Anti-Allergic Activity of a Platycodon Root Ethanol Extract

Platycodon grandiflorum (Campanulaceae) is used as traditional medicine in Asian countries. In Korean traditional medicine, Platycodon root has been widely used since ancient times as a traditional drug to treat cold, cough and asthma. However, its effects on bone marrow-derived mast cell (BMMC)-mediated allergy and inflammation mechanisms remain unknown. In this study, the biological effect of Platycodon root ethanol extract (PE) was evaluated in BMMC after induction of allergic mediators by phorbol 12-myristate 13-acetate (PMA) plus calcium ionophore A23187 (A23187) stimulation. The effect of PE on the production of several allergic mediators, such as interleukin-6 (IL-6), prostaglandin D2 (PGD2), leukotriene C4 (LTC4), β-Hexosaminidase (β-Hex) and cyclooxygenase-2 (COX-2) protein, was investigated. The results demonstrate that PE inhibits PMA + A23187 induced production of IL-6, PGD2, LTC4, β-Hexosaminidase and COX-2 protein. Taken together, these results indicate that PE has the potential for use in the treatment of allergy

Impact of Lower Urinary Tract Symptoms and Depression on Health-Related Quality of Life in Older Adults

Purpose We aimed primarily to investigate the level of health-related quality of life (HRQoL), lower urinary tract symptoms (LUTS), and depression in older adults and secondly to identify the impact of LUTS and depression on HRQoL. Methods A community-based cross-sectional study was conducted from April to November 2010. Participants were recruited from five community senior centers serving community dwelling older adults in Jeju city. Data analysis was based on 171 respondents. A structured questionnaire was used to guide interviews; the data were collected including demographic characteristics, body mass index, adherence to regular exercise, comorbidities (hypertension, diabetes mellitus, and osteoarthritis), depression, urinary incontinence, LUTS (measured via the International Prostate Symptom Score [IPSS]), and HRQoL as assessed by use of the EQ-5D Index. Stepwise multiple regression analysis was used to test predictors of HRQoL. Results Eighteen percent (18.6%) of the respondents reported depressive symptoms. The mean LUTS score was 8.9 (IPSS range, 0 to 35). The severity of LUTS, was reported to be mild (score, 0 to 7) by 53% of the respondents, moderate (score, 8 to 19) by 34.5%, and severe (score, 20 to 35) by 12.5%. HRQoL was significantly predicted by depression (Partial R2=0.193, P<0.01) and LUTS (Partial R2=0.048, P=0.0047), and 24% of the variance in HRQoL was explained. Conclusions LUTS and depression were the principal predictors of HRQoL in older adults

Optimization of extraction-free protocols for SARS-CoV-2 detection using a commercial rRT-PCR assay

Abstract In the ongoing global fight against coronavirus disease 2019 (COVID-19), the sample preparation process for real-time reverse transcription polymerase chain reaction (rRT-PCR) faces challenges due to time-consuming steps, labor-intensive procedures, contamination risks, resource demands, and environmental implications. However, optimized strategies for sample preparation have been poorly investigated, and the combination of RNase inhibitors and Proteinase K has been rarely considered. Hence, we investigated combinations of several extraction-free protocols incorporating heat treatment, sample dilution, and Proteinase K and RNase inhibitors, and validated the effectiveness using 120 SARS-CoV-2 positive and 62 negative clinical samples. Combining sample dilution and heat treatment with Proteinase K and RNase inhibitors addition exhibited the highest sensitivity (84.26%) with a mean increase in cycle threshold (Ct) value of + 3.8. Meanwhile, combined sample dilution and heat treatment exhibited a sensitivity of 79.63%, accounting for a 38% increase compared to heat treatment alone. Our findings highlight that the incorporation of Proteinase K and RNase inhibitors with sample dilution and heat treatment contributed only marginally to the improvement without yielding statistically significant differences. Sample dilution significantly impacts SARS-CoV-2 detection, and sample conditions play a crucial role in the efficiency of extraction-free methods. Our findings may provide insights for streamlining diagnostic testing, enhancing its accessibility, cost-effectiveness, and sustainability

Oncogenic Ras-mediated downregulation of Clast1/LR8 is involved in Ras-mediated neoplastic transformation and tumorigenesis in NIH3T3 cells

Oncogenic Ras proteins transform cells by way of multiple downstream signaling pathways that promote the genesis of human cancers. However, the exact cellular mechanisms by which downstream targets are regulated are not fully understood. Here, we show that oncogenic Ras reduced Clast1/LR8 transcript levels in mouse NIH3T3 fibroblasts and human WI38 fibroblasts. Clast1/LR8 transcript was undetectable in H460, A549, and H1299 cells showing high Ras activity, but was relatively abundant in DMS53 cells displaying low Ras activity. We also showed that K-Ras siRNA restored Clast1/LR8 expression in H460 and A549 cells, and that inhibitors of DNA methylation and histone deacetylation reversed oncogenic H-Ras-mediated suppression of Clast1/LR8 transcription. Additionally, ectopic expression of Clast1/LR8 inhibited serum-stimulated phosphorylation of ERK1/2 and Akt in H-RasV12-transformed NIH3T3 cells. We further showed that the expression of Clast1/LR8 interfered with oncogenic Ras-induced NIH3T3 cell transformation and invasion. Finally, our results showed that Clast1/LR8 inhibited Ras-induced proliferation of, and tumor formation by, oncogenic H-RasV12-transformed NIH3T3 cells in vivo. This study identifies the downregulation of Clast1/LR8 as a potentially important mechanism by which oncogenic Ras-mediated neoplastic transformation occurs. (Cancer Sci 2010).This research was supported by Chosun University, 2003.Schubbert S, 2007, NAT REV CANCER, V7, P295, DOI 10.1038/nrc2109Chang HC, 2006, CANCER RES, V66, P8413, DOI 10.1158/0008-5472.CAN-06-0685Maeda Y, 2006, BRAIN RES, V1104, P18, DOI 10.1016/j.brainres.2006.05.068Bild AH, 2006, NATURE, V439, P353, DOI 10.1038/nature04296Chang IY, 2005, CANCER RES, V65, P6811Rong R, 2005, ONCOGENE, V24, P4867, DOI 10.1038/sj.onc.1208660Akino K, 2005, GASTROENTEROLOGY, V129, P156, DOI 10.1053/j.gastro.2005.03.051Pruitt K, 2005, J BIOL CHEM, V280, P23363, DOI 10.1074/jbc.M503083200Jiang K, 2004, MOL CELL BIOL, V24, P5565, DOI 10.1128/MCB.24.12.5565-5576.2004Chang HC, 2004, CELL SIGNAL, V16, P675, DOI 10.1016/j.cellsig.2003.11.001Ordway JM, 2004, ONCOGENE, V23, P3737, DOI 10.1038/sj.onc.1207483Soejima K, 2003, ONCOGENE, V22, P4723, DOI 10.1038/sj.onc.1206510Malumbres M, 2003, NAT REV CANCER, V3, P459, DOI 10.1038/nrc1097Huang E, 2003, NAT GENET, V34, P226Downward J, 2003, NAT REV CANCER, V3, P11, DOI 10.1038/nrc969ULKU AS, 2003, CANC TREAT RES, V115, P189Bardeesy N, 2002, NAT REV CANCER, V2, P897, DOI 10.1038/nrc949Dammann R, 2000, NAT GENET, V25, P315ZUBER J, 2000, NAT GENET, V24, P1441Barradas M, 1999, EMBO J, V18, P6362Contente S, 1999, MOL CELL BIOCHEM, V194, P79Lurton J, 1999, AM J RESP CELL MOL, V20, P327Lorentz O, 1999, ONCOGENE, V18, P87Rosen K, 1998, CURR BIOL, V8, P1331Campbell SL, 1998, ONCOGENE, V17, P1395RodriguezViciana P, 1997, CELL, V89, P457WHITE MA, 1995, CELL, V80, P533COWLEY S, 1994, CELL, V77, P841LOWY DR, 1993, ANNU REV BIOCHEM, V62, P851BOS JL, 1989, CANCER RES, V49, P4682YOU M, 1989, P NATL ACAD SCI USA, V86, P3070RODENHUIS S, 1988, CANCER RES, V48, P5738BRADLEY MO, 1986, P NATL ACAD SCI USA, V83, P5277