CYB5R3 functions as a tumor suppressor by inducing ER stress-mediated apoptosis in lung cancer cells via the PERK-ATF4 and IRE1α-JNK pathways.

Cytochrome b5 reductase 3 (CYB5R3) is involved in various cellular metabolic processes, including fatty acid synthesis and drug metabolism. However, the role of CYB5R3 in cancer development remains poorly understood. Here, we show that CYB5R3 expression is downregulated in human lung cancer cell lines and tissues. Adenoviral overexpression of CYB5R3 suppresses lung cancer cell growth in vitro and in vivo. However, CYB5R3 deficiency promotes tumorigenesis and metastasis in mouse models. Transcriptome analysis revealed that apoptosis- and endoplasmic reticulum (ER) stress-related genes are upregulated in CYB5R3-overexpressing lung cancer cells. Metabolomic analysis revealed that CYB5R3 overexpression increased the production of nicotinamide adenine dinucleotide (NAD+) and oxidized glutathione (GSSG). Ectopic CYB5R3 is mainly localized in the ER, where CYB5R3-dependent ER stress signaling is induced via activation of protein kinase RNA-like ER kinase (PERK) and inositol-requiring enzyme 1 alpha (IRE1α). Moreover, NAD+ activates poly (ADP-ribose) polymerase16 (PARP16), an ER-resident protein, to promote ADP-ribosylation of PERK and IRE1α and induce ER stress. In addition, CYB5R3 induces the generation of reactive oxygen species and caspase-9-dependent intrinsic cell death. Our findings highlight the importance of CYB5R3 as a tumor suppressor for the development of CYB5R3-based therapeutics for lung cancer.

Development and effects of a non-face-to-face forest therapy program for nurses during the COVID-19 pandemic.

AIM: In this study, we developed a non-face-to-face forest therapy program using videos and applied it to nurses working in hospitals during the prolonged COVID-19 situation to confirm the effect on their mental health. METHOD: This study was a randomized control group pretest-posttest, and 27 clinical nurses in the experimental group and 28 clinical nurses in the control group participated. The program developed forest therapy videos and three city videos each. The experimental group watched the forest therapy video and the control group watched the city video and stress and happiness were measured through pre-test and post-test. RESULTS: The stress level of clinical nurses who applied the non-face-to-face forest therapy program had a significant reduction effect compared to the control group on day 2 (t = -2.239 P = .026) and day 3 (t = -3.188, P = .003). On the other hand, there was no significant effect in happiness in both groups. In addition, repeated measures analysis of variance statistical analysis confirmed that the stress level of the experimental group significantly decreased over time (F = 10.578, P < .001). CONCLUSION: The non-face-to-face forest therapy program is significant in that it had a positive effect on relieving stress by conducting a randomized controlled study targeting clinical nurses working in various hospitals.

Effects of aromatherapy on sore throat, nasal symptoms and sleep quality in adults infected with COVID-19: A randomized controlled trial.

Background: Patients with coronavirus disease 2019 (COVID-19) usually complain of fever, cough, and sore throat. This study examined the effects of aromatherapy on sore throat, nasal symptoms, stress, fatigue, and sleep quality by administering it to adults with post-COVID-19 condition. Methods: This study was conducted in a randomised controlled design. Its target population were adults who were released from COVID-19 quarantine treatment within 45 days from infection onset and capable of performing daily activities after isolation treatment. The participants were randomised into aromatherapy group (AG) and control group (CG). To test experimental treatment effects, the levels of sore throat, nasal symptoms, stress, fatigue and sleep quality were measured at the baseline (pre-test) and after the trial (post-test), using the numerical rating scale for sore throat, stress and fatigue, the Total Nasal Symptoms Score for nasal symptoms, and the Korean Version of Modified Leeds Sleep Evaluation Questionnaire for quality of sleep. Results: After experimental treatment, there was a significant difference in sore throat in AG compared to CG on the 3rd day (t=-2.022 p=0.048) and 4th day (t=-2.450, p=0.017) of treatment. There was also a significant difference in fatigue between AG and CG on the 2nd day(t=-2.748, p=0.008), 3rd day (t=-2.948, p=0.005) and 4th day (t=-3.084, p=0.003) of treatment. There was no significant difference in TNSS, stress, and sleep quality between the two groups after the experimental treatment. Conclusion: Inhaling aroma essential oils reduced sore throat and fatigue in adults with post-COVID-19 condition, demonstrating the feasibility of aromatherapy as an effective treatment. Trial registration: The study was registered with Clinical Research Information Service (KCT0008029).

DDIAS, DNA damage-induced apoptosis suppressor, is a potential therapeutic target in cancer.

Increasing evidence indicates that DNA damage-induced apoptosis suppressor (DDIAS) is an oncogenic protein that is highly expressed in a variety of cancers, including colorectal cancer, lung cancer, breast cancer, and hepatocellular carcinoma (HCC). The discovery of DDIAS as a novel therapeutic target and its role in human cancer biology is fascinating and noteworthy. Recent studies have shown that DDIAS is involved in tumorigenesis, metastasis, DNA repair and synthesis, and drug resistance and that it plays multiple roles with distinct binding partners in several human cancers. This review focuses on the function of DDIAS and its regulatory proteins in human cancer as potential targets for cancer therapy, as well as the development and future prospects of DDIAS inhibitors.

Development and Evaluation of a Blended Learning Mindfulness Program for High School Students During the COVID-19 Pandemic.

Many adolescents worldwide suffer from stress or unhealthy emotional states such as depression. There is a trend toward limited physical contact via social distancing practices that developed during the coronavirus disease 2019 (COVID-19) pandemic. An experimental study aimed at investigating the effects of a mindfulness program on stress, concentration, self-esteem, and self-control in high school students. A 10-week mindfulness intervention was provided to the experimental group (n = 89) from September-November 2020, while the control group (n = 89) received general health education. Four weeks after the program, the experimental group showed reduced stress and improved concentration, self-esteem, and self-control compared to baseline.The blended learning mindfulness program is effective improving concentration and should be incorporated into the formal high school curriculum.

Factors Affecting Zero-Waste Behaviours of College Students.

This study evaluated the recognition and attitude toward microplastic and zero waste among college students and investigated the factors influencing their zero-waste behaviours. The study was conducted from 20 August 2021 to 10 September 2021, including students at a university in G metropolitan city, Republic of Korea. A total of 196 data were analysed. Statements were developed to verify how the use of disposables and the recognition, attitude, and behaviours related to zero waste were affected during the COVID-19 pandemic. Family type and usage of disposables were the factors affecting zero-waste behaviour in Model 1. In Model 2, which included the subcategory of zero-waste recognition, the health effects of microplastics and environmental preservation were significant factors. In Model 3, which included the subcategory of zero-waste attitude, the health effects of microplastics (ß = 0.149, p = 0.016), use of eco-friendly products (ß = 0.342, p < 0.001), and environmental preservation (ß = 0.317, p < 0.001) were significant factors. The use of plastic products increased dramatically during the COVID-19 pandemic. Research and education are needed to promote zero-waste behaviours with a focus on microplastics. Raising awareness of the health effects of microplastics can enhance the effectiveness of education.

Synaptotagmin 11 scaffolds MKK7-JNK signaling process to promote stem-like molecular subtype gastric cancer oncogenesis.

BACKGROUND: Identifying biomarkers related to the diagnosis and treatment of gastric cancer (GC) has not made significant progress due to the heterogeneity of tumors. Genes involved in histological classification and genetic correlation studies are essential to develop an appropriate treatment for GC. METHODS: In vitro and in vivo lentiviral shRNA library screening was performed. The expression of Synaptotagmin (SYT11) in the tumor tissues of patients with GC was confirmed by performing Immunohistochemistry, and the correlation between the expression level and the patient's survival rate was analyzed. Phospho-kinase array was performed to detect Jun N-terminal kinase (JNK) phosphorylation. SYT11, JNK, and MKK7 complex formation was confirmed by western blot and immunoprecipitation assays. We studied the effects of SYT11 on GC proliferation and metastasis, real-time cell image analysis, adhesion assay, invasion assay, spheroid formation, mouse xenograft assay, and liver metastasis. RESULTS: SYT11 is highly expressed in the stem-like molecular subtype of GC in transcriptome analysis of 527 patients with GC. Moreover, SYT11 is a potential prognostic biomarker for histologically classified diffuse-type GC. SYT11 functions as a scaffold protein, binding both MKK7 and JNK1 signaling molecules that play a role in JNK1 phosphorylation. In turn, JNK activation leads to a signaling cascade resulting in cJun activation and expression of downstream genes angiopoietin-like 2 (ANGPTL2), thrombospondin 4 (THBS4), Vimentin, and junctional adhesion molecule 3 (JAM3), which play a role in epithelial-mesenchymal transition (EMT). SNU484 cells infected with SYT11 shRNA (shSYT11) exhibited reduced spheroid formation, mouse tumor formation, and liver metastasis, suggesting a pro-oncogenic role of SYT11. Furthermore, SYT11-antisense oligonucleotide (ASO) displayed antitumor activity in our mouse xenograft model and was conferred an anti-proliferative effect in SNU484 and MKN1 cells. CONCLUSION: SYT11 could be a potential therapeutic target as well as a prognostic biomarker in patients with diffuse-type GC, and SYT11-ASO could be used in therapeutic agent development for stem-like molecular subtype diffuse GC.

Effects of Forest-Based Interventions on Mental Health: A Meta-Analysis of Randomized Controlled Trials.

Forest-based interventions are a promising alternative therapy for enhancing mental health. The current study investigated the effects of forest therapy on anxiety, depression, and negative and positive mental condition through a meta-analysis of recent randomized controlled trials, using the PRISMA guideline. Of 825 articles retrieved from databases including PubMed, EMBASE, CINAHL, Cochrane, and PsycINFO, 6 met the inclusion criteria. The results of this study showed that forest-based interventions improved the mental health of participants in the intervention groups when compared to those in the control groups. Thirty-four outcome variables were analyzed from six studies. The overall effect size of the forest therapy programs was 1.25 (95% CI = 0.93−1.57, p < 0.001), which was large and statistically significant. These findings imply that forest-based interventions can improve mental health as a nonpharmacological intervention. This study is significant in that it is a meta-analysis of mental health that included only high-quality domestic and international RCTs. In future studies, more RCTs related to various forest interventions and studies involving many participants should be undertaken, which will complement heterogeneity in future meta-analysis studies.

TNF-α Secreted from Macrophages Increases the Expression of Prometastatic Integrin αV in Gastric Cancer.

The tumor microenvironment comprising blood vessels, fibroblasts, immune cells, and the extracellular matrix surrounding cancer cells, has recently been targeted for research in cancer therapy. We aimed to investigate the effect of macrophages on the invasive ability of gastric cancer cells, and studied their potential mechanism. In transcriptome analysis, integrin αV was identified as a gene increased in AGS cells cocultured with RAW264.7 cells. AGS cells cocultured with RAW264.7 cells displayed increased adhesion to the extracellular matrix and greater invasiveness compared with AGS cells cultured alone. This increased invasion of AGS cells cocultured with RAW264.7 cells was inhibited by integrin αV knockdown. In addition, the increase in integrin αV expression induced by tumor necrosis factor-α (TNF-α) or by coculture with RAW264.7 cells was inhibited by TNF receptor 1 (TNFR1) knockdown. The increase in integrin αV expression induced by TNF-α was inhibited by both Mitogen-activated protein kinase (MEK) inhibitor and VGLL1 S84 peptide treatment. Finally, transcription of integrin αV was shown to be regulated through the binding of VGLL1 and TEAD4 to the promoter of integrin αV. In conclusion, our study demonstrated that TNFR1-ERK-VGLL1 signaling activated by TNF-α secreted from RAW264.7 cells increased integrin αV expression, thereby increasing the adhesion and invasive ability of gastric cancer cells.

Effects of Mindfulness-Based Interventions on Mental Health in Nurses: A Meta-Analysis of Randomized Controlled Trials.

Mindfulness as a positive mental health intervention approach has been increasingly applied to nurses. This meta-analysis evaluated the psychological effects of mindfulness-based interventions (MBIs) on mental health in nurses. We searched PubMed, EMBASE, Cochrane, and CINAHL up to February 2020. Randomized controlled trials (RCTs) evaluating the effects of MBIs for nurses were included. Data extraction and the risk of bias assessment were conducted by two authors independently. Standardized mean differences (SMDs) with 95% confidence intervals (CIs) were calculated using a random-effects meta-analysis. Of 370 studies retrieve from databases, nine RCTs, which involved 572 participants with 283 in an intervention group and 289 in a control group, were included in the final analysis. Compared to the control groups (no treatment, treatment as usual, or active control), MBIs reduced psychological distress such as anxiety, depression, or stress (SMD = -0.47; 95% CI, -0.67 to -0.32; I2 = 34.7; n = 17) in nurses. Also, MBIs slightly improved psychological wellbeing such as resilience, wellbeing, or quality of life (SMD = 0.28; 95% CI, 0.11 to 0.46; I2 = 0.00; n = 8). However, no statistically significant effects were found in Job related outcomes (SMD = 0.23; 95% CI, -0.01 to 0.47; I2 = 20.5; n = 6). This meta-analysis found that MBIs had beneficial effects on mental health such as psychological distress and wellbeing in nurses.

A Latent Class Analysis of Health-Related Quality of Life in Korean Older Adults.

The present study aimed to confirm latent classes in health-related quality of life (HRQOL) in older adults and investigate the characteristics of participants in each class. It aimed to provide basic data to develop interventions for each quality-of-life class by analysing the predictors of each class. Secondary data from a community health survey in G province since 2019 found a total of 41,872 participants. Of them, 9027 were 65 years or older and residing in G Province in 2019, participated in this study. Mplus 8.5 was used to conduct a latent class analysis of five domains of HRQOL. Four latent classes in the HRQOL of older adults, namely, stable type, physical disability type, emotional disability type, and crisis type were found. Certain variables predicted these classes. Based on the findings of the present study, training on functional mobility and balance to prevent falls in older populations and individualised programmes to promote mental health in them should be provided. Moreover, policies should increase medical accessibility and provide social support for older people with low-incomes. Additionally, since physical, psychological, and social health in older adults are inter-connected, a comprehensive care plan is needed to improve their HRQOL.

DGG-100629 inhibits lung cancer growth by suppressing the NFATc1/DDIAS/STAT3 pathway.

DNA damage-induced apoptosis suppressor (DDIAS) promotes the progression of lung cancer and hepatocellular carcinoma through the regulation of multiple pathways. We screened a chemical library for anticancer agent(s) capable of inhibiting DDIAS transcription. DGG-100629 was found to suppress lung cancer cell growth through the inhibition of DDIAS expression. DGG-100629 induced c-Jun NH(2)-terminal kinase (JNK) activation and inhibited NFATc1 nuclear translocation. Treatment with SP600125 (a JNK inhibitor) or knockdown of JNK1 restored DDIAS expression and reversed DGG-100629-induced cell death. In addition, DGG-100629 suppressed the signal transducer and activator of transcription (STAT3) signaling pathway. DDIAS or STAT3 overexpression restored lung cancer cell growth in the presence of DGG-100629. In a xenograft assay, DGG-100629 inhibited tumor growth by reducing the level of phosphorylated STAT3 and the expression of STAT3 target genes. Moreover, DGG-100629 inhibited the growth of lung cancer patient-derived gefitinib-resistant cells expressing NFATc1 and DDIAS. Our findings emphasize the potential of DDIAS blockade as a therapeutic approach and suggest a novel strategy for the treatment of gefitinib-resistant lung cancer.

Licochalcone A inhibits hypoxia-inducible factor-1α accumulation by suppressing mitochondrial respiration in hypoxic cancer cells.

Hypoxia-inducible factor (HIF)-1 is an important regulator of the cellular response in the hypoxic tumor environment. While searching for HIF inhibitors derived from natural products that act as anticancer agents, we found that Glycyrrhiza uralensis exerts HIF-1 inhibitory activity in hypoxic cancer cells. Among the five components of G. uralensis, licochalcone A was found to potently suppress hypoxia-induced HIF-1α accumulation and expression of HIF-1α target genes, including GLUT1 and PDK1 in HCT116 cells. Licochalcone A also enhances intracellular oxygen content by directly inhibiting mitochondrial respiration, resulting in oxygen-dependent HIF-1α degradation. Hence, licochalcone A may effectively inhibit ATP production, primarily by reducing the mitochondrial respiration-mediated ATP production rate rather than the glycolysis-mediated ATP production rate. This effect subsequently suppresses cancer cell viability, including that of HCT116, H1299, and H322 cells. Consequently, these results suggest that licochalcone A has therapeutic potential in hypoxic cancer cells.

VGLL1 phosphorylation and activation promotes gastric cancer malignancy via TGF-ß/ERK/RSK2 signaling.

We previously reported that vestigial-like 1 (VGLL1), a cofactor of transcriptional enhanced associate domain 4 (TEAD4), is transcriptionally regulated by PI3K and ß-catenin signaling and is involved in gastric cancer malignancy. However, the precise mechanism underlying the regulation of VGLL1 activation remains unknown. Therefore, we aimed to investigate the molecular mechanism underlying the transforming growth factor-ß (TGF-ß)-mediated activation of VGLL1 and the VGLL1-TEAD4 interaction in gastric cancer cells. We showed that TGF-ß enhanced VGLL1 phosphorylation and that this phosphorylated VGLL1 functioned as a transcription cofactor of TEAD4 in NUGC3 cells. TGF-ß also increased the phosphorylation of ERK and ribosomal S6 kinase 2 (RSK2) in NUGC3 cells, thereby triggering the translocation of phosphorylated RSK2 to the nucleus. Site-directed mutagenesis and immunoprecipitation experiments revealed that RSK2 phosphorylated VGLL1 at S84 in the presence of TGF-ß. Mutation of VGLL1 at S84 suppressed VGLL1-TEAD4 binding and the subsequent transcriptional activation of matrix metalloprotease 9 (MMP9). Moreover, VGLL1 peptide containing S84 suppressed the TGF-ß-induced MMP9 expression and reduced the invasion and proliferation of gastric cancer cells, whereas VGLL1 peptide containing S84A did not. Furthermore, suppression of expression or activation of VGLL1 enhances the therapeutic effects of lapatinib. Collectively, these results indicate that VGLL1 phosphorylation via TGF-ß/ERK/RSK2 signaling plays a crucial role in MMP9-mediated malignancy of gastric cancer. In addition, our study highlights the therapeutic potential of the peptide containing VGLL1 S84 for the treatment of gastric cancer.

Analysis of multidimensional factors in attempts to quit using tobacco by Korean adolescents.

BACKGROUND: This study aims to understand the extent of adolescents' attempts to quit using tobacco and the factors influencing such attempts in Korea, using a descriptive, cross-sectional design and secondary data analysis with the 2019 Youth Health Behavior Survey. METHODS: The participants were 4028 adolescent tobacco users who had used tobacco for 1 day or more in the past 30 days. The data analysis was performed using IBM SPSS/WIN 26.0 program, and multivariable logistic regression analysis was conducted using the complex sampling method module. RESULTS: A total of 68.2% of the participants attempted to quit using tobacco. We analyzed the factors for adolescents' attempts to quit using tobacco by dividing them into psychological, physical, behavioral, and environmental dimensions. The factors influencing adolescents' attempts to quit using tobacco, identified through multivariable logistic regression analysis, are as follows: participation in sports activities (OR = 1.20, 95% CI 1.01-1.41), vigorous physical activity (OR = 1.24, 95% CI 1.06-1.46), and type of tobacco product used (OR = 1.65, 95% CI 1.24-2.21) in the behavioral dimension; pictorial cigarette pack warnings (perceived smoking as unhealthy) (OR = 1.91, 95% CI 1.56-2.36), and the presence of secondhand smoking at home (OR = 1.18, 95% CI 1.01-1.38) in the environmental dimension. CONCLUSIONS: Schools and public healthcare providers must consider multidimensional factors when providing support for successful tobacco cessation in adolescents and focus particularly on elements relating to physical activity and environmental factors.

Miconazole inhibits signal transducer and activator of transcription 3 signaling by preventing its interaction with DNA damage-induced apoptosis suppressor.

DNA damage-induced apoptosis suppressor (DDIAS) facilitates the survival of lung cancer by suppressing apoptosis. Moreover, DDIAS promotes tyrosine phosphorylation of signal transducer and activator of transcription 3 (STAT3) via their interaction. Here, we identified miconazole as an inhibitor of DDIAS/STAT3 interaction by screening a chemical library using a yeast two-hybrid assay. Miconazole inhibited growth, migration and invasion of lung cancer cells. Furthermore, miconazole suppressed STAT3 tyrosine Y705 phosphorylation and the expression of its target genes, such as cyclin D1, survivin and snail but had no suppressive effect on the activation of ERK1/2 or AKT, which is involved in the survival of lung cancer. As expected, no interaction between DDIAS and STAT3 occurred in the presence of miconazole, as confirmed by immunoprecipitation assays. Mouse xenograft experiments showed that miconazole significantly suppressed both tumor size and weight in an NCI-H1703 mouse model. Tyrosine phosphorylation of STAT3 at Y705 and expression of its targets, such as cyclin D1, survivin and snail, were decreased in miconazole-treated tumor tissues, as compared with those in vehicle-treated tumor tissues. These data suggest that miconazole exerts an anti-cancer effect by suppressing STAT3 activation through inhibiting DDIAS/STAT3 binding.

DDIAS promotes STAT3 activation by preventing STAT3 recruitment to PTPRM in lung cancer cells.

DNA damage-induced apoptosis suppressor (DDIAS) regulates cancer cell survival. Here we investigated the involvement of DDIAS in IL-6-mediated signaling to understand the mechanism underlying the role of DDIAS in lung cancer malignancy. We showed that DDIAS promotes tyrosine phosphorylation of signal transducer and activator of transcription 3 (STAT3), which is constitutively activated in malignant cancers. Interestingly, siRNA protein tyrosine phosphatase (PTP) library screening revealed protein tyrosine phosphatase receptor mu (PTPRM) as a novel STAT3 PTP. PTPRM knockdown rescued the DDIAS-knockdown-mediated decrease in STAT3 Y705 phosphorylation in the presence of IL-6. However, PTPRM overexpression decreased STAT3 Y705 phosphorylation. Moreover, endogenous PTPRM interacted with endogenous STAT3 for dephosphorylation at Y705 following IL-6 treatment. As expected, PTPRM bound to wild-type STAT3 but not the STAT3 Y705F mutant. PTPRM dephosphorylated STAT3 in the absence of DDIAS, suggesting that DDIAS hampers PTPRM/STAT3 interaction. In fact, DDIAS bound to the STAT3 transactivation domain (TAD), which competes with PTPRM to recruit STAT3 for dephosphorylation. Thus we show that DDIAS prevents PTPRM/STAT3 binding and blocks STAT3 Y705 dephosphorylation, thereby sustaining STAT3 activation in lung cancer. DDIAS expression strongly correlates with STAT3 phosphorylation in human lung cancer cell lines and tissues. Thus DDIAS may be considered as a potential biomarker and therapeutic target in malignant lung cancer cells with aberrant STAT3 activation.

PI3K/AKT/ß-Catenin Signaling Regulates Vestigial-Like 1 Which Predicts Poor Prognosis and Enhances Malignant Phenotype in Gastric Cancer.

Although gastric cancer is a common cause of cancer mortality worldwide, its biological heterogeneity limits the available therapeutic options. Therefore, identifying novel therapeutic targets for developing effective targeted therapy of gastric cancer is a pressing need. Here, we investigate molecular function and regulatory mechanisms of Vestigial-like 1 (VGLL1) in gastric cancer. Microarray analysis of 556 gastric cancer tissues revealed that VGLL1 was a prognostic biomarker that correlated with PI3KCA and PI3KCB. VGLL1 regulates the proliferation of gastric cancer cells, as shown in live cell imaging, sphere formation, and in vivo xenograft model. Tail vein injection of NUGC3 cells expressing shVGLL1 resulted in less lung metastasis occurring when compared to the control. In contrast, larger metastatic lesions in lung and liver were detected in the VGLL1-overexpressing NUGC3 cell xenograft excision mouse model. Importantly, VGLL1 expression is transcriptionally regulated by the PI3K-AKT-ß-catenin pathway. Subsequently, MMP9, a key molecule in gastric cancer, was explored as one of target genes that were transcribed by VGLL1-TEAD4 complex, a component of the transcription factor. Taken together, PI3K/AKT/ß-catenin signaling regulates the transcription of VGLL1, which promotes the proliferation and metastasis in gastric cancer. This finding suggests VGLL1 as a novel prognostic biomarker and a potential therapeutic target.

Percutaneous coronary artery stenting of unprotected left main coronary artery disease using drug-eluting stents: the initial Baylor University Medical Center experience.

Significant narrowing of the left main coronary artery is a high-risk condition with significant mortality risk. Bypass surgery is the current gold-standard treatment for unprotected left main (ULM) disease. Stenting utilizing drug-eluting stents (DES) is another therapeutic option for patients with ULM disease considered too high risk for bypass surgery or for patients who simply refuse bypass surgery. We have had great initial success with ULM stenting using DES in 10 selected patients at Baylor University Medical Center. Ongoing multicenter, international randomized studies comparing percutaneous coronary intervention with DES and bypass surgery will shed more light on the best treatment strategy for ULM coronary disease.

Safety of drug-eluting stents in the coronary artery in ST-elevation myocardial infarction at a single high-volume medical center.

Several trials have shown the effectiveness of drug-eluting stents (DES) in reducing restenosis. Acute ST-elevation myocardial infarction (STEMI) has been an exclusion criterion in most trials evaluating the safety and efficacy of DES. There is recent randomized trial data evaluating the use and safety of DES for acute myocardial infarction. However, there is a need for "real world" data on the efficacy and safety of DES in STEMI. A single-center retrospective analysis was performed on 188 consecutive patients with STEMI treated with primary or rescue coronary angioplasty between March 2004 and July 2005. The study consisted of 3 groups: 115 patients treated with paclitaxel-eluting stents, 55 with sirolimus-eluting stents, and 18 with bare metal stents. Outcomes were assessed from 12 to 28 months (mean 20, median 19) for major adverse cardiac events (MACEs) including myocardial infarction, in-stent thrombosis, clinical restenosis, and death. There were 4 in-stent thromboses in the paclitaxel group (3.4%) and 2 in-stent thromboses in the sirolimus group (3.6%). The thromboses ranged from acute (within 24 hours) to as late as 8 months. Clinical restenosis occurred in 4 patients (3.4%) in the paclitaxel group and in 2 patients (3.6%) in the sirolimus. None of the 18 patients with bare metal stents had thrombosis or clinical restenosis. There were 7 total deaths, all related to complications from the index STEMI: 1 in the bare metal group, 1 in the sirolimus group, and 5 in the paclitaxel group. The postdischarge MACE rate was 7% with no deaths. In conclusion, the use of DES in acute STEMI is associated with a low postdischarge MACE rate and a 3.5% in-stent thrombosis rate, which is similar to reported rates in earlier randomized trials.