Artificial Intelligence-Enabled Electrocardiogram Improves the Diagnosis and Prediction of Mortality in Patients With Pulmonary Hypertension.

Background: Pulmonary hypertension is a disabling and life-threatening cardiovascular disease. Early detection of elevated pulmonary artery pressure (ePAP) is needed for prompt diagnosis and treatment to avoid detrimental consequences of pulmonary hypertension. Objectives: This study sought to develop an artificial intelligence (AI)-enabled electrocardiogram (ECG) model to identify patients with ePAP and related prognostic implications. Methods: From a hospital-based ECG database, the authors extracted the first pairs of ECG and transthoracic echocardiography taken within 2 weeks of each other from 41,097 patients to develop an AI model for detecting ePAP (PAP > 50 mm Hg by transthoracic echocardiography). The model was evaluated on independent data sets, including an external cohort of patients from Japan. Results: Tests of 10-fold cross-validation neural-network deep learning showed that the area under the receiver-operating characteristic curve of the AI model was 0.88 (sensitivity 81.0%; specificity 79.6%) for detecting ePAP. The diagnostic performance was consistent across age, sex, and various comorbidities (diagnostic odds ratio >8 for most factors examined). At 6-year follow-up, the patients predicted by the AI model to have ePAP were independently associated with higher cardiovascular mortality (HR: 3.69). Similar diagnostic performance and prediction for cardiovascular mortality could be replicated in the external cohort. Conclusions: The ECG-based AI model identified patients with ePAP and predicted their future risk for cardiovascular mortality. This model could serve as a useful clinical test to identify patients with pulmonary hypertension so that treatment can be initiated early to improve their survival prognosis.

Activation of M1 macrophages plays a critical role in the initiation of acute lung injury.

The goal of the present study was to investigate the role of M1 macrophages in acute lung injury (ALI). To address this, we used lipopolysaccharide (LPS)-treated wild-type and CD11b-DTR mice, and examined their M1 macrophage levels, and the extent of their inflammation and pulmonary injuries. In addition, we evaluated pulmonary function by measuring the expressions of SP-A and SP-B in infiltrated M1 macrophages. Finally, we co-cultured the mouse type II-like alveolar epithelial cells (AT-II) and mouse pulmonary microvascular endothelial cells (PMECs) with M1 macrophages in the presence of TNF-α or H2O2 and assessed them for viability and apoptosis. After LPS treatment, we observed that the number of pulmonary M1/M2 macrophages and the serum levels of interleukin-1ß (IL-1ß), tumor necrosis factor α (TNF-α), and reactive oxygen species (ROS) significantly increased. Furthermore, the increase in cytokines was accompanied with the initiation of lung injury indicated by the decreased levels of SP-A and SP-B. In macrophage-depleted CD11b-DTR mice, ALI was attenuated, serum levels of IL-1ß, TNF-α and ROS were reduced, and lung levels of monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-2 (MIP-2) were decreased. After administering TNF-α and H2O2, the proapoptotic effect of M1 macrophages on AT-II or PMECs significantly increased, the cell viabilities significantly decreased, and apoptosis significantly increased. Our results suggest that M1 macrophages are recruited to the lungs where they significantly contribute to an increase in TNF-α and ROS production, thus initiating ALI.

Sirtuin 3 Protects against Urban Particulate Matter-Induced Autophagy in Human Bronchial Epithelial Cells.

Urban particulate matter (urban PM) is a heterogeneous mixture of various types of particles originating from different sources. Exposure to high concentrations of urban PM leading to adverse health effects is evaluated by using in vitro cultures of human lung epithelial cells. However, the mechanism underlying the correlation between high concentrations of urban PM exposure and adverse health effects has not been fully elucidated; urban PM-induced oxidative stress is considered as an important mechanism of urban PM-mediated cytotoxicity. Sirtuin 3 (SIRT3), a primary mitrochondrial deacetylase, controls cellular reactive oxygen species (ROS) production, and expression of antioxidant enzymes. In this study, we examined the role of SIRT3 in the regulation of urban PM-induced oxidative stress in normal primary human bronchial epithelial cells (HBEpiCs). Cell viability showed a time- and concentration-dependent decrease when exposed to urban PM, which could indicate that the amount of lactate dehydrogenase released from the cell in response to urban PM is related to cell viability in HBEpiC. The effects of urban PM on morphological and biochemical markers of autophagy in HBEpiC were analyzed by electron microscopy and Western blotting. Overexpression of SIRT3 inhibited urban PM-induced ROS generation, while concomitantly increasing the expression of antioxidant enzymes, and decreasing NF-κB activation and release of inflammation factors. Up-regulation of SIRT3 significantly inhibited the expression of autophagy markers and autophagic vacuole formation. Our findings provide a valuable insight into the potential role of the SIRT3 enzyme in regulating urban PM-induced autophagy by mediating urban PM-induced oxidative stress, which may contribute to urban PM-induced impairment of airway epithelial cell function.

Association Between the CYP1B1 Polymorphisms and Lung Cancer Risk: A Meta-Analysis.

The previously published data on the association between the cytochrome P450 1B1 Leu432Val, Asn453Ser, and Ala119Ser polymorphisms and lung cancer risk have remained controversial. Hence, we performed a meta-analysis to investigate the association between cytochrome P450 1B1 Leu432Val, Asn453Ser, and Ala119Ser polymorphisms and lung cancer risk under different inheritance models. A total of 22 studies were identified, including 2881 cases and 3653 controls for Leu432Val polymorphism (from 13 studies), 3009 cases and 3887 controls for Asn453Ser polymorphism (from 5 studies), and 1301 cases and 2045 controls for Ala119Ser polymorphism (from 4 studies). Overall, significant association was observed between cytochrome P450 1B1 Leu432Val polymorphism and lung cancer risk (dominant model: odds ratio = 1.29, 95% confidence interval = 1.08-1.53; recessive model: odds ratio = 1.21, 95% confidence interval = 1.05-1.39; additive model: odds ratio = 1.43, 95% confidence interval = 1.21-1.69) when all the eligible studies were pooled into the meta-analysis. In the further stratified and sensitivity analyses, significantly increased lung cancer risk was also observed in caucasians and smokers. No significant association was observed between cytochrome P450 1B1Asn453Ser and Ala119Ser polymorphisms and lung cancer risk in overall analysis. In summary, this meta-analysis suggests that cytochrome P450 1B1Leu432Val polymorphism is associated with increased lung cancer risk in caucasians and smokers.

The end-of-treatment telephone response and prognosis of post-radiotherapy nasopharyngeal carcinoma patients in southern China.

Nasopharyngeal Carcinoma (NPC) patients' end-of-treatment survival status has drawn more attention in recent years. Telephone follow-up, as a most operative approach among all the clinical follow-ups, is an effective means to extend medical service to patients' home and is thus widely used in clinical practice. This study aimed to analyze the post-radiotherapy NPC patients' phone response rate and its factors, and to discuss the independent prognostic factors of NPC patients' radiotherapy. We prospectively designed a nurses-led telephone follow-up to include 2520 NPC patients who received simple radical radiotherapy between Jan. 2007 and Jun. 2012 at Sun Yat-sen University Cancer Center. The patients' response rate and its factors were calculated. Survival analysis was used to estimate the patients' survival and the influencing factors. The overall response rate was 90.5%; Patients with reserved contact type of mobile + landlinephone or landline phone had higher follow-up response rate than patients with mobile contact only; patients with 2 or more reserved contacts, and family cancer history had higher response rate than patients with only 1 number and those without family history. Patients' cumulative survival rate of 1, 3 and 5 years were 98.9%, 75.3%, 50.3%, respectively. T-staging, N-staging, higher clinical staging, with basicranial invasion were the influencing factors of the patients' poor prognosis. The telephone follow-up response was affected by reserved contact type, number of contacts and family medical history; T-staging, N-staging, higher clinical staging, with basicranial invasion were the influencing factors of the patients' poor prognosis. This study provides a scientific basis for increasing the NPC patients' end-of-treatment response and promoting the individualized clinical treatment.

Role of SIRT1 in regulation of epithelial-to-mesenchymal transition in oral squamous cell carcinoma metastasis.

BACKGROUND: The epithelial-to-mesenchymal transition (EMT) process results in a loss of cell-cell adhesion, increased cell mobility, and is crucial for enabling the metastasis of cancer cells. Recently, the enzyme SIRT1 has been implicated in a variety of physiological processes; however, its role in regulating oral cancer metastasis and EMT is not fully elucidated. Here, we propose a mechanism by which the enzyme sirtuin1 (SIRT1) regulates the EMT process in oral cancer by deacetylating Smad4 and repressing the effect of TGF-ß signaling on matrix metalloproteinase-7 (MMP7). METHODS: The roles of SIRT1 in tumor cell migration/invasion and metastasis to the lungs were investigated using the Boyden chamber assay and orthotopic injections, respectively. RNA interference was used to knockdown either SIRT1 or Smad4 expression in oral squamous cell carcinoma (OSCC) cell lines. Immunoblotting, zymographic assays, and co-immunoprecipitation were used to examine the effects of SIRT1 overexpression on MMP7 expression and activity, as well as on SIRT1/ Smad4 interaction. RESULTS: We found that compared with normal human oral keratinocytes (HOKs), SIRT1 was underexpressed in OSCC cells, and also in oral cancer tissues obtained from 14 of 21 OSCC patients compared with expression in their matched normal tissues. Overexpression of SIRT1 inhibited migration of OSCC cells in vitro, as well as their metastasis to the lung in vivo. Furthermore, up-regulation of SIRT1 in metastatic OSCCs significantly inhibited the migration and invasion abilities of OSCC cells, while concomitantly increasing the expression of E-cadherin, and decreasing the expressions of mesenchymal markers. We also identified Smad4, a TGF-ß-activated transcription factor, as a direct target protein for SIRT1. Overexpression of SIRT1 in OSCC cells led to decreased levels of acetylated Smad4, and inhibition of TGF-ß-induced signaling. By associating and deacetylating Smad4, SIRT1 enzyme can influence MMP7 expression, MMP enzyme activity, and consequently, cell migration, invasion, and tumor metastasis in OSCCs. CONCLUSIONS: These findings provide a valuable insight into the potential role of the SIRT1 enzyme in regulating cell migration and invasion in oral squamous cell carcinoma. Our findings suggest the SIRT1/Smad4/MMP7 pathway as a target for oral cancer driven by EMT.

Andrographolide downregulates the v-Src and Bcr-Abl oncoproteins and induces Hsp90 cleavage in the ROS-dependent suppression of cancer malignancy.

Andrographolide is a diterpenoid compound isolated from Andrographis paniculata that exhibits anticancer activity. We previously reported that andrographolide suppressed v-Src-mediated cellular transformation by promoting the degradation of Src. In the present study, we demonstrated the involvement of Hsp90 in the andrographolide-mediated inhibition of Src oncogenic activity. Using a proteomics approach, a cleavage fragment of Hsp90α was identified in andrographolide-treated cells. The concentration- and time-dependent induction of Hsp90 cleavage that accompanied the reduction in Src was validated in RK3E cells transformed with either v-Src or a human truncated c-Src variant and treated with andrographolide. In cancer cells, the induction of Hsp90 cleavage by andrographolide and its structural derivatives correlated well with decreased Src levels, the suppression of transformation, and the induction of apoptosis. Moreover, the andrographolide-induced Hsp90 cleavage, Src degradation, inhibition of transformation, and induction of apoptosis were abolished by a ROS inhibitor, N-acetyl-cysteine. Notably, Hsp90 cleavage, decreased levels of Bcr-Abl (another known Hsp90 client protein), and the induction of apoptosis were also observed in human K562 leukemia cells treated with andrographolide or its active derivatives. Together, we demonstrated a novel mechanism by which andrographolide suppressed cancer malignancy that involved inhibiting Hsp90 function and reducing the levels of Hsp90 client proteins. Our results broaden the molecular basis of andrographolide-mediated anticancer activity.

STRESS-responsive deacetylase SIRT3 is up-regulated by areca nut extract-induced oxidative stress in human oral keratinocytes.

Areca chewing is an important environmental risk factor for development of oral premalignant lesions and cancer. Epidemiological evidence indicates that areca chewing is tightly linked to oral carcinogenesis. However, the pathogenetic impacts of areca nut extract (ANE) on normal human oral keratinocytes (HOKs) are unclear and possibly involve oxidative stress via redox imbalance. Sirtuin 3 (SIRT3) is a member of the sirtuin family of proteins that play an important role in regulating cellular reactive oxygen species (ROS) production. Recent studies have confirmed that ANE and other areca ingredients can induce ROS. In this study, we examined the role of SIRT3 in the regulation of ANE-induced ROS in HOK cells. We examined HOK cell viability following treatment with various ANE concentrations. ANE-induced cytotoxicity increased in a dose-dependent manner and was approximately 48% at a concentration of 50 µg/ml after 24 h. SIRT3 expression and enzyme activity were up-regulated in HOK cells by ANE-induced oxidative stress. Additionally, we identified that SIRT3 controls the enzymatic activity of mitochondrial proteins, such as forkhead box O3a (Foxo3a) transcription factor and antioxidant-encoding gene superoxide dismutase 2 (SOD2), by deacetylation in HOK cells. Moreover, SIRT3-mediated deacetylation and activation of Foxo3a promotes nuclear localization in vivo. These findings suggest that SIRT3 is an endogenous negative regulator in response to ANE-induced oxidative stress and demonstrate an essential role for redox balance in HOK cells.

Role of SIRT3 in the regulation of redox balance during oral carcinogenesis.

BACKGROUND: Sirtuins (SIRT1-7) are a family of NAD-dependent deacetylases, which play an important role in regulating cancer tumorigenesis; however, their role in oral cancer has been controversial. SIRT3 is localized in the mitochondria, where it deacetylates and activates several enzymes involved in cellular redox balance and defense against oxidative damage. RESULTS: We found that compared with normal human oral keratinocytes (HOK), SIRT3 is highly expressed in oral squamous cell carcinoma (OSCC) cell lines, but the enzymatic deacetylation is significantly reduced. We also sequenced the entire coding region of SIRT3 and found the same mutation in 2 different OSCC cell lines. This point mutation is located in close proximity to the active site of deacetylase in the SIRT3 protein, and reduces the overall enzymatic efficiency of deacetylation. Furthermore, up-regulation of SIRT3 inhibited the cell growth of OSCCs and decreased the levels of basal reactive oxygen species (ROS) in both OSCC lines. To verify that the SIRT3 sequence variation was associated with oral carcinogenesis, we sequenced the SIRT3 gene from 21 OSCC patients, and 5 of the 21 patients (23.8%) carried the heterozygous missense mutation, p.Val208Ile. The heterozygous missense mutation in these patients was present in gremlin DNA isolated from both normal and tumor tissues. CONCLUSIONS: Our findings provide a valuable insight into the potential role of SIRT3 in the development of oral squamous cell carcinoma, by showing that a non-synonymous point mutation in SIRT3 contributes to reduced catalytic activity of the protein and affects redox balance in OSCCs.

The application value of contrast-enhanced ultrasound in the differential diagnosis of pancreatic solid-cystic lesions.

OBJECTIVE: To retrospectively determine the accuracy of baseline ultrasound (BUS) and of contrast-enhanced ultrasound (CEUS) in the differential diagnosis of pancreatic solid-cystic lesions. METHODS: Fifty-four pancreatic solid-cystic lesions in 52 patients were examined with BUS and CEUS, two different seniority radiologists read the images independently, Receiver operating characteristic (ROC) analysis was used to evaluate the diagnostic value of BUS and CEUS in the diagnosis of benign or malignant pancreatic solid-cystic lesions, the diagnostic consistency between different seniority radiologists was evaluated by Kappa statistics. RESULTS: Among the 54 lesions, there were pancreatic cyst five cases, pancreatic pseudocyst twenty cases, pancreatic cystadenoma eight cases, pancreatic cystadenocarcinoma seven cases, intraductal papillary mucinous neoplasm of pancreas (IPMN) three cases, pancreatic carcinoma combined liquefied six cases, solid-pseudopallary tumor of pancreas (SPTP) three cases, pancreatic myopericytoma one case, pancreatic lymphangioma one case. After ROC analysis, the areas under the ROC curve (Az) were 0.752 by BUS, 0.928 by CEUS to resident radiologist, and 0.896 by BUS, 0.954 by CEUS to staff radiologist. The correct diagnosis rate of specific disease was 42.6% by BUS, 64.8% by CEUS to staff radiologist (P<0.05), and 33.3% by BUS, 53.7% by CEUS to resident radiologist (P<0.05). The interobserver agreement in CEUS is higher than that in BUS, the Kappa value was 0.889 ± 0.062 and 0.428 ± 0.126 respectively. CONCLUSION: Compared with BUS, CEUS can significantly enhance the diagnostic rate of pancreatic solid-cystic lesions.

4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone is correlated with 8-hydroxy-2'-deoxyguanosine in humans after exposure to environmental tobacco smoke.

Cigarette smoking and exposure to environmental tobacco smoke (ETS) are important risk factors for many cancers. However, exposure doses have usually not been quantitatively assessed in human studies. In humans 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and its glucuronate conjugate (defined as total NNAL) are the major metabolites of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, a cigarette-specific carcinogen. Although animal studies have shown that exposure to cigarette smoke increases tissue oxidative DNA damage, the relationship between cigarette smoke and 8-hydroxydeoxyguanosine (8-OHdG) is not consistent in human studies. In the present study, we have developed a simple, sensitive, and robust LC-MS/MS method for quantifying total NNAL and 8-OHdG concentrations in human plasma. We quantified total NNAL and 8-OHdG in plasma as well as 8-OHdG in urine of 121 healthy male subjects. Total NNAL levels were significantly higher in ever-smokers than in never-smokers. Furthermore, total NNAL levels in plasma were increased with numbers of cigarettes smoked per day in ever-smokers. It suggests that total NNAL in plasma is a good biomarker for cigarette smoke exposure. After stratifying by smoking status and adjusting for age, ETS exposure and occupation category, total NNAL was associated with plasma and urinary 8-OHdG in never-smokers, but not in ever-smokers. Since total NNAL levels in nonsmokers represented the ETS exposure, it appears that 8-OHdG levels are dose-dependently correlated with their ETS exposure dose. Furthermore, this correlation supports the hypothesis that oxidative DNA damage is one of major adverse effects induced by ETS exposure in humans.

The potentially inappropriate prescription of new drug: thiazolidinediones for patients with type II diabetes in Taiwan.

PURPOSE: To examine the potentially inappropriate prescription of thiazolidinediones (TZD). METHODS: Data on TZD prescriptions were collected from Taiwan's National Health Insurance dataset from 2001 to 2006. TZDs were considered inappropriately prescribed when they were prescribed to patients who were (1) under 18 years old, (2) pregnant, who had (3) type 1 diabetes, (4) severe heart failure, (5) hepatic insufficiency, or (6) renal insufficiency and taking TZD + metformin in combination. We aggregated potentially inappropriate prescriptions of TZD for each health-care institution in each month starting from March 2001, when TZD was introduced to Taiwan's market. RESULTS: The potentially inappropriate prescription of TZD increased from 9.41% in 2001 to 12.50% in 2006. Prior inappropriate prescription led to a 0.06% (95%CI: 0.04-0.08) further increase in its later inappropriate prescription. Accumulated months of experience prescribing TZD was found associated with higher proportion of inappropriate prescription of TZD (0.03%, 95%CI: 0.01-0.05). However, it was negatively associated with new incidence of inappropriate prescription of TZD (-0.20, 95%CI: -0.22 to -0.18). The greater the volume of prior TZD prescription (-0.87%, 95%CI: -0.93 to -0.81) and the greater the number of accumulated months since adoption (-0.14%, 95%CI: -0.16 to -0.12), the greater the decrease in rates of new inappropriate prescriptions. CONCLUSIONS: Along with the quick penetration of the new DM drug came an increased possibility that it would be prescribed inappropriately, a trend that persisted over time.

ISO-1, a macrophage migration inhibitory factor antagonist, inhibits airway remodeling in a murine model of chronic asthma.

Airway remodeling is the process of airway structural change that occurs in patients with asthma in response to persistent inflammation and leads to increasing disease severity. Drugs that decrease this persistent inflammation play a crucial role in managing asthma episodes. Mice sensitized (by intraperitoneal administration) and then challenged (by inhalation) with ovalbumin (OVA) develop an extensive eosinophilic inflammatory response, goblet cell hyperplasia, collagen deposition, airway smooth muscle thickening, and airway wall area increase, similar to pathologies observed in human asthma. We used OVA-sensitized/challenged mice as a murine model of chronic allergic airway inflammation with subepithelial fibrosis (i.e., asthma). In this OVA mouse model, mRNA and protein of macrophage migration inhibitory factor (MIF) are upregulated, a response similar to what has been observed in the pathogenesis of acute inflammation in human asthma. We hypothesized that MIF induces transforming growth factor-ß1 (TGF-ß1) synthesis, which has been shown to play an important role in asthma and airway remodeling. To explore the role of MIF in the development of airway remodeling, we evaluated the effects of an MIF small-molecule antagonist, (S,R)3-(4-hy-droxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester (ISO-1), on pathologies associated with the airway-remodeling process in the OVA mouse model. We found that administration of ISO-1 significantly mitigated all symptoms caused by OVA treatment. In addition, the treatment of OVA-sensitized mice with the MIF antagonist ISO-1 significantly reduced TGF-ß1 mRNA levels in pulmonary tissue and its protein level in bronchial alveolar lavage fluid supernatants. We believe the repression of MIF in the ISO-1 treatment group led to the significant suppression observed in the inflammatory responses associated with the allergen-induced lung inflammation and fibrosis in our murine asthma (OVA) model. Our results implicate a possible function of MIF in the pathogenesis of chronic asthma and suggest that MIF might be an important therapeutic target for airway remodeling.

Pharmaceutical penetration of new drug and pharmaceutical market structure in Taiwan: hospital-level prescription of thiazolidinediones for diabetes.

This study used Taiwan's National Health Insurance claim database (years 2000-2005) to examine how thiazolidinediones (TZD), a new class of drugs for diabetes, penetrated into Taiwan's hospitals, and its association with the concentration of all diabetes drugs at the hospital level. We collected 72 monthly summaries of diabetes prescriptions from all hospitals in Taiwan. Hospital-level pharmaceutical concentration was measured by penetration of TZD, defined as monthly market share of TZD in each hospital. Concentration of diabetes drugs was measured by Herfindahl-Hirschman indices. We found a negative association (coefficient = -0.3610) between TZD penetration and concentration of diabetes drug but a positive association between penetration of TZD and the volume of prescribed diabetes drugs (coefficient = 0.4088). In conclusion, hospital characteristics and volume of services determined the concentration of pharmaceuticals at the institution level, reflecting the heterogeneous competition between pharmaceutical companies within each hospital. Institution-level pharmaceutical concentration influences the adoption and penetration of new drugs.

The effect of changing reimbursement policies on quality of in-patient care, from fee-for-service to prospective payment.

OBJECTIVE: Using insurance claims for hemorrhoidectomies, we examined the effect of Taiwan's Bureau of National Health Insurance's case payment system, a fixed case payment rate method used to reimburse health care providers for in-patient care. DESIGN: This observational natural experimental study examined changes in medical care that occurred between two phases: the 9 months before case payment system was implemented on 1 October 1997 and the 9 months afterwards. The changes were analyzed by performing linear regressions with interaction between hospital type and the implementation of case payment system. SETTING: This study was based on total claim data from National Health Insurance. STUDY PARTICIPANTS: A total of 23 638 hemorrhoidectomy insurance claims. MAIN OUTCOME MEASURES: Length of stay, number of medical services, and number of drug prescriptions. Medical services were stratified into those that were considered minimal requirements and those considered optional by the Bureau of National Health Insurance. RESULTS: Over the 18-month period, the number of patients increased by 23.7%. After the case payment system was implemented, length of stay decreased by 0.59 days (P < 0.0001), the number of minimally required services increased by 2.19 to 4.24 items (P < 0.0001), the number of optional service items decreased by 0.32 items (P < 0.0001), and drug prescription decreased slightly by 0.58 to 0.99 items (P < 0.0001) per hospitalization. CONCLUSIONS: The case payment system successfully shortened length of stay without significantly sacrificing the provision of services.

The effect of Taiwan's tax-induced increases in cigarette prices on brand-switching and the consumption of cigarettes.

The effect of raising cigarette taxes to reduce smoking has been the subject of several studies, which often treat the price of cigarettes as an exogenous factor given to smokers who respond to it by adjusting their smoking behavior. However, cigarette prices vary with brand and quality, and smokers can and do switch to lower-priced brands to reduce the impact of the tax on the cost of cigarettes as they try to consume the same number of cigarettes as they had before a tax hike. Using data from a two-year follow-up interview survey conducted before and after a new cigarette tax scheme was imposed in Taiwan in 2002, this study examines three behavioral changes smokers may make to respond to tax-induced cigarette price increase: brand-switching, amount consumed, and amount spent on smoking. These changes were studied in relation to smoker income, before-tax cigarette price, level of addiction, exposure to advertizing, and consumer loyalty. We found that smokers, depending upon exposure to advertizing, level of consumer loyalty and initial price of cigarettes, switched brands to maintain current smoking habits and control costs. We also found that the initial amount smoked and level of addiction, not price, at least not at the current levels in Taiwan, determined whether a smoker reduced the number of cigarettes he consumed.

Public opinion regarding earmarked cigarette tax in Taiwan.

BACKGROUND: Cigarette taxation has been perceived by academics and policy-makers as one of the most effective ways of reducing the use of cigarettes. On January 1 2002, the Taiwan government imposed a New Taiwan (NT) 5 dollars per pack tax earmarked for the purpose of tobacco control. This study uses a survey collected prior to taxation to assess public attitudes toward cigarette taxation, public beliefs about the effectiveness of cigarette taxation at reducing cigarette use and public opinions about the allocation of this tax revenue. METHODS: Data were drawn from a national face-to-face interview on cigarette consumption in 2000. A total of 3,279 adults were aged 18 to 64 years; 49.9% of whom were male and 50.1% female, and with a smoking prevalence of 49.1% and 4.1%, respectively. The attitudes toward cigarette tax were analysed using multi-logit regressions. We analysed by logistic regression the potential changes in smoking behaviour that smokers might make in response to the five NT (New Taiwan) dollar earmarked tax on cigarettes per pack. We summarized public opinions about the allocation of earmarked tax revenue using descriptive statistics. RESULTS: Current smokers (OR = 0.34) and former smokers (OR = 0.68) were less likely to support the cigarette tax than non-smokers. A favourable attitude toward the tax was positively associated with personal monthly income, especially among females. Among male smokers, the possibility of reducing/quitting smoking in response to the five-NT-dollar tax was negatively associated with the monthly expense for smoking. The two most frequently-suggested areas to receive money from the revenue collected from the earmarked tax were health education and cancer subsidy. CONCLUSIONS: Smoking status and economic factors determine the attitude and potential responses of people toward the cigarette tax. Taiwan's five NT-dollar earmarked tax for cigarettes may have only a limited effect upon the reduction in cigarette use.