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Articles by J. Y Park
Total Records ( 8 ) for J. Y Park
  E. H Koh , M Kim , K. C Ranjan , H. S Kim , H. S Park , K. S Oh , I. S Park , W. J Lee , M. S Kim , J. Y Park , J. H Youn and K. U. Lee
 

Nitric oxide (NO) stimulates mitochondrial biogenesis. We recently reported that adiponectin synthesis is regulated by mitochondrial function in adipocytes. This study was undertaken to test the hypothesis that endothelial NO synthase (eNOS) plays an important role in adiponectin synthesis by producing NO and enhancing mitochondrial function in adipocytes. We examined the effects of eNOS knockdown on adiponectin synthesis in 3T3-L1 adipocytes and also examined plasma adiponectin levels and the mitochondria in adipose tissue of eNOS knockout (eNOS–/–) mice with and without chronic administration of a NO donor. In cultured 3T3-L1 adipocytes, eNOS siRNA decreased rosiglitazone-induced adiponectin secretion, which was associated with decreases in mitochondrial proteins and biogenesis factors. Plasma adiponectin concentrations were reduced in adult eNOS–/– mice compared with age-matched wild-type mice. Mitochondrial contents in adipose tissue were reduced in eNOS–/– mice, and this was associated with decreased expression of mitochondrial biogenesis factors, increased levels of 8-hydroxyguanosine, a biomarker of oxidative stress, and morphological abnormalities in mitochondria. Rosiglitazone-induced increases in adiponectin expression and mitochondrial content were also reduced significantly in eNOS–/– mice. Chronic administration of a NO donor reversed mitochondrial abnormalities and increased adiponectin expression in adipose tissue of eNOS–/– mice. eNOS plays an important role in adiponectin synthesis in adipocytes by increasing mitochondrial biogenesis and enhancing mitochondrial function.

  J. Y Park , K Matsuo , T Suzuki , H Ito , S Hosono , T Kawase , M Watanabe , I Oze , T Hida , Y Yatabe , T Mitsudomi , T Takezaki , K Tajima and H. Tanaka
 

The main lifestyle contributor to acetaldehyde exposure is the drinking of alcoholic beverages, but tobacco smoke also makes some contribution. Although acetaldehyde is associated with upper aerodigestive tract cancer risk, in accordance with genetically determined acetaldehyde metabolism, it is unclear whether lung cancer, a representative smoking-related cancer, is associated with acetaldehyde or genes impacting its metabolism. We conducted a case–control study to examine possible interaction between smoking and aldehyde dehydrogenase 2 (ALDH2) Glu504Lys polymorphism (rs671) on the risk of lung cancer in Japanese. Subjects were 718 lung cancer cases and 1416 non-cancer controls enrolled in the Hospital-based Epidemiologic Research Program at Aichi Cancer Center. Lifestyle factors, including smoking, were determined by self-administered questionnaire. We applied pack-years (PY; categorized into five levels: never, <15, <30, <45 and ≥45) as a marker of cumulative exposure to smoking. The impact of smoking, ALDH2 genotype, and their interaction on lung cancer risk were assessed by odds ratio (OR) and 95% confidence interval adjusted for potential confounders. Adjusted ORs for PY <15, <30, <45 and ≥45 relative to never smokers among those with Glu/Glu or Glu/Lys were 1.39, 1.80, 3.44 and 6.25, respectively (P-trend = 1.4 x 10–30). In contrast, ORs among Lys/Lys were 1.01, 10.2, 11.4 and 23.2, respectively (P-trend = 2.6 x 10–7). Interaction between ALDH2 genotype (Glu/Glu + Glu/Lys versus Lys/Lys) and cumulative smoking dose was statistically significant (P = 0.036) and was consistently observed in the analysis among never-drinkers (interaction P = 0.041). These results suggest that ALDH2 Lys/Lys, a null enzyme activity genotype, modifies the impact of smoking on the risk of lung cancer.

  J. Y Park , P. y Wang , T Matsumoto , H. J Sung , W Ma , J. W Choi , S. A Anderson , S. C Leary , R. S Balaban , J. G Kang and P. M. Hwang
 

Rationale: Exercise capacity is a physiological characteristic associated with protection from both cardiovascular and all-cause mortality. p53 regulates mitochondrial function and its deletion markedly diminishes exercise capacity, but the underlying genetic mechanism orchestrating this is unclear. Understanding the biology of how p53 improves exercise capacity may provide useful insights for improving both cardiovascular as well as general health.

Objective: The purpose of this study was to understand the genetic mechanism by which p53 regulates aerobic exercise capacity.

Methods and Results: Using a variety of physiological, metabolic, and molecular techniques, we further characterized maximum exercise capacity and the effects of training, measured various nonmitochondrial and mitochondrial determinants of exercise capacity, and examined putative regulators of mitochondrial biogenesis. As p53 did not affect baseline cardiac function or inotropic reserve, we focused on the involvement of skeletal muscle and now report a wider role for p53 in modulating skeletal muscle mitochondrial function. p53 interacts with Mitochondrial Transcription Factor A (TFAM), a nuclear-encoded gene important for mitochondrial DNA (mtDNA) transcription and maintenance, and regulates mtDNA content. The increased mtDNA in p53+/+ compared to p53–/– mice was more marked in aerobic versus glycolytic skeletal muscle groups with no significant changes in cardiac tissue. These in vivo observations were further supported by in vitro studies showing overexpression of p53 in mouse myoblasts increases both TFAM and mtDNA levels whereas depletion of TFAM by shRNA decreases mtDNA content.

Conclusions: Our current findings indicate that p53 promotes aerobic metabolism and exercise capacity by using different mitochondrial genes and mechanisms in a tissue-specific manner.

  S. T Kim , J. Y Park , J Lee , J. O Park , Y. S Park , H. Y Lim , W. K Kang and S. H. Park
  Objective

Malignant peritoneal mesothelioma is a rare neoplasm that accounts for ~1 per 1 million has limited data regarding its frontline therapy. We investigated the treatment outcomes in patients with malignant peritoneal mesothelioma receiving frontline cisplatin-based combination chemotherapy.

Methods

We analyzed 14 patients with malignant peritoneal mesothelioma who had been treated by frontline cisplatin-based combination chemotherapy between January 2005 and March 2009. The chemotherapeutic agent added to platinum was gemcitabine in one patient, cyclophosphamide–doxorubicin in three patients and pemetrexed in 10 patients.

Results

The confirmed overall response rate was 35.7% and the disease control rate was 71.4%. In all patients, two complete responses and three partial responses were observed (overall response rate, 35.7%). Stable disease was observed in five patients (35.7%). The median progression free survival was 4.4 months (95% CI, 0.6–9.0) and the median overall survival was 20.1 months (95% CI, 12.7–28.5). There was significant differences for progression free survival (P = 0.031) according to the different chemotherapeutic agents (pemetrexed versus non-pemetrexed agents) added to platinum. Grade 3 or 4 hematologic toxicities included leukopenia in one patient and anemia in three patients. There were no Grade 3 or 4 non-hematologic toxicities or treatment-related deaths.

Conclusion

The platinum-based combination chemotherapy showed moderate activity and a favorable toxicity profile as a frontline treatment for patients with malignant peritoneal mesothelioma. Pemetrexed in combination with platinum showed improved survival outcomes as compared with other combination regimens combined with platinum.

  J. Y Park , P. N Mitrou , J Keen , C. C Dahm , L. J Gay , R. N Luben , A McTaggart , K. T Khaw , R. Y Ball , M. J Arends and S. A. Rodwell
 

The tumour suppressor p53 is one of the most commonly altered genes in colorectal cancer (CRC) development. Genetic alterations in p53 may therefore be associated with postulated lifestyle risk factors for CRC, such as red meat consumption. In the European Prospective Investigation into Cancer and Nutrition-Norfolk study, we examined whether detailed estimates of dietary and lifestyle factors measured at baseline related to later development of p53 mutations in CRCs. After 10-year follow-up, there were 185 incident CRCs of which 34% had somatic p53 mutations (p53+). We observed significantly higher mean intakes of alcohol, total meat and red meat, in the group with p53 mutations and advanced Dukes’ stage disease (daily alcohol intake was 7 and 12 g for p53– and p53+ cases, respectively, P = 0.04; daily total meat intake was 69 and 100 g for p53– and p53+ cases, respectively, P = 0.03 and daily red meat intake was 39 and 75 g for p53– and p53+ cases, respectively, P = 0.01). Each 50 g/day increment in total meat intake was associated with having p53 mutations in cases with advanced Dukes’ stages [odds ratio (OR): 3.43, 95% confidence interval (CI): 1.47–7.96]. Similarly, each 50 g/day increment in red meat intake was also significantly associated with having consistent p53 mutations in cases with advanced Dukes’ stages (OR: 2.42, 95% CI: 1.18–4.96). These effects of total meat or red meat intake and advanced Dukes’ stages were independent of age, sex, body mass index, smoking and alcohol intake. Furthermore, P values for interaction between daily total meat or red meat intake and Dukes’ stages were statistically significant in multivariable models (Pinteraction < 0.001). Our results suggest that p53 mutations accelerate progression of CRC to advanced Dukes’ stage in association with higher meat especially red meat intakes.

  J. Y Shin , Y. Y Choi , H. S Jeon , J. H Hwang , S. A Kim , J. H Kang , Y. S Chang , D. R Jacobs , J. Y Park and D. H. Lee
 

Although shortened telomeres have been found in many cancers, elongated telomere length has been observed as an early response after low-dose treatment with various chemical carcinogens in vitro and animal experiments, suggesting low-dose exposure to carcinogenic chemicals may function as a tumour promoter at the very early stage of carcinogenesis in humans. This cross-sectional study was performed to examine whether low-dose exposure to persistent organic pollutants (POPs), lipophilic xenobiotics that mainly bioaccumulate in adipose tissue, is associated with telomere length of peripheral blood leukocytes in apparently healthy persons. Telomere length was measured using quantitative polymerase chain reaction method in 84 apparently healthy Koreans. Among various POPs, serum concentrations of organochlorine (OC) pesticides, polychlorinated biphenyls (PCBs) and polybrominated diphenylethers were measured. Most OC pesticides and PCBs were positively and significantly associated with telomere length with correlation coefficients from about +0.25 to +0.35. The strongest associations were observed with p,p'-dichlorodiphenyldichloroethylene, PCB99, PCB153, PCB180, PCB183 and PCB187. When we examined adjusted means of telomere length by quintiles of POPs, the steeper increases of telomere length tended to be observed within relatively lower ranges of POPs. Besides serum concentrations of POPs, none of the other variables studied, including age, were associated with telomere length in this study. We found that telomere length was increasing across low doses of exposure to POPs in which the majority of study subjects were found, suggesting that low-dose POPs may act as a tumour promoter in carcinogenesis in humans.

  F. E Pfefferkorn , D Bello , G Haddad , J. Y Park , M Powell , J Mccarthy , K. L Bunker , A Fehrenbacher , Y Jeon , M. A Virji , G Gruetzmacher and M. D. Hoover
 

Friction stir welding (FSW) is considered one of the most significant developments in joining technology over the last half century. Its industrial applications are growing steadily and so are the number of workers using this technology. To date, there are no reports on airborne exposures during FSW. The objective of this study was to investigate possible emissions of nanoscale (<100 nm) and fine (<1 µm) aerosols during FSW of two aluminum alloys in a laboratory setting and characterize their physicochemical composition. Several instruments measured size distributions (5 nm to 20 µm) with 1-s resolution, lung deposited surface areas, and PM2.5 concentrations at the source and at the breathing zone (BZ). A wide range aerosol sampling system positioned at the BZ collected integrated samples in 12 stages (2 nm to 20 µm) that were analyzed for several metals using inductively coupled plasma mass spectrometry. Airborne aerosol was directly collected onto several transmission electron microscope grids and the morphology and chemical composition of collected particles were characterized extensively. FSW generates high concentrations of ultrafine and submicrometer particles. The size distribution was bimodal, with maxima at ~30 and ~550 nm. The mean total particle number concentration at the 30 nm peak was relatively stable at ~4.0 x 105 particles cm–3, whereas the arithmetic mean counts at the 550 nm peak varied between 1500 and 7200 particles cm–3, depending on the test conditions. The BZ concentrations were lower than the source concentrations by 10–100 times at their respective peak maxima and showed higher variability. The daylong average metal-specific concentrations were 2.0 (Zn), 1.4 (Al), and 0.24 (Fe) µg m–3; the estimated average peak concentrations were an order of magnitude higher. Potential for significant exposures to fine and ultrafine aerosols, particularly of Al, Fe, and Zn, during FSW may exist, especially in larger scale industrial operations.

  J. Y Park , G Ramachandran , P. C Raynor , L. E Eberly and G. Olson
 

Recently, the appropriateness of using the ‘mass concentration’ metric for ultrafine particles has been questioned and surface area (SA) or number concentration metrics has been proposed as alternatives. To assess the abilities of various exposure metrics to distinguish between different exposure zones in workplaces with nanoparticle aerosols, exposure concentrations were measured in preassigned ‘high-’ and ‘low-’exposure zones in a restaurant, an aluminum die-casting factory, and a diesel engine laboratory using SA, number, and mass concentration metrics. Predetermined exposure classifications were compared by each metric using statistical parameters and concentration ratios that were calculated from the different exposure concentrations. In the restaurant, SA and fine particle number concentrations showed significant differences between the high- and low-exposure zones and they had higher contrast (the ratio of between-zone variance to the sum of the between-zone and within-zone variances) than mass concentrations. Mass concentrations did not show significant differences. In the die cast facility, concentrations of all metrics were significantly greater in the high zone than in the low zone. SA and fine particle number concentrations showed larger concentration ratios between the high and low zones and higher contrast than mass concentrations. None of the metrics were significantly different between the high- and low-exposure zones in the diesel engine laboratory. The SA and fine particle number concentrations appeared to be better at differentiating exposure zones and finding the particle generation sources in workplaces generating nanoparticles. Because the choice of an exposure metric has significant implications for epidemiologic studies and industrial hygiene practice, a multimetric sampling approach is recommended for nanoparticle exposure assessment.

 
 
 
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