Toxoplasma gondii Inhibits Apoptosis in Infected Cells by Caspase Inactivation and NF-κB Activation

Our experiments aimed to clarify the mechanism by which host cell apoptosis is inhibited by infection with the intracellular protozoan parasite, Toxoplasma gondii (T. gondii). Mouse spleen cells were cultured in 6-well plates with RPMI 1640/10% FBS at 37℃, in a 5% CO2 atmosphere. Apoptosis of spleen cells was induced by actinomycin-D (AD) treatment for 1 h prior to infection with T. gondii. A variety of assays were used to assess the progression of apoptosis: DNA size analysis on agarose gel electrophoresis, flow cytometry with annexin V/PI staining, and analysis of expression levels of Bcl-2 family and NF-κB mRNA and proteins by RT-PCR, Western blotting, and EMSA. Additionally, transmission electron microscopy (TEM) was performed to observe changes in cell morphology. Fragmentation of DNA was inhibited in spleen cells treated with AD and T. gondii 5 h and 18 h post infection, respectively, and flow cytometry studies showed a decreased apoptotic rates in AD and T. gondii treated spleen cells. We observed decreased expression of Bax mRNA and protein, while levels of Bcl-2 mRNA remained constant in spleen cells treated with AD and T. gondii. Caspase 3 and PARP were inactivated in cells treated with AD and T. gondii, and increased levels of cleaved caspase 8 were also observed. Analysis of EMSA and Western blot data suggests that activation of transcription factor NF-κB may be involved in the blockade of apoptosis by T. gondii. TEM analysis showed nuclear fragmentation and chromatin condensation occurring in spleen cells treated with AD; however, such apoptosis-associated morphological changes were not observed in cells treated with both AD and T. gondii tachyzoites. Together, these data show that T. gondii infection inhibits AD induced apoptosis via caspase inactivation and NF-κB activation in mouse spleen cells

Primary Culture of Central Neurocytoma: A Case Report

A seventeen-year-old female patient was admitted with sudden-onset of headache and vomiting. Brain magnetic resonance imaging demonstrated a heterogeneously enhancing tumour in the left lateral ventricle. The tumour was removed and confirmed as a central neurocytoma (CN). For the residual tumour in the left lateral ventricle, gamma knife stereotactic radiosurgery was done at fifteen months after the initial surgery. Tumour recurred in the 4th ventricle at 5 yr after initial surgery. The tumour was removed and proved as a CN. In vitro primary culture was done with both tumours obtained from the left lateral ventricle and the 4th ventricle, respectively. Nestin, a neuronal stem cell marker was expressed in reverse Transcriptase-Polymerase Chain Reaction of both tumors. Both tumours showed different morphology and phenotypes of neuron and glia depending on the culture condition. When cultured in insulin, transferrin selenium and fibronectin media with basic fibroblast growth factors, tumour cells showed neuronal morphology and phenotypes. When cultured in the Dulbeco's Modified Essential Media with 20% fetal bovine serum, tumors cells showed glial morphology and phenotypes. It is suggested that CN has the characteristics of neuronal stem cells and potential to differentiate into mature neuron and glial cells depending on the environmental cue

Elevated RalA activity in the hippocampus of PI3K gamma knock-out mice lacking NMDAR-dependent long-term depression

Phosphoinositide 3-kinases (PI3Ks) play key roles in synaptic plasticity and cognitive functions in the brain. We recently found that genetic deletion of PI3K gamma, the only known member of class IB PI3Ks, results in impaired N-methyl-D-aspartate receptor-dependent long-term depression (NMDAR-LTD) in the hippocampus. The activity of RalA, a small GTP-binding protein, increases following NMDAR-LTD inducing stimuli, and this increase in RalA activity is essential for inducing NMDAR-LTD. We found that RalA activity increased significantly in PI3K gamma knockout mice. Furthermore, NMDAR-LTD-inducing stimuli did not increase RalA activity in PI3K gamma knockout mice. These results suggest that constitutively increased RalA activity occludes further increases in RalA activity during induction of LTD, causing impaired NMDAR-LTD. We propose that PI3K gamma regulates the activity of RalA, which is one of the molecular mechanisms inducing NMDAR-dependent LTD.open1

Prediction of strawberry fruit yield based on cultivar-specific growth models in the tunnel-type greenhouse

The strawberry growth and fruit yield of five Korean cultivars in the tunnel-type greenhouse predicted using their growth. The number of leaves, petiole length, leaf length and width, crown diameter, and the ratio of red and far-red (RFR) of the five Korean cultivars were measured during the cultivation period. The number of leaves of all cultivars exhibited a similar trend during this period; the plant and petiole length of ‘Maehyang’ were the longest, leaf length exhibited similar trends in all five cultivars except for ‘Jukhyang’, the leaf width of ‘Arihyang’, was the longest, and crown diameter of ‘Keumsil’ was the thickest. The leaf length, crown diameter, and RFR were associated with the fruit yield in the multiple linear regression. When a single model was used to predict the yield of all five cultivars, the correlation between expected yield and actual yield was r = 0.53. When cultivar-specific models were built for the prediction, the correlation increased to r = 0.77. The results indicated that the fruit yield of strawberry cultivars could be better predicted by considering cultivar-specific information, so it may be necessary to consider individual cultivars specifically rather than all cultivars simultaneously

Mortality Trends in Chest-Abdominal Trauma Patients Before and After the Establishment of Trauma Centers in South Korea

Purpose We sought to assess mortality trends in chest-abdominal trauma patients, before and after the implementation of the Project Supporting Establishment of Trauma Centers (PSETC) in the Republic of Korea. Methods Data from the National Health Insurance Service claims database between 2009 to 2017 were analyzed. Patients with chest-abdominal trauma were defined as those with relevant main diagnosis codes and claims for emergency medical management fees. Mortality and cumulative data were analyzed for each year to compare mortality before and after the establishment of regional trauma centers across Korea (2014). Results In total, 29,127 patients were included in the analysis. While the annual incidence of trauma-related chest-abdominal injuries increased, mortalities decreased. In particular, the trauma incidence rate among patients over 50 years increased during the study period. Mortalities at trauma centers did not change year by year after the PSETC. Before and after 2014, when trauma centers operated under the PSETC, mortalities decreased [trauma cases before the PSETC; n = 14,321 (mortality 5.61), after the PSETC; n = 14,806 (mortality 4.96)]. Conclusion The number of patients treated for chest-abdominal injuries increased from 2009 to 2017 in Korea, whereas mortalities decreased over the same period

Does Changing Inhaler Device Impact Real-Life Asthma Outcomes? : Clinical and Economic Evaluation

This study was funded by Mundipharma Korea Limited (Seoul, Korea).Peer reviewedPostprin

Blockade of cannabinoid 1 receptor improves glucose responsiveness in pancreatic beta cells

Cannabinoid 1 receptors (CB1Rs) are expressed in peripheral tissues, including islets of Langerhans, where their function(s) is under scrutiny. Using mouse beta-cell lines, human islets and CB1R-null (CB1R(-/-)) mice, we have now investigated the role of CB1Rs in modulating beta-cell function and glucose responsiveness. Synthetic CB1R agonists diminished GLP-1-mediated cAMP accumulation and insulin secretion as well as glucose-stimulated insulin secretion in mouse beta-cell lines and human islets. In addition, silencing CB1R in mouse cells resulted in an increased expression of pro-insulin, glucokinase (GCK) and glucose transporter 2 (GLUT2), but this increase was lost in cells lacking insulin receptor. Furthermore, CB1R(-/-) mice had increased pro-insulin, GCK and GLUT2 expression in cells. Our results suggest that CB1R signalling in pancreatic islets may be harnessed to improve beta-cell glucose responsiveness and preserve their function. Thus, our findings further support that blocking peripheral CB1Rs would be beneficial to beta-cell function in type 2 diabetes