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Cardiac tamponade (CT) is a rare but potentially lethal complication associated with central venous catheters (CVCs). We present a 6-year-old boy who developed CT after CVC insertion in the right internal jugular vein, with its tip in the inferior vena cava. Initially, he was hospitalized to a tertiary hospital with presumptive diagnoses of pneumonia and left ankle cellulitis. Three days after CVC placement, he developed CT, manifesting as recurrent episodes of hypotension and bradycardia. Once a bedside echocardiography showed CT, pericardiocentesis was performed, resulting in successful resuscitation. Pericardiocentesis revealed a milk-appearing pericardial fluid, indicating chylopericardium. The boy also underwent debridement and joint irrigation of the left ankle, which turned out to be osteomyelitis. Although CVC tips in most reported CVC-related CTs have been commonly located in the right atrium, our case featured a tip located in the inferior vena cava. Additionally, chylopericardium was likely due to the extravasation of total parenteral nutrition fluid, rather than the usual causes, such as recent thoracic surgery. Understanding the mechanisms behind chylopericardium associated with CVCs and timely pericardiocentesis is crucial for improving the outcomes.

Bronchopulmonary dysplasia (BPD) and pulmonary hypertension (PH) are potentially fatal complications in prematurely born infants. Extracorporeal membrane oxygenation (ECMO) may be a life-saving option for managing infants with BPD and PH. We present 2 patients who were successfully weaned off mechanical ventilators (MVs) through the application of ECMO. The patients were transferred to our institution after receiving MV care for 8 and 10 months, respectively, for BPD and PH. We were able to remove the patients from MVs after a period of ECMO-mediated lung rest. Although more research is required to determine specific criteria for ECMO use in patients with BPD and PH, our clinical experiences may contribute to the early application of ECMO in MV-dependent patients.

Background: Identifying critically ill patients at risk of cardiac arrest is important because it offers the opportunity for early intervention and increased survival. The aim of this study was to develop a deep learning model to predict critical events, such as cardiopulmonary resuscitation or mortality. Methods: This retrospective observational study was conducted at a tertiary university hospital. All patients younger than 18 years who were admitted to the pediatric intensive care unit from January 2010 to May 2023 were included. The main outcome was prediction performance of the deep learning model at forecasting critical events. Long short-term memory was used as a deep learning algorithm. The five-fold cross validation method was employed for model learning and testing. Results: Among the vital sign measurements collected during the study period, 11,660 measurements were used to develop the model after preprocessing; 1,060 of these data points were measurements that corresponded to critical events. The prediction performance of the model was the area under the receiver operating characteristic curve (95% confidence interval) of 0.988 (0.975–1.000), and the area under the precision-recall curve was 0.862 (0.700–1.000). Conclusions: The performance of the developed model at predicting critical events was excellent. However, follow-up research is needed for external validation.

Objectives To identify bacterial contamination rates of laryngoscope blades and handles stored in emergency crash carts by hospital and area according to the frequency of intubation attempts. Methods One hundred forty-eight handles and 71 blades deemed ready for patient use from two tertiary hospitals were sampled with sterile swabs using a standardized rolling technique. Samples were considered negative (not contaminated) if no colonies were present on the blood agar plate after an 18-hour incubation period. Samples were stratified by hospital and according to the frequency of intubation attempts (10 attempts per year) using the χ2-test and Fisher exact test. Results One or more species of bacteria were isolated from 4 (5.6%) handle tops, 20 (28.2%) handles with knurled surfaces, and 27 (18.2%) blades. No significant differences were found in microbial contamination levels on the handle tops and blades between the two hospitals and two areas according to the frequency of intubation attempts. However, significant differences were found between the two hospitals and two areas in the level of microbial contamination on the handles with knurled surfaces (p

Issues like why students felt far from physics and did not choose physics as their prime learning option are familiar in education. This paper aims to study the effectiveness of the STEM-Project-Based learning module in physics on students' personal interest and sensemaking and effort. This research used the quasi-experimental model, employing a two-group pre-survey-post-survey design. Quantitative data were collected using the Colorado Learning Attitude about Science Survey (CLASS) instrument at two selected schools in Sabah, Malaysia, and Seoul, Korea. The sample size was 88 Form 4 students in Malaysia and 66 second-year high school students in Korea who learned classical mechanics. The students were divided into two groups, respectively, i.e., the experimental group (Malaysia=44, Korea=33) and the control group (Malaysia=44, Korea=33). Participants in the experimental group were intervened with the integrated STEM-PBL physics module, whilst participants in the control group learned physics through a conventional approach for eight weeks. Participants in both groups were then administered a pre-survey before and post-survey after the intervention. This research showed that the integrated STEM-PBL physics module significantly improved students' personal interest, and sense-making and effort after the intervention. The paper also highlighted the research's implications and suggestions.

Adiponectin plays multiple critical roles in modulating various physiological processes by binding to its receptors. The functions of PEG-BHD1028, a potent novel peptide agonist to AdipoRs, was evaluated using in vitro and in vivo models based on the reported action spectrum of adiponectin. To confirm the design concept of PEG-BHD1028, the binding sites and their affinities were analyzed using the SPR (Surface Plasmon Resonance) assay. The results revealed that PEG-BHD1028 was bound to two heterogeneous binding sites of AdipoR1 and AdipoR2 with a relatively high affinity. In C2C12 cells, PEG-BHD1028 significantly activated AMPK and subsequent pathways and enhanced fatty acid β-oxidation and mitochondrial biogenesis. Furthermore, it also facilitated glucose uptake by lowering insulin resistance in insulin-resistant C2C12 cells. PEG-BHD1028 significantly reduced the fasting plasma glucose level in db/db mice following a single s.c. injection of 50, 100, and 200 μg/Kg and glucose tolerance at a dose of 50 μg/Kg with significantly decreased insulin production. The animals received 5, 25, and 50 μg/Kg of PEG-BHD1028 for 21 days significantly lost their weight after 18 days in a range of 5–7%. These results imply the development of PEG-BHD1028 as a potential adiponectin replacement therapeutic agent.

This study investigated the protective mechanisms of triphlorethol-A, isolated from Ecklonia cava, against oxidative stress-induced DNA base damage, especially 8-oxoguanine (8-oxoG), in Chinese hamster lung fibroblast V79-4 cells. 8-Oxoguanine DNA glycosylase-1 (OGG1) plays an important role in the removal of 8-oxoG during the cellular response to DNA base damage. Triphlorethol-A significantly decreased the levels of 8-oxoG induced by H2O2, and this correlated with increases in OGG1 mRNA and OGG1 protein levels. Furthermore, siOGG1-transfected cell attenuated the protective effect of triphlorethol-A against H2O2 treatment. Nuclear factor erythroid 2–related factor 2 (Nrf2) is a transcription factor for OGG1, and Nrf2 combines with small Maf proteins in the nucleus to bind to antioxidant response elements (ARE) in the upstream promoter region of the OGG1 gene. Triphlorethol-A restored the expression of nuclear Nrf2, small Maf protein, and the Nrf2-Maf complex, all of which were reduced by oxidative stress. Furthermore, triphlorethol-A increased Nrf2 binding to ARE sequences and the resulting OGG1 promoter activity, both of which were also reduced by oxidative stress. The levels of the phosphorylated forms of Akt kinase, downstream of phosphatidylinositol 3-kinase (PI3K), and Erk, which are regulators of OGG1, were sharply decreased by oxidative stress, but these decreases were prevented by triphlorethol-A. Specific PI3K, Akt, and Erk inhibitors abolished the cytoprotective effects of triphlorethol-A, suggesting that OGG1 induction by triphlorethol-A involves the PI3K/Akt and Erk pathways. Taken together, these data indicate that by activating the DNA repair system, triphlorethol-A exerts protective effects against DNA base damage induced by oxidative stress.

Recently, we demonstrated that butin (7,3′,4′-trihydroxydihydroflavone) protected cells against hydrogen peroxide (H2O2)-induced apoptosis by: (1) scavenging reactive oxygen species (ROS), activating antioxidant enzymes such superoxide dismutase and catalase; (2) decreasing oxidative stress-induced 8-hydroxy-2'-deoxyguanosine levels via activation of oxoguanine glycosylase 1, and (3), reducing oxidative stress-induced mitochondrial dysfunction. The objective of this study was to determine the cytoprotective effects of butin on oxidative stress-induced mitochondria-dependent apoptosis, and possible mechanisms involved. Butin significantly reduced H2O2-induced loss of mitochondrial membrane potential as determined by confocal image analysis and flow cytometry, alterations in Bcl-2 family proteins such as decrease in Bcl-2 expression and increase in Bax and phospho Bcl-2 expression, release of cytochrome c from mitochondria into the cytosol and activation of caspases 9 and 3. Furthermore, the anti-apoptotic effect of butin was exerted via inhibition of mitogen-activated protein kinase kinase-4, c-Jun NH2-terminal kinase (JNK) and activator protein-1 cascades induced by H2O2 treatment. Finally, butin exhibited protective effects against H2O2-induced apoptosis, as demonstrated by decreased apoptotic bodies, sub-G1 hypodiploid cells and DNA fragmentation. Taken together, the protective effects of butin against H2O2-induced apoptosis were exerted via blockade of membrane potential depolarization, inhibition of the JNK pathway and mitochondria-involved caspase-dependent apoptotic pathway

The objective of this study was to elucidate the cytotoxic mechanism of Compound K, with respect to the involvement of reactive oxygen species (ROS) and the mitochondrial involved apoptosis, in HT-29 human colon cancer cells. Compound K exhibited a concentration of 50% growth inhibition (IC50) at 20 μg/mL and cytotoxicity in a time dependent manner. Compound K produced intracellular ROS in a time dependent fashion; however, N-acetylcysteine (NAC) pretreatment resulted in the inhibition of this effect and the recovery of cell viability. Compound K induced a mitochondria-dependent apoptotic pathway via the modulation of Bax and Bcl-2 expressions, resulting in the disruption of the mitochondrial membrane potential (Δψm). Loss of the Δψm was followed by cytochrome c release from the mitochondria, resulting in the activation of caspase-9, -3, and concomitant poly ADP-ribosyl polymerase (PARP) cleavage, which are the indicators of caspase-dependent apoptosis. The apoptotic effect of Compound K, exerted via the activation of c-Jun NH2-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), was abrogated by specific MAPK inhibitors. This study demonstrated that Compound K-mediated generation of ROS led to apoptosis through the modulation of a mitochondria-dependent apoptotic pathway and MAPK pathway.

Ionizing radiation has different biological effects according to dose and dose rate. In particular, the biological effect of low-dose radiation is unclear. Low-dose whole-body gamma irradiation activates immune responses in several ways. However, the effects and mechanism of low-dose radiation on allergic responses remain poorly understood. Previously, we reported that low-dose ionizing radiation inhibits mediator release in IgE-mediated RBL-2H3 mast cell activation. In this study, to have any physiological relevance, we investigated whether low-dose radiation inhibits allergic responses in activated human mast cells (HMC-1(5C6) and LAD2 cells), mouse models of passive cutaneous anaphylaxis and the late-phase cutaneous response. High-dose radiation induced cell death, but low-dose ionizing radiation of