, but whether LXs are involved in BML-111-mediated protection from acute injury is unclear still. METHODS: We established models of acute liver/lung injury and confirmed them with histopathology and myeloperoxidase (MPO) measurements. BML-111, a lipoxin receptor agonist, was applied to mimic the effects of LXs. The contents and activities of angiotensin converting enzyme(ACE) and angiotensinconverting enzyme 2 (ACE2) were measured through ELISA and activity assay kits respectively. Angiotensin II (AngII), angiotensin-(1-7) (Ang-1-7), AngII type 1 receptor (AT1R), and Mas receptor were quantified with ELISA and Western blot. RESULTS: Models of acute injury were established successfully and BML-111 protected LPS-induced acute lung injury and LPS/D-GalN-induced acute liver injury. BML-111 repressed the activity of ACE, but increased the activity of ACE2. BML-111 decreased the expression levels of ACE, AngII, and AT1R, meanwhile increased the levels of ACE2, Ang-(1-7), and Mas. Furthermore, BOC-2, an inhibitor of lipoxin receptor, reversed all the effects. CONCLUSION: BML-111 could protect against acute injury via regulation RAAS.

[Establishment of animal models of orchitis: Advances in studies].

Male infertility is becoming a concern of the world. Studies show that testicular inflammation is closely related to male infertility, which often manifests itself in low sperm count and motility and even the loss of fertility. In recent years, testicular inflammation-induced male infertility is arousing more and more attention, which adds to the significance of its study. It is imperative to establish stable and reliable animal models for further research on orchitis-induced spermatogenetic dysfunction and the mechanisms of spermatogenesis. This article presents an overview of recent studies on the establishment of animal models of orchitis to provide some reference for researchers in the relevant fields.

The anti-inflammatory effect of BML-111 on COPD may be mediated by regulating NLRP3 inflammasome activation and ROS production.

The aim of this study is to investigate whether the lipoxin receptor agonist BML-111 exerts a protective effect against inflammation in a mouse model of chronic obstructive pulmonary disease (COPD) by regulating NLRP3 inflammasome activation and reactive oxygen species (ROS) production. In this study, mice were randomly divided into the following five groups: control group (Control), COPD model group (Model), BML-111 low-dose group (Low-BML), BML-111 high-dose group (High-BML) and Dexamethasone group (Dex). NLRP3 involvement and oxidative stress were evaluated. Differential cell counts in the BALF were calculated to obtain a reliable enumeration of each cell type, and the levels of TGF-ß, TNF-α, IL-1ß, and IL-10 in BALF were evaluated using ELISA. We found that the white blood cell and lymphocyte numbers in the BALF were significantly lower in the High-BML group than in the Model group. ELISA of the BALF showed that BML-111 reduced TGF-ß and IL-1ß levels to some extent. HE staining showed various degrees of reduction in inflammatory cell infiltration in the bronchopulmonary tissue and blood vessels of the Low-BML, High-BML and Dex groups. Measurement of oxidative stress showed that SOD activity was significantly upregulated and that the increase in MDA content was prevented in the High-BML and Dex groups. According to the Western blotting analysis, the levels of NLRP3, Cleaved-IL-1ß and Cleaved-caspase-1 were decreased and Nrf-2 was increased to various extents in the Low-BML, High-BML and Dex groups. Based on these findings, BML-111 may prevent NLRP3 inflammasome activation and inhibit ROS production via upregulation of Nrf-2, thereby exerting an anti-inflammatory effect on COPD model mice.

Lipoxin A4 attenuates LPS-induced acute lung injury via activation of the ACE2-Ang-(1-7)-Mas axis.

Previous studies have reported that lipoxin A4 (LXA4) and the angiotensin I-converting enzyme 2 (ACE2), angiotensin-(1-7) [Ang-(1-7)], and its receptor Mas [ACE2-Ang-(1-7)-Mas] axis play important protective roles in acute lung injury (ALI). However, there is still no direct evidence of LXA4-mediated protection via the ACE2-Ang-(1-7)-Mas axis during ALI. This work was performed using an LPS-induced ALI mouse model and the data indicated the following. First, the animal model was established successfully and LXA4 ameliorated LPS-induced ALI. Second, LXA4 could increase the concentration and activity of ACE2 and the levels of Ang-(1-7) and Mas markedly. Third, LXA4 decreased the levels of TNF-α, IL-1ß, and reactive oxygen species while increasing IL-10 levels. Fourth, LXA4 inhibited the activation of the NF-κB signal pathway and repressed the degradation of inhibitor of NF-κB, the phosphorylation of NF-κB, and the translocation of NF-κB. Finally, and more importantly, BOC-2 (LXA4 receptor inhibitor), MLN-4760 (ACE2 inhibitor), and A779 (Mas receptor antagonist) were found to reverse all of the effects of LXA4. Our data provide evidence that LXA4 protects the lung from ALI through regulation of the ACE2-Ang-(1-7)-Mas axis.

Prenylflavonoids from the Twigs of Artocarpus nigrifolius.

Two new prenylated flavones, artocarnin A (2) and carpachromenol (12), together with 13 known prenylflavonoids (1, 3-11, 13-15) were isolated from the twigs of Artocarpus nigrifolius for the first time. Their structures were elucidated by high resolution-electrospray ionization (HR-ESI)-MS, NMR spectroscopic analysis, and in comparison with the reported data. Compounds 1-15 were evaluated for their antiproliferative effects against SiHa and SGC-7901 human cancer cell lines in vitro. The most active compound, eleocharin A (10), showed significant cytotoxicity on SiHa cells (IC50=0.7±0.1 µM) and inhibitory activity against SGC-7901 cells (IC50=8.3±0.2 µM) and could be considered as potential lead compound for further development of novel anti-tumor agents.

Grape seed proanthocyanidin extract protects against perfluorooctanoic acid-induced hepatotoxicity by attenuating inflammatory response, oxidative stress and apoptosis in mice.

Grape seed proanthocyanidin extract (GSPE) is a rich source of proanthocyanidins with multiple biological activities and potential health benefits. In the present study, we investigated the protective effect of GSPE against liver injury caused by perfluorooctanoic acid (PFOA) in mice and its possible mechanisms of action. Simultaneous treatment with GSPE for 14 consecutive days attenuated the functional and morphological changes in the liver of PFOA-exposed mice. Furthermore, simultaneous supplementation of GSPE reduced the production of inflammatory cytokines IL-6 and TNF-α, increased the expression of Nrf2 and its target antioxidant genes superoxide dismutase and catalase, and decreased the production of malondialdehyde and hydrogen peroxide in the liver of mice exposed to PFOA. Moreover, GSPE supplementation up-regulated the expression of anti-apoptotic protein Bcl-2 and down-regulated the expression of pro-apoptotic proteins p53 and Bax, with a decreased activity of caspase-3 in the liver of PFOA-treated mice. These findings suggest that GSPE ameliorates PFOA-induced inflammatory response, oxidative stress and apoptosis in the liver of mice.

Astrocyte elevated gene-1 promotes progression of cervical squamous cell carcinoma by inducing epithelial-mesenchymal transition via Wnt signaling.

OBJECTIVE: The aim of this study was to investigate the association of astrocyte elevated gene-1 (AEG-1) with epithelial-mesenchymal transition of cervical squamous cell carcinoma (CSCC) and the underlying mechanisms. METHODS: The expression of proteins was determined by immunohistochemistry in tissues. Overexpression and knockdown of AEG-1 in SiHa cells were achieved by stable AEG-1 gene transfection (SiHa-AEG-1+) and AEG-1-siRNA (SiHa-AEG-1-), respectively. The cellular levels of messenger RNA and proteins were assessed with reverse transcription polymerase chain reaction and Western blotting, respectively. The cell invasion capacity was assessed by the chamber invasion assay. RESULTS: AEG-1 was overexpressed in clinical CSCC and associated with lymph node metastasis, parametrial involvement, stromal invasion, and vascular invasion. A high level of vimentin and a low level of E-cadherin were also detected in the cancer tissues. AEG-1 expression was positively correlated with vimentin expression and negatively with E-cadherin expression in CSCC tissues. In addition, high level of AEG-1 was related to unfavorable prognosis of CSCC. On a cellular level, overexpression of AEG-1 was found to lead to an up-regulation of vimentin and a down-regulation of E-cadherin on messenger RNA and protein level in SiHa cells, whereas AEG-1 knockdown led to a contrary result. Meanwhile, the nuclear levels of NF-κB p65 and ß-catenin were also increased in SiHa-AEG-1+, whereas their nuclear levels were decreased in SiHa-AEG-1-. Inhibition of Wnt signaling significantly reduced vimentin level and enhanced E-cadherin level in SiHa-AEG+, but inhibition of NF-κB signaling did not. SiHa-AEG-1+ and SiHa-AEG- showed an enhanced and a decreased invasive capacity, respectively. The enhanced invasiveness of SiHa-AEG-1+ was weakened by inhibition of Wnt signaling. CONCLUSIONS: AEG-1 was associated with the progression of CSCC by promoting epithelial-mesenchymal transition via Wnt signaling pathway.

Molecular characterization and expression analysis of the autophagic gene beclin 1 from the purse red common carp (Cyprinus carpio) exposed to cadmium.

Beclin 1, the mammalian orthologue of yeast Atg6, has a central role in autophagy, which has been linked to diverse biological processes including immunity, development, tumor suppression, lifespan extension, etc. However, the relevant study about Beclin 1 is rare in fish compared with mammals. In this study, we isolated Beclin 1 gene from the kidney tissue of common carp (Cyprinus carpio) using rapid amplification of cDNA ends (RACE). The deduced amino acid sequence of cloned Beclin 1 comprised 447 amino acids, which showed approximately 80.7% identity and 88.9% similarity to human Beclin 1. It possessed a typical Bcl-2 homology domain 3 (BH3) and an evolutionarily conserved domain (ECD). Phylogenetic analysis demonstrated that common carp Beclin 1 formed a clade with zebrafish Beclin 1. To explore the relationship between Beclin 1 and cadmium (Cd)-induced injury, a Cd exposure experiment was conducted. The result showed that Cd content was significantly increased in a dose-dependent manner in kidney after Cd exposure. Swelling and vacuolation of renal tubular epithelial cells, and glomerular hyalinization were observed. Renal leukocyte infiltration was diffusely distributed in the interstitial tissue. Real-time quantitative RT-PCR analysis revealed that the mRNA transcript level of Beclin 1 was markedly up-regulated in a dose-dependent and time-dependent manner after exposure to Cd. Similarly, Western blot analysis indicated that its protein level was significantly elevated in a dose-dependent manner after Cd treatment. All the results indicate that the common carp Beclin 1 gene may play a regulatory role against Cd toxicity.

An observational study of the secondary effects of a local smoke-free ordinance.

INTRODUCTION: The secondary, sometimes unintended effects of smoke-free ordinances have not been thoroughly evaluated. In this observational study, we evaluated the association of a local ordinance implemented in Madison, Wisconsin, with changes in public disturbances; smoking, drinking, and bar-going behaviors in the general population; and smoking and drinking behaviors among university students. METHODS: We obtained data from 4 sources: police records, key informant interviews, a community survey, and an undergraduate survey. Except for interviews, which we conducted postenactment only, we compared measures before and after the ordinance was put into effect. RESULTS: We found no evidence of association of the ordinance with public disturbances. We found that the ordinance was not associated with changes in smoking rates, drinking rates, or bar-going in the general population, although bar-going decreased among the 16% of the general adult population who smokes (from 84% in 2005 to 70% in 2007, P < .001). Student smoking rates also decreased (from 23% in 2005 to 16% in 2007, P < .001), but student binge drinking did not change. CONCLUSION: The study adds unique information to the evidence base on the effect of smoke-free policies, finding little evidence of their secondary, unintended effects. With the addition of these results to existing evidence, we conclude that the potential health benefits of smoke-free ordinances outweigh the potential harms from unintended effects.

Smoking, barriers to quitting, and smoking-related knowledge, attitudes, and patient practices among male physicians in China.

INTRODUCTION: Successful interventions to reduce the high rate of smoking among male physicians in China might contribute to reduction in tobacco use in the country overall. Better characterization of smoking, barriers to quitting, and smoking-related knowledge, attitudes, and patient practices in this physician population will help plan such interventions and provide baseline data to evaluate their effectiveness. METHODS: A self-administered survey of smoking-related knowledge, attitudes, behaviors, and patient practices was conducted among health care professionals in 2 large teaching hospitals in China. RESULTS: Of 103 male physicians, those who smoked (n = 51) had a more limited knowledge of smoking-related disease and were less likely to advise patients to quit smoking compared with nonsmoking physicians (n = 52). More than one-fourth (29%) of nonsmoking physicians accepted gift cigarettes, and these physicians were less likely to ask their patients about their smoking status than those who did not accept gift cigarettes. Seventy-five percent of smokers reported that their hospitals did not help them quit, and only 19% reported receiving training in how to help their patients quit. CONCLUSION: High rates of smoking, gifting of cigarettes, limited support for physician quitting, and limited training on cessation approaches may compromise the ability of male physicians in China to effectively treat their patients who smoke.

Media campaigns to promote smoking cessation among socioeconomically disadvantaged populations: what do we know, what do we need to learn, and what should we do now?

Little is known about whether media campaigns are effective strategies to promote smoking cessation among socioeconomically disadvantaged populations or whether media campaigns may unintentionally maintain or widen disparities in smoking cessation by socioeconomic status (SES). This paper presents a systematic review of the literature on the effectiveness of media campaigns to promote smoking cessation among low SES populations in the USA and countries with comparable political systems and demographic profiles such as Canada, Australia and Western European nations. We reviewed 29 articles, summarizing results from 18 studies, which made explicit statistical comparisons of media campaign effectiveness by SES, and 21 articles, summarizing results from 13 studies, which assessed the effectiveness of media campaigns targeted specifically to low SES populations. We find that there is considerable evidence that media campaigns to promote smoking cessation are often less effective, sometimes equally effective, and rarely more effective among socioeconomically disadvantaged populations relative to more advantaged populations. Disparities in the effectiveness of media campaigns between SES groups may occur at any of three stages: differences in meaningful exposure, differences in motivational response, or differences in opportunity to sustain long-term cessation. There remains a need to conduct research that examines the effectiveness of media campaigns by SES; these studies should employ research designs that are sensitive to various ways that SES differences in smoking cessation media effects might occur.