Partial Pericardial Defect Incidentally Discovered During Coronary Bypass Surgery

A 71-yr-old male patient with three vessel coronary artery disease underwent a coronary artery bypass graft. The patient was found to have a large pericardial defect at the apex of the heart that measured approximately 18 cm in circumference. The edge of the pericardial defect impinged on the epicardial coronary arteries. The left phrenic nerve descended via the dorsal boundary of the pericardial defect. Following coronary artery bypass grafting, the pericardial defect was repaired with a polytetrafluorethylene patch. The patient had an uncomplicated postoperative course

Simulated microgravity with floating environment promotes migration of non-small cell lung cancers

A migration of cancer is one of the most important factors affecting cancer therapy. Particularly, a cancer migration study in a microgravity environment has gained attention as a tool for developing cancer therapy. In this study, we evaluated the proliferation and migration of two types (adenocarcinoma A549, squamous cell carcinoma H1703) of non-small cell lung cancers (NSCLC) in a floating environment with microgravity. When we measured proliferation of two NSCLCs in the microgravity (MG) and ground-gravity (CONT), although initial cell adhesion in MG was low, a normalized proliferation rate of A549 in MG was higher than that in CONT. Wound healing results of A549 and H1703 showed rapid recovery in MG; particularly, the migration rate of A549 was faster than that of H1703 both the normal and low proliferating conditions. Gene expression results showed that the microgravity accelerated the migration of NSCLC. Both A549 and H1703 in MG highly expressed the migration-related genes MMP-2, MMP-9, TIMP-1, and TIMP-2 compared to CONT at 24 h. Furthermore, analysis of MMP-2 protein synthesis revealed weaker metastatic performance of H1703 than that of A549. Therefore, the simulated microgravity based cancer culture environment will be a potential for migration and metastasis studies of lung cancers

Association between shift work and obesity among female nurses: Korean Nurses’ Survey

Background: Shift work has been hypothesized as a risk factor for obesity. In this study, we investigated the association between current shift work and body mass index (BMI) among female nurses in Korea. The relationship between duration of shift work and BMI of the participants was also evaluated. Methods: This cross-sectional survey evaluated participants in the Korean Nurses’ Survey, conducted from October to December 2011, using web-based self-administered questionnaires. A total of 9,989 nurses were included among 10,000 who registered on the survey web site (5,287 shift workers and 4,702 non-shift workers). Current shift workers were divided into tertiles of shift work duration (0.08–3.00 years, n = 1,732; 3.08–6.75 years, n = 1,731; and 6.83–38.00 years, n = 1,686). The BMI thresholds of overweight and obesity were ≥23 kg/m2 and ≥25 kg/m2, respectively. Data were analyzed using SPSS software. Results: Mean participant age was 33.2 ± 8.6 years and the mean BMI was 20.9 ± 2.5 kg/m2. There were statistically significant differences in current smoking status, regular drinking habit, dietary habits, regular exercise, sleep problems and self-perceived health status according to duration of shift work. The overall prevalence of overweight/obesity (18.6%) and obesity (7.4%) increased significantly as shift work duration increased from the lowest to highest tertile (P for trend <0.001). Multivariate logistic regression analysis revealed no association between current shift work and BMI. However, after adjusting for potential confounders, the participants with the longest duration of shift work were 1.63 (95% CI, 1.22–2.17) times more likely to be overweight or obese than those with the shortest duration. There was a significant positive association between obesity and shift work duration in the unadjusted analysis; however, it was attenuated and no longer significant in the multivariate model. Conclusions: The duration of shift work was positively associated with prevalence of overweight/obesity in nurses in Korea. Although these findings need to be confirmed in prospective studies, they suggest that special attention should be paid to female nurses with a long duration of shift work

Exogenous 8-hydroxydeoxyguanosine attenuates doxorubicin-induced cardiotoxicity by decreasing pyroptosis in H9c2 cardiomyocytes

Doxorubicin (DOX), which is widely used in cancer treatment, can induce cardiomyopathy. One of the main mechanisms whereby DOX induces cardiotoxicity involves pyroptosis through the NLR family pyrin domain containing 3 (NLRP3) inflammasome and gasdermin D (GSDMD). Increased NAPDH oxidase (NOX) and oxidative stress trigger pyroptosis. Exogenous 8-hydroxydeoxyguanosine (8-OHdG) decreases reactive oxygen species (ROS) production by inactivating NOX. Here, we examined whether 8-OHdG treatment can attenuate DOX-induced pyroptosis in H9c2 cardiomyocytes. Exposure to DOX increased the peroxidative glutathione redox status and NOX1/2/4, toll-like receptor (TLR)2/4, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) expression, while an additional 8-OHdG treatment attenuated these effects. Furthermore, DOX induced higher expression of NLRP3 inflammasome components, including NLRP3, apoptosis-associated speck-like protein containing a c-terminal caspase recruitment domain (ASC), and pro-caspase-1. Moreover, it increased caspase-1 activity, a marker of pyroptosis, and interleukin (IL)-1β expression. All these effects were attenuated by 8-OHdG treatment. In addition, the expression of the cardiotoxicity markers, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) was increased by DOX, whereas the increase of ANP and BNP induced by DOX treatment was reversed by 8-OHdG. In conclusion, exogenous 8-OHdG attenuated DOX-induced pyroptosis by decreasing the expression of NOX1/2/3, TLR2/4, and NF-κB. Thus, 8-OHdG may attenuate DOX-induced cardiotoxicity through the inhibition of pyroptosis.This research was funded by a grant from the National Research Foundation of Korea (NRF) grant (2020R1A2C200652811) (to K.H.S.) and Korea Environment Industry & Technology Institute (KEITI) through ‑Core Technology Development Project for Environmental Diseases Prevention and Management Program, funded by Korea Ministry of Environment (MOE) (2021003310006) (to K.H.S.

Effect of fermented sarco oyster extract on age induced sarcopenia muscle repair by modulating regulatory T cells

Sarcopenia is an age-related, progressive skeletal muscle disorder involving the loss of muscle mass and strength. Previous studies have shown that γ-aminobutyric acid (GABA) from fermented oysters aids in regulatory T cells (Tregs) cell expansion and function by enhancing autophagy, and concomitantly mediate muscle regeneration by modulating muscle inflammation and satellite cell function. The fermentation process of oysters not only increases the GABA content but also enhances the content of branched amino acids and free amino acids that aid the level of protein absorption and muscle strength, mass, and repair. In this study, the effect of GABA-enriched fermented sarco oyster extract (FSO) on reduced muscle mass and functions via Treg modulation and enhanced autophagy in aged mice was investigated. Results showed that FSO enhanced the expression of autophagy markers (autophagy-related gene 5 [ATG5] and GABA receptor-associated protein [GABARAP]), forkhead box protein 3 (FoxP3) expression, and levels of anti-inflammatory cytokines (interleukin [IL]-10 and transforming growth factor [TGF]-β) secreted by Tregs while reducing pro-inflammatory cytokine levels (IL-17A and interferon [IFN]-γ). Furthermore, FSO increased the expression of IL-33 and its receptor IL-1 receptor-like 1 (ST2); well-known signaling pathways that increase amphiregulin (Areg) secretion and expression of myogenesis markers (myogenic factor 5, myoblast determination protein 1, and myogenin). Muscle mass and function were also enhanced via FSO. Overall, the current study suggests that FSO increased autophagy, which enhanced Treg accumulation and function, decreased muscle inflammation, and increased satellite cell function for muscle regeneration and therefore could decrease the loss of muscle mass and function with aging

Synthesis and Characterization of Poly(Ethylene Glycol) Based Thermo-Responsive Hydrogels for Cell Sheet Engineering

The swelling properties and thermal transition of hydrogels can be tailored by changing the hydrophilic-hydrophobic balance of polymer networks. Especially, poly(N-isopropylacrylamide) (PNIPAm) has received attention as thermo-responsive hydrogels for tissue engineering because its hydrophobicity and swelling property are transited around body temperature (32 °C). In this study, we investigated the potential of poly(ethylene glycol) diacrylate (PEGDA) as a hydrophilic co-monomer and crosslinker of PNIPAm to enhance biological properties of PNIPAm hydrogels. The swelling ratios, lower critical solution temperature (LCST), and internal pore structure of the synthesized p(NIPAm-co-PEGDA) hydrogels could be varied with changes in the molecular weight of PEGDA and the co-monomer ratios (NIPAm to PEGDA). We found that increasing the molecular weight of PEGDA showed an increase of pore sizes and swelling ratios of the hydrogels. In contrast, increasing the weight ratio of PEGDA under the same molecular weight condition increased the crosslinking density and decreased the swelling ratios of the hydrogels. Further, to evaluate the potential of these hydrogels as cell sheets, we seeded bovine chondrocytes on the p(NIPAm-co-PEGDA) hydrogels and observed the proliferation of the seed cells and their detachment as a cell sheet upon a decrease in temperature. Based on our results, we confirmed that p(NIPAm-co-PEGDA) hydrogels could be utilized as cell sheets with enhanced cell proliferation performance

Addition of oh8dG to Cardioplegia Attenuated Myocardial Oxidative Injury through the Inhibition of Sodium Bicarbonate Cotransporter Activity

The biomarker 8-hydroxy-2&prime;-deoxyguanosine (oh8dG) is derived from oxidized nucleic acids or products of oxidant-mediated DNA damage. Enhanced sodium bicarbonate cotransporter (NBC) activity is caused by reactive oxygen species (ROS) production in ventricular myocytes. Thus, we hypothesized that cardioplegia-solution-mediated ROS generation may be involved in the regulation of NBC activity in cardiomyocytes and that oh8dG treatment may modulate ROS and associated NBC activity. Langendorff-free cardioplegia-arrested cardiac strips and cardiomyocytes were isolated to determine the NBC activity and effects of oh8dG on oxidative-stress-mediated cardiac damage markers. We first determined the histidine-tryptophan-ketoglutarate (HTK) solution mediated NBC activity in cardiac strips and cells. The oh8dG treatment attenuated NBC activity in the electroneutral or electrogenic form of NBC. Additionally, exposure to HTK solution induced ROS, whereas co-administration of oh8dG attenuated ROS-mediated NBC activity, reduced ROS levels, and decreased the expression of apoptotic markers and fibrosis-associated proteins in cardiac cells. The oh8dG-administrated cardiac tissues were also protected from enhanced HTK-induced damage markers, heat shock protein 60 and polyADP-ribose. Our results show that oh8dG has a protective role against myocardial oxidative damage and provides a useful treatment strategy for restoring cardiac function

Pyrogallol-Phloroglucinol-6 6-Bieckol on Attenuates High-Fat Diet-Induced Hypertension by Modulating Endothelial-to-Mesenchymal Transition in the Aorta of Mice

Endothelial-to-mesenchymal transition (EndMT), which is involved in the development of various cardiovascular diseases, is induced by dyslipidemia or obesity. In dyslipidemia, the increased levels of oxidized low-density lipoproteins (oxLDL) upregulated the lectin-type oxidized LDL receptor 1 (Lox-1), which then upregulated the down signaling pathways of PKC-α/MMPs/TGF-β/SMAD2 or 3 and increased the EndMT. In this study, we investigated the effect of pyrogallol-phloroglucinol-6,6-bieckol (PPB), which is a compound of Ecklonia cava (E. cava), on decreased blood pressure (BP) by attenuating the EndMT in a high-fat diet- (HFD-) fed animal model. We also investigated PPB’s attenuation effect on EndMT in oxLDL-treated mouse endothelial cells as an in vitro model. The results indicated that, in the aorta or endothelial cells of mice, the HFD or oxLDL treatment significantly increased the expression of Lox-1/PKC-α/MMP9/TGF-β/SMAD2/SMAD3. The PPB treatment significantly decreased its expression. In contrast, the HFD or oxLDL treatment significantly decreased the expression of the EC markers (PECAM-1 and vWF) while the PPB treatment significantly increased them. Moreover, the HFD or oxLDL treatment significantly increased the expression of the mesenchymal cell markers (α-SMA and vimentin) while PPB treatment significantly decreased them. PPB decreased the intima-media thickness and extracellular matrix amount of the aorta and attenuated the BP, which was increased by the HFD. In conclusion, PPB attenuated the upregulation of Lox-1/PKC-α/MMP9/TGF-β/SMAD2 and 3 and restored the EndMT in HFD-fed animals. Moreover, PPB showed a restoring effect on HFD-induced hypertension

Attenuating Effects of Dieckol on Endothelial Cell Dysfunction via Modulation of Th17/Treg Balance in the Intestine and Aorta of Spontaneously Hypertensive Rats

Disruptions of the Treg/Th17 cell balance and gut barrier function are associated with endothelial dysfunction. Dieckol (DK) obtained from Ecklonia cava and E. cava extract (ECE) decreases blood pressure by reducing inflammation; however, it has not been elucidated whether DK or ECE modulates the Treg/Th17 balance, changes the gut epithelial barrier, or decreases endothelial cell dysfunction. We evaluated the effects of ECE and DK on gut barrier and the Treg/Th17 balance in the intestine and aorta, with regard to endothelial dysfunction, using the spontaneously hypertensive rat (SHR) model. The level of Th17 cells increased and that of Treg cells decreased in the intestine of SHRs compared to normotensive Wistar Kyoto (WKY) rat. These changes were attenuated by ECE or DK treatment. Additionally, the serum IL-17A level increased in SHRs more than WKY; this was decreased by ECE or DK treatment. The level of Treg cells decreased and that of Th17 cells increased in the aorta of SHRs. These changes were attenuated by ECE or DK treatment. The NF-κB and IL-6 levels were increased in SHRs, but these changes were reversed by ECE or DK treatment. Endothelial cell dysfunction, which was evaluated using peNOS/eNOS, nitrate/nitrite ratio, and NADPH oxidase activity, increased in the aorta of SHRs, but was decreased by ECE or DK treatment. The Treg/Th17 balance in the intestine and aorta of SHRs was attenuated and endothelial cell dysfunction was attenuated through the Th17/NF-κB/IL-6 pathway by ECE or DK